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Valerie I. Leek - Patho Phlash! Pathophysiology Flash Cards-F.A. Davis Company (2011)

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Patho Phlash!
Pathophysiology Flash Cards
Valerie I. Leek, MSN, RN, CMSRN
F. A. DAVIS COMPANY
• Philadelphia
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F. A. Davis Company
1915 Arch Street
Philadelphia, PA 19103
www.fadavis.com
Copyright © 2012 by F. A. Davis Company
Copyright © 2012 by F. A. Davis Company. All rights reserved.
This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or
by any means, electronic, mechanical, photocopying, recording,
or otherwise, without written permission from the publisher.
Printed in China
Last digit indicates print number: 10 9 8 7 6 5 4 3 2 1
Senior Acquisitions Editor: Thomas A. Ciavarella
Director of Content Development: Darlene D. Pedersen
Senior Project Editor: Meghan Ziegler
Design and Illustration Manager: Carolyn O’Brien
As new scientific information becomes available through basic and clinical
research, recommended treatments and drug therapies undergo changes.
The author(s) and publisher have done everything possible to make this
book accurate, up to date, and in accord with accepted standards at the
time of publication. The author(s), editors, and publisher are not responsible for errors or omissions or for consequences from application of the
book, and make no warranty, expressed or implied, in regard to the contents of the book. Any practice described in this book should be applied by
the reader in accordance with professional standards of care used in regard
to the unique circumstances that may apply in each situation. The reader is
advised always to check product information (package inserts) for changes
and new information regarding dose and contraindications before administering any drug. Caution is especially urged when using new or infrequently
ordered drugs.
Authorization to photocopy items for internal or personal use, or the internal or personal use of specific clients, is granted by F. A. Davis Company
for users registered with the Copyright Clearance Center (CCC)
Transactional Reporting Service, provided that the fee of $.25 per copy is
paid directly to CCC, 222 Rosewood Drive, Danvers, MA 01923. For those
organizations that have been granted a photocopy license by CCC, a separate system of payment has been arranged. The fee code for users of the
Transactional Reporting Service is: 8036-2493-X/12 0 + $.25.
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Dedication
To my husband, David, and my sons, Jeffrey and Zachary, thank you for your love and
support.
To my family and friends, thank you for giving me latitude when I seemed glued to my computer
screen.
To my granddaughter, Cadence, just keep growing healthy and strong. Nona loves you.
In remembrance of my Uncle Tommy and my friends Reuel and Sharon.
Acknowledgments
Thank you to all my past and present students. It is such a privilege to teach. I learn
something new every day by the interesting inquiries from all of you that stimulate my
thinking!
Thank you to all the wonderful people at F. A. Davis Company, including Tom, Meghan,
and Julie. You have the gift of making hard work seem pleasant!
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Reviewers
Joyce B. Ceresini, ADN, BSN
Anatomy/Med-Surg Instructor
Lebanon County Career & Technical School
Lebanon, Pennsylvania
Gary Gudlin RN, MSN, Ed. M
Senior Program Manager PSU Outreach
Pennsylvania State University
Bethlehem, Pennsylvania
JoEllen Kubik, RN, MA, LMSW
Assistant Professor
Allen College
Waterloo, Iowa
Andrea R. Mann, MSN, RN
Instructor, Third Level Chair
Frankford Hospital School of Nursing
Philadelphia, Pennsylvania
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Debra Morrison, RN, BScn, MN (c)
Academic Coordinator: Practical Nursing Program
Faculty: Practical Nursing, Critical Care E-learning, online Patho.Anatomy and Physiology
Durham College
Oshawa, Ontario
Mary J. Sletten, DM(c)m MSN, RN
Associate Professor
Dona Ana Community College
Las Cruces, New Mexico
Janet C. Stradtman, MSN, RN, CCRN, CNE, CNS
Assistant Director
Firelands Regional Medical Center School of Nursing
Sandusky, Ohio
Debbie Tavernier MSN, RN, BSN, School Nurse Credential
Associate Professor of Nursing
California State University Stanislaus
Turlock, California
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Icons
Gastrointestinal System Disorders
Cardiovascular System Disorders
Endocrine System Disorders
Respiratory System Disorders
Urologic System Disorders
Sensory System Disorders
Immune System Disorders
Dermatologic System Disorders
Musculoskeletal System Disorders
Mental Health Disorders
Nervous System Disorders
Women’s Health and Perinatal
Disorders
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Abbreviations
AAA
ABG
ABI
ac
ACE
AChE
AChR
ACLS
ACTH
ADH
ADHD
ADLs
AED
AF
AFB
AGC
AIDS
ALL
ALP
ALS
ALT
AMI
abdominal aortic aneurysm
arterial blood gases
ankle-brachial index
before meals
angiotensin-converting enzyme
acetylcholinesterase
acetylcholine receptor
advanced cardiac life support
adrenocorticotropic hormone
antidiuretic hormone
attention-deficit/hyperactivity
disorder
activities of daily living
antiepileptic drug
atrial fibrillation
acid-fast bacillus
atypical glandular cells
acquired immunodeficiency
syndrome
acute lymphocytic leukemia
alkaline phosphatase
amyotrophic lateral sclerosis
alanine aminotransferase
acute myocardial infarction
AML
ANA
ANP
anti-CCP
APAP
aPTT
ARDS
AS
ASA
ASC
ASCA
ASC-US
AST
AV
AVM
AVP
BBB
BCG
acute myelogenous
(myeloblastic) leukemia
antinuclear antibody
atrial natriuretic peptide
anticyclic citrullinated
peptide
acetaminophen
activated partial
thromboplastin
acute respiratory distress
syndrome
aortic stenosis
acetylsalicylic acid
atypical squamous cells
anti–Saccharomyces cerevisiae
antibody
ASC of undetermined
significance
aspartate aminotransferase
atrioventricular
arteriovenous malformation
arginine vasopressin
bundle branch block
bacille Calmette-Guérin
BCP
BD
BHS
bid
BMI
BMS
BMT
BNP
BP
BPH
bpm
BRM
BROW
BSA
BSE
BUN
BUN
BX
C&S
CA
Ca+
Ca++
CABG
CAD
birth control pills
Buerger’s disease
beta-hemolytic streptococci
two times a day
body mass index
bone marrow suppression
bone marrow transplant
brain natriuretic peptide
blood pressure
benign prostatic hyperplasia
beats per minute
biologic response modifier
barley, rye, oats, and wheat
body surface area
breast self-examination
blood urea nitrogen
blood urea nitrogen
biopsy
culture and sensitivity
coronary artery
serum calcium
calcium
cardiac artery bypass graft
coronary artery disease
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cap
CBC
CBI
CBT
CD4
CD8
CEA
CFTR
CHF
CIN
CK
CK-MB
CLL
CML
CNS
CO
COMT
COPD
COX-2
CPHSS
capsule
complete blood count
continuous bladder irrigation
cognitive behavioral therapy
T-helper cells
cytotoxic cells
carcinoembryonic antigen
cystic fibrosis transmembrane
regulator
congestive heart failure
cervical intraepithelial
neoplasia
creatine kinase
serum creatine kinase,
myocardial bound
chronic lymphocytic
leukemia
chronic myelogenous
leukemia
central nervous system
cardiac output
catechol-O-methyltransferase
chronic obstructive pulmonary
disease
cyclooxygenase 2 inhibitors
Cincinnati Prehospital
Stroke Scale
creatine phosphokinase
continuous passive motion
cardiopulmonary
resuscitation
CR
controlled release
CREST
calcinosis, Raynaud’s
phenomenon, esophageal
dysfunction, sclerodactyly,
telangiectasia (cluster of
features of systemic sclerosis
scleroderma)
CRP
c. reactive protein
CRS-R
Conners Rating Scales–Revised
CS
cardiogenic shock
CS
cesaerean section
CSF
cerebrospinal fluid
CSF
colony-stimulating factor
CT
computerized tomography
CV
cardiovascular
CVA
cardiovascular accident
CVC
central venous catheter
CVP
central venous pressure
CXR
chest x-ray
D5/0.9
5% dextrose and normal
NaCl
saline solution (0.9% NaCl)
D5/1/2/NS 5% dextrose and half normal
saline solution (0.45% NaCl)
CPK
CPM
CPR
5% dextrose in water
diastolic blood pressure
dermatology
dual-energy x-ray
absorptiometry
DFV
Doppler flow velocimetry
DHT
dihydrotestosterone
DI
diabetes insipidus
DIC
disseminated intravascular
coagulation
DISIDA
diisopropyl iminodiacetic
(scan)
acid (cholescintigraphy)
DJD
degenerative joint disease
DKA
diabetic ketoacidosis
dL
deciliter
DMARD disease-modulating
antirheumatic drug
DNA
deoxyribonucleic acid
DRE
digital rectal examination
DSM-IV-TR Diagnostic and Statistical
Manual of Mental Disorders,
4th Edition, Text Revision
DTR
deep tendon reflexes
DTs
delirium tremens
DVT
deep vein thrombosis
ECG
electrocardiogram
ECHO
echocardiography
D5W
DBP
Derm
DEXA
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ECMO
ECT
EEG
EENT
EF
EGD
ELISA
EMA-IgA
EMG
EMS
Endo
EP
EPS
ER
ERCP
ESR
ESRD
ESWL
ET-1
ETOH
extracorporeal membrane
oxygenation
electroconvulsive therapy
electroencephalogram
eye, ear, nose, and throat
ejection fraction
esophagogastroduodenoscopy
enzyme-linked immunosorbent assay
immunoglobulin A
antiendomysial
electromyography
emergency medical services
endocrine
extrapyramidal
extrapyramidal symptoms
extended-release
endoscopic retrograde
cholangiopancreatography
erythrocyte sedimentation
rate
end-stage renal disease
extracorporeal shock wave
lithotripsy
endothelin-1
ethal alcohol
F and E
FAP
FBS
FDA
FFP
FHT
FISH
G, g, gm
GABA
GABAB
GABRB3
GB
GERD
GFR
GGT
GH
GI
GnRH
GTT
GU
fluid and electrolyte
familial adenomatous
polyposis
fasting blood sugar
U.S. Food and Drug
Administration
fresh frozen plasma
fetal heart tone
fluorescence in situ
hybridization
gram
gamma-aminobutyric acid
gamma-aminobutyric acid
type B
GABAA receptor gene
Guillain-Barré
gastroesophageal reflux
disease
glomerular filtration rate
gamma-glutamyl transferase
growth hormone
gastrointestinal
gonadotropin-releasing
hormone
glucose tolerance test
genitourinary
GVHD
H&H
H1N1
H2
H5N1
HAART
HAV
HBV
HCP
Hct
HCV
HDL
HDV
HELLP
HEPA
HER2
HEV
Hgb
HGSIL
graft-versus-host disease
hematocrit and hemoglobin
hemagglutinin type 1 and
neuraminidase type 1
histamine 2
hemagglutinin type 5 and
neuraminidase type 1
highly active antiretroviral
therapy
hepatitis A
hepatitis B
health-care professional
hematocrit
hepatitis C
high-density lipoproteins
hepatitis D
hemolysis, elevated liver
enzymes, low platelets
high-efficiency particulate
air
human EGF (epidermal
growth factor) receptor 2
hepatitis E
hemoglobin
high-grade squamous
intraepithelial lesion
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HIDA
(scan)
HIV
HLA
HOB
HPV
HR
HRT
HTN
HSIL
HSV
I&O
ICD
ICP
ICS
IDM
IgE
IgG
IL-1
IL-8
INR
IOL
IOP
hepatobiliary iminodiacetic
acid (cholescintigraphy)
human immunodeficiency
virus
human leukocyte antigen
head of bed
human papillomavirus
heart rate
hormone replacement therapy
hypertension
high-grade squamous
intraepithelial lesion
herpes simplex virus
intake and output
implantable cardioverter
defibrillator
intracranial pressure
intercostal space
infants of diabetic mothers
immunoglobulin E
immunoglobulin G
interleukin 1
interleukin 8
international normalized
ratio
intraocular lens
intraocular pressure
IVP
JNC 7
K+
KOH
KS
KUB
LDH
LDL
LEEP
LFT
LLQ
LOC
LP
LR
LSIL
LVAD
MAO-B
MELD
MG
Mg+
MgSO4
intravenous pyelogram
The Seventh Report of the Joint
National Committee on Prevention,
Detection, Evaluation, and
Treatment of High Blood Pressure
potassium
potassium hydroxide
Karposi’s sarcoma
kidney-ureter-bladder
lactate dehydrogenase
low-density lipoprotein
loop electrosurgical excision
procedure
liver function tests
left lower quadrant
level of consciousness
lumbar puncture
lactated Ringer’s (solution)
low-grade squamous
intraepithelial lesion
left ventricular assist device
monoamine oxidase-B
Model for End-Stage Liver
Disease
myasthenia gravis
magnesium
magnesium sulfate
MI
MM
MRgFUS
MRI
NAA
NG
NGT
NK
NMDA
NMJ
NMS
NPO
NSAIDs
O2
OCD
OmpC
ORIF
OSHA
OTC
PA
PABA
myocardial infarction
multiple myeloma
MR-guided focused ultrasound surgery
magnetic resonance imaging
nucleic acid amplification
nasogastric
nasogastric tube
natural killer
N-methyl D-aspartate
neuromuscular junction
neuroleptic malignant
syndrome
nil per os (nothing by mouth)
nonsteroidal antiinflammatory drugs
oxygen
obsessive-compulsive
disorder
outer membrane porin C
open reduction with internal
fixation
Occupational Safety and
Health Administration
over-the-counter
placenta abruption
para-aminobenzoic acid
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PaCO2
PAD
P-ANCA
PAO2
Pap
PCOS
PCR
PD
PD
PDA
PE
PEEP
PET
PFT
pH
PIH
PIPIDA
(scan)
PND
PP
partial pressure of carbon
dioxide in alveolar gas
peripheral arterial disease
perinuclear antineutrophil
cytoplasmic antibody
alveolar oxygen partial
pressure
Papanicolaou
polycystic ovarian syndrome
polymerase chain reaction
Parkinson’s disease
peritoneal dialysis
patent ductus arteriosus
pulmonary embolism
positive end-expiratory
pressure
positron emission tomography
pulmonary function test
potential of hydrogen
pregnancy-induced
hypertension
99mTc-para-isopropylacetanilido-iminodiacetic acid
(cholescintigraphy)
paroxysmal nocturnal
dyspnea
placenta previa
PRBCs
PSA
PSV
PT
PUBS
PUVA
PVC
PVR
QFT-G
R/O
RA
RAIU
RBC
RD
RF
RFT
RLQ
ROM
RSV
RUQ
SA
SAD
SARS
SBP
packed red blood cells
prostate-specific antigen
peak systolic velocity
prothrombin time
percutaneous umbilical
blood sampling
psoralen ultraviolet A
premature ventricular
contraction
peripheral vascular resistance
QuantiFERON-TB Gold
rule out
rheumatoid arthritis
radioactive iodine uptake
red blood cell
Raynaud’s disease
rheumatoid factor
renal function tests
right lower quadrant
range of motion
respiratory syncytial virus
right upper quadrant
sinoatrial
seasonal affective disorder
severe acute respiratory
syndrome
systolic blood pressure
SCI
SDAT
SERM
SGA
SIADH
SJS
SLE
SNS
SOB
SPECT
SPF
SSRI
STD
T3
T4
T6
TB
TEE
TEN
TENS
spinal cord injury
senile dementia of the
Alzheimer type
selective estrogen receptor
modulator
small-for-gestational-age
syndrome of inappropriate
diuretic hormone
Stevens-Johnson syndrome
systemic lupus erythematosus
sympathetic nervous system
shortness of breath
single-photon emission
computed tomography
skin protection factor
selective serotonin reuptake
inhibitor
sexually transmitted disease
triiodothyronine
tetraiodothyronine
thoracic nerve pair 6
tuberculosis
transesophageal
echocardiogram
toxic epidermal necrolysis
transcutaneous electrical
nerve stimulation
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TG
THR
TKR
TN
TNF
TNF-I
TNF-α
TNM
TPN
thyroglobulin
total hip replacement
total knee replacement
trigeminal nerve
tumor necrosis factor
tumor necrosis factor
inhibitors
tumor necrosis factor alpha
tumor-node-metastasis
total parenteral nutrition
TPO
TRAP
criteria
TSH
tTG
TUMA
thyroid peroxidase
tremor, rigidity, akinesia
or postural instability
bradykinesia, and
postural instability
thyroid-stimulating
hormone
antitransglutaminase
transurethral microwave
antenna
TURP
UC
US
UTI
UV
V/Q
VF
VT
WBC
transurethral resection of
the prostate
ulcerative colitis
ultrasound
urinary tract infection
ultraviolet
ventilation/perfusion
ventricular fibrillation
ventricular tachycardia
white blood cell
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Introduction
Students who study alterations in health states
must learn to link assessment data, laboratory
and diagnostic studies, medical and surgical
treatment, possible complications, client
teaching, and important findings in order to
develop a comprehensive understanding of
specific disease management. After many years
of health instruction, watching learners
attempt to synthesize and integrate client information, I noticed that the novice learner in
health care had difficulty connecting all the
pieces of the puzzle. It is for this reason that I
developed Patho Phlash. These cards make the
connection between all the aspects of disease
management.
Each card is a brief but comprehensive snapshot of an alteration in health. Pharmacological
interventions are listed in drug classes, ideally
used with Pharm Phlash Pharmacology Flash
Cards. Using these cards gives the learner all
of the important information necessary to adequately prepare for care of any client.
Key memory aids are “Clue” boxes for selfassessment of knowledge and “Remember” or
mnemonics to help identify important assessment or care information. Fifty NCLEX style
questions formatted self-tests on the DavisPlus
Web site are available for knowledge application
by students and assignments by faculty.
The cards include body system icons to
remind the learner which system is affected, and
a list of common abbreviations for easy reference. The front of each card has the name of
the disorder with its phonetic spelling along
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with a Clue box. On the back of each card you
will find
1. Pathophysiology
2. Assessment and Diagnostic Findings
3. Complications
4. Medical and Surgical Treatment
5. Keep in Mind (includes information to be
taught to the client)
6. Make the Connection, which is crucial
information to remember about assessment and treatment for that disorder
This learning system does not replace a comprehensive medical-surgical book or pharmacology text. It is a tool that integrates all aspects of
medical and nursing inquiry and treatment of
disease states. Students who utilize these cards
with Pharm Phlash will have at their fingertips
completely integrated information to deal with
diseases. Best of all, the cards can be easily
carried in their pocket! Best of luck to all!
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Page 1
GASTROINTESTINAL
Celiac Disease, 1
Gastritis, 2
Gastroesophageal Reflux Disease, 3
Histal Hernia, 4
Peptic Ulcer Disease, 5
Gastric Cancer, 6
Obesity, 7
Hepatitis, 8
Abdominal Hernias, 9
Laënnec’s Cirrhosis, 10
Liver Cancer, 11
Esophageal Varices, 12
Pancreatitis, 13
Cholecystitis, 14
Pancreatic Cancer, 15
Bowel Obstruction, 16
Ulcerative Colitis, 17
Colon Cancer, 18
Diverticulosis, 19
Appendicitis, 20
Crohn’s Disease, 21
Peritonitis, 22
Hemorrhoids, 23
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Gastrointestinal Disorders
1
Celiac Disease
(se-le-ak di-zez)
Clue: Diagnostic or Clinical Findings
Bloating, diarrhea, rashes, anemia,
malnutrition, and failure to thrive.
+ Hydrogen breath test.
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Gastrointestinal Disorders
Pathophysiology
• Malabsorption disorder caused by antibody
•
•
response to gluten or gliadin proteins in barley,
rye, oats (some), and wheat (BROW) affecting
up to 1% of U.S. population.
Damages small intestinal villi; prevents fat, iron,
calcium, and B-vitamin absorption.
Genetic link that is not well understood, but
human leukocyte antigen (HLA), of which the cell
surface receptor type protein human leukocyte
antigen (HLA-DQ) is one, is found in family
members with a high incidence of celiac disease;
pediatric and adult clients affected.
Assessment and Diagnostic Findings
• Diarrhea, steatorrhea, cramps, hyperactive bowel
sounds, dermatitis herpetiformis (rash).
• Complete blood count (CBC) with differential,
•
vitamin and iron profile, and antibody tests
(immunoglobulin A antiendomysial [EMA-IgA],
IgA/IgG, antitransglutaminase antibodies [ATA])
elevation.
Screening with endoscopic biopsy, hydrogen
breath test, and DEXA scan.
1
Complications
• Anemia due to B-vitamin and iron deficiency.
• Osteoporosis and osteopenia (calcium
malabsorption).
• Hemorrhage (vitamin-K deficiency related to
decreased B-vitamin activity in bowel).
• Neuropathies and mental status changes
(Remember: B vitamins are for Brain/Blood).
• Bowel cancers and autoimmune organ destruction.
Medical Care and Surgical Treatment
• Antirheumatics and tumor necrosis factor inhibitors.
• Monoclonal antibodies.
• Corticosteroids and other immunosuppressants.
Keep in Mind
• Awareness of BROW-containing foods, food
fillers, and pharmaceutical agents is important.
Make the Connection
• Monitor I&O, calories, and stools.
• Assess for development of vesicular rash on
knees, elbows, and buttocks.
• Monitor for SOB, pallor, poor pulse oximetry
(anemia), and bleeding tendencies (vitamin K).
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Gastrointestinal Disorders
2
Gastritis
(gas-tri-tis)
Clue: Diagnostic or Clinical Findings
Epigastric burning or discomfort
associated with tobacco use,
alcohol ingestion, stress, or
NSAID use.
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Gastrointestinal Disorders
Pathophysiology
• Gastric mucus forms a physical and chemical
•
•
barrier, protecting the epithelial cells lining the
stomach and trapping bicarbonate between the
mucus and the cells.
Hydrogen production outpaces bicarbonate production during physiologic or psychological stress.
Common gastric irritants include alcohol, stress,
tobacco, caffeine, NSAIDs, Helicobacter pylori
(H. pylori) bacteria, and shock.
Assessment and Diagnostic Findings
• Complaints of epigastric pain or burning, hyper•
•
acidity of the stomach, eructation, pressure, nausea and vomiting, or hematemesis in severe cases.
CBC with differential to screen for pernicious
anemia.
Endoscopy with direct visualization of inflammation
with biopsy urease testing, urea breath test, and
IgG antibody test for H. pylori.
Complications
• Upper gastric bleeding, peptic ulcer disease with
possible perforation and peritonitis.
• Mental status changes and pernicious anemia
are common with vitamin-B12 deficiencies
2
(Remember: B vitamins are for Brain/Blood),
especially in the elderly.
Medical Care and Surgical Treatment
• Proton pump inhibitors, Pepto-Bismol, H2 blockers, and antibiotics.
• Antacids, coating agents, prostaglandin-containing
agents may be utilized.
• PRBC cell infusion and vasopressin in cases of
hemorrhage.
• Perforation may require gastric reduction surgery.
Keep in Mind
• Avoid gastric mucosal irritants.
• Avoid and channel psychological and physiologic
stress.
Make the Connection
• Assess intake/use of gastric irritants.
• Chemotherapy and radiation treatments over the
stomach are atypical causes of severe gastritis.
• Chronic use of over-the-counter medications for
gastritis may lead to alteration in absorption
of other medications and nutrients (↑pH).
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Gastrointestinal Disorders
3
Gastroesophageal Reflux
Disease (GERD)
(gas-tro-e-sof-a-je-al re-fluks di-zez)
Clue: Diagnostic or Clinical Findings
Chest pain or severe burning
occurring within an hour of
eating. Discomfort is worse when
lying down after meals and may
occur during the night.
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Gastrointestinal Disorders
Pathophysiology
• Meals that are large, high-fat, spicy, or consumed
•
concurrently with alcohol cause relaxation of the
lower esophageal sphincter, allowing hydrochloric
acid and pepsin present in gastric contents to
reflux, or pass back, into the esophagus.
The esophagus is easily damaged by acidic gastric
contents, resulting in inflammation, edema, and
scarring over time.
Assessment and Diagnostic Findings
• Chest pain and burning within an hour of meals.
• Endoscopy with biopsy and pH measurement.
• Barium swallow.
Complications
• Scarring of the esophageal tissue that can cause
•
•
narrowing of the esophagus and noncompliance
of the lower esophageal sphincter.
Chronic irritation of the esophagus may lead to
Barrett’s esophagus (a dysplastic change of normal squamous cells to columnar epithelial cells in
areas of irritation), and esophageal CA.
Respiratory difficulties related to aspiration of
acidic gastric contents; pain with respiration.
3
Medical Care and Surgical Treatment
• Antacids, H2 blockers, proton pump inhibitors,
•
•
coating agents, prostaglandins, antiemetics that
increase emptying.
Dilation of the esophagus if narrowing occurs.
Nutritional and lifestyle changes.
Keep in Mind
• Avoid large, fatty meals; alcohol use; and tobacco
use.
• Clothing should be loose around the waist.
• Sit upright for 2 hours after eating; don’t eat
•
within 3 hours of retiring; elevate the head of the
bed (HOB) 6–8 inches using shock blocks.
Consume liquids separately from meals to avoid
stomach distention.
Make the Connection
• Assess lifestyle choices for clients with
GERD and teach accordingly.
• Rule out cardiac problems that mimic GERD.
• Monitor for signs of chemical pneumonia and
respiratory problems, especially in very young and
very old or debilitated clients.
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Gastrointestinal Disorders
4
Hiatal Hernia
(hi-a-tal her-ne-a)
Clue: Diagnostic or Clinical Findings
Burning, chest pain, heartburn,
dysphagia, GERD, a feeling of
fullness.
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Gastrointestinal Disorders
Pathophysiology
• A weakness in the hiatus of the diaphragm
•
coupled with intra-abdominal pressure forcing
protrusion of the stomach and esophagus
upward through the hiatus.
Hiatal hernias include the “sliding” type and the
“rolling” type.
Assessment and Diagnostic Findings
•
•
Discomfort increases when lying down and decreases
when standing or sitting upright after meals.
Endoscopy; barium swallow with x-ray, fluoroscopy, and swallowing studies can show the
upward displacement of the stomach.
Complications
• Scarring and narrowing of the esophagus with
noncompliance of the lower esophageal sphincter.
• Chronic irritation of the esophagus may lead to
Barrett’s esophagus and esophageal CA.
• Respiratory difficulties related to aspiration of
acidic gastric contents, pain with respiration.
Medical Care and Surgical Treatment
•
Antacids, H2 blockers, proton pump inhibitors,
coating agents, prostaglandins, antiemetics that
increase gastric motility and emptying.
4
• Dilation of the esophagus if narrowing occurs.
• Fundoplication, a surgical procedure in which the
•
fundus is wrapped around the lower esophagus,
stabilizes the upper stomach, preventing herniation.
Nutritional counseling.
Keep in Mind
• Clothing should be loose around the waist.
• Sit upright for 2 hours after eating; don’t eat
•
•
within 3 hours of retiring; elevate the head of the
bed (HOB) 6–8 inches using shock blocks.
Consume several small meals daily instead of
three large meals.
Consume liquids separately from meals to avoid
stomach distention.
Make the Connection
• Rule out cardiac problems that mimic
hiatal hernia symptoms.
• Monitor for signs of chemical pneumonia and
respiratory problems, especially in very young and
very old or debilitated clients.
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Gastrointestinal Disorders
5
Peptic Ulcer Disease
(pep-tik ul-ser di-zez)
Clue: Diagnostic or Clinical Findings
Gnawing, burning pain in either the
midepigastric area 2–4 hours after
meals or the left epigastric area
with meals.
Weight loss and presence of melena.
Low H&H.
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Gastrointestinal Disorders
Pathophysiology
• Eighty percent of all peptic ulcer disease is caused
•
•
•
by Helicobacter pylori (H. pylori) infection that causes
inflammation and erosion of the mucosal barrier
in the stomach.
Gastric mucus provides a physical and chemical
barrier, protecting the epithelial cells lining the
stomach and trapping bicarbonate between the
mucus and the cells.
Hydrogen production outpaces bicarbonate
production during physiologic or psychological
stress.
Common gastric irritants or contributors to
gastritis include alcohol, stress, tobacco, NSAIDs,
H. pylori bacteria, and shock.
Assessment and Diagnostic Findings
•
•
•
Duodenal ulcer: Midepigastric pain 2–4 hours
after meals, relieved with food intake.
Gastric ulcer: Left epigastric pain that increases
with food intake, especially 1–2 hours after
meals; hematemesis is more common than
melena.
Urea breath test, IgG antibody test for H. pylori,
H. pylori culture, barium swallow with x-ray, EGD.
5
Complications
• Bleeding, anemia, perforation with peritonitis or
•
•
pancreatitis (severe back pain) or obstruction
(pyloric scarring), upper gastrointestinal (GI) bleed.
Gastric cancer (chronic irritation and regeneration
of cells).
Dumping syndrome after subtotal gastrectomy.
Medical Care and Surgical Treatment
• Antibiotics, proton pump inhibitors, H2 blockers,
coating agents, antacids.
• Vagotomy.
• Subtotal gastrectomy.
Keep in Mind
• Avoid spicy foods, alcohol, tobacco, and caffeine;
manage stress; eat small, frequent bland meals.
Make the Connection
• Monitor CBC for anemia.
• Assess patterns of pain and weight loss.
• Assess emesis for frank bleeding or coffee-ground
appearance; test stools for melena.
• In the acute stage, the client will be NPO.
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Gastrointestinal Disorders
6
Gastric Cancer
(gas-trik kan-ser)
Clue: Diagnostic or Clinical Findings
Indigestion, anorexia, weight loss,
nausea and vomiting, anemia,
melena. Pain relieved
by antacids.
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Gastrointestinal Disorders
Pathophysiology
• Epithelial cells undergo mutation related to
•
chronic irritation or exposure to carcinogens.
Cells that are damaged must be replaced. The
chance of a mutation occurring is proportional
to the rate of new cell growth.
Implicated causes are chronic or autoimmune
gastritis; exposure to lead dust, grain dust, glycol
ethers, or leaded gasoline; or a diet high in
smoked fish or meats.
Assessment and Diagnostic Findings
• Indigestion that responds to antacids.
• Anorexia and weight loss, nausea and vomiting,
gastric distention.
• Complete blood count (CBC) reveals anemia.
Stool is positive for occult blood.
• Barium swallow with x-ray, gastric fluid analysis
for cytology, serum gastrin levels.
• Positive diagnosis is made by gastroscopy and biopsy.
Complications
• Nutritional deficit.
• Metastasis.
• Bleeding, perforation, and peritonitis.
• Death.
6
Medical Care and Surgical Treatment
• Subtotal or total gastrectomy.
• Dumping syndrome related to subtotal or total
gastrectomy.
• Chemotherapy and radiation, biological therapies.
Keep in Mind
• Manage stress.
• Pain medication should be taken before the pain
is severe.
• Teach pre- and postoperative therapies (nasogastric [NG] tube will be in place after gastrectomy).
• Teach the side effects of chemotherapy and radiation and how to mitigate them.
Make the Connection
• Monitor nutritional status with daily or
•
•
•
weekly weights and laboratory values like total
protein, CBC, and blood chemistries.
If client is on chemotherapy, monitor for
hyperuricemia.
Assess for excessive diarrhea or nausea, and cold
sweats (dumping syndrome).
Assist with psychosocial needs.
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Gastrointestinal Disorders
7
Obesity
(o-be-si-te)
Clue: Diagnostic or Clinical Findings
BMI >30 kg/m2, degenerative joint
disease, type 2 diabetes, total
cholesterol >200 mg/dL.
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Gastrointestinal Disorders
Pathophysiology
• Behavioral, genetic, medication, or hormonal
etiology.
• Imbalance between food energy consumed and
energy expended.
Assessment and Diagnostic Findings
•
•
Overweight is defined as a body mass index
(BMI) of 25 to <30 kg/m2.
Obesity is defined as a BMI of >30 kg/m2.
Complications
7
• Bariatric surgery:
• Roux-en-Y.
• Gastric banding.
Keep in Mind
• Reduction of 500 kilocalories (kcal) per day
results in weight loss of 1–2 lb/wk.
• Walking for 30–60 minutes daily is the safest
method of exercise.
• Prevention of obesity is the goal. Eat a variety of
colorful foods and exercise 35 minutes daily.
• Degenerative joint disease (DJD).
• Cardiovascular, renal, and neural damage related
•
•
•
•
•
to hypertriglyceridemia and hypercholesterolemia,
resulting in atherosclerosis.
Enlargement and infiltration of the liver with fat.
Type 2 diabetes mellitus.
Dumping syndrome related to bariatric surgery.
Intertriginous skin breakdown.
Dyspnea.
Medical Care and Surgical Treatment
• Total hip, knee, and ankle replacement.
• Angioplasty or coronary bypass surgery.
• Oral antidiabetic agents or insulin therapy.
• Dialysis.
Make the Connection
• Monitor I&O carefully following bariatric
•
•
•
surgery. Once gastric leaking is ruled out, the
client may begin taking 1–2 ounces of liquids
per meal.
Rupture of the gastric pouch after bariatric
surgery may occur with excessive food intake.
Behavioral interventions must be coupled with
surgical intervention.
Monitor cardiac and respiratory status when an
approved diet and exercise regimen is prescribed.
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Gastrointestinal Disorders
8
Hepatitis
(hep-a-ti-tis)
Clue: Diagnostic or Clinical Findings
Lethargy, malaise, headache,
anorexia, low-grade fever, right
upper quadrant pain, jaundice.
Elevated ALT and AST levels.
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Gastrointestinal Disorders
Pathophysiology
• Inflammation of the liver caused by direct cellular
•
•
•
•
injury and secondary injury by the immune
response; those with a lesser immune response
may become carriers rather than infected.
Hepatitis A (HAV): Spread by the oral-fecal route.
Hepatitis B (HBV; often coexistent with hepatitis D
[HDV]): Spread by blood and body fluids.
Hepatitis C (HCV): Spread by contact with contaminated blood, IV drug use, unprotected sex.
Hepatitis E (HEV): Spread by contaminated water.
Assessment and Diagnostic Findings
• Preicteric phase: Weeks to months depending on
•
•
type; characterized by malaise, lethargy, nausea,
vomiting.
Icteric phase: Characterized by jaundice, pale
stools, dark tea-colored urine, and rashes.
↑ ALT and AST, ↑ bilirubin, presence of virusspecific antigen, prothrombin time >11.6 seconds,
↑ ESR, ↑ serum ammonia levels, abnormal
hepatocytes revealed through liver biopsy.
Complications
• Acute or chronic liver failure and encephalopathy.
• Hemorrhage; liver cancer.
8
Medical Care and Surgical Treatment
• Avoid hepatotoxic medications like acetaminophen.
• Bedrest; avoid injections to prevent hemorrhage.
• Small, frequent meals that contain high calories,
•
high protein (titrate protein to ammonia levels),
low sodium, and moderate fluid intake.
Immunoglobulin therapy on exposure; hepatitis A
and B vaccination for prevention.
Keep in Mind
• Teach client dietary regimen, to rest, and avoid
hepatotoxic substances.
• Report confusion, asterixis, abdominal distention, or edema of legs/feet.
Make the Connection
• Monitor ALT, AST, bilirubin, stool and
urine color, mental status, and presence of
ascites.
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Gastrointestinal Disorders
9
Abdominal Hernias
(ab-dom-i-nal her-ne-a)
Clue: Diagnostic or Clinical Findings
Abdominal area that bulges out,
especially when intra-abdominal
pressure is ↑. Gentle pressure can
cause reduction or popping back
of the abdominal contents.
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Gastrointestinal Disorders
Pathophysiology
• A weakness in the abdominal wall allows the
•
•
•
•
bowel or omentum, along with peritoneal tissue,
to herniate outward. Weakened areas include the
umbilical area, along the linea alba, incisional
areas, and areas that have not completely closed
after birth (the inguinal rings).
Umbilical hernias are caused by incomplete
closure of the umbilical orifice and commonly
occur in children and obese clients.
Ventral hernias are caused by weakness in the
linea alba and are aggravated by obesity.
Inguinal hernias are caused in both males and
females by incomplete closure of the inguinal rings.
Incisional hernias occur after underlying muscle is
cut and scar tissue forms, weakening the area.
Assessment and Diagnostic Findings
• May be reducible.
• Straining causes the hernia to protrude.
• Inguinal hernias may cause a dragging feeling or
occasional discomfort.
• May be present in newborn males with hydrocele.
• Diagnosed through physical examination,
computerized tomography (CT) scan, magnetic
9
resonance imaging (MRI), or direct
endoscopy.
Complications
• Incarcerated or strangulated hernia results in
necrosis of the bowel or omentum, which is a
surgical emergency.
Medical Care and Surgical Treatment
• Stool softeners or bulk laxatives to prevent straining at stool.
• Herniorrhaphy or hernioplasty (open or closed
surgical procedure).
Keep in Mind
• Postsurgical care includes avoidance of coughing
or straining.
• Males need to use ice packs and elevate the
scrotum.
• Avoid lifting, driving, and sexual activity as
prescribed.
Make the Connection
• Assess ventral hernias for bowel sounds.
• Assess for pain that may be a sign of strangulation.
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Gastrointestinal Disorders
10
Laënnec’s Cirrhosis
(la-e-neks si-ro-sis)
Clue: Diagnostic or Clinical Findings
Chronic condition associated with
alcohol consumption. Elevated ALT
and AST, ascites, and edema
in the lower extremities.
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Gastrointestinal Disorders
Pathophysiology
• Chronic heavy consumption of alcohol causes
inflammation of the cells of the liver.
• Fatty infiltration of the liver occurs related to
•
decrease in fatty acid oxidation and increase in
gluconeogenesis. The liver enlarges first.
The stellate cells to produce fibrous connective
tissue and becomes resistant to blood flow from
the portal vein; portal HTN and ascites result.
Assessment and Diagnostic Findings
• ↑ GGT and ALP, abnormalities in hepatocytes
revealed by liver biopsy.
• ↑ ALT, AST, and bilirubin levels.
• Anorexia, nausea, vomiting, right upper quadrant
•
•
•
•
discomfort, presence of ascites and lower extremity
edema, enlarged liver, pruritus.
Presence of alcohol withdrawal symptoms.
Pale stools, dark tea-colored urine, jaundice.
History of alcohol abuse; starburst hemorrhages
under the skin.
B-vitamin deficiency, (Remember: B vitamins
are for Blood/Brain), as in wet beriberi.
Complications
• Chronic liver failure, encephalopathy, and death.
10
• Portal hypertension, ascites, edema.
• Hepatorenal syndrome.
• Hemorrhage, bleeding esophageal varices.
Medical Care and Surgical Treatment
• Nutritional assessment and dietary intervention:
• Small, frequent high-calorie, low-sodium meals.
• Protein is titrated according to the serum
ammonia levels.
• Lactulose for high ammonia levels; diuretics
and/or albumin for ascites.
• Alcohol cessation program.
• Paracentesis to remove ascitic fluid if respiratory
embarrassment occurs.
• Transjugular intrahepatic portosystemic shunt.
Keep in Mind
• Teach client to avoid hepatotoxic substances.
Make the Connection
• MELD score indicates the likely survival of
the client for 90 days (score ranges from 6 to 40).
• Assess laboratory values, respiratory and mental
status; assess.
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Gastrointestinal Disorders
11
Liver Cancer
(liv-er kan-ser)
Clue: Diagnostic or Clinical Findings
Elevated ALT and AST, ascites,
edema in the lower extremities,
↑ bilirubin.
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Gastrointestinal Disorders
Pathophysiology
• Chronic irritation of hepatocytes or surrounding
parenchyma causes mutation of cells.
• The liver is a common site of mastastasis.
Assessment and Diagnostic Findings
• ↑ ALT and AST, ↑ ALP and ↑ bilirubin level.
• Anorexia, nausea, vomiting, right upper quadrant
•
•
•
discomfort, presence of ascites and lower extremity
edema, enlarged liver, pruritus.
Presence of alcohol withdrawal symptoms.
Pale stools, dark tea-colored urine, jaundice.
Liver biopsy is positive for carcinoma.
Complications
• Chronic liver failure, encephalopathy, and death.
• Portal hypertension, ascites, edema.
• Hepatorenal syndrome.
• Hemorrhage; bleeding esophageal varices.
Medical Care and Surgical Treatment
• Chemotherapy, radiation, biologic therapies, and,
rarely, liver transplantation.
• Nutritional assessment and dietary intervention:
• Small, frequent high-calorie, low-sodium meals.
• Protein is titrated according to the serum
ammonia levels.
11
• Lactulose for high ammonia levels; diuretics
and/or albumin for ascites.
• Alcohol cessation program.
• Paracentesis to remove ascitic fluid, if respiratory
embarrassment occurs.
• Transjugular intrahepatic portosystemic shunt.
Keep in Mind
• Avoid hepatotoxic substances as much as
possible.
• Manage stress with counseling.
• Teach the side effects of chemotherapy and radiation therapy.
Make the Connection
• Offer pain medication and antiemetics
around the clock or by patient-controlled system.
• Monitor laboratory values, respiratory ease, and
signs of bleeding.
• Intra-arterial chemotherapy is shown to be less
toxic to the body.
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Gastrointestinal Disorders
12
Esophageal Varices
(e-sof-a-je-al var-i-sez)
Clue: Diagnostic or Clinical Findings
Oral hemorrhage in the presence
of portal hypertension.
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Gastrointestinal Disorders
Pathophysiology
• Dilation of the veins of the esophagus occurs related
to portal hypertension from chronic liver disease.
• The walls of the veins become thin and can spontaneously rupture and cause massive bleeding.
• Ingestion of fibrous or fried foods can scratch
and rupture the varices.
Assessment and Diagnostic Findings
•
•
Endoscopic examination for dilated areas of the
esophagus.
Portal hypertension (resistance to blood flow
through the liver).
12
• Transfusion of packed red blood cells (PRBCs),
•
volume expanders (e.g., albumin), and fresh frozen
plasma (FFP) for clotting factors (if necessary).
Sclerotherapy done with an esophagogastroduodenoscopy (EGD).
Keep in Mind
• Avoid hard, fried, or fibrous foods if diagnosed
with enlarged esophageal varices.
• After sclerotherapy, chest pain may occur for
72 hours. Report worsening pain not responding
to the prescribed analgesic.
Complications
• Hemorrhage.
• Fluid and electrolyte imbalance.
Make the Connection
• Monitor the airway carefully when using
Medical Care and Surgical Treatment
• Infusion of vasopressin to stop the hemorrhage.
• Tamponade (pressure) on the varices with a
Sengstaken-Blakemore tube, which has three
lumens. One drains the stomach contents, another
inflates a balloon in the fundus of the stomach,
and the last inflates a long balloon in the esophagus. The esophageal balloon pressure should be
maintained between 20 and 25 mm Hg.
•
•
•
tamponade. Be ready to quickly deflate or cut the
lumens of the esophageal balloon in cases of respiratory distress.
Assess the complete blood count (CBC), blood
pressure, and pulse for hypovolemia and anemia.
Start venous access.
Unrelieved pain after sclerotherapy could indicate
esophageal perforation.
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Gastrointestinal Disorders
13
Pancreatitis
(pan-kre-a-ti-tis)
Clue: Diagnostic or Clinical Findings
Severe midline abdominal pain that
radiates to the flank, spine, and back,
worsening with extension of the legs
or ingestion of food. Elevated ALT and
AST, amylase, lipase, and glucose.
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Gastrointestinal Disorders
Pathophysiology
• The outlet of the pancreas may become blocked
•
•
due to inflammation, mechanically (gallstones),
or by the digestive enzymes being prematurely
activated while they are still in the pancreas.
Protease causes dilation and permeability of
the capillaries, allowing fluid to move from the
pancreas to the retroperitoneal space. If fluid
loss is severe, shock may occur.
Protease initiates a chain reaction of inflammation that results in conversion of prothrombin to
thrombin, causing DIC.
Assessment and Diagnostic Findings
• ↑ ALT and AST, amylase, lipase, ALP, bilirubin,
LDH, potassium, and glucose.
• CT scan and US to show infiltrates in the
retroperitoneal and pleural spaces.
• Pain in the abdomen with guarding. Pain is less•
ened by drawing the knees up and worsened by
extension.
Low blood pressure and ↑ pulse indicate shock.
Complications
• Shock, respiratory distress.
• Renal failure.
13
• Signs of hemorrhage: Turner’s sign (a purple
discoloration in the flanks) and Cullen’s sign
(a purple discoloration around the umbilicus).
Medical Care and Surgical Treatment
• IV infusion of fluids, volume expanders, and
PRBCs.
• Oxygen, IV analgesics (meperidine rather than
•
morphine to lessen spasm of the sphincter of
Oddi), and antiemetics.
NPO to avoid worsening autodigestion.
Keep in Mind
• Chronic alcohol ingestion is a causative factor in
pancreatitis.
• Cholelithiasis may cause mechanical obstruction.
Make the Connection
• Monitor pain level and medicate as needed.
• Assess vital signs for ↑ pulse and ↓ blood
pressure.
• Monitor amylase and lipase levels and F and E
levels.
• Assess for Turner’s or Cullen’s sign.
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Gastrointestinal Disorders
14
Cholecystitis
(ko-le-sis-ti-tis)
Clue: Diagnostic or Clinical Findings
Right upper quadrant pain that
radiates to the right scapula.
Murphy’s sign is present.
↑ Amylase and bilirubin.
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Gastrointestinal Disorders
Pathophysiology
• Presence of gallstones causes mechanical
•
•
•
obstruction of bile from the gallbladder. Stasis
of bile attracts bacteria, which adds to the
inflammation.
Small gallstones enter the cystic duct and cause
severe colicky pain as the duct’s peristaltic waves
press on the stone.
The gallbladder becomes fibrotic and does not
release bile effectively into the duodenum.
Pressure of gallstones on the gallbladder walls
can cause necrosis.
Assessment and Diagnostic Findings
• Severe right upper quadrant (RUQ) pain (biliary
•
•
•
•
colic) radiating to the right scapula, especially
after a fatty meal, and lasting for 4–6 hours;
nausea and vomiting.
Murphy’s sign, in which the client is unable to
take a deep breath when the examiner places
pressure over the lower liver border.
Low-grade temperature elevation, elevated WBC
count.
↑ Serum amylase levels, ↑ bilirubin, jaundice.
PIPIDA, DISIDA, or HIDA nuclear medicine scans.
14
• Ultrasound of the gallbladder.
• Endoscopic retrograde cholangiopancreatography
(ERCP) with contrast.
Complications
• Sepsis, gallbladder perforation, peritonitis.
• Adenocarcinoma of the gallbladder.
Medical Care and Surgical Treatment
• Low-fat diet, meperidine for pain, antispasmodics,
antiemetics, oral gallstone dissolution medications.
• Laparoscopic or classic cholecystectomy.
• Extracorporeal shock wave lithotripsy (ESWL).
Keep in Mind
• Avoid high-fat meals preoperatively. Postoperatively,
reintroduce fats into the diet gradually.
• A T tube may be inserted temporarily after
cholecystectomy for drainage of bile if the cystic
duct was explored.
Make the Connection
• Assess pain patterns and medicate as needed;
assess for Murphy’s sign.
• Monitor laboratory values and vital signs.
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Gastrointestinal Disorders
15
Pancreatic Cancer
(pan-kre-at-ik kan-ser)
Clue: Diagnostic or Clinical Findings
Weight loss, anorexia; ↑ amylase,
lipase, and bilirubin. ↑ vitamin D
intake may be preventative.
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Gastrointestinal Disorders
Pathophysiology
• Mutation of cells in the pancreas occurs from
genetic factors or chronic irritation.
• Tumors are most commonly found in the head of
the pancreas and are large.
• Metastasis by direct extension to the stomach,
gallbladder, liver, and duodenum occurs rapidly.
• Tumors in the body of the pancreas metastasize
rapidly via blood and lymph.
Assessment and Diagnostic Findings
• ↑ ALP, glucose, and bilirubin.
• If the cancer causes obstruction, ↑ amylase and
lipase levels are seen.
• Needle biopsy guided by ultrasound revealing
cancer cells.
• ERCP.
• CT scan and MRI.
Complications
• DVT and CVA are commonly associated with
•
pancreatic cancer. The tumor secretes substances
similar to trypsin or protease that convert prothrombin to thrombin and increase clotting
factors in the blood.
Diabetes mellitus.
15
•
•
Postoperative infection, fistula formation,
peritonitis, paralytic ileus, malabsorption
disorder.
Death: pancreatic cancer has a poor prognosis.
Medical Care and Surgical Treatment
• Total or partial pancreatectomy when the tumor
is located in the head of the pancreas.
• Whipple’s procedure, which involves removal of
the head of the pancreas, the duodenum, and
parts of the stomach. Chemotherapy and/or
radiation.
Keep in Mind
• Manage pain and stress of illness.
• Monitor glucose level; report bruising.
• Take digestive enzymes as ordered.
Make the Connection
• Monitor pain level and medicate as needed.
• Assess laboratory values, electrolytes, albumin,
vital signs, weight and nutritional status.
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Gastrointestinal Disorders
16
Bowel Obstruction
(bow-el ob-struk-shun)
Clue: Diagnostic or Clinical Findings
High-pitched bowel sounds,
abdominal distention and pain.
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Gastrointestinal Disorders
Pathophysiology
• Mechanical obstruction occurs when a tumor or
•
•
hard stool lodges in the intestine or when the
bowel twists (volvulus) or telescopes within itself
(intussusception). Pressure builds on the walls of
the intestine, decreasing perfusion, which can
lead to necrosis of the bowel.
Adhesions from prior abdominal surgeries
cause scar tissue causing mechanical
obstruction.
Paralytic obstruction results from a temporary
cessation in nerve conduction.
Assessment and Diagnostic Findings
• Abdominal pain, thirst, and malaise.
• Abdominal distention and visible loops of bowel.
• Intractable vomiting, eventually of fecal material;
no stools.
• F and E imbalance (dehydration).
• CT scan.
• ↑ WBC and H&H.
Complications
• Necrosis and perforation of the bowel.
• Peritonitis.
16
• Mental status changes or cardiovascular abnormalities related to electrolyte imbalance.
Medical Care and Surgical Treatment
• NPO.
• Decompression with an NGT.
• Bowel resection.
• F and E replacement.
• Antibiotics, antiemetics, and analgesics.
Keep in Mind
• The NGT is used until the obstruction is resolved
(self-resolution or with surgery).
• Report nausea immediately, because the NGT
may be occluded.
Make the Connection
• Monitor all clients with past abdominal
surgeries for signs of bowel obstruction.
• Bowel sounds are more active and high pitched
at the area of obstruction.
• Assess vital signs, pain level, and laboratory
values for infection; assess F and E status.
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Gastrointestinal Disorders
17
Ulcerative Colitis
(ul-ser-a-tiv ko-li-tis)
Clue: Diagnostic or Clinical Findings
Daily passage of six or more bloody
mucus stools associated with
abdominal pain.
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Gastrointestinal Disorders
Pathophysiology
• Inflammation and hemorrhage in small areas of
•
•
•
•
the mucosal layer of the colon cause abscesses to
form (crypt abscesses). The necrotic areas slough
off, causing ulcer formation that extends to the
submucosal layer of the bowel.
Blood in the colon causes hypertonicity of the
bowel contents and acts as a laxative.
Pseudopolyps (ragged edges of the mucosal layer).
Incidence is greatest in the second, third, and
sixth decades of life, a genetic link exists; probable autoimmune disease.
Lesions begin in the rectum and spread proximally.
Assessment and Diagnostic Findings
• Weight loss, diarrhea with blood and mucus,
cramping and abdominal pain.
• F and E imbalance.
• CBC, colonoscopy with bowel biopsy, presence of
fissures, fistulas.
• Arthritis, skin lesions, inflammatory eye disorders,
altered liver function studies.
• P-ANCA, ASCA, OmpC testing.
Complications
• Anemia.
17
• Bowel perforation, peritonitis, and CA.
• Bowel cancer.
Medical Care and Surgical Treatment
• Antirheumatics, tumor necrosis factor (TNF)
•
•
inhibitors, anti-inflammatory medications;
corticosteroids and immunosuppressants; bulk
laxatives (gel the stool, ↓ diarrhea).
Partial bowel resection or colectomy.
NPO during the acute phase; IV or TPN.
Keep in Mind
• Avoid spicy foods and high-residue foods.
• Expect remissions and exacerbations; avoid stress.
• Avoid persons with infections while on anti•
inflammatories, antirheumatics, TNF inhibitors,
or corticosteroids; teach care of ostomy.
Support groups for ulcerative colitis are helpful.
Make the Connection
• Monitor number and characteristics of
•
stools; assess laboratory values for anemia and
electrolyte imbalances.
Assess vital signs and pain level frequently.
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Gastrointestinal Disorders
18
Colon Cancer
(ko-lon kan-ser)
Clue: Diagnostic or Clinical Findings
Stool is positive for blood.
A change in bowel habits
has occurred.
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Gastrointestinal Disorders
Pathophysiology
• Mutation of epithelial cells of the colon from the
chronic irritation of inflammatory bowel disease,
familial adenomatous polyposis (FAP; early onset
of polyps in the colon that become malignant),
removal of the gallbladder, increased fat in the
diet, and ingestion of carcinogens.
18
Medical Care and Surgical Treatment
• Bowel resection with or without ostomy creation.
• Chemotherapy and/or radiation.
• Analgesics, antiemetics.
Keep in Mind
• Provide preoperative teaching concerning naso-
Assessment and Diagnostic Findings
• Change in bowel habits (constipation or diarrhea).
• Change in shape of stool due to obstructing
lesion.
• Virtual colonoscopy by computed tomographic
(CT) scan, colonoscopy with biopsy, barium
enema revealing polyps or tumors; stool for
occult blood is positive (polyps and tumors tend
to bleed).
Complications
• Bleeding.
• Obstruction, necrosis, bowel perforation with
peritonitis.
• Metastasis to the lymph system and liver, resulting in death.
• After bowel resection, anastomotic leak, and
peritonitis.
•
•
gastric tube (NGT), deep breathing, incentive
spirometer, exercise, use of antiemetics and analgesics, and early ambulation.
Awareness of the side effects of chemotherapy
and/or radiation and their mitigation is important.
Support groups for colon cancer are helpful;
teach ostomy care.
Make the Connection
• Monitor laboratory tests for elevated liver
enzymes to detect metastasis.
• Assess vital signs and pain level.
• Teach ostomy care and assess ability of the client
for self-care.
• Assess complete blood count (CBC) for immuno-
suppression related to chemotherapy or radiation.
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Gastrointestinal Disorders
19
Diverticulosis
(di-ver-tik-u-lo-sis)
Clue: Diagnostic or Clinical Findings
History of constipation and
poor bowel habits.
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Gastrointestinal Disorders
Pathophysiology
• Small herniations of the sigmoid and descending
•
•
colon that occur when pressure within the bowel
and abdomen is high.
Related to poor bowel habits, constipation, and
straining at stool.
When diverticula become inflamed by seeds or
other residue entering them, diverticulitis results.
Assessment and Diagnostic Findings
• Diverticulosis is asymptomatic.
• Barium enema or computed tomographic (CT)
•
•
scan shows multiple small pouches, usually on
the sigmoid colon.
Diverticulitis presents with pain in the left lower
quadrant (LLQ); bleeding may be present and
necessitate transfusion with packed red blood
cells (PRBCs) or surgery (bowel resection).
Stool for occult blood may be positive.
Complications
• Infection, colon perforation with peritonitis.
Medical Care and Surgical Treatment
• Diverticulosis: High-fiber diet; adequate fluid and
exercise to encourage healthy bowel habits.
19
• Diverticulitis (acute phase): Nothing by mouth
(NPO); rest the gut; intravenous fluids.
• Diverticulitis (surgical intervention): Bowel resection.
• Diverticulitis (convalescent phase): Increase to a
soft, low-fiber, low-residue diet and avoid all
foods with nondigestible seeds or shells; once
healed, slowly resume normal diet, adding fiber.
Keep in Mind
• When the signal comes for a bowel movement,
•
•
do not ignore it because doing so causes water
loss from the stool and promotes constipation.
Use bulk laxatives; eat raw vegetables and fruits,
fiber-containing grain; increase fluid intake and
exercise for healthy bowel habits.
Do not strain at stool.
Make the Connection
• Assess for rebound tenderness at the LLQ
if diverticulitis is suspected.
• Monitor complete blood count (CBC); monitor
stool for occult blood.
• Teach proper dietary habits for the presenting
condition.
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Gastrointestinal Disorders
20
Appendicitis
(a-pen-di-si-tis)
Clue: Diagnostic or Clinical Findings
Rebound tenderness at McBurney
point, ↑ WBC.
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Gastrointestinal Disorders
Pathophysiology
• Inflammation of the appendix by obstruction,
usually by fecalith. The small stones may enter,
causing more inflammation by exerting pressure
and abrasiveness on the walls of the appendix.
Assessment and Diagnostic Findings
•
•
•
•
•
Temperature elevation, ↑ white blood count (WBC).
Guarding, limping on ambulation, rebound tenderness at McBurney point (midpoint between
the umbilicus and the right iliac crest).
Computed tomographic (CT) scan and ultrasound show enlargement of the appendix.
Rectal examination reveals enlarged appendix.
If appendix has ruptured, abdominal rigidity is
evident; if appendix is abscessed, no bowel
sounds are heard over the right lower quadrant
(RLQ), and pain increases.
Complications
• Rupture and peritonitis.
• Abscess.
Medical Care and Surgical Treatment
• Laparoscopic resection.
• Drainage of abscess.
• Antibiotics, analgesics.
20
Keep in Mind
• A nasogastric tube (NGT) may be in place briefly
•
•
•
until bowel function returns to prevent nausea
and vomiting; diet is increased once bowel
function returns to normal.
Pain medication should be taken only after diagnosis; no enemas should be used prior to coming
to the emergency department.
Take nothing by mouth (NPO).
Lying in side-lying or semi-Fowler’s position will
decrease pain.
Make the Connection
• Monitor complete blood count (CBC) for
WBC elevation.
• Assess pain patterns, including rebound tenderness at McBurney point.
• Watch for any increase in pain and decreased
bowel sounds in the RLQ.
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Gastrointestinal Disorders
21
Crohn’s Disease
(kronz di-zez)
Clue: Diagnostic or Clinical Findings
Diarrhea, weight loss, cobblestone
appearance in the small bowel.
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Gastrointestinal Disorders
Pathophysiology
• Inflammatory bowel disease affecting mostly
•
•
•
•
•
women from adolescence to the third decade
of life.
Cobblestone appearance of the bowel wall related
to interspersed areas of inflammation and healthy
tissue; also called regional enteritis.
Inflammation occurs mainly in the small intestine
above the cecum and spreads proximally.
Affects the submucosa, causing strictures,
scarring, fissures, and fistulas.
Disease involves both genetic and autoimmune
factors.
Crohn’s disease affects the entire bowel wall.
21
Medical Care and Surgical Treatment
• Antirheumatics and TNF inhibitors,
•
•
corticosteroids, immunosuppressants,
anti-inflammatories.
Ileostomy or bowel resection. Surgery is not a
cure; the enteritis will spread.
Dietary intervention with folate, calcium,
flaxseed, and fish oil.
Keep in Mind
• Avoid spicy foods and high-residue foods.
• Expect remissions and exacerbations; avoid stress.
• Avoid persons with infections.
• Support groups for Crohn’s disease are helpful.
Assessment and Diagnostic Findings
• Cramps and diarrhea that occur with food intake.
• Remissions and exacerbations.
• F and E imbalance.
• CBC, bowel biopsy, presence of fissures, fistulas.
• P-ANCA, ASCA, OmpC testing.
Complications
• Anemia and malnutrition.
• Fissures, fistulas, stricture/obstruction, bowel perforation with peritonitis.
Make the Connection
• Monitor I&O, calories, and characteristics
and number of stools.
• Assess laboratory values for anemia and inflammatory markers.
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Gastrointestinal Disorders
22
Peritonitis
(per-i-ta-ni-tis)
Clue: Diagnostic or Clinical Findings
Rebound tenderness and rigidity
over the abdominal wall.
Decreased bowel sounds.
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Gastrointestinal Disorders
Pathophysiology
• Inflammation of the sterile peritoneal cavity by
introduction of bacteria via invasive procedures,
open bowel surgeries, or perforation of intraabdominal organs whose normal flora contain
bacteria.
Assessment and Diagnostic Findings
• Generalized abdominal pain and rigidity.
• If perforation is the cause, pain localizes to the
area of the perforation and leak.
• ↑ White blood count (WBC), temperature
increase, tachycardia.
• Absence of bowel sounds (peristalsis) over the
affected area.
Complications
• Septicemia.
• Hypovolemia with fluid shifts into the
peritoneum.
• Shock and death.
Medical Care and Surgical Treatment
• Nothing by mouth (NPO).
• Exploratory surgery; abscess drainage and infiltration with antibiotic solution.
22
• Intravenous antibiotics, analgesics.
• Organ repair if caused by a perforation; placement of a nasogastric tube (NGT) if bowel is
perforated.
Keep in Mind
• Teach pre- and postoperative care and expecta•
tions (early ambulation, deep breathing, leg
exercises).
Explain the illness and the use of antibiotic
therapy.
Make the Connection
• Assess for return of bowel sounds.
• Monitor CBC for normalization of WBC levels.
• Assess function of all organ systems.
• Support cardiorespiratory functions as needed.
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Gastrointestinal Disorders
23
Hemorrhoids
(hem-o-roydz)
Clue: Diagnostic or Clinical Findings
History of constipation. Frank
blood on the stool. Painful
anal lesions.
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Gastrointestinal Disorders
Pathophysiology
• Varicosities of the veins of the anus related to
increased intra-abdominal pressure.
• Occur during pregnancy as the weight of the
•
•
fetus compresses the inferior vena cava, causing
congestion of the veins in the anus (as well as
the legs).
Poor bowel habits and constipation contribute to
the etiology.
Internal hemorrhoids occur above the internal
sphincter; external hemorrhoids occur below the
external sphincter.
Assessment and Diagnostic Findings
• Frank red blood on stools.
• External hemorrhoids are visible. When inflamed,
they are large and red and usually encircle the
anus. Careful examination should be done of
these lesions to determine whether they are blue,
light-colored, or black, which could indicate
ischemia or necrosis of the overlying skin.
Complications
• Pain, bleeding, and infarction of the skin above
the lesions.
23
Medical Care and Surgical Treatment
• Prevent straining at stool and constipation.
• Nutritional consultation.
• Anti-inflammatory topical medication, analgesics.
• Sitz baths, side-lying positions, ice packs.
• Sclerotherapy.
• Rubber-band ligation.
• Laser, cryotherapy, or surgical removal.
Keep in Mind
• Avoid constipation by eating adequate fiber-rich
foods; increase fluids and exercise.
• Encourage good hygiene.
Make the Connection
• Monitor affected site for improvement.
• Sitz baths can lower blood pressure and cause
syncope, so monitor the client carefully.
• Assess stools for bright red blood.
• Assess hemorrhoids for color.
• Postoperatively, monitor for bleeding, infection,
and pain.
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ENDOCRINE
Hyperpituitarism, 24
Hypopituitarism, 25
Diabetes Insipidus, 26
Syndrome of Inappropriate
Antidiuretic Hormone, 27
Cushing’s Syndrome, 28
Addison’s Disease, 29
Hyperthyroidism, 30
Hypothyroidism, 31
Diabetes Mellitus Type 1, 32
Diabetes Mellitus Type 2, 33
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Endocrine Disorders
24
Hyperpituitarism
(hi-per-pi-tu-i-tar-ism)
Clue: Diagnostic or Clinical Findings
Excess growth hormone, abnormal
lipid level, high blood glucose
levels. Adults experience arthritis,
visual changes, and enlarged
hands and feet.
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Endocrine Disorders
Pathophysiology
• Hyperfunction of the pituitary is almost
always caused by an adenoma.
• GH, from the anterior pituitary, is secreted in
•
•
•
•
•
•
large amounts, resulting in gigantism in children
and acromegaly in the adult.
Acromegaly is characterized by growth of bone,
connective, and soft tissue.
Hands and feet become enlarged; larynx
enlarges; vertebral growth often results in
kyphosis; teeth become displaced; enlargement
and erosion of the sella turcica causes visual
changes and headache.
Metabolic alteration causes fats to become
the initial energy burned, resulting in ketosis.
GH–induced insulin resistance, along with
glycogen release by the liver, causes DM.
Other anterior pituitary hormones are inhibited.
Fatty acid metabolism is altered causing
atherosclerosis.
Excess soft tissue of the soft palate cause sleep
apnea.
Assessment and Diagnostic Findings
• ↑ GH, ↑ LDL.
24
• Enlarged feet and hands, deep voice, arthritis,
insulin resistance, headache, sleep apnea.
• CT scan and MRI to detect pituitary tumor.
Complications
• MI, CHF, DM.
• Sleep apnea, dysphagia.
• Arthritis, osteoporosis, and chronic bone pain.
• Cancer from GH.
Medical Care and Surgical Treatment
• Dopamine agonists, GH inhibitors (somatostatin).
• Radiation therapy or hypophysectomy.
Keep in Mind
• Monitor the glucose level, report excessive
snoring, and report difficulty swallowing.
Make the Connection
• Remember: Following transsphenoidal
hypophysectomy, assess all drainage for glucose,
indicating CSF leak.
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Endocrine Disorders
25
Hypopituitarism
(hi-po-pi-tu-i-ta-rizm)
Clue: Diagnostic or Clinical Findings
Short stature in children accompanied
by weakness, low blood glucose, and
delayed sexuality and stunted growth
of sexual organs.
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Endocrine Disorders
Pathophysiology
• Growth hormone (somatropin) is deficient
•
•
related to an ablative pituitary tumor or failure
of the gland to develop.
Dwarfism, in the child, and mental slowness.
In adults, decreased GH leads to central accumulation of body fat and related problems with
cardiovascular health.
Assessment and Diagnostic Findings
• Growth of a child well below the 25th
percentile.
• Developmental delay.
• Weakness, hypoglycemia, “apple fat,” and skin
changes in adults.
• GH levels, GH stimulation test in response to
induced hypoglycemia.
• MRI and CT scan to detect presence of pituitary
tumor.
Complications
• Cardiovascular disease in adults and untreated
children.
• Short stature, mental retardation.
• Headache and visual changes in cases of pituitary
tumor.
25
Medical Care and Surgical Treatment
• Somatropin.
• Hypophysectomy.
• Hypoglycemia treated with dietary intervention.
Keep in Mind
• Report any bone pain or limping after starting
somatropin therapy.
• Growth is possible as long as the epiphyseal disks
are not closed.
• Adults should be under the care of a health professional if GH or secretagogues are used.
Make the Connection
• Monitor glucose levels, growth patterns,
•
sexual organ development, and thyroid function
tests.
Measure long-bone growth bilaterally; note any
change in gait, which may be a sign of a slipped
epiphyseal disk, in which growth is occurring only
in one area of the disk.
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Endocrine Disorders
26
Diabetes Insipidus
(di-a-be-tez in-si-pi-dus)
Clue: Diagnostic or Clinical Findings
Low specific gravity of urine <1.005.
Urinary output in excess of
5–15 liters daily.
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Endocrine Disorders
Pathophysiology
•
•
•
•
ADH or AVP is secreted by the posterior pituitary gland and is responsible for reabsorption
of water by the kidney.
DI is caused by a deficiency of ADH and excess
loss of water through urination. Urinary output
can be in excess of 5–15 L daily.
DI can be caused by drugs like lithium; surgical
removal of the pituitary; and nephrogenic DI.
Psychogenic DI (not true DI) is caused by a desire
to drink large amounts of fluids (water intoxication); alcohol ingestion causes a temporary DI
resulting in dehydration.
Assessment and Diagnostic Findings
•
•
•
•
•
•
Polyuria, nocturia, excessive thirst, poor skin turgor.
Hypovolemia, dehydration, and electrolyte
imbalance.
Specific gravity of urine of <1.005; ↓ urine
osmolality.
↓ ADH levels following administration of hypertonic saline solution or fluid restriction (should ↑).
Water deprivation test.
CT scan and MRI to detect presence of a
pituitary tumor.
26
Complications
• Hypovolemic shock.
• Electrolyte imbalances.
• Enlarged bladder.
Medical Care and Surgical Treatment
• Hypophysectomy in presence of pituitary tumor.
• Replacement of ADH.
• Hypotonic fluid replacement (0.45% sodium
chloride solution).
• Sulfonylureas that increase sensitivity to ADH
and thiazide diuretics (slow urine output in the
absence of ADH).
Keep in Mind
• Monitor daily weight (report an increase of
•
•
greater than 2 lb in 1 day), and keep a diary of
intake and output (I&O) after start of therapy.
Take extra fluids if thirst occurs.
Comply with medication regimen.
Make the Connection
• Monitor vital signs, I&O, urine specific
gravity, and serum electrolytes.
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Endocrine Disorders
27
Syndrome of Inappropriate
Antidiuretic Hormone
(sin-drom uv in-a-pro-pree-et
an-ti-di-u-ret-ik hor-mon)
Clue: Diagnostic or Clinical Findings
High blood pressure, low serum
osmolality, bounding pulse,
seizures.
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Endocrine Disorders
Pathophysiology
• SIADH occurs when ADH does not decrease in
•
•
response to a low serum osmolality, leading to
fluid overload.
Frequently, SIADH is associated with cancers of
the lung, pancreas, and Hodgkin’s disease.
ADH may hypersecrete in the presence of head
trauma or tumor or as a complication of diabetes
insipidus treatment.
Assessment and Diagnostic Findings
• Weight gain, bounding pulse, increased blood
pressure, crackles.
• Dilutional hyponatremia with signs and symp•
•
•
•
toms of headache, personality changes, nausea,
diarrhea, seizure, and coma (cerebral edema).
Serum osmolality <275 mOsm/kg; serum ADH ↑.
Lethargy, muscle cramps and weakness.
History of cancer, especially oat cell cancer of the
lung.
Water load test.
Complications
•
Mental status changes, weakness, lethargy, muscle
cramps related to dilution of electrolytes.
27
• Seizures, coma, cerebral and pulmonary edema,
and death.
Medical Care and Surgical Treatment
• Oral salt, hypertonic solutions, loop diuretics,
and fluid restriction (1,000 mL/24 hr).
• Demeclocycline.
• Treatment of underlying cancer.
Keep in Mind
• Monitor fluid restriction adherence, monitor daily
weight (report gain of >2 lb/24 hr), encourage
fluids high in sodium (ice chips may satisfy thirst
without adding to fluid intake), maintain diary
of I&O.
Make the Connection
• Monitor for change in mental status
•
•
•
(Glasgow Coma Scale may be used in severe
cases).
Monitor serum osmolality, urine output, daily
weight, and urine specific gravity.
Monitor serum electrolytes (135–145 mEq/L).
Auscultate lungs for crackles or diminished
breath sounds in the bases.
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Endocrine Disorders
28
Cushing’s Syndrome
(koosh-ingz sin-drom)
Clue: Diagnostic or Clinical Findings
Moon face, buffalo hump,
truncal obesity, ↑ serum glucose,
↓ potassium (K+), ↑ serum sodium.
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Endocrine Disorders
Pathophysiology
• Hormones secreted by the adrenal cortex are
•
•
the body’s stress hormones (glucocorticoids and
mineral corticoids).
Cushing’s disease is caused by excess cortisol
secretion related to excess ACTH secretion, while
Cushing’s “syndrome” is related to consumption
of exogenous cortisol.
May be caused by secreting tumor of the lungs or
adrenal glands.
Assessment and Diagnostic Findings
• Weight gain, moon face, buffalo hump, truncal
•
•
obesity, osteoporosis, glucose intolerance and
secondary diabetes, slow wound healing, striae,
bruising, bone marrow suppression and hyperpigmentation of the skin.
↑ Serum sodium and ↓ serum potassium.
Plasma and urine cortisol and plasma ACTH are
elevated.
Complications
• Masked infection, WBC activity, ↓ platelets.
• Cardiac arrhythmias; atherosclerosis.
• Pathologic bone fracture.
• Diabetes mellitus.
28
Medical Care and Surgical Treatment
• Hypophysectomy or adrenalectomy if indicated.
• Treatment for secondary diabetes and insulin
resistance.
• Exogenous cortisol dosage change or given every
other day.
Keep in Mind
• Teach client to monitor blood glucose; modify
•
dietary intake to low calorie, high protein,
high K+, and low Na+.
Report any signs of infection (e.g., sore throat).
Make the Connection
• Monitor cardiac rhythm strip, serum
potassium, and serum sodium.
• Monitor daily weights and I&O; administer potassium supplements, if ordered.
• Encourage weight-bearing exercise.
• Monitor CBC and for any signs of infection.
• Monitor wound healing.
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Endocrine Disorders
29
Addison’s Disease
(ad-i-sonz di-zez)
Clue: Diagnostic or Clinical Findings
Tanned appearance to skin, low
blood pressure, ↓ serum glucose,
↓ serum sodium (Na+), ↑ serum
potassium (K+).
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Endocrine Disorders
Pathophysiology
• The adrenal cortex secretes hormones necessary
•
•
•
to react to stress (physical or psychological).
They include glucocorticoids, aldosterone, and
sex hormones (sugar, salt, and sex).
In primary hypofunction of the adrenal gland,
the adrenal hormones are not secreted in adequate amounts; in secondary hypofunction of
the adrenal glands, insufficient pituitary secretion
of ACTH occurs.
Primary Addison’s disease may be autoimmune.
Adrenalectomy may cause Addison’s.
Assessment and Diagnostic Findings
of the skin, ↓ BP, ↓ serum
• Hyperpigmentation
Na+, ↑ K+, ↓ serum glucose levels.
• Anorexia, weight loss, confusion, psychosis.
• Low urine sodium and cortisol levels; ↑ pituitary
output of serum ACTH (primary); ↑ blood urea
nitrogen (BUN) related to dehydration.
Complications
• Inability to respond to stress; Addisonian crisis.
• Arrhythmias.
• Coma and death from hypoglycemia.
29
Medical Care and Surgical Treatment
• Replacement of corticosteroids and aldosterone
given daily in divided doses in times of stress.
Keep in Mind
rest
• Teach compliance with medication regimen;
+
•
•
as needed; and high-calorie, moderate-Na , and
↓K+ diet.
Client must learn to assess his or her BP.
Wear a MedicAlert bracelet.
Make the Connection
•+ Monitor BP, blood glucose, serum Na+,
and K levels; weight, Addisonian crisis.
• Monitor cardiac rhythm strip data.
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Endocrine Disorders
30
Hyperthyroidism
(hi-per-thi-royd-izm)
Clue: Diagnostic or Clinical Findings
Restlessness, irritability,
heat intolerance, ↓ TSH,
↑ T3 and T4.
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Endocrine Disorders
30
Pathophysiology
• The thyroid gland hormones are responsible for
•
•
•
•
carbohydrate, protein, and fat metabolism
required by the body cells and for calcium regulation (in tandem with the parathyroid glands).
Primary hyperthyroidism (Graves’ disease) is
caused by excess thyroid hormone secretion
(T3 and T4).
Secondary hyperthyroidism is caused by hypersecretion of thyroid-stimulating hormone (TSH)
by the pituitary gland.
A thyroid tumor may also cause hypersecretion of
thyroid hormones or TSH.
Exposure to radiation is another causative factor.
Assessment and Diagnostic Findings
•
•
•
pressure, restlessness, decreased mental acuity,
and delirium.
Goiter (enlargement of the thyroid gland).
Hypothyroidism after treatment.
Visual changes related to exophthalmos.
Medical Care and Surgical Treatment
• Subtotal thyroidectomy.
• Radioactive iodine treatment.
• Thyroid-suppressing medications.
Keep in Mind
• Report temperature increase, increased blood
pressure, or change in mental status; manage
stress, maintain nutritional status, and take rest
breaks.
• Weight loss despite increased appetite, heat intol•
•
•
erance, irritability, nervousness, tremor, tachycardia, palpitations, inability to sit still or rest.
↓ Serum TSH, ↑ serum T3 and T4.
Thickening of the skin on the anterior legs.
Exophthalmos.
Complications
• Thyrotoxic crisis (thyroid storm) characterized by
very high temperature, tachycardia, high blood
Make the Connection
• Monitor vital signs, serum TSH, and
cardiac rhythm strip data.
• Assess for nodules palpated on the thyroid.
• In the case of radioactive iodine treatment,
remind the client he or she will have to be in
isolation.
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Endocrine Disorders
31
Hypothyroidism
(hi-po-thi-royd-izm)
Clue: Diagnostic or Clinical Findings
Lethargy, mental slowness, heavy
menstrual periods in women,
↑ TSH, ↓ T3 and T4.
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Endocrine Disorders
Pathophysiology
• The thyroid gland is responsible for metabolism
•
•
•
•
of carbohydrates, fats, and protein according to
body requirements.
Primary hypothyroidism (myxedema) occurs when
the thyroid gland does not secrete adequate
thyroid hormone.
Secondary hypothyroidism is related to hyposecretion of thyroid-stimulating hormone (TSH)
by the pituitary gland or overtreatment of
hyperthyroidism.
Low levels of thyroid hormone decrease metabolism in the body.
Hashimoto’s thyroiditis is an autoimmune
disorder that destroys thyroid tissue.
Assessment and Diagnostic Findings
• Fatigue; weight gain; lethargy; mental slowness;
•
bradycardia and heart failure; dry skin; coarse,
dry hair; feeling cold all the time; menorrhagia in
women; shortness of breath; decreased sweating.
↑ TSH and ↓ T3 and T4 in primary disease.
Complications
• Myxedema coma triggered by physical or psychological stress and resulting in subnormal
31
temperature, decreased respiration, decreased
cardiac output, renal failure, nonpitting edema
of extremities, death from respiratory failure.
Medical Care and Surgical Treatment
• Synthetic thyroid hormone replacement therapy.
Keep in Mind
• Teach that full effects of the hormone
replacement may take from days to a week.
• Report palpitations or shortness of breath after
hormone replacement therapy.
Make the Connection
• Monitor TSH level.
• Assess cardiac rhythm strip data when beginning
synthetic hormone replacement.
• Teach client to report signs and symptoms of
hyperthyroidism or myxedema.
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Endocrine Disorders
32
Diabetes Mellitus Type 1
(di-a-be-tez mel-i-tus type 1)
Clue: Diagnostic or Clinical Findings
Polyuria, polydipsia, polyphagia,
↑ serum glucose levels that
persist.
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Endocrine Disorders
Pathophysiology
• The pancreas secretes insulin from the beta cells
•
•
(islets of Langerhans) in response to elevated
blood glucose levels.
In primary diabetes mellitus type 1, the beta cells
are destroyed by an autoimmune reaction.
In secondary diabetes mellitus type 1, the beta
cells are damaged by cancer of the pancreas or
other diseases like pancreatitis and cystic fibrosis.
Assessment and Diagnostic Findings
• Elevated fasting blood glucose levels, elevated
postprandial glucose levels.
• Weight loss, polyuria, polydipsia, polyphagia.
• Elevated glycohemoglobin levels, acetone breath
(smells like alcohol/fermented fruit).
Complications
• Neuropathy, nephropathy, retinopathy.
• Diabetic ketoacidosis (DKA).
• Hypoglycemia (the most common complication
after treatment with insulin is begun).
• Infertility related to sexual dysfunction.
Medical Care and Surgical Treatment
• Carbohydrate counting; dietary regimen should
be similar day to day with increase in calories if
physical activity is increased.
32
• Synthetic or animal-derived insulin given
subcutaneously.
• Treatment of DKA with intravenous hypotonic
•
saline solution with regular insulin added. Once
the glucose begins to normalize, potassium
replacement is necessary.
Pancreas transplant; transplantation of beta cells
into the liver via the portal vein.
Keep in Mind
• Monitor glucose level before meals and at bed•
time. Report hypoglycemia in the middle of the
night (Somogyi effect) or increase in the morning
(dawn phenomenon).
Encourage client to carry a simple sugar or glucose at all times, wear a MedicAlert bracelet,
examine his or her feet for lesions, and report
visual problems or pain in arms/legs.
Make the Connection
• Teach the client to rotate sites for insulin
administration and to follow dietary regimen.
• Monitor glycosylated hemoglobin and serum
glucose levels; monitor for complications.
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Endocrine Disorders
33
Diabetes Mellitus Type 2
(di-a-be-tez mel-i-tus type 2)
Clue: Diagnostic or Clinical Findings
Sedentary lifestyle. Polyuria,
polyphagia, and polydipsia.
Elevated serum glucose levels.
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Endocrine Disorders
33
Pathophysiology
•
•
Type 2 diabetes increases in incidence with
obesity, poor diet, and sedentary lifestyle as
the cells of the body become resistant to
insulin.
Genetic link (10 new gene variants that affect
blood glucose and insulin levels have been
identified); type 2 diabetes is affecting more
children related to poor diet and obesity.
Assessment and Diagnostic Findings
• Elevated fasting blood glucose levels, elevated
postprandial glucose levels.
• Weight loss, polyuria, polydipsia, polyphagia.
• Elevated glycohemoglobin levels.
Complications
• Neuropathy, nephropathy, retinopathy.
• Metabolic syndrome (syndrome X), character-
•
ized by elevated waist circumference (apple
fat), reduced high-density lipoprotein levels,
elevated blood pressure, fasting glucose levels
of >100 mg/dL. This syndrome is related to
atherosclerosis and cardiac events.
Hyperosmolar nonketotic syndrome, in
which stress from illness causes extreme
•
increases in the blood glucose level without
ketosis.
Death.
Medical Care and Surgical Treatment
• Oral hypoglycemic agents and drugs to lower
•
•
•
insulin resistance; insulin may be required if these
medications are ineffective or if the client is ill
(increases glucose levels).
Nutritional consult and exercise regimen.
Assessment of cardiac status with stress testing,
lipid profile, cardiac rhythm strip.
Renal tests.
Keep in Mind
• Monitor blood glucose level ac and hs. Learn the
•
•
•
symptoms of low blood glucose and report if it
occurs.
Follow dietary, exercise, and medication regimen.
Check feet for sores.
Report sensation or vision changes.
Make the Connection
• Monitor HgbA1c and serum glucose levels;
monitor for complications.
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Page 3
UROLOGIC
Urinary Tract Infection, 34
Urethritis, 35
Pyelonephritis, 36
Glomerulonephritis, 37
Nephrotic Syndrome, 38
Polycystic Kidney Disease, 39
Hydronephrosis, 40
Renal Calculus, 41
Rhabdomyolysis, 42
Acute Renal Failure, 43
Chronic Renal Failure, 44
Overactive Bladder, 45
Renal Artery Stenosis, 46
Epididymitis, 47
Benign Prostatic Hyperplasia, 48
Bladder Cancer, 49
Prostate Cancer, 50
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Urologic Disorders
34
Urinary Tract Infection
(u-ri-nar-e trakt in-fek-shun)
Clue: Diagnostic or Clinical Findings
Urinary frequency, urgency, dysuria,
bacterial count of >100,000/mL
of urine.
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Urologic Disorders
Pathophysiology
• Occurs more frequently in women because of
anatomy and age-related structural changes.
• UTIs can also occur as a result of obstructive disease, invasive therapies, and incontinence issues.
• Most UTIs (95%) are caused by contamination
•
•
•
and ascension in the urethra by normal flora
from the rectum.
Causative agents are Escherichia coli; Staphylococcus
saprophyticus; and to a lesser extent Klebsiella
species, Proteus mirabilis, Staphylococcus aureus, and
Pseudomonas aeruginosa.
The normal mucin-surface glycosaminoglycans
are overwhelmed and bacteria become adherent
to bladder surfaces.
Soap in bathwater causes UTIs in children.
Assessment and Diagnostic Findings
• Chills, temperature elevation, dysuria, frequency,
•
urgency, frank blood in urine, urethral spasm,
and pyuria or strong ammonia smell of urine.
Urine culture showing bacterial count of
>100,000/mL indicates infection. The presence
of RBCs, WBCs, hyaline casts, and positive leukocyte esterase and nitrite in urinalysis.
34
• Residual urine of >50 mL immediately after
voiding (bladder scans).
• Voiding cystourethrogram or KUB x-ray showing
obstruction.
Complications
• Ascending infection.
• Urosepsis.
Medical Care and Surgical Treatment
• Antibiotics and urinary analgesics.
• Transurethral resection of the prostate or lithectomy for obstructions.
• Complementary ingestion of cranberry capsules,
which are shown to prevent adherence of
bacteria.
Keep in Mind
• Increase fluid intake when on treatment, and complete all antibiotics as ordered.
Make the Connection
• Recurrent infections or those caused by
unusual organisms must be investigated.
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Urologic Disorders
35
Urethritis
(u-re-thri-tis)
Clue: Diagnostic or Clinical Findings
Dysuria, blood in the urine or ejaculate
in a male. Discharge from the urethra.
History of unprotected sex. In women,
pelvic pain.
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Urologic Disorders
Pathophysiology
• More common in men but can occur in women;
•
also characterized by inflammation and colonization of the urethra by Escherichia coli, Neisseria
gonorrhoeae, Chlamydia trachomatis, herpes simplex,
or cytomegalovirus.
Infectious agents may ascend and affect the
prostate and infiltrate the lymph nodes in the
groin area. In women, these agents can ascend
to infect the pelvic area and may be a cause of
infertility.
Assessment and Diagnostic Findings
•
•
•
•
Culture and sensitivity and treatment with antiinfective to which the organism is sensitive.
In males, symptoms are dysuria, blood or pus in
urine and semen, swollen lymph nodes in the
groin area, swollen testicles, purulent discharge
from the penis, sore throat, and fever.
In women, symptoms include dysuria, dyspareunia,
vaginal discharge, pelvic pain, sore throat, and
fever.
Cervical cultures, rectal culture, penile cultures,
joint fluid culture, Gram stain, and throat
culture.
35
Complications
• Infertility.
• Diffuse infection that spreads to joints, heart
valves, and meninges.
• Spread to other sexual partners.
Medical Care and Surgical Treatment
• Ceftriaxone, azithromycin, or penicillin.
• Sexual counseling and reporting to public health
department as indicated.
• Urinary analgesics.
Keep in Mind
• Men may not become symptomatic for 1 month
after contact with infectious agents.
Make the Connection
• It is important to diagnose this condition
early to prevent systemic infection and infertility.
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Urologic Disorders
36
Pyelonephritis
(pi-e-lo-ne-fri-tis)
Clue: Diagnostic or Clinical Findings
Chills, fever, tenderness over the
costovertebral angle, dysuria,
elevated WBCs.
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Urologic Disorders
Pathophysiology
• Usually an ascending urinary tract infection (UTI)
•
caused by a failure of the “washout” mechanism
of urine and protective mucin gel. Causative
agents are usually Escherichia coli and, to a lesser
extent, Staphylococcus aureus.
Kidney pelvis structures may be damaged by
ongoing infection, leading to nephron damage
and renal failure.
36
Keep in Mind
• Recognize signs and symptoms of UTI so that
spread to the kidneys may be avoided.
• Use complementary agents, like cranberry juice or
•
•
capsules, to prevent adherence of bacteria to
bladder area (trigone is most easily breached).
Take entire antibiotic prescription as directed.
Ensure that urine culture is collected properly
(midstream).
Assessment and Diagnostic Findings
• Pyuria.
• Urinalysis and culture findings showing white
blood cells singly, in clumps, or in casts.
• Bacteria count of >100,000/mL of urine.
• Low specific gravity and osmolarity.
• Slightly alkaline urine pH.
• Proteinuria, glycosuria, and ketonuria.
Complications
• Chronic renal failure.
Medical Care and Surgical Treatment
• Antibiotics (e.g., sulfonamides, fluoroquinolones,
nitrofurantoin, penicillins) and urinary analgesics.
If drugs are given intravenously (IV), hospitalization is required.
Make the Connection
• Monitor for dysuria.
• Assess costovertebral angle for tenderness.
• Assess urinalysis and urine culture.
• Identify risk factors for UTI.
• Remember: The kidneys are inextricably linked to
the bloodstream, so infections in the kidney may
quickly become overwhelming infections of the
blood, and the reverse is also true.
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Urologic Disorders
37
Glomerulonephritis
(glo-mer-u-lo-ne-fri-tis)
Clue: Diagnostic or Clinical Findings
Hypertension; oliguria; smoky, frothy
urine. Urinalysis shows RBCs, casts,
and protein.
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Urologic Disorders
Pathophysiology
• The glomerulus is formed from tufts of arteriolar
•
•
capillaries fed by an afferent arteriole and drained
by an efferent arteriole that have thin basement
membrane composed of a proteinous matrix
and a layer of epithelial cells with footlike outpouches. Blood plasma is forced through these
thin structures by a pressure gradient into
Bowman’s capsule and the renal tubule.
A number of toxins, diseases, and organisms
can cause inflammation and damage to this
basement membrane.
In poststreptococcal infection, antigens are
deposited in the basement membrane of the
glomerulus. When antigen/antibody complexes
form, the immune system destroys them, setting
up large areas of inflammation and damage to
surrounding structures.
37
• High BUN, creatinine, and creatinine/BUN ratio
(>20:1); elevated antistreptolysin O titer.
• US of the kidney, renal biopsy, or CT scan.
Complications
• Renal failure.
Medical Care and Surgical Treatment
• Steroidal and nonsteroidal anti-inflammatory
agents; antibiotics, if indicated.
• Sodium and fluid restriction, antihypertensive
agents, and diuretics.
• Dialysis may be necessary; bedrest.
Keep in Mind
• All suspected streptococcal infections require culture specimen analysis, completion of treatment,
and verification of negative culture.
Assessment and Diagnostic Findings
Make the Connection
• Hypertension; smoky, frothy urine from RBCs and
•
protein; oliguria; edema; periorbital edema tenderness over the costovertebral angle; and flank pain.
Adventitious lung sounds or absent lung sounds
and generalized edema.
• Monitor laboratory values, pulse oximetry,
•
BP urinalysis results; serum chemistry for worsening azotemia.
Monitor level of consciousness and daily weights;
maintain strict I&O measurements.
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Urologic Disorders
38
Nephrotic Syndrome
(ne-frot-ik sin-drom)
Clue: Diagnostic or Clinical Findings
Elevated LDL cholesterol and
triglycerides, proteinuria, frothy urine
from protein and lipids, decreased
immunoglobulins lost in urine.
Massive edema.
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Urologic Disorders
Pathophysiology
• Nephrotic syndrome is an umbrella term encom-
•
•
passing disorders that result from glomerular
damage. Damage to the basement membrane
results in loss of blood components that would
otherwise remain in circulation.
Large amounts of protein and immunoglobulins
are lost in the urine. Hyperlipidemia and hypertriglyceridemia occur as the liver responds to the
low protein levels. Triglycerides and LDL are also
lost in the urine, to some extent adding to the
frothy appearance.
Protein loss causes loss of intravascular fluid
into the interstitial spaces, but low glomerular
filtration rate still results in hypertension.
Assessment and Diagnostic Findings
• Hypertension, hyperlipidemia, hypertriglyceridemia, loss of antibodies (immunoglobulins).
• Foamy urine.
• Azotemia (increased nitrogenous wastes).
• Hypercoagulability.
Complications
• Thrombosis and embolism.
38
• Generalized edema, CHF, pleural effusion, and
HTN.
• Atherosclerosis.
• Renal failure.
• Infections from loss of immunoglobulins.
Medical Care and Surgical Treatment
• Antihypertensive agents, lipid-lowering drugs,
diuretics.
• Anticoagulant therapy, corticosteroids.
• Sodium and water restrictions; protein is titrated
•
based on serum nitrogenous wastes and estimate of
protein loss in the urine (low to moderate amount).
Dialysis.
Keep in Mind
• Report sudden weight gain or change in mental
or urinary status.
Make the Connection
• Monitor I&O, daily weights, abdominal
circumference, and vital signs.
• Monitor laboratory values for worsening
azotemia and complications of thrombosis.
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Urologic Disorders
39
Polycystic Kidney
Disease
(pol-e-sis-tik kid-ne di-zez)
Clue: Diagnostic or Clinical Findings
Hypertension, headaches, and
hematuria. Ultrasound shows
fluid-filled cysts.
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Urologic Disorders
Pathophysiology
• Hereditary disorder causing cystic formation in
the cortex or medulla of the kidney.
• Cysts may develop from pressure buildup in the
tubules and can progress to the entire kidney.
• Glomerular filtration rate (GFR) decreases.
• Stasis of fluid in the cysts predisposes to repeated
urinary tract infection (UTI).
• Persons with this hereditary disease are at high
risk for aneurysms in the brain and diverticulosis
related to body system formation during the
embryonic period.
Assessment and Diagnostic Findings
• Elevated blood pressure, UTIs and hematuria.
• Ultrasound revealing cysts in the kidney.
• Subjective findings of discomfort in the flank and
lower back.
Complications
• Urosepsis.
• Hypertension.
• Renal failure.
39
• Aneurysm in the brain.
• Diverticulosis in the colon.
• Cyst formation in other organs.
Medical Care and Surgical Treatment
• Antibiotic therapy and antihypertensives.
• Dialysis or renal transplant.
Keep in Mind
• Report signs and symptoms of UTI (frequency,
urgency, pyuria, and hematuria).
• Report change in mental status and prolonged,
severe headache.
Make the Connection
• Remember: Decrease in GFR will result in
hypertension.
• Because this disease is associated with brain
aneurysm, it is important to keep hypertension
under control.
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Urologic Disorders
40
Hydronephrosis
(hi-dro-nef-ro-sis)
Clue: Diagnostic or Clinical Findings
Obstruction of urine outflow from
the kidney related to lithiasis, tumor,
outflow obstruction from the bladder.
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Urologic Disorders
40
Pathophysiology
• Unilateral or bilateral swelling of the renal cap-
•
•
sule from regurgitant urine related to outflow
obstruction. Because the renal capsule is fibrous,
internal functional structures (nephrons) are
destroyed.
Causes may include renal system lithiasis; tumors
of the kidneys, ureters, or bladder; enlargement
of the prostate; or stricture of the urethra.
May occur with continuous bladder irrigation
(CBI) if a clot obstructs outflow of irrigant and
urine or with an obstructed Foley catheter.
•
•
•
removal of tumor, lithectomy, dilation of strictures, careful monitoring of urinary output during
CBI or when an indwelling Foley catheter is in
place).
Nephrostomy tubes and/or stent placement.
Nephrectomy, if necessary.
Antibiotics for repeated UTI.
Keep in Mind
• Report repeated UTI symptoms to the health-care
professional.
• Report flank pain, especially if post-TURP.
Assessment and Diagnostic Findings
• Flank and back pain.
• If insidious onset, urinary tract infections (UTIs)
begin to occur because of urine stasis.
Complications
• Renal failure.
• Urosepsis.
Medical Care and Surgical Treatment
• Removal or mitigation of the obstruction
(transurethral resection of the prostate [TURP],
Make the Connection
• Remember: Monitor intake and output
carefully during CBI.
• As they grow, renal system cancers can physically
obstruct kidney outflow at any point from the
hilus of the kidney to the urethra.
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Urologic Disorders
41
Renal Calculus
(re-nal kal-ku-lus)
Clue: Diagnostic or Clinical Findings
KUB or US shows one or more masses
in the kidneys, ureters, or bladder.
Renal colic in the flank that radiates
downward, nausea, vomiting, and
costovertebral tenderness.
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Urologic Disorders
Pathophysiology
• Men are affected more than women, and stone
•
•
•
•
formation is usually unilateral. Once stones have
formed, repeated formation is likely.
Irritation of the epithelial cells that line the tubules.
Dehydration causes more solute to be present
in the urine.
Persons prone to stone formation may lack
inhibitor proteins and stones may recur.
Small stones (<5 mm) usually are passed in the
urine.
Assessment and Diagnostic Findings
• Repeated urinary tract infection (UTI), hematuria
from stasis of urine.
• Calculi, hydronephrosis, and hydroureter can be
•
•
•
diagnosed by KUB x-ray, retrograde pyelography,
or ultrasound (US).
Renal colic, genital pain, nausea, vomiting, and
diarrhea.
24-hour urine for creatinine clearance.
Urinalysis and urine pH.
Complications
• Hemorrhage and hypovolemic shock.
• Urosepsis.
41
• Hydronephrosis and hydroureter.
• Renal failure with repeated stone formation.
Medical Care and Surgical Treatment
• Nephrolithotomy, pyelolithotomy, lithotripsy,
chemolysis, and nephrostomy tubes.
• Pain medication.
• Dietary changes: increase fluid intake. Acid-ash
diet for calcium, struvite, and calcium oxalate
stones. Calcium added to the diet binds with
oxalates and is eliminated in the stool. Struvite
stones are formed in the presence of infections
and an alkaline environment. Alkaline-ash diet for
uric acid stones.
Keep in Mind
• Stone formation seems to be hereditary. Alter diet
as necessary and force fluids.
Make the Connection
• Monitor for characteristic pain,
hematuria, and repeated UTI.
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Urologic Disorders
42
Rhabdomyolysis
(rab-do-mi-ol-i-sis)
Clue: Diagnostic or Clinical Findings
Azotemia, edema, hypertension,
hematuria, arrhythmias. Common
causative drugs are cholesterollowering agents.
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Urologic Disorders
42
Pathophysiology
• Results from crush injuries (compartment syn•
drome), the toxic effect of drugs or chemicals on
skeletal muscle, extremes of exertion, sepsis,
shock, electric shock, and severe hyponatremia.
Lipid-lowering drugs (e.g., statins, niacin, and/or
fibrates) are among the commonly prescribed
drugs that cause damage to skeletal muscle fibers
that are released into the bloodstream and accumulate in renal tubules.
Assessment and Diagnostic Findings
• Elevated levels of serum or urine myoglobin or
creatine kinase (CK).
• Hematuria, elevated potassium levels, low
calcium levels, and metabolic acidosis.
• Arrhythmias related to altered electrolyte levels.
• Azotemia and decreased glomerular filtration rate
(GFR).
Complications
•
Renal failure and death.
Medical Care and Surgical Treatment
• Hydrate to achieve urine output of between 200
and 300 mL/hr. If urine output does not increase
•
•
•
with hydration, loop and osmotic diuretics are
prescribed to promote diuresis.
Dialysis may be needed if renal failure develops.
Urinary alkalinization with sodium bicarbonate
increases myoglobin solubility in the urine and
assists its elimination from the body. The patient
with rhabdomyolysis should also be monitored
closely for electrolyte disturbances (hypocalcemia, hyperkalemia) and dysrhythmias, with
corrections being made as quickly as possible.
Bedrest throughout the acute illness phase.
Keep in Mind
• Report any muscle tenderness immediately if taking a cholesterol-lowering drug.
Make the Connection
• Monitor closely for electrolyte disturbances
(hypocalcemia, hyperkalemia) and dysrhythmias.
• Remember: Crush injuries may cause renal
failure.
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Urologic Disorders
43
Acute Renal Failure
(a-kut re-nal fal-yer)
Clue: Diagnostic or Clinical Findings
Azotemia, anuria, or oliguria.
Precipitated by severe hypotension,
use of diagnostic contrast dyes, or
structural damage to nephrons.
Elevated K+ and decreased Na+ in
serum. Elevated creatinine and BUN.
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Urologic Disorders
Pathophysiology
• Acute damage to nephrons associated with severe
•
•
•
hypotension, use of contrast dyes, or damage to
skeletal muscle fibers that accumulate in the
nephron tubules.
Three stages: The oliguric stage (less than 400 mL/
24 hr), lasting 2 weeks (better prognosis) to several
months (poor prognosis).
The diuretic phase, characterized by a normal
output of low-quality urine lasting up to a
month. The recovery phase, which may last up to
1 year. The quality of urine in this phase
improves, but full recovery is not guaranteed.
Prerenal conditions are those that decrease perfusion of the kidneys. Intrarenal failure includes
incidents that damage the nephrons.
Postrenal failure is caused by obstruction, resulting in hydronephrosis.
Assessment and Diagnostic Findings
• Hypertension, azotemia, change in LOC,
nausea, vomiting, fatigue, anemia.
• Low urine sodium level (<10 mEq/L).
• CBC showing anemia and platelet dysfunction,
azotemic pericarditis, and acidosis.
43
Complications
• Azotemic encephalopathy; acute renal failure
becomes chronic renal failure.
• Hypertension, CHF, anemia, osteomalacia or
osteoporosis with spontaneous fracture, and pulmonary edema.
Medical Care and Surgical Treatment
• Bedrest; treatment of the underlying cause.
• Restriction of protein intake, fluid, sodium,
•
•
potassium, and phosphorus while in renal
failure.
Erythropoietin injections, antihypertensives,
diuretics, vitamin D supplementation, and
calcium supplements with meals.
Dialysis or transplant.
Keep in Mind
• Hydrate well prior to and following studies using
contrast dyes; report changes in voiding.
Make the Connection
• Renal failure carries with it the
3 Ds—dialysis, donor, or death.
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44
Chronic Renal Failure
(kron-ik re-nal fal-yer)
Clue: Diagnostic or Clinical Findings
History of diabetic nephropathy,
hypertension, glomerulonephritis, or
an autoimmune disease (systemic
lupus erythematosus [SLE]).
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Urologic Disorders
44
frost, sexual dysfunction, and accumulation of
drugs in the body.
Pathophysiology
• Gradual destruction of the nephrons and reduc-
tion of GFR. Acute renal failure, diabetic
nephropathy, and hypertension are the most
common causes, but abnormalities of the kidney,
autoimmune disorders, and chronic infection or
cancer are also causes.
Assessment and Diagnostic Findings
• Hypertension, worsening azotemia, change in
•
•
LOC, nausea, vomiting, fatigue, anemia, electrolyte imbalances, and abnormal DEXA scan.
Low urine sodium level (<10 mEq/L).
CBC showing anemia and platelet dysfunction,
azotemic pericarditis, and acidosis.
Complications
• Increasing azotemia, ESRD, uremic
•
•
•
encephalopathy, and sites for hemodialysis
becoming exhausted.
Infection from peritoneal dialysis (PD) from
peritoneal catheter access (peritonitis).
Infected or clotted hemodialysis shunt or
graft.
HTN, arrhythmias, azotemic pericarditis, peptic
ulcers, change in LOC/coma, pruritus, uremic
Medical Care and Surgical Treatment
• Diet+ high in calories+and ++low in phosphorus,
•
•
•
•
Na , protein, and K ; Ca supplements (PhosLo)
with meals, vitamin D; fluid restriction (titrated).
Hemodialysis or PD-insertion of peritoneal
catheter.
Erythropoietin injections, iron supplements.
Antihypertensives and diuretics.
Kidney transplant.
Keep in Mind
• It is important to know the blood glucose level
and blood pressure to avoid renal complications.
Make the Connection
• Monitor laboratory results; monitor for
peritonitis (cloudy peritoneal return). Check graft
for bruit/thrill.
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Urologic Disorders
45
Overactive Bladder
(o-ver-ak-tiv blad-der)
Clue: Diagnostic or Clinical Findings
Urgency, frequency, and stress
incontinence related to autonomic
and structural anomalies of
the bladder.
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Urologic Disorders
Pathophysiology
• Overactive bladder is thought to be caused by
•
•
excessive parasympathetic impulses to the detrusor muscle of the bladder, initiating the micturition response.
Also, structural anomalies resulting from pelvic
relaxation syndrome decrease the angle of the
bladder, causing undue pressure on the neck of the
bladder and abnormal stretch of the transitional
cells, which again triggers the micturition response.
Neurogenic causes may include chronic neurologic
illnesses (e.g., multiple sclerosis) that unintentionally stimulate motor function and the micturition
reflex arc, making the bladder more active.
Assessment and Diagnostic Findings
• Ultrasound (US) examination of the bladder for
residual urine.
• Endoscopic examination of the bladder.
• Subjective history of stress incontinence, frequency,
and urgency.
Complications
• Incontinence and social inhibition.
• Urinary tract infections, especially if the bladder
is at an abnormal angle due to pelvic relaxation.
45
Medical Care and Surgical Treatment
• Anticholinergics to block parasympathetic
impulses.
• Behavioral modification exercises for bladder
retraining and Kegel exercises.
• Dietary changes to reduce fluids that cause
diuresis; decreased fluid intake prior to bed.
Keep in Mind
• Anticholinergic medications may cause drowsi-
•
•
ness; dry mouth; warm, flushed skin; changes in
vision; and, in some clients, changes in mental
status. Troublesome side effects should be
reported.
Side effects may diminish with time.
Behavioral modification exercises and Kegel
exercises are very effective for this condition.
Make the Connection
• Monitor frequency and urgency.
• Monitor for side effects of anticholinergic
medications (blind as a bat, mad as a hatter,
dry as a bone, red as a beet, and hot as a hen).
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46
Renal Artery Stenosis
(re-nal ar-ter-e ste-no-sis)
Clue: Diagnostic or Clinical Findings
Onset of severe hypertension in the
absence of glomerular disease, renal
failure, or pheochromocytoma.
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Urologic Disorders
Pathophysiology
• Hypertension occurs when the renal artery
•
becomes narrowed and incapable of transmitting
blood to the kidney. The response is activation of
the renin-angiotensin-aldosterone mechanism to
increase vasoconstriction, further increasing the
blood pressure.
Young women usually develop renal stenosis from
fibromuscular dysplasia; older adults develop it
from chronic atherosclerotic disease.
Assessment and Diagnostic Findings
• Computed tomography (CT) scan or magnetic
•
•
resonance imaging (MRI) of the kidney with
contrast.
Duplex ultrasound of the kidney.
Renal artery angiography.
Complications
• Cerebrovascular accident (CVA), retinopathy,
heart disease, vascular disease, and nephropathy
of the uninvolved kidney (if unilateral).
46
Medical Care and Surgical Treatment
• Renal artery angioplasty.
• Medications, especially angiotensin-converting
enzyme (ACE) inhibitors.
Keep in Mind
• Report headache or changes in vision immediately.
• Have blood pressure assessed at every health-care
visit.
Make the Connection
• Structural anomalies must be ruled out
before standard treatment with antihypertensive
agents is begun.
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47
Epididymitis
(ep-i-did-i-mi-tis)
Clue: Diagnostic or Clinical Findings
Painful inflammation of the back
of the testes. The scrotum is
erythematous.
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Urologic Disorders
Pathophysiology
• Infection and inflammation of the epididymis, the
•
•
•
•
tube along the back side of the testes in which
sperm mature and are stored, can be the result of
several events.
In older men, regurgitation of urine from excessive bladder pressure when trying to urinate in
the presence of an enlarged prostate can force
urine into the vas deferens to the epididymis,
causing infections with bacteria such as
Escherichia coli.
Infections with sexually transmitted organisms occur
with frequency in young, sexually active males.
Congenital structural abnormalities in young children predispose them to infection.
Trauma results from excessive pressure exerted on
the epididymis.
47
Complications
• Sexually transmitted diseases (STDs) may persist
and cause infertility and abnormalities in other
organ systems (valvular disease, neurologic deficits).
Medical Care and Surgical Treatment
• Antibiotic therapy.
• Bedrest, scrotal elevation, and ice pack application.
• Oral analgesics and antipyretics.
• Sexual counseling.
Keep in Mind
• Appropriate protection from STD must be used
(condoms).
• Difficulty urinating must be reported to the
health-care provider.
• Scrotal protection should be worn when strenuous
activity resulting in scrotal pressure is planned.
Assessment and Diagnostic Findings
• Scrotum is painful to touch; usually unilateral
involvement. Ambulation is difficult.
• Urinalysis, Gram stain, and urine culture showing
infection.
• Possible pyuria and penile discharge.
Make the Connection
• Assess laboratory results.
• Maintain bedrest in the acute phase, with scrotal
elevation and intermittent use of ice packs.
• Counsel the person with an STD that the sexual
partner must be treated as well.
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48
Benign Prostatic
Hyperplasia
(be-nin pros-tat-ik hi-per-pla-ze-a)
Clue: Diagnostic or Clinical Findings
Difficulty starting or maintaining urinary
stream, dribbling of urine, urgency
and frequency in men approaching or
in the fifth decade of life.
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Urologic Disorders
Pathophysiology
• Enlargement of glandular tissue in the periurethral
•
•
area of the prostate under the influence of testosterone, particularly DHT.
Estrogen is also implicated, as it makes the gland
more susceptible to DHT.
The prostatic urethra narrows as the prostate
gland enlarges, causing partial, or eventually total,
obstruction of urine outflow from the bladder.
Assessment and Diagnostic Findings
• Decrease in urinary stream, difficulty starting the
•
•
flow of urine, frequency and urgency, incomplete
emptying of the bladder, dribbling of urine,
overflow incontinence, and nocturia.
Urinary tract infections from urine stasis; epididymitis from pressure in the bladder forcing
urine into the ejaculatory ducts.
Digital rectal examination for assessment of
enlargement, urinalysis, prostate-specific antigen
(PSA), and serum creatinine level to determine
the level of obstruction.
Complications
• Hydronephrosis, hydroureter, and diverticular
lesions of the bladder from pressure of attempted
voidings.
48
Medical Care and Surgical Treatment
• Alpha-adrenergic antagonists.
• DHT- and testosterone-blocking medications.
• Herbals like saw palmetto.
• TUMA.
• Prostatic balloon dilation.
• Transurethral resection of the prostate (TURP).
Keep in Mind
• Report difficulty passing urine to the health-care
provider.
• Medications used for benign prostatic hyperplasia
(BPH) can cause significant side effects like ↓ BP
or feminization (DHT blockers).
Make the Connection
• If untreated, prostatic enlargement can
cause hydronephrosis and renal failure.
• The PSA test is done serially from age 40.
• If a TURP is done, monitor I&O from the CBI
carefully to prevent postoperative hydronephrosis;
output should exceed instillation amount.
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Bladder Cancer
(blad-der kan-ser)
Clue: Diagnostic or Clinical Findings
Painless hematuria, pelvic pain,
lower back discomfort, and changes
in voiding patterns.
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Urologic Disorders
Pathophysiology
• More common in middle-aged males than in females.
• Strong association with cigarette smoking.
• Exposure to industrial pollutants (e.g., aniline dyes).
• The tumor-node-metastasis (TNM) method of staging the cancer determines prognosis and treatment.
• Over time, dysplastic changes occur in the
urothelium. With chronic irritation, these areas
of dysplasia are replaced by malignant cells. The
cells may form small cancers that remain in the
urothelium or may become invasive and metastatic to the liver, lungs, and bones.
Assessment and Diagnostic Findings
• Urine for cytology; urine culture.
• Intravenous pyelogram (IVP) to assess invasion of
other urinary structures.
• Cystoscopy with biopsy is the only definitive diagnostic method.
Complications
• Hydronephrosis, hydroureter, renal failure, and
hemorrhage.
• Removal of the bladder with urinary diversion
may result in urinary tract infection or sepsis if
not cared for properly.
49
• Metastasis and death.
Medical Care and Surgical Treatment
• Surgery, radiation, chemotherapy, bacille
•
Calmette-Guérin (BCG) bladder instillations to
prevent return of cancer cells.
Surgeries after cystectomy include incontinent urinary diversion, continent urinary diversion using a
Kock pouch, or formation of a neobladder (or
new bladder) using a part of the intestines.
Keep in Mind
• Report blood in the urine immediately.
• If surgery for bladder cancer has been performed
and a urinary diversion is done, care for area
aseptically.
Make the Connection
• Monitor laboratory and urinalysis results
for infections and nitrogenous waste levels.
• Teach client how to care for urinary diversions.
• Explain that incontinence is sometimes a problem
with orthotopic or neobladder formation.
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Prostate Cancer
(pros-tat kan-ser)
Clue: Diagnostic or Clinical Findings
Late symptoms include signs of urinary
obstruction, pain in the lumbar or hip
area, weight loss, and weakness. Urine
outflow may be impaired.
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Urologic Disorders
Pathophysiology
• Prostatic glandular cells mutate and grow under
the influence of testosterone and DHT.
• Prostate cancer late in life is usually slow
growing (↓ testosterone levels).
• Metastatic spread into other urinary and repro•
ductive structures is through lymph and blood
vessels.
The TNM system is used to grade the cancer and
make a prognosis.
Assessment and Diagnostic Findings
• Symptoms are usually late in the disease, so PSA
and DRE should be done in males older than 40.
• Elevated prostatic acid phosphatase.
• Late symptoms include hematuria, signs of
•
urinary obstruction, weight loss, anemia, and
pain in the boney structures of the pelvic girdle.
Definitive diagnosis is made by a transrectal
ultrasound-guided prostatic biopsy.
Complications
• Complications of chemotherapy include nausea,
vomiting, alopecia, hyperuricemia, and bone
marrow suppression; radiation causes burns, skin
breakdown, and scarring of internal tissue.
50
• Metastatic disease.
• Tumors that obstruct urinary outflow and may
result in hydronephrosis and renal failure.
Medical Care and Surgical Treatment
• Testosterone-suppressing medications.
• Radiation therapy (external beam or implanted
radioactive seeds) and/or chemotherapy.
• Radical prostatectomy; TURP.
• Orchiectomy to decrease testosterone levels.
Keep in Mind
• Early detection is key.
• Medications and surgeries may cause feminization and permanent erectile dysfunction.
Make the Connection
• Monitor I&O, calorie count, and stool
characteristics.
• Assess for development of vesicular rash on
knees, elbows, and buttocks.
• Monitor for anemia and bleeding tendencies.
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IMMUNE SYSTEM
Anaphylaxis, 51
Scleroderma, 52
Systemic Lupus Erythematosus, 53
Hashimoto’s Thyroiditism, 54
Sjögren’s Syndrome, 55
Acquired Immunodeficiency
Disease, 56
Kaposi’s Sarcoma, 57
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51
Anaphylaxis
(an-a-fi-lak-sis)
Clue: Diagnostic or Clinical Findings
Sudden onset of wheezing, edema
of airway, hypotension, tachycardia,
feeling of impending doom and
anxiety.
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Immune Disorders
Pathophysiology
• Severe type I hypersensitivity reaction in which
•
IgG antibodies attached to mast cells, previously
sensitized to an antigen, are reactivated. The
most common antigenic material is derived from
foods or insect stings.
Chemical mediators are released, the most
common of which are histamine, proteases,
chemotactic factors, leukotrienes, prostaglandin D,
cytokines, and interleukins 1, 3, 4, 5, and 6). These
mediators cause vasodilation and fluid shift from
the intravascular to the interstitium.
Assessment and Diagnostic Findings
•
•
Erythema, angioedema, urticaria (hives),
stridor, wheezing, decrease in BP, and
increase in pulse.
Change in level of consciousness, drowsiness.
Complications
• Shock, respiratory and cardiac failure.
• Renal ischemia.
51
Medical Care and Surgical Treatment
• Emergency care includes use of an EpiPen.
• IV fluids, IV vasopressors, corticosteroids,
•
•
epinephrine, antihistamines, and histamine 1
(H1)-receptor and H2-receptor blockers.
Supplemental oxygen will be needed and airway
support.
Electrocardiogram (ECG) monitoring.
Keep in Mind
• Teach that severe allergy an occur at any time after
first occurance.
• Families with a member who has food or other
allergies should have an EpiPen on hand.
Make the Connection
• Anaphylaxis causes shock. Remember:
shock = ↓ BP, ↑ pulse.
• Remember: ↓ HOB, ↑ legs. Keep client warm.
• Start an IV for fluid and drug administration.
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Immune Disorders
52
Scleroderma
(skler-a-der-ma)
Clue: Diagnostic or Clinical Findings
Taut face without wrinkles. Calcium
deposits. + ELISA for ANA and
other antibodies. Raynaud’s
phenomenon.
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Immune Disorders
Pathophysiology
• An autoimmune disease.
• Women are affected more often than men;
•
•
disorder often has periods of exacerbation and
remission.
The skin, connective tissue, and internal organs
are affected. Insoluble collagen is overproduced
and deposited in the skin and other organs, causing inflammation. Inelastic rather than supple
edema results. A common finding is “stone face,”
which is the result of this hardening of the skin.
There is a strong association (95%) with
Raynaud’s phenomenon.
Assessment and Diagnostic Findings
• Pitting edema of the upper extremities followed
by tightening of the tissue.
• The face will have no wrinkles.
• Arthritis and decreased range of motion occur.
• The kidneys, lungs, heart, and gastrointestinal
tract are also affected.
• Skin biopsies and ELISA testing for anti-Scl-70
and anticentromere antibodies.
• Kidney function tests, pulmonary function tests,
electrocardiogram, and x-ray studies.
52
Complications
• CREST syndrome: calcinosis (calcium deposits),
•
Raynaud’s phenomenon, esophageal immotility,
sclerodactyly, and telangiectasia.
Dysphagia and aspiration risk; pneumonia and
desaturation of blood from lung noncompliance;
arrhythmias; and necrosis of fingertips, toes, and
nose from Raynaud’s vasculitis.
Medical Care and Surgical Treatment
• Immunosuppressants.
• Vasodilating agents.
• Careful and consistent physical therapy and
occupational therapy.
• Extremities must be kept warm.
Keep in Mind
• Report any signs of illness (e.g., sore throat) immediately.
• Physical activity helps to keep the body supple. Be as
independent as possible.
Make the Connection
• Scleroderma presents a body image
problem, so psychological counseling is essential.
• Monitor lung, renal, and cardiac function.
• Passive and active ROM.
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Immune Disorders
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Systemic Lupus
Erythematosus
(sis-tem-ik lu-pus er-i-the-ma-to-sis)
Clue: Diagnostic or Clinical Findings
Butterfly rash, arthritis, malaise,
Raynaud’s phenomenon, peripheral
neuropathy, change in vision and
renal status; round lesions on head
cause hair loss.
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Immune Disorders
Pathophysiology
• Immune system antibodies attack “self.” Females
•
•
are affected more than males. A hereditary predisposition exists.
Discoid lupus causes skin plaques that tend to
occur on the face, ears, and hair. Wherever they
appear, the area is inflamed and becomes scarred.
Alopecia results in affected areas in the hair.
Systemic lupus erythematosus (SLE) causes
changes in the dermatologic, cardiovascular,
musculoskeletal, hematologic, gastrointestinal,
renal, and ophthalmologic systems—all related to
inflammation from overreaction of the immune
system.
53
• Peritonitis from chronic inflammation and scarring of abdominal and intestinal vasculature.
• Visual changes or blindness.
• Severe arthritic changes.
Medical Care and Surgical Treatment
• Antirheumatics and tumor necrosis factor
inhibitors.
• Corticosteroids and other immunosuppressants.
Keep in Mind
• Teach signs of heart disease, like SOB.
• Teach signs of kidney inflammation.
• Eat a healthy diet, stay active, get adequate rest,
and wear a MedicAlert bracelet.
Assessment and Diagnostic Findings
• ELISA for SLE-specific antibodies; antinuclear
antibody (ANA); and nonspecific inflammatory
studies, like complete blood count with differential (CBC with diff), erythrocyte sedimentation
rate, and kidney function tests.
Complications
•
•
•
Myocarditis, myocardial infarction, and pericarditis.
Renal failure.
Thrombocytopenia, anemia.
Make the Connection
• Monitor laboratory results and clinical
•
condition. Refer to a rheumatologist if butterfly
rash and arthritis occur.
Immunosuppressant therapy puts the client at
risk for infection and pseudodiabetes.
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Immune Disorders
54
Hashimoto’s Thyroiditis
(ha-she-mo-toz thi-royd-i-tis)
Clue: Diagnostic or Clinical Findings
Goiter, periods of insomnia, anxiety,
muscle and joint aches, weight
changes, hair loss, and fertility
problems that are mixed symptoms
of hyper- and hypothyroidism.
TSH may be normal or elevated.
T3 and T4 are low.
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Immune Disorders
Pathophysiology
• Usually a disease of older women with a history
of autoimmune disease.
• Autoantibodies are produced to fight TSH. TSH
•
•
is not destroyed and instead binds with its receptors in the thyroid gland, causing symptoms of
hyperthyroidism.
As the thyroid gland becomes infiltrated with
lymphoid tissue and plasma cells it enlarges and
hypothyroidism occurs.
Episodic hyperthyroidism can occur, so symptoms may swing back and forth from hyperthyroidism to hypothyroidism.
Assessment and Diagnostic Findings
• Elevated levels of serum TG antibodies and TPO
•
•
•
54
• Fatigue, depressive illness, and mental dullness.
• Anorexia, constipation, facial puffiness, and
dry skin.
Medical Care and Surgical Treatment
• Evidence shows that low-dose thyroid hormone
therapy may reduce destruction of the thyroid
gland.
Keep in Mind
• Report any signs of chest pain when therapy
•
•
using immunofluorescent assay. TSH may be
elevated or normal. T3 and T4 levels ↓.
Needle biopsy of the thyroid.
↑ RAIU.
Visible goiter or enlarged thyroid gland on US.
Complications
• Atherosclerosis, bradycardia, hypotension, and
chest pain.
begins. It takes a few weeks for the drug to
reduce symptoms.
Report any thoughts of suicide.
Stay active and follow a low saturated-fat diet.
Make the Connection
• Remember: Starting thyroid replacement
•
hormones with a sluggish heart can precipitate an
angina attack or myocardial infarction. Monitor
the client’s electrocardiogram.
Adjust dietary regimen as condition changes.
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Immune Disorders
55
Sjögren’s Syndrome
(sho-grenz sin-drom)
Clue: Diagnostic or Clinical Findings
Blurred vision, thick secretions,
decreased sense of taste, dysphagia,
xerostomia, and dry nasal membranes.
Antiribonucleoprotein serum antibodies
and + rheumatoid factor in the absence
of rheumatoid arthritis.
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Immune Disorders
Pathophysiology
• Autoimmune illness in which the lacrimal and
•
•
•
salivary glands are attacked by autoantibodies
and T lymphocytes.
Can occur alone or with other autoimmune
diseases.
Occurrence is mainly seen in older women.
Sjögren’s syndrome is associated with a 40%–60%
increase in the chance of developing non-Hodgkin’s
lymphoma.
Assessment and Diagnostic Findings
• Blurred vision, burning and itching of the eyes,
•
•
•
•
Schirmer’s test (ability to wet a test strip placed
under the eyelid).
Decreased sense of taste; thick secretions; dysphagia; dry, cracked oral mucous membranes;
enlarged parotid glands; lower lip salivary
biopsy.
Dry nasal membranes, thick secretions in the
bronchi and lungs.
Synovitis, vaginal dryness with frequent Candida
infection, and vasculitis.
Anemia, leukopenia, and elevated ESR.
55
Complications
•
Corneal abrasion, choking, pneumonia,
anorexia, non-Hodgkin’s lymphoma, dyspareunia, tachycardia, and primary biliary cirrhosis.
Medical Care and Surgical Treatment
• Artificial tears, cyclosporine eye drops, effective
•
and thorough mouth care, sugarless gum or
candies, sips of water, a cholinergic preparation
to induce salivation, and artificial saliva.
Antimalarials and immunosuppressants.
Keep in Mind
• Report xerostomia, dysphagia, and chronic
dry eye.
Make the Connection
• Observe ability to swallow.
• Protect eyes from excessive dryness to prevent
corneal abrasion.
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Immune Disorders
56
Acquired
Immunodeficiency Disease
(a-kwird im-u-no-de-fish-en-se di-zez)
Clue: Diagnostic or Clinical Findings
Lymphadenopathy, night sweats, and
presence of rare opportunistic illness.
T-helper (CD4) cells <500 cells/mm3,
T-killer (cytotoxic) (CD8) cells
<375 cells/mm3, change in the
CD4/CD8 ratio (normal 0.9–1.9),
and measurable viral load.
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Immune Disorders
Pathophysiology
• Macrophages process foreign antigens and present antigenic material to the T-helper cells (CD4).
• The CD4 transfer this information to the T and
•
B lymphocytes. In HIV, a retroviral particle
(RNA strand) wrapped in a glycoprotein coat
(gp120 receptor) with p24 viral protein invades
the CD4 cell. The CD4 cell and macrophage are
the immune cells affected and destroyed.
Once the CD4 cell count drops below
200 cells/mm3, the client is diagnosed with
AIDS. Other diagnostic criteria include the
presence of an opportunistic infection.
Assessment and Diagnostic Findings
• CD4 and CD8 counts, CD4/CD8 ratio abnormality,
and viral load.
• GI wasting through opportunistic diarrheal
•
•
infection and by alterations in enteral epithelial
function by the viral particles.
AIDS dementia complex.
Opportunistic disease; ELISA is repeated after one
positive result and confirmed by Western blot
analysis.
56
Complications
• Kaposi’s sarcoma and lymphomas, AIDS
dementia, fungal meningitis, and tuberculosis.
• Pneumocystis carinii pneumonia, Mycobacterium
avium complex, and other pneumonias.
• Septicemia, toxoplasmosis, cytomegalovirus
retinitis, cervical cancer and Candida infections,
GI infections, and wasting.
Medical Care and Surgical Treatment
• HAART, fusion inhibitors (injectable only), and
•
integrase inhibitors. Monotherapy with a nucleoside transcriptase inhibitor is administered only
during pregnancy and the neonatal period.
Once an opportunistic infection occurs, prophylactic treatment is added to the daily medical regimen.
Keep in Mind
• Avoid smoking, unprotected sex, and organic
foods, and take medications as ordered.
Make the Connection
• Monitor CD4/CD8 ratios, viral load, and
presence of opportunistic infection.
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57
Kaposi’s Sarcoma
(kap-o-sez sar-ko-ma)
Clue: Diagnostic or Clinical Findings
Red-to-purple macules, papules,
and nodules seen in persons with
AIDS. First seen usually on the
mucous membranes.
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Immune Disorders
Pathophysiology
• A rare lymphatic malignancy of the endothelial,
•
•
•
rather than connective, tissue characterized by
red-to-purple macules, papules, or nodules.
Lesions are first seen on the skin or mucous
membranes but may involve the internal
organs.
A rare cancer commonly related to AIDS.
In patients with AIDS, KS is believed to be
sexually acquired by infection with the human
herpesvirus 8.
57
Medical Care and Surgical Treatment
• Chemotherapy and radiation treatment, biotherapy
•
Keep in Mind
• Do not have unprotected sex, as this cancer may
•
Assessment and Diagnostic Findings
• Classic form is found on the lower extremities
•
and dorsal area of the feet. The type associated
with AIDS is found on the upper extremities and
on the mucous membranes.
Biopsy provides the only definitive diagnosis.
Complications
• Damage to organ systems by metastasis.
• Overgrowth and blockage of lymph, blood
vessels, gastrointestinal and accessory tract,
and organ exocrine function.
(interferon alfa-2b), cryotherapy, and hormone
therapy.
Treatment with HAART.
be spread in this way and there are many strains of
human immunodeficiency virus that can be spread.
Do not smoke, as many infective organisms can
be present in cigarette paper.
Make the Connection
• Monitor complete blood cell count and
•
•
•
uric acid level during chemotherapy to assess for
bone marrow suppression and hyperuricemia.
Assess the skin (portal of entry and portal of exit)
during radiation therapy.
Provide reverse isolation if leukopenic; avoid fresh
flowers and organic foods.
Counseling.
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MUSCULOSKELETAL
Osteoarthritis, 58
Gouty Arthritis, 59
Rheumatoid Arthritis, 60
Osteoporosis, 61
Osteomalacia, 62
Osteomyelitis, 63
Paget’s Disease, 64
Sprain, 65
Fracture, 66
Compartment Syndrome, 67
Total Joint Replacement, 68
Herniated Nucleus Pulposus, 69
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Osteoarthritis
(os-te-o-ar-thri-tis)
Clue: Diagnostic or Clinical Findings
Pain and stiffness in the weightbearing joints and the vertebral
column due to wear and tear
or obesity.
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Pathophysiology
• The matrix of cartilage is composed of chondro•
cytes imbedded in proteoglycan molecules, which
are large and osmotic, drawing fresh synovial
fluid into the joint.
With excess wear and tear, the chondrocytes
become inflamed and release inflammatory mediators (cytokines), causing a cascade of events that
includes formation of protease, which break down
the proteoglycan molecules. Eventually, the cartilage becomes worn and misshaped. Streaks and
dents in the cartilage become cracks. Synovial
fluid leaks into the underlying bone, causing cysts.
The underlying layer of the cartilage can no longer
be an effective shock absorber. Bone spurs form.
Assessment and Diagnostic Findings
• Pain with or following activity that subsides with
rest. More likely to occur after age 40.
• CT scan or MRI scan are diagnostic.
• Arthroscopy may be done to both diagnose and
treat articular and bony malformations.
Complications
• Ankylosis of joints, with resulting immobility and
chronic pain.
58
• Heberden’s and Bouchard’s nodes, which are
painful nodes in the fingers.
• Vertebral osteoarthritis can result in muscle
spasm and pressure on nerves.
Medical Care and Surgical Treatment
• Anti-inflammatory and immunosuppressants like
DMARDs and TNF-I.
• Muscle relaxants and application of cold and
heat therapy.
• Joint replacement surgery, if necessary.
Keep in Mind
• Walking and swimming can replace high-impact
exercise. Weight loss is necessary if obese.
• Take anti-inflammatory agents with food, and
report any signs of infection immediately.
Make the Connection
• Inactivity should never be advocated.
Clients should know that if you don’t use it, you
lose it.
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Gouty Arthritis
(gowt-e ar-thri-tis)
Clue: Diagnostic or Clinical Findings
Acute pain and swelling in a joint,
usually the great toe (unilaterally).
High serum uric acid levels.
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Musculoskeletal Disorders
Pathophysiology
• In gouty arthritis, uric acid crystals are deposited
in the joints and other connective tissues. The
concentration in synovial fluid is higher than in
plasma, so the crystals cause excessive inflammation in the joint. Joints affected are usually those
at the distal area of the body, as uric acid crystals
are affected by gravity. Called “the rich man’s disease” because many of the foods that contain
purines are considered those consumed by the
wealthy.
Assessment and Diagnostic Findings
• Hyperuricemia, high-purine diet, painful joints,
and possible gouty lesions near joints.
• Attacks of gout precipitated by excessive alcohol
•
ingestion, dehydration, illness/stress, and medications like diuretics, aspirins, cyclosporine, levodopa, aminophylline, niacin, and antibiotics
used to treat tuberculosis.
Arthroscopy with joint fluid aspiration for uric
acid crystals and white blood cells.
Complications
• Pain and immobility during acute attacks.
59
• Soft nontender tophi can occur on the extremities
•
near joints. These may become open sores (ulcers)
if the skin is not cared for properly.
Possible uric acid kidney stone formation.
Medical Care and Surgical Treatment
• Anti-inflammatory agents, uricosuric agents,
and probenecid; increasing daily fluid intake to
2,000–3,000 mL.
Keep in Mind
• Avoid aspirin and diuretics as well as high-purine
foods.
• Consume alcohol in small amounts, if at all.
• Find healthy outlets for stress.
Make the Connection
• Remember: Gouty arthritis is very painful. Give
anti-inflammatory drugs, such as colchicine.
• Force fluids, and teach the client the importance
of remaining hydrated.
• Monitor uric acid levels, and assist the client in
choosing low-purine foods and drugs.
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Rheumatoid Arthritis
(roo-ma-toyd ar-thri-tis)
Clue: Diagnostic or Clinical Findings
Swan neck deformity or ulnar
deviation of the metacarpophalangeal
joints. Fatigue, flu-like symptoms
may accompany exacerbations of
the disease. Elevated ESR; RF and
CCP antibodies present.
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Musculoskeletal Disorders
Pathophysiology
• Rheumatoid arthritis is a systemic disease known
•
•
•
•
to be genetic and autoimmune in nature. Women
are affected more than men.
Rheumatoid factor (RF) antibodies react with
IgG, forming immune complexes in the body
and in the synovial joints.
Granulocytes phagocytize the immune complexes
and release toxins into the tissue and into the
joints.
Synovitis occurs as well as increased formation of
blood vessels in the synovial walls, which contributes to production of vascular pannus.
The area of inflammation is “walled off” in an
attempt to heal injured tissue causing more
immobility and destruction.
Assessment and Diagnostic Findings
• Presence of RF, anti-CCP antibodies,
WBC elevation, and ↑ ESR.
• Synovial fluid examination reveals a significant
number of neutrophils.
• Low-grade temperature, flu-like symptoms,
bilateral joint inflammation, joint deformities
like swan neck deformity, and nodal formation.
60
Complications
• Pain, joint deformity, ankylosis, and immobility.
• Vasculitis, scleritis, pulmonary and cardiac
inflammation, and leukopenia.
Medical Care and Surgical Treatment
• Salicylates, NSAIDs, gold salts, TNF inhibitors,
DMARDs, and corticosteroids.
• Surgery for joint replacement.
• Physical and occupational therapy to maintain
function.
Keep in Mind
• Take all anti-inflammatory agents with food.
Report any signs of infection immediately.
Make the Connection
• Monitor CBC for signs of infection while
on anti-inflammatory agents.
• Assist with ROM exercises to maintain function.
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Osteoporosis
(os-te-o-por-o-sis)
Clue: Diagnostic or Clinical Findings
Loss of bone density (by DEXA scan)
seen mainly in females who weigh
less than 140 lb at menopause and
have never used estrogen-replacement
therapy. The mnemonic is ABONE
(A = age, B = bulk, ONE = one never
on estrogen).
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Musculoskeletal Disorders
Pathophysiology
• Healthy bone is living tissue that is dynamic in
•
•
nature. Osteoclasts resorb bone, while osteoblasts
lay down new bone. In this way, healthy bone is
always remodeled. Bone remodeling occurs under
the influence of hormones and from normal body
movement and weight-bearing activities.
At menopause, estrogen withdrawal causes
inflammatory mediators and immune cells that
encourage the differentiation of osteoclasts and
increase their life span. Osteoblasts, or bone
creators, are less active.
As osteoporosis progresses, this trabecular framework is diminished and may be totally resorbed.
Bone density decreases.
61
and prolonged immobility.
• DEXA scan of the hip, spine, and first four vertebrae; serial heights; US of bone; and CT scan.
Complications
• Falls resulting in hip fracture.
• Pathologic fractures.
Medical Care and Surgical Treatment
• SERMs, biphosphonates, calcitonin hormone,
and recombinant human parathyroid hormone.
• HRT Weight-bearing exercise.
• Calcium and vitamin D supplements.
Keep in Mind
• The client with confirmed osteoporosis should
Assessment and Diagnostic Findings
• Risk factors include Caucasian or Asian ancestry,
postmenopausal status, weight of less than 140 lb
at menopause, sedentary lifestyle, history of
rheumatoid arthritis, low calcium and vitamin D
consumption, excessive alcohol consumption,
smoking and caffeine intake. Secondary risks are
associated with endocrine imbalance, steroid use,
sleeping tablets, cancer treatment, kidney disease,
•
•
wear well-fitting shoes (no slip-ons) and clear all
clutter (e.g., throw rugs) from walking areas.
Assistive devices (e.g., walkers) may decrease the
chance of falls and fractures.
Teach importance of DEXA scan.
Make the Connection
• Give calcium with meals. Observe for
esophagitis related to SERM therapy.
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Osteomalacia
(os-te-o-mal-a-she-a)
Clue: Diagnostic or Clinical Findings
Softening of bone causing bowed
legs in children and soft or brittle
bones in adults. Bone pain is often
present with muscle weakness.
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Musculoskeletal Disorders
Pathophysiology
• Bone mineralization is diminished because of lack
of calcium or vitamin D.
• Vitamin D absorbed by exposure of the skin to
•
•
sunlight must be activated by two organs, first
the liver and then the kidney. Any disorders of
these organs decreases vitamin D availability.
The disease is more prevalent in women because
of their increased need for calcium.
Osteomalacia is seen more frequently in persons
with low sun exposure.
Assessment and Diagnostic Findings
• X-ray (sometimes showing transverse pseudo-
fractures believed to be stress fractures that
have not been remodeled), laboratory tests for
serum calcium and phosphorus, bone scan, and
bone biopsy.
Complications
• Deformity of bone and teeth.
• Change or closure of the epiphyseal growth plate
in children, resulting in stunted growth.
• Muscle weakness.
62
Medical Care and Surgical Treatment
• Treatment of the underlying condition.
• Biliary disease may require that pancreatic
•
enzymes be given to absorb vitamin D and
calcium from the diet.
In renal disease, supplemental calcium, phosphate binders, and vitamin D supplements are
used.
Keep in Mind
• Moderate exposure to the sun with skin SPF 15
sunscreen.
• Dietary intake of supplemented foods, like dairy
products and dark green leafy vegetables. Visit
choosemyplate.gov
Make the Connection
• Monitor laboratory values; do serial
height and gait assessment.
• Bracing of upper and lower extremities may be
necessary in severe cases.
• Monitor for scoliosis and other vertebral
abnormalities.
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Osteomyelitis
(os-te-o-mi-el-i-tis)
Clue: Diagnostic or Clinical Findings
Increased temperature with pain and
inflammation over the affected bone;
elevated WBC and ESR. Bone biopsy
positive for infection.
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Musculoskeletal Disorders
Pathophysiology
• Bone infection with microorganisms that can
•
•
occur in compound fracture as well as in surgical
intervention (direct inoculation), spread from
surrounding tissue (e.g., cellulitis [contiguous
spread]), and infection of the bone from sepsis
(hematogenesis).
When the bone becomes infected, the inflamed
area forms an abscess that impairs blood flow to
the intramedullary area. Bone death occurs, the
periosteum peels away from the ostium, and
dead bone (sequestrum) forms. The sequestrum
can fall from the bone, causing more pressure
and decreased blood flow to other boney areas.
Sinuses commonly form that allow pus and
debris to escape from the bone to the outer skin.
Assessment and Diagnostic Findings
63
Complications
• Amputation of the affected limb to decrease the
chance of death from septic shock.
• Repeated surgical procedures to remove diseased
bone (sequestrectomy).
Medical Care and Surgical Treatment
• IV and oral antibiotic therapy for long periods of
time.
• Sterile wound dressing changes.
• Sequestrectomy.
Keep in Mind
• Avoid osteomyelitis by carefully controlling blood
•
glucose levels and checking the feet each evening
for pressure areas.
Report any sore areas where a soft tissue injury
has occurred.
• History and physical, x-ray, complete blood count
•
(CBC), elevated erythrocyte sedimentation rate
(ESR), positive bone biopsy for infection, positive
blood culture, magnetic resonance imaging
(MRI), and computed tomography (CT) scan.
A history of diabetic foot ulcers and cellulitis is
considered a risk factor.
Make the Connection
• Teach clients the importance of tight
•
glycemic control and to check for ill-fitting shoes,
dentures, and other prosthetics.
Assess sites of infection carefully; monitor CBC
and ESR.
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Paget’s Disease
(paj-ets di-zez)
Clue: Diagnostic or Clinical Findings
Enlarged bone mass and deformity of
the femur, skull, vertebrae, or pelvis,
usually in older adults. Increased
serum ALP, increased urine
hydroxyproline (measured by Pyrilinks
and Osteomark), increased urine
and serum calcium.
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Musculoskeletal Disorders
Pathophysiology
• A disease of older adults in which osteoclastic
•
•
•
activity is followed by an exaggerated response by
osteoblasts resulting in enlargement of bone.
There are three phases: (1) the active phase
(reabsorption); (2) the mixed phase (osteoblast
activity); and (3) the inactive phase, in which the
osteoblastic phase has exceeded the osteoclastic
activity.
Increased vasculature around the bones.
The femur, skull, vertebrae, and pelvis are most
often affected.
Assessment and Diagnostic Findings
• X-ray showing enlargement and deformity of
bone.
• Nuclear bone scans showing “hot spots” of
abnormally rapid bone cell turnover that appear
overgrown or have a mosaic pattern; increased
ALP. Pyrilinks and Osteomark urine tests, which
measure markers of bone resorption, are elevated
in Paget’s disease.
Complications
• ↓ cardiac output related to vasodilation.
• Pain and deformities.
64
• Nerve palsies.
• Calcified aortic stenosis.
• Decreased rib cage compliance and
pneumonia.
Medical Care and Surgical Treatment
• Calcitonin, biphosphonates, and
•
•
anticancer/antibiotic agents (e.g., plicamycin) to
suppress osteoclasts and osteoblasts.
Anti-inflammatory agents.
Analgesics.
Keep in Mind
• Report pain level on a 0–10 scale and any
dizziness or dyspnea.
• Report any bleeding of the gums or from any orifice while under treatment.
Make the Connection
• Monitor CBC for low platelet level with
plicamycin therapy.
• Titrate analgesic levels to keep pain level <3.
• Monitor serum and urine studies to assess
effectiveness of therapy.
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Sprain
(sprane)
Clue: Diagnostic or Clinical Findings
Pain, swelling, and heat around
a recently injured joint, usually
the ankle.
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65
Pathophysiology
• The ligaments, the strong connective tissue bands
•
that secure bone to bone, are affected. The most
likely joint is the ankle.
The ligaments may be slightly torn or completely
torn with disconnection from and a piece of the
bone attached to the torn ligament.
Assessment and Diagnostic Findings
• Rapid swelling and pain of the joint.
• Limited ability to function.
• X-ray, necessary to differentiate a sprain from a
fracture, is done usually after the extremity
swelling has diminished.
Complications
• Poor healing with change in range of motion.
Medical Care and Surgical Treatment
• RICE method: rest the extremity; apply ice to
decrease swelling; confine or compress the
•
•
extremity by using an ACE wrap, cast, or brace;
and elevate the extremity to decrease tissue
edema.
Assistive devices are necessary for mobility.
Muscle relaxants or anti-inflammatory agents may
be used.
Keep in Mind
• Keep the injured area elevated as much as
possible and avoid weight bearing.
• Allow time for adequate repair.
Make the Connection
• Sprains have to be assessed for a fracture
being present.
• Remember: Ligaments hold bone to bone;
tendons hold muscle to bone (more involved
in strains).
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66
Fracture
(frak-chur)
Clue: Diagnostic or Clinical Findings
Tenderness, pain, or deformity over
an area of injury. Crepitation may
be heard or felt; range of motion
is decreased.
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Musculoskeletal Disorders
Pathophysiology
• Healthy bone is living tissue that is dynamic in
•
•
•
•
nature. Osteoclasts resorb bone, while osteoblasts
lay down new bone. In this way, healthy bone is
always remodeled.
A fracture is a disruption in the bone structure
caused by trauma or pathology.
Closed fractures do not disrupt the integrity of the
skin; open fractures are called compound because
they break through the skin as well as disrupt the
integrity of the bone.
Fracture types are comminuted, impacted, greenstick, oblique, longitudinal, and transverse.
Fractures heal by forming a blood clot at the site and
attracting cells to the site. The fracture site is known
as a callus at week 1, and by week 6, osteoclasts have
resorbed dead bone and osteoblasts have remodeled
the site. Complete healing is usually in 1 year.
Assessment and Diagnostic Findings
• X-ray, CT scan, and MRI.
• CBC++ to assess blood loss internally or externally.
• CA and ESR to assess tissue damage.
Complications
• Fat embolism.
66
• Infection, neurologic damage, compartment
syndrome, and thrombophlebitis.
Medical Care and Surgical Treatment
• Analgesics, skin traction using balanced traction
or an external fixator.
• ORIF.
• Closed reduction.
• Electrical stimulation and bone grafting in cases
in which the bone does not mend.
Keep in Mind
• If a fall involves the hip, report deep groin pain in
the absence of x-ray data (a positive sign).
• Report any unusual smells from a cast; do not
scratch under the cast.
Make the Connection
• Monitor vital signs for signs of infection,
petechial hemorrhage, or dyspnea.
• Watch for color, motion, and sensitivity and
“palm” cast.
• Encourage mobility exercises for the unaffected
side to combat thromboembolism.
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67
Compartment Syndrome
(com-part-ment sin-drom)
Clue: Diagnostic or Clinical Findings
Neurovascular assessment of injured
area, usually by crush injury or
fracture, includes severe pain,
pallor, pulselessness, paresthesia,
paralysis, and coolness to
the touch.
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Musculoskeletal Disorders
Pathophysiology
• In a traumatic injury (e.g., fractures caused by
•
•
automobile accident or crush injury), soft tissue
swelling occurs. The soft tissue in this case is the
muscle. Every muscle compartment is surrounded
by connective tissue called fascia.
Fascia compresses the swelling tissue, causing
loss of vascularity to tissue and nerves. The muscle tissue is essentially being strangled in its own
covering.
Less problematic compartment syndrome is seen
in exertional compartment syndrome and stress
fracture.
67
• Rhabdomyolysis and renal failure.
• Infection.
Medical Care and Surgical Treatment
• Restoring blood flow by performing a fasciotomy.
Once pressure is relieved and the swelling goes
down, the fascia and skin are closed. Skin grafting may be required.
Keep in Mind
• Report excessive pain after any sports injury.
• Report skin that is cool to the touch distal to any
wrap or cast.
Assessment and Diagnostic Findings
Make the Connection
• Neurovascular assessment of injured area, usually
•
by crush injury or fracture, includes severe pain,
pallor, pulselessness, paresthesia, paralysis, and
coolness to the touch.
Excessive pain is the first clue.
• Time is muscle. Is it important to
•
Complications
• Necrosis of the affected tissue.
• Paralysis of the extremity.
• Volkmann’s contracture.
•
recognize compartment syndrome to prevent
complications and deformity.
Remember: When muscle fibers are injured, they
may gain access to the bloodstream and filter
into the nephrons, causing renal failure.
Watch for signs of infection in the area of the
fasciotomy or graft.
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68
Total Joint Replacement
(to-tal joint re-plas-ment)
Clue: Diagnostic or Clinical Findings
Replacement of the femoral head
and placement of an acetabular cup
(THR) (hip), or replacement of the
femoral and tibial ends of the knee
by metal and the knee cap by a
button (TKR).
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Musculoskeletal Disorders
Pathophysiology
• Persons with problems like chronic osteoarthritis
pain, avascular necrosis of the femoral head, or
systemic lupus erythematosus (SLE) cannot perform activities of daily living (ADLs) and require
the joint be replaced by prosthetic devices.
Assessment and Diagnostic Findings
• Preoperatively, the client exhibits severe decrease
in range of motion and increased pain with ADLs.
• Baseline neurovascular assessment is performed.
• Postoperatively, the complete blood count (CBC)
•
is monitored for blood loss and infection; neurovascular assessments are done every 4 hours.
Total hip replacement (THR) clients have legs
abducted and may not sit with hips flexed at
greater than a 90-degree angle. Total knee
replacement (TKR) clients have the affected leg
(legs) in continuous passive motion (CPM)
machines, which move the knee to greater angles
as directed by the orthopedist.
Complications
• Thrombophlebitis and embolism.
• Infection.
• Hip or knee dislocation.
68
• Sepsis in the joint or blood.
• Skin breakdown.
• Hemorrhage.
Medical Care and Surgical Treatment
• Prophylactic antibiotics.
• Blood transfusion if necessary (autologous
replacement if possible).
• Analgesia.
• Assessment of neurovascular status.
• Assessment of neurologic status in the elder adult.
• Flowtron boots or compression stockings; early
ambulation (non–weight-bearing).
Keep in Mind
• Teach THR clients to not cross their legs or sit at
greater than a 90-degree angle.
• Report pain or chills immediately.
Make the Connection
• Monitor CBC for hemorrhage and infection.
• Monitor and report the neurovascular status of
the affected leg distal to the surgery.
• Remember that orthopedic surgery is very bloody,
so the need for transfusion exists.
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69
Herniated Nucleus
Pulposus
(her-ne-at-ed nu-kle-us pul-po-sis)
Clue: Diagnostic or Clinical Findings
Pain and numbness in the arm or
headaches on the affected side
(cervical), or pain and numbness
radiating down the sciatic nerve
in the leg (lumbar).
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Musculoskeletal Disorders
Pathophysiology
• The vertebrae have cushions or intervertebral
•
•
disks between them to absorb shock and to keep
the nerve roots away from the boney areas.
Disks can herniate out of the normal position,
and the annulus fibrosus tears. The inner portion
(nucleus pulposus) pushes outward and places
pressure on a nerve root.
The most common sites are the cervical and
lumbar areas.
Assessment and Diagnostic Findings
• Cervical disk herniation causes numbness and tin•
•
gling in the affected arm, neck spasm, pain, and
(in some cases) migraine headache.
Lumbar disk herniation causes numbness, pain,
and tingling in the affected leg. Muscle spasm is
common. Heel-toe walking is not possible
because of discomfort. Severe herniation is the
only type that would cause incontinence.
MRI, with and without contrast, will show
herniation of the disk.
Complications
• Hemorrhage, nerve root damage, and reherniation, and altered mobility after surgery.
69
• Infection after surgery.
Medical Care and Surgical Treatment
• Analgesics, muscle relaxants, physical therapy,
•
minimally invasive balloon vertebroplasty, TENS
unit, skin traction, and corticosteroid injections
directly into the disk area.
Surgical laminectomy (frontal approach for
cervical, posterior approach for lumbar).
Keep in Mind
• Report any numbness or problems with mobility
after surgery.
• Report chills or other signs of infection.
• Spinal fusions will limit range of motion.
Make the Connection
• Monitor neurovascular status of the
•
•
arms (cervical surgery) or of the legs, bladder,
and bowel (lumbar surgery).
Log-roll the client after surgery.
Monitor CBC and ability to perform ADLs
without pain.
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NERVOUS SYSTEM
Meningitis, 70
Concussion, 71
Skull Fracture, 72
Epidural and Subdural Hematoma, 73
Huntington’s Disease, 74
Spinal Cord Injury, 75
Autonomic Dysreflexia, 76
Spinal Shock, 77
Cerebral Aneurysm, 78
Tonic-Clonic Seizures, 79
Absence Seizures, 80
Myoclonic Seizures, 81
Atonic Seizures, 82
Simple Partial Seizures, 83
Complex Partial Seizures, 84
Cerebrovascular Accident, 85
Multiple Sclerosis, 86
Myasthenia Gravis, 87
Trigeminal Neuralgia, 88
Parkinson’s Disease, 89
Alzheimer’s Disease, 90
Bell’s Palsy, 91
Amyotrophic L ateral Sclerosis, 92
Guillain-Barré Syndrome, 93
Encephalitis, 94
Malignant Hyperthermia, 95
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Nervous System Disorders
70
Meningitis
(men-in-ji-tis)
Clue: Diagnostic or Clinical Findings
Nuchal rigidity and pain as the
meninges are stretched by moving the
legs or flexing the neck to the chin.
Turbid CSF with low glucose and
high protein.
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Pathophysiology
• The meninges include the dura matter, arachnoid
•
•
•
•
layer, and pia matter; and surround the brain and
spinal cord.
Causative agents include bacteria, viruses,
mycobacteria, fungi, amebas, cancer, and noninfectious sources. Entrance via the respiratory
system is most common.
Infections that occur close to the CNS, basilar fracture, CNS surgery or presence of an indwelling
shunt, and blood-borne illnesses cause meningitis.
TNF-α and IL-1 are major mediators of inflammation that increase permeability and transit of the
causative agent through the blood–brain barrier.
Inflammation causes ↑ ICP in meningitis.
Assessment and Diagnostic Findings
• Fever and symptoms of ICP, including change in
•
LOC, headache, nausea, vomiting, nuchal rigidity
(positive Kernig’s and Brudzinski’s signs), lethargy,
photophobia, seizures, pupil dilation, decorticate or
decerebrate posturing, and pulse pressure changes.
LP shows turbid CSF, and ↓ glucose and ↑ protein
levels. Infectious cell count, Gram stain or C&S.
70
• CBC, procalcitonin testing, MRI.
• Eye fundus examination showing papilledema.
Complications
• Seizures; residual hearing, vision, or cognitive
defects; and death.
Medical Care and Surgical Treatment
• Quiet, darkened, nonstimulating environment.
Cooling blanket for high temperature.
• Antimicrobials, antipyretics, steroids, pain
medication, and (rarely) surgical drainage of
abscesses.
Keep in Mind
• Vaccines are recommended for the most common
forms of bacterial meningitis (Haemophilus influenzae
type b in infants and children, and Neisseria meningitidis in college-aged children).
Make the Connection
• Change in LOC is often the first sign.
• Monitor CBC and Glasgow Coma Scale assessments; elevate the head with neck straight.
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Concussion
(kon-kush-un)
Clue: Diagnostic or Clinical Findings
A blow to the head resulting
in changes in LOC.
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Pathophysiology
• Also known as traumatic brain injury, concussion
•
is caused by a nonpenetrating, or closed, head
injury. Mechanisms of injury include acceleration
injury, deceleration injury, or a combination
of both. Rotational injuries cause traumatic
shearing of the brain tissue. Most injuries are
related to automobile accidents, but playing
contact sports and falls are also frequent
causes.
After injury, the compromised cells require
increased glucose in order to remain alive.
However, with the onset of cerebral edema, the
capillary bed may become displaced from the
cells by fluid. With decreased blood flow,
neuronal loss can continue to occur.
Assessment and Diagnostic Findings
• Change in LOC that may include confusion,
•
difficulty concentrating, amnesia, brief loss of
conciousness, ICP (direct or MRI measurement of
≥15 mmHg), widening pulse pressure, and decorticate or decerebrate posturing.
CT scan, MRI ICP measurement >15 mm Hg,
and PET.
71
Complications
• ICP, brain herniation, diabetes insipidus, and vital
sign instability.
• Posttraumatic syndrome characterized by a permanent impairment of cognitive or motor function.
Medical Care and Surgical Treatment
• Control ICP by pharmacologic means or by
•
mechanical hyperventilation with barbiturateinduced coma and temperature control.
Initiate invasive ICP monitoring and ventricular
drainage; elevate head and keep neck straight.
Keep in Mind
• Head trauma is cumulative, so repeated blows
to the head can cause irreversible damage.
• Teach clients that prevention is the best
approach. Wear appropriate headgear when
engaging in activities such as bike riding, skating,
skiing, or playing contact sports. Helmet use does
not guarantee that brain trauma will not occur.
Make the Connection
• Any change in LOC after head injury
warrants medical care and monitoring.
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Skull Fracture
(skul frak-chur)
Clue: Diagnostic or Clinical Findings
Severe head trauma resulting in an
area of open-skull injury that presents
as crepitus, CSF leak, or a depressed
area in the skull.
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Pathophysiology
• Loss of integrity of the cranial bones and/or
•
•
meninges causing damage to the underlying brain
tissue and creation of an avenue of infection to
the CNS.
Types include linear, comminuted, depressed,
compound, and basilar.
Acute cerebral edema and ICP occur from
neuronal damage, hemorrhage, inflammation,
infection, potassium leaking to the extracellular
space, and lactate buildup from glycolysis.
Assessment and Diagnostic Findings
• Amnesia, brief loss of consciousness, or signs of
increased ICP.
• CT scan, or skull x-ray to detect fracture, MRI ICP
reading.
• Leakage of CSF from cranial orifices.
• Battle’s sign or raccoon sign.
Complications
• ICP, brain herniation, diabetes insipidus, and vital
sign instability.
• Permanent impairment of cognitive or motor
function.
72
Medical Care and Surgical Treatment
• Control ICP by pharmacologic means or by
•
•
mechanical hyperventilation with barbiturateinduced coma and temperature control.
Initiate invasive ICP monitoring and ventricular
drainage; elevate head and keep neck straight.
Reduction of fracture, including removal of
penetrating bone.
Keep in Mind
• After head trauma, an area that is depressed
rather than swollen requires immediate care.
Make the Connection
• Monitor CT, MRI, or PET imaging.
• Maintain a record of vital signs and Glasgow
Coma Scale readings.
• Monitor ICP reading.
• Check any clear drainage for glucose or
concentric circles forming on a dressing.
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Epidural and Subdural
Hematoma
(ep-i-dur-al and sub-du-ral he-ma-to-ma)
Clue: Diagnostic or Clinical Findings
Head injuries that may be arterial
or venous in nature, causing ICP and
change in LOC. May cause rapid
ICP or be insidious, chronic, or
become fatal.
73
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Pathophysiology
• Traumatic brain injury that is nonpenetrating and
•
•
•
caused by rotational injury, acceleration injury,
deceleration injury, or both.
Epidural hematomas are arterial, so symptoms
are more severe due to rapid accumulation of
blood above the dural layer.
Subdural hematomas are venous, so symptoms
may be more insidious.
These hematomas may occur together.
Assessment and Diagnostic Findings
• CT scan, MRI scan, and x-ray of the skull.
• Increased ICP with decreased LOC, headache,
dizziness, nausea, vomiting, vital sign changes
like temperature increase, hemiparesis, unequal
pupil dilation, decorticate or decerebrate
posturing, ICP measurement by invasive or
noninvasive MRI measurement of ≥15 mm Hg.
Complications
• ICP, brain herniation, diabetes insipidus, and vital
sign instability.
• Hemiparesis, chronic neurologic injury, or
death.
73
Medical Care and Surgical Treatment
• Control ICP by pharmacologic means, steroids, or
•
•
by mechanical hyperventilation with barbiturateinduced coma and temperature control.
Initiate invasive ICP monitoring and ventricular
drainage; elevate head and keep neck straight.
Surgical evacuation of hematoma and repair of
bleeding vessels.
Keep in Mind
• Teach clients that prevention is best approach.
Wear appropriate headgear when engaging in
activities such as bike riding, skating, skiing, or
playing contact sports. Helmet use does not
guarantee that brain trauma will not occur.
Make the Connection
• Monitor CT, MRI, and ICP measurements.
Maintain Glasgow Coma Scale assessments.
• Monitor vital signs; keep head elevated and neck
straight to lessen ICP.
• Elderly clients and alcoholics may develop
insidious subdural hematoma.
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Huntington’s Disease
(se-le-ak di-zez)
Clue: Diagnostic or Clinical Findings
Onset of jerking movements of the
upper extremities, face, and neck
progressing to the rest of the body
accompanied by progressive psychotic
behavior. Genetic testing reveals
mutation of the IT15 gene resulting
in huntingtin protein.
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Pathophysiology
• A disorder that causes a mutation in the IT15
•
•
gene that results in transcription of an abnormal
protein called huntingtin protein. Abnormalities
in DNA trigger cellular death. Cells affected are
those that control motor and cognitive function.
An autosomal dominant disorder; each offspring
of an affected parent has a 50% chance of
inheriting the disorder.
Onset may be in childhood or in midlife.
Assessment and Diagnostic Findings
74
Medical Care and Surgical Treatment
• Antipsychotic medications, antidepressants, and
antichoreic medications.
• Research is ongoing regarding fetal nerve tissue
transplant, but there is no cure.
Keep in Mind
• Teach clients and caregivers that soft foods and
•
• Personality changes, inappropriate behaviors,
•
•
•
labile moods, depression, and suicidal
tendencies.
Paranoia with irritability, anxiety, and aggressive
behavior.
Choreiform movements.
Video swallowing test for dysphagia.
Complications
• Aspiration pneumonia.
• Choking.
• Progressive loss of social and physical skills,
leading to debilitation and death.
thickened liquids will be substituted in the diet to
assist in swallowing effectively.
Teach caregivers that jerking movements are not a
sign of aggression but that aggression can occur.
Make the Connection
• The client with Huntington’s disease must
•
•
make end-of-life decisions at the onset of
symptoms.
Genetic counseling and testing must be available
to anyone with a history of Huntington’s disease.
Assess respiratory function, breath sounds, and
ability to swallow.
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75
Spinal Cord Injury
(spi-nal kord in-jur-e)
Clue: Diagnostic or Clinical Findings
Loss of sensation, movement, or
both after trauma to the neck,
thorax, lumbar, or sacral area.
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75
substance abuse, skin breakdown, and autonomic
dysreflexia.
Pathophysiology
• Nerve fibers of the spinal cord are nonregenerative.
• Central cord syndrome results in weakness or
•
•
•
•
paralysis that affects the upper extremities more
than the lower extremities.
Anterior cord syndrome, caused by trauma or
ischemia results in weakness and decreased pain
and temperature sensation below the damaged
area.
Posterior cord syndrome causes ataxia, but
strength and sensation are preserved.
Brown-Séquard syndrome results in paralysis
on the affected side and sensation loss on the
opposite side of injury.
Cauda equina syndrome results in bowel and
bladder dysfunction and some leg paresthesia.
Medical Care and Surgical Treatment
• Immobilize the client, apply traction, and support
•
•
the respiratory and vital functions. IV access
required for fluids and medications. Injuries above
C4 will result in respiratory depression.
Support bowel and bladder function.
Surgically stabilize the vertebrae.
Keep in Mind
• Teach clients that they must remain immobile.
• Clients need to know that there is a “wait and
see” time frame for some types of injuries, but
they must be kept apprised and participate in the
plan of care.
Assessment and Diagnostic Findings
• Abnormalities in sensation, temperature sense,
•
or motor function that occur in patterns that
suggest the type of injury.
MRI scan.
Complications
• Infection, deep vein thrombosis, orthostatic
hypotension, spinal shock, depression and/or
Make the Connection
• Monitor all vital functions and oxygenation;
assess CBC.
• Maintain immobilization; check sensation/motor
function; assess skin, bowel, and bladder.
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Autonomic Dysreflexia
(aw-to-nom-ik dis-re-flek-se-a)
Clue: Diagnostic or Clinical Findings
In spinal cord injuries above T6,
sudden onset of headache, nasal
stuffiness, high BP, and flushed skin
above the level of injury.
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Pathophysiology
• SCI above T6 receive peripheral sensory impulses
•
•
from below the injury via the spinothalamic tract
that stimulates a large sympathetic release of
norepinephrine, dopamine β-hydroxylase, and
dopamine. These neurotransmitters cause vasoconstriction (↑ BP) and skin pallor below the area
of injury.
The brainstem reacts to the ↑ BP by parasympathetic nervous innervation above the level of
injury.
Relieving the noxious stimuli stops the sensory
signal and therefore the sympathetic response.
76
Complications
• Cerebrovascular accident or hemorrhage; retinal
hemorrhage.
• Myocardial infarction.
Medical Care and Surgical Treatment
• Antihypertensive medications as needed.
• Remove the noxious stimuli to stop the dysreflexia.
Keep in Mind
• Teach clients with SCI above T6 about symptoms
and to report them immediately.
• If clients are capable, they should self-catheterize
if symptoms begin.
Assessment and Diagnostic Findings
• Blood pressure elevation that can be as high as
300 mm Hg systolic.
• Flushing of skin above the thoracic SCI, nasal
stuffiness, headache, and bradycardia.
• Pallor of the skin below the thoracic SCI with
piloerection.
• Bladder distention, bowel impaction, UTI,
ingrown toenail, pressure sores, wrinkled bed
linen, or pain below the level of the SCI are
causes.
Make the Connection
• Monitor vital signs.
• Assess for full bladder or rectal impaction first,
and then conduct systematic assessment for
stimuli.
• Monitor CBC, I&O, and urine C&S.
• Turn client every 2 hours.
• Teach and assess bladder and bowel training
activities.
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77
Spinal Shock
(spi-nal shok)
Clue: Diagnostic or Clinical Findings
Period of time after SCI in which
there is no motor or sensory
transmission. Can last a day to
several months.
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Pathophysiology
• SCI causes a concussion-like injury to neurons
•
•
•
•
known as spinal shock in which neurons below
the level of the SCI are incapable of any sensory
or motor transmission.
Cytokines cause an inflammatory condition in the
affected neurons.
Phase 1 spinal shock is characterized by the
absence of all reflex arcs below the SCI.
Phase 2 spinal shock is characterized by the return
of some of the reflex arcs, which signals the beginning of the end of spinal shock.
Phase 3 and 4 are characterized by strong reflexes
that occur with minor stimulation and may be
followed by autonomic dysreflexia, hyperreflexia,
and clonus.
Assessment and Diagnostic Findings
• Hypotonia, areflexia, and paralysis below the level
of SCI.
• Bulbocavernosus reflex elicitation and assessing
for anal sphincter contraction.
Complications
• Skin breakdown; osteoporosis.
77
• Depression of the client with spinal shock waiting
to know the extent of injuries.
• Respiratory infection; hemodynamic fluctuation.
• Spasticity; autonomic dysreflexia.
Medical Care and Surgical Treatment
• Immobilization to prevent any further injury.
• Steroids and other anti-inflammatory agents.
Keep in Mind
• Teach clients that the extent of their injuries
cannot be assessed until spinal shock ends.
Make the Connection
• Monitor for return of reflexes, spasticity,
or clonus.
• Assess breath sounds and institute a respiratory
care program.
• Monitor blood chemistry for F&E and CBC for
infection.
• Assess skin and utilize pressure-relieving methods
while maintaining immobilization for SCI.
• Support the client psychologically.
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78
Cerebral Aneurysm
(ser-a-bril an-u-rizm)
Clue: Diagnostic or Clinical Findings
Sudden onset of a severe headache,
ICP, change in LOC, and motor
dysfunction and dilation of pupil
on affected side.
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Nervous System Disorders
Pathophysiology
•
•
The endothelial lining of vessel walls become
damaged, lose elasticity, and become vulnerable to rupture. Contributing conditions include
HTN, atherosclerosis, natural presence of arterial bifurcation, and congenital high-pressure
areas such as AVMs.
Ruptured aneurysms have abnormally high levels
of inflammatory cell infiltration.
Assessment and Diagnostic Findings
• Cerebral angiography can precisely diagnose an
•
•
•
•
•
aneurysm by outlining the abnormal dilation or
outpouching of vessels.
MRI with contrast is diagnostic and shows
abnormal outpouching of vessels.
Dilation of the pupil on the affected side,
headache, nausea and vomiting, change in LOC,
and other signs of ICP.
Motor dysfunction of cranial nerve VI resulting in
abnormal gaze.
Motor dysfunction of one or both limbs on the
side opposite the ruptured aneurysm.
Abnormal Glasgow Coma Scale score.
78
Complications
• Rebleeding after surgical repair.
• Vasospasm leading to widespread ischemia.
• Hydrocephalus.
Medical Care and Surgical Treatment
• Antihypertensives.
• Smoking cessation program.
• Catheterization and placement of a coil or other
material to fill a small aneurysm.
• The stalk of a berry aneurysm can be clipped
surgically; others may be wrapped to prevent
rupture; some are resected and reanastomed.
Keep in Mind
•
Teach clients to report severe headaches,
especially accompanied by nausea/vomiting;
have yearly physicals; stop smoking; and limit
alcohol consumption.
Make the Connection
• Monitor ICP, Glasgow Coma Scale score,
and vital signs.
• Assess psychological status.
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Tonic-Clonic Seizures
(ton-ik klon-ik se-zhurz)
Clue: Diagnostic or Clinical Findings
Presence of an aura followed by loss
of consciousness with alternating
cycles of stiffness and jerking
movements lasting 1–2 minutes.
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Pathophysiology
• Tonic-clonic seizures are generalized seizures.
• Pathology includes an area of hyperexcitable
neurons. This is the epileptogenic focus.
Assessment and Diagnostic Findings
• EEG identifies the epileptogenic focus and
seizure threshold.
• Client reports having a sensory warning prior to
onset of a seizure (aura).
• The tonic phase is accompanied by laryngeal
•
•
•
spasm, autonomic reaction with increase in
pulse and BP, and increased mucus secretion.
This phase lasts approximately 20 seconds.
The clonic phase is characterized by alternating
atonia and spasm and lasts approximately
30 seconds; the client may be incontinent as
the urinary sphincter relaxes.
The entire seizure usually does not exceed
1–2 minutes.
The postictal phase follows the seizure and
is characterized by amnesia of the seizure,
confusion, lethargy, muscle pain, and
embarrassment.
79
Complications
• Status epilepticus and death.
• Injury to the head or body, biting of the lips or
tongue, vertebral compression fractures.
• Interpersonal relationship interruption.
Medical Care and Surgical Treatment
• AEDs; ketogenic diet.
• Resection or ablation of the epileptogenic focus.
• Vagal nerve stimulation; corpus callosotomy.
Keep in Mind
• Teach clients they may drive again when seizures
are certified as being controlled.
• Stress may increase the need for AEDs.
• Comply with serum AED levels.
Make the Connection
• Protect the client from injury; never insert
anything into the mouth during the seizure.
• Time the seizure; monitor serum level of AEDs;
monitor CBC for ↓ WBC.
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Absence Seizures
(ab-sens se-zhurz)
Clue: Diagnostic or Clinical Findings
Usually a disease of children; the
child appears to be daydreaming
and has no recall of the event.
Abnormal EEG.
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Pathophysiology
• Generalized seizures that may be due to alternat•
ing gamma-aminobutyric acid type B (GABAB)
receptor–mediated inhibition alternating with
glutamate-mediated excitation.
Calcium channel abnormalities are also implicated
in the genesis of absence seizures.
Assessment and Diagnostic Findings
• Electroencephalogram (EEG) showing abnormal
spikes alternating with slow-wave patterns.
• Staring episodes that look like daydreaming.
• Mutation in the GABAA receptor gene (GABRB3).
Complications
• Educational and behavioral problems related to
unrecognized seizures.
Medical Care and Surgical Treatment
• Antiepileptic drugs (AEDs).
80
Keep in Mind
• Teach clients, caregivers, and teachers about the
illness.
• Medication regimens must be followed to prevent
further seizures.
• Teach that serum blood levels of AEDs will be
measured.
• Teach side effects (lethargy, sleepiness) of AEDs.
• The need for AEDs increases with stress.
Make the Connection
• Monitor serum AED levels.
• Monitor vital signs.
• Provide emotional support to the family; impress
upon the family that this illness can be controlled
with little risk to or interruption of the development of the child.
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Myoclonic Seizures
(mi-o-klon-ik se-zhurz)
Clue: Diagnostic or Clinical Findings
Brief, sudden jerking motion
bilaterally, with EEG showing
abnormal waveforms.
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Pathophysiology
• A generalized seizure with juvenile onset. The
•
•
cerebral cortex, subcortical, and spinal areas are
believed to be involved in the development of
myoclonic seizures. The electrical discharge from
the cortex produces stimulation of the muscles
through the motor centers.
Acetycholine (excitatory), serotonin (inhibitory),
and GABA (inhibitory) neurotransmitters are
present in mismatched amounts in this disorder.
The mechanism of myoclonic seizure disorder is
related to restless leg syndrome.
Assessment and Diagnostic Findings
• Involuntary jerking motion of limbs, soft palate,
and other areas that occurs bilaterally.
• CT scan and MRI to rule out physiologic abnormalities of the brain.
• EEG identifies the epileptogenic focus.
• Loss of consciousness cannot be determined due
to the brevity of the seizure; however, myoclonic
seizures can progress to tonic-clonic seizures.
Complications
• Falls and injury from tripping.
• May progress to tonic-clonic seizures.
81
• Some forms of myoclonic seizure can be associated with cognitive delay and progressive brain
dysfunction.
Medical Care and Surgical Treatment
• AEDs; ketoginec diet.
• Vagal nerve stimulation.
• Focal resection; corpus callosotomy.
Keep in Mind
• Teach clients and family members that myoclonic
•
seizure activity can occur during sleep or immediately after awakening.
Loss of consciousness is rare, but a period of
confusion may occur.
Make the Connection
• Monitor serum concentrations of AEDs to
assure therapeutic levels.
• Monitor CBC to assess for BMS.
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Atonic Seizures
(a-ton-ik se-zhurz)
Clue: Diagnostic or Clinical Findings
Sudden loss of muscle tone
causing a “drop attack.”
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Pathophysiology
• Classified as a generalized seizure, with juvenile
•
onset lasting into adulthood. The cerebral cortex,
subcortical, and spinal areas are believed to be
involved in the development of generalized
seizures. The electrical discharge from the cortex
produces stimulation of the muscles through the
motor centers.
Evidence indicates that an abnormality exists
among neurotransmitters (e.g., gammaaminobutyric acid [GABA]) or in calcium,
potassium, or sodium channel activity.
Assessment and Diagnostic Findings
• May experience an aura and have sweating and
piloerection.
• Electroencephalogram (EEG) showing abnormal
wave patterns.
• Computed tomography (CT) scan and magnetic
resonance imaging (MRI) to rule out other brain
pathology.
Complications
• Injury related to loss of tone and falls.
82
Medical Care and Surgical Treatment
• Antiepileptic drugs (AEDs).
• Vagal nerve stimulation.
• Focal resection; corpus callosotomy.
• Ketogenic diet.
Keep in Mind
• Teach clients and family members about the
nature of the disorder and its treatments.
• Blood tests will be done to monitor serum AED
levels.
Make the Connection
• Monitor serum concentrations of AEDs to
assure therapeutic levels.
• Monitor complete blood count (CBC) to assess
for bone marrow suppression.
• Assess CT scan and MRI for abnormalities in
brain structure.
• Provide emotional support; refer to support
group.
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Simple Partial Seizures
(Focal)
(sim-pl par-shul se-zhurz fo-kal)
Clue: Diagnostic or Clinical Findings
Lip smacking, picking at clothing,
or chewing behaviors of which the
client is unaware. Consciousness
is not lost.
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Pathophysiology
• Simple partial seizures, or focal seizures, arise
•
•
•
from one hemisphere of the brain, usually in the
temporal lobe.
May spread to the parietal lobe, causing transient
paresthesias of the body on the opposite side of
the epileptogenic focus, usually beginning in the
finger, arm, and hand and then spreading to the
leg and face.
Neurotransmitter abnormalities, especially in
gamma-aminobutyric acid (GABA), as well as calcium, potassium, or sodium channel abnormalities, may produce the abnormal electrical charge.
Simple partial seizures may spread and become a
generalized seizure.
Assessment and Diagnostic Findings
• Juvenile onset lasting into late adulthood.
• Electroencephalogram (EEG) showing abnormal
wave patterns.
• Computed tomography (CT) scan and magnetic
•
resonance imaging (MRI) to rule out other brain
pathology.
Automatisms (e.g., fondling oneself, chewing,
lip smacking).
83
Complications
• Psychosocial implications if automatisms are
present.
• May spread and become a generalized seizure.
Medical Care and Surgical Treatment
• Antiepileptic drugs (AEDs).
• Vagal nerve stimulation.
• Focal resection.
• Corpus callosotomy is controversial.
• Ketogenic diet.
Keep in Mind
• Teach clients and family members about the
nature of the disorder and its treatments.
• Blood tests are done to monitor serum AED levels.
Make the Connection
• Monitor serum concentrations of AEDs to
assure therapeutic levels.
• Monitor complete blood count (CBC) to assess
for bone marrow suppression.
• Assess CT scan and MRI for abnormalities in
brain structure.
• Provide emotional support; refer to support group.
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Complex Partial Seizures
(Psychomotor)
(kom-pleks par-shul se-zhurz si-ko-mo-tor)
Clue: Diagnostic or Clinical Findings
Staring, running away, picking at
clothing, or standing still with
lip smacking or other socially
awkward behavior. May lose
consciousness.
84
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Pathophysiology
• Complex partial seizures arise from one hemisphere of the brain, usually in the temporal lobe.
• May spread and become a generalized seizure.
• Neurotransmitter abnormalities, especially in
•
gamma-aminobutyric acid (GABA), as well as
calcium, potassium, or sodium channel abnormalities, may produce the abnormal electrical
charge.
Loss of consciousness occurs and may last
2–15 minutes.
Assessment and Diagnostic Findings
• Electroencephalogram (EEG) showing abnormal
wave patterns.
• Computed tomography (CT) scan and magnetic
•
resonance imaging (MRI) to rule out other brain
pathology.
Automatisms (e.g., fondling oneself, chewing,
lip smacking, running away, screaming,
masturbating).
Complications
• Psychosocial implications if automatisms are
present.
• May spread and become a generalized seizure.
84
Medical Care and Surgical Treatment
• Antiepileptic drugs (AEDs).
• Vagal nerve stimulation.
• Focal resection.
• Corpus callosotomy is controversial.
• Ketogenic diet.
Keep in Mind
• Teach clients and caregivers the nature of these
seizures and that they may spread.
• Teach caregivers not to yell at the client or tell the
client to stop the behavior because doing so is
not helpful; rather, keep the client safe.
Make the Connection
• Monitor serum concentrations of AEDs to
assure therapeutic levels.
• Monitor complete blood count (CBC) to assess
for bone marrow suppression.
• Assess CT scan and MRI for abnormalities in
brain structure.
• Provide emotional support; refer to support group.
• Do not attempt to restrain the client unless he or
she is in danger.
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85
Cerebrovascular
Accident
(ser-e-bro-vas-ku-lar ak-si-dent)
Clue: Diagnostic or Clinical Findings
Inability to form words, drooping
of the face, or inability to see out
of one eye.
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Nervous System Disorders
Pathophysiology
• Result of a thrombotic block to blood flow or
•
•
•
bleeding into the brain that drastically diminishes
blood flow to the neurons, causing the cerebrovascular accident (CVA).
Injured cells fill up with free zinc ions that are
believed to hasten their demise.
Production of glutamate increases the metabolic
needs of the already depleted neurons.
Inflammation causes cerebral edema.
Assessment and Diagnostic Findings
• CT scan (first) and MRI to determine if the CVA
•
•
•
•
is a result of ischemia related to a thrombus or a
hemorrhage.
Hemianopsia and facial droop on affected side,
aphasia or dysphasia, and paresthesia or paralysis on the opposite side of the CVA.
The CPHSS is performed, and if any one of the
three criteria is positive, the client is brought to
the hospital for assessment.
ECG to rule out atrial fibrillation; ↑ BP.
A severe headache will be present in hemorrhagic
stroke.
85
Complications
• Death.
• Permanent loss of function; unilateral neglect.
• Depression, poor judgment, seizures, and PE.
• Increased ICP and respiratory insufficiency.
Medical Care and Surgical Treatment
• Thrombolytic therapy.
• Antiplatelet therapy; antidysrhythmic medications; oxygenation; cardiac monitor.
• Suction as necessary; liquids are thickened.
• Surgical intervention for hemorrhagic stroke.
Keep in Mind
• Teach clients to have their BP and blood lipids
checked and to report any CVA signs.
Make the Connection
• Closely monitor laboratory tests and
hemodynamic status in the acute phase.
• Provide physical and occupational therapy; assess
ability to swallow effectively.
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86
Multiple Sclerosis
(mul-ti-pl skle-ro-sis)
Clue: Diagnostic or Clinical Findings
Exacerbating and remitting periods
of degenerating motor function.
The MRI shows demyelination of
the white matter of the brain.
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Nervous System Disorders
Pathophysiology
• Exacerbating and remitting disease characterized
•
•
by demyelination of brain white matter, damage to
axons, and decreased number of oligodendrocytes
in the CNS affecting young adults (ages 20–40)
and women more than men.
Autoimmune inflammatory disease involving
cell-mediated (T-cell) and antibody (B-cell)
activity.
Exacerbation of symptoms can be caused by
extreme heat or cold, fatigue, infection, stress, or
pregnancy.
Assessment and Diagnostic Findings
• Visual problems (one eye at a time), with eye pain
•
•
•
•
during eye movement; diplopia; slurred speech
and dysarthria; vertigo; tinnitus; nystagmus;
ataxia; and dysphagia.
Numbness and weakness of limbs, spastic or
flaccid bladder, urinary incontinence, constipation,
and sexual dysfunction.
Mood lability.
CSF assessment for oligoclonal IgG.
Magnetic resonance imaging (MRI) reveals
sclerotic plaques.
86
Complications
• Immobility issues.
• Accidents and risk for falls; decreased cognitive
function; alteration in family relationships.
• Respiratory infections; death.
Medical Care and Surgical Treatment
• Beta-interferons, corticosteroids, or adrenocorticotropic hormone.
• Antidepressants, antispasmodics, and anticholinergics.
• Plasmapheresis.
• Physical therapy and rest periods.
Keep in Mind
• Teach clients to avoid stress and extremes of
temperature and to report respiratory infections.
Make the Connection
• Evaluate respiratory status; have client use
incentive spirometry.
• Encourage self-care and stress reduction; provide
emotional support.
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Myasthenia Gravis
(mi-as-the-ne-a gra-vis)
Clue: Diagnostic or Clinical Findings
Ptosis of one eyelid.
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Nervous System Disorders
Pathophysiology
• Meaning “grave muscle weakness,” MG is an
•
•
autoimmune disease that produces antibodies
that attack AChR in the NMJ of skeletal muscles.
ACh molecules are inactivated by the enzyme
AChE, which is abundantly present at the NMJ.
The disease involves periods of exacerbation and
remission.
87
Medical Care and Surgical Treatment
• Cholinesterase-inhibiting drugs; steroids;
plasmapheresis.
Keep in Mind
• Teach clients to take their medication on arising
and before eating breakfast.
• Report excessive weakness, nausea, vomiting,
constriction of pupils, and dyspnea.
Assessment and Diagnostic Findings
• Antibodies to muscle striations in serum.
• Weakness with activity and return of muscle
strength after rest.
• Ptosis of eyelids when asked to gaze upward for
•
•
•
•
2 minutes; weakness in chewing and swallowing,
speaking, and breathing.
Exacerbations caused by stress.
EMG to rule out nerve damage.
Tensilon test.
Respiratory function tests.
Complications
• Cholinergic crisis; myasthenic crisis.
• Aspiration and choking.
• Respiratory failure; death.
Make the Connection
• Avoid medications that interfere with
therapy.
• Monitor clients on calcium channel blockers,
•
beta blockers, antibiotics, and antidysrhythmics,
as these may interfere with muscle contraction.
Assess muscle function; auscultate lungs and
review pulmonary function tests.
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88
Trigeminal Neuralgia
(tri-jem-in-al nu-ral-je-a)
Clue: Diagnostic or Clinical Findings
Severe knife-like facial pain unilaterally
in response to movement of the
musculature of the face, a touch,
or cool breeze.
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Nervous System Disorders
Pathophysiology
• Vascular compression or other structural disor•
•
ders of the vasculature cause inflammation of the
fifth cranial nerve, or TN.
Inflammation and compression cause demyelination and remyelination of the nerve. This
abnormal myelination causes abnormal sensory
discharge, felt by the client as intense pain.
Trigger zones include the lips, upper or lower
gums, cheeks, forehead, and side of the nose.
Assessment and Diagnostic Findings
• Burning, jabbing or knife-like pain in the face on
one side.
• Triggers include a slight touch, a cold breeze,
•
•
•
chewing, talking, face washing, teeth brushing,
shaving, and eating.
Tearing and frequent blinking on the affected side.
Attacks are rare during sleep.
CT scan and MRI to rule out other disorders.
Complications
• Avoidance behaviors.
• Bone marrow suppression from drugs to treat
TN; loss of corneal sensation from nerve blocks
and ablative therapies.
88
Medical Care and Surgical Treatment
• Anticonvulsants and benzodiazepines.
• Nerve block with a local anesthetic.
• Radiofrequency ablation to destroy some of the
nerve branches.
• Gamma knife therapy.
Keep in Mind
• Teach clients to protect their eyes if corneal sen-
sation is lost as a result of treatment. Artificial
tears and an eye patch should be used (eye patch
during sleep).
Make the Connection
• Encourage normal activity.
• Report attacks and implement pharmacologic
intervention as necessary.
• Assess corneal sensation after ablative therapies.
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89
Parkinson’s Disease
(par-kin-sonz di-zez)
Clue: Diagnostic or Clinical Findings
Mask-like facial expression, soft and
monotonous voice, drooling,
dysphagia, and shuffling gait.
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Nervous System Disorders
Pathophysiology
• Under the cerebral cortex are interconnected
•
areas of gray matter (basal ganglia), which are
involved in controlling voluntary movement.
Adjacent to the basal ganglia are cells of the substantia nigra that produce the neurotransmitter
dopamine necessary to produce smooth and
coordinated muscle movement. Death of cells
in the substantia nigra leads to decreased levels
of dopamine production, and impairment of
EP tract.
As dopamine levels decrease, acetylcholine levels
increase.
Assessment and Diagnostic Findings
• MRI to rule out other conditions.
• Lewy bodies, found in the cortex.
• TRAP criteria.
Complications
• Orthostatic hypotension, falls, constipation,
•
painful joints from stiffness and tremor, and
communication problems.
Loss of quality of life, depression, swallowing
difficulty, and dementia in later stages related to
the disease or treatment.
89
• Parkinsonian crisis triggered by physical or
emotional stress.
Medical Care and Surgical Treatment
• Dopamine agonists, MAO-B inhibitors, COMT
inhibitors, and anticholinergics.
• Pallidotomy; embryonic stem cell therapy.
Keep in Mind
• Teach clients tricks to overcome “freezing”; add
•
fiber and liquids to the diet; report any psychological problems (hallucinations or depression).
Avoid tyramine-containing foods.
Make the Connection
• Monitor side effects of medication.
• Avoid meperidine (fatal interaction with MAO-B
inhibitors).
• Assess ability to chew and swallow.
• Assess for worsening of symptoms.
• Provide emotional support, assess for pain.
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Alzheimer’s Disease
(alts-hi-merz di-zez)
Clue: Diagnostic or Clinical Findings
Short-term memory loss, forgetfulness,
confusion, and inability to recognize
loved ones or self.
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90
Pathophysiology
• Neuropathologic findings in SDAT include amy•
•
•
loid plaques, neurofibrillary tangles, and synaptic
and neuronal cell death.
Degeneration occurs first in the hippocampus,
(short-term memory), then damage spreads to
the temporal area. Frontal damage causes
personality changes and incontinence.
Acetylcholine levels in the cerebral cortex become
deficient.
Ventricles of the brain become larger as the
brain tissue is destroyed. The brain shrinks in
size.
Assessment and Diagnostic Findings
• Stage 1 (the forgetfulness stage) is characterized
•
•
by episodes of losing personal items, forgetting
appointments, and jealousy.
Stage 2 (the confusional stage) is characterized
by transient loss of recognition of loved ones and
self, inability to do simple mathematic calculations, depression, anxiety, and hyperorality.
Stage 3 (the dementia stage) is characterized by
psychosis, permanent loss of memories of loved
ones, severe sleep disorders and “sundowning,”
•
incontinence, decreased appetite, and respiratory
compromise.
MRI, PET scan, and SPECT scans may reveal
areas of tangles, plaques, and decreased cell
metabolism respectively.
Complications
• Inability to achieve caloric needs.
• Respiratory compromise leading to pneumonia.
• Incontinence and skin breakdown.
• Immobility resulting in death.
Medical Care and Surgical Treatment
• Acetylcholinesterase inhibitors; NMDA receptor
antagonists.
• Cognitive therapy, reality orientation, pet therapy,
validation therapy, reminiscence therapy.
Keep in Mind
• Teach family to assist clients with ADLs.
• Arrange for respite care services.
Make the Connection
• Utilize recall of past events in order to
communicate with those with severe dementia;
monitor I&O and dietary intake.
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91
Bell’s Palsy
(bellz pawl-ze)
Clue: Diagnostic or Clinical Findings
Unilateral drooping of the face;
inability to blink the eye.
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Nervous System Disorders
Pathophysiology
• Inflammation thought to be caused by autoim•
•
mune, viral, bacterial, or traumatic processes of
the seventh cranial nerve (facial nerve), causing
interruption of nerve transmission.
Motor control is lost usually on one side of the
face, although it can occur bilaterally (1%).
More likely to occur in pregnancy, immune dysfunction (e.g., human immunodeficiency virus),
or diabetes.
Assessment and Diagnostic Findings
• Drooping of the face unilaterally; inability to
blink the eye.
• Electromyogram (EMG) may be done to confirm
nerve dysfunction.
• Computed tomography (CT) scan to rule out
cerebrovascular accident.
Complications
• Damage to the cornea of the eye through drying
or rubbing against the pillow during sleep. Pain
described as burning or “cold” in the eye and
facial area.
91
Medical Care and Surgical Treatment
• Steroids, antibiotics, antiviral medications, and
B-vitamin supplements.
• Eye patch and frequent application of artificial
tears.
Keep in Mind
• Teach the client to gently massage the face and
ear to ease pain.
• Teach the client to use analgesics as needed and
as prescribed.
• Disorder may be self-limiting or become a chronic
condition.
Make the Connection
• Medicate the client for pain based on a
scale of 0–10 when pain level is at 4 or above.
• Assess the affected eye for inflammation, which
could be a sign of corneal irritation.
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Nervous System Disorders
92
Amyotrophic Lateral
Sclerosis
(a-mi-o-tro-fik lat-er-al skle-ro-sis)
Clue: Diagnostic or Clinical Findings
Fasciculations and atrophy of muscle
groups with progressive weakness; a
degenerative neuromuscular disease.
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Nervous System Disorders
Pathophysiology
• Also known as Lou Gehrig’s disease, ALS is a progressive neurodegenerative disease.
• The upper and lower motor neurons degenerate
•
•
and form scar tissue, disrupting nerve transmission and leading to muscle atrophy.
Results in swallowing and breathing difficulty.
A genetic link is suspected as the cause. Onset is
usually between ages 40 and 70 years and more
prevalent in men than in women; survival varies
from 3–10 years or more.
Assessment and Diagnostic Findings
• Fasciculation and atrophy of muscle, with
progressive weakness.
• Intellect is intact.
• Difficulty chewing and swallowing.
• Difficulty clearing respiratory secretions.
• CSF analysis, EEG, nerve biopsy, and EMG may
be done to rule out other disorders.
• Blood enzymes may be increased due to muscle
atrophy.
Complications
• Aspiration; respiratory compromise.
92
• Incontinence.
• Immobility issues; death.
Medical Care and Surgical Treatment
• Muscle relaxants and benzodiazepines for spasticity.
• Quinine for muscle cramps.
• Riluzole to reduce motor neuron destruction.
• Physical and occupational therapy, massage,
mobility aids, and enteral feedings.
• Air mattresses to reduce skin breakdown.
• Respiratory suctioning and supplemental oxygen.
Keep in Mind
• Teach the client and caregivers how to preserve
the skin, respiratory function, and activity level.
• Provide information regarding mobility devices
and computer-assisted communication devices.
Make the Connection
• Assess respiratory function and ability to
clear secretions.
• Provide a method of communication.
• Monitor for skin breakdown; institute a turning
schedule.
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Nervous System Disorders
93
Guillain-Barré Syndrome
(ge-yan ba-ra sin-drom)
Clue: Diagnostic or Clinical Findings
Paralysis of the legs, ascending to
the upper body. May affect the ability
to breathe on one’s own.
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Nervous System Disorders
Pathophysiology
• GB syndrome (inflammatory polyneuritis), is an
•
•
•
inflammatory disorder characterized by a distinct
progression of paralysis. GB often follows a viral
infection. Occurs in those older than age 45 years
and with higher frequency in Caucasians than in
African Americans.
Peripheral nerves are infiltrated by immune cells
that lead to inflammation and demyelination of
the axon. Paralysis begins in the legs and ascends.
If the disease reaches the lungs, respiratory support is required. The plateau stage is the most
severe, but it signals the end of the progression;
remyelination occurs and the symptoms regress.
A descending form of the disease exists.
Miller-Fisher syndrome causes ataxia and extra
ocular paralysis but no respiratory or sensory loss.
Assessment and Diagnostic Findings
•
•
•
LP for CSF. Shows ↑ protein.
EMG and nerve conduction velocity tests.
Pulmonary function tests.
Complications
• Respiratory failure, infections, depression, and
anxiety.
93
• Immobility, skin breakdown, PE, muscle atrophy,
and DVT.
Medical Care and Surgical Treatment
• Plasmapheresis.
• Ventilation and supplemental oxygen.
• Steroids.
Keep in Mind
• Teach clients and caregivers measures will be
•
taken to mitigate symptoms; temporary ventilator
support may be needed.
Teach about the normal progression of the
disease.
Make the Connection
• Provide emotional support and diversion.
• Manage pain; assess for skin integrity, nutritional
status.
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Nervous System Disorders
94
Encephalitis
(en-sef-a-li-tis)
Clue: Diagnostic or Clinical Findings
Inflammation of the brain leading to
ICP, most frequently caused by viruses
(e.g., West Nile virus), parasites,
toxins, bacteria, vaccines, or fungi.
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Nervous System Disorders
Pathophysiology
• Neurons are damaged and inflamed, leading to
cerebral edema and increased ICP.
• Causative agents are viruses, ticks, mosquitoes,
•
parasites, toxins, bacteria, vaccines, or fungi.
Those with a compromised immune system,
the very young, and the very old are especially
at risk.
Herpes simplex virus may be the most common
non-insect-borne cause of the disease.
Assessment and Diagnostic Findings
• Elevated temperature, headache, nausea, vomiting,
and general malaise.
• Ataxia, altered sleep patterns, tremors, and
hemiparesis.
• CT scan, MRI, and LP to assess CSF. CT scan and
MRI diagnose cerebral edema. CSF shows an
increased WBC and protein level, and normal
glucose levels.
Complications
• Seizures, motor deficits, personality changes,
blindness, and cognitive deficits.
• Brain herniation and death.
94
Medical Care and Surgical Treatment
• AEDs, antipyretics, analgesics, sedatives, and corticosteroids.
• ICP monitoring through invasive methods or
noninvasive MRI.
• Antiviral medications IV.
Keep in Mind
• Teach client and family members about the
disorder.
• To decrease cerebral edema, maintain a calm
environment with little stimuli.
• Teach that the goal of ventilator and medication
therapy is to reduce ICP.
Make the Connection
• ICP is made worse by noxious stimuli;
keep the client calm and the environment quiet.
• Monitor CBC, ABGs, and ICP measures.
• Assess for skin breakdown.
• Monitor ventilation; clear respiratory passages
only when needed to reduce ICP increases.
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Nervous System Disorders
95
Malignant Hyperthermia
(ma-lig-nant hi-per-ther-me-a)
Clue: Diagnostic or Clinical Findings
Temperature increase and muscle
rigidity following exposure to
anesthetics. Creatinine and BUN
levels increase. Urine is brown
in color.
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Nervous System Disorders
Pathophysiology
• Autosomal dominant disorder in which exposure
•
•
to a certain anesthetic agent causes temperature
increase and muscle rigidity.
Affects skeletal muscle tissue primarily. Free
ionized calcium concentration can increase
to damaging levels and cause multiple contractions of skeletal muscle. The temperature may
rise to over 105°F from repeated contractions.
The hypermetabolic state causes lactate formation, resulting in acidosis.
95
Medical Care and Surgical Treatment
• Discontinue the anesthetic immediately.
• Cooled intravenous dantrolene and IV fluids to
clear myoglobin from the kidneys.
• Cooling blanket; antipyretics.
Keep in Mind
• Teach client to report any personal or family
history of side effects with anesthesia.
Make the Connection
Assessment and Diagnostic Findings
• Familial link.
• Temperature increase following exposure to an
anesthetic.
• Muscle rigidity and sore muscles.
• Dark brown urine (myoglobin in urine); renal
insufficiency due to rhabdomyolysis.
• Blood chemistry.
Complications
• Arrhythmia; death.
• Renal failure.
• Destruction of brain tissue; seizure.
• Muscle tissue is destroyed by rapid
•
•
contraction due to excess calcium. As muscle is
destroyed, myoglobin is released and flows via
the bloodstream to the kidneys, which may
cause acute tubular necrosis; adequate
hydration is necessary to flush the kidneys.
Monitor blood chemistry for elevated levels of
enzymes, creatinine, and BUN.
Temperature must be reduced to normal by
antipyretics and cooled intravenous fluid.
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Page 7
CARDIOVASCULAR
Coronary Artery Disease, 96
Angina Pectoris, 97
Myocardial Infarction, 98
Congestive Heart Failure, 99
Cardiogenic Shock, 100
Atrial Fibrillation, 101
Ventricular Tachycardia, 102
Ventricular Fibrillation, 103
Pericarditis, 104
Myocarditis, 105
Rheumatic Endocarditis, 106
Cardiomyopathy, 107
Deep Vein Thrombosis, 108
Aortic Stenosis, 109
Venous Stasis Ulcer, 110
Varicose Veins, 111
Peripheral Artery Disease, 112
Buerger’s Disease, 113
Raynaud’s Disease, 114
Aortic Aneurysm, 115
Hypertension, 116
Leukemia, 117
Multiple Myeloma, 118
Graft-Versus-Host Disease, 119
Metabolic Acidosis, 120
Metabolic Alkalosis, 121
Respiratory Acidosis, 122
Respiratory Alkalosis, 123
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Cardiovascular System Disorders
Coronary Artery Disease
(kor-o-na-re ar-ter-e di-zez)
Clue: Diagnostic or Clinical Findings
Shortness of breath with activity in
a client with risk factors for heart
disease such as a history of elevated
blood lipids, smoking, poor dietary
habits, sedentary lifestyle, and obesity.
96
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Cardiovascular System Disorders
Pathophysiology
• CAD results in interruption of blood flow that
•
•
•
can cause ischemia or infarction as a result of
atherosclerosis.
The inflammation attracts low-density lipoproteins (LDL) and binds them to the site. The
triglyceride core of the LDLs is spilled into the
underlayer of the intima. Macrophages envelop
these fats and are now termed “foam cells.”
This is the “fatty streak” seen in early stages of
atherosclerosis. As the area enlarges, more LDL,
macrophages, platelets, and smooth muscle
fibers are drawn to the site and accumulate
under the intima, narrowing the vessel.
This causes reduced blood flow and higher blood
pressure in the small coronary vessels.
Assessment and Diagnostic Findings
• Crp to diagnose inflammation in the body; serum
lipid profile to assess cholesterol and LDL.
• Stress test with thallium nuclear imaging (areas
not well perfused are seen as “cold spots”).
• Stress echocardiography; ECG abnormalities.
• Ultrafast CT scan to detect calcium deposits in
the arteries.
96
• Cardiac catheterization is the gold standard for
diagnosis.
Complications
• Activity intolerance with angina pectoris; myocar•
dial infarction that can result in permanent heart
muscle damage and heart failure.
Arrhythmias because of loss of perfusion to the
conduction system.
Medical Care and Surgical Treatment
• Dietary changes; lipid-lowering drugs.
• Cardiac catheterization with balloon angiography
and stent placement, depending on severity.
• CABG.
Keep in Mind
• Teach clients that CAD may be genetic, but there
are modifiable risk factors (e.g., cessation of
smoking, healthy diet, exercising).
Make the Connection
• Lifestyle changes can reverse CAD. Assess
shortness of breath with activity.
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Cardiovascular System Disorders
97
Angina Pectoris
(an-ji-na pek-tor-is)
Clue: Diagnostic or Clinical Findings
Chest pain referred to the jaw, neck,
upper arms, and scapulae that is
usually associated with activity, cold
weather exercise, or smoking. Usually
subsides with rest.
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Cardiovascular System Disorders
Pathophysiology
• The coronary arteries that feed the heart muscle
•
•
become occluded with atherosclerotic plaque.
Increased oxygen demands cannot be met
because of narrowing and noncompliance to
dilation. Ischemic pain results and is referred to
the jaw, inner upper arms, sternum, and between
the scapulae.
Causative events include the 4 Es—eating a large
meal, excitement, environment (very cold or very
hot), and exercise—as well as smoking.
Types include stable angina; variant angina
(Prinzmetal’s), unstable angina, which can easily
lead to MI; and silent ischemia, usually experienced by older adults, that damages the heart
without pain.
Assessment and Diagnostic Findings
• ECG, exercise ECG, graded testing exercise, and
•
•
chemical stress testing with radioisotope imaging
(showing “cold spots” or areas of diminished
cellular metabolism).
Stress ECHO.
Crp ↑; cardiac enzymes.
97
Complications
• MI; permanent heart muscle damage leading to
heart failure.
Medical Care and Surgical Treatment
• Cardiac catheterization with balloon angioplasty
and stent placement.
• CABG.
• Vasodilators, calcium channel blockers, beta-
adrenergic blockers, angiotensin-converting
enzyme inhibitors, angiotensin II receptor blockers,
lipid-lowering drugs, and antiplatelet drugs.
Keep in Mind
• Teach the client about healthy diet, exercise, and
avoiding triggers of angina.
• Teach the client about use of nitroglycerin.
Make the Connection
• Anginal attacks and MI must be differ-
entiated. Cardiac enzymes and ECG assist in
diagnosis. Until an MI is ruled out, angina
should be treated as an MI.
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Cardiovascular System Disorders
Myocardial Infarction
(mi-o-kar-de-al in-fark-shun)
Clue: Diagnostic or Clinical Findings
Severe chest pain that refers to the
jaw, upper arms, neck, and scapula
and is described as “crushing.”
Accompanied by shortness of breath,
elevated BP, and sweating.
98
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Cardiovascular System Disorders
Pathophysiology
• When blood flow diminishes to the heart muscle,
•
•
•
the sympathetic nervous system is activated,
raising the blood pressure and heart rate. This
increases the oxygen and glucose needs of the
cardiac cells.
Cardiac necrosis from lack of perfusion occurs
centrally, surrounded by varying levels of ischemic
tissue radiating outward from the site.
Necrotic cardiac tissue will never resume its prior
ability to contract but rather will form scar tissue.
Damage can occur to the pacing system of the
heart, causing lethal arrhythmias.
98
Medical Care and Surgical Treatment
• Thrombolytics, antiplatelet drugs, antidysrhyth•
mic agents, oxygen, morphine sulfate, nitrates,
vasodilators, beta blockers, and angiotensinconverting enzyme inhibitors.
Cardiac catheterization with stent placement;
CABG.
Keep in Mind
• Prevention of atherosclerosis by healthy lifestyle is
best; some people are genetically predisposed.
• Teach clients the signs and symptoms of MI so
they will seek treatment in time.
Assessment and Diagnostic Findings
• ECG changes (ST segment elevation).
• Abnormalities in a 12-lead ECG.
• Elevation of cardiac enzymes.
• Elevated pulse and blood pressure; decreased
oxygen saturation.
• CBC showing an elevation of white blood cells;
electrolyte abnormalities.
Complications
• Lethal dysrhythmias, cardiogenic shock, valvular
insufficiency, heart failure, and sudden death.
Make the Connection
• Women have atypical signs and symptoms
•
•
(nausea, indigestion, and maybe no pain), but if
they present with shortness of breath or other
symptoms, diagnostic tests should be performed.
There is a 6-hour window for thrombolytic therapy,
but following “60 minutes to treatment” guideline
is best. “Time is muscle.”
Defibrillator access in public areas saves lives of
those with arrhythmia.
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99
Congestive Heart Failure
(kon-jes-tiv hart fal-yer)
Clue: Diagnostic or Clinical Findings
Elevated BNP, edema in the
extremities, shortness of breath,
crackles and pleural effusion,
jugular vein distention,
hepatomegaly, and
splenomegaly.
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Cardiovascular System Disorders
Pathophysiology
• The heart is a double pump. Any structural
damage to the pump will cause heart failure.
• Left-sided heart failure causes backup of fluid in
the lungs.
• Right-sided heart failure causes backup of fluid in
the inferior and superior venae cavae.
• Preload becomes extensive and afterload is difficult
to overcome because of ↑ PVR.
Assessment and Diagnostic Findings
• SOB; crackles or diminished breath sounds at the
•
•
lung bases; presence of third and fourth heart
sounds; orthopnea; cough; pale, clammy skin;
anxiety; and restlessness.
CXR revealing pleural effusion and/or atelectasis,
increased pulmonary wedge pressures, transesophageal echocardiogram (TEE) showing
decreased ejection fraction and low cardiac
output, exercise or pharmacologic stress test
demonstrating poor myocardial perfusion
pattern, ECG abnormalities.
ABG showing a decreased PaO2; elevation of
endothelin 1 (ET-1), a vasoconstrictor, and ANP
and BNP elevation.
99
Complications
• PND related to pleural effusion, hepatomegaly
and splenomegaly, left ventricular thrombus/
embolus, and cardiogenic shock.
Medical Care and Surgical Treatment
• Oxygen, high Fowler’s position, bedrest,
IV opioids, IV inotropic agents, IV vasodilators,
IV human B-type natriuretic peptide, ventricular
assist device, hemodynamic monitoring, and
daily weights.
Keep in Mind
• Yearly physical examinations, proper diet,
exercise, and medications can prevent heart
failure.
Make the Connection
• Monitor daily weights, urinary output,
breath sounds, and BNP for improvement.
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100
Cardiogenic Shock
(kar-de-o-jen-ik shok)
Clue: Diagnostic or Clinical Findings
Following MI, sudden onset of low
BP, poor perfusion, tachycardia,
and arrhythmias.
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Cardiovascular System Disorders
Pathophysiology
• AMI leads to decreased contractility of either the
•
•
•
right or left ventricle, decreasing cardiac output
to all body organ systems.
CS may be caused by pericarditis and resulting
cardiac tamponade.
Stenosis of heart valves or sustained arrhythmia
can cause CS.
Drugs, used for preexisting hypertension, angina,
or arrhythmias, may reach toxic levels and
cause CS.
Assessment and Diagnostic Findings
•
•
•
•
•
•
Jugular venous distention, cyanosis, muffled heart
sounds, crackles and wheezes in the lung bases,
and extra heart sounds.
BP of less than 90 mm Hg lasting more than
30 minutes; ECG showing ST-segment elevation
that indicates AMI.
Cold extremities; change in mental status.
Urine output of less than 20–30 mL/hr.
Increased cardiac enzymes.
CBC indicating inflammation, electrolyte levels,
ABG for acidosis, BNP, and coagulation studies.
100
Complications
• Cardiopulmonary arrest, fatal arrhythmias, renal
failure, thromboembolus, and stroke.
Medical Care and Surgical Treatment
• Inotropic agents, phosphodiesterase enzyme
•
•
inhibitors, platelet aggregation inhibitors,
vasodilators, natriuretic peptides, vasopressors,
and opioid analgesics.
Hemodynamic monitoring.
LVAD; intra-aorta balloon pump.
Keep in Mind
• Teach clients the early signs and symptoms of
AMI and to seek care immediately.
Make the Connection
• Monitor urine output, BP, cardiac output,
pulse oximetry, and ECG.
• Keep the environment calm; reassure the client to
decrease sympathetic outflow.
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101
Atrial Fibrillation
(a-tre-al fi-bril-a-shun)
Clue: Diagnostic or Clinical Findings
Irregular R-R intervals
Palpitations, skipping heartbeats,
or vertigo perceived.
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Cardiovascular System Disorders
Pathophysiology
• Atrial fibrillation (AF), or quivering of the atria,
•
•
•
is caused by repeated reentry of stimuli to the
atrioventricular (AV) node.
Loss of atrial kick.
Stimulation of the sympathetic nervous system,
as well as increasing age, illness (e.g., hyperthyroidism), and the stress of surgery may initiate AF.
Types of AF include paroxysmal, persistent,
permanent, and lone.
Assessment and Diagnostic Findings
• ECG shows no P waves, and the rhythm is irregu•
•
•
larly irregular with shortened QRS complex.
PR interval cannot be measured.
Client may complain of palpitations, skipped
heartbeats, and anxiety.
CBC, cardiac enzymes, thyroid function tests,
serum drug levels, serum toxicology, and blood
chemistry to assess for infection, MI, thyrotoxicosis, toxicity of prescribed cardiac drugs or side
effects of over-the-counter or street drugs, renal
failure, or abnormalities of electrolytes.
CXR or TEE to evaluate for structural or inflammatory disease.
101
Complications
• Stasis of blood causes formation of thrombi,
•
which can lead to CVA, MI, or pulmonary
embolism (PE).
Left ventricular failure.
Medical Care and Surgical Treatment
• Intravenous anticoagulants, antiarrhythmic
•
agents, cardiac glycosides, beta-adrenergic
blockers, and calcium channel blockers.
Electrical cardioversion, pacemaker, implantable
cardioverter defibrillator (ICD), ablation or maze
procedure (cardiac catheterization approach), or
open-heart maze procedure.
Keep in Mind
• Teach clients, especially those with preexisting
cardiac conditions, to report palpitations.
• Teach clients the importance of monitoring
laboratory values.
Make the Connection
• Monitor ECG and INR and PT levels
carefully. Report any SOB that may indicate PE.
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Cardiovascular System Disorders
Ventricular Tachycardia
(ven-trik-u-lar tak-e-kar-de-a)
Clue: Diagnostic or Clinical Findings
Client may be lightheaded or
unconscious and pulseless.
102
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Cardiovascular System Disorders
Pathophysiology
• In ventricular tachycardia (VT), the ventricles
•
•
•
•
replace the sinoatrial (SA) node as the pacemaker
of the heart.
PVCs often precede VT.
VT may be caused by MI, myocardial irritability,
and cardiomyopathy.
Abnormally low levels of K+, Ca++, and Mg+;
digoxin toxicity; RA, SLE, and respiratory acidosis.
Cardiac catheterization and pacing wires.
102
Medical Care and Surgical Treatment
• Defibrillation; administration of antiarrhythmics,
•
Keep in Mind
• Teach clients to seek emergency medical services
for any incidence of chest pain, dizziness, or
syncope because prehospital stabilization can
increase chances of survival.
Assessment and Diagnostic Findings
• ECG shows rapid ventricular rhythm, absent
•
•
P waves, no PR interval, and QRS complex
greater than 0.11 seconds.
Client may become diaphoretic and report
sudden dyspnea, palpitations, lightheadedness,
nausea, and chest pain. The client may lose
consciousness and become pulseless.
Blood chemistry, cardiac enzymes, ABGs, and
serum digoxin levels are assessed.
Complications
• Sustained VT can progress to ventricular
fibrillation and death.
• CHF following repeated episodes.
vasopressors, and oxygen according to ACLS
protocol.
Replacement of electrolytes; magnesium administration to relax ventricular myocardium.
Make the Connection
• Clients with severe preexisting cardiac
•
•
conditions may have VT and should be on
telemetry.
Remember: check the client not only the ECG.
Monitor electrolyte levels, serum drug levels, and
cardiac enzymes.
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Cardiovascular System Disorders
Ventricular Fibrillation
(ven-trik-u-lar fi-bril-a-shun)
Clue: Diagnostic or Clinical Findings
Loss of consciousness, no peripheral
pulses or blood pressure.
103
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Cardiovascular System Disorders
Pathophysiology
• VF is associated with CAD, MI, and structural or
•
•
inflammatory cardiac conditions. It may be precipitated by antiarrhythmic drug administration, atrial
fibrillation, cardioversion, and hypoxic states.
VF causes include hyperkalemia and hypomagnesemia, cardiac catheterization and placement of
pacemaker wires.
Congenital conditions that predispose to VF
include Marfan’s syndrome, tetralogy of Fallot,
Kawasaki’s disease, long QT syndrome, and
Wolff-Parkinson-White syndrome also predispose
to VF.
Assessment and Diagnostic Findings
• ECG shows an irregular rhythm with no P wave,
PR interval, or QRS complex.
• Clients lose consciousness immediately, are pulseless, and have no BP.
• Cyanosis, respiratory arrest, circulatory collapse,
and pupil dilation occur.
Complications
• Death.
• Cerebral anoxia, aspiration pneumonia, defibrillation injury, and repeated VF episodes.
103
Medical Care and Surgical Treatment
• Immediate defibrillation, oxygen therapy, intuba•
•
tion, and administration of antiarrhythmics,
anticholinergics, and vasopressors according
to ACLS protocol.
CABG for perfusion problems.
ICD for those with known risk.
Keep in Mind
• Encourage all clients and family members to learn
•
CPR and to use AEDs for personal safety and
promotion of public health.
Teach clients to activate emergency services if
experiencing any chest pain.
Make the Connection
• Follow ACLS protocols and algorithms to
increase the likelihood of client survival.
• Defibrillate immediately; monitor oxygen saturation, ECG, and vital signs continuously.
• Follow safety protocols for use of defibrillators.
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104
Pericarditis
(per-i-kar-di-tis)
Clue: Diagnostic or Clinical Findings
Pericardial friction rub. Substernal
radiating chest pain that increases in
intensity with deep inspiration or lying
flat. Pain is somewhat relieved by
sitting upright and leaning forward.
CBC and ESR may indicate inflammation
or infection is present.
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Cardiovascular System Disorders
Pathophysiology
• Pericarditis is an inflammation of the pericardial
•
•
sac. The pericardial sac is a fibrous tissue layer
that surrounds the heart. Under normal circumstances, it contains and is bathed with approximately 25–50 mL of serous fluid. In pericarditis,
the volume may increase to 1,500 mL.
Many diseases, conditions, and drugs can inflame
the pericardial sac.
Hemopericardium may be caused by trauma and
in-hospital procedures.
Assessment and Diagnostic Findings
• Radiating substernal chest pain that increases
•
with deep inspiration or lying flat and is somewhat relieved by sitting upright and leaning
forward, dyspnea, low-grade fever, cough, and
pericardial friction rub.
CBC and ESR to detect infection and inflammation; ECG shows ST-T wave elevation; echocardiogram shows pericardial effusions; CT scans
and MRI can show the status of the pericardial
tissue and effusions; blood chemistries to
detect uremia; pericardiocentesis fluid analysis
to determine the causative agent.
104
Complications
• Pericardial effusion (an accumulation of fluid in
the pericardium).
• A large pericardial effusion impairs cardiac filling,
causing shock or death.
• Constrictive pericarditis leads to heart failure.
Medical Care and Surgical Treatment
• Drug therapy depends on the causative factor.
• Pericardiocentesis; creation of a pericardial
window or use of a balloon pericardiotomy for
chronic or persistent pericarditis.
Keep in Mind
• Teach clients to seek emergency medical care if
experiencing dyspnea or chest pain.
Make the Connection
• Monitor ECG, oxygen saturation, and
ease of breathing after pericardiocentesis.
• Assess clients undergoing invasive cardiac
procedures for postprocedure pericarditis.
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105
Myocarditis
(mi-o-kar-di-tis)
Clue: Diagnostic or Clinical Findings
Fever, chest pain, and activity
intolerance.
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Cardiovascular System Disorders
Pathophysiology
• The myocardium is infiltrated by inflammatory cells
leading to necrosis of muscle cells and fibrosis.
• Causes include viral, bacterial, protozoan, and
fungal infections.
• Inflammatory and autoimmune causes or
•
exposure to chemicals or toxins, and radiation
therapy.
Women who are pregnant, those undergoing
radiation therapy to the chest area, and the
elderly are also at risk.
Assessment and Diagnostic Findings
•
•
•
•
•
•
CBC and ESR to detect infection and inflammation; cardiac troponin I is elevated; ECG shows
ST-segment elevation and Q-wave development,
and may show complete heart block and BBB;
ECHO shows ↓ CO and ↓ EF.
MRI shows areas of inflammation.
Temperature elevation and chest pain.
Signs of heart failure.
Endomyocardial biopsy to examine the cells of
the myocardium for damage and causative agent.
PCR identification of a viral infection in myocardial biopsy tissue.
105
Complications
• Pericarditis, arrhythmias, chronic dilated
cardiomyopathy, and heart failure.
Medical Care and Surgical Treatment
• Anticoagulants for thromboembolus development.
• Angiotensin-converting enzyme inhibitors,
•
beta-adrenergic blockers, loop diuretics, and
cardiac glycosides.
Temporary pacemaker or heart transplant.
Keep in Mind
• Teach clients to report new onset of dyspnea or
swelling of ankles immediately.
• Activity will be limited after diagnosis, maybe
permanently.
• Teach about heart transplantation.
Make the Connection
• Monitor for worsening signs of heart failure
and for pericarditis (pericardial friction rub) and
chest pain.
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Cardiovascular System Disorders
Rheumatic Endocarditis
(roo-mat-ik en-do-kar-di-tis)
Clue: Diagnostic or Clinical Findings
Fever, chest pain, dyspnea, cough,
arthritic symptoms, chorea, and ankle
edema develop 2–3 weeks after strep
throat (beta-hemolytic streptococci).
106
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Cardiovascular System Disorders
Pathophysiology
• BHS that cause throat infection or impetigo travel
•
•
•
to the bloodstream, causing bacteremia. The BHS
infect the heart typically 2–3 weeks after the initial
infection. May occur in clients in childhood and
recur as rheumatic endocarditis at any age.
All layers of the heart are affected, with
generalized inflammation of all heart structures.
The endocardium is affected by vegetation
deposited on the valves.
The end result of cardiac structural anomalies
is CHF.
Assessment and Diagnostic Findings
• Tachycardia, heart murmur, pericardial friction
•
•
•
rub, chest pain, fever, polyarthritis, subcutaneous nodules, arthralgia, dyspnea, cough, and
abdominal pain.
ECG shows PR interval lengthening.
ECHO shows abnormal movement of the mitral
valve.
Antistreptolysin O titer greater than 250 IU/mL
and throat culture positive for BHS; CBC and
ESR indicating infection and inflammation.
106
Complications
• Thromboemboli.
• Mitral or aortic valve stenosis; CHF.
Medical Care and Surgical Treatment
• Antipyretics as needed and long-term antibiotic
therapy.
• Treatment of heart failure.
• Mitral valvulotomy, percutaneous balloon
valvuloplasty, or mitral valve replacement.
Keep in Mind
• Teach clients that any sore throat or outbreak of
impetigo must be examined by culture, treated,
and reexamined by culture to ensure the infection
has been cured.
Make the Connection
• Monitor CBC for improvement.
• Monitor client for pericardial friction rub and
symptoms of heart failure.
• Monitor oxygen saturation and activity tolerance;
offer restful activities.
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107
Cardiomyopathy
(kar-de-o-mi-op-a-the)
Clue: Diagnostic or Clinical Findings
Dyspnea, fatigue, edema of the
ankles, and possible atypical chest
pain occurring with rest and not
relieved with nitrates. MRI shows
enlargement of the heart muscle
or chambers.
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Cardiovascular System Disorders
Pathophysiology
• Enlargement of the heart muscle or chambers of
the heart that causes heart failure.
• Major types: dilated and restrictive.
• Causes: Heredity, myocarditis, chronic alcohol or
cocaine use, HIV, thiamine or zinc deficiencies,
infections; or autoimmune disease.
107
Medical Care and Surgical Treatment
• Anticoagulants and antiarrhythmias.
• Medications and procedures are related to type.
Keep in Mind
• Teach family members how to perform CPR and
to seek emergency medical care if the client
experiences dyspnea, chest pain, or syncope.
Assessment and Diagnostic Findings
• Angina, arrhythmias, dyspnea, fatigue, syncope,
and S3 gallop rhythm.
• ECHO, shows abnormal myocardial thickness or
large chamber size.
• ECG shows arrhythmias.
• Cardiac catheterization to visualize chamber size
and contractility.
• Cardiac MRI to visualize heart wall and chamber
size.
Complications
• Congestive heart failure.
• Hypertrophic type may cause enlargement of the
•
septum that blocks the aortic valve resulting in
abnormal heart rhythms and sudden death.
Thromboemboli.
Make the Connection
• Monitor vital signs, oxygen saturation,
•
and for worsening signs of congestive heart
failure and monitor ECG for arrhythmias.
Remember: PE, MI, or CVA can occur if thromboemboli are produced. Monitor INR and PT.
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108
Deep Vein Thrombosis
(dep van throm-bo-sis)
Clue: Diagnostic or Clinical Findings
Positive Homans’ sign, redness or
warmth in an area of pain in the leg,
and edema unilaterally in the arm
or leg.
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Cardiovascular System Disorders
Pathophysiology
• Causes of DVT include venous stasis, vessel wall
•
•
•
injury, and hypercoagulability. Perinatally, women
are at increased risk because of excess clotting
factors.
Areas where blood flows more slowly, usually
where veins are bending are more prone to DVT.
Postsurgery clients are at greater risk due to ↓
activity.
Septicemia resulting in hemolysis and dehydration can contribute to DVT.
Assessment and Diagnostic Findings
• Unilateral pitting edema in the affected extremity,
with pain and erythema over the site.
• Positive Homans’ sign.
• D-dimer test showing fibrin degradation
products.
• Duplex ultrasonography detects the occlusion
and changes in venous flow.
• Impedance plethysmography shows slowed
venous outflow from the affected area.
• MRI to image iliac or inferior vena caval sites.
• CT venography shows DVT.
108
Complications
• Massive PE, MI, or CVA from thromboembolus.
Medical Care and Surgical Treatment
• Anticoagulants and thrombolytics, followed by
outpatient warfarin treatment.
• Compression stockings and early ambulation.
• Thrombectomy; vena caval filter placement.
Keep in Mind
• Teach the client to report swelling, pain, or
warmth in an extremity.
• Seek immediate medical attention if sudden
dyspnea occurs.
• Teach the client to move about on airplanes and
long car rides.
Make the Connection
• Never repeat a positive Homans’ assessment.
• Monitor platelets and clotting time.
• Have client maintain bedrest; as ordered.
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Cardiovascular System Disorders
109
Aortic Stenosis
(a-or-tik ste-no-sis)
Clue: Diagnostic or Clinical Findings
Presence of a loud, harsh midsystolic,
crescendo–decrescendo murmur that
radiates to the side of the neck and
down the left sternal border or apex.
Heard loudest at the second right
ICS. Low BP, fatigue, dizziness,
and chest pain.
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Cardiovascular System Disorders
Pathophysiology
• AS develops from thickening, scarring, calcification, vegetation, or fusing of the flaps of the valve.
• Left ventricular hypertrophy occurs as the sympathetic nervous system is activated to compensate
for low cardiac output. When compensatory
mechanisms fail, heart failure results.
Assessment and Diagnostic Findings
• Presence of a loud, harsh midsystolic, crescendo–
•
•
•
•
decrescendo murmur that radiates to the side of
the neck and down the left sternal border or
apex. Heard loudest at the second right ICS.
Low BP, fatigue, vertigo or syncope, palpitations,
and angina chest pain.
CXR and ECG show enlargement of the left
atrium and ventricle.
Two-dimensional and Doppler echocardiography
show impaired movement of the aortic valve,
decreased cardiac output, and lowered ejection
fraction.
Cardiac catheterization shows increased ventricular
pressure and decreased cardiac output.
Complications
• CHF; pulmonary edema.
109
Medical Care and Surgical Treatment
• Prophylactic antibiotic therapy; anticoagulant
therapy.
• Valvotomy for young adults; valve replacement in
older adults.
Keep in Mind
• Teach clients to report any episodes of chest
pain, vertigo, or syncope immediately.
• Teach clients to seek immediate medical care
for chest pain.
• If a valve replacement is performed, teach the
client the importance of maintaining anticoagulant therapy and keeping laboratory appointments to assess effectiveness of therapy.
Make the Connection
• Monitor the INR and PT in clients with
valve replacement and on warfarin therapy.
• Assess for bleeding, assess platelet count, and
assess CBC for anemia.
• Remember: Microorganisms can grow on the
valves, forming vegetation that can embolize.
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Cardiovascular System Disorders
110
Venous Stasis Ulcer
(ve-nus sta-sis ul-ser)
Clue: Diagnostic or Clinical Findings
Ulcer that occurs on the lower
extremities in the presence of edema
and brown, leathery skin. Described
as “wet” and exudes a large amount
of serous fluid.
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Cardiovascular System Disorders
Pathophysiology
• Blood is not returned efficiently to the heart and
•
•
venous pressure ↑ in the lower extremities. The
↑ venous pressures cause backflow of blood into
the capillary exchange beds and leakage of serous
fluid containing wastes into the interstitial space.
Edema in the interstitial space prevents capillary
access for all cells and can be severe.
Increased pressure in a vein causes a small rupture that becomes a deeper wound that cannot
heal because of poor capillary access to inflammatory agents, oxygen, and glucose. The wound
ulcerates because of inflammatory substances
trapped in the subcutaneous tissue, damaging the
valves in the veins and exuding serous fluid.
Assessment and Diagnostic Findings
• Edema of the extremities, with brown, leathery
skin.
• Culture of the ulcer obtained.
• CBC to R/O infection.
Complications
• Infection, nonhealing chronic ulcerations that
affect the client’s quality of life; reulceration.
• Permanent damage to the valves in the veins.
110
Medical Care and Surgical Treatment
• Unna’s boot compression bandage is wrapped
with the leg elevated.
• Pentoxifylline therapy.
• Skin grafts and artificial cultured skin.
• Clients are instructed to walk, as tolerated.
Keep in Mind
• Teach the importance of elevating the legs;
walking as tolerated to ↑ use of skeletal muscle
pump.
Make the Connection
• Assess for healing when the compression
boots are removed (every 2–7 days).
• If skin grafts are used, the area should not be
disturbed until skin buds are seen.
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Cardiovascular System Disorders
111
Varicose Veins
(var-i-kos vanz)
Clue: Diagnostic or Clinical Findings
Visible, tortuous, bulging veins that
cause discomfort in the leg and
changes in body image.
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Cardiovascular System Disorders
Pathophysiology
• Venous return in the body is dependent on the
•
•
muscular contractions of the skeletal muscle
pump. Competency of the valves within the veins
cause forward flow that is eventually returned to
the heart.
In pregnancy, the pressure of the fetus causes
venous hypertension, and hormones make the
valves less competent, which ↑ incidence of varicose veins of the legs and anus to occur.
Superficial varicosities are more visible than more
deeply located varicosities.
Assessment and Diagnostic Findings
• Visible tortuous veins seen on the legs or hemor•
•
rhoids seen around the anus. Varicosities can
also occur in the esophagus because of portal
hypertension.
Contrast venography, MRI, and color-flow duplex
US that show blood pooling.
Clients complain of pain, pressure, or a dragging
sensation in the legs.
Complications
• Thromboembolisms, venous ulcerations, and
bleeding varicosities.
111
Medical Care and Surgical Treatment
• Sclerosing agents.
• Endovenous laser therapy, radiofrequency abla•
tion, ambulatory phlebectomy, and the traditional
saphenectomy with saphenofemoral ligation.
Corticosteroids and other immunosuppressants.
Keep in Mind
• Teach clients to utilize compression stockings if
•
they stand in one place for a prolonged period
of time; teach them to plantar flex and dorsiflex
the foot and ankle, and shift their weight from
leg to leg.
Teach pregnant clients to elevate the legs
frequently.
Make the Connection
• Assess whether the client who has
undergone treatment is using compression
stockings.
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Cardiovascular System Disorders
Peripheral Arterial
Disease
(per-if-er-al ar-te-re-al di-zez)
Clue: Diagnostic or Clinical Findings
Symptoms occur late in the disease
and include intermittent claudication
in the calves associated with activity.
Color changes in the legs, with hair
loss and dry, flaky skin, may occur.
112
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Cardiovascular System Disorders
Pathophysiology
• PAD is caused by progressive narrowing of the lumen
of the arteries by atherosclerotic plaque buildup.
• If arteries are totally occluded, necrosis and
ulceration (gangrene) develop, and the limb is
no longer viable.
Assessment and Diagnostic Findings
• The 5 Ps: pulselessness, paralysis, paresthesia,
pain, and pallor.
• Heaviness and pain in the legs after a short
period of exertion that are relieved by rest.
• ABI measures BP in the upper and lower extremi•
•
•
•
•
ties. The BP taken after a brief period of exercise in
the client with PAD shows a drop in the ankle BP,
indicating constriction and decreased perfusion.
Doppler US measures the velocity of blood flow.
MRI shows images of plaque in arteries.
Plethysmography and angiography to visualize
blood flow through the extremity.
Lipid panel and a total blood chemistry to assess
electrolytes and nitrogenous wastes.
D-dimer test to assess for fibrin degradation
products; Crp and interleukin 6 to assess for
inflammatory markers.
112
Complications
• Thromboembolism, CVA, and MI.
• Necrosis, arterial ulcerations, gangrene, and
amputation.
Medical Care and Surgical Treatment
• Anticoagulants; pentoxifylline.
• Vasodilators and calcium channel blockers.
• Amputation.
Keep in Mind
• Teach client to have yearly physicals and blood
work to detect risks for atherosclerosis.
• Eat a healthy diet and exercise daily.
Make the Connection
• Monitor dependent and elevated extremities
•
in the client with PAD. Palpate for pulses; report
loss of pulse, mottling, or cold extremities.
Monitor anticoagulant therapy and glucose levels.
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Cardiovascular System Disorders
113
Buerger’s Disease
(burg-erz di-zez)
Clue: Diagnostic or Clinical Findings
A disease of young men who
smoke. Thrombi develop in the
legs, occluding circulation. “Your
cigarettes or your legs” is often
the choice.
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Cardiovascular System Disorders
Pathophysiology
• BD also known as thromboangiitis obliterans is a
•
disease of recurrent inflammation of the small
and medium arteries of the legs that results in
thrombus formation.
Young men (aged 25–40) who smoke are affected.
It is thought that substances in the tobacco products trigger an autoimmune response in these
young men. Vasospasm and loss of arterial blood
flow occurs.
Assessment and Diagnostic Findings
• The 5 Ps: pulselessness, paralysis, paresthesia,
pain, and pallor.
• Heaviness and pain in the legs after a short
period of exertion that are relieved by rest.
• ABI measures BP in the upper and lower extremi-
•
•
•
ties. The BP taken after a brief period of exercise
in the client with PAD shows a drop in the
ankle BP, indicating constriction and decreased
perfusion.
Doppler US measures the velocity of blood flow.
MRI shows images of plaque in arteries.
Plethysmography and angiography to visualize
blood flow through the extremity.
113
Complications
• Necrosis, arterial ulcerations, gangrene, and
amputation.
Medical Care and Surgical Treatment
• Anticoagulants; pentoxifylline to increase red
blood cell flow.
• Vasodilators and calcium channel blockers.
• Amputation.
• Smoking cessation program.
Keep in Mind
• Teach the client the importance of smoking
cessation.
• Refer client to a support group for those with
Buerger’s disease.
Make the Connection
• The legs will be purple-red when
•
•
dependent and show pallor when elevated;
palpate for pulses.
Maintain anticoagulant and vasodilator therapy.
Assess the effectiveness of smoking cessation
program and support group interactions.
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114
Raynaud’s Disease
(re-noz di-zez)
Clue: Diagnostic or Clinical Findings
Vasospasm and vasoconstrictive
ischemia of the tips of the nose,
fingers, hands, feet, and toes when in
contact with cold objects or cold
temperatures.
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Cardiovascular System Disorders
Pathophysiology
• A disease of women, RD causes vasospasm and
•
•
vasoconstrictive ischemia of the tips of the nose,
fingers, hands, feet, and toes when in contact
with cold objects or cold temperatures. Ischemia
is followed by a period of hyperemia. Diagnosis is
made when the ischemic attacks occur for 2 or
more years.
Endothelin 1 and angiotensin may be causative
agents.
Secondary RD is associated with autoimmune/
collagen disorders and persons with occupations
that involve vibratory tools like jackhammers.
Assessment and Diagnostic Findings
• CBC to assess for blood disorder, BUN and
•
•
creatinine to assess renal and hydration status,
PT and aPTT to assess the clotting cascade;
serum glucose; and thyroid panel to assess for
metabolic disorders. Diagnostics for autoimmune and collagen disorders are also ordered.
Calcitonin gene-related peptide, which is a
vasodilator, is found to be decreased in RD.
Neuropeptide Y, a vasoconstrictor, is found in
high levels in secondary RD.
114
Complications
• Digital ulceration, tissue loss, and gangrene.
Medical Care and Surgical Treatment
• ACE inhibitors, angiotensin-receptor antagonists,
•
•
•
vasodilators, SSRI, analgesics, and local infiltration with lidocaine.
Digital sympathectomy.
Pharmaceutical-grade omega-3 fatty acid.
Biofeedback; avoiding contact with cold; smoking
cessation.
Keep in Mind
• Teach the client to insulate the hands, feet, and
face from cold temperatures and to never smoke.
• Report ischemic events immediately.
Make the Connection
• Assess color, sensation, and temperature
in digits and nose; smoking cessation program.
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Cardiovascular System Disorders
115
Aortic Aneurysm
(a-or-tik an-u-rizm)
Clue: Diagnostic or Clinical Findings
Abdominal pain, nausea, or fullness
relieved by position change. Pulsating
mass in the abdomen. Auscultation
with the bell of the stethoscope for a
bruit adjacent to the umbilicus.
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Cardiovascular System Disorders
Pathophysiology
• Bulging or ballooning of the aorta due to athero-
•
•
sclerosis, hypertension, chronic obstructive pulmonary disease, smoking, trauma, or congenital
anomaly. Commonly found in the abdominal
aorta (abdominal aortic aneurysm [AAA]). Tends
to run in families with Marfan’s syndrome.
Types include fusiform, saccular, and dissecting.
May be completely asymptomatic until it
ruptures.
Assessment and Diagnostic Findings
• Abdominal pain, nausea, or fullness relieved by
position change. Pulsating mass in the abdomen.
• Auscultation with the bell of the stethoscope for
a bruit adjacent to the umbilicus.
• US screening for men aged 50 or older or those
with a family history.
• MRI showing a enlarged black mass; aortography
showing the outline of the aortic abnormality.
• Spiral CT scan with contrast revealing the
calcified rim of the aneurysm.
Complications
• Rupture of the aneurysm, cardiac arrest,
hemorrhage, shock, and death.
115
Medical Care and Surgical Treatment
• Monitoring of the size of the aneurysm.
• Antihypertensive agents for BP management.
• Smoking cessation program.
• Surgical intervention with open surgical repair or
endovascular grafting.
Keep in Mind
• Teach clients with a first-degree relative with AAA
•
the risk factors and symptoms to report, and
encourage screening by ultrasound.
Teach clients at risk to maintain therapy with
antihypertensive agents, avoid smoking, and have
yearly examinations.
Make the Connection
• The rate of rupture increases with age
or surgery.
• Assess BP and advise clients undergoing surgical
repair to avoid lifting heavy objects.
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Cardiovascular System Disorders
116
Hypertension
(hi-per-ten-shun)
Clue: Diagnostic or Clinical Findings
BP readings of greater than 119 mm Hg
systolic or greater than 79 mm Hg
diastolic classify the client as
prehypertensive. The client may have
no symptoms or, in severe cases,
headache and nosebleed.
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Cardiovascular System Disorders
Pathophysiology
• BP is determined by CO, which is determined by
•
heart rate multiplied by the stroke volume. The
heart rate can be affected by stimulation of the
SNS responding to arterial baroreceptors that
measure BP and by chemoreceptors that measure
CO2 levels. Other mechanisms that alter BP
include the renin-angiotensin-aldosterone system,
exercise, emotions, and taking medications that
cause vasoconstriction. High blood pressure damages the intima of arteries, making way for infiltration of macrophages, muscle fibers, cholesterol,
and fatty acids that form atherosclerotic plaque.
PVR is the resistance to blood flow through
arterioles creating a high afterload.
Assessment and Diagnostic Findings
116
Complications
• Atherosclerosis and vessel damage; cerebrovascu•
lar accident (CVA) and myocardial infarction
(MI), and resulting congestive heart failure (CHF).
Nephropathy and retinopathy due to poor
perfusion.
Medical Care and Surgical Treatment
• Diuretics, antihypertensives, and lifestyle changes.
• Smoking cessation program.
Keep in Mind
• Teach clients to change modifiable risk factors,
avoid added salt, decrease caffeine intake, drink
alcohol modestly, take prescribed medications
regularly, and manage stress through exercise or
meditative means.
• Systolic BP should ideally be less than 120 mm Hg
•
and diastolic BP should be less than 79 mm Hg
(JNC 7).
Hypertension is diagnosed if the average BP
readings taken on two separate occasions is
greater than 139 mm Hg systolic and
greater than 89 mm Hg diastolic.
Make the Connection
• Assess BP carefully in the correct way with
the correctly sized cuff, the client seated, and the
sphygmomanometer at heart level. Take the BP
after 5 minutes of rest.
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117
Leukemia
(loo-ke-me-a)
Clue: Diagnostic or Clinical Findings
Low-grade fever, lymphadenopathy,
bleeding tendency, infections, and
anemia. Bone marrow biopsy shows
many immature WBCs.
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Cardiovascular System Disorders
Pathophysiology
• Leukemia can be acute or chronic and affect
•
lymphocytes, monocytes, granulocytes, erythrocytes, and platelets. Due to a mutation in the
stem cells of the bone marrow, immature WBCs
(blasts), proliferate uncontrollably in the bone
marrow, lymph tissue, and spleen. In the bone
marrow, the immature and ineffective WBCs
crowd the normal WBCs, RBCs, and platelets,
greatly reducing their number.
Types include ALL, AML, CLL, CML.
Assessment and Diagnostic Findings
•
•
•
•
•
CBC showing many immature WBCs, low RBC
count, and low platelet count.
Bone marrow aspiration, with cell count showing
many immature blasts.
Genetic testing for the Philadelphia chromosome
(CML).
LP for identification of blasts in CSF to determine
CNS involvement.
Low-grade fever, pallor, weakness, SOB, bone pain,
headache, and confusion.
117
Complications
• Thrombocytopenia, petechiae and bleeding,
infection, GVHD, and severe anemia.
Medical Care and Surgical Treatment
• Chemotherapy, radiation therapy, stem cell
transplant, and bone marrow transplant.
Keep in Mind
• Teach clients that ALL in children has a high cure
rate (cancer-free for 5 years or more).
• Clients with leukemia should use soft toothbrushes,
eat foods of moderate temperature, avoid organic
vegetables, take frequent rest periods, and report
fever immediately.
Make the Connection
• Monitor the CBC, vital signs, and oxygen
saturation levels frequently.
• Maintain reverse isolation in the client undergoing
BMT.
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Cardiovascular System Disorders
118
Multiple Myeloma
(mul-ti-pl mi-e-lo-ma)
Clue: Diagnostic or Clinical Findings
Pathologic fractures from severe
osteoporosis, bleeding tendency,
infections, and anemia affecting those
in the fifth to seventh decades of life.
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Cardiovascular System Disorders
Pathophysiology
• Mutation of plasma cells (type of B-lymphocyte)
•
that infiltrate the bone marrow, bone tissue, liver,
spleen, lymph nodes, lungs, adrenal glands,
kidneys, skin, and GI tract.
MM has a poor prognosis.
Assessment and Diagnostic Findings
• Bone pain, especially in the back or ribs, joint
pain, low-grade fever, and general malaise.
• Pathologic fractures and spinal cord compression, hypercalcemia, and pneumonia.
• CBC shows anemia, WBC fluctuation, and
decreased platelets.
• X-ray, CT scan, bone scans, and MRI show severe
osteoporosis.
• Urine is positive for M-type gamma globulins
known as Bence-Jones protein (24-hour urine).
• Bone marrow biopsy confirms the presence of
immature plasma cells.
Complications
• Bone destruction, pathologic fracture, spinal cord
•
compression with loss of bowel and bladder control, and renal calculi from hypercalcemia; GVHD.
Recurrent infections, pneumonia, and sepsis.
118
Medical Care and Surgical Treatment
• High-dose steroids, IV biphosphonates, thalidomide, and analgesics.
• Treatment of hypercalcemia, hyperuricemia,
dehydration, respiratory infection, renal calculi.
• High-dose chemotherapy with stem cell transplant and external beam radiation therapy.
Keep in Mind
• Teach the client to drink plenty of fluids, walk as
tolerated, and avoid injury.
• Report fever, pain, or paresthesias immediately.
Make the Connection
• Monitor the CBC, vital signs, oxygen
saturation, and breath sounds frequently.
• Ambulation as tolerated.
• Lift the client with a lift sheet gently; provide
passive and active range of motion.
• Encourage fluid intake of up to 4 liters daily;
medicate for pain as needed.
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Cardiovascular System Disorders
119
Graft-Versus-Host
Disease
(graft vur-sus host di-zez)
Clue: Diagnostic or Clinical Findings
Approximately 31/2 months following
solid organ, bone marrow, or stem
cell transplant, damage to the
epithelial cells of the skin, GI tract,
and hepatocytes occurs from an
immune attack initiated by the
transplanted tissue.
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Cardiovascular System Disorders
Pathophysiology
• GVHD can occur following solid organ, bone
•
•
•
marrow, or stem cell transplant. The graft cells
recognize the host cells as foreign.
Phase 1 of GVHD involves the host tissue that
has been prepared for transplant by use of
chemotherapy and radiation therapy. The injured
tissue releases cytokines, which stimulate the
host’s CD4+ cells.
In phase 2 of GVHD, activated CD4+ cells cause
the graft to activate T killer cells and NK cells that
mount an immune response against susceptible
tissues of the host (epithelial tissue, GI tract, and
hepatocytes).
In phase 3 of GVHD, immune cells and cytokines
begin to damage host tissues.
Assessment and Diagnostic Findings
• CBC shows anemia, thrombocytopenia, and an
•
•
elevation in eosinophils; Howell-Jolly bodies are
identified in the peripheral blood smear.
Elevated serum levels of IL-2 receptor alpha, TNF
receptor 1, IL-8, and hepatocyte growth factor;
elevated LE and liver biopsy.
US, CT scan, and Doppler studies to assess the liver.
119
• Endoscopic examination of the GI tract.
Complications
• Graft failure, hemorrhage, infection, and liver
failure that may lead to death.
• Permanent scarring of epithelium of skin and
GI tract.
Medical Care and Surgical Treatment
• Removal of graft T cells.
• Immunosuppressive agents, DMARDs, and
anti-TNF agents.
• Plasmapheresis of host CD4+ cells.
Keep in Mind
• Teach the client that prior to bone marrow or
stem cell transplant, immunosuppressive and
steroid drugs may be given.
Make the Connection
• Monitor serial CBC, liver enzymes, and
blood chemistries. Remember: This disease
occurs 3 1/2 months after graft.
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120
Metabolic Acidosis
(met-a-bol-ik as-i-do-sis)
Clue: Diagnostic or Clinical Findings
ABG shows pH of less than 7.35,
PCO2 in the range of 35–45 mm Hg
or decreasing
to compensate, and
_
HCO3 of less than 22 mEq/L.
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Cardiovascular System Disorders
Pathophysiology
• Normal pH of the body is 7.35–7.45. ABG analy•
•
•
•
sis diagnoses metabolic acidosis; pH is low, CO2
is within normal_range or decreasing to compensate, and HCO3 is low.
Buffering systems are initiated by the body when
the pH goes out of range. The first to react are
cellular buffers. In metabolic acidosis, H+ are
absorbed into the cells, causing a shift of K+ into
the extracellular area.
The lungs are the second buffering system to
activate. When pH is low, CO2 is released
through rapid and deep respirations.
The kidneys are the last buffering system to
activate; and it may take as long as 1–2 days
for them to begin to affect pH. In metabolic
acidosis, the kidneys secrete H+.
Causes include diarrhea (loss below the waistlose base), CRF, lactic acidosis, salicylate poisoning, methanol and alcohol poisoning, paraldehyde poisoning, and diabetic ketoacidosis.
Assessment and Diagnostic
Findings
_
• Low pH and low HCO3 . The value of the anion gap
may be high, low, or normal; guides further testing.
120
• Serum osmolality; blood chemistry analysis for
azotemia, electrolytes, and high fasting glucose
levels; Kussmaul’s respirations; change in mental
status; ECG changes.
Complications
• Prolonged acid-base imbalance will lead to death.
Medical Care and Surgical Treatment
• IV administration of sodium bicarbonate; correction of electrolytes.
Keep in Mind
• Teach the client about toxic materials in the
environment.
• Teach the client the signs and symptoms of
diabetes mellitus and the importance of
maintaining a normal blood glucose level.
Make the Connection
• Monitor laboratory values, mentation,
acetone breath, and ECG.
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Cardiovascular System Disorders
121
Metabolic Alkalosis
(met-a-bol-ik al-ka-lo-sis)
Clue: Diagnostic or Clinical Findings
ABG shows pH of greater than 7.45,
PCO2 in the range of 35–45 mm Hg
or rising
to compensate, and
_
HCO3 of greater than 26 mEq/L.
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Cardiovascular System Disorders
Pathophysiology
• Normal pH of the body is 7.35–7.45. The ABG
•
•
•
•
diagnoses metabolic alkalosis, pH is high, CO2 is
within normal
range or increasing to compensate,
_
and HCO3 is high.
Buffering systems are initiated by the body when
the pH goes out of range. The first to react are
cellular buffers. In metabolic alkalosis, H+ are
released from the cells, causing a shift of potassium ions (K+) into the cells.
The lungs are the second buffering system to
activate. When pH is high, CO2 is held by slow,
shallow respirations.
The kidneys are the last buffering system to
activate, and it may take as long as 1–2 days
for them to begin to affect pH. In metabolic
alkalosis, the kidneys hold H+.
Causes include persistent vomiting; gastrointestinal suction; diarrhea; and use of loop
diuretics, antacids, licorice, glucocorticoids,
and mineralocorticoids.
Assessment and Diagnostic Findings
• Urine chloride less than 20 mEq/L; hypocalcemia
and hypokalemia; ABG analysis.
121
• Abnormalities on electrocardiogram (ECG).
Complications
• Prolonged changes in pH level of the body.
• Tetany, seizures, change in mentation, hypoventila+
tion and hypoxemia, and lethal arrhythmias (K ).
Medical Care and Surgical Treatment
• Carbonic anhydrase inhibitors, IV hydrochloric
acid preparations, potassium-sparing diuretics,
ACE inhibitors, K+ and Ca supplements, corticosteroids, nonsteroidal fluid replacement, and fluid
replacement.
Keep in Mind
• Teach clients about metabolic alkalosis, especially
in the case of vomiting for prolonged periods, and
to seek medical care if mental status changes occur
or if they have tremors.
Make the Connection
• Monitor ABGs and other laboratory
values. Check both Chvostek’s and Trousseau’s
signs to detect low calcium levels and ECG for
arrhythmias related to low K+ levels.
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Cardiovascular System Disorders
Respiratory Acidosis
(res-pir-a-to-re as-i-do-sis)
Clue: Diagnostic or Clinical Findings
ABG shows pH of less than 7.45,
than 45 mm Hg,
PCO2 of greater
_
and HCO3 within range or rising
to compensate.
122
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Cardiovascular System Disorders
Pathophysiology
• Normal pH of the body is 7.35–7.45. The ABG
•
•
•
•
analysis diagnoses respiratory
acidosis; pH is low,
_
CO2 is high, and HCO3 is within normal range
or rising to compensate.
Buffering systems are initiated by the body when
the pH goes out of range. The first to react are
cellular buffers. In respiratory acidosis, H+ are
absorbed into the cells, causing a shift of K+ out
of the cells.
The lungs are the second buffering system to
activate. When pH is low, CO2 is released
through rapid and deep respirations.
The kidneys are the last buffering system, and it
may take as long as 1–2 days for them to begin
to affect pH. In respiratory acidosis, the kidneys
secrete H+.
Causes include COPD, hypoventilation, sleep
apnea, and drug use that suppresses respiratory
function.
Assessment and Diagnostic Findings
• ABG analysis, CBC for polycythemia, drug
screens, and CXR.
122
Complications
•
Chronic hypoxemia leading to polycythemia,
pulmonary hypertension, and cor pulmonale;
mental status changes; cerebral edema; and
papilledema. Death may occur.
Medical Care and Surgical Treatment
• Bronchodilators, ventilation support, mechanical
•
or, naloxone or flumazenil for opioid and benzodiazepine overdosages, and theophylline.
Surgical interventions for obesity and sleep
apnea.
Keep in Mind
• Teach the client to avoid smoking, use oxygen
as directed, and maintain a healthy weight.
• Teach the client about sleep study programs.
Make the Connection
• Monitor ABGs, ventilation status, and
CBC for polycythemia.
• Assess Glasgow Coma Scale score for cerebral
edema; assess for papilledema.
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Cardiovascular System Disorders
Respiratory Alkalosis
(res-pir-a-to-re al-ka-lo-sis)
Clue: Diagnostic or Clinical Findings
ABG shows pH of greater than
7.45, PCO2 of_ less than 35 mm Hg,
and HCO3 within the range of
22–26 mEq/L or decreasing to
compensate.
123
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Cardiovascular System Disorders
Pathophysiology
• Normal pH of the body is 7.35–7.45. The ABG
•
•
•
•
analysis diagnoses respiratory
alkalosis; pH is
_
high, CO2 is low, and HCO3 is within normal
range or decreasing to compensate.
Buffering systems are initiated by the body when
the pH goes out of range. The first to react are
cellular buffers. In respiratory alkalosis, H+ are
released from the cells, causing a shift of K+ into
the cells.
The lungs are the second buffering system to
activate. When pH is high, CO2 is held by
slow, shallow respirations.
The kidneys are the last buffering system to
activate, and it may take as long as 1–2 days
for them to begin to affect pH. In respiratory
alkalosis, the kidneys hold H+.
Causes include pain, anxiety, fever, CVA, tumor,
and trauma.
Assessment and Diagnostic Findings
serum chemistries for intracellular
• ABG analysis;
+
+
•
shifts of Na , K , and phosphates; and LFT, as respiratory alkalosis may be caused by liver failure.
CBC showing a reduced hematocrit.
123
• CXR and VQ scans to identify pulmonary
infection, pneumothorax, or PE.
• Brain MRI to R/O tumor.
Complications
• Cerebral vasoconstriction leading to seizures.
• Hyperventilation causing paresthesias, dyspnea,
and chest pain.
• ECG changes related to hypocapnia; BP changes.
Medical Care and Surgical Treatment
• Rebreathing of CO2 and treatment of underlying
conditions.
Keep in Mind
• Teach the client methods for relieving
hyperventilation.
Make the Connection
• Monitor ABG; assist to calm the client;
monitor CBC and imaging studies.
• Institute seizure precautions if necessary; monitor
the ECG and vital signs.
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Page 8
RESPIRATORY
Bronchiectasis, 124
Asthma, 125
Emphysema, 126
Chronic Bronchitis, 127
Pneumothorax, 128
Cystic Fibrosis, 129
Acute Respiratory Distress Syndrome
(ARDS), 130
Severe Acute Respiratory Syndrome
(SARS), 131
Pulmonary Embolism, 132
Pneumonia, 133
Pleural Effusion, 134
Influenza, 135
Legionnaires’ Disease, 136
Lung Cancer, 137
Histoplasmosis, 138
Sarcoidosis, 139
Mesothelioma, 140
Tuberculosis (TB), 141
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Respiratory Disorders
124
Bronchiectasis
(brong-ke-ek-ta-sis)
Clue: Diagnostic or Clinical Findings
Dyspnea, cyanosis, expectoration of
large amounts of foul-smelling mucus.
↓ RBC, weight loss. Rhonchi heard on
auscultation.
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Respiratory Disorders
Pathophysiology
• Chronic dilation of the bronchi and bronchioles
due to inflammation.
• Inflammatory process destroys elasticity of
smooth muscle in the airways.
• Chronic infections occur in dilated areas that
retain mucus and obstruct airways.
• Can be localized or diffuse; associated with
childhood diseases (e.g., measles), influenza, or
tuberculosis.
Assessment and Diagnostic Findings
• Recurrent respiratory infections, foul-smelling
•
•
mucus from accumulation of infected secretions,
rhonchi over bronchi and diminished breath
sounds in the lung bases.
High-resolution CT scan, CBC with differential,
ABG, oxygen saturation.
Bronchoscopy for diagnosis and palliative
treatment.
Complications
• Anemia due to poor dietary intake (dyspnea).
• Respiratory acidosis; atelectasis, pneumonia.
• Chronic obstructive disease.
• Necrosis of bronchi and bronchioles.
124
Medical Care and Surgical Treatment
• Antibiotics, bronchodilators, mucolytics, expectorants, supplemental oxygen, leukotriene inhibitors.
• Postural drainage; limiting of activity level.
• Bronchoscopy for palliative treatment.
• Segmental lobectomy.
Keep in Mind
• Teach importance of influenza and pneumonia
vaccination.
• Postural drainage must be continued on an
outpatient basis; discontinue smoking.
Make the Connection
• Assess for oxygen saturation by pulse
oximetry as well as for worsening dyspnea.
• Auscultate lungs every 4 hours, and perform
postural drainage.
• Assess characteristics of cough and mucus.
• Remember: When there is collection and stasis
of mucus, viruses and bacteria have a perfect
medium in which to grow and cause infection.
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Asthma
(az-ma)
Clue: Diagnostic or Clinical Findings
Expiratory wheeze on auscultation,
rapid onset, difficult expiration,
nonproductive cough, “chest is tight,”
and ↓ O2 saturation.
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Pathophysiology
125
aminophylline drip.
• Reactive inflammatory disorder associated with
• Small, frequent high-calorie, high-protein meals.
• Limiting of activity level.
•
Keep in Mind
•
exposure to allergens, viral infection, pollution,
smoking, or extremes of temperature.
Chronic inflammation results in fibrosis and
narrowing of bronchiole passageways, leading
to air trapping, bronchospasm, and increased
dead air space.
Mast cells, active in inflammation, release
histamine, prostaglandins, leukotrienes, and
bradykinin.
Assessment and Diagnostic Findings
• Sudden onset of nonproductive cough, expiratory
•
wheeze, dyspnea, “tight chest,” ↑ expiratory
effort and prolonged expiratory cycle, diaphoresis, and tachycardia.
ABG (acidosis), blood and sputum for eosinophils,
↑ serum IgE, abnormal PFTs, and CXR, allergy skin
testing.
Complications
• Status asthmaticus; acute respiratory failure.
Medical Care and Surgical Treatment
• Beta2-agonist bronchodilators, leukotriene
inhibitors, supplemental O2, corticosteroids, IV
• Environment should be free of allergen-laden
materials like carpets and drapes.
• Stop smoking; have a rescue inhaler available at
all times (beta2-agonist).
• Increase fluid intake; maintain a healthy diet.
• Monitor asthma with a peak flowmeter.
• Avoid temperature extremes.
• Vaccinate for influenza and pneumonia.
Make the Connection
• Monitor for exacerbation of condition,
respiratory failure, and status asthmaticus.
• Monitor breathing pattern, auscultate lungs every
4 hours, and monitor with pulse oximetry.
• Remember: Daily assessment with the peak
flowmeter is integral to treating exacerbations
early.
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Emphysema
(em-fi-se-ma)
Clue: Diagnostic or Clinical Findings
Barrel or pigeon chest, dyspnea, the
“pink puffer,” ↑ PaCO2, chronic
respiratory acidosis, and hypoxic
respiratory drive.
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Pathophysiology
• A chronic disorder in which the alveolar struc-
•
tures distend, lose elasticity, rupture, or coalesce,
resulting in damage and destruction to the pulmonary capillary bed, air trapping, and increased
dead air space.
Cigarette smoking and an inherited deficiency
of α1-antitrypsin are cocontributors to the
disease. ↓ α1-antitrypsin results in elastase secreted from neutrophils that can digest elastin and
other alveolar structures.
Assessment and Diagnostic Findings
• Pursed lip breathing, a prolonged expiratory
•
•
respiratory cycle, barrel or pigeon chest, and use
of accessory muscles to breathe; difficult inspiration and chronic cough with thick sputum.
Abnormal CXR, and PFTs, sputum analysis, ABG.
Clubbing of fingers, diminished breath sounds,
orthopnea, dyspnea on exertion.
Complications
• Cor pulmonale, recurrent respiratory infections,
and respiratory failure.
• Hypoxia and confusion.
126
Medical Care and Surgical Treatment
• Bronchodilators, expectorants, mucolytics,
supplemental O2, corticosteroids, antibiotics.
• Lung volume reduction surgery.
• Limiting of activity level.
Keep in Mind
• Teach pursed lip breathing. O2 may be needed at
home.
• Vaccinate for influenza and pneumonia.
• Suggest small, frequent nutrient-dense meals.
↑ fluids.
Make the Connection
• Monitor I&O, calorie count; offer small
high-calorie, high-protein meals frequently.
• Assess O2 saturation, ABG, breathing pattern;
clients may like a fan blowing on them.
• Remember: Keep O2 at low levels; hypoxic
respiratory drive.
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Chronic Bronchitis
(kron-ik brong-ki-tis)
Clue: Diagnostic or Clinical Findings
A history of a chronic productive
cough of more than 3 months’ duration
for more than 2 consecutive years;
the “blue bloater.”
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Respiratory Disorders
Pathophysiology
• Chronic Inflammation by IL-8 and cytokines of
•
the mucous membrane lining the bronchi and
bronchioles. Excess mucus is produced, and the
mucociliary pump ceases to function properly,
causing chronic congestion. Common in smokers.
Chronic bronchitis results in a fibrotic, noncompliant airway and pulmonary hypertension.
Assessment and Diagnostic Findings
• Cough with expectoration for at least 3 months
•
•
•
for more than 2 consecutive years, with dyspnea
and cyanosis.
The “blue bloater” related to cor pulmonale;
clubbing of the fingernails.
Fever, headache, fatigue, and nausea.
Along with clinical findings, abnormal, CXR scans,
MRI, ABGs, and abnormal PFTs.
Complications
• Worsening right-sided CHF.
• Chronic bouts of pneumonia and hospitalization.
• Colonization of antibiotic-resistant organisms.
• Development of oxygen dependency as pulmonary
function worsens.
• Death from pneumonia and/or heart failure.
127
Medical Care and Surgical Treatment
• Bronchodilators, mucolytics, diuretics, oxygen
•
•
supplementation, anti-infective drugs, nebulizer
treatments, incentive spirometry, antihypertensives,
ACE inhibitors, and inotropic drugs and betaadrenergic blockers.
Smoking cessation program.
Lung-reduction surgery.
Keep in Mind
• Teach clients that the effects of smoking.
• Teach clients that vaccination against
influenza and pneumonia are necessary.
• Teach clients to report SOB, symptoms of infection, or sudden weight gain immediately.
Make the Connection
• Monitor diagnostic chest x-rays, CT scan,
or MRI for improvement.
• Monitor ABGs and pulse oximetry.
• Weigh the client daily during acute episodes of
right-sided CHF.
• Plan care according to activity tolerance.
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Pneumothorax
(nu-mo-tho-raks)
Clue: Diagnostic or Clinical Findings
Sudden sharp pain in the chest area,
SOB, ↓ O2 saturation, absent breath
sounds in the affected lung.
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Respiratory Disorders
Pathophysiology
• Potential space created by the visceral and pari-
•
etal pleura creates negative pressure in that area.
Once breached by trauma or a pathologic event,
negativity is lost and the potential space becomes
an actual space that fills with air (pneumothorax)
or blood (hemothorax).
Positive pressure in the pleural space presses
against the lung tissue, causing atelectasis ↓ gas
exchange.
128
• For lung collapse related to pathology (injury
•
to the pleura from disease), a thoracotomy
with evacuation of accumulated fluid offers
relief.
Recurrent pneumothorax may require pleurodesis.
Keep in Mind
• The chest tube may be in place for several days.
• Bronchodilators, coughing and deep breathing
exercises, and frequent x-rays are needed.
Assessment and Diagnostic Findings
• Sudden, sharp pleural pain; dyspnea; anxiety; SOB.
• Absent breath sounds in affected lung field, uneven
chest movement, ↓O2 saturation, hemoptysis.
• ABG abnormalities and CXR showing atelectasis.
Complications
• Mediastinal shift with respiratory distress.
• Respiratory acidosis.
• Subcutaneous emphysema.
Medical Care and Surgical Treatment
• Depending on the size of the pneumothorax
(>30%), placement of a chest tube exerts suction
in the pleural space, restoring negative pressure.
Make the Connection
• Monitor O2 saturation, auscultate lungs
•
•
every 4 hours, and palpate thorax for subcutaneous emphysema.
Remind client to ask for pain medication as needed,
especially if the chest tube is being removed.
Remember: Monitor the blood pressure carefully
for hypotension following evacuation of a
large amount of fluid from the pleural space.
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Cystic Fibrosis
(sis-tik fi-bro-sis)
Clue: Diagnostic or Clinical Findings
Meconium ileus at birth is the earliest
sign. Later, respiratory, gastrointestinal,
and reproductive dysfunction.
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Respiratory Disorders
Pathophysiology
• Autosomal recessive disorder that affects chro•
•
mosome 7, which normally produces a protein
CFTR that affects movement of Na+ and Cl– ions.
All secretions of exocrine glands of the respiratory,
gastrointestinal, and reproductive tracts become
thick and obstruct normal flow.
Sweat glands do not reabsorb sodium, so salt
depletion in sweat can occur.
Assessment and Diagnostic Findings
• CXR, testing of sweat electrolytes, PFTs, fat absorp•
tion; pancreatic enzymes for infants who present
with a meconium ileus and children with repeated
or severe pulmonary disease.
Genotype testing of the parents and child.
Complications
• Obstruction to pancreatic exocrine function.
Chronic pancreatitis and secondary type 1 DM.
• Potentially fatal recurrent respiratory episodes of
•
•
infections and atelectasis; thorax may become
barrel-shaped due to respiratory effort.
Steatorrheic stools, malnutrition, hypovitaminosis;
and bowel obstruction.
Sterility.
129
Medical Care and Surgical Treatment
• Pancreatic enzymes.
• Antibiotics for respiratory episodes, chest percussion, supplemental O2, ABG, CXR, CBC.
• Lung transplant.
• Genetic counseling.
Keep in Mind
• The disease is chronic, and clients usually have
shortened life spans (3 or 4 decades).
• Chest percussion and pancreatic enzyme replacement must be continued.
• Vaccination for influenza and pneumonia are
recommended for high-risk individuals.
Make the Connection
• Monitor PFTs and O2 saturation;
auscultate lungs sounds every 4 hours.
• Monitor stools; assess for small-bowel obstruction.
• Assess labs for hypovitaminosis and low total
protein.
• Remember: Help families emotionally.
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Acute Respiratory Distress
Syndrome (ARDS)
(a-kut res-pir-a-to-re dis-tres sin-drom)
Clue: Diagnostic or Clinical Findings
Rhonchi and crackles on auscultation,
↓ O2 saturation after sepsis,
near-drowning, or aspiration
of gastric contents.
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Pathophysiology
• Destruction of alveolar walls and capillary beds
•
caused by stimulation of immune mediators that
↓O2 exchange by fibrosis and edema.
Immune mediators are also stimulated by
traumatic events.
Assessment and Diagnostic Findings
• Rapid breathing; air hunger.
• CXR showing consolidation to complete “white
•
•
•
out”; symptoms of noncardiogenic right-sided
CHF.
ABG and pulse oximetry showing decreased
oxygenation.
Auscultation revealing rhonchi, crackles, and
areas of absent breath sounds over areas of
consolidation.
Cool skin, cyanosis, peripheral edema.
Complications
• Acute respiratory failure with a 50% or greater
mortality rate.
• Respiratory acidosis.
• Multisystem organ failure; shock.
130
Medical Care and Surgical Treatment
• Intubation and ventilation with PEEP.
• Hemodynamic monitoring for CO; daily weigh•
•
ing to assess fluid retention; use of diuretics,
antibiotics, and inotropic agents; ECG
monitoring.
Intravenous support; transfusion of PRBC for
oxygen transport.
Enteral feedings; intermittent prone positioning
for increased oxygenation.
Keep in Mind
• Teach clients about mechanical ventilation.
• Will require serial x-rays, laboratory tests, and
central IV catheters.
Make the Connection
• Monitor central venous pressure, lung
sounds, ABG, pulse oximetry, and ECG.
• Monitor I&O strictly.
• Monitor for signs of shock, assess serial CXR, and
provide aseptic ventilator care.
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Severe Acute Respiratory
Syndrome (SARS)
(se-ver a-kut res-pir-a-to-re
dis-tres sin-drom; sarz)
Clue: Diagnostic or Clinical Findings
Cough, rhonchi, crackles, and
worsening respiratory symptoms
after exposure to the coronavirus.
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Respiratory Disorders
Pathophysiology
• Exposure to the coronavirus by droplet inhalation
•
or contact. The SARS virus can live 6 hours on
the hands.
After contact with the SARS coronavirus, immune
mediators cause inflammation, edema, and pneumonia by blocking gas exchange and resulting in
filling of the alveoli with fluid.
Assessment and Diagnostic Findings
• Auscultation revealing rhonchi, crackles, and
•
•
diminished lung sounds in areas of consolidation;
fever; myalgia; cough.
Liver function tests (LFTs) showing elevation;
complete blood count (CBC) for low white blood
cell (WBC) and platelet counts; chest x-ray and
chest computed tomography (CT) for areas of
consolidation; electrolyte panel for low potassium and low sodium; polymerase chain reaction
(PCR) and antibody test for SARS.
Recent trips to countries with SARS.
131
• Intubation and ventilation possibly required if the
client’s status worsens.
• Hemodynamic monitoring for cardiac output;
•
Keep in Mind
• Teach ventilator-dependent clients about intense
physical and psychosocial care they will receive.
• Serial x-rays, arterial blood gas (ABG), blood
transfusion, central venous catheters, and intensive care are needed.
Make the Connection
• Strict infection control must be followed.
• Monitor central venous pressure, lung sounds,
Complications
• Acute respiratory failure and death.
Medical Care and Surgical Treatment
• Antivirals, antibiotics, steroids, supplemental O2.
daily weighing to assess fluid retention; use of
diuretics, antibiotics, and inotropic agents; continuous electrocardiogram (ECG) monitoring.
Intravenous support; transfusion of packed red
blood cells (RBCs) for oxygen transport.
•
•
ABG, pulse oximetry, and electrocardiogram
(ECG).
Monitor intake and output (I&O) strictly.
Monitor for signs of shock, assess serial chest
x-rays, and provide aseptic ventilator care.
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Pulmonary Embolism
(pul-mo-ne-re em-bo-lizm)
Clue: Diagnostic or Clinical Findings
Rapid onset of dyspnea, chest pain,
anxiety, feeling of impending doom,
and hemoptysis.
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Respiratory Disorders
Pathophysiology
• Thrombus formation in the deep veins from an
•
•
ineffective cardiac pump; atrial fibrillation; the
presence of increased clotting factors; or lack of
movement of the musculoskeletal pump, delaying
blood movement back to the heart.
Emboli may also consist of air, fat, amniotic
fluid, and bacteria.
The thrombus occludes pulmonary circulation,
impairing gas exchange.
Assessment and Diagnostic Findings
•
•
Anxiety, dyspnea, diaphoresis, fear, feeling of
impending doom, chest pain, abnormal auscultatory findings, hemoptysis, syncope, and
hypotension.
CXR for obstruction, ECG for arrhythmias or
signs of right ventricular hypertrophy, ABG
showing decreased oxygenation, V/Q scan
abnormality, peripheral Doppler studies for
DVT, spiral CT scan of the lung to visualize PE,
D-dimer test, and pulmonary angiography.
132
Complications
• Right-sided CHF, shock, and sudden death.
Medical Care and Surgical Treatment
• Supplemental O2, suctioning, frequent auscultation of the lungs, hemodynamic support.
• Anticoagulants, thrombolytics, inotropics,
diuretics, antiarrhythmics, IV morphine.
• Embolectomy.
Keep in Mind
• Identify and decrease risk factors for PE.
• Prophylaxis of atrial fibrillation with warfarin.
Make the Connection
• Remember: Assess extremities of
•
bed-bound clients every shift. Look for unilateral
edema of the arms or legs to identify DVT
formation.
Assess vital signs for shock; support the anxious
client; be ready to support ventilation and
hemodynamic state.
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Pneumonia
(nu-mo-ne-a)
Clue: Diagnostic or Clinical Findings
Productive cough, chills, dyspnea,
pain on inspiration.
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Respiratory Disorders
Pathophysiology
• Acute inflammation of lung tissue by inhalation
•
of droplets containing viral particles, bacteria,
fungi, parasites, or irritating chemicals.
Inflammatory mediators in lung tissue cause
edema and filling of alveoli with serous fluid
and mucus.
Assessment and Diagnostic Findings
133
Medical Care and Surgical Treatment
• Antibiotics, bronchodilators, expectorants,
antipyretics, pulse oximetry.
Keep in Mind
• Vaccination for influenza and pneumonia reduces
risk of pneumonia.
• Respiratory toileting and infection control
measures are necessary.
• Rhonchi, crackles, and wheezes on auscultation.
•
Auscultation over areas of consolidation are
diminished; over these areas, the spoken word is
clearly heard (not the case in air-filled areas).
Temperature elevation; productive cough characterized by green, yellow, or rusty sputum.
Chest x-ray or computed tomography (CT) for
consolidation, complete blood count (CBC) for
elevated white blood count (WBC), arterial blood
gas (ABG) for ↓ O2 level, sputum analysis for
causative agent with culture and sensitivity (C&S)
test and Gram stain.
Complications
• Pulmonary edema.
• Respiratory failure and death.
Make the Connection
• Auscultate lungs every 4 hours; assess
•
•
vital signs; monitor intake and output (I&O);
position in semi-Fowler’s to high Fowler’s position; assess pulse oximetry reading every 4 hours.
Assess breathing patterns; give supplemental O2
(humidified if necessary).
Teach infection control measures.
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Pleural Effusion
(ploo-ral e-fu-zhun)
Clue: Diagnostic or Clinical Findings
Dyspnea, diminished breath sounds
over affected area, pleural friction
rub.
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Respiratory Disorders
Pathophysiology
• The pleural space is the visceral and parietal
•
lining of the outer lungs. Negative pressure or a
vacuum exists in this space.
If the lining becomes damaged or diseased, or
experiences oncotic pressure changes (lung cancer,
pulmonary tuberculosis [TB], lung abscess,
congestive heart failure, ascites, chronic renal
disease, chest trauma), the space loses its
negative pressure and expands into a space
that presses on the lung in that cavity.
134
Medical Care and Surgical Treatment
• Thoracentesis or placement of chest tube.
• Antibiotics, steroids, and analgesics.
• Cancer-causing pleural effusions are assessed by
•
Keep in Mind
• Shortness of breath (SOB) should be reported
Assessment and Diagnostic Findings
• Cough, dyspnea, diminished breath sounds
•
over the affected area, asymmetric expansion
of the chest, presence of pleural friction rub on
inspiration.
Complete blood count (CBC) with differential
showing an increase in white blood count (WBC)
(infection); chest x-ray; thoracentesis and cytology
to find the cause of the effusion; client history.
•
•
immediately, especially if diagnosed with chronic
lung disorders.
Vaccination for influenza and pneumonia is
recommended for high-risk clients.
Infection control and splinting the chest for
effective coughing are important.
Make the Connection
• Remember: Carefully assess blood pressure
Complications
• Mediastinal shift with pressure on unaffected
lung.
• Respiratory distress.
the oncologist to determine the most efficacious
treatment.
Pleurodesis (talc placed in pleural space to cause
a scar to prevent further effusion).
•
•
(BP) after thoracentesis, as removal of fluid
depletes total circulating volume.
Place client in high-Fowler’s position, medicate
before chest tube removal, and limit activities.
Monitor for SOB and poor pulse oximetry.
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Influenza
(in-floo-en-za)
Clue: Diagnostic or Clinical Findings
Fever, myalgia, respiratory and
gastrointestinal symptoms.
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Respiratory Disorders
Pathophysiology
• A viral syndrome that is spread as aerosolized
•
•
•
particles (airborne) and causes systemic inflammatory reactions of myalgia, fever, respiratory
symptoms, and gastrointestinal symptoms.
Strains are varied, and influenza vaccine is
developed anew each season on the basis of
identified strains. H1N1 influenza (swine flu)
and H5N1 (bird flu) are relatively new strains
causing concern.
Influenza can easily become pandemic without
vaccination.
The very young, very old, and those with
chronic disease are at most risk for death from
complications.
135
Medical Care and Surgical Treatment
• Antiviral medications, which must be started
•
Keep in Mind
• Vaccination for influenza strains is essential in
high-risk populations but contraindicated in
persons allergic to eggs.
Make the Connection
Assessment and Diagnostic Findings
• History of contact with an infected person.
• Complete blood count (CBC) with differential,
vital signs, culture for strain (if necessary), breath
sounds, visualization of postnasal drip by
oropharyngeal examination.
Complications
• Pneumonia.
within 48 hours of onset of symptoms to be most
effective.
Analgesics, bronchodilators (if necessary),
culture, antibiotics for secondary infection,
electrolyte solutions for gastrointestinal symptoms, and resting of the gut.
• Monitor intake and output (I&O), vital
signs, and breath sounds.
• Teach clients that vaccines are in forms with
•
either killed or weakened virus; therefore, they
are unable to cause influenza.
Vaccination may result in a low-grade temperature or soreness at injection site related to local
and systemic inflammation and production of
antibodies.
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Legionnaires’ Disease
(le-ju-nerz di-zez)
Clue: Diagnostic or Clinical Findings
Dry cough, myalgia, abnormal lung
sounds. Exposure to contaminated
water droplets.
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Respiratory Disorders
Pathophysiology
• Legionella bacteria is inhaled from contaminated
•
•
water supplies (e.g., from air conditioner vents,
spas, respiratory equipment), causing pneumonialike symptoms. Thrives at temperatures from
90°–105° F.
Headache, myalgia, fever, diarrhea. Incubation
period of 2–10 days.
Results in Legionnaire’s disease or a lesser
influenza-like illness known as Pontiac fever.
Assessment and Diagnostic Findings
• Persons at risk include middle-aged or older
•
adults who smoke cigarettes or have chronic lung
disease and those whose immune systems are
compromised by diabetes, renal failure, organ
transplantation, cancer, or AIDS.
Sputum culture, bronchial washings, blood
serology for antibody titer; or antigen testing of
urine.
136
Medical Care and Surgical Treatment
• Erythromycin given early and throughout the
course of the disease is the treatment of choice.
• Rifampin (used only with other antibiotics).
• Macrolides and fluoroquinolones are effective.
• Penicillin, cephalosporins, and aminoglycosides.
• Antiemetics for vomiting.
• CBC, ABG, CXR.
Keep in Mind
• Maintain infection control practices.
• Encourage coughing and deep breathing exercises;
use incentive spirometer.
Make the Connection
• Monitor intake and output (I&O) and
character of stools; assess and treat emesis.
• Assess breath sounds every 4 hours; monitor ease
Complications
• Pneumonia.
• Respiratory failure leading to death.
•
•
of respiration, pulse oximetry, ABGs, and vital
signs; perform chest percussion; and provide
frequent oral hygiene care.
Assess for neurologic deterioration.
Use sterile water for humidification.
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Lung Cancer
(lung kan-ser)
Clue: Diagnostic or Clinical Findings
Persistent cough, weight loss, history
of or current cigarette smoking.
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Respiratory Disorders
Pathophysiology
• Exposure to chronic irritants or carcinogens cause
•
•
•
•
cell mutation, resulting in oncogene stimulation
and loss of genetic material from chromosome 3.
Cells in early differentiation that mutate are more
aggressive than more mature cells.
Cancers are evaluated using the TNM method.
Cancer cells divide more rapidly and are more
metabolic than normal body cells. Secreting cancers cause damage to the body by hypersecretion.
Cancer in the lung may be the primary site or a
metastatic secondary site from a distant body
area.
137
• Hyperuricemia as a side effect of cancer treatment
and cancer cells killed.
Medical Care and Surgical Treatment
• Radiation, chemotherapy, immunotherapy,
corticosteroids, TomoTherapy.
• Lobectomy or pneumonectomy.
• CBC, electrolytes, serial CXRs or other imaging.
Keep in Mind
• Encourage smoking cessation, yearly checkups,
and learning the warning signs of cancer.
Make the Connection
Assessment and Diagnostic Findings
•
•
Persistent cough, wheezing, dyspnea, fever, weight
loss, anorexia, pleural friction rub, hoarseness.
CXR, bronchoscopy and biopsy, sputum for
cytology, MRI, CT scan, PET scan, US.
Complications
• Superior vena cava syndrome.
• Pleural effusions.
• Cardiac tamponade.
• Monitor F and E, skin and underlying
•
•
structures (radiation); provide antiemetics
(chemotherapy).
Monitor CBC for ↓ RBC, and ↓ WBC.
Support the psychosocial needs of the client and
family; medicate for pain as needed.
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Histoplasmosis
(his-to-plaz-mo-sis)
Clue: Diagnostic or Clinical Findings
Cough, fever.
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Pathophysiology
• Systemic fungal disease caused by dimorphic
fungus Histoplasma capsulatum.
• Organism grows in soil enriched with bird droppings. Fungal spores form that are then inhaled.
• Once at body temperature, fungal spores change
to the yeast form in the alveoli. The yeast is then
absorbed through the regional lymphatics and
into the bloodstream. Cellular immunity occurs
2–3 weeks after infection.
138
• Decreasing neurologic status.
Medical Care and Surgical Treatment
• Intravenous amphotericin B, ketoconazole,
itraconazole.
• Immunosuppressed clients will be on fluconazole
for life.
Keep in Mind
• Immunosuppressed clients who are human
Assessment and Diagnostic Findings
• Fever, cough.
• Fever, anemia, enlargement of the spleen and liver,
•
leukopenia, pneumonia, adrenal necrosis, and
gastrointestinal tract ulcers in disseminated disease. Chronic pulmonary histoplasmosis produces
lung cavitations similar to those in tuberculosis.
Positive histoplasmin skin test or urine antigen
test, and rising complement fixation and agglutination titers. Confirmed by stained tissue biopsy
or culture of H. capsulatum from sputum, blood,
lymph nodes, or bone marrow.
Complications
• Pleural effusion, cardiac tamponade.
•
immunodeficiency virus (HIV) positive or are
undergoing chemotherapy or radiation should
avoid exposure to soil that may be contaminated
with bird droppings.
Encourage client to report cough or fever immediately.
Make the Connection
• Monitor breath sounds every 4 hours,
•
vital signs, liver function tests (LFTs), and gastrointestinal pain indicating ulceration.
Monitor chest x-ray for tuberculosis-like cavitations; complete blood count (CBC) for anemia
and blood chemistry for catecholamines.
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Sarcoidosis
(sar-koyd-o-sis)
Clue: Diagnostic or Clinical Findings
Fever, myalgia, night sweats, anorexia,
weight loss, fatigue, with progressive
lung noncompliance and SOB.
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Pathophysiology
• Granulomatous disorder primarily of the lungs,
•
•
•
•
skin, eyes, and lymphatics thought to have a
genetic link. Other organs affected are the heart,
bones, joints, liver, and kidneys.
Genetic clusters include mainly African Americans
and Scandinavians. Environmental influences
are considered as genetic triggers. Affects those
40 years of age and younger.
Hilar lymphadenopathy occurs, then progresses
to lymphocytic alveolitis. Skin lesions, peripheral
lymphadenopathy, interstitial nephritis, iritis,
hepatomegaly and splenomegaly can also occur.
Symptoms and complications are related to
malabsorption.
Can result in pulmonary fibrosis or associated
right-sided heart failure (cor pulmonale).
139
• Abnormalities on chest x-ray, electrocardiogram
(ECG), histology; rule out histoplasmosis and
tuberculosis (TB).
Complications
• Cor pulmonale and progressive pulmonary
fibrosis leading to death.
• Kidney, liver, and eye damage.
Medical Care and Surgical Treatment
• Corticosteroids and other immunosuppressants.
Keep in Mind
• Report dry cough that does not remit, night
sweats, and shortness of breath (SOB).
• Teach client about the nature of the illness, its
low mortality rate, and the use of corticosteroids.
Assessment and Diagnostic Findings
• Signs of inflammation, such as temperature
elevation, and other flu-like symptoms.
• History of night sweats.
• T-cell lymphocytopenia, increased monocyte
count, allergy panel testing for common
allergens.
Make the Connection
• Monitor pulse oximetry reading, chest
•
x-rays, ease of respiration, and signs of rightsided heart failure.
Assess for symptoms associated with corticosteroid therapy and intervene when noted.
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Mesothelioma
(mes-o-the-le-o-ma)
Clue: Diagnostic or Clinical Findings
Cough, SOB, history of asbestos
exposure.
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Pathophysiology
• Mesothelia is a single layer of flat cells that line
•
the pleural, peritoneal, and pericardial cavities.
Exposure to asbestos through inhalation causes
infiltration by the short asbestos fibers into
these cells. Peritoneal infiltration is thought to
occur by coughing up and swallowing the
asbestos fibers.
Cells mutate causing changing DNA, and activating oncogenes.
140
Medical Care and Surgical Treatment
• Chemotherapy, radiation (external beam and
implanted).
• Lobectomy and pneumonectomy.
• Pleurodesis for repeated pleural effusion.
Keep in Mind
• Follow the OSHA guidelines for working with
asbestos products.
• Those with history of asbestos exposure should
have frequent health screenings.
Assessment and Diagnostic Findings
• A good history assists with diagnosis.
• CT scan, CXR, MRI, bronchoscopy or thoracoscopy with biopsy.
• Genotypes show abnormalities in chromosome
22 and rearrangement of the arms of chromosomes 1, 3, 6, and 9.
Complications
Make the Connection
• Monitor for SOB, vital signs, pulse
•
• Spread to the peritoneal cavity, chest wall, and
lymph nodes.
• Pleural effusion, dysphagia, superior vena cava
syndrome.
•
oximetry, electrolytes, CBC, and pleural effusions.
Auscultate the breath sounds every 4 hours.
Remember: If the client has had a pneumonectomy,
there is no chest tube, and the affected lung is
placed down or in semi- to high-Fowler’s position. In the case of a lobectomy, a chest tube is
in place. The client is placed in semi- to highFowler’s position.
Radiation may cause dysphagia, candidiasis of the
esophagus.
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141
Tuberculosis (TB)
(tu-ber-ku-lo-sis)
Clue: Diagnostic or Clinical Findings
Fatigue, weight loss, anorexia, night
sweats, low-grade fever, productive
cough, hemoptysis, chest pain,
anxiety.
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Pathophysiology
• Mode of transmission: The tubercle bacilli are
•
spread by the airborne route. The mycobacteriumcontaining droplet nuclei circulate in the air. A
T-cell–mediated response occurs, walling off the
lesion (Ghon tubercle), inactivating the disease.
The Ghon tubercle affects the hilar region first. If
the client becomes immunosuppressed, the Ghon
necrose cavitates then may release the organism
into the lung.
Assessment and Diagnostic Findings
141
Medical Care and Surgical Treatment
• Combination of four antibiotics. Based on immu•
•
Keep in Mind
• After exposure or vaccination with BCG, the
• History; chest x-ray (lesions more likely in the
•
•
upper lobes); Mantoux test revealing TB or induration of >15 mm in clients with normal immune system function; sputum smears and culture for AFB.
NAA; QFT-G test done on blood specimen with
results given in 24 hours. The QFT-G test result is
unaffected by having received the BCG vaccine.
Auscultation of chest reveals adventitious breath
sounds.
Complications
• Obstructive respiratory disease, respiratory failure, and death.
nity, 6–9 or more months of antibiotic therapy
may be needed. Monthly AFB sputum test until
two tests are negative in a row.
Adequate nutrition, weekly weights, bronchodilators, chest percussion.
Airborne isolation in a negative pressure room.
•
•
Mantoux test will always be positive, so CXR will
have to be done.
Expect health-care providers wear special masks
while in the room.
Compliance with the medical regimen is essential
for personal and public health. Teach about the
side effects.
Make the Connection
• Monitor for SOB, poor pulse oximetry,
presence of lymphadenopathy, vital signs, and
night sweats, wear fit-tested HEPA mask.
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SENSORY
Cataracts, 142
Acute Angle-Closure Glaucoma, 143
Primary Open-Angle Glaucoma, 144
Retinal Detachment, 145
Macular Degeneration, 146
Diabetic Retinopathy, 147
Conductive and Sensorineural Hearing
Loss, 148
Otitis Media, 149
Otitis Externa, 150
Mastoiditis, 151
Otosclerosis, 152
Labyrinthitis, 153
Ménière’s Disease, 154
Acoustic Neuroma, 155
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Cataracts
(kat-a-rakts)
Clue: Diagnostic or Clinical Findings
Difficulty driving at night because of
excessive glare. Opacity of the lens on
ophthalmologic examination.
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Pathophysiology
• Opacity of the lens can occur at any age, including
•
•
•
congenitally. However, most cataract formation
occurs over age 40 years and most commonly in
the elderly. Types include subcapsular; nuclear;
and cortical.
In nuclear (age-related) cataract formation, the
center and outer areas of the lens start to produce more protein strands that begin to aggregate in the center portion of the lens and form
strata by folding. As strata forms, the center
portion of the lens opacifies and yellows as the
protein fibers accumulate.
Women who take HRT are at a greater risk, and
women who take HRT and consume significant
amounts of alcohol are at an even greater risk.
Exposure to UV light is another risk factor.
Assessment and Diagnostic Findings
• Ophthalmoscope and slit lamp microscope
exams reveal opacity of the lens.
• Subjective reports include difficulty reading small
print, difficulty seeing in bright light, seeing halos
around objects, and difficulty driving at night
because of glare.
142
Complications
• Intraoperative floppy iris syndrome (α-blocker
•
therapy), which can cause the iris to suddenly
constrict during surgery.
Retinal detachment, macular edema, IOP, hemorrhage; IOL implant dislocation.
Medical Care and Surgical Treatment
• Phacoemulsification of the old lens, with insertion of an IOL.
Keep in Mind
• Discuss all daily medications with the surgeon,
especially α-adrenergic blockers.
• Recovery time is very fast.
Make the Connection
• Monitor vital signs and visual acuity
pre- and postoperatively.
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Acute Angle-Closure
Glaucoma
(a-kut ang-gl klo-shur glaw-ko-ma)
Clue: Diagnostic or Clinical Findings
Unilateral redness and pain in the eye,
headache, nausea, and vomiting. Client
may see halos in the visual field around
lights. Tonometry measurement may
exceed 50 mm Hg.
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Pathophysiology
• Highest risk group is Asian or Inuit women over
age 45 years or persons with nearsightedness.
• In glaucoma, the anterior chamber experiences
•
•
outflow problems, with fluid and pressure increases. Because it is an enclosed fibrous capsule, the
eye is unable to swell without causing pressure on
important structures like the choroid retina and
optic nerve.
Causes the outflow area of the iris/corneal
angle to become narrow because of bunching
of the iris as the pupil dilates. Prolonged pupil
dilation, can cause an episode of mild or emergent severity. A mild episode may be relieved by
sleep and relaxation.
Trauma to the eye can also produce the same
type of symptoms, which create a medical and
surgical emergency.
Assessment and Diagnostic Findings
• Tonometry that measures IOP. Gonioscopy that
visualizes and assesses the angle of the anterior
chamber during eye exam.
143
Complications
• Partial or total blindness.
• Systemic effects of eye drops.
• Postsurgical infection.
Medical Care and Surgical Treatment
• Laser surgery that creates an opening from the
•
•
anterior chamber to posterior chamber; may be
done on the unaffected eye as prophylaxis.
Miotic agents, carbonic anhydrase inhibitors,
adrenergic agonists, or beta-adrenergic blockers.
In acute episodes, corticosteroids to reduce
inflammation, osmotic diuretics, analgesics,
antiemetics, and bedrest.
Keep in Mind
• Avoid long periods of time in the dark, stress,
and any medication that may produce mydriasis.
Make the Connection
• Assess for eye redness, nausea, vomiting,
and seeing rainbows around objects.
• Remember: This is a medical and surgical
emergency. Time is vision.
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Primary Open-Angle
Glaucoma
(pri-ma-re o-pen ang-gl glaw-ko-ma)
Clue: Diagnostic or Clinical Findings
Bilateral, usually painless loss of vision.
May see halos around objects and
experience mild aching in the eyes
or headaches. Tonometry measurement
⬎20 mm Hg.
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Pathophysiology
• This is the most common type of glaucoma, with
•
•
insidious onset in persons older than 35 years of
age. The only risk factors are black race, trauma
to the eye, and chronic use of corticosteroids by
any route.
In glaucoma, the anterior chamber experiences
outflow problems, with fluid and pressure
increases on the choroid layer, the retina, and
optic nerve.
In the darkly pigmented eye, iris pigment may
flake off and occlude the iridocorneal angle.
Assessment and Diagnostic Findings
• Tonometry measurements exceed 12–20 mm Hg.
• Gonioscopy to assess the anterior angle.
• Ophthalmoscopic examination with pupil dilation.
• GDx Access device scan, which utilizes an infrared
laser to assess damage to retinal fibers.
Complications
• Gradual visual loss and blindness.
• Systemic effects of eye drops.
• Postsurgical infection.
144
Medical Care and Surgical Treatment
• Miotic agents, carbonic anhydrase inhibitors,
adrenergic agonists, or beta-adrenergic blockers.
• Argon laser trabeculoplasty, trabeculectomy, or
cyclocryotherapy.
Keep in Mind
• Eye examinations with tonometry must be
continued on a regular basis.
• Eye drops must be continued for life; wear a
MedicAlert bracelet and always carry medications.
• Occlude the lacrimal duct for 1 full minute after
administration of eye drops to prevent systemic
effects.
Make the Connection
• Tonometry is the most important aspect
of diagnosis for most clients.
• Monitor for systemic effects of eye drops, especially in the elderly.
• Administration of eye drops is done with sterile
technique; the applicator does not touch the eye.
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145
Retinal Detachment
(ret-i-nal de-tach-ment)
Clue: Diagnostic or Clinical Findings
Visual abnormalities of seeing flashing
lights or sparks, floaters, loss of
peripheral vision, and eventually
nothing, like a curtain falling over
the visual field.
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Pathophysiology
• Disorders in vision, like myopia, may predispose
•
•
the peripheral retina to come away (traction)
from the choroid layer.
Rhegmatogenous detachment can occur during
intraocular surgery if traction is applied to the
retina, causing vitreous fluid to flow into a hole
between the retina and choroid layer, resulting in
detachment. Trauma to the head and eyes may
cause this type of detachment.
Exudative or serous detachment occurs in persons
with hypertension or intraocular tumors in which
serous fluid leaks between the retina and choroid.
145
Medical Care and Surgical Treatment
• Argon laser reattachment.
• Cryosurgery.
• Scleral buckling.
• Less common procedures include pneumatic
retinopexy.
• Electrodiathermy uses heat to drain fluid from the
area between the choroid and retina.
Keep in Mind
• Report any sudden changes in vision, especially
after trauma.
• Be aware of the signs and symptoms of retinal
detachment after cataract surgery.
Assessment and Diagnostic Findings
• Loss of peripheral vision, flashing lights, floaters,
or total loss of part of the visual field.
• Indirect ophthalmoscopic visualization of the
Make the Connection
• Retinal detachment will cause death of
retina.
Complications
• Permanent visual loss in the area of detachment.
• IOP.
• Recurrent detachment.
•
rods and cones in the area of detachment unless
interventions are initiated quickly.
The client must comply with postsurgical limitations on activity in order to allow the procedure
to correct the detachment.
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Macular Degeneration
(mak-yoo-ler de-jen-er-a-shun)
Clue: Diagnostic or Clinical Findings
Most commonly, a gradual, age-related
loss of central, near, or color vision.
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Pathophysiology
• The central fovea of the retina is rich in cones
•
•
•
(color vision) and is responsible for clear central
vision.
Risk factors include being an older (⬎75 years)
female, white, a smoker; having hyperlipidemia;
and consuming little antioxidant-containing
foods.
Dry or atrophic age-related macular degeneration
causes pigmental changes in the fovea, which can
be visualized on examination. Drusen (pale yellow
spots) appear on the macula, showing areas that
no longer function. This is the most common
type.
Wet or exudative age-related macular degeneration occurs when vitreous fluid and/or blood leak
under the macula. The onset of this type is sudden, and it may be treated with an argon laser,
as in retinal detachment.
Assessment and Diagnostic Findings
• Progressive loss of central and near vision in the
dry type; sudden onset in the wet type.
• Visual acuity tests.
146
• Color vision test.
• IV fluorescein angiography.
• Amsler grid for initial and ongoing self-diagnosis.
Complications
• Central blindness.
Medical Care and Surgical Treatment
• Dry type: few options other than low-vision
lenses.
• Wet type: argon laser therapy, vascular endothelial
growth factor inhibitors.
Keep in Mind
• Teach coping skills for clients with loss of central
vision.
Make the Connection
• Monitor Amsler grid findings to assess
visual stability or loss.
• Monitor IOP and for infection following argon
laser therapy.
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Diabetic Retinopathy
(di-a-bet-ik ret-in-op-a-the)
Clue: Diagnostic or Clinical Findings
Those with a history of poorly controlled
diabetes experience gradual central
visual field changes that can progress
to flashing lights and cessation of
vision (retinal detachment). On
ophthalmoscopic examination,
cotton-wool spots and tortuous,
dilated vessels are seen.
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Pathophysiology
• Background retinopathy is caused by microa•
•
•
neurysms that form on the retinal capillaries and
leak blood. The client may experience visual
changes caused by inflammation.
The preproliferative stage of retinopathy is characterized by edema of the retina with blocked and
infarcted blood flow.
The proliferative stage of retinopathy is characterized by twisting of vessels, with neovasculature growing into the optic disk and obscuring
the retina. The neovasculature leaks easily.
Traction may occur as a result of the twisting
and leaking of these vessels and cause retinal
detachment.
Disorder has a genetic link.
147
Medical Care and Surgical Treatment
• Tight blood glucose control, especially during the
first 5 years following diagnosis of diabetes.
• Vitrectomy is done if leakage of blood has
•
Keep in Mind
• Retinopathy can be avoided with tight control
of blood glucose levels through diet, lifestyle
changes, and medication.
Make the Connection
• Teach diabetic clients how to keep their
Assessment and Diagnostic Findings
• Change in visual acuity testing.
• Ophthalmoscopic examination with dilation of
the pupil.
• Retinoangiography.
Complications
• Visual loss.
• Retinal detachment.
occurred under the retina. The vitreous humor is
drained and replaced with saline or silicon oil.
Argon laser therapy or sclera buckling is needed
if retinal detachment occurs.
blood glucose levels in the normal range.
• Teach diabetic clients to undergo a complete
•
•
visual examination with pupil dilation at least
yearly.
Monitor blood glucose level and provide periodic
visual acuity tests.
Listen to subjective complaints of the client or
family about visual changes.
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Conductive and
Sensorineural
Hearing Loss
(kon-duk-tiv and sen-so-re-nu-ral her-ing los)
Clue: Diagnostic or Clinical Findings
Acquired or congenital inability to
discriminate sound, resulting in
impaired hearing. History of ototoxic
drug use. Weber’s and Rinne’s tests
are abnormal.
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Pathophysiology
• Hearing loss is a common problem in the elderly,
but it may occur at any age.
• Efficient hearing is accomplished by appropriate
•
•
conduction of sound into the inner ear.
Conduction of sound is accomplished by vibration of the tympanic membrane that is connected
to the malleus. The malleus, incus, and stapes
transmit the vibration to the oval window of the
inner ear. The oval window vibrates and causes
movement of endolymph within the cochlea that
stimulates sensorineural receptors within the
cochlea. Transmission to the acoustic nerve sends
information to the brain for interpretation.
Conductive hearing loss can result from increased
cerumen, foreign bodies in the ear canal, cysts,
tumors, otosclerosis, or stiffened or scarred tympanic membrane.
Sensorineural hearing loss occurs through damage to sensory nerves caused by complications of
infections, use of ototoxic drugs, neuromas, arteriosclerosis, chronic exposure to noise, and aging.
148
Assessment and Diagnostic Findings
• Abnormal Weber’s and Rinne’s tests.
• Hearing loss indicated by subjective methods as
well as audiometric testing.
Complications
• Changes in family processes and relationships
with friends; safety issues.
Medical Care and Surgical Treatment
• Use of cerumen-reducing topical solutions.
• Anti-infectives and anti-inflammatories.
• Hearing aids, cochlear implants.
• Stapedectomy for otosclerosis.
Keep in Mind
• Lipreading can assist in hearing.
• Clean hearing aid and replace batteries as directed.
Make the Connection
• Face the person with hearing loss while
speaking; use gestures or word boards.
• Assess if the client has heard you by writing a
question about the conversation.
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Otitis Media
(o-ti-tis me-de-a)
Clue: Diagnostic or Clinical Findings
Fever and pain in the ear. Otoscopic
examination reveals a reddened and
swollen tympanic membrane. Usually
associated with colds and allergies.
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Pathophysiology
• Otitis media is common in infants and children
•
•
and results in accumulation of fluid in the middle
ear because their short, horizontal eustachian
tubes allow exudates from colds and allergens
access to the inner ear.
Causative microorganisms are viruses and bacteria.
Other risks include respiratory infections, daycare attendance, lower socioeconomic status,
exposure to secondhand smoke or wood-burning
stoves, allergies, excessive use of a pacifier, and
feeding with a propped bottle.
Assessment and Diagnostic Findings
• Ear pain, drainage of fluid from the ear canal,
ear tugging, and hearing loss.
• Elevated temperature, irritability, headache,
lethargy, anorexia, and vomiting.
• History of a recent upper respiratory infection or
allergies.
• Elevated WBC count, altered Weber’s and Rinne’s
tests.
149
Complications
• Tympanosclerosis.
• Cholesteatoma.
• Mastoiditis.
• Hearing loss.
Medical Care and Surgical Treatment
• Vaccination against Streptococcus pneumoniae.
• Antibiotics, decongestants, analgesics,
antipyretics, and heat or cold application.
• Low-dose antibiotics.
• Myringotomy with ventilation tubes.
Keep in Mind
• Do not smoke around children.
• Vaccination can reduce the number and severity
of inner ear infections.
• Breastfeeding for at least 3 months ↓ incidence.
Make the Connection
• Assess the tympanic membrane and ability
to hear (bilaterally). Assess tympanic membrane
for redness and swelling.
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Otitis Externa
(o-ti-tis eks-tur-na)
Clue: Diagnostic or Clinical Findings
Pain in the external auditory canal.
The canal may swell shut. Pain is
elicited by pressure on the tragus.
Often called “swimmer’s ear.”
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Pathophysiology
• Infection or inflammation of the external auditory
•
canal caused by a contact allergy, an acute bacterial infection, or a fungal infection.
Diabetics and immunosuppressed clients may
experience invasion of the infection into the base
of the skull, resulting in deep bone infection.
150
Keep in Mind
• Use a mild alcohol solution or an over-the-counter
•
Assessment and Diagnostic Findings
Make the Connection
• Pain in the auditory canal (elicited by pushing on
the tragus of the ear), fever.
• Otoscopic examination reveals a reddened,
•
swollen ear canal. This infection may exist by
itself or with otitis media.
Elevated white blood cell (WBC) count shown on
complete blood count (CBC); altered Weber’s
and Rinne’s test.
Complications
• Otitis media.
• Mastoiditis.
• Hearing loss.
Medical Care and Surgical Treatment
• Antibiotics, corticosteroid given by mouth or as
drops, and analgesics.
drying agent to dry water in the ear canal after
swimming.
Report ear pain immediately to prevent otitis
media and severity of infection.
• Bacteria and other organisms like to grow
•
•
in moist, warm, dark environments like the ear
canal.
Assess the ears carefully in the adolescent or
adult who swims frequently.
Teach the client to hold the head to one side to
drain water from ears completely and to follow
up with a drying agent.
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Mastoiditis
(mas-toyd-i-tis)
Clue: Diagnostic or Clinical Findings
Pain behind the ear, with fever and
chills, usually after ear or sinus
infection.
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Pathophysiology
• Inflammation of the mastoid sinuses, usually as a
•
•
•
result of the spread of infection from acute otitis
media.
Occurs rarely because of the availability of
antibiotics for otitis media.
Causative organisms usually are the same as those
causing otitis media (e.g., Streptococcus species,
Haemophilus influenzae, Staphylococcus aureus),
although on some occasions, mycobacteria or
fungi may cause the disease.
Chronic infection of the frontal sinuses may cause
this secondary infection.
Assessment and Diagnostic Findings
•
•
•
Pain behind the ear and sometimes fever and
systemic symptoms (e.g., malaise, chills).
Physical examination may reveal redness and
tenderness behind the affected ear, with swelling
of the external auditory canal.
Magnetic resonance imaging (MRI) or computed
tomography (CT) scan showing inflammation or
abscess of the mastoid bone.
151
Complications
• Brain abscess.
• Meningitis.
Medical Care and Surgical Treatment
• Intravenous (IV) antibiotics followed by PO outpatient medications and close follow-up.
• Mastoidectomy or other neurosurgical procedures
if infection has spread to beneath the periosteum
or if intracranial infection or thrombosis of neighboring veins develops.
Keep in Mind
• Treat sinus and ear infections when symptoms
occur to prevent complications and secondary
infection.
Make the Connection
• Monitor level of consciousness in the
context of a comprehensive neurologic assessment.
• Gain IV access and watch for irritability of the
neurologic system.
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Otosclerosis
(o-to-skle-ro-sis)
Clue: Diagnostic or Clinical Findings
Progressive hearing loss, especially with
low or soft tones. Rinne’s test for bone
conduction is normal, but Weber’s test
shows lateralization to the most affected
ear. Tinnitus may be evident.
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Pathophysiology
• The cause of this condition is unknown, and is
more common in women (worsens in pregnancy).
• The condition may begin in the adolescent years
and occurs bilaterally.
• Due to chronic inflammation in the inner ear, bone
remodeling by the osteoclasts and osteoblasts
occurs, causing excessive spongy bone growth
around the stapes and the oval window, resulting
in ankylosis and conductive hearing loss.
Assessment and Diagnostic Findings
• Whispered voice test shows decreased hearing;
low-tone deafness, tinnitus.
• Rinne’s test is normal for bone conduction,
•
but Weber’s test shows lateralization to the most
affected ear.
Audiometric tests and CT scan and MRI
determine the extent of sclerosis.
Complications
• Progressive hearing loss.
• Postsurgical brain infection, dizziness, nausea,
vomiting, and movement of prosthetic inserted
after stapedectomy.
152
Medical Care and Surgical Treatment
• Stapedectomy with prosthetic.
• Postoperatively, the client is positioned with the
•
operative ear upward, perhaps with a plug or
dressing to prevent infection that could travel to
the brain.
Antiemetics are given as well as instructions not
to cough, sneeze, vomit, or travel by air for a
given time.
Keep in Mind
• Teach to notify the surgeon immediately if the
client develops a cold postoperatively.
Make the Connection
• Conduct neurologic examinations
periodically.
• Monitor vital signs frequently.
• Position the client on the unaffected side.
• Give antiemetics or other medications necessary
to prevent loss of prosthetic.
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Labyrinthitis
(lab-i-rin-thi-tis)
Clue: Diagnostic or Clinical Findings
Vertigo, tinnitus. Weber’s and Rinne’s
tests indicate conductive or sensorineural
hearing loss. Fever, elevation in WBCs,
nausea, and vomiting may occur.
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Sensory Disorders
Pathophysiology
• Inflammation of the inner ear caused by bacterial
•
•
or viral microorganisms that enter the inner ear
from the middle ear, meninges, or bloodstream.
Serous labyrinthitis can occur after toxic intake of
alcohol or drugs.
Diffuse suppurative labyrinthitis is caused by
acute or chronic otitis media, mastoiditis, or
mastoid surgery.
153
Medical Care and Surgical Treatment
• Antibiotics or antiviral agents.
• Mild sedatives, antiemetics, and antihistamines.
• Bedrest.
Keep in Mind
• Ringing in the ears should always be investigated
by the health-care provider.
Assessment and Diagnostic Findings
• Complete blood count (CBC) to diagnose infection (increased WBC count or shift to the left).
• Nystagmus on the affected side.
• Weber’s and Rinne’s tests to assess for conductive or sensorineural hearing loss.
• Presence of tinnitus.
Complications
• Loss of cochlear function and hearing loss.
• Spread of infection to neurologic structures.
Make the Connection
• Counsel clients with tinnitus and hearing
•
loss on methods to mitigate problems that will be
encountered.
Assess for dizziness, as this may be a safety issue
for the client and his or her family.
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Ménière’s Disease
(man-e-arz di-zez)
Clue: Diagnostic or Clinical Findings
Ear fullness, tinnitus, and vertigo.
Sweating, nausea, and vomiting may
occur. Movement of the head makes
symptoms worse.
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Sensory Disorders
Pathophysiology
• Excessive endolymph in the compartment of the
•
•
•
•
inner ear, possibly from a blockage of endolymph
reabsorption.
Recurring episodes of hearing loss, tinnitus, vertigo, and aural fullness, often resulting in gradually
progressive hearing loss.
Exacerbations may occur suddenly and last for as
long as 24 hours.
When one ear is affected, the other ear will
become involved in approximately 50% of cases.
Injury, infections, endocrine disorders, and vascular disorders may be causative.
154
Medical Care and Surgical Treatment
• Bedrest and keeping the head still during acute
episodes is the most effective treatment.
• Antihistamines, sedatives, corticosteroids, and
diuretics.
• A low-sodium diet.
• Endolymphatic shunt.
• Balance training exercises.
• Discontinue smoking.
Keep in Mind
• Report dizziness and tinnitus to the health-care
provider.
Assessment and Diagnostic Findings
• Electronystagmography, caloric stimulation,
rotational tests, and Romberg’s test.
• Auditory assessment, x-rays, CT scan, and MRI
studies are performed to assess quantity of
endolymph in the inner ear and extent of hearing
loss accompanying the disorder.
Complications
• Postoperative brain infection.
• Hearing loss.
Make the Connection
• Monitor for balance and hearing problems.
• Neurologic assessments, and monitor CBC.
• Counsel the client concerning balance training
exercises, safety, and adherence to low-sodium
diet.
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Acoustic Neuroma
(a-koos-tik nu-ro-ma)
Clue: Diagnostic or Clinical Findings
Hearing loss, headache (wakes the client
or is worse with sneezing or coughing),
facial numbness, balance problems, and
tinnitus.
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Pathophysiology
• Benign tumor of the Schwann cells of cranial
nerve VIII.
• Linked with neurofibromatosis type 2.
Assessment and Diagnostic Findings
• Drooling, facial drooping, and dilation of pupil
on affected side.
• Computed tomography (CT) scan, magnetic
•
•
•
resonance imaging (MRI) to assess size and
location of lesion.
Electronystagmography to assess extent of
vertigo.
Test of hearing and brainstem function (brainstem auditory evoked response).
Caloric stimulation test.
Complications
• Postoperative brain infection.
• Radiation therapy after radiosurgery can result in
nerve damage and hearing loss.
• Without treatment, the tumor can continue to
•
press on structures, causing increasing discomfort
and loss of function.
Hydrocephalus.
155
Medical Care and Surgical Treatment
• Surgery.
• Stereotactic radiosurgery.
• Treatment of inflammation with corticosteroids.
• Antihistamines for dizziness; analgesics for
headache.
Keep in Mind
• Benign tumors will not metastasize but will
grow and cause pressure on other structures,
possibly resulting in serious problems (e.g.,
hydrocephalus, hearing loss, and progressive
pain and dizziness).
Make the Connection
• Monitor postsurgically for infection by
watching the complete blood count (CBC).
• Assess hearing and facial movement after surgical
or radiosurgery procedures.
• Monitor neurologic status.
• Counsel client on what to expect from treatment
or choosing not to have treatment.
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DERMATOLOGIC
Skin Cancer, 156
Contact Dermatitis, 157
Eczema, 158
Cellulitis, 159
Psoriasis, 160
Herpes Zoster, 161
Herpes Simplex, 162
Paronychia, 163
Impetigo, 164
Scabies, 165
Pediculosis Capitis, 166
Acne Vulgaris, 167
Stevens-Johnson Syndrome and Toxic
Epidermal Necrolysis, 168
Tinea, 169
Verruca, 170
Superficial and Partial-Thickness
Burns, 171
Full-Thickness Burns, 172
Rosacea, 173
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Skin Cancer
(skin kan-ser)
Clue: Diagnostic or Clinical Findings
Skin lesion with asymmetry, irregular
borders, color changes, and >6 mm
diameter.
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Dermatologic Disorders
Pathophysiology
• Mutation of cells of the skin that occurs from
chronic exposure to the sun or other irritants.
• Basal cell cancer (the most common; cells in the
•
lowest layer of the epidermis), squamous cell
(cells of the middle layer of the epidermis), or
melanoma (the most deadly form; melanocytes in
the bottom layer of the epidermis).
Cells lose normal functional properties and can
metastasize to other organs (melanoma).
Assessment and Diagnostic Findings
• Unusual lesion or change in a mole.
• ABCD criteria: Is it asymmetric? Are the borders
•
irregular? Is the color unusual (ranges from tan,
black, and brown to white, blue, and red). Is
the diameter greater than 6 mm?
• Basal cell lesions are curled; squamous cell
lesions reveal underlayer of tissue and are red,
scaly, or have drainage; melanomas are darkly
pigmented.
Diagnosis made by excision and biopsy of the
melanoma or Mohs’ chemosurgery technique, in
which thin layers of skin are shaved and examined
for cancerous cells (basal and squamous).
156
Complications
• Metastasis to internal organs and death.
Medical Care and Surgical Treatment
• Excision and biopsy; Mohs’ chemosurgery for
basal and squamous cell cancers.
• Chemotherapy, radiation, TomoTherapy, interleukin, interferon.
Keep in Mind
• Avoid prolonged sun exposure; wear SPF 30 or
greater sun block.
• Maintain yearly skin checks with the dermatologist.
Make the Connection
• Monitor skin lesions and apply ABCD
criteria.
• If client is undergoing cancer treatment, assess
for nausea, vomiting, CBC, electrolytes, site
of radiation, and problems with underlying
structures.
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Contact Dermatitis
(kon-takt der-ma-ti-tis)
Clue: Diagnostic or Clinical Findings
Patterned skin eruption after contact with
an irritant or allergen.
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Dermatologic Disorders
Pathophysiology
• Irritant contact dermatitis is caused by chemicals
•
like detergents; allergic contact dermatitis is a
cell-mediated type IV hypersensitivity reaction to
an allergen (poison ivy, tape, and jewelry are
some examples).
Areas affected may show mild erythema or vesicles and bullae and are referred to as eczema.
Assessment and Diagnostic Findings
• Areas of erythema, vesicles, or bullae that appear
in a pattern.
• Allergy to the metal in a client’s watch will
result in a rash localized in that area.
• Exceptions: poison ivy leaves, in which the sap
may aerosolize if leaves are burnt, or photosensitivity, which is a reaction to exposure to the sun,
usually caused by use of drugs like diuretics,
antipsychotics, or antibiotics, producing a more
extensive rash not occurring in area of clothing.
Complications
• Infection.
• Rash occurring in the eye.
157
• Respiratory distress, as in cases of severe latex
allergy.
Medical Care and Surgical Treatment
• Corticosteroids topically, orally, or intraocularly.
• Lesions should be lightly wrapped.
Keep in Mind
• Allergy testing should be done to prevent further
outbreaks.
• Avoid the allergen.
Make the Connection
• Take a good history; look to see if the
lesions have a distinct pattern.
• Apply corticosteroids; watch for adrenal insufficiency (↓ Na, ↑ K, ↓ BP).
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Eczema
(ek-ze-ma)
Clue: Diagnostic or Clinical Findings
Presence of a vesicular rash that may
occur on any skin surface, including
under the eyes. Asthma is often a
comorbid illness.
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158
than steroid creams except in severe outbreaks.
Tacrolimus and pimecrolimus inhibit the actions
of T lymphocytes, mast cells, dendritic cells, and
keratinocytes. Ointment forms are preferable.
Pathophysiology
• Type I hypersensitivity disorder, genetically linked,
•
•
with a family history of hay fever, asthma, or
atopic dermatitis.
Infantile forms are vesicular, cheeks are pale, and
Dennie-Morgan folds may be present under the
eyes. Adults usually have dry leathery areas that
are either more or less pigmented than surrounding tissue and appear in the antecubital and
popliteal areas.
The pruritic lichenified (dry, leathery) lesions can
spread to the hands, feet, eyelids, and neck.
Keep in Mind
• Family histories of asthma or hay fever place
other family members at greater risk.
• Allergy skin testing should be done so contact
with allergens can be avoided.
• Scratching the skin should be avoided to decrease
the chance of secondary infection.
Assessment and Diagnostic Findings
• Areas of vesicular eruption in infants; dry, leathery
Make the Connection
• Assess skin care habits and take a good
areas in adolescents and adults.
Complications
•
Secondary infection.
family history.
• Assess discomfort and medicate with antihista-
Medical Care and Surgical Treatment
• Warm water baths with a hypoallergenic soap or
colloidal substances like oatmeal.
• Moisturizers.
• Antihistamines for itching, topical immune modulators (tacrolimus and pimecrolimus) rather
•
mines to prevent scratching of the skin. Show
how to lightly tap the area rather than scratch for
relief.
Assess for adrenal insufficiency if topical or oral
steroids are used.
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Cellulitis
(sel-u-li-tis)
Clue: Diagnostic or Clinical Findings
Patchy erythema and edema in the
extremities in the absence of DVT. May
be more prevalent in those with diabetes
or peripheral vascular disease.
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Dermatologic Disorders
Pathophysiology
• Bacteria infiltrate skin, bypassing normal skin
barriers, and release toxins in the subcutaneous
tissue. Comorbid illnesses like diabetes and
peripheral vascular disease increase the incidence.
Assessment and Diagnostic Findings
159
Keep in Mind
• Educate clients at risk about proper skin and foot
care.
• Clients should not use heating pads if they have
decreased sensation in the extremities as they may
be burned.
• Acute onset of edema, patchy erythema, some-
times vesicles and pain with systemic signs and
symptoms of inflammation, like fever, pain, and
sweating. Lymph nodes in the region may be
swollen.
Complications
• Possible deep vein thrombosis (DVT) forming due
to inactivity.
• Spreading infection and possible necrosis of
tissue.
Medical Care and Surgical Treatment
• Antibiotics.
• Elevate the limb.
• Warm, moist soaks.
Make the Connection
• Monitor the skin if client is using warm,
moist soaks, to prevent maceration.
• Assess for allergy to antibiotics.
• Teach clients that any injury (bruising, ulcerations,
ingrown toenails, and hangnails) can result in
cellulitis.
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Psoriasis
(so-ri-a-sis)
Clue: Diagnostic or Clinical Findings
Patches of papules or plaques with silvery
scale. The underlying skin is
erythematous.
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Dermatologic Disorders
Pathophysiology
• T cell–mediated autoimmune disorder characterized by silvery scale on an erythematous base.
• Abnormal growth of keratinocytes and dermal
blood vessels.
• Precipitating factors may be any that stimulate
•
the T-cell lymphocytes (e.g., trauma, stress,
infections, and medications).
Histologic studies show increased epidermal cell
turnover; white blood cells (WBCs) are found in
the stratum corneum.
Assessment and Diagnostic Findings
• History, presence of typical lesions. Client may
report improvement with sun exposure.
• Histologic studies showing defects in keratinocyte
differentiation (filaggrin and involucrin gene
mutation), increased presence of plasma proteins
and Ig G.
Complications
• Secondary infections to skin shedding.
• Adrenal insufficiency from corticosteroid use.
160
Medical Care and Surgical Treatment
• Topical moisturizers, keratolytic agents, retinoids;
•
•
coal tar products; anthralin; corticosteroids (topical or PO); calcipotriene; and antihistamines.
Psoralenscoupled with PUVA phototherapy.
Disease-modifying antirheumatic drugs
(DMARDs; e.g., methotrexate), biologic agents
(e.g., etanercept), and intralesional cyclosporine.
Keep in Mind
• Support groups are in place because psoriasis
can be psychosocially disruptive.
• Sun exposure and swimming in salt water will
help clear or reduce the severity of lesions, but
excess sun exposure increases risk for skin cancer.
Make the Connection
• Monitor the extent of the lesions.
• Watch for bleeding or secondary infection.
• Watch for signs of adrenal insufficiency (↓ Na, ↑
K, ↓ BP).
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161
Herpes Zoster
(her-pez zos-ter)
Clue: Diagnostic or Clinical Findings
“Dew drops on a red leaf.” Painful
vesicular lesions unilaterally occurring
along sensory nerve pathways.
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Dermatologic Disorders
Pathophysiology
• Caused by varicella zoster virus, identical to that
which causes chickenpox.
• The herpes virus lies latent in the nerve tissue and
•
•
reactivates with stress or decreased immunity or
in clients with a malignancy or an injury to the
spine or cranial nerve.
Breakouts follow the course of sensory nerves, dermatomes, or cranial nerves and occur unilaterally.
Eruptions last may last from 5 days to 5 weeks.
Even when the lesions are gone, a postherpetic
neuralgia exists and persists.
Assessment and Diagnostic Findings
• Painful unilateral vesicular lesions following a
sensory nerve, dermatome, or cranial nerve.
• Vesicles cause an erythema on the skin because of
161
• Scarring.
• Systemic infection.
Medical Care and Surgical Treatment
• Antivirals orally, topically, or intravenously.
• Analgesics, corticosteroids if no systemic
infection occurs.
• Antibiotics for secondary infection.
Keep in Mind
• Persons with risk factors should avoid persons
with varicella zoster infection.
• Antiviral medications will shorten the course of
the illness.
• Lesions should not be scratched.
• The infectious period is 1–2 days prior to the
lesions erupting to when the lesions are dry.
the acute inflammation.
Complications
• Postherpetic neuralgia, persistent dermatomal
•
•
pain, and hyperesthesia, which can last for weeks
or months.
Ophthalmic herpes zoster can affect eyesight.
Hearing loss, tinnitus, paralysis, and vertigo as
postherpetic cranial nerve problems.
Make the Connection
• Clients with herpes zoster in the hospital
setting should be isolated for infection control.
• Monitor vital signs and skin for secondary
infection.
• Assess pain level and medicate as necessary.
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Herpes Simplex
(her-pez sim-plex)
Clue: Diagnostic or Clinical Findings
Painful, itchy, vesicular lesion on the lips
or in the nose. May also occur in the
genital area.
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Dermatologic Disorders
Pathophysiology
• Caused by the herpes simplex virus (HSV). There
•
are two types: HSV-I occurs above the waist, and
HSV-II occurs below the waist.
Occurs through direct contact, respiratory
droplet, or fluid exposure. After exposure, the
virus lies dormant in the nerve ganglia where the
immune system cannot destroy it. Stress of any
kind can cause the virus to reactivate.
162
• Daily antiviral medication is given orally for
prevention of genital herpes outbreak.
Keep in Mind
• Lesions are infectious a couple of days prior to
outbreak to the time the lesions are crusted.
• Herpes I and II cannot be cured, only suppressed.
• Genital herpes is spread most commonly by sexual
contact.
Assessment and Diagnostic Findings
• Tingling sensation or itching as the vesicle erupts.
• Area is swollen and erythematous.
Complications
• Type II (genital herpes), if present during vaginal
•
birth, can cause blindness or acute neurologic
problems in the newborn such as herpes
encephalitis.
A herpetic lesion on the eye requires ophthalmologic care.
Medical Care and Surgical Treatment
• Antiviral medication topically or orally, which will
shorten the duration of the outbreak.
Make the Connection
• Teach the client about type I and
type II HSV.
• Avoid contact with lesions; wear appropriate
protective gear.
• Teach about antiviral medication and its side
effects and action.
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Paronychia
(par-o-nik-e-a)
Clue: Diagnostic or Clinical Findings
Erythema around the base of the nailbed
in persons who frequently, as a result of
employment, have their hands in water
or are nailbiters or thumb suckers.
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Dermatologic Disorders
Pathophysiology
• Acute or chronic condition in which the protec•
tive barrier between the nail and the nail fold is
breached by bacteria or fungus, causing erythema
and pain.
Can occur in persons whose hands are often in
water and in those who engage in thumb sucking
or nail/cuticle biting.
163
Keep in Mind
• Keep nails moisturized, and care for cuticles
carefully.
• Dry hands after thoroughly washing them.
• Do not bite the nails or cuticles.
Make the Connection
• Assess the site carefully; look for the nail
Assessment and Diagnostic Findings
• Erythema and pain around and at the nail fold,
which can spread.
• Antiretroviral drug use (indinavir) predisposes to
this illness in HIV+ persons.
• Potassium hydroxide 5% smears; potassium
hydroxide (KOH) wet mounts from scrapings or
discharge (hyphae).
Complications
• A run-around infection of the nail.
• Loss of the nail.
Medical Care and Surgical Treatment
• Warm soaks; a drain if necessary; antibiotics or
antiviral medications orally or topically.
lifting from the nailbed.
• Apply warm soaks and give medications as
ordered.
• Teach the client to stop nail biting and use anti•
bacterial hand sanitizers as needed at places of
employment.
Apply antibacterial moisturizers.
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Impetigo
(im-pe-ti-go)
Clue: Diagnostic or Clinical Findings
Honey-colored crusts on the lips mouth,
nose, hands, or perineum; usually in
children. Shallow vesicles that
rupture easily.
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Dermatologic Disorders
Pathophysiology
• Superficial bacterial infection of the skin caused
by staphylococci, streptococci, or both.
• Vesicles or bullae are preceded by discolored
spots.
• Vesicles or bullae rupture, leaving honey-colored
crusts.
• Infection spreads outward.
164
Keep in Mind
• Teach that the lesions are a bacterial infection, so
medical regimen should be followed.
• Parents should teach their child not to scratch
the lesions because the infection can spread.
• Child should not come in contact with other
children until crusts are dry and antibiotics have
been taken for 24 hours.
Assessment and Diagnostic Findings
• Pruritus, weeping vesicles, bullae, and crusts.
• Cultures can be taken for confirmation.
Complications
• Systemic infection, rarely necrotizing fasciitis,
or toxic shock syndrome.
Medical Care and Surgical Treatment
• Antibacterial soap; topical and systemic
antibiotics.
Make the Connection
• Clean the area carefully.
• Administer antibiotics and antibiotic ointment as
ordered.
• Assess for diminution of lesions.
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Scabies
(ska-bez)
Clue: Diagnostic or Clinical Findings
Grayish brown pruritic threadlike lesions
with black dot at the end between fingers,
toes, axillae, groin, buttocks, and
abdominal areas.
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Dermatologic Disorders
Pathophysiology
• Impregnated female scabies mite burrows under
the skin and lays eggs. An inflammatory response
occurs 30–60 days after initial contact.
165
Keep in Mind
• Scabicides do not have to be applied above the
neck; keep on only for prescribed time, no longer.
• Teach that infestations like scabies are common-
Assessment and Diagnostic Findings
•
•
•
Grayish brown threadlike lesions with black dot
at the end found between fingers, toes, axillae,
groin, buttocks, and abdominal areas.
Pruritus.
Skin scraping shows mite under microscope.
Complications
• Secondary infection from scratching.
• Spreads from person to person easily, so it can
become epidemic in school-aged children and
their families.
Medical Care and Surgical Treatment
• Application of a scabicide (e.g., Permethrin
topical cream or Lindane lotion).
• Wash clothing and other items with which the
infected person came into contact.
•
place among schoolchildren and discourage from
feeling judged.
Scabies are easily passed person to person, so all
persons in contact with the infected person are to
be treated.
Make the Connection
• Monitor lesions; wear protective gear.
• Advise the infected person not to scratch the
lesions.
• Support the family’s psychosocial needs.
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166
Pediculosis Capitis
(pe-dik-u-lo-sis ka-pi-tis)
Clue: Diagnostic or Clinical Findings
Itching of the scalp. Magnifying glass
assessment reveals white or translucent
eggs adhered to hair shaft near the skin
or movement of insects in the hair.
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Dermatologic Disorders
Pathophysiology
• Infestation of the head by Pediculus humanus capitis
(head louse).
• Female louse lays eggs at night on a hair shaft
close to the skin; eggs appear white or clear.
• Eggs hatch 7–10 days later.
• Itching of the scalp is produced by the insects
crawling and by their saliva on the scalp. Lice bite
and feed on human blood. They are approximately
2 mm in length.
Assessment and Diagnostic Findings
• Itching.
• Nits observable on hair shaft by magnifying glass.
• Usually found in the hair at the occipital area
and nape of the neck, but can spread anywhere,
even to eyebrows and eyelashes.
Complications
• Secondary infection from itching and scratching
the skin on the scalp.
• Spreads easily, so anyone with contact can
become infected.
Medical Care and Surgical Treatment
• Shampoos and conditioners that contain pediculicidal agents (e.g., Lindane, RID, NIX).
166
• Small-tooth comb to remove nits.
Keep in Mind
• Wash all clothing, hats, and bedding in hot
water.
• Pediculicidal spray can be used on items that
cannot be laundered, like carpet or large pillows.
• Vacuum carpets and other surfaces.
• Soak combs and other hair management items in
the pediculicidal solution.
• Do not leave shampoo on longer than directed,
as it is a toxic agent meant to kill insects.
• In the case of a child, report the infestation to
•
the school nurse so anyone in contact can be
treated.
Support the child to prevent feelings of
embarrassment.
Make the Connection
• Use gloves and tongue blades when
looking for lice or nits.
• Nits are difficult to remove and are adhered tightly
to the hair shaft.
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167
Acne Vulgaris
(ak-ne vul-ga-ris)
Clue: Diagnostic or Clinical Findings
Whitehead, blackheads, or cysts on the
face, neck, upper back, chest, and
shoulders, usually in adolescents, but
can occur in adults.
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Dermatologic Disorders
Pathophysiology
• Skin disorder of the sebaceous glands and their
hair follicles.
• Androgens, stress, strong soaps or cosmetics,
•
•
or genetic factors cause an increase in sebum
secretion.
Pilosebaceous ducts are blocked with accumulated
debris causing inflammation and bacterial
infiltration.
Lesions may be on face, neck, chest, upper back,
and shoulders.
Assessment and Diagnostic Findings
• Erythematous areas with open comedones
(whiteheads) or closed (blackheads).
• Presence of papules, pustules, nodules, and in
severe cases, cysts.
Complications
• Scarring, especially if the acne is cystic.
• Psychosocial implications.
Medical Care and Surgical Treatment
•
•
Topical antibiotics in combination with desquamation agents.
Oral antibiotics in combination with desquamation agents or retinoids.
167
• Oral retinoids.
• Intralesional injections with corticosteroids.
• Comedones extraction.
• Chemical peels or collagen injections for scars.
Keep in Mind
• Lesions should not be manipulated or
“squeezed.”
• Oral retinoids require that females use a reli-
able method of birth control and produce a
negative pregnancy test prior to the start of
therapy. Monthly LFTs will be performed. Skin
structures will be very dry and will require a
moisturizer. Report depressive symptoms.
Make the Connection
• Acne causes psychosocial effects.
• Assess for improvement once therapy is begun.
• If using oral retinoids, make certain adequate
teaching is done about prevention of pregnancy
and monthly LFTs. Assess for signs of depression
in the client on these medications.
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168
Stevens-Johnson
Syndrome and Toxic
Epidermal Necrolysis
(ste-venz-jon-son sin-drom;
toks-ik ep-i-der-mal ne-krol-i-sis)
Clue: Diagnostic or Clinical Findings
Flu-like symptoms or macular rash after
starting sulfa drugs, antibiotics, or
antiepileptics.
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Dermatologic Disorders
Pathophysiology
• Altered drug metabolism causes a T cell–mediated
reaction in the keratocytes.
• A macular rash spreads rapidly and forms vesicles
•
and bullae in the epidermis and in the mucous
membranes, which necrose and slough.
Stevens-Johnson syndrome (SJS) involves 10%
of body surface area, while toxic epidermal
necrolysis (TEN) involves 30%.
Assessment and Diagnostic Findings
• About 1–3 weeks after a drug is started,
flu-like symptoms and conjunctivitis occur.
• Large bullae that are easily broken will slough
•
•
•
•
over a period of 1–3 days. Nails, eyebrows, and
internal mucosal structures may be lost.
Nikolsky’s sign. Painful oral crusts, erosions, and
genital problems exist in most cases.
Cough, pulmonary edema, and
hypoxemia.
Glomerulonephritis and hepatitis may develop.
Histology shows necrotic epithelial tissue.
168
Complications
• Fluid loss and electrolyte imbalance.
• Respiratory failure.
• Acute renal and hepatic failure.
Medical Care and Surgical Treatment
• Transfer to a burn unit.
• F & E replacement.
• Prophylaxis for infection.
• Corticosteroids.
Keep in Mind
• Report any flu-like symptoms or rash after start-
ing therapy with any medication, seek immediate
medical care.
Make the Connection
• Maintain strict monitoring of I&O; provide
fluid replacement based on total surface area.
• Monitor pulse oximetry, CBC, LFTs, RFTs, and
electrolyte panel.
• If client is placed on a ventilator, provide aseptic
ventilator care and suctioning.
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169
Tinea
(tin-e-a)
Clue: Diagnostic or Clinical Findings
Reddened lesions that have a scaly
appearance. Lesions may form circular
areas, reddened raised areas, or, between
toes, crevasses that can be deep and
bloodless.
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Dermatologic Disorders
Pathophysiology
• Tinea infections or dermatophytoses occur
•
•
when skin is impaired by exposure to a moist
environment.
Infections may occur through direct contact with
infected humans, animals, or objects.
Superficial mycotic infections include:
Tinea pedis.
Tinea capitis.
Tinea corporis.
Tinea versicolor.
Tinea cruris.
Tinea unguium.
Tinea barbae.
Assessment and Diagnostic Findings
169
Complications
• Secondary infection from altered skin integrity.
• Alopecia.
Medical Care and Surgical Treatment
• Topical and oral antifungal agents.
• Corticosteroids for severe hypersensitivity
reactions (kerion).
Keep in Mind
• Teach clients to keep area clean and dry.
• Tinea capitis and tinea pedis are easily spread
•
• Superficial types are characterized by scaling,
•
slight itching, reddish or grayish patches, and
dry brittle hair that is easily extracted with the
hair shaft.
Deep lesions are flat, reddish, kerion-like areas
studded with dead or broken hairs. Permanent
alopecia may occur in these areas.
by direct contact; tinea capitis is also spread by
animals.
Nonsynthetic or cotton socks and underwear
help decrease the incidence or severity of tinea
infections.
Make the Connection
• Assess for sites in moist areas that are
•
reddened, have a scaly appearance, or form a
circular lesion.
Assess effectiveness of topical antifungals.
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170
Verruca
(ver-roo-ka)
Clue: Diagnostic or Clinical Findings
Pink or light pink growths that cluster on
skin structures. Occasionally, these
lesions are flattened and found on the
facial area.
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Dermatologic Disorders
Pathophysiology
• Benign papillomas, or warts, are caused by
•
•
human papillomaviruses (HPVs) that are spread
through cracks in the skin; genital warts are
spread by sexual contact.
Various types are commonly seen:
Verruca vulgaris (common warts).
Verruca filiformis are found on the eyelids, face,
and neck and project from the skin.
Verruca plana (flat warts).
Verruca plantaris (plantar warts).
Condyloma acuminata (genital warts).
These growths usually clear in time, but the
immune system reacts very slowly to their
presence.
170
Medical Care and Surgical Treatment
• Keratolytic agents, plaster that breaks down the
verruca, and freezing with liquid nitrogen.
• Intralesional bleomycin injections.
• Laser surgery and electrosurgery.
• Antiviral therapy.
• Duct tape (on for 6–7 days, off for 12 hours, and
repeat).
Keep in Mind
• Teach females the connection between genital
warts and cervical cancer.
• Warts can be self-limiting, but removal methods
do exist.
• Wart removal can cause scarring.
Assessment and Diagnostic Findings
• Irregular thickening of the skin layers (stratum
spinosum and stratum corneum) in typical areas.
• Differentiated from other growths by biopsy.
Complications
• Scarring.
• Cervical cancer from condyloma acuminata.
Make the Connection
• Assess areas affected by verrucae and
apply topical removal agents as ordered.
• Assess effectiveness.
• Refer to dermatologist or gynecologist for
verrucae removal.
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Dermatologic Disorders
Superficial and
Partial-Thickness Burns
(soo-per-fish-al and par-shal thik-nes birns)
Clue: Diagnostic or Clinical Findings
Redness of the skin resembling sunburn
or redness and mottling of the skin with
blister formation after contact with a
thermal source.
171
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Dermatologic Disorders
Pathophysiology
• Thermal or chemical injury to skin, the extent
of which is expressed as body surface area.
• Superficial (first-degree) burns are likened to
•
•
sunburn and affect only the epidermis. Partialthickness (second-degree) burns involve the
epidermis and some portion of the dermis.
Second-degree burns are characterized by blister
formation.
Deep second-degree burns take longer to heal
and may cause scarring.
First- and second-degree burns are painful
because of intact free nerve endings for sensory
pain transmission.
Assessment and Diagnostic Findings
• Redness of the skin resembling sunburn that is
very painful.
• Red, mottled skin with blisters that blanch on
171
the hand, the client will require referral to a burn
center for treatment, especially if the burn is a
deep second-degree burn.
Medical Care and Surgical Treatment
• Silvadene or other antibiotic creams; analgesics
(usually morphine sulfate for severe pain).
• Original Biobrane or Integra Artificial Skin for
deep second-degree burns of the hands.
• Assess respiratory status if the client was exposed
to smoke and heat.
Keep in Mind
• Teach the client about the extent of the burn and
what kind of treatment to expect.
• The client must maintain adequate fluid intake
and a nutritious diet.
• Any treatment regimen, like creams or occlusive
dressings, must be maintained.
pressure and then refill; very painful.
Complications
• Edema, pain, and secondary infection with
second-degree burns.
• If burn occurs in the perineal area, over a large
surface area, or involves the entire surface of
Make the Connection
• Monitor I&O, pain level, electrolytes, and
nutritional status.
• Assess for healing or infection.
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172
Full-Thickness Burns
(ful thik-nes birns)
Clue: Diagnostic or Clinical Findings
Tough, leathery, or charred skin surface
that is brown, tan, red, or black. The skin
does not blanch and is painless.
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Dermatologic Disorders
Pathophysiology
• Thermal, chemical, or electrical source destroys
all layers of the skin (third-degree burns).
• Severe edema from protein loss and increased
capillary permeability.
Assessment and Diagnostic Findings
• Tough, leathery, or charred skin that is brown,
•
•
•
•
tan, red, or black; does not blanch; and is
painless.
Progressive dyspnea from hot air burns.
Progressive edema, ↓ BP, ↑ HR; rule of nines to
assess BSA burned.
CBC shows decreased RBCs.
Decreased renal output or hemoglobin in the
urine.
Complications
• Shock from massive fluid loss to death.
• Respiratory distress.
• Secondary infection.
Medical Care and Surgical Treatment
• LR IV for fluid resuscitation with albumin infusion based on BSA burned; transfer to burn
center; fluids must be sufficient to keep urine
clear of hemoglobin.
172
• Respiratory support.
• Allograft, autograft, xenograft or cultured skin
that must not be disturbed.
• Antibiotics, morphine sulfate, TPN, and pressure
suits to reduce scarring.
Keep in Mind
• Client and family must be kept apprised of the
situation to reduce anxiety.
• Client will require reverse isolation when stable;
débridement is done with anesthesia.
Make the Connection
• Assess BSA affected by using the rule of
nines for adults and children.
• Prepare to infuse a large volume of LR in the
first 24 hours.
• Monitor vital signs for shock; monitor I&O; and
monitor urine for color (must not be maroon).
• Medicate with morphine sulfate IV as needed.
• Support the family and client.
• Apply splints or pressure suits as needed.
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173
Rosacea
(ro-za-se-a)
Clue: Diagnostic or Clinical Findings
Client’s skin appears flushed. States that
sun exposure, eating or drinking hot
foods or liquids, and alcohol make the
condition worse.
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Dermatologic Disorders
Pathophysiology
• Chronic inflammatory process that often coexists
with acne that looks like blushing.
• Thought to be caused by leakage of fluid and
•
•
•
inflammatory mediators into the dermis.
Inflammation may persist because of bacterial
infiltration in the area.
The main types of rosacea are the following:
• Telangiectatic (marked by the appearance of
spidery blood vessels on affected skin).
• Papulopustular (bumpy/pustular lesions).
• Phymatous (nasal scarring and deformity).
• Ocular (involving the lids, lashes, or conjunctiva).
The condition is common, especially in persons
of Northern European ancestry. It usually is
noted first between the ages of 30 and 50.
Women are affected more often than men.
Assessment and Diagnostic Findings
• Blushing or redness of the cheeks, nose, and
eyelids, with acne-like outbreaks that are worsened by sun exposure, ingestion of hot liquids
or foods, and alcohol (especially wine).
173
Complications
• Rhinophyma (thickening and bumpy deformity of
the nose and cheeks).
Medical Care and Surgical Treatment
• Metronidazole or azelaic acid topically.
• Oral antibiotics.
• Rhinophyma requires laser treatment, dermabra-
sion, cryosurgery, or excision of excess tissue by a
plastic surgeon.
Keep in Mind
• Clients with rosacea must be treated to prevent
worsening.
• Teach clients to avoid hot foods and liquids,
exposure to the sun, and alcohol.
Make the Connection
• Monitor skin for improvement during
treatment.
• Reinforce teaching about foods, alcohol, and sun
exposure.
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MENTAL HEALTH
Generalized Anxiety Disorder, 174
Posttraumatic Stress Disorder, 175
Panic Disorder, 176
Phobias, 177
Obsessive-Compulsive Disorder, 178
Conversion Disorder, 179
Dissociative Amnesia, 180
Mania, 181
Depression, 182
Bipolar Disease, 183
Schizophrenia, 184
Attention Deficit-Hyperactivity
Disorder (ADHD), 185
Alcoholism, 186
Borderline Personality Disorder, 187
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174
Generalized Anxiety
Disorder
(jen-er-al-ized ang-zi-e-te dis-or-der)
Clue: Diagnostic or Clinical Findings
Excessive worry or anxiety that cannot
be controlled, causing interference with
normal activities of daily living.
Symptoms must have occurred for
at least 6 months.
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Mental Health Disorders
Pathophysiology
• Anxiety is produced by stimulation of the
autonomic nervous system. Neurotransmitters
involved in the anxiety response include gammaaminobutyric acid (GABA), serotonin, epinephrine, and norepinephrine. A prolonged, abnormal
fight-or-flight response occurs to normal stimuli.
Assessment and Diagnostic Findings
• According to the Diagnostic and Statistical Manual
•
•
of Mental Disorders, 4th Edition, Text Revision
(DSM-IV-TR), symptoms must be associated
with the following: feeling easily fatigued,
irritability, sleep disturbances, difficulty concentrating, restlessness, and muscle tension.
Autonomic activity causes cold sweats, sweaty
palms, dry mouth, nausea or diarrhea, urinary
frequency, difficulty swallowing and eating, an
exaggerated startle response, and depressive
symptoms.
PET and SPECT scans reveal increases in metabolism in the brain.
Complications
• Panic disorder and phobia development.
174
• Disturbances in family processes.
• Loss of ability to function in society.
• Depression that can lead to psychosis or suicide.
Medical Care and Surgical Treatment
• Cognitive behavioral therapy, along with anxiolytic
and antidepressive agents.
• Electroconvulsive therapy (ECT).
• Group therapy.
Keep in Mind
• Exercise, diet, and social activity are part of
therapy.
Make the Connection
• “Offer yourself” to the client (“I will stay
•
•
with you until you feel better”) and use empathy.
Walk along with clients who need to pace.
Use open-ended questions (“Tell me about . . .”).
Be aware of the defense mechanisms.
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175
Posttraumatic Stress
Disorder
(post-traw-mat-ik stres dis-or-der)
Clue: Diagnostic or Clinical Findings
Acute anxiety and distress related
to flashbacks or memories of a
traumatic event.
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Mental Health Disorders
Pathophysiology
• Severe psychological distress after traumatic
•
•
•
events (e.g., war, criminal assault, accidents,
natural disasters, rape).
The amygdala of the brain is hyperactive in PTSD.
Activation of the amygdala causes activation of
the autonomic nervous system, and the adrenal
system. The sympathetic nervous system
produces many of the symptoms of PTSD,
which are prolonged by the adrenal hormones.
According to the Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision (DSM-IV-TR),
symptoms must last at least 1 month. Onset may
occur at any time after the traumatic event.
175
Complications
• Depression, suicide, and homicide.
• Loss of family processes and social withdrawal.
Medical Care and Surgical Treatment
• Treatment of substance abuse.
• Anxiolytic and antidepressant agents.
• ECT.
• Group therapy and cognitive behavioral therapy.
Keep in Mind
• Family therapy will help enlist assistance for the
client at home.
Make the Connection
Assessment and Diagnostic Findings
• “Offer yourself” to the client
• Flashbacks or reexperiencing the horrifying event.
• Avoidance behavior:
•
•
Memory disturbances.
Irritability.
Sleep disturbances.
Psychological or social withdrawal and substance
abuse.
EEG changes, and PET scan showing ↑ in brain
metabolism.
•
•
•
•
(“I will stay with you until you feel better”) and
use empathy. Walk along with anxious clients
who need to pace and ensure they are safe.
Use open-ended questions (“Tell me about....”).
Be aware of the defense mechanisms.
Reexperiencing traumatic events can be very
disturbing to the client.
Use crisis management theory.
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Mental Health Disorders
176
Panic Disorder
(pan-ik dis-or-der)
Clue: Diagnostic or Clinical Findings
Sudden feeling of impending doom,
going crazy, unreality, and fear
accompanied by palpitations,
numbness of the arms, chest
discomfort, and dizziness.
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Mental Health Disorders
Pathophysiology
• Symptoms are recurrent.
• The cycle of panic is attributable to “fear of the
fear.” Dreading an attack brings one on.
• Physical symptoms are related to the sympathetic
and adrenal systems.
• Several hypotheses exist as to cause: a disorder
in serotonin sensitivity, hypersensitivity to
catecholamines, sensitivity to lactate, decreased
inhibition to GABA, hypersensitivity in neuroanatomy producing abnormal signals for fight
or flight, and genetics.
Assessment and Diagnostic Findings
• Differential diagnosis must be made, especially to
rule out hypoglycemia and mitral valve prolapse.
• PET scan shows abnormalities of brain metabo•
lism. Lactate infusion can precipitate a panic
attack.
Chest discomfort, palpitations, dyspnea, numbness and tingling of extremities, depersonalization and dizziness, feelings of impending doom,
nausea, choking, chills, cold sweats, and hot
flashes.
176
Complications
• Development of phobias,↑ functioning socially.
• Disturbances in family processes.
• Loss of ability to function in society.
• Depression and substance abuse.
Medical Care and Surgical Treatment
• Anxiolytic and/or antidepressant agents along
with cognitive behavioral therapy.
• Electroconvulsive therapy (ECT) for severe
depression.
• Group therapy; treatment of substance abuse.
Keep in Mind
• Once stable, the client can use therapeutic techniques to recognize the self-limiting nature of a
panic attack.
Make the Connection
• Offer yourself to the client (“I will stay
•
with you”). Walk along with clients who need to
pace.
Use crisis theory to assure that the client knows
he or she is safe.
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Mental Health Disorders
177
Phobias
(fo-be-az)
Clue: Diagnostic or Clinical Findings
Irrational fear of an object, place,
situation, thing, or person that causes
avoidance behaviors.
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Mental Health Disorders
Pathophysiology
• According to the Diagnostic and Statistical Manual
•
•
of Mental Disorders, 4th Edition, Text Revision
(DSM-IV-TR), phobia development is strongly
associated with anxiety disorders. A phobia
occurs when an object, place, situation, thing,
or person causes a sympathetic nervous system
(autonomic) response that results in anxiety.
The trigger of anxiety becomes a phobia.
A phobia can become so severe that all social
contact is lost.
A simple phobia is one associated with fear of
common things (e.g., spiders, heights).
177
Medical Care and Surgical Treatment
• Cognitive behavioral therapy; group therapy.
• Desensitization therapy (a long process).
• Anxiolytic and antidepressant agents.
Keep in Mind
• Once stabilized, the client can gradually be intro•
Make the Connection
• It is crucial to offer yourself to the client
Assessment and Diagnostic Findings
• Fear, anxiety, and panic when faced with the
object of the phobia.
• Tachycardia and dyspnea.
• An intense desire to escape.
Complications
• Social phobia and agoraphobia result in loss
of social contacts and isolation.
• Phobias are associated with anxiety and depression, so suicide can be a complication.
duced to the phobic object or situation in a
therapeutic setting.
Phobias can be overcome.
•
•
•
•
(“I will stay with you until you feel better”) and
use empathy (“I understand your discomfort”).
Walk along with anxious clients who need to pace.
Use open-ended questions (“Tell me about....”).
Be aware of the defense mechanisms that clients
will use to ease their discomfort.
Use crisis management theory. Make certain the
client knows he or she is safe, especially if using
desensitization therapy.
Utilize appropriate medication therapy to
decrease the client’s anxiety.
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Mental Health Disorders
178
Obsessive-Compulsive
Disorder
(ob-sess-iv kom-pul-siv dis-or-der)
Clue: Diagnostic or Clinical Findings
Rituals are performed a specific number
of times and in a specific sequence to
decrease unpleasant thoughts.
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Mental Health Disorders
Pathophysiology
•
•
•
•
According to the Diagnostic and Statistical Manual
of Mental Disorders, 4th Edition, Text Revision
(DSM-IV-TR), an obsession involves recurrent,
intrusive, and persistent thoughts, impulses, or
images that cause excessive anxiety. The obsession is known to be irrational yet cannot be
ignored. Attempts to suppress the obsession
become rituals known as compulsions.
The DSM-IV-TR defines a compulsion as a repetitive act or ritual.
The client with obsessive-compulsive disorder
(OCD) spends a great deal of time on the
ritualistic behavior.
There is a genetic predisposition for OCD.
178
Complications
• Severe interruption in social and family processes.
• Depression, suicide, or homicide.
Medical Care and Surgical Treatment
• Selective serotonin reuptake inhibitors and
anxiolytic agents.
• Cognitive behavioral therapy.
Keep in Mind
• If behaviors are interfering with activities of daily
living, it is time to seek help.
• An obsession can be controlled with medication.
Make the Connection
• “Offer yourself” to the client (“I will stay
Assessment and Diagnostic Findings
•
•
•
•
Ritualistic hand washing, “checking for” safety,
opening and closing drawers a certain number
of times, and other repetitive, time-consuming
behaviors.
Severe anxiety is experienced if the compulsion is
not completed.
Some obsessions and compulsions are violent or
sexual in nature.
MRI may show increase in size of caudate nucleus.
•
•
•
•
with you until you feel better”) and use empathy.
Walk along with anxious clients who need to
pace.
Use open-ended questions (“Tell me about....”).
Be aware of the defense mechanisms.
Use crisis management theory.
Monitor LFTs during antidepressant drug therapy.
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Mental Health Disorders
179
Conversion Disorder
(kon-ver-zhun dis-or-der)
Clue: Diagnostic or Clinical Findings
Somatization of anxiety that results in
paralysis, blindness, or other physical
symptoms for which no medical
explanation can be found. The client
seems indifferent to the loss of
function.
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Mental Health Disorders
Pathophysiology
• A somatoform disorder in which neurologic
•
•
symptoms (e.g., blindness, paralysis, loss of
touch) may occur as a result of anxiety. According
to the Diagnostic and Statistical Manual of Mental
Disorders, 4th Edition, Text Revision (DSM-IV-TR),
symptoms cannot be intentional or explained by
any medical tests.
Impulses to the brain are misinterpreted or
rerouted by an anxiety response, resulting in
perceptual abnormalities. An anxiety- or stressproducing event precedes onset of the conversion
disorder. Women are affected more than men.
Neurotransmitters affected in this disorder are
serotonin and norepinephrine.
Assessment and Diagnostic Findings
• Neurologic deficit with no medical explanation.
• MRI, CT scan, and other symptom-specific
•
•
examinations are performed to rule out physical
causes.
“La belle indifference.”
Primary gain (avoidance behavior) and secondary
gain (attention).
179
Complications
• Comorbid depression and risk of suicide.
• Deterioration of the personality.
• Failure to diagnose actual neurologic conditions.
Medical Care and Surgical Treatment
• Anxiolytic and antidepressive agents.
• Cognitive behavioral therapy.
Keep in Mind
• Teach clients methods for keeping stress under
control.
Make the Connection
• “Offer yourself” to the client (“I will stay
with you”) and use empathy (“I understand your
discomfort”).
• Never reveal doubt that the illness is real.
• Use open-ended questions (“Tell me about....”).
• Be aware of the defense mechanisms.
• Use crisis management theory.
• Monitor LFTs during antidepressant therapy.
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180
Dissociative Amnesia
(dis-o-shi-a-tiv am-ne-ze-a)
Clue: Diagnostic or Clinical Findings
Inability to remember stressful events.
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Pathophysiology
•
•
•
A dissociative disorder is caused by a traumatic
occurrence. The areas of the brain associated
with memory recall and storage (the limbic and
hippocampal areas) may be traumatized by
childhood events or by unbearable events later
in life.
According to the Diagnostic and Statistical Manual
of Mental Disorders, 4th Edition, Text Revision
(DSM-IV-TR), the client must have experienced
at least two occurrences of amnesia for an
event as well as impaired social or familial
processes.
Repression.
Assessment and Diagnostic Findings
• After a traumatic event, the client cannot recall
•
•
any details of the event. This may be a temporary
or permanent loss of recall.
Early-life trauma may not be recalled later in life.
Imaging studies conducted to rule out physical
cause.
Complications
• Overuse of repression; poor coping skills.
• Recall can cause severe trauma.
180
• Loss of family or social contacts.
• Suicide or homicide.
• Self-medication (substance abuse).
Medical Care and Surgical Treatment
• Cognitive behavioral therapy.
• Crisis management.
• Anxiolytic and antidepressant agents.
Keep in Mind
• Teach coping skills once the client is stabilized.
Make the Connection
• Clients may become assaultive when
memory returns.
• If client is pacing, walk along with him or her to
communicate and provide company.
• “Offer yourself” to the client (“I will stay with
you”) and use empathy.
• Use crisis theory and assure safety.
• Monitor LFTs during antidepressant therapy.
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Mania
(ma-ne-a)
Clue: Diagnostic or Clinical Findings
Mental disorder characterized by
excessive excitement, restlessness,
delusions of grandeur, and poor
judgment.
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Pathophysiology
• According to the Diagnostic and Statistical Manual
•
of Mental Disorders, 4th Edition, Text Revision
(DSM-IV-TR), the client must have experienced
at least three persistent episodes of grandiose
thoughts, excessive need to speak characterized
by flight of ideas, decreased need for sleep, poor
judgment, and irritability.
Imbalance in levels of norepinephrine, serotonin,
dopamine, and hormones.
Assessment and Diagnostic Findings
• Hyperactivity, hypersexuality, hyperreligiosity,
•
•
impulsiveness, poor nutritional status, substance
abuse, and sleep disturbances.
MRI and PET scan may show disturbances in
metabolic function of the brain (prefrontal and
temporal).
Cortisol levels may be abnormal.
Complications
• Severe interference with societal, familial, and
legal processes.
• Worsening substance abuse and decline of
nutritional status.
• Sexually transmitted disease.
181
Medical Care and Surgical Treatment
• Long-term treatment with mood stabilizers, anti•
depressant agents, anticonvulsants, antipsychotic
agents, and calcium channel blockers.
Cognitive behavioral therapy.
Keep in Mind
•
Compliance with therapy is important to
success.
Make the Connection
• “Offer yourself” to the client
(“I will stay with you”) and use empathy.
• If the client is pacing, walk along with him or her.
• Offer finger foods so the active client can walk
and eat.
• A one-on-one therapeutic setting is more
effective.
• Monitor CBC for low WBC, and monitor drug
levels and LFTs during mood stabilizer, antidepressant, and anticonvulsant therapy.
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Depression
(de-presh-un)
Clue: Diagnostic or Clinical Findings
Persistent sadness, hopelessness, feelings
of guilt, inability to concentrate,
decreased interest in daily activities,
changes in appetite, insomnia or
excessive sleep, and recurrent thoughts
of death or suicide.
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Pathophysiology
• Changes in brain tissue metabolism and blood
•
•
flow, particularly in the prefrontal cortex
(decreased) and the amygdala (increased).
Changes in the ability of receptors to bind with
neurotransmitters (e.g., serotonin, norepinephrine); increase in reuptake of neurotransmitters
before they can bind with receptors and
increased destruction of neurotransmitters by
monoamine oxidase, which deaminates serotonin and norepinephrine.
Less ability to handle stress related to altered
hypothalamus-pituitary-adrenal system.
Assessment and Diagnostic Findings
• MRI and PET scan abnormalities. ↓ blood flow
•
•
•
and metabolism in the prefrontal cortex but ↑ in
the amygdala.
Low serum cortisol levels.
Sleep study abnormalities.
According to the Diagnostic and Statistical Manual
of Mental Disorders, 4th Edition, Text Revision
(DSM-IV-TR), symptoms of depression must represent a significant deviance from normal activity that is present for greater than 2 weeks.
182
Complications
• Psychosis, suicide attempts, and death.
• Severe interference with family and societal
processes; self-medication (substance abuse).
Medical Care and Surgical Treatment
• Anxiolytic, mood stabilizing, antipsychotic, and
antidepressant agents.
• ECT; light therapy (if associated with SAD).
• Cognitive behavioral therapy with a one-on-one
structured therapeutic setting (until stable).
Keep in Mind
• Teach clients that side effects will lessen with
time, and some require dietary restrictions.
• Persons with major depression can recover
completely.
Make the Connection
• “Offer yourself” to the client (“I will stay
with you until you feel better”) and use empathy.
• Use open-ended questions (“Tell me about....”).
• Be aware of the defense mechanisms.
• Monitor LFTs during antidepressant therapy.
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Bipolar Disorder
(bi-pol-ar dis-or-der)
Clue: Diagnostic or Clinical Findings
Cycling through periods of depression
and mania. Rapid cycling (four episodes
per year) indicates a more severe illness.
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183
poor nutritional status, substance abuse, and
sleep disturbances.
Pathophysiology
• Changes in brain tissue metabolism and blood flow,
•
•
•
particularly in the prefrontal cortex (decreased) and
the amygdala (increased). Strong genetic link, and
women are affected more than men.
Imbalance in neurotransmitters. Epinephrine and
norepinephrine are increased in the manic phase,
and serotonin and norepinephrine are decreased
in the depressive phase.
Less ability to handle stress (hypothalamuspituitary-adrenal system).
Sleep disturbances related to neurotransmitter
imbalances.
Assessment and Diagnostic Findings
• MRI and PET scan.
• Sleep study abnormalities.
• According to the Diagnostic and Statistical Manual of
Mental Disorders, 4th Edition, Text Revision (DSM-IVTR), symptoms of bipolar disorder such as persistent sadness, hopelessness, feelings of guilt,
inability to concentrate, decreased interest in
daily activities, changes in appetite, insomnia or
excessive sleep, and recurrent thoughts of death
or suicide alternate with periods of hyperactivity,
hypersexuality, hyperreligiosity, impulsiveness,
Complications
• Psychosis, suicide attempts, and death.
• Severe interference with family and societal
processes, self-medication, and substance abuse.
Medical Care and Surgical Treatment
• Anxiolytic, mood stabilizing, antidepressant, and
antipsychotic agents.
• ECT; light therapy (if associated with SAD).
• CBT with a one-on-one structured therapeutic
milieu.
Keep in Mind
• Teach the client about the disorder and the need
for periodic blood tests.
Make the Connection
• “Offer yourself” to the client (“I will stay
•
with you”) and use empathy (“I understand your
discomfort”). A one-on-one therapeutic setting is
most effective. Offer nutrient-dense finger foods
during the manic phase.
If the client is pacing, walk along with him or her.
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Schizophrenia
(skiz-o-fren-e-a)
Clue: Diagnostic or Clinical Findings
Often described by the 4 As (autism,
avolition, anhedonia, and associative
looseness). Schizophrenia means “split
mind,” with a chasm occurring between
the client and the environment. High
dopamine levels are present.
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Mental Health Disorders
Pathophysiology
• The neurotransmitter dopamine is excessively
abundant. Changes in brain metabolism.
• Genetic links are not as strong as once thought
•
•
but still place relatives at greater risk of developing schizophrenia (onset adolescense; early
adulthood).
Alterations in perception and thought, including
delusions (fixed thoughts) and hallucinations
(auditory is the most common but can involve all
the senses).
Difficulty with expression of thought.
Assessment and Diagnostic Findings
• PET scans.
• High dopamine levels.
• The 4 As: autism, avolition, anhedonia, and
associative looseness.
• Delusions, hallucinations, difficulty expressing
•
•
oneself (associative looseness, neologisms,
echolalia, and word salad).
Depersonalization.
Behavioral problems.
184
Complications
• Increasing anxiety, depression, and suicide.
• Severe interference with social and family processes.
• Substance abuse.
Medical Care and Surgical Treatment
• Anxiolytic, mood stabilizing, antidepressant,
and antipsychotic agents; ECT with CBT.
Keep in Mind
• Teach the client to report return of hallucinations
and types and how to cope.
• Teach the client about side effects of medications
and to report movement problems.
Make the Connection
• Monitor CBC for low WBC count.
• Check the blood glucose levels (atypical antipsychotics).
• Assess the effectiveness of medication and CBT.
• Ensure the client’s safety by providing structure.
• Watch carefully for signs of tardive dyskinesia,
akathisia, and pseudoparkinsonism. Clients with
movement disorders should be referred to a
movement specialist immediately.
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185
Attention
Deficit-Hyperactivity
Disorder (ADHD)
(a-ten-shun def-i-sit hi-per-ak-tiv-i-te dis-or-der)
Clue: Diagnostic or Clinical Findings
Child or adult with difficulty focusing,
finishing projects, listening to
instructions, and sitting still who
also shows emotional lability.
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Mental Health Disorders
Pathophysiology
• PET scans show decreased metabolic activity in the
•
•
•
frontal lobes and basal ganglia; EEG readings show
↓ wave activity in the same area.
PET scans show ↑ metabolism in the primary
sensory and sensorimotor areas. There is no
specific lesion. ADHD is believed to be an error in
myelination.
Affects boys and men more than girls and women.
Inability to wait, impatience, bursts of anger, and
an inability to sit still; difficulty finishing projects,
focusing, and following directions and often
appears to be staring off into space.
Assessment and Diagnostic Findings
• Abnormal PET scan and EEG showing ↓ activity,
•
•
•
particularly in the right frontal lobe, and
increased activity in the thalamus and sensorimotor areas.
Diagnosis is often made by complaints of parents
and teachers about behaviors.
Developmental assessment.
CRS-R are administered along with intelligence
and psychological tests to differentiate behavioral
problems from other mental or physical disorders.
185
Complications
• Poor self-esteem, difficulty with school work.
• Substance abuse (self-medication).
Medical Care and Surgical Treatment
• Psychostimulants.
• Cognitive behavioral therapy.
• Social skills training.
Keep in Mind
• Clients with ADHD may benefit from activities
•
like massage, music therapy, yoga, and
chiropractic manipulation.
Dietary management is important.
Make the Connection
• Monitor weight and sleep habits of clients
on medications.
• Interview parents to assess the degree of improvement seen in their child.
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Alcoholism
(al-ko-hol-izm)
Clue: Diagnostic or Clinical Findings
Smell of alcohol on breath, ataxia,
slurred speech, and inappropriate affect;
or shaking if abstinent.
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Mental Health Disorders
Pathophysiology
• Alcoholism is genetically linked.
• Alcohol is very lipid-soluble and enters the
brain easily. Once there, it acts on GABA receptors, promoting a depressant and pleasurable
effect. The action of other drugs (e.g., heroin)
on the opioid and dopaminergic centers is
similar to that of alcohol, cross-addictions
occur.
186
• Dietary intervention.
• CBT with social coping skills and group session
with community follow-up.
Keep in Mind
• Teach that alcoholism adversely affects social, intimate, and financial aspects of an entire family.
• Alcohol adversely affects physiology, resulting in
many health problems.
Assessment and Diagnostic Findings
• Changes in mood, judgment, and sexual practices.
• May exhibit ataxic gait, slurred speech, and
Make the Connection
• Watch for DTs from several hours to
nystagmus; ETOH smell on breath.
Complications
• Addiction.
• Severe interference with family and social processes.
• Withdrawal, Wernicke-Korsakoff syndrome, cirrhosis of the liver, diabetes, metabolic syndrome,
and increased blood lipid levels.
Medical Care and Surgical Treatment
• Antidepressant agents (tricyclic), opioid-receptor
inhibitors, acamprosate, disulfiram, folic acid,
thiamine, anticonvulsants, magnesium sulfate,
and sedatives.
several days after the last drink.
• Monitor LOC and for seizure activity during acute
withdrawal.
• Monitor blood chemistries for LFTs nutritional
•
•
assessment, GGT, and blood ETOH level. Check
for cross-addictions.
Monitor the effectiveness of drug therapy.
Check compliance with therapy. Most inpatient
facilities provide 28 days of treatment for alcohol
withdrawal and then facilitate follow-up with
Alcoholics Anonymous in the community.
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187
Borderline Personality
Disorder
(bor-der-lin per-sun-al-i-te dis-or-der)
Clue: Diagnostic or Clinical Findings
Substance abuse; impulsive, “needy”
behavior. Self-destructive behavior
(suicide attempts) for attention.
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Mental Health Disorders
Pathophysiology
• The personality develops as a normal part of
•
neurophysiology, coupled with environmental
factors. Components of the client’s genetic
framework react to what is external, creating
the outer and inner persona.
Changes in the prefrontal cortex may be responsible for the personality changes exhibited by those
with personality disorders. Affects women more
than men.
Assessment and Diagnostic Findings
• MRI may show reduction in size of the prefrontal
cortex.
• Splitting.
• Self-destructiveness, inappropriate affect, attention seeking; difficulty maintaining relationship,
manipulation, and impulsiveness with angry
outbursts.
Complications
• Substance abuse.
• Psychosis with paranoia.
• Depression.
• Suicide attempts and death.
187
Medical Care and Surgical Treatment
• Antidepressant, antipsychotic, and mood stabilizing agents.
• CBT with clearly delineated boundaries.
Keep in Mind
• Teach the client about the importance of medications and about possible side effects.
• Develop a contract with the client to report any
thoughts of suicide.
• Tell the client of the boundaries of the therapeutic
relationship.
Make the Connection
• Monitor the CBC for WBC depletion
during anticonvulsive therapy.
• Monitor the drug levels of mood stabilizers and
anticonvulsants.
• Monitor the LFTs during antidepressant therapy.
• Set limits and restate them frequently.
• Realize that the client will show desired behaviors
in order to attain favors.
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WOMEN’S HEALTH
Leiomyomas, 188
Cervical Cancer, 189
Polycystic Ovarian Syndrome, 190
Breast Cancer, 191
Pregnancy-Induced Hypertension, 192
Placenta Previa, 193
Placenta Abruption, 194
Persistent Fetal Circulation, 195
Patient Ductus Arteriosus, 196
Neonatal Sepsis, 197
ABO Blood Type Incompatibility, 198
Rh Incompatibility, 199
Meconium Aspiration Syndrome, 200
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Women’s Health and Perinatal Disorders
Leiomyomas
(li-o-mi-o-maz)
Clue: Diagnostic or Clinical Findings
Heavy menstrual periods with resulting
low H&H. May feel pressure, heaviness,
or pain in the pelvis.
188
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Pathophysiology
• Estrogen is dominant in the proliferative phase
•
•
of the menstrual cycle and acts on the endometrial
layer and is also responsible for proliferation of
abnormal uterine cells that grow under its
influence.
Benign tumors or growths that usually occur
in the corpus of the uterus. Subserosal myoma
(forms under the outer serous layer of the
uterus and may become pedunculated); intramural myomas (grow within the myometrium)
and submucosal myomas (endometrial layer
and may cause excessive menstrual bleeding).
Fibrous connective tissue surrounds the body of
the tumor.
Assessment and Diagnostic Findings
•
•
•
•
Pelvic examination showing enlargement of the
uterus, or the mass may be felt.
Ultrasound, CT scans, and MRI.
Menorrhagia, which may lower the H&H
significantly.
Uterine fundus examination after childbirth may
reveal irregular and bumpy feel of the uterine
fundus.
188
Complications
• Torsion and ischemia of pedunculated tumors.
• Hypermenorrhea with chronic anemia.
• Dyspareunia, infertility.
• Pain on voiding or defecation.
Medical Care and Surgical Treatment
• Antiestrogen medications, GnRH agonist.
• Hysterectomy; myomectomy.
• MRgFUS.
• Uterine artery embolization.
Keep in Mind
• Teach clients that uterine fibroids rarely become
cancerous and will shrink in menopause.
• Report excessively heavy periods, dyspnea,
fatigue, or pain.
Make the Connection
• Monitor CBC for anemia, as well as US,
CT scan, and MRI results.
• Pelvic examination.
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Women’s Health and Perinatal Disorders
Cervical Cancer
(ser-vi-kal kan-ser)
Clue: Diagnostic or Clinical Findings
History of recurrent STD, especially HPV
infection. Abnormal Pap smear. Late
signs are vaginal bleeding, dyspareunia,
and pelvic pain.
189
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Women’s Health and Perinatal Disorders
Pathophysiology
• Squamous cells on the outer cervix, chronically
•
•
irritated, undergo dysplasia from antigenic or
infectious material from STD, especially HPV, or
multiple sexual partners. Glandular cells on the
uterine side of the cervix can undergo dysplasia
from chronic irritation of smoking, infection
with HIV that lowers immunity, or having several pregnancies.
LSIL, and HSIL are squamous cells (afffected by
HPV) that are likely to progress to cancer. CIN
followed by the numbers 1, 2, or 3 describes the
thickness of the lining of the cervix that contains
abnormal cell growth.
Pap smear results and grade (low or high) guide
treatment regimen.
Assessment and Diagnostic Findings
• Pap smear reports are classified as negative, intraepithelial lesions, or malignancies.
• Possible reports of serosanguineous bleeding or
pelvic pain during or after sex.
• Presence of risk factors, e.g., HPV.
189
Complications
• Infertility after treatment.
• Metastasis and death.
Medical Care and Surgical Treatment
• Gardasil, a vaccine that prevents infection with
•
four types of HPV that cause the majority of
cervical cancers and HPV outbreaks.
LEEP cryotherapy, laser therapy, conization of the
cervix, and hysterectomy.
Keep in Mind
•
•
Gynecologic visits are advised in the early
teenage years. Pap smears and vaccination
against HPV can prevent cervical cancer.
Teach client to use barrier methods to prevent
pregnancy and STDs.
Do not start smoking, or try to quit.
Make the Connection
• Early detection is essential for favorable
outcome.
• Remember: High-grade lesions contain less differentiated cells and are more likely to be cancerous.
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Women’s Health and Perinatal Disorders
Polycystic Ovarian
Syndrome
(pol-e-sis-tik o-va-re-an sin-drom)
Clue: Diagnostic or Clinical Findings
US or CT scan shows multiple ovarian
cysts. Clinically irregular menstrual
periods, hirsutism, high FBS, and
infertility.
190
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Women’s Health and Perinatal Disorders
Pathophysiology
•
190
Medical Care and Surgical Treatment
PCOS is a genetically linked female endocrine
disorder that results in chronic anovulation,
hyperinsulinemia that triggers androgen hormone
release, type 2 DM, lipid abnormalities, hirsutism
and thinning scalp hair, infertility, and ovarian
cysts.
• Etiology is unknown. Also known as SteinLeventhal syndrome.
• Insulin sensitivity drugs and oral hypoglycemic
agents.
• Lipid-lowering agents, along with diet and weight
reduction regimens.
• Calcium and vitamin D for oocyte maturation
and prevention of osteoporosis.
• BCP and GnRH agonists.
Assessment and Diagnostic Findings
• Teach the client not to smoke.
• Teach how to manage type 2 DM.
• Although it is more difficult, it is possible to
• Irregular menstrual periods, anovulation, and
infertility.
• High FBS; type 2 DM; elevated LDL and ↓ HDL;
•
↑ testosterone levels; and ovarian cysts on US or
CT scan.
Obesity, acne, hirsutism, and male-pattern
baldness.
Complications
• Metabolic syndrome and heart disease.
• Endometrial cancer.
• Complications of diabetes.
• Infertility; osteoperosis.
Keep in Mind
become pregnant with medical assistance.
Make the Connection
• Monitor FBS, lipid panel, bone density
scans, hormone levels, and weight.
• Assess effectiveness of insulin sensitivity drug.
• Assess effectiveness of BCP.
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Women’s Health and Perinatal Disorders
Breast Cancer
(brest kan-ser)
Clue: Diagnostic or Clinical Findings
Firm, painless, fixed, irregularly shaped
lump usually found in the upper outer
quadrant of the breast. Mammogram
reveals a mass, usually with
calcification.
191
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Women’s Health and Perinatal Disorders
Pathophysiology
• Overstimulation of estrogen.
• TP53 mutation, (protection against tumor
growth).
• Genetic anomalies (e.g., BRCA1, BRCA2, TP53)
•
•
increase the risks of developing breast cancer and
ovarian cancer.
Women develop cancer more than men.
Risk factors are ↑ age, ↓ immunity, HRT,
personal or family history of breast cancer,
high-fat diet, alcohol intake, early menarche,
late menopause, no pregnancy or late pregnancy,
and no or short breastfeeding.
Assessment and Diagnostic Findings
•
•
•
•
•
Breast examinations done by a professional.
Mammograms, US, MRI, and PET scans.
Fine-needle biopsy, surgical excision and BX,
ductal lavage, and sentinel lymph node examination.
Tumor markers: CA 15.3, TRUQUANT, CA 27.29,
CA 125, and CEA.
FISH testing for excessive HER2-positive
receptors.
191
Complications
• Metastasis to bone, lungs, liver, and other distant
sites.
• Side effects of radiation, chemotherapy, SERMs,
and BRMs.
• Body image disturbances as a result of surgery.
Medical Care and Surgical Treatment
• Surgery (curative, palliative, or prophylactic).
• Radiation, chemotherapy, BMT.
• Trastuzumab (Herceptin), which blocks HER2
receptors, aromatase inhibitors, and SERMs.
Keep in Mind
• BSE monthly, yearly professional examinations,
and mammograms as directed.
Make the Connection
• Early detection increases survival rate.
• Monitor blood chemistries, tumor markers, and
CBC for anomalies.
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Women’s Health and Perinatal Disorders
Pregnancy-Induced
Hypertension
(preg-nan-se in-dusd hi-per-ten-shun)
Clue: Diagnostic or Clinical Findings
Hallmark signs include elevated blood
pressure, nondependent edema, and
proteinuria in the second or third
trimester of pregnancy.
192
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Women’s Health and Perinatal Disorders
Pathophysiology
• PIH, also known as preeclampsia, may be caused
•
•
•
•
by a vasospastic disorder of the placenta leading
to a endothelial dysfunction and placental release
of factors such as sFlt-1.
Endothelial dysfunction leads to capillary permeability, resulting in nondependent edema,
weight gain, pulmonary edema, hemoconcentration, edema in the retina, and edema in the
brain tissue.
BP ↑ is caused by an abnormal response to
angiotensin II and epinephrine, and an imbalance among prostaglandins, prostacyclin, and
thromboxane A2, resulting in vasoconstriction
and vasospasm.
Proteinuria is the result of HTN and
subsequent damage to vessel walls.
Severe PIH is characterized by HELLP syndrome.
192
• SBP ↑ of 30 mm Hg or DBP ↑ of 15 mm Hg, the
•
presence of protein in the urine (5 g/24 hr or
more), retinal changes, and oliguria.
Oligohydramnios (by US), nonreassuring fetal
heart tones, or small-for-dates fetus.
Complications
• HELLP syndrome.
• Renal failure, coma, and seizures.
• Placental insufficiency leads to a SGA neonate.
Medical Care and Surgical Treatment
• Delivery of the fetus; continued treatment with IV
Mg SO4; environmental control; and blood work
for LFT, platelets, and RBCs.
Keep in Mind
• Teach clients the importance of prenatal visits
and that PIH may require hospitalization.
Assessment and Diagnostic Findings
• The risk of PIH is increased in adolescence and
primigravidas older than 35, diabetics, and
women with preexisting vascular problems or
multiple pregnancies.
Make the Connection
• Continuous monitoring of DTR, blood
pressure, and FHR are necessary while on MgSO4.
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Women’s Health and Perinatal Disorders
Placenta Previa
(pla-sen-ta pre-ve-a)
Clue: Diagnostic or Clinical Findings
Painless, frank red vaginal bleeding at
or after 20 weeks’ gestation.
193
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Women’s Health and Perinatal Disorders
Pathophysiology
• In PP, the placenta implants in the lower rather
•
•
than the upper uterine area. When the cervix
begins to dilate and move up the uterine wall in
preparation for delivery of the fetus, the placenta
may dislodge due to traction, causing bleeding
and decreased oxygen delivery to the fetus.
There are three types: PP centralis (total or
complete PP) in which the placenta has been
implanted in the lower uterine segment and completely covers the internal cervical os; PP lateralis
(low marginal implantation) and PP marginalis
(partial or incomplete PP).
Risk factors include uterine scarring, previous
pregnancy or cesarean section, Asian ethnicity,
smoking, and age over 35 years.
193
• Premature delivery or cesarean section.
• Placenta accreta.
Medical Care and Surgical Treatment
• Less extensive previa may require conservative
•
•
treatment (e.g., rest, avoidance of sexual intercourse, no vaginal examinations).
Severe vaginal bleeding necessitates hospitalization, blood replacement, cesarean section, and
monitoring of fetal well-being.
Double setup operating room.
Keep in Mind
• Teach clients to report any vaginal drainage.
• Encourage clients to attend all prenatal and US
examinations.
Assessment and Diagnostic Findings
• Transabdominal and intravaginal US.
• Painless vaginal bleeding around the time of
delivery.
Complications
• Placenta abruption or vasa previa.
• Hemorrhage.
Make the Connection
• Vaginal bleeding can result in both
maternal shock and fetal/neonatal hypoxia.
• Monitor FHR and scalp potential of hydrogen
(pH).
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Women’s Health and Perinatal Disorders
Placenta Abruption
(pla-sen-ta a-brup-shun)
Clue: Diagnostic or Clinical Findings
Rigid, painful abdomen. Nonreassuring
fetal heart tones with late decelerations.
Maternal signs of shock or DIC.
194
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Pathophysiology
• Placenta abruption (PA), the sudden dislodgment
of the placenta from the uterine wall, is classified
according to type and severity:
• Grade 1 PA (vaginal bleeding with mild uterine
tenderness and mild uterine tetany, where only
10%–20% of the placenta is detached).
• Grade 2 PA (uterine tenderness and uterine
tetany, with or without uterine bleeding, fetal
distress, or maternal shock where 20%–50%
of the placenta is detached).
• Grade 3 PA (severe uterine tetany and maternal
shock, fetal demise is imminent or has occurred,
maternal or fetal DIC, and more than 50% of
the placental surface is detached).
Assessment and Diagnostic Findings
• A history of PIH, cocaine use, automobile accident,
or domestic violence.
• Painful, rigid abdomen with or without visible
vaginal bleeding.
• Signs of maternal shock.
• Nonreassuring FHTs, with prolonged late decel-
erations of the fetal heart rate and low scalp pH.
194
Complications
• Maternal and/or fetal death.
• Maternal shock; DIC.
• Possible hysterectomy.
Medical Care and Surgical Treatment
• Delivery may be vaginal or by emergency CS.
• Blood replacement.
• Treatment of DIC.
Keep in Mind
• Teach client to report any vaginal drainage, pain,
dizziness, or shortness of breath.
• Report absence of fetal movement.
Make the Connection
• Remember: PA can be present without
visible bleeding if the abruption is central.
• Monitor the FHT tracing, fetal scalp pH, and
maternal vital signs.
• IV to replace fluids and/or blood, administer
oxygen, and assist in cesarean delivery.
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Women’s Health and Perinatal Disorders
Persistent Fetal
Circulation
(per-sis-tint fe-tal sir-ku-la-shun)
Clue: Diagnostic or Clinical Findings
Shunting of blood from the right to
the left side of the heart through the
foramen ovale and ductus arteriosus
after birth, causing hypoxemia.
195
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Women’s Health and Perinatal Disorders
Pathophysiology
• Antenatal blood circulation includes three shunts.
•
•
The lungs are bypassed by two shunts, the foramen ovale, and the ductus arteriosus. The last is
the ductus venosus that bypasses the liver.
Following birth and adequate ventilation pressures, the foramen ovale closes and the ducts
collapse.
Hypoxia and high carbon dioxide levels increase
vasoconstriction in the lungs causing pulmonary
hypertension that interferes with closure of the
shunts and PFC occurs in small-for-gestationalage (SGA) neonates, infants of diabetic mothers (IDM), and those with a traumatic delivery.
195
Complications
• Without intensive care, the neonate will not
survive.
Medical Care and Surgical Treatment
•
•
•
Keep in Mind
• Apprise the parents tactfully of the neonate’s
Assessment and Diagnostic Findings
•
•
•
•
Onset of respiratory distress at or shortly
following delivery, with cyanosis, tachypnea,
tachycardia, and low oxygen saturation levels
with administration of 100% oxygen.
Meconium aspiration syndrome.
Abnormal chest x-ray.
Diaphragmatic hernia.
Supplemental 100% oxygen by endotracheal
tube and ventilator. May use a high-frequency
ventilator.
Neuromuscular paralyzing agents and nitric oxide
inhalation.
ECMO.
•
condition, the causes, and the required equipment. Encourage visits to the neonatal intensive
care unit.
Teach parents that diaphragmatic hernia requires
surgical intervention.
Make the Connection
• Carefully monitor the bilateral breath
sounds, CXR (should reveal 9–10 “ribs of air”),
ABG, pulse oximetry, pulse, respiration, and
blood pressure.
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Women’s Health and Perinatal Disorders
Patent Ductus Arteriosus
(pat-ent duk-tus ar-ter-e-o-sis)
Clue: Diagnostic or Clinical Findings
Persistent murmur. Weight loss,
difficulty with feedings, and
desaturation of oxygen with
activity.
196
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Women’s Health and Perinatal Disorders
Pathophysiology
• Antenatal blood circulation includes three shunts
•
•
one of which is ductus arteriosus, which shunts
oxygenated blood from the pulmonary artery to
the aorta (a right-to-left shunt).
A PDA following birth will become a left-to-right
shunt related to pulmonary vascular resistance
causing excessive blood flow to the pulmonary
area and left atria, as well as left ventricle congestion and decreased systemic flow via the aorta.
Occurs in preterm infants; girls are affected more
often than boys; more likely to occur in neonates
with Downs syndrome or those exposed to rubella
during gestation.
196
Medical Care and Surgical Treatment
• Prostaglandin therapy.
• Transcatheter device closure.
• Direct surgical ligation.
Keep in Mind
• Reinforce teaching about PDA repair.
• Teach clients that the child with PDA repair will
be able to resume normal activity levels.
• Preterm children will “catch up” developmentally
based on the level of prematurity at birth.
Make the Connection
• Assess for murmurs in neonates carefully.
Assessment and Diagnostic Findings
• Murmur on auscultation.
• Echocardiogram shows left-to-right shunt.
• Tachypnea, difficulty feeding, sweating, and
weight loss.
Complications
• Ventilator assistance for breathing.
• Pulmonary hypertension.
• Infective endocarditis.
•
•
Perform a four-extremity blood pressure assessment and carefully grade and report to the
neonatal cardiologist. Provide continuous monitoring of vital signs and oxygen saturation levels.
Monitor weight daily.
Assess feeding problems and sweating.
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Women’s Health and Perinatal Disorders
Neonatal Sepsis
(ne-o-na-tal sep-sis)
Clue: Diagnostic or Clinical Findings
Temperature instability, tachypnea, and
cyanosis. Amniotic fluid may have
an abnormal odor.
197
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Women’s Health and Perinatal Disorders
Pathophysiology
• Usually an ascending infection caused by
•
Escherichia coli, Listeria monocytogenes, or group B
streptococci related to premature rupture of
membranes, maternal chorioamnionitis, or premature birth in which immunity is severely limited.
Sepsis may occur as a result of invasive therapies
(e.g., umbilical catheters; fetal surgery).
Assessment and Diagnostic Findings
• Amniotic fluid may have a foul odor.
• CBC may show a high WBC count and the
presence of bands (immature WBC).
• Gastric fluid analysis shows a high neutrophil
count.
• Blood and urine cultures are positive.
• CSF may be cloudy or have a high protein and
low glucose level and culture positive for bacteria.
• Possible temperature instability (subnormal tem•
•
peratures), tachypnea, tachycardia, and possible
need for supplemental oxygen administration.
CXR may show infiltrates.
↑ CRP; erythrocyte sedimentation rate is high.
197
Complications
• Neonatal death.
Medical Care and Surgical Treatment
• Sepsis work-up.
• Temperature, respiratory, and nutritional support
(IV TPN).
Keep in Mind
• Clients must report any vaginal drainage and be
assessed for rupture of membranes.
• Comply with recommendations regarding neonatal visits and testing for infection with group B
streptococci and other infectious organisms.
Make the Connection
• Subnormal temperature, bulging fontanel,
abnormal flexion or limpness, tachypnea,
cyanosis, or other signs and symptoms must be
reported and acted upon immediately.
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Women’s Health and Perinatal Disorders
ABO Blood Type
Incompatibility
(a-b-o in-kom-pa-ti-bil-i-te)
Clue: Diagnostic or Clinical Findings
Jaundice that occurs in the first
24 hours of life. Maternal blood type
is type O.
198
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Women’s Health and Perinatal Disorders
Pathophysiology
• Mothers with type O blood carrying fetuses with
•
•
type A, B, or AB blood are at risk for having a
neonate with an ABO incompatibility problem if
their antibodies are IgG antibodies.
IgG antibodies readily cross the placenta and begin
to hemolyze the fetal red blood cells (RBCs).
The fetal/neonatal liver is too immature to
process the bilirubin produced from the RBC
breakdown, and this results in early-onset
jaundice.
Assessment and Diagnostic Findings
198
Medical Care and Surgical Treatment
• Phototherapy.
• Exchange transfusion.
Keep in Mind
• Keep prenatal appointments and comply with all
laboratory testing.
• Explain the work-up associated with early-onset
jaundice.
• Teach parents about phototherapy and exchange
transfusion.
• Teach parents how to care for the neonate during
treatment.
• Yellow/orange coloration to the sclera and skin.
• Serum bilirubin levels are elevated within the first
12–24 hours.
• Indirect Coombs’ test on maternal blood detects
antibodies to the fetus’s blood type.
• Fetal anemia can be monitored noninvasively by
Doppler flow velocimetry (DFV), which measures
the peak systolic velocity (PSV) in the middle
cerebral artery.
Complications
• Kernicterus.
• Anemia.
Make the Connection
• Early onset of jaundice requires a
•
differential diagnosis of blood incompatibilities,
neonatal sepsis, or trauma at birth with
hematoma formation.
Serial bilirubin levels are measured by heel-stick
method approximately every 6–8 hours to assess
effectiveness of treatment.
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Women’s Health and Perinatal Disorders
Rh Incompatibility
(r-h in-kom-pa-ti-bil-i-te)
Clue: Diagnostic or Clinical Findings
Rh-negative woman carrying an
Rh-positive fetus.
199
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Women’s Health and Perinatal Disorders
Pathophysiology
• A pregnant woman with no Rh antigen, known as
Rh0(D), on her RBCs is Rh negative. Additionally,
there are no antibodies against the Rh antigen in
her serum. If the fetus she is carrying is Rh positive, there should not be antibodies produced that
cross the placenta. However, at delivery of the
fetus, when maternal and fetal bloods finally mix,
the maternal immune system is activated to produce anti-Rh antibodies. If no treatment is provided, the next Rh-positive fetus the woman carries
will have its RBCs attacked by the anti-Rh antibodies, producing a condition called erythroblastosis fetalis, a potentially fatal condition in which
most or all of the fetal RBCs are destroyed.
Assessment and Diagnostic Findings
• Blood and Rh factor typing, along with a screen
•
•
for antibodies, are done at the first prenatal
visit. The antibody screen is performed again at
28 weeks. Rh0(D) immune globulin (RhoGAM)
is given to prevent sensitization.
PUBS may be done to assess the fetal blood type,
degree of hemolysis, and bilirubin levels.
Amniocentesis.
199
• Direct Coombs’ testing will indicate that antibodies are attached to RBCs, destroying them.
Complications
• Neonatal heart failure, high bilirubin levels,
kernicterus, edema (hydrops), and renal failure.
Medical Care and Surgical Treatment
• RhoGAM must be given to the woman within
•
72 hours after delivery to prevent sensitization
problems with subsequent pregnancies.
If the neonate survives, aggressive therapy with
phototherapy, hydration, and other symptomatic treatment in an intensive care nursery is
necessary.
Keep in Mind
• Teach clients to keep all prenatal appointments.
• Explain the significance of being Rh negative.
Make the Connection
• There will be no problem with this
disorder if the fetus is also Rh negative; the
mother must be Rh negative and the fetus
Rh positive for this disorder to occur.
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Women’s Health and Perinatal Disorders
Meconium Aspiration
Syndrome
(me-ko-ne-um as-pi-ra-shun sin-drom)
Clue: Diagnostic or Clinical Findings
Amniotic fluid, stained with meconium,
is aspirated by the fetus/neonate,
causing acute respiratory distress.
200
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Women’s Health and Perinatal Disorders
Pathophysiology
• Causes include intrauterine stress, such as PIH,
•
•
•
postmaturity (aging placenta), intrauterine
hypoxia and asphyxia, and infection.
Fetal stress may produce increased intestinal
peristalsis, anal sphincter relaxation, and expulsion of meconium into the amniotic fluid.
Fetus breathing in utero, or with the first few
breaths of air after delivery, causes aspirated
meconium-stained fluid to enter the lungs.
Alveoli of the lungs can be infiltrated by the
meconium, causing atelectasis or the blockage
of bronchiolar passages.
Assessment and Diagnostic Findings
• Rupture of membranes reveals meconium-stained
fluid.
• Often meconium-stained fluid is accompanied by
nonreassuring FHTs.
• Laryngoscopic examination reveals meconium
below the level of the vocal cords.
• Acute respiratory distress develops.
Complications
• Low oxygen saturation levels.
• Respiratory acidosis, atelectasis.
• Death.
200
Medical Care and Surgical Treatment
• Immediate suction when the fetal head is delivered.
• Suction of meconium below the vocal cords.
• Ventilator, high-frequency ventilator, or ECMO
therapy.
• Nitric oxide inhalation therapy and surfactant
therapy.
• Administration of prophylactic antibiotic therapy,
IV TPN.
Keep in Mind
• Teach client to report rupture of membranes and
the color and character of the fluid.
• Apprise the client of the condition of the neonate
and encourage visitation to the nursery.
Make the Connection
• Nonreassuring FHTs (late decelerations
•
and variable decelerations) are signs of fetal
distress.
Staff present at deliveries must be trained to
suction and visualize vocal cords and to begin
respiratory support in cases of meconium-stained
fluid.
2693_Leek_Divider Tab.qxd
INDEX
References
Index
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Index
A
Abdominal hernias, 9
ABO blood type
incompatibility, 198
Absence seizures, 80
Acne vulgaris, 167
Acoustic neuroma, 155
Acquired immunodeficiency
syndrome, 56
Acute angle-closure
glaucoma, 143
Acute renal failure, 43
Acute respiratory distress
syndrome (ARDS), 130
Addison’s disease, 29
Alcoholism, 186
Alzheimer’s disease, 90
Amyotrophic lateral
sclerosis, 92
Anaphylaxis, 51
Angina pectoris, 97
Aortic aneurysm, 115
Aortic stenosis, 109
Appendicitis, 20
Asthma, 125
Atonic seizures, 82
Atrial fibrillation, 101
Attention deficit-hyperactivity
disorder (ADHD), 185
Autonomic dysreflexia, 76
B
Bell’s palsy, 91
Benign prostatic hyperplasia,
48
Bipolar disorder, 183
Bladder cancer, 49
Borderline personality
disorder, 187
Bowel obstruction, 16
Breast cancer, 191
Bronchiectasis, 124
Buerger’s disease, 113
C
Cardiogenic shock, 100
Cardiomyopathy, 107
Cataracts, 142
Celiac disease, 1
Cellulitis, 159
Cerebral aneurysm, 78
Cerebrovascular accident,
85
Cervical cancer, 189
Cholecystitis, 14
Chronic bronchitis, 127
Chronic renal failure, 44
Colon cancer, 18
Compartment syndrome, 67
Complex partial seizures, 84
Concussion, 71
Conductive hearing loss, 148
Congestive heart failure, 99
Contact dermatitis, 157
Conversion disorder, 179
Coronary artery disease, 96
Crohn’s disease, 21
Cushing’s syndrome, 28
Cystic fibrosis, 129
D
Deep vein thrombosis, 108
Depression, 182
Diabetes insipidus, 26
Diabetes mellitus
type 1, 32
type 2, 33
Diabetic retinopathy, 147
Dissociative amnesia, 180
Diverticulosis, 19
E
Eczema, 158
Emphysema, 126
Encephalitis, 94
Epididymitis, 47
Epidural hematoma, 73
Esophageal varices, 12
F
Fracture, 66
Full-thickness burns, 172
G
Gastric cancer, 6
Gastritis, 2
Gastroesophageal reflux
disease, 3
Generalized anxiety disorder,
174
Glomerulonephritis, 37
Gouty arthritis, 59
Graft-versus-host disease,
119
Guillain-Barré syndrome, 93
H
Hashimoto’s thyroiditis, 54
Hemorrhoids, 23
Hepatitis, 8
Herniated nucleus pulposus, 69
Herpes simplex, 162
Herpes zoster, 161
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Hiatal hernia, 4
Histoplasmosis, 138
Huntington’s disease, 74
Hydronephrosis, 40
Hyperpituitarism, 24
Hypertension, 116
Hyperthyroidism, 30
Hypopituitarism, 25
Hypothyroidism, 31
I
Impetigo, 164
Influenza, 135
K
Kaposi’s sarcoma, 57
L
Labyrinthitis, 153
Laënnec’s cirrhosis, 10
Legionnaires’ disease, 136
Leiomyomas, 188
Leukemia, 117
Liver cancer, 11
Lung cancer, 137
M
Macular degeneration, 146
Malignant hyperthermia, 95
Mania, 181
Mastoiditis, 151
Meconium aspiration
syndrome, 200
Ménière’s disease, 154
Meningitis, 70
Mesothelioma, 140
Metabolic acidosis, 120
Metabolic alkalosis, 121
Multiple myeloma, 118
Multiple sclerosis, 86
Myasthenia gravis, 87
Myocardial infarction, 98
Myocarditis, 105
Myoclonic seizures, 81
N
Neonatal sepsis, 197
Nephrotic syndrome, 38
O
Obesity, 7
Obsessive-compulsive
disorder, 178
Osteoarthritis, 58
Osteomalacia, 62
Osteomyelitis, 63
Osteoporosis, 61
Otitis externa, 150
Otitis media, 149
Otosclerosis, 152
Overactive bladder, 45
P
Paget’s disease, 64
Pain disorder, 176
Pancreatic cancer, 15
Pancreatitis, 13
Parkinson’s disease, 89
Paronychia, 163
Partial-thickness burns, 171
Patent ductus arteriosus, 196
Pediculosis capitis, 166
Peptic ulcer disease, 5
Pericarditis, 104
Peripheral arterial disease, 112
Peritonitis, 22
Persistent fetal circulation,
195
Phobias, 177
Placenta abruption, 194
Placenta previa, 193
Pleural effusion, 134
Pneumonia, 133
Pneumothorax, 128
Polycystic kidney disease, 39
Polycystic ovarian syndrome,
190
Posttraumatic stress disorder,
175
Pregnancy-induced
hypertension, 192
Primary open-angle
glaucoma, 144
Prostate cancer, 50
Psoriasis, 160
Pulmonary embolism, 132
Pyelonephritis, 36
R
Raynaud’s disease, 114
Renal artery stenosis, 46
Renal calculus, 41
Respiratory acidosis, 122
Respiratory alkalosis, 123
Retinal detachment, 145
Rh incompatibility, 199
Rhabdomyolysis, 42
Rheumatoid arthritis, 60
Rheumatoid endocarditis,
106
Rosacea, 173
S
Sarcoidosis, 139
Scabies, 165
Schizophrenia, 184
Scleroderma, 52
Sensorineural hearing loss,
148
Severe acute respiratory
syndrome (SARS), 131
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Simple partial seizures, 83
Sjögren’s syndrome, 55
Skin cancer, 156
Skull fracture, 72
Spinal cord injury, 75
Spinal shock, 77
Sprain, 65
Stevens-Johnson syndrome,
168
Subdural hematoma, 73
Superficial burns, 171
Syndrome of inappropriate
antidiuretic hormone, 27
Systemic lupus
erythematosus, 53
T
Tinea, 169
Tonic-clonic seizures, 79
Total joint replacement, 68
Toxic epidermal necrolysis,
168
Trigeminal neuralgia, 88
Tuberculosis (TB), 141
U
Ulcerative colitis, 17
Urethritis, 35
Urinary tract infection, 34
V
Varicose veins, 111
Venous stasis ulcer, 110
Ventricular fibrillation, 103
Ventricular tachycardia, 102
Verruca, 170