MEDICAL-SURGICAL
Layer of the Heart:
Endocardium ( inner ) - facilitates blood flow,
contains valve & chambers
Myocardium ( middle ) - contracting muscle,
cardiac muscle
Pericardium ( outer )
o Layer of Pericardium

Visceral ( epicardium )

Pericardial ( 5-20cc of
fluid ) serves as cushion,
lubricant

Parietal
-
AV valves ( atrioventricular valves ) “Atria”
o 1 way flow of blood

Tricuspids ( right atria )

Bicuspids/ Mitral ( left
atria )
SL valves ( semilunar valves )

Pulmonary SL valve

Aortic SL valve
Ventricle contract : Semi Lunar valve open
( AV valve closed )
Ventricle relax : Semi Lunar valve closed ( blood filling )
( Av valve open )
Myocardium
Endocardium
Visceral
(epicardium)
Circulation:
left
from
Vena
cava
to
Lungs
deoxygenated
Pulmonary
circulation
Pulmonary
veins
System
oxygenated
Systemic
circulation
Valves & Chambers:
Bundle of HIS
Intranodal tract
AV node
Bundle branches
Right Purkinje
Left Purkinje
Cardiac Cycle
Two main phase
o Systole : contraction / ejection
o Diastole : relaxation / refill

Difference between
Systolic & Diastolic is
the PULSE PRESSURE
( PP: 30 – 40cpm ) narrowed pulse – hypovolemia
( PP: 60cpm ) wided pulse – increased in Stroke volume
Fibrous layer
right
SA node
Coronary Artery
Pericardial
cavity
Parietal
(pericardium)
Conduction System
SA node ( sinoatrial node ) main pacemaker
of the heart : 60 – 100bpm
AV node ( atrioventricular node ) 2nd
pacemaker of the heart : 40 – 60bpm
Bachmann’s node ( node in the left atrium )
Branch out from ascending aorta
Right Coronary Artery – supplying the Right
Atrium / Right Ventricle / inferior portion of Left
Ventricle
Left Coronary Artery
o Circumflex – supplying the Left
Atrium / posterior portion of Left
Ventricle
o Left Anterior Descending Artery
(LADA) – supplying the Left
Ventricle /Apex
Electrophysiologic Properties
A – utomacity –
C – ontractility – transmit impulse
C – onductivity – contraction
E – xcitability – respond to stimuli
R – efractiones – ability to finish a response
before initiating another response.
Cardiac Output
Amount of blood pump by the heart
particularly by the left ventricle per minute
Stroke Volume (SV) – amount of blood pump by the
heart in every beat
SV
=
amt (ml)
Beat
Contractility : ( Inotropic ) ability of cardiac
muscle to contract
Preload : amount of the blood from the
ventricle after the end of diastolic phase
(Frank Staring Law : the greater the stretch,
the better the pump)
o Venous returns
o Regurgitation of the blood
Afterload : resistance of LV must surpass as
the heart pump blood to the circulation
o Systemic resistance ( HPN )
o Blood viscosity ( DM. polycythemia
vera, multiple myeloma )
Heart Rate ( HR ) – number of heart beat per minute
HR
=
Beats
Minute
Formula: Cardiac Output
CO
=
amt (ml)
Beat
X
Beats
Minute
HEART RATE & STROKE VOLUME REGULATOR
Autonomic Response
Symphatetic Nervous System ( SNS )
( Fight or Flight Response )
o Norepinephrine (adrenal gland)
kidney
o Dilated pupils(compensate)
Mydriatic
o Constricted blood vessel
o Increased SV/HR
Parasymphathetic Nervous System ( PNS )
o Rest & Digest Response
Baroceptors
o Pressure detectors ( common
carotid, right atrium, aortic arc )
Chemoreceptors
o Chemical detectors ( O2, CO2, pH )
o Aortic arc, carotid bodies
o CO2 : 35 – 35mmHg ( normal )
volatile gas
o O2 : 80 – 100mmHg ( normal )
o CO2 + H2O = H2CO3 (carbonic acid )
increased pH level
Proprioceptors
o Stretch detectors ( tendons )
Electrocardiograph ( ECG )
-
Vertical : impulse
Horizontal : duration
Small box : 1mm/.04sec
Big box : 5mm / .2sec
Isoelectric line : straight/ middle line
-
Deflection : raise & falls of line ( wave )
Wave : line deviated from isoelectric line
( P wave )
Complex : group of continuous waves
( QRS complex )
Segment : isoelectric line between waves
( ST segment )
Interval : wave + segment ( PR interval )
P wave – atrial depolarization
PR segment – conduction delay from SA node – AV
node
QRS complex – ventricular depolarization
ST segment – early ventricular repolarization
PR – atrial depolarization + conduction delay of
SA node – AV node
T wave – ventricular repolarization
U wave – unknown
Before:
Assess for allergy ( seafoods : iodine/contrast
dye )
Assess for bleeding parameters
Assess for kidney function
Administer pre medication as ordered
Patient usually sedated ( valium )
After:
CBR / monitor V/S
Prevent bleeding
Immobilized affected extremities
Do circulation assessment
Angiography / Arteriography
is a test that uses an injection of a liquid dye
to make the arteries easily visible on X-rays
Laboratories ( cardiovascular function )
Blood component
Electrode Placement
Right arm – white / Right leg - green
Left arm – black / Left leg – red
Chest Electrode Placement
1st Node – 4th ICS right of sternum
2nd Node – 4th ICS left of sternum
3rd Node – between the 2nd & 4th node
4th Node – 5th ICS left
5th Node – 6th ICS left
6th Node – axillary line
Holters Monitoring ( activity diary )
Stress Testing ( threadmill test )
Detection of level of activity
o Ischemic heart disease
o Chest pain
o Evaluate effectiveness of activity
o Develop cardiac rehab.program
Echocardiograph
Ultrasound of the heart
Supine position: HOB elevated 15 – 20 degree
Slightly turned to the left side
Chest Xray
Magnetic Resonance Imaging ( MRI )
The MRI scan uses magnetic and radio waves,
meaning that there is no exposure to X-rays
or any other damaging forms of radiation.
Cardiac Fluoroscopy
Cardiac Catherization
Introduction of radiopaque venous catheter
o Right radial / antecubital
o Left brachial / femoral
RBC
WBC ( leukocytes )
Platelets (thrombocytes )
3
Normal value ( mm )
4-6 million
4,5000-11,000
150,0000- 450,000
Erythrocyte Sedimentation Rate ( ESR )
It is a common hematology test that is a nonspecific measure of inflammation
Male : < 15 – 20mm/hr
Female : < 25 – 30mm/hr
Blood Urea Nitrogen ( BUN )
10 – 20mg/dl ( normal )
Easily affected by hydration status
Blood Lipids
NPO ( 10 – 12hrs )
Serum cholesterol: < 200mg/dl
Triglycerides : 100 – 200mg/dl
Auscultation : ( Heart Sound )
S1 – apex – lubb – closure of AV valve (
contracting / ejecting ) systole phase
S2 – base – dub – closure of SL valve (
relaxation / refill ) diastole phase
S3 – above 30y.o – ventricular gallop ( rapid
ventricular refill )
S4 – atrial gallop ( resistance to ventricular
refill )
o Summation gallop ( S1, S2, S3, S4 )
nd
Aortic – 2 ICS right sternum
Pulmonic – 2nd ICS left sternum
th
Mitral – 5 ICS midclavicular line
th
Tricuspid – 5 ICS left sternum
Stethospcope
Diaphragm – hi pitch ( heart, lung ,
abdominal sound )
Bell – low pitch
-
Decubitus Angina : ( occurs when ever
standing or lying )
Silence Ischemia : ( no manifestation but
appear in laboratory test )
CM:
ANGINA PECTORIS
Paroxysm chest pain ( myocardial ischemia )
Pathogenesis: imbalanced in demand ( cardiac output )
& supply ( myocardial tissue perfusion )
Precipitating Factor:
Coronary Atherosclerosis – narrowing of
artery ( fatty deposit )
Coronary Thrombosis / Embolism
Hypertension ( HPN ) – increased in afterload
Decreased blood flow with shcok
Direct Trauma
Polycythemia Vera
Coronary Artery Spasm
Etiology:
Physical Exertion
Environment / Extreme Weather
Digestion Every Meal
Eating a heavy meal
Valsalva Maneuver
Emotion Stress
Sexual Excitation
Hot Bath or Shower
Types of Angina Pectoris
Stable / Exertional Angina : predictable
Unstable Angina : unpredictable (
Intermittent Coronary Syndrome )
Variant Angina : “ Prinzmetal” (even at rest)
Intractable Angina : chronic ( resistant to
medication / treatment )
Post Infarction Angina : ( myocardial
infarction )
Intractable Angina : ( more responsive to
medication )
Nocturnal Angina : ( occurs when sleeping )
-
Pain ( lactic acidosis )
o Substernal, crushing or squeezing
o Radiate from neck to arms up to
back
o Unaffected by inspiration /
expiration
Pallor
Palpitation / Tachycardia
Dizziness / Faintness
Dyspnea
DX test:
ECG, Stress Test, cardiac Catheterization,
Cardiac Enzymes
NI:
CBR ( decreased demand )
Oxygenation
Lifestyle modification
Medication
o Nitrates ( nitroglycerine )
vasodialtion of coronary artery :
decreased demand & afterload (
heart ) : 3 – 6 months
o Calcium Channel Blocker ( VAND )
Verapamil, Anlodipine, Nicardipine,
Diltiazem

calcium – innervating
muscular movement
o Antilipidemic – “statin” : prevent
atherosclerosis
o Beta Adrenergic Blockers “olol”
o Antiplatelet : ( ASA ) Acethy
Salicylic Acid
o Anticouagulant : Heparine
Surgical:
PTCA ( Percutaneous Transluminal Coronary
Angioplasty )
Vascular Stent
Laser Angioplasty
Atherectomy
CABG ( Coronary Artery Bypass Graft )
MYOCARDIAL INFARCTION
Heart attack : formation of localized necrotic
areas in the myocardium
Risk factor:
CAD ( Coronary Artery Disease )
atherosclerosis
Elevated cholesterol level
Smoking ( damage the endothelium:
vasospasm ) nicotine
HPN, DM, stress ( increased the workload /
afterload )
Classification of MI
Transmural Infarct : starts in the myocardium
going to pericardium & endocardium
Sub endocardial Infarct : starts in the
myocardium going to endocardium
Intramural Infarct : isolated / patchy &
localized myocardium death
3 areas developed ( after MI )
Area of Infarction : O2 totally deprived (
damage is irreversible ) Q wave pathologic
Area of Injury : damage is reversible ( cell is
viable as long as collateral circulation is
present ) ST segment elevation
Area of Ischemia : blood circulation is only
reduced ( most of the time it is not damage )
T wave inverted
CM:
Prolonged pain ( > 3o min )
Unrelieved by Nitroglycerin
Crushing Severe Radiating Pain
Levines Sign
Anxiety / apprehension ( increased
restlessness )
Feeling of Doom
Pallor, Cyanosis, coolness of extremities
Mild fever ( hard to assess ), dyspnea,
leukocytosis
Nausea & vomiting ( nasovagal stimuli )
Syncope ( sudden loss of consciousness )
DX studies:
Cardiac Enzymes ( most accurate )
CK ( Creatinine Phophokinase ) 26 -174u/L

CKmB ( myocardial ) O –
5% total ( normal )

CKmM ( damage muscle
tissue )

CKbB ( reflects brain
tissue damage )
LDH ( Lactate Dehydroginase ) 90 – 176u/L

LDH1 (.2 - .36u/L)

LDH2 (.35 - .46u/L)(heart)
LDH3 – LDH4 – LDH5 ( liver )
LDH1 > LDH2 (flipped)
LDH1 < LDH2 (normal)
Complication of MI
Dysrrhythmia : Vtach ( emergency )
CHF : increased inotropic activity
Cardiogenic Shock : pump failure ( #1 cause
of death )
Post Infarction Angina
Pericarditis : Transmural Infarct
Pulmonary Edema : ( CHF )
TX:
Goal:
o Prevent further tissue injury
o Decreased cardiac workload
o Increased O2
NI:
O2 ( nasal cannula )
CBR : 24 – 48hrs w/o bathroom
Semi-fowlers ( immediate phase )
Monitor Cardiac function ( ECG )
o Continuous ECG monitoring
o Blood pressure ( cardiogenic shock )
Lifestyle Modification ( diet, exercise )
o Low salt – fat
o Compliance to treatment
Pharmacotherapy:
Morphine Sulfate ( Opiate Analgesic )
o Severe pain – SNS – increased CW
Nitroglycerin ( Nitrates )
o Vasodilation – decreased CW /
Afterload ( dilation of coronary
artery )
Thrombolytics ( dissolve clot / thrombus )
fibrinolysis process
o Best given in the 1st 6hrs
o Streptokinase, Urokinase,
-
-
-
-
-
o Tissue Plasminogen Activator
o Monitor patient for bleeding
Benzodiazepine ( Anxiolytic )
o Diazepam/Lorazepam

Valium : ( relaxation )

Flumazenil : ( antidote )
Anticoagulant (prevent thrombus formation)
o Heparin
o Coumadin
Anitplatellet
o ASA : ( Acethyl Salicylic Acid )
platelet aggregation
o Dipyridamole ( Persatin )
o Clopidogrel ( Flavix )
Beta Adrenergic Blockers ( SNS )
o Beta1 – heart ( Propanolol /
Atenolol )
o Beta 2 – lungs
Laxatives ( Lactulose ) prevent bowel
straining
o Valsalva Maneuver (contraindicated
to HF )
o Rectal Temp. ( stimulate vagal
response / bradycardia )
CONGESTIVE HEART FAILURE
Inability of heart to maintain cardiac output
Cause by impaired pumping activity
Classification
Types of CHF
R-sided CHF
L-sided CHF
Forward
failure
Lungs
System
Backward
failure
Vena cava
Lungs
Ejection fraction : % of blood pump by the ventricle
after a diastolic phase
Manifestation:
RSCHF:
o JVD,
o Peripheral edema
o Hepatomegaly
o Spleenomegaly, nausea & vomiting,
o Feeling of bloutedness,
o Ascites (peritoneal cavity fluid)
o Decreased urine output
o Anasarca ( generalized edema)
LSCHF:
o Crackles/rales ( pulmonary edema )
o Increased ventilation
o Cough
o Dyspnea
o Paroxysimal Nocturnal Dyspnea
o Decreased urine output
Direct damage to the heart
o Myocarditis
o Ventricular Aneurysm ( cells dilated
/ turn back to normal size )
o Ventricular Overload

Increased Preload: mitral
/ aortic regurgitation, VSD
( ventricular septal
defect), ASD( atrial septal
defect ) IVF overload

Increased Afterload:
aortic / pulmonary valve
stenosis, HPN
o Constriction of Left Ventricles

Pericarditis, cardiac
tamponade ( constriction
of ventricle / rapid
accumulation of
pericardial fluid ),
restrictive
cardiomyopathy
( HYDRATION STATUS : weight is the best indication )
TX:
Promote oxygenation
Promote rest & activity
Facilitate fluid balance
Providing skin care
Promote nutrition
Promote elimination
Pharmacotherapy:
Digitalis therapy: “ treatment of choice”
o Digoxin ( Lanoxin )
-
-
-
MOA:
+ inotropic effect ( inc. SV )
- chronotropic effect ( dec. HR )
Maintenance drug: ( digitalis toxicity )
o Nausea & vomiting ( early stage )
o Visual disturbances : yellow – green
halo vision ( snowy vision )
o Dysrhythmia / Arrhythmia
(dangerous)
o Assess:

PR: ( bradycardia )
+

K level ( hypokalemnia )

3.5 – 5mEq/L

Potentiates
digitalis toxicity
Vasodilators: ( Hydralizine )
o Calcium channel blockers ( VAND )

Verapamil

Amlodipine

Nicardipine

Diltiazem
Symphatomemitics:
o Dopamine / Dobutamine ( severe
HF )
Diuretics therapy:
o Loop diuretics ( Furosemide )
o K+ wasting diuretics

Best given in the morning
monitor UO/BP
VALVULAR HEART DISEASE
Mitral Valve Disease
MITRAL STENOSIS
Narrowing of the mitral valve
Manifestation:
Initially assympthomatic
Diastolic murmur ( abnormal heart sounds )
Dyspnea
Atrial fibrillation / hypertrophy
o Chamber quivering
o Thrombus formation
MITRAL REGURGITATION
Incompetent mitral valves
Manifestation:
Dyspnea / fatigue
Atrial fibrillation
High pitch systolic murmur
LSCHF ( manifestation )
-
MITRAL VALVE PROLAPSED
Manifestation:
Dyspnea / fatigue
Systolic click
Chest pain & palpitation
Aortic Valve Disease
AORTIC VALVE STENOSIS
Narrowing of the aortic valve
Manifestation:
Dyspnea, syncope, chest pain
Left Ventricular Hypertrophy
LSCHF ( manifestation )
AORTIC REGURGITATION
Manifestation:
Corrigans ( water hammer pulse ) quick sharp
pulse / suddenly collapse
High pitch diastolic murmur
Tricuspid Valve Disease
TRICUSPID VALVE REGURGITATION / STENOSIS
RSCHF like symptom
Dyspnea, syncope
PULMONIC VALVE DISEASE
RSCHF like symptom
Dyspnea, syncope
TX:
Depend on the clinical manifestation
Valvular Repair
o Commissurotomy ( commissure )
o Annuloplasty ( annulos )
o Chordoplasty ( chordate tindenae )
o Leaflet repair
Valvular Replacement
o Mechanical ( synthetic )
o Tissue ( living organism )
Valvular Graft / Tissue ( living organism )
o Xenograft / Heterograft (non
human )
o Homograft ( human source )
o Isograft ( same person )
INFLAMMATORY DISEASE OF THE HEART
PERICARDITIS
Causes:
Mechanical injury to the heart ( invasive )
Infection ( viral :HIV / bacteria :
streptococcal. Staphylococcal, entero )
Tumor ( metastasis )
o Lungs, blood, lymph
Connective Tissue Disease ( SLE ) Systemic
Lupus Erythematus
Common Complication:
Heart failure
Cardiac tamponade
Manifestation:
Chest pain ( aggravated by supine position &
relieve by sitting and leaning forward )
Pericardial Friction Rub ( scratchy high pitch
sound )
Sign & symptoms of inflammation ( increased
ESR, leukocytosis, fever )
DOB & fatigue ( oxygenation problem )
MYOCARDITIS
Caused by infection
Manifestion:
Murmur & Summation Gallop rhythm
Sign of Infection / Inflammation
DOB & fatigue
Complication:
Thrombus
Heart failure
Cardiomyopathy ( dysfunction of the heart/
myocardial defect-disease )
INFECTIVE MYOCARDITIS
Manifestation:
Signs of infection ( fever )
DOB & fatigue
Splinter Hemorrhages ( strain blood in the
nails )
Oslers nodes ( painful nodules in the fingers )
Janeways Lession ( flat macules : palm/soles )
pinkish – purflish
TX:
Promote oxygenation
Facilitate proper rest activity pattern
Administer medication ( CANADA )
o C-orticosteroid (anti-inflammatory)
o A-ntiplatelet
o N-SAID’s
o A-ntibiotics
o D-Igoxin
o A-ntidysrhthmia
CARDIAC DYSRHYTHMIA
NORMAL SIGN RHYTHM
Originate from SA node
Atrial/ ventricular rate ( normal )
PR interval / QRS complex ( normal )
P : QRS ratio 1 : 1
SINUS BRADYCARDIA
Sinus node creates / slower than normal rate
( 60bpm ) SA node
PR interval / QRS complex ( normal )
Causes:
o Metabolic rate ( hypothyroidism )
o Sleep decreased metabolic rate
o Vagal stimuli ( valsalva, sunctioning
increased ICP )
TX:
Sinus Bradycardia that lead to Bradycardia
o Atropine Sulfate ( anticholinergic )
.5mg – 3mg “ treatment of choice”
Bradycardia ( IDEA )
o I-soprotenolol
o D-opamine
o E-pinephrine
o A-tropine
SINUS TACHYCARDIA
SA node ( adult 100bpm )
Faster than normal
Causes:
Stress / hypermetabolic rate
Medication ( aminophylline )
o IDEA
o Illicit drugs ( shabu )
PR interval / QRS complex (normal)
Rates exceed 100bpm
TX:
Digoxin (- ) chronotropic
Calcium Channel Blockers “ VAND ”
Beta Adrenergic Blockers ( decreased
contractility & HR ) “olols”
MOST COMMON DYSRHYTHMIA
ATRIAL FLUTTER
SA node is not the main pacemaker
Ectopic atrial focus captures heart rhythm
Conduction defect on the atrium
SAW TOOTHED ( atrial rate 250 – 400bpm )
PR interval is difficult to determine
o
P / QRS ratio 2:1, 3:1, 4:1 so on……
ATRIAL FIBRILLATION
Atrial quivers ( 300 – 600bpm )
Multiple rapid impulses ( many foci )
No definitive P wave
PR interval cannot measured
VENTRICULAR DYSRRHYTHMIA
PVC ( premature ventricular contraction)
Ectopic beat originating from ventricle
Conducted before the next sinus
PVC of 6 or more is life threatening (>6/min)
Occurs in repetitive patterns / alternating
repetitive pattern / continuous repetitive
pattern
o Bigeminy ( N-PVC ) 2nd turn
rd
o Trigeminy ( N-N-PVC ) 3 turn

Couplet ( 2x PVC )

Triplet ( 3x PVC )
QRS complex may be unifocal ( same foci ),
multi-focal ( came from different foci )
VENTRICULAR TACHYCARDIA
Irritable focus on the ventricle ( emergency )
Ventricular rate ( 100 – 200 )
Ventricular no time to refill
QRS complex prolonged ( .12sec/complex )
Risk for asystole
VENTRICULAR ASYSTOLE
Absence of QRS complex
No heart beat, palpable pulse
No respiration
Need immediate treatment
Causes: ( SSSCAT )
o S-evere hypoxia ( cerebral )
o S-evere electrolyte imbalance
o S-hock
o C-ardiac tamponade
o A-cidosis
o T-ension Pneumothorax
TX:
Artificial Cardiac Pacemaker
Antiarrhythmic drugs
CLASS I ( fast sodium channel blocker )
o CLASS IA - moderate depression of
depolarization but prolonged
repolarization ( Procainamide )
-
CLASS IB – minimal depression of
depolarization but prolonged
repolarization ( Lidocaine )
o CLASS IC – marked depression of
depolarization / no effect on
repolarization ( Propafenone )
CLASS II ( beta adrenergic blocker ) increased
automacity /conduction
CLASS III prolonged repolarization/
Amiodanone
CLASS IV ( calcium channel blocker )
Pacemaker
Indication:
Permanent normal impulse / temporary
slower than formation
Pacing mode
By demand ( if heart needs a demand )
By set ( settings )
Cardioversion
Delivery of Electrical Current
Synchronized with patient electrical event
Send electrical impulse: QRS complex
Elective procedure
Starts with low voltage
Client is awake ( sedated )
Defibrillation
Immediate & synchronized
Toc: V-fib & pulse less
Emergency
Starts with high voltage
Unconscious
ECG is monitored
Conduction defects
st
1 degree AV block ( impulse is send &
receive ) in slower rate
nd
2 degree AV block ( not all impulse is
received ) if sympyomatic – treatment
Atropine Sulfate
rd
3 degree AV block ( totally no impulse is
received ) sympyomatic – treatment Atropine
Sulfate / pacemaker
RHEUMATIC HEART DISEASE
Preceded by GABHS infection
o Sore throat, impetigo
Inflammatory disease of the heart ( valves is
affected )
CM:
HYPERTENSION ( HPN )
Shortness of breath
Heart murmur
Tachycardia
Fever
Subcutaneous nodules
Erythema marginatum
Chorea
DX test:
Elevated ASO titer ( anti streptolysin O )
Elevated ESR
TX:
CBR ( 24hr )
Increased CHO, CHON
Medication:
ASA
Corticosteroid
Penicillin
CARDIOMYOPATHY
Form of cardiac dysfunction
DCM ( Dilated Cardiomyopathy )
HCM ( Hypertropic Cardiomyopathy )
RCM ( Restrictive Cardiomyopathy )
ACM ( Arrhytmogenic Cardiomyopathy )
Unclassified
CM:
Sign & symptoms is progressive
CHF ( manifestation )
Chest pain & palpitation
Dizziness & syncope
(+) S3 & S4
Enlarged heart
Complication:
Severe HF
Lethal dysrrhythmia ( death )
TX:
Identify /manage cause if possible
Treat heart failure
Low sodium diet
Exercise & rest
Anti dysrrhythmia / anticoagulant
Surgical Management:
Heart transplant
RAAS ( renin angiotensin aldosteron system )
BP ( signals )
kidney ( renin )
Angiotensin 1
( weak
vasoconstriction )
ace
inhibitors
(lungs )
renin converts
Angiotensinogen
( liver )
converts
angiotensin 1 to
Angiotensin 2
initiates
( strong vasoconstriction )
adrenal
cortex
( to release )
Cathecholamines ( epinephrine / norepinephrin )
Glucocortecoid ( costisol ) blood sugar
Mineralocortecoid ( aldosteron )
sodium
reabsorption /
potassium
excretion
sodium attracts H20
( plasma ) CBV
Abnormal elevation of BP
SBP > 140 : DBP > 90
Systemic Hypertension
Risk factor:
Age, gender, genetic factor, lifestyle, stress
Determinants of BP
BV – CBV ( increased BV – increased pressure)
Peripheral Vascular Resistance ( afterload )
Cardiac Output
Compliance of blood vessel( change in
diameter of lumen )
Blood viscosity
Blood pressure regulator
Main factor of BP
o CBV ( Circulating Blood Volume )
o Systemic Vascular Resistance
o Intrinsic Regulators

RAAS ( renin angiotensin
aldosteron system )
BP

ANP ( anti natriuretic
peptide)
ANP ( anti natriuretic peptide)
BP
atria is stretch
ANP is release
Kidney
Excrete sodium
sodium attracts
( H2O )
BP
H2O ( plasma ) CBV

ADH (anti diuretic
hormone) vasopressin (
target the kidney to
increased the
permeability of collecting
tubules – reabsortion of
H2O in the system –

o
decreased urine output (
concentrated )

pituitary gland /
hypophysis

posterior/neuro
hypophysis

anterior/adeno
hypophysis
Catecholamine
(epinephrine /
norepinephrine)
emergency stress
hormone
(vasoconstriction :
increased HR
(tachycardia) increased
SV = increased CO
Classification of HPN:
Primary HPN ( idiopathic ) no cause
Secondary HPN ( resulted from a
complication from existing disease
Hypertensive Crisis
o MAO inhibitor + Tyramine = HPN
crisis
Malignant HPN
White coat HPN
CM:
Headache
Epistaxis
Dizziness, unsteadiness, blurred vision
Tinnitus
Complication of HPN:
Heart : ( MI, dysrrhythmia, CHF, IHD )
Eyes : ( retinopathy, blurred vision )
Brain : ( hemorrhagic CVA, stroke imbolic,
thrombotic, hemorrhagic )
Kidney : renal failure ( HPN 2nd leading causes
of CRF ) hypertensive nephrosclerosis
Peripheral Blood Vessel : aneurysm,
gangrene
TX:
Healthy Lifestyle
o Maintain IBW
o Regular exercise
o Stress reduction
o Proper diet
Advise to have regular consultation
Pharmacologic Treatment
Diuretics
-
Thiazide – affect the Nephron
(kidney) Decreased CBV / Increased
UO

Hydrochlorothiazide

Chlorothiazide

Methylchlorothiazide

affects the
kidneys ( Distal
Convulated
Tubules ) – after
the Loop of
Henle
o Loop Diuretics – Potassium Wasting
Diuretics ( hypokalemia )

Furosemide

Bumetamide

Ethacrynic Acid

Affects the
kidneys (
Ascending Loop
of Henle )
o Potassium Sparing Diuretics
(common effects hyperkalemia /
dehydration)

Spironolactone

Amiloride
Symphatolytics
Destruction of Symphathetic Response
o Beta Adrenergic Blockers
decreased HR & contractility (olol)
Types of Beta Adrenergic Blockers

Cardio Selective ( beta 1 )
Heart

Metraprolol

Atenolol

Besoprolol

Non Cardio Selective (
beta 2 ) Lungs

Propanolol

Tinolol
Side Effects :

Hypotension

Bradycardia

Brochospasm

Fatigue

Weakness
o Alpha Adrenergic Blockers
o
o
o
o
o
Blocks stimulation resulting to
vasodilation - decrease BP ( zosin )

Doxazosin

Prazosin

Terazosin
Direct Acting Vasodilator
Relaxation of smooth muscle
(tunica media)

Hydralizine

Monoxide
Central Alpha 2 Agonist
Decrease contractility / vasodilation

Methyldopa ( Aldomet )

Clonidine ( Catapress )
Calcium Channel Blockers ( VAND )
- Increase contraction &
vasodilation ( increase Calcium
uptake of cell ) - Calcium initiate
the Sliding Filament Theory

Verapamil

Amlodipine

Nicardipine

Diltiazem
ACE Inhibitors
Block Angiotensin 1 to convert to
Angiotensin 2 ( pril )

Captopril

Enalapril

Lisinopril
ARB’s - Angiotensin2 Receptor
Blocker blocks Angiotensin2
receptors (sartan ) - decreased BP

Lozartan

Irbesartan

Telmisartan
NI:
-
Monitor S/E ( orthostatic hypotension ) - Ask
the client to rise up slowly or dangle feet
Advise client to take drugs on REGULAR
BASIS ( maintenance )
Always promote safety
PERIPHERAL VASCULAR DISORDER
DX:
Venography – indirect visualization of vein (
contrast dye )
Angiopgraphy – indirect visualization of
artery ( contrast dye )
-
Vascular Endoscopy – direct visualization of
blood vessel
-
Assess allergy to Iodine ( seafood allergy )
Increase IFO
Apply pressure function site ( prevent
bleeding )
NI:
DEEP VEIN THROMBOSIS
Cause:
VIRCHOWS TRIAD
Vessel wall injury
o Trauma
o Substance abuse – nicotine
Venous stasis
o Stagnant blood
o Prolonged standing / sitting
Hypercoagubility of the blood
o Pregnant
o Women using pills ( fibrinogen )
CM:
( + ) Homan’s Sign
o Outstanding sign
o Pain in the Calves ( dorsiflex )
o Pathognomonic sign
Warm skin / tender to touch
Redness / Edema
Pulmonary embolism ( dangerous ) emboli
can impede pulmonary blood vessel
( phlegmonic cerulea dolens )
Massive edema ( ileu-femoral vein )
TX:
CBR ( elevate legs )
Compression stocking ( morning / upon
awakening / before rising in bed
Perform peripheral circulatory assessment
( 5P’s)
Pain/Pulse/Pallor/Paresthesia/Paralysis
Do not massage affected leg
Anticoagulant
Heparin ( immediately effective )
o MOAdmission – subcutaneous or
TIV
o MOAction – inhibits action of
thrombin
o Antidote ( protamine sulfate )
o Monitor – PTT & APTT (20 – 39sec)

1.5 – 2.5X the higher
laboratory control
-
Warparin ( 3 – 4 days effective )
o Inhibits synthesis of Vit.K ( per
OREM )
o Antidote ( Vit.K )
o Monitors

PT ( 9 – 12sec )

1.5 – 2X normal
laboratory
control

INR(1) normal

2–3
PTT – Partial Thromboplastin Time
PT – Prothrombin Time
APTT – Activated Partial Thromboplastin Time
INR – International Normalized Ratio
VARICOSE VEINS
Distended – protruded veins
Cause:
Incompetent Valve
Etiology:
Hereditary
Prolonged standing / sitting
Venous hypertension
Congenital
CM:
Dilated purplish – tortuous veins
Edema – Pain
Feeling of fullness / heaviness in the veins
( + ) Trendelenburg Test
TX:
Sclerotheraphy ( palliative treatment than
curative )
Vein stripping / Ligation ( curative )
NI:
Health teaching
Use anti-embolitic stockings
Avoid wearing restrictive clothing
Avoid prolonged standing / sitting
RAYNAUD PHENOMENON
Vasospasm ( arteries / arteriols )
Assessment:
Abnormal tissue discoloration
Numbness, tingling, swelling
NI:
Perform peripheral circulatory assessment
(5P’s)
-
Instruct client to avoid precipitating
environment ( exposure to cold environment)
Avoid stress / smoking
Pharmacotheraphy
Vasodilators ( Calcium Channel Blockers )
(FUCKN )
F-emale ( high risk )
U-pper extremities
C-yanosis
K-( Cold )
N-numbness / tingling sensation
AORTIC ANEURYSM
Abnormal dilation of aorta
Located along the aorta
Types:
Fussiform – dilation in both side
Dissecting – separation of layer of arteries
Saccular – aneurysm in 1 side
Location:
Thoracic
Abdominal
#1 predisposing factor ( atherosclerosis )
Most feared complication ( HPN rupture )
Assessment:
Thoracic
o Pain ( swallowing )
o Hoarseness of voice ( dysphagia )
o Syncope(sudden loss of
consciousness)
Abdominal
o Pulsating mass in the abdomen
o Pain ( abdominal - lower back )
o Bruit on the aorta
DX:
Ct scan, abd. ultrasound, arteriography
TX:
Goal:
o Limit progression
o Prevent rupture ( Dacron graft )
prosthesis
NI:
Antihypertensive drugs
Surgical treatment ( Dacron Graft )
BUERGER DISEASE
Throm Anginitis Obleterans
Occlusive disease medium / small arteries &
veins
-
#1 precipitating factors ( tobacco )
-
Brocks ( complete repair )
CM:
Pain ( intermittent claudication )
Cool / numb
Diminished pulse
Complication:
Ulceration
Gangrenous foot
Management:
Eliminate smoking
Medication:
Calcium Channel Blocker
Antiplatelet
Surgery:
Symphalectomy
Amputation
CONGENITAL HEART DISEASE ( Cyanotic / Acyanotic)
Cyanotic: ( starts with letter T )
Right – Left Shunting ( deoxygenated blood is
circulating in the systemic circulation )
Acyanotic:
Left – Right Shunting ( oxygenated blood is
going to the pulmonic circulation )
CYANOTIC HEART DISEASE
Tetralogy of Fallot
o 4 anomalies

P-ulmonic Stenosis

V-entricule Septal Defect

O-ver-riding of the Aorta

R-ight Ventricular
Hypertrophy
S/S:
Cyanosis
Polycythemia ( increase RBC )
Severe Dyspnea
TET spell ( severe acute hypoxic attack )
Management:
Oxygenation
Knee – chest position
Pharmacotheraphy
Morphine Sulfate ( decrease oxygen
consumption )
Surgery :
Blalock – Taussig Procedure ( palliative )
TRICUSPID ATRESIA
Ended in a blinded pouch
S/S:
Cyanosis
Polycythemia
DOB
Management:
FONTAN procedure
TRANSPOSITION OF THE GREAT ARTERIES
Largest arteries ( aorta / pulmonary )
S/S:
Cyanosis
Poycythemia
DOB
Management:
Rashkind procedure ( palliative )
Mustard procedure ( complete repair )
TRUMCUS ARTERIOSUS
Aorta / Pulmonary artery branch out ina
single artery
S/S:
Cyanosis
Polycythemia
DOB
Management:
Modified Rastelli procedure ( surgical )
ACYANOTIC HEART DEFECT
ASD / VSD
Cyanosis appears in severe case
DOB
Murmur
DX:
Cardiac catheterization
ECG
MRI & CT scan
Management:
Open Heart Surgery ( ECMO )
PDA ( Patent Ductus Arteriosus )
CM:
Continuous machinery murmur
DX:
Cardiac catheterization
ECG
MRI & CT scan
Management:
Indomethacin ( NSAID’s ) strong affinity to
heart
Ligation of PDA ( surgical ) inhibit steroids
( prostaglandin )
COARCTATION OF THE AORTA
Narrowed portion of the aorta
Manifestation:
Weak / absent pulse ( lower extremities )
Strong pulse ( upper extremities )
BP changes
DX:
Cardiac catheterization
ECG
MRI & CT scan
Management:
Closed Heart Surgery
BLOOD DISORDER ( Hematological )
Blood ( 4 -6 liter ) ( 7.35 – 7.45pH ) ( 380C )
Plasma ( 90% water ) CHON – liver
o Albumin ( osmotic / oncotic
pressure )
o Fibrinogen ( clotting )
o Globulin ( immune system )
o Other substance

Nutrient

Waste / metabolic ( urea )

Hormone
Blood elements ( formed cell )
o RBC ( biconcave / annucleated )

90 – 120 days expired
3

4 – 6 million / mm

Provide wider space for
Oxygen

No ATP ( low consuming
cellular activity )

M: 14 – 18g/dl

F: 12 – 16g/dl
o Heme ( iron ) Globin ( protein )
o Hematocrit :

Can be affected by
plasma ( decrease plasma
– decrease hematocrit )

M: 42 – 52%

F: 35 – 47%

Hemoconcentration

decrease
plasma/
decrease Hct.

Hemodilution

Increase
plasma/
decrease Hct
Erythropoiesis ( erythropoietin ) process of
producing RBC
Reticulocyte ( immature RBC )
o 1 day circulating in the body &
become matured
Hematopoiesis
Stem cell – (hemocrytoblast) – myeloid /lymphoid
Myeloid
o Reticulocyte
o RBC, platelet, WBC
Lymphoid
o Lymphocyte

T- Lymphocyte (cell
mediated immune
system)

B- Lymphocyte ( humoral
mediated immune
system)
WBC ( white blood cell ) LEUKOCYTE
Myeloid
o WBC

Neutrophils ( 40 – 70% )

Active
phagocytes

Eosinophil (1 – 4% )

Kill parasitic
worms – stop
chemical for
inflammation

Basophil ( 0 – 1% )

Contain
histamine (
activate
inflammation )

Lymphocyte ( 20 – 45% )

T- Lymphocyte

B- Lymphocyte

Monocyte ( 4 – 8% )

Become
macrophage
(much greater
than neutrophil)
PLATELETS ( Thrombocytes )
150,000 – 450,000 mm3
Granular fragments of megakaryocyte
Prevent bleeding
Platelet aggregation
Platelet adhesion
DISORDER OF THE BLOOD ( RBC )
ANEMIA
Oxyhemoglobin ( oxygen connect to RBC )
bright red
Primary problem: decrease availability of oxygen going
to the tissue or fast hemolysis
Common manifestation of Anemia: ( PWET )
P-allor
o Oxygenation problem
W-eakness
o Decrease O2
E-asy fatigability
o Decrease O2
T-achycardia
o Compensation
Severe:
Chronic:
-
SOB
Chest pain
Koilonychia ( spoon shape nail )
Amenorrhea
Brittle hair / nail
IDA ( IRON DEFICIENCY ANEMIA )
Microcytic – smaller than normal
Hypochromic – amount of RBC in the
hemoglobin
Causes:
Blood lost
Gastrointestinal malabsorption
Dietary inadequate
Increase metabolic demand
TX:
Nursing Intervention:
Promote iron rich food
o Heme - animals
o Non heme – plants
Medical management:
Blood transfusion as needed
Administer iron supplement
Iron supplement
Oral:
o Ferrous Sulfate – gastric irritation
o Oral liquid – use straw
Parenteral: ( Iron Dextran )
o Administer through Z track ( do
not massage )
o Do not give tea, antacid, milk
o Stool appear dark
o Common Side Effects:

Constipation ( increase
OFI – increase fiber )
FOLATE DEFICIENCY ANEMIA
Deficiency of folic acid
Macrocytic & Hyperchromic RBC
o Folic acid is responsible for
synthesis of RBC maturation
Causes:
Poor dietary intake / malnutrition ( folate )
Malabsorption disorder
Alcoholism
TX:
Folic rich food
Folic supplement 1mg / day ( PO )
PERNICIOUS ANEMIA ( Megaloblastic Anemia )
Decreased Vit.B12
Vit. B12 is responsible to RBC maturation
Etiology:
Total / Partial gastric surgery
Malabsorption disorder
Deficiency intake - rare ( intrinsic factor )
DX test:
CBC
Schilling test ( for absorption of vit.B12 ) 24hr
urine collection
CM:
Red beefy tongue
Manifestation of anemia
Jaundice ( massive hemolysis )
Neurological impairment ( psychosis )
o Vit. B12 maintain integrity of myelin
sheath
TX:
-
Vit.B12 supplementation
Blood transfusion
APLASTIC ANEMIA
Characteristic by bone marrow hypoplasia
o Immature bone marrow
Result to Pancytopenia ( decrease RBC / WBC
/ platelet )
Causes:
Congenital
Radiation
Medication
Infection
DX:
CBC
Bone marrow aspiration
CM
Anemia
Leukopenia ( recurrent infection )
Thrombocytopenia
TX:
Anemia:
o Activity pacing ( promote
oxygenation )
Prevent infection:
o Provide isolation

Strict

Reverse
Encourage hygiene
Avoid raw / fresh fruit / vegetable
Bleeding precaution:
Avoid sharp object
Minimize invasive procedure
Avoid contract sport
Medical management:
Bone marrow transplant
Blood transfusion
SICKLE CELL ANEMIA
Hgb is replace by Hgb S
Inherited
Resulting to severe chronic anemia
Causes: ( DISH )
D-ehydration ( #1 causes )
I-nfection
S-tress
H-ypoxia
Types of Sickle Cell:
Vaso occlusive ( painful )
-
Splenic Sequestration ( spleen )
Aplastic ( decrease RBC / WBC / platelet )
o Parnovirus ( decrease red bone
marrow )
-
Blood smear
Sickle turbidity test
Amniocentesis
-
Prevent DISH
During crisis
o Promote oxygenation during
hydration
DX:
NI:
THALASSEMIA
Inherited group of hemolytic anemia
Cause by few hemoglobin peptide chain
Resulting to decrease Hgb & life span
Common for Mediterranean blood
4 forms:
Thalassemia Minor
o Silent carrier
Thalassemia Major
o Very severe
Thalassemia Intermedian
o Moderate severe w/ hemolysis
Thalassemia Tract
o Mild microcytic anemia
Sign & Symptoms:
Frontal brossing
Maxillary prominence
Splenomegaly
Hemosiderosis ( iron overload )
DX:
PBS ( Peripheral Blood Smear )
Hgb electrophoresis
CBC
TX:
Goal: Supportive Treatment
No known cure
Blood transfusion
Admission of Deferoxime ( iron overload )
Spleenectomy
OTHER DISORDER ( RBC )
POLYCYTHEMIA
Increase RBC
POLYCYTHEMIA VERA
Primary ( hyperactive bone marrow )
Increase RBC / WBC / platelet
SECONDARY POLYCYTHEMIA
Release of erythropoietin
Complication:
Thrombosis
Increased cardiac workload
DISORDER OF WBC
LEUKEMIA
Malignant disorder characterized by rapid &
unregulated proliferation of immature WBC
Classification:
ALL – Acute Lymphocyte Leukemia
AML – Acute Myeloid Leukemia
CLL – Chronic Lymphocyte Leukemia
CML – Chronic Myeloid Leukemia
Causes:
Idiopathy ( cannot pin point causes )
Viral infection
Familiar susceptibility ( carcinogenic genes )
Genetic disorder
Radiation and Chemical
Theories / CA ( cellular aberration )
Failure of the immune response theory
Cellular transformation & dearrangement
CM:
Decrease mature WBC / RBC / platelet
Bone pain & Arthalgia ( pain in the joint
w/out inflammation )
Hepato – Spleenomegaly
Abdominal pain
Sign & symptoms of electrolyte imbalance
DX test:
Bone marrow aspiration
PBS ( Peripheral Blood Smear )
CBC
Medical management:
Chemotherapy
Bone marrow transplant
BT
NI:
Prevent bleeding
Prevent infection
Promote oxygenation
BLEEDING DISORDER
DIC ( Dissimenated Intravascular Coagulation )
Acquired thrombotic / Hemorrhagic
syndrome
Abnormal activation of clotting & fibrolysis
Causes:
-
Severe massive infection ( septicemia )
Obstetric complication
Malignancy
Hemolytic transfusion reaction
Shock
ABNORMAL CLOTTING
Manifestation:
Coolness / Cyanosis ( extremities )
Pain ( extremities )
Dyspnea / Adventitious breath sound
Altered mental status
Complication:
Pulmonary Embolism (most feared
complication)
DVT ( deep vein thrombosis )
CVA ( cerebro vascular accident ) embolic
MI ( myocardial infarction ) coronary artery
ABNORMAL BLEEDING
Manifestation:
Internal / External bleeding
DX:
Decrease platelet / fibrinogen
Prolonged PT & PTT
Complication:
Hemorrhage ( most common cause of death )
TX:
Treat underlying cause
Replacement therapy:
FFP ( fresh frozen plasma )
Cryoprecipitate – platelet transfusion
Anticoagulant
HEMOPHILLIA ( specific )
Deficiency in specific coagulation factors
Pattern of inheritance ( X linked recessive )
Male: manifest
Female: carrier
Most common type:
Hemophilia A (deficiency in clotting factor 8)
Hemophilia B (Christmas hemophilia)
Hemophilia C (deficiency in clotting factor 11)
Assessment:
Sudden bleeding
Abnormal bleeding during trauma
Hemorthorosis ( bleeding of joints )
-
Excessive bleeding
-
Same as the other bleeding disorder
TX:
NI:
-
WOF sign of bleeding
Institute bleeding precaution
Monitor vital sign ( hypovolemic shock )hypo
tachy-tachy
If already present ( control bleeding )
o I-ce
o C-ompress
o E-levate
Medical management:
Replacement therapy
Antifibrinolytic medication ( stops dissolving
of clot )
o Amicar
o Tranexamic acid
VON WILLEBRAND DISEASE
Deficiency or defect on vWf
o vWf – initiates platelet aggregation
/ adhesion – potentiates clotting
factor
CM:
Bleeding especially in the mucus membrane
Prolonged bleeding time
Decrease vWf ( clotting factor 8 )
TX:
Same as hemophilia
Pharmacotherapy
Humate P ( alphate )
ATP ( AUTO IMMUNE THROMBOCYTOPENIC
PURPURA)
Idiopathic
Immune destruction of platelet
Usually viral infection
Suppressor T cell cannot stop immune
response
Destroy other cell
Infected thrombocytopenic purpura (dengue)
CM:
Bleeding from gums & nares
Bruising
Petechiae
Menorrhagia
TX:
Platelet transfusion
-
Immunesuppresant
Bleeding precaution
MULTIPLE MYELOMA
Malignant disease of plasma cell
Rapid B – cell proliferation
CM:
Normochromic / Normocytic anemia
Back pain
Decrease WBC / platelet
Bone pain / fracture ( osteoclast –
destruction )
o Bone ( hydroxyl apatite crystals )
Hypercalcemic ( renal failure )
Complication:
Bleeding
Anemia
Infection
Renal failure ( hypercalcemia )
DX procedure:
(+) Bence Jones Protein ( urine / blood )
FNAB – fine needle aspiration biopsy
o
bone marrow
TX:
Chemotherapy
Alpha interpheron
Radiation
Hydration ( viscos blood due to plasma )
Pain management
RESPIRATORY SYSTEM
PHYSIOLOGIC DEAD SPACE ( nares – bronchi )
Nares
Nasal cavity
Vestibule – inner portion of nasal cavity
Vibrissae – tiny hair in the nasal cavity
Pharynx
Vasopharynx
Oropharynx
Laryngopharynx
Larynx
Voice box ( cartilagenious epithelium )
Epigloittis ( guardian of the airway )
Thyroid cartilage ( largest cartilage in the
larynx ) “ adams apple “
Vocal chords ( vibration – phonation )
Trachea
Wind pipe ( cartilage with smooth muscle )
Carina ( point were before trachea separates)
Bronchi
Right
Left
Segmental bronchi
o Sub – segmental bronchi
o Bronchioles
o Terminal bronchioles
o Respiratory bronchioles
Basic Functional Unit ( Lungs ) ALVEOLI
Alveolar duct
Alveoli
o Alveoli 1 ( gas exchange )
o Alveoli 2 ( surfactant production )
Muscle responsible for breathing:
Diaphragm
Intercostals’ muscle
Pleura ( parietal ) – Outside cover of the lungs ( serous
membrane )
Visceral pleura – Inside cover of the lungs
Prinic nerve – innervations of the diaphragm
RESPIRATION ( an act of breathing )
External ( lungs – environment )
Internal ( blood cells – capillaries )
3 process:
Ventilation: movement of air in & out of the
lungs
Diffusion: exchange of gas ( higher pressure –
lower pressure )
Perfusion: availability / movement of blood
for transport
Pneumocytes:
o Type 1 - located in the alveoli
o Type 2 - surfactant
o Type 3 - phagocyte
Respiratory Center
Medulla Oblongata: primary center of
respiration
Pons: helps the regulation of respiration
o Pneumotoxic center – responsible
5
o Apneustic center – deep &
prolonged inspiration
Chemoreceptor: detects the level of
respiratory gases & blood pH
Proprioreceptors: detects amount of stretch
Lung Volume
Tidal volume


o
In & out of air with normal breath
( 500ml )
Inspiratory reserve volume
o Amount of extra air that can be
inhaled beyond the tidal volume (
3100ml )
Expiratory reserve volume
o Amount of air that can be exhaled
of the normal breath ( 1200ml )
Residual volume
o Amount of air that remain in the
lungs after a forceful expiration (
1200ml )
Assessment:
Inspection:
Signs of respiratory distress
o Nasal flaring
o Alteration of LOC
o Rapid respiration
o Skin discoloration
o Used of accessory muscle

Sternocleidomastoid

Pectoris major / minor

Trapezius
Rate & depth of respiration:
Eupnea ( normal )
Bradypnea ( <12cpm )
Tachypnea ( >24cpm )
Hypoventilation ( decrease rates & depth )
Hyperventilation ( increase rates & depth )
hypercapnia / Kussmaul Respiration
Apnea ( absence of breathing
Cheyne stroke ( progress apnea prolonged )
Boit’s respiration
Thoracic inspection:
AP diameter to Lateral diameter ( 1: 2 ratio )
4 main chest deformities:
Barrel chest (1;1 ratio - increase AP diameter)
COPD
Funnel chest ( pectus excavatum )
Pigeon chest ( pectus carinatum )
Kyposcoliosis
Thoracic Palpation & Inspection:
Respiratory excursion ( 3 -5cm )
o Measure the symmetry / extent of
lung expansion
Tactile fremitus
o Spoken voice transmit low
frequency vibration

Abnormal findings
Increase tactile fremitus

Consolidation of
the lungs

Pneumonia

Tumor

Fibrosis
Decrease tactile fremitus

Increase
amount of air in
the lungs

COPD

Pneumothorax
Percussion tones
Resonance / long-hollow /normal
Flat / short extremely dull / pleural perfusion
Dull / moderate /may indicate consolidation
Tympanic / moderate drumlike /
Hyperresonance / very long booming / COPD
Auscultation:
NORMAL BREATH SOUND
Bronchial
Bronchio
Vesicular
Vesicular
Manubrium
area (upper)
Bronchi (mid)
Base of Lungs
Pitch
High
Amplitude
Loud
Moderate
Moderate
Low
Low
ADVENTITIOUS BREATH SOUND
Crackles ( rales ) coarse / fine - pulmonary edema
Air passing to a fluid ( mucus )
Gurgles ( ronchi ) pneumonia
Air passing to a narrowed passage w/ fluid
Friction rub
Inflammation of the pleural surfaces
Wheezes ( asthma )
Voice sound ( ask the client to say ninety nine / eee )
Egophony
Bronchopony
Whispered pectoriloquy
DX procedure:
Chest Xray ( radiograph )
Sputum specimen
o Sputum C & S ( identify pathogen /
antibiotics )
o AFB staining ( detects TB bacilli )
o Cytologic examination
Mantoux test
o Read after 48 – 72hrs
o
-
-
-
-
Result:

(+) induration of 10mm or
more

(+) induration of 5mm or
more ( HIV )
Bronchoscopy ( direct visualization –
endoscope)
o Consideration:

NPO ( check for gag reflex
)

Pre op meds ( atropine
sulfate )

WOF complication
Bronchography ( visualization through the
use of radiopaque
o Consideration:

Check for allergy ( iodine )

NPO ( 8 -12 hrs before )

Pre op med
ABG ( measure dissolve oxygen & carbon
dioxide in the arterial blood )
Lung biopsy
o Transbronchospic biopsy /
bronchoscopy
o Percutaneous needle biopsy
o Open lung biopsy / chest surgery
Pulse oximetry ( measure O2 saturation )
O2% in the capillary blood
Lung scan
o Intervention

Assess for allergy to dye
SINUSITIS
Inflammation of sinus
Causes:
URTI ( upper respiratory tract infection ) ,
smoking, allergic rhinitis
Assessment:
Pain:
o Maxillary
o Frontal
o Ethmoid
o Sphenoid
Fever
Cough & runny nose
TX:
NI:
-
Rest & increase OFI
Warm pack ( pain )
Administer medication prescribed
o Decongestant ( phenylephrine )
o Antihistamine ( chlorphenamine )
o Antipyretic ( paracetamol )
Surgical Intervention:
FESS ( functional endoscopic sinus surgery )
Caldwell – Luc surgery
Ethmoidectomy / Ethmoidotomy
Sphenoidectomy
Osteoplastic flap surgery
-
CANCER OF THE LARYNX
Risk factor:
Substance abuse ( smoking )
Voice abuse ( persistent voice hoarseness - #1
initial sign )
Environmental pollutant
Chronic laryngitis
Assessment:
Persistent voice hoarseness
Mass at the anterior part of the neck
Persistent cough & sore throat
Dyspnea / dysphagia ( burning sensation –
swallowing )
Pain radiating to ear ( metastasis )
-
TX:
-
Symptomatic treatment based on
manifestation
Treatment includes surgery, chemotherapy,
radiation
Surgical Intervention:
Laryngofissure-thyrotomy (partial
laryngotomy )
o Removal of parts of larynx
Total Laryngectomy
o All laryngeal structures are remove
includes the hyoid bone, epigloittis,
cricoids cartilage, 3 tracheal ring
-
Proximal airways:
o >2mm in diameter
o Increase number of Goblet cell
o Enlarged in submucosal gland
Goblet gland grandular epithelium )
produce musin result to excessive
mucus & decrease diameter in lumen of
airways.
Peripheral airways:
o <2mm in diameter
o Thickening of the air wall
o Peribronchial fibrosis ( fibrous
connective tissue )
Lung parenchyma ( functional unit )
o Decrease elastic recoil
CHRONIC BRONCHITIS ( COPD )
Presence of cough & sputum production
Increase mucus secreting cell
Narrowing of the bronchial lumen
Alveoli become damage ( fibrosis )
EMPHYSEMA ( BARREL CHEST ) COPD
Abnormal destruction & distention of alveoli
Impaired diffusion
Increase dead space
Reduction in the size of the capillary bed
At high risk for the developing col pulmonade
Col pulmonade – R-sided CHF related to
pulmonary distention ( COPD )
Risk factors:
Exposure to tobacco
Air pollution
Occupational exposure
Genetic abnormalization
Assessment:
T.fremitus
Percussion
Auscultation
Emphysema
decrease
hyperresonance
C.bronchitis
normal
resonance
decrease
intensity
normal
DX:
COPD ( CHRONIC OBSTRUCTIVE PULMONARY
DISEASE)
Progressive chronic airway mutation that is
not fully reversible
Associated with abnormal inflammatory
response ( structural changes )
Structural changes in COPD
-
-
Pulmonary function test
o FEV – false expiratory volume
o FVC – functional vital capacity
o RV – residual value
ABG:
o Decrease PO2 : increase PCO2
( >45mmHg)
-
CBC:
o
Polycythemia ( increase RBC )
CM:
Chronic cough
Sputum production
Dyspnea on exertion
Adventitious breath sound
Weight loss
Signs of respiratory distress
Clubbing of fingernails
Polycythemia
Barrel chest
Decreased tactile fremitus & hyperresonance
Complication:
Respiratory insufficiency
Respiratory failure
Pneumonia
Atelectasis
Pneumothorax
TX:
Avoid smoking and sir pollutant
Increase OFI ( if not contraindicated ) to
liquify mucus
Promote rest
Oxygen supplementation ( in times of
exacerbation / 1-3LMP ) O2 narcosis
CPT ( chest percussion therapy )
Pharmacotherapy:
Antitussives ( suppress cough )
o Dextrometorphan ( Codeine )

s/e: drowsiness
Expectorant & mucolytic
Bronchodilator
Antihistamine
Steroids ( anti inflammatory )
Leukotrine inhibitors
Antibiotic
BRONCHIOSTATIS
Chronic reversible dilation of the bronchi &
bronchioles
Predisposing factor:
Airway injury / obstruction
Recurrent / long term pulmonary infection
Abnormal host defense
Idiopathic cost
CM:
Chronic cough
-
Purulent sputum
Hemoptysis
Clubbing
Recurrent pulmonary infection
-
-
CT scan
-
DX:
TX:
Avoid cigarette & air pollutant
Increase OFI ( if not contraindicated )
Promote rest
Oxygen supplementation
CPT
Pharmacotherapy:
Antitussives ( suppress cough )
o Dextrometorphan ( codeine )

s/e: drowsiness
Expectorant & mucolytic
Bronchodilator
Antihistamine
Steroids ( anti inflammatory )
Leukotrine inhibitors
Antibiotic
ASTHMA
Chronic reversible and diffuse airways
inflammation
Hyper responsive of the airway resulting to
o Bronchospasm
o Mucosal edema
o Mucus production
CM:
Cough
Wheezing ( expiratory )
Chest tightness / dyspnea
Other sign of respiratory distress
Assessment:
Tactile fremitus ( normal to decrease )
Percussion ( resonance to hyperresonance )
Auscultation ( wheeze )
TX:
Identify / prevent precipitating factors
Promote oxygenation
Alleviate anxiety
Pharmacotherapy:
Inhaled corticosteroid ( acute attack )
o Busemide
o Beclomethasone
o Monetasone
Systemic ( long term )
o Betaprednisolone
o Prednisone
o Prednisolone
Methylxanthines ( bronchodilators )
o Theophylline
Beta 2 agonist ( bronchodilators )
o LABA ( long acting beta adrenergic
agonist )

Salveterol

Albuterol ( SR ) sustain
release
o SABA ( short acting beta
adrenergic agonist )

Salbutamol

Metaproterenol

Terbutaline
o Mast cell inhibitors ( histamine )

Cromolyn sodium
o Leukotrine inhibitors

Zafirlukast

Montelukast
o Anticholinergic ( decrease mucus
secretion )

Ipatropium
CYSTIC FIBROSIS ( Mucuvisidosis )
Chronic disorder resulting to hyperactivity of
the exocrine gland
Most common life shortening inherited
Result:
Chronic airway obstruction
Infection
Malabsorption
CM:
Failure to pass meconium ( meconium ilues )
Sign of respiratory distress
Thick mucus production
Cyanosis / clubbing
Steatorrhea ( recurrent plug infection )
Recurrent long infection
Frosting of the skin or salty taste sweat
DX:
Iontophoresis of Pilocarpine test ( sweat
chloride test ) < 60meq/L
TX:
Promote effective airway
CPT
Reduce risk factor for respiratory infection
Lifestyle modification
Supplemental oxygen
Pharmacotherapy:
Antibiotic
Anti inflammatory
Leukotrine ( mast cell inhibitors )
PHARYNGITIS
Painful inflammation of the pharynx
Causes:
Viral / bacterial
CM:
Fiery red pharyngeal membrane
Enlarged & tender cervical lymphnodes
Malaise / masalgia
Fever
Headache
LARYNGITIS
Inflammation of the larynx
Causes:
Voice abuse
Exposure to dust & chemical
Smoking
GERD ( gastro esophageal reflux disorder )
Manifestation:
Hoarseness of voice
Aphonia
Severe cough
Subjective complain of tickling
Management:
Avoid irritants
Rest the voice
Steam inhalation
Increase OFI
Pharmacotherapy:
Corticosteroid
Antibiotic
Expectorant
Omeprazole ( proton pump inhibitor ) GERD /
decrease HCl cheyne
ATELECTASIS
Collapse of alveoli
Causes:
Altered breathing pattern ( guillian baire
syndrome ) shunt
Retained secretion
Prolonged supine positioning
Reduced lung volume
-
Surgical procedure
Accumulation of excessive pleural fluid
CM:
Progressive dyspnea
Percussion flat
Auscultation ( decreased to absent)
DX findings:
Xray
Pulse oximetry & ABG
Prevention:
Frequent turning
Early mobilization
Strategies to expand the lungs
Secretion management techniques
Management:
Endotracheal intubation
Mechanic ventilation
Treat underlying cause
RESPIRATORY INFECTION
LTB ( Laryngo – Tracheo Bronchitis )
Most common in infant & children less than 3
y.o
CM:
Fever
Nausea & vomiting
Nasal flaring
1 – hoarseness,stridor,cough or barky cough
2 – inspiratory stridor, intercoastal retraction
3 – lower rib retraction, use of accessory
muscle
4 – intermittent respiration, permanent
cyanosis, cessation of breathing
Laboratory study:
ABG
Throat swab
Chest – neck Xray
Causes:
Parainfluenza virus
Bacterial infection
Management:
Promote mucus secretion
Steam inhalation
Advise to rest
Oxygen administration
Pharmacotherapy:
Corticosteroid
Antibiotic
Bronchodilator
-
Severe case : inhalation
EPIGLOITTITIS
Emergency condition of the URTI
Resulting to airway obstruction
Sign & symptoms:
Sudden onset
Pooling of the saliva
Hoarseness
Tripod position
Leaning forward with tongue protrusion
High fever
Sign of respiratory distress
Management:
Comfortable position
Do not use tongue depressor
Steam inhalation
Pharmacotherapy:
Antibiotic
Corticosteroid
Vaccination: HIB ( humane influenza type B )
PNEUMONIA
Inflammation of the lung parenchyma
Resulting to consolidation of the alveoli space
Classification:
CAP
HAP - nosocomial
Aspiration
Opportunistic ( immunocompromised )
Hypostatic ( prolonged bed rest )
Etiology:
Bacterial pneumonia
o Streptococcus pneumonia ( CAP )
o Staphylococcus aureus ( HAP )
o Pseudomonas aureginosa
o Klebsiella pneumonia
Non bacterial pneumonia
o Mycoplasma pneumonia
o Pneumocytic car inii ( HIV )
o Influenza parainfluenza virus
Assessment:
Rusty sputum
Fever & chills
Sign of respiratory distress
Sign of URTI
Anxiety & confusion
Tactile fremitus increased
Percussion: dull
-
Auscultation: crackles
Egophony
Bronchopony
Whispered pectoriloqy
2
3
TX:
Promote thermoregulation
Promote rest
Promote sputum expectoration
Promote infection control
Antibiotic:
Macrolide ( Azithromycin / clindamycin /
erythromycin )
Cephalosporin
Penicillin
Flouroquinolone ( floxacin)
PTB ( Pulmonary Tuberculosis )
Infectious diseases affecting the lungs
parenchyma
Mycobacterium ( anaerobe )
Sensitive to heat & UV ray
CM:
Fever
Cough
Night sweat
Weight loss
Shortness of breath
Chest / back pain
Risk factor:
Close contact to patient w/ active PTB
Immunocompromised status
Substandard lungs
Healthcare worker
DX:
CXR ( ideal )
Mantoux test ( Tb bacilli )
o (+) 10mm- general population
o (+)5mm
o DSSM ( direct sputum smear
microscopy ) interpret
Classification ( PTB )
Category
1
Type of PTB patient
-New (-)DSSM
-New(-)DSSM w/
extensive
parenchymal lesion
on CXR
-EPTB
Treatment
intensive
continuation
RIPE
RI
4
-Treatment failure
-Relapse
-New(-)DSSM w/
minimal
parenchymal lesion
on CXR
-chronic/still smear
positive after
supervised
retreatment
RIPES
RIE
RIPE
RI
DOTS
Management:
Goal of treatment:
Prevent spread of diseases
Promote recovery
Weight loss
Medication:
Rifampicin – red - orange discoloration ( normal )
Isoniacid – increase vit.b6 ( pyridoxine ) causes
peripheral neuritis
Pyrazinamide – photosensitivity
Ethambutol – optic neuritis
Streptomycin – category 2 patient
Hepatotoxicity / Ototoxicity
Single dose ( separate preparation )
Fix ( single tablet medicine ) Fixcom/ Quadtab
MDR ( multi drug regimen ) avoid develop PTB regimen
– reduce side effect
TB
Cancer
Chest pain / Trauma
Assessment:
Chest pain
SOB
Pleural friction rub
DX findings:
Xray
Thoracentesis ( removal of fluid – pleura )
TX:
TUC
Promote comfort
Promote oxygenation
HISTOPLASMOSIS
Systemic fungal disease
Common in rural / Midwest / southern area
Not spread from human to human ( chicken /
dove )
o Fecal transmission
Assessment:
Similar to PTB & pneumonia
Cough
Joint pain
Malaise
DX:
CXR
Histoplasmin skin test
TX:
Antifungal ( Ampothericin B / Polymycin B )
PLEURAL EFFUSION
Accumulation of excessive fluid ( pleura )
Type:
Hemothorax ( blood )
Pyothorax ( emphysema ) pus/ inflammation
Hydrothorax ( serous fluid )
Common cause:
Pulmonary infection
Iatrogenic
Neoplastic tumor
Trauma
Connective tissue disease
Complication:
Atelectasis
Hypovolemic shock
CM:
Sudden sharp chest pain
Tachycardia / tachypnea
Assessment:
Tactile fremitus ( absent )
Percussion: dull to flat
Auscultation: decrease to absent
TX:
C – hest drainage ( 5th – 6th ICS )
H – igh fowlers
O – xygen
P – ain management
A – BG
PLEURISY / PLEURITIS
Inflammation of the pleura
Causes:
Pneumonia
URTI
PNEUMOTHORAX
Accumulation of fluid in the pleural space
CM:
SOB
Restlessness
Types:
-
o
Sudden sharp chest pain
Tracheal deviation
Tachycardia / tachypnea
Cyanosis
Open pneumothorax
o Penetrating chest injury
o Wound is large enough to move air
in / out
o Tidal volume diminished ( decrease
ventilation )
Tension pneumothorax
o Accumulation of pressure
o Disease or injury ( emphysema )
o Air is traped ( inspiration )
Complication:
Lung collapsed
Mediastinal shift ( dangerous )
Assessment:
Signs & symptoms are bought by underlying
diseases
Tactile fremitus: decreased
Percussion: hyperresonant
Auscultation: absent breath sound
Pleuritic pain
SORD
DX:
-
CXR
Thoracentesis
-
TUC
Promote oxygenation
CHOPA
TX:
ACUTE RESPIRATORY FAILURE ( ARF )
Deterioration in the gas exchange function of
the lungs
Resulting to:
Caused by failure in the ventilation /
oxygenation mechanism
Cause:
Ventillary failure ( acute respiratory failure )
o Impairment CNS ( head trauma,
CVA, infection )
o Neuromascular dysfunction ( ALS –
amyotropic lateral sclerosis /
Guillan Barre Syndrome, M. gravis)
-
Muscular dysfunction ( chest
trauma, malnutrition, kyphosis )
Oxygenation failure ( COPD, lung infections )
o Constrictive lung disease (
pneumothorax, pleural effusion)
CM:
SORD
Air hunger
Tachycardia / Tachypnea
Cyanosis
Diaphoresis
Alteration of LOC
Complication:
Respiratory arrest
TX:
TUC
Oxygenation therapy
Endotracheal intubation
Mechanical ventilation
Monitor respiratory status
ACUTE RESPIRATORY DISTRESS SYNDROME
Severe form of acute lung injury
Caused by diffuse alveolar damage
CM:
Sudden & progressive pulmonary edema
o Increased bilateral infiltrates in CXR
o Hypoxemia unresponsive to oxygen
therapy
o Absence of elevated atrial pressure
Common cause:
Aspiration
Drug overdose
Hematologic disorder
Shock / trauma
Major surgery
Embolism
CM:
Sudden ( 4 – 48hrs onset )
Severe dyspnea
SORD
Dry cough ( sticky )
Fine crackles
DX:
ABG ( decrease oxygen / increase carbon
dioxide)
CXR
BNP ( brain natriaretic peptide ) /
endocardiography
TX:
-
Oxygen therapy
Positioning ( orthopnic, high fowlers, semi
fowlers )
Promote comfort
Intubation / mechanical intubation
Avoid anxiety
PULMONARY EDEMA
Excessive accumulation of fluid in the lung
tissue / alveolar spaces
CM:
SORD
Air hunger
Frothy sputum
Assessment:
Tactile fremitus; normal
Percussion: resonant
Auscultation: crackles
TX:
Treat fluid volume excess
Alleviate anxiety
Promote oxygenation
o Proper positioning
o CPT
o Oxygen therapy
o Suctioning / coughing exercise
In severe cases:
o Intubation ( ET )
o Mechanical ventilation
PULMONARY EMBOLISM
Obstruction in the pulmonary artery
Common cause:
PVD ( peripheral vascular disease )
Fat embolism
Multiple trauma
Immobility
Hypercoagubility
SARCOIDOSIS
Multi system, granulomatous disease
Hypersensitivity response to one or more
exogenous agents
Etiology:
Idiopathic
Pulmonary changes:
Granuloma infiltration & fibrosis
CM:
Depend on the system affected
General manifestation:
Anorexia
Fatigue
Fever
Specific pulmonary manifestation:
Dyspnea
Cough / hemoptysis
DX:
X ray / CT scan
Biopsy
TX:
Symptomatic treatment
Corticosteroid
Cytotoxic
Immnunosuppressive
PNEUMOCONIOSES
Occupational diseases of the lung
Non neoplastic alteration of the lungs
Causes:
Inhalation of mineral / inorganic dust
o Asbestosis
o Coal worker pneumoconiosis ( black
lung )
Result:
Pulmonary fibrosis
Parenchymal changes
Manifestation:
SORD
Cough
Chest pain
TX:
Symptomatic treatment
Avoid exposure to industrial dust
LUNG CANCER
Predisposing factor:
Cigarette smoking
Chronic exposure to industrial dust
Emphysema ( pre cancerous cell )
Genetics
Types:
Squamous cell ( good prognosis )
Adenocarcinoma ( good prognosis )
Oat cell ( poor prognosis )
Undifferentiated ( poor prognosis )
Manifestation:
Asymptomatic ( early stage )
-
Cough
Dyspnea
Adventitious breath sound
Chest pain
SORD
-
CXR / CT scan
Bronchoscopy
Biopsy ( #1 )
-
Surgical
o Pneumonectomy (removal of the
lung )
Unaffected side ( chest drainage )
o Lobectomy ( removal of the lobe )
o Segmentectomy
o Wedge resection ( removal of the
tumor regardless of the segment )
o Decortation ( stripping of the
fibrous membrane – enclosing the
lung )
Chemotherapy
Promote oxygenation
Radiation
Alleviate pain
o Narcan / Morphine ( narcotic
antagonist ) monitor respiratory
rate - < 12cpm
o Site of metastasis

Brain, Liver, Adrenal
gland, Bone
DX:
TX:
-
-
FLAIL CHEST
Crushing chest injury ( 2 adjacent ribs )
Manifestation:
Paradoxical breathing ( other part is not
expanding when breathing )
Signs of SORD
TX:
Promote oxygenation
Surgery ( chest surgery )
CARBON MONOXIDE POISONING
CO takes up the space of O2 in the RBC
resulting to hypoxia
Exposure to inadequately vented combustion
device
CM:
SORD
-
Headache
Vertigo ( feeling that environment is moving )
Paralysis
-
Hyperbanic pressure
Remove patient from immediate area of
poisoning
Initiate CPR immediately
Administer oxygen
Monitor VS
Intubation / Mechanical ventilation
TX:
-
RESPIRATORY MODALITIES
Oxygen Therapy
O2 concentration in room air ( 21% )
Factor related to O2 transport
Cardiac output
Arterial O2 content ( 96 – 100% O2
saturation)- V-D-P
Hg concentration ( decrease. RBC )
Metabolic requirement ( increase metabolic
rate & O2)
Indication:
Hypoxemia / Hypoxia
Types of hypoxia
Hypoxemia hypoxia ( dec. O2 concentration
in RBC – tissue )
Circulatory hypoxia ( blood flow ) CHD – PVD
Anemic hypoxia ( anemia )
Histotoxic hypoxia ( certain substance )
cyanide
Intervention:
Continuous assessment
Humidify O2 if indicated
Reduce risk for fire ( O2 highly combustible
gas )
OXYGEN ADMINISTRATION DEVICE
Low flow system:
Partial O2 Is Inspire
Nasal cannula: 1 – 6 LPM ( 22% – 42% )
-
Indication : need for low to medium O2
concentration
Advantage: comfortable for longer period
Disadvantage: drying of the nasal mucosa
( variable FiO2 ) fraction of inspired O2
Simple mask: 6 – 8 LPM ( 40% - 60% )
Indication: low to medium ( short term )
Advantage: able to gather O2
Disadvantage: uncomfortable ( variable FiO2)
Partial Rebreather Mask:
With Reservoir bag: 8 – 11 LPM ( 50% - 75% )
Indication: moderate
Non Rebreather:
Reservoir bag + Additional valves: 12 LPM ( 80% -100%)
Indication: high O2 concentration (
deteriorating O2 status )
High flow system: “ no room air “
Venturi mask: 4 – 5 LPM ( 24% - 40% )
-
T – Piece/Tracheostomy Collar: 8 – 10 LPM ( 30% 100% )
o
o
o
o
Indication: useful in weaning Pt. in mechanical
ventilator
Oxygen toxicity
Risk:
o Too high ( above 80% )
o Too long ( longer than 48hrs )
Result: inc. O2 radicals ( anti radicals – anti
oxidants / Vit. E )
Oxygen narcosis / COPD
Incentive spirometry ( method of deep breathing
exercise / visual feedback ) encourage Pt. to breathe
deeply & slowly
Indication: Atelectasis ( risk )
Patient Education:
Proper positioning: upright / semi fowlers
Breathing exercise
o 10x a day / 10 breaths each hour ( 3
sec. intervals ) allow coughing –
best in waking hours
o Splint incision
ET ( Endotracheal Intubation )
most reliable / accurate
Indication: precise FiO2
-
Indication: any person who cannot maintain
adequate airways
Pt. need mech. Ventilation
Passes with the aid of Laryngoscope
May be useful for not longer that 3
weeks
Client cannot talk / increase
secretion which is thicker
Ensure 1 way flow of air
o
Tracheostomy
Opening of the trachea (
temporary/permanent )
Indwelling tube is inserted
Indication: by pass an upper airway
obstruction / for long term use of mech.
Ventilator
Mechanical Ventilation
Indication: during surgery, severe head injury
or inadequateventilation
Types:
Pressure cycled
o It delivers flow of air until it reaches
preset pressure ( commonly for
short term )
o Limitation; volume of air vary as the
resistance or compliance change
Time cycled
o It delivers flow of air until it reaches
preset time ( commonly used –
infant/newborn )
o
Volume of air receives is regulated
by the length of inspiration
Volume cycled
o Most commonly used
o Volume of air is preset
o Constant/ adequate breath despite
of varying pressure
Non invasive positive pressure ventilation
Mode of ventilation
Controlled:
o Tidal volume / rate is set
o For patient who cannot initiate
respiratory effort
o Mechanical ventilator is in total
control
o If the client attempt to initiate
breath the ventilator block it
Assist Controlled:
o Commonly used
o
-
Alarms
-
Tidal volume / ventilator rate is
preset
o When the client initiates breath the
ventilator deliver the preset tidal
volume
Synchronized Intermittent Mandatory
Ventilation:
o Tidal volume / ventilator is preset
o Allows the patient breath on his
own effort and the tidal volume is
between the ventilator and client
breath.
High pressure alarms
o When ventilator receives resistance

Secretions,
bronchospasm,

Displaced tube

When the clients cough,
gags or bite the tube
Low pressure alarms
o Detects fast flow of air

Ventilator disconnection

Leak on ventilator of
patient cuffs
Chest Physio Therapy ( Cpt )
Includes:
Postural drainage
Chest percussion
Vibration
Goal:
Decrease bronchial secretion
Coughing Exercise
Position: sitting
Inhale slowly through the nose, exhale
through purse lips and cough twice during
exhalation
Note: for splint incision area to prevent
dehiscence / evisceration
Chest Drainage
Fluid:
Indication:
After thoracic surgery
Pneumothorax / pleural effusion
Purpose:
Remove excess fluid / air
Re expand the lungs
Restore negative pressure
Collection Chamber
Blood / Fluids
Maintain ( - ) pressure
Monitor / Report
o 100ml / Hr
o Sudden increase in bright red color
Water Seal Chamber
Note for patency
No bubbling ( leak )
Stop flanctuation
o Obstruction / Full expansion
Suction Controlled Chambers
With 20mm of sterile NSS
With gentle continuous bubbling
Absent of bubbling
o Not enough suctioning
o Vigorous leakage
80% TBW ( infant )
60% TBW ( male )
50% TBW ( female )
Function of fluid
Maintain blood volume
Transport gas & nutrients
Chemical cellular function
Eliminate waste ( urea )
Intake & Output
Intake ( 2600ml)
o Oral
1300ml
o Water in food
1000ml
o Metabolism
300ml
Output ( 2600ml )
o Urine
1300ml
o Stool
200ml
o Insensible

Lungs
300ml

Skin
600ml
Movement of body fluids
Colloid oncotic & osmotic pressure
Pulling force ( moving in )
Plasma ( oncotic ) albumin ( CHON )
Solutes ( osmotic ) sodium
Osmolarity ( mOsm/L ) / Osmolality (
mOsm/kg )
o Measures the concentration of the
solution
o 270 – 300mOsm/L ( kg )
Hydrostatic pressure
Pushing force ( moving out )
Fluid regulation
Kidney
Main organ for excretion & regulation of F&E
( urine )
3 process:
o Glomerular filtration
o Tubular reabsorption
o Tubular secretion
ANP ( Anti Natriuretic Peptide ) sodium
Atrium of the heart( stretch )
Potent diuretic / reduce thirst
Thirst mechanism ( earliest sign of FVD )
o Dry mouth ( xerostamia )
o Hyperosmolarity
ADH ( Anti Diuretic Hormone) - vasopressin
Released by Neurohyphopysis
Synthesize in the Hypothalamus
FLUID & ELECTROLYTES
Amount & Composition:
Intracellular: ( 2/3 fluid )
Extracellular :
Intravascular ( 3L ) plasma ( 90%)
Interstitial ( 11 – 12L ) lymphatic fluid
Transcellular (1L ) specific function
o Cerebrospinal, pericardial,
pancreatic, pleural, intraocular,
biliary, peritoneal, synovial fluid
-
Increase serum osmolarity. ADH is produced
– collecting ducts become permeable
RAAS ( Renin Angiotensin Aldosterone System )
Juxtaglomerular cell of the kidney initiates
RAAS
Baroreceptors ( pressure detectors )
Osmoreceptors ( osmolarity detectors )
-
Electrolytes
Active chemicals in the plasma ( ions )
Functions:
Maintaining fluid balance
Acid base regulation
Transmitting neuromuscular reaction
Dynamic transport of F&E
Passive ( - )ATP
o Diffusion ( H – L ) particles
o Osmosis ( L – H ) water
o Filtration ( H – L movement of
F & E in a semi permeable
membrane
Active ( + )ATP
o Sodium – Potassium pump (
balance the potassium )
FLUID VOLUME DISTURBANCES
HYPOVOLEMIA
Fluid volume deficit
When loss of ECF exceed the intake of fluid
Fluid not sufficient to meet the fluid needs of
the body
Causes:
Inadequate fluid intake
Risk:
NPO
Comatose
Impaired mental status
Lack of access of fluid ( rare )
Abnormal fluid loss
Vomiting
Diarrhea
GI suctioning
Colostomy
Excessive sweating
Hemorrhage
Disorder that increase fluid loss
DI ( decrease ADH )
DM
o Polyfagia
o Polydypsia
o Polyuria
ARF ( diuretic phase )
Hyperthyroidism
o Increase metabolic rate
o Diaphoresis
Adrenal insufficiency
o Addisons disease.
o Regulate

Sugar

Salt

Sex
Third space fluid shifting
Fluid accumulate in a certain parts of the
body which is not necessary ( non functional )
o Pathologic in origin
o Disease
o Burns edema
Types
Isotonic
o Electrolytes loss equals to Fluid
loss
Hypotonic
o Electrolyte loss less than or equals
to Fluid loss
Hypertonic ( most common )
o Fluid loss greater than Electrolyte
loss
CM:
Thirst
Decreased skin turgor
Weight loss
Oliguria / concentrated urine
o 1.02 – 1.025cc/hr
Weal / rapid HR
Flattened neck vein
Delayed capillary refill
Warm, dry skin
Muscle weakness & cramps
Sunken fontanels & eyeballs
Assessment & DX findings
Blood osmolarity
Hematocrit ( decrease in plasma )
Urine specific gravity
Low central venous pressure
( 2 – 6mmHg )
Changes in V/S ( hypo-tachy-tachy )
TX:
Goal
-
Fluid replacement
TUC
-
Promote safety
Oral care & skin care
Encourage OFI ( mild – moderate )
Monitor for V/S, I & O, weight & LOC
NI:
WHO
No dehydration
DOH
Mild dehydration
5 – 10% TBW
Some
dehydration
Moderate dehydration
(Insatiable thirst)
10% TBW
Severe
dehydration
Severe dehydration
(too weak to move )
< 5%TBW
HYPERVOLEMIA
Fluid volume excess
Result from either:
o Increase in water / sodium
o Decrease in water / sodium
excretion
Types
Isotonic
o Electrolytes equals to Fluid
Hypertonic
o Electrolyte greater than Fluid
Hypotonic ( most common )
o Electrolyte less than or equals to
Fluid
Causes:
Excessive IVF therapy ( fluid overload )
Renal failure ( oliguric phase ) CRF – ESRD
(anemia)
Long term corticosteroid ( Na+ reabsorption )
SIADH
CHF
CM:
Edema
Distended neck vein
Abnormal lung sounds
SOB
Polyuria ( diluted urine ) except SIADH
Assessment & DX findings:
Blood osmolarity
Hematocrit
-
BUN ( renal function test)
Urine specific gravity
Bounding pulse rate
Increase BP
-
Prevent further fluid overload
TUC
-
Restrict fluid & Na+ intake
Monitor V/S ( bp ), I & o, weight & LOC
WOF complication
TX:
NI:
-
NI:
-
ELECTROLYTE IMBALANCE
SODIUM IMBALANCE NA+
135 – 145meq/L ( normal )
Primary determinant of Osmolarity
Responsible for excitability of the
neuromuscular junction
Regulated by ADH, ANP, RAAS & thirst
mechanism
HYPONATREMIA
Less than 135meq/L
Causes:
Inadequate intake
Increased excretion
o Vomiting, diarrhea, excessive
diaphoresis & dieresis of fluid /
sodium
Water excess ( dilutional hyponatremia )
o Excessive intake of hypotonic fluids
o Disorders that result to water
retention
S/S:
Anorexia, Nausea & Vomiting
Headache & Dizziness
Alteration of LOC
Muscle cramps & Weakness
Edema & Low BP
Laboratory findings
Serum sodium
Urine sodium
Urine specific gravity
Osmolarity
TX:
Sodium replacement
o Hyper Osmolar Demyelination
(complication of Na+ replacement)
<12meq/L for 24hrs
Water restriction for dilutional
hyponatremia
TUC
Enforce high sodium diet
o Avoid SPC ( sauce, process food,
canned goods
Promote safety
HYPERNATREMIA
Greater than 145meq/L
Causin crenation ( shrinking of cell )
Causes:
Decreased sodium excretion
o Corticosteroid
o Cushing syndrome ( hyper activity
of adrenal gland )
o Conn’s disease
Increased sodium intake
Decreased water intake
Increased water loss
Assessment
Thirst
Dry sticky mucus membrane
Flush skin ( hyperemia )
Peripheral / pulmonary edema
Oliguria
Increase deep tendon reflexes
Alteration of LOC
Laboratory findings
Serum sodium
Urine sodium
Urine specific gravity
Osmolarity
TX:
Increase fluid
Restrict sodium
Promote sodium excretion
Promote safety
Monitor V/S and I & O
POTASSIUM IMBALANCE (K+)
3.5 – 5meq/L
Major intracellular cation
Important for neuromuscular function
Regulated by kidney & aldosteron
HYPOKALEMIA
Below 3.5meq/L
Causes:
Decreased potassium intake
Excessive potassium loss
o Use of diuretics / corticosteroid
o Vomiting & diarrhea
o Disorder that increase K+ excretion
Movement from ECF to ICF
o Alkalosis
o Hyperinsulinism
CM:
Cardiovascular
o Weak, Thready pulse & Hypotension
o Dysrhythmia
Respiratory
o Shallow & Ineffective respiration
Neuromuscular
o Confusion, Lethargy & Coma
o Muscle weakness, Leg carmaps &
Paresthesia
o Deep Tendon Hyporeflexia
Gastro Intestinal
o Decreased motility
DX:
ECG changes
o Flat or inverted T wave
o Low ST segment
o High U wave
Complication
Dysrhythmia
Metabolic alkalosis
Respiratory failure
TX:
Potassium replacement
o Encourage intake of K+ ( ABCPOT )

Avocado / Apricot

Banana

Carrot / Cantalope

Potato

Orange

Tomato
Administer K+ supplement
TUC
Provide sympthomatic treatment
WOF complication
Remember: UNANO
U – rine output greater than 30cc/hr
N – ever via Bolus
A – ssess IV site ( phlebitis )
N – not more than 1meq/10cc (PNSS)
`
O – n cardiac monitor if greater than
10meq/hr
HYPERKALEMIA
Greater than 5meq/L
Causes:
Excessive intake of K+ rich food/ medication
Decreased K+ excretion
o Use of Potassium Sparing Diuretics
o Renal failure
o Adrenal failure
Movement of K+ from ICF – ECF
o Tissue damage
o Acidosis
CM:
Cardiovascular
o Dysrhythmia
Respiratory
o DOB ( late )
Neuromuscular
o Early

Muscle twitching & spasm
o Late

Muscle weakness, flaccid
& paralysis
Gastro Intestinal
o increased motility
DX: findings
ECG changes
o Tall peaked T wave
o Wide QRS complex
o Prolonged PR intervals
o Flat P wave
Complication
Dysrhytmia
Metabolic acidosis
Respiratory failure
TX:
Restrict K+ intake
Dialysis
WOF complication
Pharmacotherapy
Potassium excreting diuretics
Polysterine Sulfonate ( Kayexalate ) Na+ resin
exchange
Regular insulin & IV glucose
Calcium Gluconate
Sodium Bicarbonate
CALCIUM IMBALANCE ( CA+ )
8.6 – 10.2meq/dl ( serum)
Regulated by PTH & Calcitonin ( thyroid )
1% serum - 99% bone ( hydroxyl apatite
crystals )
Bone strength / density
Calcium is inversely proportional to
Phosphorus
Function
-
Forms:
-
Transmission of nerve impulse
Necessary for blood coagulation
Cloting factor #4
Decreases cellular membrane permeability
o Decrease Serum Ca+ stimulate the
Parathyroid gland to secrete PTH
which will trigger Osteoclastic
activity
o Increase serum Ca+ stimulate
Parathyroid gland to secrete
Calcitonin which trigger
Osteoblastic activity
Ionized: (4.5 – 5.1mg/dL ) 50% physiologic
active
Bound / Complexed ( citrate/phosphate )
HYPOCALCEMIA
Less than 8.6mg/dL
Causes:
Decrease Ca+ absorption
Inadequate intake of Ca+
Inadequate intake of Vit. D
Malabsorption (Cronhs disease/ulcerative
colitis)
ESRD
Disorder resulting to Steatorrhea
Hypoparathyroidism
Increase Ca+ excretion
Renal disease ( diuretic phase )
Massive blood transfusion ( citrate )
anticoagulant
Hyperphosphatemia
Pancreatitis ( lipolysis ) increase FFA – Ca+
binds to FFA
CM: Fast & High
CNS:
Tingling sensation & Seizures
GI:
Increased peristalsis
CV:
Dysrhytmia
RESP:
Laryngospasm
MUSCOSKELETAL:
Muscle spasm, & Tetany ( + )Trousseaus &
Chvostek sign
Risk for:
TX:
-
Osteoporosis
Bone fracture
Bleeding
High Ca+ diet
Calcium supplementation
Promote safety
Monitor Cardio – Respiratory function
( dysrhytmia )
Pharmacotherapy
Calcium Gluconate 10%
Aluminum Hydroxide ( Amphogel )
phosphate binding agent
HYPERCALCEMIA
Greater than 10.2mg/dL
Causes:
Increase Ca+ absorption / intake
Decrease Ca+ excretion
Increase Ca+ resorption
o Hypothyroidism
o Malignancy ( ectopic PTH )
o Immobility stimulate Osteclast
(physical stress stimulate
Osteoblast )
o Hemoconcentration
o Use of Thiazide Diuretics
CM: Low & Slow
Decrease neuromuscular activity
o Muscle weakness
o Diminished ( absent of deep tendon
reflex )
o Lethargy & Coma
ECG changes
Gastro Intestinal disturbances
o Anorexia, nausea & Vomiting
o Decrease Bowel movement
Formation of Renal Calculi
Decrease Bone density
TX:
Decrease calcium in diet
WOF complication of hypercalcemia
Increase OFI
Pharmacotherapy
PNSS
Phosphorus
Calcitonin
Mithracin (antineoplastic antibiotic)
decrease serum Ca+
MAGNESIUM IMBALANCES ( MG+ )
1.6 – 2.3meq/L
Necessary for Carbohydrates & Protein
metabolism
Inhibits the production of Acethylcholine (
muscular contraction )
HYPOMAGNESEMIA
Less than 1.6meq/L ( vasoconstriction )
Causes:
Insufficient Mg+ intake
Increase Mg+ secretion
Assessment: High & Fast
Cardiovascular
o ECG chages
o Tachycardia ( hypertension )
Neuromuscular
o (+) Trousseaus & Chvostek sign
o Hyperreflexia
o Tetany & Seizures
o Muscle twitching
TX:
Increase Mg+ diet
Promote safety
WOF complication
Pharmacotherapy
Mg+ sulfate ( IV )
o B – lood pressure
o U – rine output ( oliguria: 30cc/hr )
o R – espiratory rate ( <12cpm )
o P – atellar reflex ( absent )
HYPERMAGNESEMIA
Greater than 2.3meq/L
Causes:
Excessive intake of Mg+
Decreased Mg+ excretion
Assessment: Low & Slow
-
-
Neuromuscular
o Hypoflexia
o Drowsiness / Lethargy
o Skeletal muscle weakness
Cardiovascular
o ECG changes
o Bradycardia / hypotension
Respiratory depression
TX:
Decrease Mg+ in diet
D/C of Mg+ based antacid
Pharmacotherapy
Diuretics
Calcium Gluconate ( antidote to Mg+ toxicity)
IV Therapy
Purpose:
Replacement therapy ( F & E )
Provide vascular access ( blood products
medication )
Types of solution
Colloids ( Albumin / Dextran )
Increasevascular volume rapidly
Tonicity ( strength to provide osmotic forces )
o Isotonic ( same osmolarity as body
fluids ) 154meq/ L ( Na+/CL+ )

9% NaCl

PNSS ( plain normal saline
solution )
o Hypotonic ( lower osmolarity – fluid
moves out to ICF – cell will swell –
Lysis ( rupture ) 7.7meq/L = NaCl

( Less than 9% is
hypotonic )

.45%NaCl ( half strength)
NSS

25% dextrose in water

2% dextrose in water

Precaution:
pulmonary
edema, cerebral
edema, heart
failure, increase
ICP
o Hypertonic ( higher osmolarity –
increase osmotic pressure )

3% NaCl ( 513 me/L of
NaCl )

5% NaCl (856meq/L of
NaCl )

Lactate Ringer – cell
shrink – Crenate
Lactate Ringer ( Hartman Solution )
Na+:
130meq
Cl+:
109meq
Lactate
28meq
K+:
4meq
Ca+:
3 meq
Parenteral Nutrition
Least desire option
Nutrition via Vein
Indication
Severely dysfunctional or non functional GI
Need to rest GI ( severe abdominal surgery )
Need to meet high nutritional requirement
Types of PN ( 5 – 70% vary CHO )
TPN
Large concentration of CHO >10%
Long term PN ( > 1 week insertion )
Intrajugular / Subclavian ( > 1 week - < 1
month )
o PICC ( Peripheral Inserted Central
Catheter ) > 1 month ( antecubital
vein) x ray
PPN
Small concentration ( < 10% CHO )
Short term PN ( < 1 week )
Arm
Complication
H – yperglycemia
A – ir embolism ( ask patient to perform
valsalva maneuver
P – neumothorax
I – nfection
ACID – BASE IMBALANCE
Concentration of H+ ion ( 7.35 – 7.45pH )
< 7.35pH ( acidosis )
o Respiratory acidosis ( inc. H2CO3 )
o Metabolic alkalosis ( dec. HCO3 )
> 7.45pH ( alkalosis )
o Respiratory alkalosis ( dec H2CO3 )
o Metabolic alkalosis ( inc. HCO3 )
REGULATORY SYSTEM OF BLOOD PH
Carbonic Acid – Bicarbonic System
Normal ratio: 20:1 ( Henderson - Hasselbach
equation )
20 : 1
HCO3
( Kidney )
Hour / Days
-
o
o
o
o
H2CO3
( Lungs regulates amount of
CO3 )
Seconds / Hours
Carbonic acid is controlled by retention or
excretion of carbon dioxide
Bicarbonate is released / excreted by kidney
Potassium plays an exchange role
H+ exchange to potassium (compensation )
Plasma – Protein System
Have the ability to attract or release
hydrogen ions ( albumin – strongest )
Respiratory Acidosis
Carbonic acid excess
Cause:
Carbon dioxide retention
Disorder that result to respiratory disorder
o B-rain trauma
o A-sthma
o H-ypoventilation
o A-telectasis
o P-neumonia
o E-mphysema
o P-ulmonary edema
o U-se of CNS depressants
CM:
Increase Blood pressure, Heart rate,
Repsiratory rate
Increase ICP ( cerebral vasodilation ) acidosis
Depression of CNS
o Disorientation
o Drowsiness

Monroe Kellie Hypothesis
( cranium close cavity )

Brain Herniation
(dangerous )
NI:
TUC
Promote / Monitor oxygenation
Monitor electrolyte value
Prepare for ET / Mechanical ventilation
WOF complication
Respiratory alkalosis
Carbonic acid deficit
Cause:
Carbon dioxide over excretion
Disorder resulting to respiratory alkalosis
o Hyperventilation
Hysteria & Anxiety
Fever
Pain
Over ventilation by mechanical
ventilation
CM:
-
Light headedness ( initial )
Sign of hypokalemia
Tachycardia
Tetany / Muscle twitching
Seizures ( over stimulated CNS )
-
Alleviate anxiety
Encourage proper breathing pattern
Promote CO2 breath
Monitor electrolytes
NI:
METABOLIC ACIDOSIS
Bicarbonate acidosis or deficit
Cause:
Diabetic Ketoacidosis ( faster than ketone
rate oxidation )
Excessive ingestion of ASA
Insufficient CHO metabolism
Malnutrition
Renal failure
Severe diarrhea
CM:
Kussmaul Respiration (increase rate / depth)
Sign of hyperkalemia
Drowsiness / Lethargy
Coma
TX:
Fluid replacement
Promote safety
Pharmacotherapy
Sodium Bicarbonate
o TUC
o WOF complication
METABOLIC ALKALOSIS
Bicarbonate excess
Cause:
Excessive vomiting
Gastrointestinal suctioning
Hyperaldosteronism
Massive blood transfusion ( citrate repel /
bind to H+ )
CM:
Hypoventilation
-
Sign of hypokalemia
Tetany & muscle twitching
Seizures
TX:
Safety
Pharmacotherapy
NaCl ammonium chloride
Carbonic Anhydrase Inhibitors
o Identify & TUC
o WOF complication
ABG ( ARTERIAL BLOOD GAS )
Normal values:
PO2 ( 80 – 100mmHg )
pH ( 7.35 – 7.45pH )
o Acidosis ( < 7.35 )
o Alkalosis ( > 7.45 )
PCO2 ( 35 – 45mmHg )
o Acidosis ( > 45mmHg )
o Alkalosis ( < 35mmHg )
PHCO3 ( 22 – 26mmHg )
o Acidosis ( < 22mmHg )
o Alkalosis ( > 26mmHg )
Steps:
1st
Analyze the data:
Ex.
pH:
7.23
( acidosis )
PCO2:
21
( acidosis )
PCO3:
27
( alkalosis )
nd
2
Identify etiology
Check for the same value of pH
pH 7.23( acidosis)
PCO2(acidosis)= respiratory
acidosis
3rd
Check or identify compensation (if normal)
PCO2:
21 ( acidosis )
PCO3:
27 ( alkalosis )
Compensated
th
4
Identify the degree ( totally / partially )
If the pH is normal ( totally )
GENITO – URINARY SYSTEM
Maintain homeostasis by regulating fluid
component & volume
o
-
-
-
Kidney
-
Ureter
-
T12 – L3 vertebra ( costovetebral angle )
Retroperitoneal area
Enclosed by fibro renal capsule ( shiny
appearance – fatty layer – adipose tissue )
attach to muscular wall
25 – 30mm
Transport urine ( renal pelvis – bladder )
Obliquely inserted ( ureterovesicular
sphincter ) urinary reflux
Urethra
5 – 7 inches ( male )
o Posteriorly – Lateraly to prostate
1 ½ - 2 ½ inches ( female )
o Risk for UTI
Bladder
Reservoir of urine
Detruser muscle / smooth muscle ( excreting
urine )
1000cc maximum capacity ( disorder )
400 – 500cc ( physiologic )
200 – 250cc ( void reflex )
Stretch receptor stimulate detruser muscle
Cortex
o Superficial parts of the kidney
Medulla
o Innermost part of the kidney that
contains the renal/medullary
pyramids
o Contains calyces that collects urine

Calyces - branch into the
renal pelvis ( basin like
cavity )
Adrenal glands ( located in the top of the
kidney )
Nephrons ( urine formation ) basic functional unit of
the kidney
-
-
-
-
-
-
-
3 parts of kidney
Parts:
-
-
-
Afferent arteriole
o The artery that subdivides into the
capillaries that compose the
glomerulus
Bowman's capsule
o The cup-shaped capsule that
encompasses the glomerulus and
draws filtrate from the blood
Brush border
-
Microscopic protrusions that
increase the surface area for
reabsorption
Cortical nephron
o A nephron whose loop of Henle
does not extend past the cortex
Distal convoluted duct
o The portion of the renal tubule in
the nephron between the
ascending limb of the loop of Henle
and the collecting duct
Efferent arteriole
o The artery that is formed when the
capillaries in the glomerulus
converge
Filtrate
o The fluid in the renal tubule which
consists of water, urea, salts, and
other small molecules found in
blood
Filtration
o The process by which filtrate enters
the renal tubule without allowing
blood
Glomerulus
o A ball of capillaries that secretes
filtrate into the Bowman's capsule
Juxtamedullary nephron
o A nephron whose loop of Henle
extends past the cortex and well
into the medulla
Loop of Henle
o A long, narrow portion of the renal
tubule which extends into the
deeper tissue of the kidney
Peritubular capillaries
o The capillaries that weave around
and between the proximal and
distal convoluted tubules
Podocytes
o Selectively permeable cells on the
capillaries of the glomerulus that
allow water and small solutes into
the Bowman's capsule, but not
blood
Proximal convoluted duct
o The portion of the renal tubule in
the nephron between the
Bowman's capsule and the
descending limb of the loop of
Henle
Reabsorption
o The movement of substances from
the filtrate back into the interstitial
fluid so as to be readmitted into the
blood stream
Renal tubule
o The tube through which filtrate
passes as it is converted into urine
in the nephron
Secretion
o The addition of plasma solutes into
the filtrate from the interstitial fluid
How does kidney works?
Kidney – blood supplied – renal arteries – nephrons (
separate waste – clean bloods )
Waste ( ammonia, urea, excess fluids &
electrolytes )
Clean blood ( renal veins to circulation )
Process:
Glomerular filtration
Tubular reabsorption
Tubular secretion
Cystoscopy – direct visualization of Urethra, Bladder &
Urethral opening using a cystoscope
NI:
Before:
Must secure a consent
Lithotomy position
After:
Increase fluid intake ( to promote urination )
Assess urine output ( pink tinged color is
normal within 24hrs )
Relieve discomfort ( hot seat bag / warm
compress )
KUB ( kidney, urethra, bladder x-ray visualization )
NI:
Bowel preparation as ordered
o Laxative ( night before procedure )
o Enema ( morning before procedure)
Assure that the procedure is painless
IVP ( intravenous pyelography )
Indirect visualization with contrast medium
NI:
Before:
Written consent
Assess for allergy to iodine
o Antihistamine – allergy
o Epinephrine – anaphylactic shock
Bowel preparation
After:
Increase fluid intake ( for excretion of dye )
Assess voiding pattern ( to determine
excretion of dye )
UTZ ( ultrasound )
Soundwave
Deyecys tumor, obstruction & cyst
NI:
Bowel preparation
Distend the bladder ( drink 2 – 3 glass of
water 3omin before procedure )
Renal biopsy – removal of living renal tissue for
microscopic examination. Most accurate in malignancy
& cancer.
NI:
Before:
Check for bleeding parameters ( inr, apt, ptt,
pc )
Mild sedation is done
Prone position
Local anesthesia
Ask client to hold breath
After:
Bed rest
Monitor for bleeding & V/S ( hypo-tachytachy
Increased oral fluid intake
Risk:
Bleeding
Infection
Function of kidney
Remove waste
Regulate fluid &electrolyte
Restore pH balance
Nephrotoxic agent
A – minoglycoside
N – SAIDs
T – etracycline
A – ntineoplastic
V – ancomycin
A – mpothericin B
Type of shock
Cardiogenic
Anaphylactic
Septic
Hypovolemic
Neurogenic
-
Distributive
DISORDER OF GENITO-URINARY TRACT
RENAL FAILURE
CHRONIC RENAL FAILURE ( CRF )
Gradual & progressive loss of renal function
Irreversible
Cause:
DM ( diabetic nephropathy )
HPN ( hypertension nephrosclerosis )
Chronic Glomerulonephritis
Autoimmune disorders ( incompetent
suppressor T-cell )- SLE / Lupus nephritis
Advancement of acute renal failure
Staging: CRF
( old )
Renal impairment
40 – 50% GFR
Renal insufficiency
20 – 40% GFR
Renal failure
10 – 20% GFR
ESRD
<10% GFR
( new )
Stage I
> 90ml/min
Stage II
60 – 89ml/min
Stage III
30 – 59ml/min
Stage IV
15 – 29ml/min
Stage V
< 15ml/min
CM:
Inability to excrete metabolic waste
o Increased BUN & serum creatinine

BUN: 10 – 20mg/dl

Creatinine: .6 – 1.2mg/dl
o Stomatitis & GI bleeding
o Urineferous breath
o Hyperpigmentation ( increase
urochrome )
o Uremic frost ( severe dryness/
itchiness of the skin )
o Decrease libido
Complication
Renal Encephalopathy
Inability to secrete erythropoietin
o Severe & Chronic Anemia
Inability of the kidney to regulate fluid &
electrolyte
o Oliguria
o Edema
o Hyperkalemia
o Hypermagnesemia
-
o Sodium imbalances
o Metabolic acidosis
Inability to activate Vit.D
Urine
output
Electrolyte
Urine
< 4L/day
Oliguric
phase
>Dilutional
hyponatremia
>Hyperkalemia
concentrated
4L/day
Diuretic
phase
>True
hyponatremia
>Hypokalemia
diluted
o
o
o
o
>Increase BP,
BUN, creatinine
>Pulmonary
edema
>fluid volume
excess
>decrease BP
>Hypovolemic
Shock
>fluid volume
deficit
Hypercalcemia
Hyperphosphatemia
Hyperparathyroidism
Hyperosteodysthropy
TX:
-
-
-
-
Fluid restriction ( 800cc/day )
Electrolyte control
Proper diet
o Increase CHO
o Decrease CHON,Na+,K+ & fluid
Treat complication
o Anemia ( epoitin alfa / epogen alfa
– subQ )
o GI disturbances
o CHF
o HPN
Dialysis
Renal transplant
o
GVHD – graft vs. host disease
( immunosuppressant ) – cyclosporin
( prograft/prednisone )
Promote comfort
ACUTE RENAL FAILURE
Sudden loss of renal function
Reversible
Cause:
Pre renal ( decrease renal perfusion – before kidney )
Renal artery obstruction
Infarction
Cardiac disorder
Hypovolemia
Shock
Intra renal ( inside the kidney )
Pigment nephropathy
Acute tubular necrosis
Acute glomerulonephritis
Acute pyelonephritis
Nephrotoxicity
Post renal ( obstruction of renal outflow )
Benign prostatic hyperplasia
Blood clots
Calculi
Tumor
Phase:
Onset: from exposure to precipitating factor
Oliguric / Anemic phase ( 1 – 3 weeks )
Diuretic phase ( 1 week )
Recovery phase ( 1 – 2 years ) 80% recovery
DIALYSIS
Acute renal failure & chronic renal failure
with severe fluid excess, electrolyte
imbalances
2 types:
Coupling ( 1x use )
Reprocessing ( 4x use – ideally ) ( 6x
maximum )
HEMODIALYSIS
Requires vascular access ( subclavian, intra
jugular, femoral )
Dialyzate solution ( non sterile )
Indication
Acute renal replacement ( temporary )
Chronic renal replacement ( permanent )
Types of vascular access
AV graft
o Surgical connection ( synthetic
blood vessel ) GORETEX
o For geriatric patient with
inadequate blood vessel ( 1 month )
External AV graft
o Outside the body
o Silastic cannula
AV fistula
o Most common form
o Anastomosis ( 1 – 2 months )
Subclavian / intrajugular / femoral vein
catheter
o 6 weeks ( risk for infection )
Nursing care:
Arm precaution on patient with AV access
Assess for patency of AV access
o Bruit ( auscultate )
o Thrill ( palpate )
Monitor V/S & LOC ( q30 )
Omit hypertensive medication ( 24hrs )
Promote comfort ( 3 – 4hrs / 2 – 3weeks )
Monitor weight
o Actual weight - Target weight
Assess for bleeding ( heparin bolus )
Provide adequate nutrition ( first 2hrs patient
can eat anything )
Complication
Air embolism ( rare )
Infection ( reprocessing or reuse of dialyzer )
Painful muscle cramps ( incompliant patient )
Dialysis encephalopathy ( aluminum toxicity /
dialyzate solution is not good )
Disequilibrium syndrome ( CNS disturbances )
st
o 1 timer ( decrease duration of HD )
PERITONEAL DIALYSIS
No dialyzer
Peritoneum acts as a dialyzing membrane
Dialyzate solution ( sterile )
Indication
Susceptible to rapid fluid , electrolyte &
metabolic changes duing HD ( 36 – 48hrs )
Insertion
Site: 3 – 5cm below umbilicus ( avascular )
TENCKHOOF CATHETER
Nursing care
1st few bottle will have pink tinged drainage
Warm the dialyzate ( to promote vasodilation
) removal of extra waste & avoid abdominal
cramping
WOF peritonitis ( cloudy drainage
If drain stops put patient in side lying position
Process:
Infusion ( introduce dialyzate ) 5 – 10min
Dwelling ( solution stay in the peritoneum
membrane ) 20 – 30min
Drainage ( drain the solution ) 10 – 20min
o Clamp ( regulator )
o Dialyzate ( increase dextrose
content )
o Every 1 cycle – 2L
CAPD( continuous ambulatory peritoneal dialysis )
URINARY CALCULI
Stone in the urinary tract
70% of stone formed in the kidney
Types of stone
Alkaline stone
o Calcium phosphate
75%
o Calcium oxalate
o Struvite - staghorn

Magnesium

Ammonia

Phosphate

Urease splitting
microorganism

Klebsiella

Pseudomonas

Staphylococcus

Streptococcus
Acidic stone
o Uric acid ( hyperuricemia )

Gout ( inherited disorder
of urine metabolism )
o Cystine stone ( malabsorption of
cystine )
Most common causes
Hypercalcemia
Urinary stasis
Dehydration
Elevated uric acid
UTI
Diagnostic procedure
KUB
IVP
CT scanning
Renal UTZ
CM:
Renal colic ( sudden severe sharp pain from
lumbar – abdominal – testicle )
GI disturbances ( nerve plexus – genito
intestinal reflex )
o Anorexia / vomitting
o Diarrhea / constipation
Changes in bladder pattern
o Dysuria
o Urine frequency
TX:
Increase oral fluid intake
Strain all urine
Pain management
Nutritional therapy
Calcium phosphate stones
o
Acid ash diet ( cranberries,
plums,prunes )
o Low calcium/phosphate diet
Calcium oxalate stones
o Acid ash diet
o Low calcium / oxalate diet
Struvite
o Acid ash diet
o Low phosphorus diet
Uric acid stones
o Alkaline ash diet

Fruits except CPP
o Low purine diet
Cystine stone
o Alkaline ash diet
Medical intervention
Pharmacotherapy
Calcium stones
o Aluminum Chloride / Calcibind
Phosphate stones
o Amphogel
Uric stones
o Allupurinol
Stone removal
Extracorporeal Shockwave Lithotripsy
Surgery
Nephrolithotomy
Pyelolithotomy
Ureterolithotomy
NEPHROTIC SYNDROME
Caused by glomerular drainage / increased
glomerular permeability
Risk factor
Not a specific disease ( complication )
Malignancy
DM / HPN
Toxins
CM:
Proteinuria ( albuminemia )
Microscopic or no hematuria
Hypoalbuminemia
Edema
Elevated serum cholesterol
o Breaking down of lipoprotein
Malaise / easy fatigability
Irritability / headache
TX:
Medical management
o Bed rest
o High protein diet
o Low sodium diet
Pharmacotherapy
o Anitlipidemics ( statin )
o Diuretics
o Plasma / volume expanders
NI:
-
Monitor hydration status
Promote safety
GLOMERULONEPHRITIS
Inflammation of glomerular capillaries
Cause
Post infection ( GABHS )
Auto immune disorders
o Antigen antibody complex
Type
Acute ( 2 – 3 weeks after streptococcal
infection)
Chronic ( slow progression)
Assessment
Proteinuria
Periorbital / facial edema
Cloudy smoky urine
Pallor
Irritability / lethargy
Hypertension
Severe sign of ARF ( oliguric phase )
Laboratory findings
Elevated Aso titer
Increased BUN / creatinine
NI:
Monitor V/S & hydration status
Limit activity / provide safety measure
WOF complication
Pharmacotherapy
Diuretic
Antihypertensive ( ACE inhibitors )
Anitibiotics
PYELONEPHRITIS
Inflammation of renal pelvis ( basin like )
Cause
Ascending infection ( urine )
Systemic spread of infection ( blood )
2 types
Acute pyelonephritis ( enlarge kidney /
interstitial infiltration )
-
Chronic pyelonephritis ( contracted & scar
kidney )
CM:
Fever & chills
Leukocytosis
Bactenuria & Pyuria
Flank pain
Dysuria ( kidney punch )
DX procedure
UTZ
CT scan
IVP
TX:
Usually on outpatient basis ( if not
complicated )
Increase oral fluid intake
Antibiotic ( 2 weeks )
o Fluoroquinolone
o Cotrimaxazole
o Cephalexin
Uralgesic ( phenizopyridine ) pyridium
o Red orange urine ( normal
o Absence of pain to test efficiency
WILMS TUMOR
Encapsulated tumor of the kidney
Rapid proliferation of the rhinoblast
Assessment
Non tender mass
Hematuria
Lethargy
Anorexia
DX:
UTZ
CT scan
MRI
TX:
Surgical removal of tumor
o Chemotherapy / radiation

Before - for tumor to
shrink

After – to prevent
metastasis or recurrent
URINARY TRACT INFECTION
Urethra ( urethritis )
Ureter ( ureteritis )
Baldder ( cystitis )
Female is high at risk
E. coli ( most common causative agent )
Risk factor
Incomplete bladder emptying
Immunosuppresion ( iatrogenic/pathogenic )
Instrumentation
DM
Pregnancy
CM:
F-requency
U-rgency
C-hills
K-( cloudy urine )
E-levated temperature
D-ysuria
S-uprapubic pain
DX:
Routine urinalysis
o Increase WBC
o Bacteruria
o Pyuria
Urine C&S
NI:
Increase oral fluid intake
Acidify urine ( CPP)
Relieve pain ( pyridium )
4W
o Water therapy
o Wash after sex
o Wear cotton underwear
o Wife ( front to back )
Avoid urinary stasis
Empty bladder after sex
Pharmacotherapy
Uralgesic ( phenazopyridine )
Urinary antiseptic
Antibiotic
o Fluoroquinolone ( floxacin )
o Sulfonamides ( sulfadiazine )
At risk : Steven Johnson Syndrome ( crystanuria )
Exposure to radiation
Common site of metastasis
Liver
Bones
Lungs
Assessment
Painless hematuria ( initial sign / most
characteristics )
Dysuira ( late sign )
Urinary frequency
Urgency
DX:
Bladder wash specimen
Biopsy
NI:
Treatment for cancer ( surgical intervention )
Cystectomy ( urinary diversion )
o ILEAL CONDUIT ( ileum is cut and
connected through anastomosis
Cutaneous ureterostomy
Indiana pouch (straight catheter for draining)
BLADDER CANCER
Papillomatous growth ( pre cancerous )
Undergoes malignant change
Infiltrate bladder cell wall
Common among males
Predisposing factors
Cigarette smoking
Exposure to industrial chemicals
TX:
Surgical intervention
Transurethral resection of the prostate
o Continuous bladder irrigation
Suprapubic prostectomy
Retropubic prostectomy
Perinial prostectomy
BPH ( BENIGN PROSTATIC HYPERPLASIA )
Prostate enlargement
Cause is unknown
Resulting to comprehension of the urethra
Complication
Renal failure
UTI
Renal calculi
Assessment
Nocturia
Frequency, urgency, hesitancy
Increased residual urine
Decreased projectile force of the urine
Hematuria
DX:
Cystoscopy
UTZ
Digital rectal examination
ENDOCRINE
2 types
CM:
o
o
-
Exocrine ( w duct )
Endocrine ( w/ out duct )
Pineal Gland
is a small endocrine gland in the vertebrate
brain. It produces the serotonin derivative
melatonin, a hormone that affects the
modulation of wake/sleep patterns and
seasonal functions.
Pituitary Gland
o
Located at the selia turcica inferiorly of the hypothalamus (
controlled )
Composed of 2 parts
Anterior ( adenohypophysis ) glandular
Posterior ( neurohypophysis ) nervous (+
feedback mechanism )
o Oxytocin

Milk let down reflex

Increase uterine
contraction
o ADH ( vasopressin )

Controlled osmolarity

Controlled water
reabsorption
DIABETES INSIPIDUS
Decrease ADH
Inability of the renal tubules to retain water
DX:
Water deprivation test
o No water intake ( 8 – 12 hours)
Polyuria
Polydypsia
Constipation
Signs of FVD
TX:
-
Fluid replacement
Monitor V/S & LOC
Monitor hydration status
TUC
o Tumor, surgery stroke,
trauma,infection
Pharmacotherapy
Desmopressin acetate ( DDVAP )
Vasopressin ( pitressin )
Clofibrate ( antilipidemic medication)
SIADH
Excessive water retention
Cause
Brain trauma ( increase ICP )
Cushing triad hyper brady brady
Ectopic ADH production
o Some cell are capable of producing
hormone ( lung carcinoma, CNS
infection, stroke, trauma )
CM:
Edema
Weight gain
HPN
Hyponatremia
Signs of hypovolemia
Decrease urine output ( concentrated )
TX:
Fluid restriction
Monitor V/S
Assess cardio respiratory function
Assess neurological assessment
o Cerebral edema - most feared
o Cushing triad
o Widen pulse pressure
Monitor hydration status
TUC
Pharmacotherapy
Demeclocycline ( Declomycin )
o Antagonize effect of ADH in the
kidney
Diuretics ( loop diuretics )
ADENOHYPOPHYSIS
Samatotropin ( growth hormone )
Stimulates growth
Affect CHO, CHON & fat metabolism
Antagonizing effect of insulin ( hyperglycemia
Prolactin
Necessary for breast development and
lactation
TSH ( thyroid stimulating hormone )
T3 & T4 - Responsible fpr production of TSH
Adrenocorticoid hormone
Stimulates adrenal cortex
MSH ( melanocyte stimulating hormone )
Signals to the brain have effects on appetite
and sexual arousal.
Gonadtropic hormone
TSH & LH
Development of secondary hormone
HYPERPITUITARISM
Hyper function of adenohypophysis
Related disorder
Acromegaly / Gigantism
Gigantism ( increase GH before closure of
epiphyseal plate / lengthening of the bone )
o Epiphyseal line – not active
Acromegaly ( increase GH after closure of
epiphyseal plate / widening of the bone )
Cushing syndrome
Galactorrhea ( excessive milk production )
Hormonal imbalances
TX:
Surgery
Transphenoidal hypophysectomy
o Removal of pituitary – lifetime
hormone replacement therapy

Insition site ( between
upper lip & upper gum
Pharmacotherapy
Bromocriptine ( Parlodel ) only effective in
inhibiting growth hormone
HYPOPITUITARISM
Hypo function of anterior pituitary gland
SSTT & CNS infection
Related disorder
Pituitary dwarfism
-
Panhypopituitarism ( Simon disease )
Post partum pituitary necrosis
o Post partal hemorrhage ( Shechan
disease )
-
HRT ( hormonal replacement therapy )
TUC
TX:
THYROID GLAND
T3 ( triiodothyronine )
T4 ( thyroxine )
o Regulate metabolism
o T3 ( 5x more potent than T4 )
steady metabolic rate
o Stimulates SNS response
CNS underdevelopment ( neurological & psychological
disturbance )
Thyrocalcitonin
Inhibits osteoclastic activity
DX:
TSH assay ( .2 – 5.4mu/ml )’
o Primary hypothyroidism ( problem
is in the thyroid gland itself ) –
decrease T3 – T4 / increase TSH
assay
o Secondary hypothyroidism or
(problem is in the stimulation ) –
increase T3 – T4 / decrease TSH
o Hyperthyroidism – increase T3 – T4
/ decrease TSH assay
T3 : 80 – 230ng/dL (decrease hypothyroidism)
T4 : 5 – 12mcg /dL (increase hyperthyroidism)
Radioactive iodine uptake
Iodine123 ( radionuclide isotope )
o Measure the absorption of iodine
isotope
o Normal value:

3 – 10% at 24hour urine
specimen
-
GOITER
Thyroid scan
o Radio isotope of iodine is
administered before scanning
o Identify nodules ( hot & cold areas )
using gamma camera

Hot ( hyperactivity )

Cold ( hypoactivity )
-
Enlargement of thyroid gland due to increase
TSH
My occur with
o Hyperthyroidism & hyperplasia of
thyroid cell
o Hypothyroidism : Hyperthropy
o Euthyroidism - decrease intake of
iodine
Common types of Goiter
Endemic Goiter
Goiter belt area:
o ( far from sea ) no seafoos w/c is
rich in iodine
o Mountainous regions ( goitrogenic
foods )

Cabbage

Radish

Turnips

Sweet potato

Spinach
Sporadic Goiter
Goitrogenic drugs
o Antithyroid hormones
o Lithium - manic patients
Attention Deficit Hyperactive Disorder
o Methyl Phynedate
o ASA ( acethyl salicylic acid ( inhibits
the production of TSH )
HYPERTHYROIDISM
Increase T3 – T4 & metabolic rate
Metabolism – sum of all biochemical reaction
inside the body
Hypersecretion of thyroid
Incidence higher in females
Graves disease
Most common form
Related to: Stress and infection
Cause: Idiopathic
CM:
High – fast – wet except men ( amenorrhea )
High
Increase neurologic status
Increase BP
Increase temperature
Fast
Fast heart rate
Fast respiratory rate
Wet
Stool & skin
Other manifestation
Heat intolerance
Enlarged thyroid gland
Exopthalmos ( bulging of eyes ) fatty pads
behind the eyes
Dalyrimple sign ( thyroid stare ) infrequent
blinking / the eyeballs irreversible
THYROID STORM ( thyroid crisis )
Severe uncontrolled hyperthyroidism
Hyperpyrexia ( 41 C ) – extreme nervousness,
palpitation, hypertensive crisis
TX:
Safety
High calorie diet
Eye care ( exopthalmos & dalyrimple signs )
Rest
Environment cool
Fluid & electrolytes replacement
Monitor V/S and LOC
Thyrotoxicesis – all clinical manifestation
Pharmacotherapy
Anti thyroid medication
o Iodides – inhibits the release of
thyroid hormones

Mix with H2O or juice,
use straw ( prevent teeth
stain )

SSKI ( saturated solution
of potassium iodide )
Lugols solution
o Thiomides – inhibits synthesis of
thyroid homones

PTU ( proyl thio uracil )

Topazole ( methimazole
carbimazole )
o Antihypertensive
Surgery
Subtotal thyroidectomy ( 5/6 areas of
thyroid )
o Pre op medication – Lugols solution
( to shrink the size of thyroid gland
/ decrease blood supply thyroid
gland
o Post operation – ensure V/S are
stable / support neck
o
o
WOF complication

Injury of the larynx (
speak every hour )

Mild hoarseness
( normal )

Severe
hoarseness (
report )

Hemorrhage

Hypocalcemia (
larygospasm)

Thyoid storm ( deadliest )
Radiation

Radioactive iodine ( I131)
NI:
-
Place client on isolation for few days
Do not use in pregnant women
Pregnancy should be delayed for 6 months
HYPOTHYROIDISM
Hyposecretion of thyroid gland
CM:
Low - Slow - dry except men ( menorrhagia )
Low
Low neurologic status
Low BP
Low temperature
Slow
Heart rate
Respiratory rate
Dry
Stool & skin
Other manifestation
Cold fatigue
Fatigue
Hyperlipidema
Loss of memory ( forgetfulness )
Myxedema Coma – extreme severe stage
Risk for respiratory failure & coma
TX:
Low calorie diet
Assess LOC
Warm environment
Monitor V/S and daily weight
Pharmacotherapy
Thyroid replacement therapy – shynthetic
thyroid hormone
o Levotherapy ( morning to prevent
insomnia / empty stomach )
DISORDER OF THE PARATHYROID GLAND
HYPOTHYROIDISM
Hyposecretion of parathyroid gland
S/S:
Hypocalcemia
Hyperphosphatemia
TX:
Hypocalcemia
o Spinach, anchovies, sardines,
o Calcium gluconate in D5W
Cause
-
-
Congenital ( decrease T3 – T4 ) slow CNS
development
Autoimmune ( myxedema )
o Cretinism ( hypothyroidism in
children)
o
Hashimoto disease ( autoimmune )
Thyroidectomy
Radioactive thyroid
HYPERTHYROIDISM
Hypersecretion of parathyroidism gland
S/S:
Hypercalcemia
Hyperphosphatemia
TX:
Hypercalcemia
o Galium nitrate
DISORDER OF THE PANCREAS
DIABETES MELLITUS
Chronic disorder of the CHO, CHON & fat
metabolism
Cause
Exact cause is still unknown
Predisposing factor
Stress
Heredity ( diabetes induced gene )
Obesity
Autoimmune
Types of DM
Type 1
Insulin dependent
Juvenile onset ( < 30 y/o )
Pathologic etiology
o
Absolute deficiency / no insulin
produced
Insulin treatment
Acute complication
o Diabetic Ketoacidosis
Type 2
Non insulin dependent
Adult onset ( > 30 y/o )
Pathologic etiology
o Lack of insulin
o Insulin resistance ( not recognized
by the cell )
Oral hypoglycemic agent treatment
Complication
o Hyperglycemic Hyperosmolar Non
Ketotic Coma
CM:
Cardinal sign ( 3-P )
o Polyuria ( due to hyperosmolar
diuresis)
o Polydypsia ( due to hyperosmolar
dehydration )
o Polyphagia ( cellular starvation )
-
Associated sign ( 3W )
o Weight loss ( due to prolonged
cellular starvation )
o Wound ( slow to heal )

Diabetic foot ( poor
circulation ) slow to heal
because protein is utilized
– slow tissue repair
o Warm & dry
High risk for ( 3-I )
Infection ( conclusive for bacterial growth )
Inadequate circulation ( atherosclerosis )
Impotent ( impaired circulation in the genital)
Complication
CAD, HPN, PVD
Diabetic nephropathy
Diabetic retinopathy ( impair retinal
circulation )
Diabetic neuropathy ( erectile dysfunction )
DX:
Measurement setting
Normal value
Fosting blood sugar
70 – 110mg/dl
Oral glucose tolerant /
challenge test
30min
2hrs
Remember DASAL:
Down phenomenon – occurs due to
nocturnal release of GH w/c antagonize
insulin
o Diurnal variation ( body clock )
o Night ( increase GH )
o Pre breakfast hyperglycemia
Allergic response – local allergy
o Pruritus
o Itchiness at IV site
Somogye phenomenon
Normal blood sugar
Hypoglycemia ( 2 – 3 am )
Increase intrinsic hyperglycemic hormone
o
GH
o
Norepinephrine / epinephrine
o
Glucagon
o
Glucocorticoids

All are potent that insulin
110 – 170mg / dl
80 – 110mg / dl
Dextrose anhydrase intake
check blood every 2hr
Glycosylated hemoglobin ( <7%
reflects the pt.blood sugar
for the past 3 – 4 months /
percentage of glucose
attached to the cell
TX:
Medication ( type 2 )
Oral Hypoglycemic Agent ( OHA ) teratogenic
ABS
o Alpha glucosidase inhibitor

Moa: decreased
absorption of CHO

Acarbose
o Biguanides

Moa: decrease insulin
resistance

Glucophage ( Metformin )
o Sulfonulureas

Moa: stimulates beta cell

“ ide “

Glipizide

Glimepiride

Glypuride

Chlorpropramide
Insulin ( type 1 )
regular insulin through IV
Rebound hyperglycemia
Tx: Decrease evening dose of insulin or
midnight snack
-
-
Aypoglycemia ( hypoglycemia )
o Very long insulin ( humalog )
o Rapid acting ( humalin R )
o Intermediate ( NPH normal neutral
hagedorn )
o Long acting ( ultra lente )
Assessment:
Tired / Tachycardia
Irritability
Restlessness
Excessive hunger
Diaphoresis ( skin cold & moist )
Lipodystrophy – hardening of the
subcutaneous tissue
o 2.54cm apart or 1 inch from the
previous site
o Do not massage injection site it
may lead to rapid absorption
o Administered insulin at room
temperature
Diet
-
Low calorie diet
High fiber diet
More complex than simple CHO
Activity & exercise
Increase glucose uptake
Monitor glucose
Acute complication
Diabetic Ketoacidosis ( life threatening
complication of DM type 1
Cause
Underdose of insulin
Illness or intection
Stress of injury
Clinical manifestation
Kaussmaul
Acetone breath
Nausea & vomiting
Abdominal pain
TX:
Insulin – insu;in drip
IV rehydration ( PNSS isotonic – to prevent
hyperglycemic rebound )
Sodium bicarbonate
HHNK ( Hyperglycemic Hyperosmolar Nonketotic )
Life threatening complication on patient with
type 2 DM
Severe hyperglycemia without ketoacidosis
Manifestation
Severe hyperglycemia and dehydration
TX:
Same with DKA ( except sodium bicarbonate )
Thyroid gland
o Adams apple / thyroid cartilage
Parathyroid gland
o Side / back of the thyroid
Thymus gland
o Mediastinal spaces
Adrenal glands
o Top of the kidney ( suprarenal )
Pancreas
o Near the stomach
Ovary & testicle
MUSCOLUSKELETAL SYSTEM
Consist:
Muscle, Tendons, Bones, Cartilage together
with the bones
Bones:
206 ( adults )
o
Skeletal ( dried up )
Function:
Locomotion / Skeletal movement ( voluntary)
Protection
Support and Lever
Blood cell production
Storage
2 major components:
Non Living Intracellular Materials:
Mineral ( calcium / phosphorus )
o Ca + Ph = hyaline apatite crystals
Bone matrix
o Collagen – Mucopolysaccharides
Living Cell:
Osteoblast ( bone building cell / formation of
bone matrix )
Stimuli
Activated by
Effect
Osteoblast
Inc. Ca+
Calcitonin
Hypocalcemic
o
o
Lamellae: ( thin sheets of
extracellular matrix ) calcified /
mineralized matrix
Lacunae: ( opening between
lamellae where osteocytes is
located )
Canaliculus ( tiny canal ) passage
way of blood
Osteoclast
Dec. Ca+
PTH
Hypercalcemic
Bone to Serum ( bone resorption )
Serum to Bone ( bone absorption )
Osteoclast ( bone resorption cell ) release of
calcitonin and phosphate from bone
Osteocytes ( mature bone cells ) maintenance
of bone matrix
Skeletal System according to Location:
Axial skeleton:
o Form a longitudinal axis ( skull,
bony thorax, vertebra )
Appendicular skeleton:
o Consist of extremities, hips,
shoulder girdle & pelvic girdle
Types of Bones according to Shape
Long ( L > W ) femur, humerus
Short ( cube ) carpal, tarsals
Flat ( skull, shoulder blades )
Irregular ( vertebrae, stirrups )
Composition of Bone structures
Cancellous Bone ( spongy ) has a small needle
like of bone ( located at epiphysis of a long
bone)
o Trabeculae: irregular layers and
surrounded by red / yellow bone
marrow ( add strength to the bone )
o Haversian systems / Osteon: ( Basic
unit of the Bone )
-
Compact bone - Dense ( smooth appearance )
o Osteon
o Lamellae

Concentric ( inside
osteon)

Circumference ( outside
osteon )

Instertitial ( in between
osteon )
o Haversian Canal / Central Canal
( parallel to the bone )
o Volksmann Canal / Perforating
Canal
( perpendicular to the bone )
*Periosteum: outer layer of the bone ( fibrous
connective tissue )
Long bone
Epiphysis: ( ending of the bone )
-
o Compact ( outside )
o Spongy ( inside )
o Articular cartilage:
o Endosteum
Diaphysis: ( shaft )
o Medullary cavity is located
o Periosteum:
o
Medullary cavity:
Red Bone Marrow
Hematopoietic Tissue
Produce stem cell ( hematoblast )
Location in adults ( Central Bone Cavity )
Function:
Formation of RBC, WBC, Platelets
CARTILAGE:
Dense connective tissue consist of fibers
embedded in a strong like gel substance
3 types
Elastic: ( elastin in each intracellular
substance )
Hyaline: ( pearly white color ) most abundant
– articulary cartilage ( end of the bones )
Fibrocartilage: 65% - 80% are H2O ( tough,
smooth, cushion )
JOINTS:
Hold the bones together
Gives the rigid skeletal mobility
Major classification:
Synarthroses ( fibrous )
o Not movable ( suture of skull )
Amphiarthroses ( cartillagenous )
o Little movement ( intervertebral )
Diarthroses ( synovial )
o Full movement ( hip, knee etc )




Ball & socket (to all
direction – full
movement)
Ellipsoidal ( gliding joint)
to all direction – limited
Hinge ( elbow – knee )
bending – in one direction
Pivot ( rotation
movement )
Bone Maintenance:
Weight bearing ( local stress )
o Activate osteoblast
o Stimulate bone formation/
remodeling
o Prolonged bed rest bone losses
calcium ( resorption ) & becomes
osteopenia & weak
Calcitrol:
o Activated form of Vit. D
o Increase amount of Ca+ in the
blood by promoting Ca+ absorption
in the GI
o Facilitates mineralization of osteoid
tissue
Calcitonin: ( serum to bone )
PTH: ( bone to serum )
Parathyroid gland ( PTH )
Bone release Ca+
Calcium concentration
in the extracellular fluid
Intestine reabsorption of Ca+
via activate Vit.D
Bursae:
Fluid filled sac ( around the joint )
Reduces friction & facilitate movement
Synovium: ( synovial membrane )
Line the capsule
Synovial fluid:
Secreted by synovium
Bone Formation: ( Osteogenesis )
Ossification
o Bone matrix is formed
o Hardening materials is deposited
(collagen fibers)
Endochondral formation
o Most of the bones
o Osteoid ( cartillage like tissue )
Intramembrous formation
o Flat bones
Bone Healing:
Kidney reabsorb of
Ca+
urinary excretion
of phosphorus
activation of
Vit.D
1.Hematoma Formation & Inflammation
Bone is damage – hematoma is precedes new
tissue formation – production of new bone
substance
2.Cellular Proliferation
Granular tissue formation – white blood
vessel & cartilage over lie the fracture
Callus form as mineral and deposited to
organize network fiber for the new bone (
fiber & cartilage )
3.Callus Ossification ( 2 – 6 weeks )
Callus form the initial clinical union of the
bone & provides enough stability to prevent
movement when bones are gently stress
4.Bone Remodelling
Consolidation & Remodeling
Complete healing ( 3 – 6 months )
Continued bone healing provides gradual
return of the injured bone to its pre injury
shape & structural strength
Factors affecting time required for healing:
Age
Displacement
Site of fracture
Nutritional level
Blood supply to the area of injury
MUSCLES:
Skeletal muscle
o Voluntary – Striated
Cardiac muscles
o Involuntary – Striated
Smooth / Visceral muscles
o Involuntary _ Non striated
Tendons connect bone to muscles. Epimysium / Fascia
cover the muscles. Muscle is composed of numerous
visible bundles called Muscle Fasciculi which is
surrounded by loose connective tissue called
Perimysium. A fasciculus is composed of several
Muscle Fibers ( contains nuclei / capillary ). Each is
surrounded by Endomysium. Inside the muscle fibers is
the basic structural and functional unit of muscle called
Sarcomere. Each sarcomere contains Actin & Myosin (
myofilament ). It also contains Z disk ( anchors the actin
myofilament ) & M disk ( anchors the myosin
myofilament ).
Functional Property of Muscle Fibers
Irritability : ability to react to a stimuli ( nerve
impulse ) voluntary
Contractility: ability to shorten with force
(adequate stimuli )
Nerve Stimulus
Motor unit:
o 1 motor neuron + all the muscle
correspond to it>
o Action potential

Electrical impulses that
controls bodily process
SKELETAL MUSCLE
Energy is consumed during muscle
contraction
Consume too much energy
Muscle fatigue:
( work > 02 supply ) unaerobic respiration
Depletion of glycogen / energy stored
Accumulation of lactic acid
Aerobic respiration:
36 ATP

6 oxygen
6 carbon dioxide
Unaerobic respiration:
2 ATP + Lactic Acid
Fascia: ( surrounded and divide muscle )
Tendons: ( fibrous connected tissue / tough ) decrease
blood supply – slower healing
Ligaments: ( fibrous connected tissue / dense &
flexible ) connect bone to another bone – decrease in
blood supply
HEALTH HISTORY
INJURY
Genetic / Familial Disposition
Congenital Talipes Equinovarus
Marfan syndrome
Osteoporosis
Osteogenesis Imperfecta
Concurrent Health Condition
Communicable
o Leprosy
o TB of the bone
Non Communicable
o COPD
o CAD
o Asthma
o CVA
Physical Activities
o Daily activity pattern
o Occupation
o Exercise pattern

F-requency

I-ntensity ( moderate )

Mild ( <50% )

Moderate ( 50%
– 70% )

Highly ( 70% )

T-ime ( 30mins / Session )
-
Recreation
Alteration in Sensation
o Pain

P-allative / Provocative

Q-uality

R-egion

S-everity

Pain Scale
( adult )
Wong – Baker
( pedia )

T-ime
Paresthesia

Tingiling sensation (
impaired circulation /
compression of nerves )
Nutritional Status
o Dietary intake
o Weight / Height ( IBW )
o
-
PHYSICAL EXAMINATION
Posture
Stand straight ( spinal curvature )
Abnormalities
Kyphosis ( increase convexity of vertebrae )
Lordosis ( sway back/exaggeration of lumbar
region )
Pride of pregnancy
Scoliosis
Lateral curvature of the spine
Idiopathic
Congenital
Damage of Paraspinal Muscle
o Polio
Muscle Assessment
Size ( atrophy )
Symmetry ( compare )
Tonicity ( palpation )
Muscle Strength
o Method

Elbow flexion / extension

Wrist flexion / extension

Grip test
Grade
5
4
3
2
1
Description
Normal muscle strength
Full ROM that can be overcome w/ increase
examiner resistance
Full ROM of muscle against gravity only is overcome
w/ slight examiner resistance
Weak movement of muscle but insufficient to
overcome gravity
Slight visible / palpable contraction ( - ) movement
0
Complete paralysis
Gait
Ask the client to walk straight
Stance face
Genu Varum ( sakang )
Genu Valgum ( piki )
Abnormal gait due to neurological disorder
Spastic Hemaparesis ( stroke )
Steppage Gait ( lower motor neuron disease )
Shuffling Gait ( Parkinson disease )
Joint
Assessment
ROM
Active / Passive ( form of intervention )
goniometer
Inflammation
o Dolor ( pain )

Compression of nerve
endings ( release
prostaglandin )
o Rubor ( redness )

Hyperemia
o Callor ( heat )

Hyperemia
o Tumor ( swelling )

Increase capillary
permeability
Laesa Function ( loss of function )
Effusion ( joint effusion )
Accumulation of excessive fluid
o Ballon sign
o Ballottement sign
Identify presence of
o Snap ( slipping of ligament in a
bony prominent )
o Crepitus ( crackling / grating sound)
ROM ( range of motion )
Head
Protraction / Retraction
Rotation
Flexion / Extension / Hyperextension
Arm
Abduction ( away the midline )
Adduction ( toward the midline )
Circumduction
Hand
Foot
6P’s
-
Pronation ( palm down )
Supanation ( palm up )
Dorsiflex
Plantar flexion
Inversion
Evesion
External rotation
Internal rotation
Pain
Pallor
Paralysis
Paresthesia
Pulselessness
Poikilothermia (inability to sustain
temperature)
Bone Marrow Aspiration ( biopsy )
Red bone marrow
Leukemia / Aplastic Anemia
Sternum / Hip bone ( posterior – superior
iliac crest ) 1 – 2ml specimen
Side lying position / Prone
Before:
Secure consent
Check bleeding parameter
After:
WOF bleeding
Apply pressure
Bone Scan
Identify - evaluate the stage cancer of the
bone
Uses contrast radioactive materials ( irritating
to bladder )
o Galium
o Thalium
o Technetium
Before:
Remove jewelry
During:
Proper positioning ( supine – patient must be
steady still )
Promote safety
After:
Increase OFI ( facilitate excretion ) patient
should urinate within 4 hours after procedure
DEXA ( Dual Energy Xray Absorptiometry )
Procedure that measure BONE MINERAL
DENSITY
Commonly used
Low dosed radiation
No special preparation only remove jewelry
Quantitative ultrasonography
Quantitative computed tomography
Roentgenography ( X-ray )
2 types:
Bone X-ray
Joint X-ray
Other types:
Multiple X-ray ( multiple views ) APL
Serial X-ray ( to identify healing process )
Contraindicated to pregnancy
Myelography
Identify – locate tumor in spinal column
X-ray of subarachnoid space
1.Create lumbar puncture ( shrimp position )
L3 – L 4 ( subarachnoid space )
5 – 10ml for exchange with contrast dye
o Hot flushes & metallic taste is
normal
2.Intervention
Before:
Check allergy to iodine
On NPO ( after liquid breakfast )
After:
Oil dye ( flat on bed – to avoid spinal
headache ) easily excreted ( 8 – 12hrs )
Water dye ( amipaque ) HOB elevated
(semifowler ) 30 – 45hrs to avoid Seizures
cause by Meningeal irritation
Precaution:
Before:
Padded side rails
Tongue guard
Decrease height of the bed
During:
Put patient in side lying position
Arthrography
Identify tear in joint capsule / ligaments &
tendons
Indirect visualization of joints
Intervention
Assess for contraindication
-
Perform ROM after injecting contrast dye
(contrast dye leak into the tear of the joint )
After:
Pain management ( NSAIDs )
Avoid bleeding ( ice )
Crackling sounds ( normal – 3 days )
Bone / Muscle Biopsy
Use to identify cancer
Intervention
Local anesthesia
Check PT – PTT
Give coagulant ( 2 – 3 days ) before & after
the procedure ( Amicar / Transxenamic Acid )
antifibrolytic medication
Apply pressure
CT scan ( Computed Tomography ) - MRI ( Magnetic
Resonance Imaging ) better view
Both are use to identify damage into tendons
& ligaments
Assess bone & soft tissue
Assess for “ Claustrophobia“
Both are contraindicated to metal inplant
ESR ( Erythrocyte Sedimentation Rate )
Non specific for inflammation
M: <20mm/hr
F: <30mm/hr
Uric acid: Gout ( inborn error in metabolism )
o Normal:

2.2 – 7mg/dl ( M )

4.2 – 8mg/dl ( F )
ANA ( Anti Nuclear Antibody )
Identify autoimmune disorder
o Measures amount of antibody that
destroys the nucleus of a normal
tissue
Normal value:
o ( - ) or < 1:40
Rheumatoid Factor ( specific )
Determine presence of auto antibody
( + ) RF is suggested of RA
< 40 IU/ml
Muscle Enzyme Test
Cretinine Phospokinase ( cK3 / cKmm )
F: 30 – 135 U/L
M: 55 – 170 U/L
Alkaline Phospoknase ( ALP – 2 )
Normal: 20 – 90 IU/L
Elevated indicates:
o Paget’s disease
o
o
o
o
o
o
Osteomalasia
Cancer of the bone
MUSCULOSKELETAL SYSTEM
Nursing management
1.Pain
Subjective assessment manifested by
Objective cues
Assess Patient perception to pain
Provide non – pharmacologic treatment to
pain
Provide pharmacologic treatment to pain
o
NSAID’s
Assessment of effectiveness to pain
measurement
2.Impaired Physical Mobility
Perform ROM exercise
Types:
o Active: ( allow patient to do ROM )
enhances joint mobility and muscle
bone
o Passive: ( nurse do the ROM )
enhances joint mobility and prevent
contractures ( comatose / paralyzed
patient )
o Active - Assistive:
o Active – Resistive: ( apply
resistance ) increase muscle power
( weight )
Provide support in ambulation w/ assistive
devices
Turn the patient every 2hrs to avoid bed
soars
Encourage mobility
Facilitate exercise
o Isotonic exercise ( change in muscle
length & tension )
o Isometric exercise ( alternate
contraction & relaxation of muscle
3.Self – Care deficit
Assess functional level of the patient
Assist patient w/ difficulty in bathing &
hygiene
o Assist W bath only when patient
has difficulties
o Provide ample time for patient to
finish the activity
Provide support for feeding problem
o Proper positioning ( high fowler )
Provide assistive device
Supervise meal time
Offer finger foods
Keep suction equipment available
TRAUMA
TRAUMATIC CONDITION
CONTUSION
Soft tissue injury cause by blunt trauma
Skin is intact
Extravasation ( blood under the skin due to
rupture blood vessel )
S/S:
Bleeding ( internal )
Swelling ( edema )
Pain ( compression of nerve ending )
Management:
Elevate parts
Cold compress in the 1st 24hrs & apply warm
compress after 24hrs
Apply pressure bandage
STRAINS
Over stretching of the muscle / tendons
Types:
Acute ( recent injury of muscle / tendon
classified by degree )
Chronic ( repeated use of the muscle beyond
physiologic needs )
Degree of acute strain
First degree ( feels stiff & sore locally )
Second degree ( tenderness over the area )
Third degree ( burning sensation )
Assessment of Strain
1
st
Assessment
Tenderness
Muscle
spasm
ROM
No loss
Edema
No / Little


2


nd
Slight ( loss
pain )
Develops early
rd
3


Cannot
move
Extreme
Ecchymosis
No / Little
Develops later
-
edema
Delayed
-
Management
1
st


Elevation
Ice
Drugs
None
Physical
therapy
Not
needed
nd
2


NSAID, muscle
relaxant
Needed
rd
3


NSAID,
muscle
relaxant
Needed
-
SPRAIN
Greater than strain
Over stretching of the ligament
Assessment of Sprain
Assessment
Tearing of
ligament
Edema /
Hematoma
Loss of
function
Weakening
of joint
Pain
st
nd
1
Minimal
2
Up to half
Localized
Increase
None
decrease
None
intact
Mild
Mild
Increase
rd
3
Complete
ruptre
Severe
Dramatic
decrease
Loss of
integrity
Severe pain
Management
1
st
nd
Elevation
Ice
Drugs


analgesics
2


NSAID, muscle
relaxant
Physical
therapy
Compression
Isometric
Needed
Bandage
Restoration
None
Protective
splint
None
General management for Strain / Sprain
R - est
I - ce
C - ompression
E – levation
FRACTURES
A break in continuity of bone
Types of Fractures
rd
3


NSAID,
muscle
relaxant
Needed
-
Casting
-
Surgery
-
-
-
Closed fracture ( simple fracture )
o No break in the skin
Open fracture ( compound / complex )
o ( + ) skin breakage
o Risk for infection
Complete fracture
o Entire cross section
Incomplete fracture
o Only portion of the bone
Greenstick
o One side portion of the bone is
broken and the other portion is
bend
Comminuted
o Several bone fragment
Depressed
o Fragment is driven down / inward
Impacted
o Bone is driven into another bone
(bone to bone )
Transversed
o Break straight across the bone
Oblique
o Angle across
Spiral
o From oblique to long shaft
Compressed
o Bone has been compressed
Stress
o Caused by repeated, prolonged or
abnormal stress
Avulsion
o Pulling away of a fragment of bone
Factors
Extrinsic factor ( stress )
Force
Rate of loading ( speed / momentum )
Intrinsic factor ( bone strength ) speed > strength
Bone capabilities
o Age
o Pre existing disease
Behavioral factor
High risk activities
Nutrition
Assessment of Fracture
Pain
Sudden / Severe Pain ( release of
inflammatory mediator ) prostaglandin
Compression & damage ( pain receptor )
Aggravated by movements
Loss of function
Compression / Damage to the nerve that
innervates
Deformity
Obvious changes
Edema formation
Disalignment of the bone
Shortening of the bone
Disalignment ( cause by muscle spasm )
Crepitation
Crackling / Grating sounds
Edema ( 24 hrs )
Hyperpermeability of surrounding blood
vessels
Numbness
Absence of sensation
Damage to the sensory nerve
Motor weakness
Ecchymosis ( after 24 hrs )
Evaluate if edema subside (ruptured
capillary)
Abnormal circulation
Poor capillary refill time
(-) pulse
Cyanosis
DX procedure
Xray is enough ( presence of fracture )
Emergency management
Immobilized any suspected fracture
Support ( splint / sling )
Do not attempt to reduce the fracture
Place clean sterile gauze
Intervention
Reduction
Cast
Fixation
Traction
Complication of fracture
Early:
Shock
Compartment syndrome
Infection
Fat embolism
Avascular necrosis
Thrombos formation
Late:
Delayed union / non union / mal union
Angulation
Fixation reaction
SHOCK
Stages
-
-
Hypovolemic shock ; low blood volume
15% blood loss
Most common cause of death for patient
with severe & multiple trauma
Non progressive
o Early compensatory stage

( increase HR, RR & slight
oliguria ) normal BP

LOC, irritable &
restlessness
Progressive
o Intermediate stage

Hypo – tachy – tachy
( release of catecholamine )

o
Decrease BP , UO (oliguria
phase) lethargy
Late ( irreversible )

Bradycardia

(-) bradypnea, palpatory
BP ( systole )

Unconscious

Sever schemia

Metabolic acidosis

Multiple organ failure

Anuric phase
-
-
Pharmacological treatment
o Cortecoisteroid ( decrease damage
to the lungs )
o Morphine ( pain management ) SNS
response, increase oxygen
consumption
Institute preventive measure
o Immobilization
o Avoid manipulation
Surgical:
EMBOLECTOMY
TX:
-
-
-
-
-
Positioning
o Divert blood to vital organs

Tredelenburg / Modified
tredelenburg position
Respiratory and Support
o Large concentration of oxygen

Mechanical ventilation

Intubation
IV infusion
o PNSS / LRS
o 3%nacl
Blood transfusion
o Blood compatibility
o Whole blood
Emergency meds
o Dopamine
o Epinephrine
o Atropine sulfate
o Dobutamine
o Sodium bicarbonate
FAT EMBOLISM
Release of fat globule ( fracture )
Stock to the lungs, brain, kidney etc.
Classical triad:
Hypoxemia
o Decrease perfusion, increase
pressure pulmonary circulation
Petechial rash
o Chest / Neck
-
Neurological alteration
o Sudden confusional stage
o Chest pain / Dyspnea
o Tachycardia
Intervention
Support respiratory function
COMPARTMENT SYNDROME
Increased tissue pressure within
compartment
Myofascia compartment
o Low ability to expand

Blood vessel

Nerve

Muscle
Edema & Hemorrhage ( fascia )
o Increase pressure compress
myofascia compartment
Assessment
Pain
Pallor
Edema
Pulselessness
Paresthesia
Medical / Nursing management
Frequent assessment
Elevate the extremities
Reduce cast pressure ( Bivalbing )
Surgical:
FASCIOTOMY
INFECTION
OSTEOMYELITIS
Most common
Assessment
Fever
Leukocytosis
Elevated ESR
Erythema
Pain
Intervention
Proper handling of open fracture
Long term antibiotic therapy
Surgery:
-
SEQUESTRECTOMY ( sequestrium ) dead
bone
BONE GRAFT
NI:
-
AVASCULAR NECROSIS
Bone death due to disrupted blood supply
Assessment
Continuous pain
Decrease sensation
NI:
Continuous assessment
Removal of necrotic tissue
FRACTURE MANAGEMENT
REDUCTION
Restore the bone to proper alignment
Types
Closed reduction
o Client is under anesthesia
o Cast may be applied
Open reduction
o Treated with internal / external
fixation, cast or traction
CAST
Types:
Function
-
Is a temporary immobilization.
Plaster of paris ( 1- 3 day )
Fiber glass ( 30 min )
To promote healing and early weight bearing.
To support, maintain and protect realigned
bone.
To prevent or correct deformity
To immobilize
Cast Application
Apply the stockinette.
Apply the wadding sheet.
Fiber glass or the plaster cast
Characteristic of a good cast
White / Shiny
Odorless
Light weight
Properly fit
Resonant on percussion
Contraindications
Pregnancy
Skin disease
Swelling
Open wound
Infection
Handle wet cast with palms of hands, not
fingers.
Cast should be allowed to air dry.
o L – ow cool dryer
o E – expose the cast
o T – urn to promote equal drying
Elevate the cast on one or two pillows during
drying.
Observe “hot spot” and musty odor, which is
signs and symptoms of infection.
Maintain skin integrity – “petalling”
Do neurovascular checks such as skin color,
skin temperature, sensation, mobility and
pulse.
Assess for vascular occlusion.
Adhesive tape petals reduce irritation at cast
edges.
Prevent complication of mobility.
Types of Cast, Molds And Indications
1. Airplane cast – for humerus and shoulder
joint with compound fracture.
2. Basket cast – for severe leg trauma with open
wound or inflammation.
3. Body cast – for lower dorso-lumbar spine
affectation.
4. Boot leg cast – for hip and femoral fracture.
5. Cast brace – for fracture of femur (distal
curve) with flexion and extension.
6. Collar cast – for cervical affectation.
7. Cylindrical leg cast – for fractured patella.
8. Delbit cast – for fracture of tibia or fibula.
9. Double hip spica cast – for fracture of hip
and femur.
10. Double hip spica mold – cervical affectation
with callus formation.
11. Frog cast – for congenital hip dislocation.
12. Functional cast – for fractured humerus with
abduction and adduction.
13. Hanging cast – for fractured shaft of the
humerus.
14. Internal rotator splint – for post hip
operation.
15. Long arm circular cast – for fractured radius
or ulna
16. Long arm posterior mold – for fractured
radius or ulna with compound affectation.
17. Long leg circular cast – for fractured tibiafibula.
18. Long leg posterior mold – for fracture tibiafibula with compound affectation.
19. Minerva cast – for upper dorsal or cervical
affectation.
20. Munster cast – for fractured radius or ulna
with callus formation.
21. Night splint – for post polio.
22. Pantalon cast – for pelvic bone fracture
23. Patella tendon bearing cast – for fractured
tibia-fibula with callus formation.
24. Quadrilateral (ischial weight bearing) cast –
for shaft of femur with callus formation.
25. Rizzer’s jacket – for scoliosis
26. Short arm circular cast – for wrist and
fingers.
27. Short arm posterior mold – for wrist and
fingers with compound affectation.
28. Short leg circular cast – for ankle and foot
fracture.
29. Short leg posterior mold – for ankle and foot
with compound affectation.
30. Shoulder spica – for humerus and shoulder
joint.
31. Single hip spica – for hip and 1 femur.
32. Single hip spica mold – for pelvic fracture
with callus formation.
33. 1 and ½ hip spica – for hip and femur.
34. 1 and ½ spica mold – for hip and femur with
compound affectation.
Cast assessment
Assessment
WOF
Color
- Pallor / Cyanosis
Temperature
- Cold Skin / Hot Spot
Sensation
- Tingling / Numbness
Mobility
- Distal Paralysis
Pulse
- Absent
Cast procedures
Petalling
o Smoothening of cast to prevent
rupture skin
-
Windowing
o Removal of a part of a cast
Bivalving
o Splitting of the cast ( xray )
Other cast complication
Compartment syndrome
-
Cast syndrome
o N&V
o Abnormal pain / Bloatedness
o ( - ) bowel sound
Plaster sores
o Itchiness / burning sensation
o Severe pain
Equipment in removal
Cast cutter
Cast spreader
Bandage scissor
Fixation
Alignment of the bone fragments
More freedom of movement
Outer Reduction & Internal Fixation ( ORIF )
Outer Reduction & External Fixation ( OREF )
Types:
Internal Fixation
May include removal of a damage
Provide immediate bone strength
o Screw
o Skeletal pin

Inside the bones
o Medullary rods
o Plates
External Fixation
Use of a rigid external support
Indication: Massive Tissue Trauma
PIN care is necessary
External frame
Connect skeletal pin ( outside the bones )
6 – 8 weeks
Nursing management
Check dressing for bleeding and infection
Empty Hemovac – evacuation of blood
Turn every 2 hours
Avoid weight bearing on affected extremities
Hypercalcemia
Constipation
Hypostatic pneumonia
Assisted devices
Walkers
Level of the hip
4 -6 inches away to feet
15 -30 degrees flexion to elbow
Lift & walk technique
Lift walkers and walk across the walker
Going up put the walker at the back
Put the walker in front
Cane
Rubber tip
C-ane
O-pposite
A-ffected
L-imb
NI:
Inspect the device
Proper positioning
Proper handling
o Greater trochanter to the femur
o 5 cm below the hips
o 4 -6 inches, 15 – 30 degrees
Proper movement
The cane and the affected leg must moves at
the same time
Prosthesis
Crutches
2-3 fingers width
2.5 – 5cm /12 inches between crutches &
armpit
30 degrees flexion
Crutch palsy
o Brachiocephalic paralysis
6 inches – 1 foot
o Gives the client broader base
The hand grip should be at waist level
Standing with crutch
Sit near the edge of the chair
Unaffected part must be near the chair
Stand using the unaffected part
Then separate the crutch
Up with the good, down with the bad
Going upstairs
o Good leg up and crutch with
weaker leg
Going down
o Bad leg then good leg
4 point crutch gait
Indication
Use if weight bearing is allowed
Pattern sequence
1. Left crutch
2. Right foot
3. Right crutch
4. Left foot then repeat
3 point crutches gait
Indication
-
Partial weight bearing or no weight bearing
on affected leg
Pattern sequence
1. Move both crutches and leg
2. The weaker lower limb forward then bear all
your weight down through the crutches
3. Move the stronger part
2 point crutches gait
Indication
Weakness in both legs on poor coordination
Pattern sequence
1. Left crutch and right foot together then the
2. Right crutch and left foot together then
repeat
Swing to gait
Indication
Patients w/ weakness of both lower
extremities
Pattern sequence
1. Advance both crutches forward while bearing
swing all weight down through both crutches.
2. Swing both legs forward at the same time
( not to pass ) the crutches
Swing through gait
Indication
Inability to fully bear weight on both legs
Pattern sequence
1. Advance both crutches forward then, while
bearing all weight down through both
crutches.
2. Swing both legs forward at the same time –
past the crutches
Other Treatment Modalities
Traction
Fulling force in two opposite side
Essential components
Traction
Forward force
Countertraction
Backward force
Friction
Purpose
Reduce muscle spasm
To immobilize
Principles of traction
Client should properly positioned
For every traction there is a countertraction
Line of full should be aligned with the
deformity
-
For traction to be effective it must be
continuous
Types of traction
Halo Femoral Traction
90 – 90 degrees
Balanced Skeletal Traction (BST)
Overhead
Crutchfield Tongs
Supracondylar area
Hemo-femoral
Severe cases of scoliosis
90-90 traction
Subtrochateric
Fracture of the femur
Types of Traction
BUCKS EXTENSION
RUSSELL TRACTION
BRYANT TRACTION
SKULL TONG / TURNING FRAME
LATERAL SKELETAL TRACTION
BALANCED TRACTION
1.
2.
3.
4.
5.
Balanced Suspension
Bucks extension traction
Bryant traction
Bootcast traction
Cotrel traction
6.
7.
8.
9.
Cervical traction
Dunlops traction
Hammocks traction
Pelvic girdle
NI:
Traction: General Principles
1. Always ensure that the weights hang freely
2. Never remove the weights
3. Maintain proper body alignment
4. Ensure that the pulleys and ropes are
properly functioning
5. Observe the patient foot drop
6. Observe for DVT
7. Provide pin care for clients in skeletal traction
8. Promote skin integrity
9. The line of pull must be in line with deformity
Braces
Immobility
Proper body alignment
Support
Treat fracture
Amputation
Removal of a body part ( limb )
Cause
Trauma ( accidental amputation )
Surgical amputation
Types
Related to preservation of the joint
Peripheral disease
o BKA – below the knee amputation
o BEA – below the elbow amputation
Extensive trauma / Disease
o AEA – above the elbow amputation
o
AKA – above the knee amputation
Mostly
Due to trauma, malignancy, arterial
insufficiency
Post Op Intervention
Monitor V/S & stump dressing
Elevate stump for 12 – 24 hours
Teach client about PHANTOM LIMB
SENSATION ( after 24 hrs )
o Stimulation of the remain limb
o Neural nerves in the brain
Provide stump care
o Maintain elastic bandage ( shrink /
shape )
When wound is healed, wash the stump daily
( avoid oil ) maceration
-
Apply pressure to the end of the stump
Encourage client to move the stump to
promote circulation
Place client with a lower extremities
amputation in a prone position twice daily
Figure of 8 method
To wrap your residual limb
ARTHRITIS
35 -45y.o ( female )
Inflammation of the joint
Types:
RHEUMATOID ARTHRITIS
Inflammatory changes of the joint
Chronic / Systemic Connective Tissue Disease
Affect the Peripheral / Synovial membrane
Factors
Genetic predisposition
Autoimmune
A/E:
o F- atigue
o E-xtreme C-old
o S-tress
o I-nfection
Immune response ( joint )
Neutrophil ( attract )
Collagen ( breakdown )
-
Destruction of synovial lining
Inflammation of synovial membrane
( Fibrous antylosis )
Panus formation ( bone antylosis )
(development of tissue with blood vessel )
Fibrous antylosis – shortening of connective tissue
Bone antylosis – fusion of the bone
Assessment finding
Pain ( esp.morning ) after a long period of
inactivity
Joint swelling / stiffness
Sign of inflammation
Fever & weight loss
Anemia
Spongy tissue
Related disorder
Sjorgen syndrome
o Decrease activity of glands

Skin

Lacrimal

Salivary
Felty syndrome
o Rheumatoid Arthritis
o Neutropenia
o Splenomegaly
DX test
Xray
o (+) bony erosion
Blood studies
o (+) rheumatoid factor, elevated
ESR,ANA & CRP (C-reactive protein)
Arthrocentesis
o Cloudy, milky & dark yellow
o (+) WBC
Medical management
Pharmacotherapy
NSAID’s ( non selective cox - inhibitor )
Cox ( prostaglandin synthesis )
o Cox1 ( stomach lining )
o Cox2 ( inflamed area )
Chryotherapy / Gold Therapy
o Gold Na+ Thromalate ( IM ) 36months / Auranofin ( PO )
Complication:
o Kidney damage
o Bone marrow depression
Steroids
o Prednisone / Cortisone
Surgical
Anthroplasty
Synovectomy
Nursing Management
Relieve Pain / Discomfort
Immobilized
Suggest application
o Cold / heat application
Promote balance in activity & rest
Increase patient mobility ( safety )
Provide diet therapy
o Increase protein / caloric diet
Prevent deformity
o Use flat / firm mattress
o Use one pillow under the head
o No pillow under the joints
o Lie prone several times
OSTEOARTHRITIS
Degenerative joint disease
Destruction of cartilage
Affects weight bearing joints
Risk factors
Increased age ( above 50 yo ) wear & tear
Obesity
Repetitive use of joints
Genetic susceptibility
Hyperactive chondrocytes ( cell in the jint
capable of destroying cartilage)
Assessment
Functional joint limitation
Bonchard Nodes ( thicken bone growth )
Heberdens Nodes ( terminal interphallegeal
joint )
Joint pain
o Assymetrical

Not systemic

Weight bearing joint
Stiffness
o Esp. morning
o Decreases with movement
DX findings
Xray
NI:
Provide relief of pain
Advise patient to reduce weight
o Aerobic exercise
o Walking
Administer prescribed medication
o NSAID’s
Position the client to prevent flexion /
deformity
Surgical Intervention
Synovectomy
Arthrodesis – fusion of a joint
o Artificial antylosis ( palliative )
Reconstructive surgery
Comparison:
Rheumatoid
-Onset is early
-Chronic systemic
-Involves the synovium
-Joints are symmetrical
-Malaise, fever, anemia
-SubQ, nodules, stiffness
-Rest the joint
-Cold/ Heat modalities
-Medication
Osteo
-Onset is late
-Non systemic
-Involve the cartilage
-Joint is unilateral
-No other symptoms
-Crepitus, stiffness
-Rest the joint
-Cold/ Heat modalities
-Medication
GOUTY ARTHRITIS
Systemic disease caused by disposition of uric
acid crystal
Cause
Primary Gout ( error in purine metabolism )
Secondary Gout ( caused by pre existing
disease )
Assessment
Severe pain
Inflammation of the joint
TOPHI formation
PODAGRA ( big toe because of gout )
Fever & malaise
Body weakness & headache
Renal stones
DX test
Serum uric acid
Uric acid stones in the kidney
(+) Urates crystal in the synovial fluid
Medication Management
Allopurinol
o Taken after meal
o WOF: allergy
Colchicines
-
o Acute attack
Probenecid
o Uricosuric drugs
-
Provide proper diet
Increase OFI
Provide alkaline ash diet
Provide bed rest during arly attack of gout
NI:
METABOLIC BONE DISORDER
OSTEOPOROSIS
Decrease in the bone mass & density
Types
Primary osteoporosis
o Above 55 yo ( female )
o Menopause ( estrogen )
Secondary osteoporosis
o Pathologic ( renal failure )
o Iatrogenic ( long term steroid
therapy )
Risk factor
Sedentary lifestyle ( immobility )
Age
Poor diet
Post menstrual
Genetics ( Caucasian / Asian )
Assessment findings
Low stature ( Dowagers back )
Bona pain
High risk for fracture
Laboratory findings
DEXA ( Dual Energy Xray Absorptiometry )
Xray
Medication management
Diet therapy
Hormone replacement therapy
Biphosphonate ( Alendronate ) decrease
osteoclastic activity
Moderate weight bearing exercise
Management of fracture
OSTEOMALACIA
Delayed mineralization
Kyphosis / Lordosis
Assessment
History
Muscle & Skeletal
Physical Examination
Gait
o Wide stance
o Waddling gait
Muscle weakness
Cones
o Deformities of the spine
o Bone breaks easily
DX testing
Radiographic resting
Laboratory studies
Serum calcium
ALP
Management
Ca+ Gluconate
Vitamin D. intake daily
Diet high in protein
UV radiation therapy
HERNIATED DISK
Nucleus Pulposus forces through the weaker
/ torned outer fibrous ring
Cause
Trauma
Strain
Joint degeneration
Assessment finding
Back pain
o Radiates to the buttocks, leg & feet
Motor & sensory loss
DX test
Laseque test
o 30 -70 degrees ( dorsiflex )
o Xray
o CT Scan
o MRI
NI:
Bed rest for several days
Heat application
Promote exercise on bed
Pelvic traction application
Provide the drugs as order
o Muscle relaxants
Provide care for Lamonectomy
Surgical
LAMONECTOMY
o Removal of the protruding disk
o Usually accompanied by insertion
of metal plates
Post operatively
Maintain bed rest
-
Log rolling technique
Never lie on prone
Hemovac drainage system
Straight back chair
OSTEOMYELITIS
Acute / Chronic infection of the acid
surrounding soft tissue
DX test
CBC
ESR
Blood culture
Reason
Open fracture
Sepsis
CM:
Fever & malaise
Inflammation
Difficulty with weight bearing
Drainage from wound site
Management
Analgesic as prescribed
COD
Maintain proper body alignment
Immobilization of affected part
Surgery if needed
Proper diet
o High caloric / protein diet
PAGET’S DIET
Oteitis Deformans
Slow progressive
Familial
Rapid osteoclastic activity ( bone resorption )
Abnormal bone formation
Assessment
Assymptomatic initially
Musculoskeletal
o Bone deformity ( bowing of the
bone ) skull, femur, tibia & vertebra
-
o Bone pain even without activity
Fracture
DX
-
Radiographic findings ( pathologic fracture )
sclerotic bones
Laboratory analysis
Increase ALP
Increase Urine Hydroxy Proline
o
Substance similar structure to
amino acid only found on collagen
Increase serum level
ORTHOPEDIC SURGERY
TOTAL HIP REPLACEMENT
Replacement of both articular surfaces of hip
joint
Indication
Osteoarthritis
Rheumatoid Arthritis
Femoral neck fracture
Avascular necrosis ( head & neck of femur )
Post op care
WOF for bleeding ( 24-48 hours / 500ml
blood )
o After 48 hrs – 1 week ( minimal
bleeding ) 100 -200cc
Pain management
o PCA ( patient control analgesia )
narcotic morphine ( 48-72hrs )

After 72hrs ( non narcotic
analgesia )
NI:
st
1 post op week ( use abductor device )
Use bed pan
Client therapy
o Use assistive device
o Methods to prevent dislocation
o Sexual activity
Avoid
-External rotation
-Prevent hip flexion
-Adduction
-Do not bend
-Do not cross the legs
Do’s
-Place trochanter walls
-Use high chair
-Used Abduction splint
-Use slip on shoes
-Keep feet flat
TOTAL KNEE REPLACEMENT
Hinged joint
Metal or Acrylic prosthesis
Indication
Osteoarthritis
Rheumatoid Arthritis
Trauma
Flexion failure
Wrong insertion
Manifestation
Unable to flex the knee ( 1st week )
NI:
1st 48hrs ( apply ice )
Wound drainage ( 200ml / 8 hrs ) 3rd day no
bleeding
Physical therapy ( aggressive ) after 8 hrs –
prevent flexion
Prescribe CPM ( control passive machine )
Keep leg elevated
Pain management ( NSAID’s )
Monitor limb neurovascular status ( 6P)
Monitor for complication
NEUROSENSORY SYSTEM
Lacrimal Apparatus
Hyperactive Lacrimal Gland
Chemical irritation
Foreign object
Emotional stress
6 Extra Occular Muscle
1
2
3
5
4
6
Cranial Nerve 3
1. Superior Rectus
2. Inferior Rectus
3. Medial Rectus
4. Inferior Oblique
Cranial Nerve 6
5. Lateral Rectus
6. Superior Oblique
Layer Of The Eye
Lacrimal gland
Produce tears ( diluted salt )
Tears
-
Outer layer ( fibrous tunic )
Lysozyme ( protects & moisten the eye )
-
-
Sclera is the opaque, fibrous, protective,
outer layer of the eye containing collagen and
elastic fiber.
Cornea is the transparent front part of the
eye that covers the iris, pupil, and anterior
chamber.
Middle layer ( vascular tunic )
Choroid provides oxygen and nourishment to
the outer layers of the retina. Rich in
melanin.
Ciliary body attach the lens and responsible
for accomodation
Iris is the colored part of the eye &
responsible for papillary reflex
Inner layer ( nervous tunic )
o Rods ( dim vision )
o Cones ( colored vision )

Fovea centralis ( bundle
of cones )
Cavities Of The Eye
Anterior cavity ( aqueous )
Refract lights ( provide nourishment to
cornea )
Drained through Trabecular Meshwork &
Canal Of Schlemm
Intraocular pressure ( 10 – 21 )
Posterior cavity / Vitreous cavity
Contains gel like substance ( maintain the
shape of the eyeball
Attachment of 3 layers
Refract lights
Lens
BICONVEX ( transparent )
Located posteriorly behind cornea & iris
Accommodation – ability of the lens to
change shape according to object distance.
Distant vision – flatten
Near vision – rounded ( risk for eye strain )
Refraction of light / Bend of light
Orbit
Bony structure of the skull which contains the
eyeball
Orbital Cavity
Space between eyeball & orbit
Retina
is a light-sensitive tissue lining the inner
surface of the eye
Optic Nerve
-
Bundle of axons
Optic Chiasm
Intersection of medial nerve
Optic Tract
Joining of medial & lateral nerve
Visual Area Of The Thalamus
Were nerve meet / receives optic tract
Visual Cortex
Interpret stimuli ( occipital lobes )
DX procedure:
Snellen Chart
Visual acuity ( sharpness of vision )
o Ability to distinguish in details
through your eyes
Numerator :
-Distance of S.C to Pt.
( 20ft )
Denominator :
-Distance wher eye can
read the same letter
20/200 ( legal blindness )
OD ( ocular dexter ) - right
OS ( ocular sinister ) – left
Ishiwara Colored Plate
Use to diagnosed color blindness
Tonometer
Indirect measurement for IOP ( indirect
ocular pressure ) 12 -21 mmhg
Increase IOP ( glaucoma )
Gonioscopy
Bio microscopic examination of the eye
Provide information regarding to the angle of
the anterior chamber
Use for glaucoma
Opthalmoscope
Visualizes ( direct ) fundus of the eye
Visualize retina
Visualize fovea centralis
Slit Lamp
Beam of light passes through the eye ( small
frequency light ) & then direct examination
follow
Done to visualize small part of the eye
Visualize different layer of the eye
Cover – Uncover Test
Diagnostic procedure for strabismus,
heterotropia & squint
Retinoscopy
Direct visualization of the eye
Perimetry
Test for peripheral vision
Corneal Reflex
Light touch to the corneal / Blinking reflex
Blinking reflex is loss in times of :
o Coma
o Anesthesia
o Death
COMMON EYED DISORDER
INJURIES
Chemical injury ( any chemical that irritate
the eye )
NI:
Immediately wash the eye
IOFB ( intraocular foreign body )
First Aid
Wash the eye ( 15mins )
Never attempt to remove foreign body
manually
BLUNT TRAUMA
Injury in the eye due to blunt object
First Aid:
Apply ice ( prevent swelling )
Manifestation
Non painful red rounded mass
Cause
Staphylococcus aureus
PENETRATING EYE INJURY
Injury due to sharp object
NI:
Put eye cover 7 rush to the hospital
SYMPHATETIC OPTHALMIA ( feared
complication) day – years after PEI
INFECTION
EYE LID DISORDER
BLEPHERITIS
Inflammation of the eye lid margin
DISORDR OF CONJUNCTIVA
CONJUNCTIVITIS
Inflammation of conjunctiva ( red eye )
Viral in origin / bacterial ( self limiting )
Manifestation
Red eye
Lacrimation
Eye discharge ( purulent )
Manifestation
Burning sensation
Irritation
Itching
Eye lashes fall apart
Cause
Bacterial / Viral
Fungal ( rare )
HORDEOLUM
Pustular infection of eyelash follicle
Manifestation
Painful red rounded mass
Cause
Staphylococcus aureus
CHALAZION
Inflammation of meibonian gland
TRACHOMA
Severe case of conjunctivitis
Chronic eye disorder
Conjunctivitis of the eyelid
TX:
C&S
Sulfonamides, Erythromysin, Tetramycin
Manifestation
Painful when blinking
Redness to eyelid
SCLERITIS
Inflammation of sclera
Manifestation
Very red eye ( hyperemia )
Painful when blinking or movement of the
eyeball
TX:
Sulfonamides, Erythromysin, Tetramycin
CORNEAL INFLAMMATION
Keratitis
Cause
Infection,
Physical
Chemical agent
Assessment
Pain – sharp radiating to frontal portion of
the head
Photophobia
Lacrimation
Blepharospasm ( sharp - frequent blinking of
the eye )
Decreased vision
TX:
-
Bacterial : MOXIFLOXIN ( fluoroquinolones )
Viral :
o TRIFLURIDINE ( Viroptic ) anti viral
o IDOXURIDINE ( IDU ) herpes
Severe cases:
Mechanical / Chemical Intervention
CORNEAL ULCERATION
Cause
Trauma
Infection ( systemic )
o Vit. deficiency ( ACE )
At risk:
AIDS
Syphilis
Systemic Lupus Erythematus
Sarcoidosis
TB
Complication
Corneal scarring ( perforation-severe )
Intraocular infection ( rare but severe )
Corneal opacity ( blindness )
TX:
Corneal Transplantation ( Keratoplasty )
Treatment for corneal perforation / opacity
Must remove 2 – 4hrs from the eye ( 4o C)
48hrs ( sterile normo saline solution )
8 – 12hrs ( refrigerate without sterile )
UVEAL TRACT DISORDER
Uveal Tract
Middle layer ( vascular tunic ) responsible for
dissemination of blood supply
Easily inflamed ( phlebitis )
UVEITIS
Cause
-
Iritis ( Iris )
Iridocyclitis ( Iris & Cyliary body )
Choroiditis ( Choroid )
Choroirentinitis ( Choroid + Retina )
Local or systemic disease
o SLE
o AIDS
o Sarcoidosis
Injury
Unidentified factors
Assessment
-
Pain ( radiating pain ) from eye to frontal &
temporal )
Blurred vision
Photophobia
Redness of the eye
Small pupil
Lacrimation
Collaborative management
Mydriasis ( atropine drops )
o Relaxation of iris
o Prevent adhesion of anterior
structure ( lens, iris & cornea )
Steroids ( anti inflammatory )
Dark glasses ( reduce photophobia )
Analgesics ( reduce pain )
RETINAL DISORDER
RETINITIS
Inflammation of the retina ( large portion of
the retina )
Assessed through opthalmoscopy ( direct
visualization of fundus of the eye )
Usually associated with chroinditis
Rare fungal retinitis
CYTOMEGALOVIRUS ( herpes group )common
viral agent
Protozoan ( toxoplasmosis gondvi )
Staphylococcus aureus ( bacteria )
Assessment
Reduced visual acuity
Changes in visual field ( narrowing )
Eye discomfort ( pain is provoked by
exposure to light / pain is slightly removed by
rest )
Photophobia
Collaboration management
Rest the eye
Protects eye from light
Mydriatics ( SMAC )
o S - copolamine
o M - ydriasil
o A – tropine sulfate
o C – yclopentolate
EXTRAOCULAR DISORDER
STRABISMUS ( squint )
Uncoordinated extraocular muscles
Unilateral
Types:
Esotropia
both eyes turns inward
-
Exotropia
the eyes are deviated outward
Hypertropia
upward
Hypotorpia
downward
Collaborative Management
Corrective Eyeglasses
Surgery:
o Tenotomy
o Resection Tucking
EYE SURGERY
General Pre Op Care
Orient ( to promote safety )
Practice covering the eyes for pediatric
patients ( 5 -7 days eye cover )
Before surgical intervention give Mydriatics
Post Op Care
-
Position ( supine or towards the unaffected
side )
Burning sensation ( 1hr after the procedure decreases gradually after 8hrs )
Eye patch & Eye shield
o To rest the eye ( 5 – 7 days ) after
procedure
o Eye patch every night for 1 month
Sensation of pressure within the eye and
sharp pain in the eye
If pressure occurs during 16hrs ( notify
physician ) it may indicate increase IOP, IO
bleeding
Miotics as prescribed
o Carbotic ( Carbachol )
o Humorsol ( Demeconium Bromide )
o Isopto Carpine ( PIlocarpine HCl )
o Floropryl ( Isoflurophate )
CATARACT
Opacity of the lens
Transparent of opaque
Etiological Factor:
Chemical changes & structural changes of
protein in lens
Degeneration of epithelial layers of lens
(older people )
Changes in density of the lens
o Low molecular weight lens protein
to high molecular weight – high
dense
Increase oxidation ( free radicals )
Classification
Primary / Senile Cataract ( 70 – 75 yo )
o Older people
Traumatic ( blunt trauma )
o Children
Congenital Cataract
o Infant acquired during pregnancy
st
o Exposure to teratogens ( 1 tri )

TORCH
T-oxoplasmosis
O-thers
R-ubella
C-ytomegalovirus
H-erpes simplex
Secondary
o
Pre existing disease (DM common)
Ss/ Sx:
-
Dimness in visual acuity
Refraction error ( rapid & marked changes )
HAZY VISION ( blurred vision )
-
-
Intracapsular cataract extraction ( ICCE )
o Removes lens & capsule
Extracapsular cataract extraction ( ECCE )
o Removes lens only
Cryoextraction (probe is inserted in 0oC temp)
Phacoemulsification – probe vibrates
Contact lens
-
Aphakic glasses – cataract glasses
TX:
-
-
Intraocular lens – synthetic distant vision for
aphakic patient
GLAUCOMA
May result to irreversible damage
Cause
Increase Intra Ocular Pressure ( normal 12 –
21 )
Infection ( uvitis )
Injury ( blunt trauma )
Hereditary – thickening of trabecular
meshwork resulting to obstruction of passage
way of aqueous humor
Narrowing of the Canal of Schlemm
TYPES
CHRONIC
o Hereditary ( similar to open angle
glaucoma )
o Narrowing of the canal of schlemm
o It will take time to develop
o Obstruction in the excretion of
aqueous humor
Ss/Sx:
Tunnel vision ( loss of peripheral vision )
Difficulty in adjusting to darkness
Colored vision disturbances
-
Headache
Halo light surrounded by a concentric shape
(rainbow color )
Dull eye pain
Management
Conservatives
o Miotics ( papillary constriction )
o Acetazolamide ( decrease aqueous
production )

Drug class: Carbonic
Anhydrase Inhibitor

MOA: decrease acqueous
humor production
o Avoid excessive fluid
Aggressive
o Principle: Improve Drainage of
Aqueous ( will create a permanent
fistula )
o Indectomy ( passage way in the Iris)
o Selerectomy ( passage way in the
sclera )
o Trabeculotomy / ectomy
o Corneoscleral therapy
o Laser therapy
ACUTE
Aqueous humor imbalance
o Increase production rather than
drainage
Displacement of Iris ( Iris blocked the aqueous
humor )
Infection
Injury or trauma
Ss/Sx:
Sever eye puss
N&V
Halo around light
Dilated pupils
Increase IOP
Management
Miotics
Diamox
Surgery
Avoid: mydriatics
Long term care:
No restriction on the use of the eyes
No fluid restriction
Medical follow up ( for life )
RETINAL DETACHMENT
-
Causes
-
Ss/Sx:
-
Separation of:
o Epithelial pigment – layer of rods
and cones ( nervous layer of retina )
o Retina ( choroid ) rare
Trauma
Intra Ocular Hemorrhage
Aphakia ( absence of lens )
Sudden severe exertion
Floating spots ( dark pigment )
Head position
Photo coagulation - increase coagulation with
use of light ( adhere the detached retina )
Cryotherapy ( cold application using
instruments )
Surgical
Scleral Buckling
o Re adhere the detach retina
o Synthetic silicon
Refractive errors
Common errors
Myopia
o Light rays focus in front of retina )
o
Due to : wide AP dimension
o Near sightedness
o Eye glasses ( concave ) long
refraction
Hyperopia / Far sightedness
o Eye ball AP dimension too short
o Light rays focus behind the retina
o Good vision for far distances
o Convex lenses
Presbyopia / Far sightedness of old age
o Gradual loss of accommodation
(loss of elasticity )
o Inability to read without holding
the material more 13ft. from the
eye
o TX: lens ( bifocal lens )
Astigmatism / Distorted sight
o Abnormal curvature of lens
o Due to variation of refractive ability
o Eyeglass ( special cylindrical lens )
MACULAR DEGENERATION
Loss of central vision
o Macular Lutea (responsible for
central vision)
o
Fovea centralis ( inside macula
lutea ) sharpest vision
Most common type : AGE related macular
degeneration ( at risk : above 60 yo )
2 types
Dry macular
80 – 90% of incidence
Non exudative
Non neo vascularization
DRUSEN ( yellow patches on retinal layer )
o No Ss/Sx if Drusen does not enter
Macula Lutea
Wet macular
Low incidence 10 – 20 %
(+) neo vascularization
Symptomatic
Ss/ Sx:
Decrease visual acuity
Blurred vision ( starting at central vision )
Central scotoma ( partial or totalblindness in
certain areas )
TX:
Wet:
Anti-Angiogenesis
o Macugen ( given once a month or
twice )
o MOA: decrease progress of neo
vascularization
Dry:
Lutein
Omega 3 ( fishes )
DX:
Amster grid
o Consist of geometric square with a
central fixation point
o Ask the patient to look at the point
o Blind spot – common to dry
macular degeneration
o Curves – common to wet macular
degeneration
Injection of Fluorescent Dye ( WET )
o Angiography
o Evaluates macular edema neo
vascularization & macular capillary
Retinal photography ( black & white )( DRY )
EAR
Auricle / Pinna ( elastic cartilages )
Collect sound waves
Auditory canal / Meatus
Transmit sound wavws from pinna to
tymphanic membrane
It has a protective function ( cerumen )
Tymphanic membrane / Ear drum
Vibrates the 3 ossicles
o Mallius
o Illcus
o Stapes
Mastoid
Air filled cavity & relieves pressure
Eustanician tube/Auditory tube
From middle ear going to nasopharynx
Opening during yawning & swallowing
Oval window
Enter the sound wave & transmit
Round window
Relieves pressure
Vestibule & Semi Circular Canal
Rich in vestibular nerves
Responsible for balance
It is compose by:
o Utericle
o Saccule
Cochlea
Consist of Organ of Conti ( responsible for
hearing )
Rich in auditory nerves
Vestibular + Auditory = Vestibular Cochlear Nerve
( CNVIII )
transfer in temporal nerve ( interpretation of
hearing )
HEARING TEST
Accuracy or degree of hearing loss
Whisper or Spoken voice test
2 ft. behind the patient
Cover 1 ear
Say 2 syllable word ( eg. Twenty )
Audiometer
Cannot measures accuracy but degree of
hearing loss only
Pure tone:
o Increase decibels = Increase hearing
loss
Speech:
o Degree of hearing loss with
interpretation
-
Watch tick test:
AUDITORY ASSESSMENT
Test to localize cause of deafness
Rinne’s test
Sound heard better: “ air vs. bone”
N = positive: “ air conduction is better “
ABN = negative : “ bone conduction is better”
Conductive hearing loss
Weber’s test
Sound heard: normal ear vs. affected ear
Better to detect : sensory neural hearing
loss
Better in affected ear ( conductive )
Normal: equal laterization
Symptoms of Ear Diseases
Deafness
Varies in severity
o Conductive ( rinne’s test )
o Sensorineural ( weber’s test )
o Mixed type
Pain
From ear itself or adjacent side
o Otalgia ( ear ache ) inflammation
o Otitis externa
o Otitis media
o Otitis interna
Ear discharges
May be
o Mucoid ( inflammation – hyper
active mucosa )
o Purulent ( infection )
o Bloody ( damages )
Vertigo
Form of dizziness characterized by moving
environment
Tinnitus
Noise in the ear ( ototoxicity )
OTOSCLEROSIS
Conductive hearing loss
Normal bone is replaced by spongy bone
Ankylosis of the foot plate of the strapes
Impaired vibration system
Assessment
Gradual hearing loss
Difficulty hearing a whisper
Paracusis : form of distortion to hearing
DX: Rinne’s test
Intervention
Hearing aid
Surgery
o Stapedectomy ( primary )
o Fenestration ( create opening )
MENIERE’S DISEASE
Endolymphatic Hydrops
Chronic
Increase in endolymphatic pressure
(endolymphatic fluid )
Assessment
Tinnitus ( earliest )
Hearing loss
Vertigo ( most common )
Intervention
Conservative : Pallative
o Bed rest
o Medication

Sedatives

Diuretics ( Diamox )

Antiemetic
(Metoclopromide )
Diet
o Low sodium ( limit fluids )
exacerbation
Planning & Implementation
Surgery
o Labyrinthectomy
o Endolymphatic Sac Decompression
o Vestibular nerve section
Inflammatory mediators ( nerve irritating
substance )
Fever
Provide environment not conducive
to bacteria
Fast metabolic rate
Potentiates interferon response
Assessment in a client with hearing loss
Turns up volume
Ask for repetition
Inappropriate answer
Leans forward to hear better
Dominates conversation
Abnormal articulation
Communicating with hearing impaired clients
Talk directly
-
Use gestures with speech
Do not shout
Use short phrases
Do not whisper in front of hearing impaired
clients
Do not smile , chew gum or cover mouth
when talking to hearing impaired clients
Other types of ear surgry
Myringoplasty
Tymphanoplasty
Ossiculoplasty
Stapedectomy
Post op: Ear surgery
Inform client
o Head still during surgery

Consciously sedated
o Get out of bed with assistance
o Avoid nose blowing ( 1 week )
o Change cotton ball ( daily )
o Lie on unoperated part
Complication of ear surgery
Facial nerve involvement
o Facial paralysis
Meningitis
Bleeding
NEUROLOGICAL SYSTEM
Nervous System
Central Nervous System
o Brain
o Spinal Cord
Peripheral Nervous System
o Motor Neuron

Somatic Nervous System

Autonomic Nervous
System

Symphathetic
Nervous System

Parasymphathe
tic Nervous
System
o Sensory Neuron

Somatic Neuron System

Visceral Neuron System
Cranial nerve ( 12 )
CN 1 – olfactory ( se )
CN 2 – optic ( se )
CN 3 – oculomotor ( mo )
CN 4 – trochlear ( mo )
CN 5 – trigeminal ( mi )
CN 6 – abducen ( mo )
CN 7 – facial ( mi )
CN 8 – auditory ( se )
CN 9 – glossopharyngeal ( mi )
CN 10 – vagus ( mi )
CN 11 – accessory ( mo )
CN 12 – hypoglossal ( mo )
Symphathetic
Fight or Flight
Dilated pupil
Increase HR & contractility
Bronchodilation
Vasoconstriction
Decrease peristalsis
o Conversion of glycogen – glucose
Inhibit bladder response
Parasymphathetic
Rest & digest
Constricted pupil
Decrease HR
Bronchoconstriction
Vasodilation
Increase digestion – secretion of enzymes
Constrict bladder
Kernicterus ( jaundice ) deadly
BILIRUBIN PRODUCTION :
RBC
Heme
o Fe
o Protoporphylin ( indirect
bilirubin ) fats soluble

Glucorine
transferase
(convert to )

Direct bilirubin (
water soluble )
Globin
Spinal Nerve / Peripheral Nervous System ( 31 )
Cervical ( 8 )
o Head , neck, diaphragm,deltoid,
biceps, wrist extender, triceps,
hands
Thoracic ( 12 )
o Chest & abdominal muscles
Lumbar ( 5 )
o Leg muscles
Sacral ( 5 )
Coccyx ( 1 )
o Bowel,bladder, sexual function
CNS ( central nervous system )
Neuron
Excitability ( ability to response to stimuli )
o External
o Internal
Permanence ( cannot regenerate )
Regenerative capacity of the cell
o Labile ( still regenerate )

Skin, respiratory tract, GI
tract
o Stable ( regenerate for a limited
time )

Liver, kidney, lungs
o Permanent
Neuroglia
Nerve glue ( group of cell )
o Support
o Depend
o Nourishes
Not capable in transmitting impulses
Types:
Astrocytes
o Nourishment of neurons
o Barrier in neuron & brain cell( 75%
of glucose )
o Forming the blood brain barrier
(semi permeable / selective )
Toxins can pass through B&B:
o B-ilirubin
o L-ead
o A-mmonia
o C-arbon monoxide
o K-etones
Oligodendrocytes
o Facilitating rapid transmitting of
nerve impulses
o Responsible in production of myelin
sheath
Migrolia
o Engulf bacteria / cellular debris
o Macropage of CNS
-
Brain: ( Microglia )
Blood: ( Monocytes / Macropages )
Liver: ( Kupfter Cell )
Lungs: ( Alveolar Macropage )
Subcutaneous: ( Histrocytes )
Intracranial Compartment:
80% ( brain mass )
10% ( CSF )
10% ( blood )
Brain Mass
Grey matter – outer cortex
o Integrative / Interpretation
White matter – inner
o Conduction of impulses
Cerebrum
Function:
o S-ensory
o I-ntegrative / Interpretation
o M-otor
1. Frontal lobe:

Sense of humor

Abstract thinking

Primitive reflex inhibited

Hypothalalmus central

Broca’s area
2. Temporal

Hearing

Short term memory
(anterograde amnesia)

Wernick’s area
3. Parietal lobe

Sensory impulses

PPTT

Pain

Pressure

Temperature

Touch
4. Occipital

Vision
5.
Rhiencephalon

Smell, libido,long term
memory ( retrograde
amnesia )
Basal Ganglia
o Parts of extrapyramidal tract
o Release of dopamine
DOPAMINE
Decrease
Parkinson & Huntington
disease
Increase
Diencephalon ( CN 1 – 2 ) - branch out

Posterior part of forebrain

Thalamus ( rely of
impulses / sensation)
Spinothalamic Tract

Hypothalamus

Center for thirst

Satiety( insulin )

Osmoreceptor

Pituitary
gland(controls)

Center for
thermoregulator
Brain Stem
o Mid Brain( CN 3-4 )

Rely of impulses
o Pons ( CN 5 – 8 )

Respiratory rhythm /
depth
o Medulla Oblongata ( CN 10 – 12 )

Controls HR, RR &
vomiting

Center for cardio receptor
- Chemoreceptor Trigger
Zone ( CTZ )
+Cerebellum
o Posture, Gait & Balance
o Muscle Tonicity
Cerebellar Test
o Romberg’s Test

Normal anatomical
position (20 – 30sec )
o Fingers to nose test

o
Identifies Dysmetria
(+FTNT)
Alternate Pronation & Suponation

Dysdiadokinesia
Assessment of the Neurologic System
Physical examination
5 categories
Cerebral function
Cranial nerve
Motor function
Sensory function
GLASGOW COMA SCALE ( Level of Consciousness )
Eye opening
4 – spontaneous
3 – to voice
2 – to pain
1 – no response
Verbal Response
5 – oriented
4 – confused
3 – inappropriate voice
2 – incomprehensive
1 – none
Motor Response
6 – obeys command
5 – localize pain
4 – withdraw to pain
3 – decorticate posture ( corticothalamic
tract )
2 – decerebrate posture ( pons )
1 – none
GCS Scoring
15 – 14 Conscious
13 – 11 Lethargy
10 – 8 Stupos
7
Coma
3
Deep Coma
Decerebrate posturing, the head is arched back, the
arms are extended by the sides, and the legs are
extended. A hallmark of decerebrate posturing is
extended elbows.
Sensory:
Body parts to brain
Motor:
Brain to body parts
Odynophagia ( painful swallowing )
Vagal nerve increase peristalsis / heart rate
Decorticate posturing present with the arms flexed, or
bent inward on the chest, the hands are clenched into
fists, and the legs extended and feet turned inward.
Peripheral Confrontation Test ( Visual Field Test )
Cranial Nerve Function:
Cranial Nerve 1 ( Olfactory )
Sensory
Sense of smell
Shift & identify aromatic subs
Cranial Nerve 2 ( Optic )
Sensory
Impulses of Vision
Check:
o Visual acuity ( Snellen Chart )
o Visual field ( PCT )
Cranial Nerve 3, 4 ,6
( 3 ) Occulomotor
( 4 ) Trochlear
( 6 ) Abducen
o Motor
o Movement of extraocular muscles
o ( CN 3 ) pupillary reflex &
accomodation
Deviation:
o Opthalmoplagia ( paralysis of
EOM)
o Diplopia ( double vision )
Cranial Nerve 5 ( Trigeminal )
Mixed
o Eyes
o Mandible
o Maxillary
Largest cranial nerve
Sensation
o Skin of the face
o Corneal reflex
Motor
o Open mouth
o Move jaw
Cranial Nerve 7 ( Facial )
Mixed
Facial sensory
Sense of taste
Motor
o Facial expression
o Close the eyelid
Cranial Nerve 8 ( Vestibulocochlear )
Sensory
Hearng acuity
Balance
Cranial Nerve 9 ( Glossopharyngeal )
Mixed
Sensory ( posterior 1/3 of the tongue )
Motor
o Swallowing
o Gag reflex
Cranial Nerve 10 ( Vagus Nerve )
Mixed
Sensory
o Throat, Abdominal & Thoracic
vicera
Motor
o PNS response of GI & Heart
Cranial Nerve 11 ( Accessory )
Motor
Movement of sternocleidomastoid &m
trapezius
Headache
Cranial Nerve 12 ( Hypoglossal )
Motor
Movement of the tongue
Assess the motor function
Assess the muscle tone & strength
o Grading of muscle strength

5/5 – movement against
gravity with strong
resistance

4/5 – movement against
gravity with some
resistance

-
-
-
3/5 – movement against
without resistance

2/5 – movement cannot
resist gravity

1/5 – trace movement

0/5 – no movement
Assessing the motor function of cerebellum
o Test for balance
o Test for coordination
Assessing the sensory function
o Evaluate symmetric areas of the
body
o Ask the patient to close eyes
Materials:

Used test tubes

Blunt / sharp object

Use wisp of cotton
Assessing the reflexes
o Deep tendon / muscle stretch
reflexes

Bicep

Tricep

Patellar

Brachioradialis
o Superficial / Cutaneous reflexes

Abdominal

Cremasteric ( inner thigh )
ascend scrotum/ testes

Gag
o Pathologic / Primitive reflexes

Babinski
Grading of reflex
0 - absent
+ - present but diminished
++ - normal
+++ - increased
++++ - hyperactive
Assessment of Brain Stem
Test for the Oculocephalic reflex
o Doll’s eye test ( eye movement
towards the opposite side )
Test for Oculovestibular reflex
o Caloric test

Assess patency of the
ears

Semifowlers position

Irrigate the ear

C – old

O – pposite

W – arm

S – ame side
Diagnostic Procedure
EEG ( Electroencephalogram )
Records electronic activity generated in the
brain especially in the grey matter
Identify seizure disease
Identify brain death
Nursing Consideration
Advise to shampoo hair before procedure
Recommend the patient not to sleep
Withhold medication that affect brain
function ( 24 – 48hrs prior )
o Antiseizure ( Penetol )
o Tranquilizer ( major / minor )
o Brain stimulant ( Amphetamine )
o Caffeine
o Methylpenedate
o Sedatives
Alpha – awake ( calm )
Beta – awake ( alert )
Delta – children
Theta – deep sleep
CT Scan
Scan the body part in successive layer
Uses narrowed xray beams
Asses allergy for contrast dye
Identify:
Intracranial bleeding
Pressure of lesion tumor
Identify changes in brain structure
o Brain atrophy
o Cerebral edema
Ares of refraction
Brain herniation
MRI
Uses magnetic waves
Contraindicated to a patient with:
Pacemaker
Orthopedic metal prosthesis
Implanted
Cerebral Angiography
Visualization of cerebral artery
o Brachial / Femoral
-
Give patient a rest after procedure / Maintain
pressure dressing
o To avoid bleeding
Lumbar Puncture
Ensure consent
Determine ability to lie still
o Side lying position with knee &
head flex
o 500ml CSF ( choroid flexus )
o Subarachnoid space ( L3 – L4 )
o 150ml ( aspirate )
Contraindicated to a patient with increase ICP
o Brain herniation
Keep flat on bed after procedure ( 6 – 12 hrs )
Increase fluid intake after procedure
Indication:
Obtain CSF analysis
Cerebrospinal Gross Analysis
o Normal color ( colorless )
o Abnormal ( pinkish color )
Measure & reduce CSF pressure ( 70 120mmHg )
Use to administer medication
Quekenstedt Test
Subarachnoid block ( assess )
Normal ( CSF pressure is increased )
Slow rise and fall in pressure indicates a
partial block
Alteration in the level of consciousness
Delirium ( acute confusional state )
Disoriented – agitated
Even without stimuli
o Hallucination ( - ) stimuli
Obtunded
Client remain drowsy when awaked
Stupor
Respond to a strong stimulus ( pain )
Confusion
Has short attention span
React to stimuli
Coma
Poor response / totally no response to stimuli
V/S maybe stable
Cerebral death
Vital sign must be maintained artificially
V/S unstable
( - ) reflex
( - ) EEG
( - ) respond
INCREASED ICP
(8 – 20 mmHg )
Predisposing factor
Increased size of brain mass
o Tumor
o Edema
Intracranial bleeding
o Intracerebral
o Subarachnoid
o Epidural hematoma
o Subdural hematoma
Inflammatory condition
o Meningitis
o Encephalitis
CSF flow problem
o Hydrocephalus
Ss/Sx;
Early sign:
Alteration of LOC
o Awaken coherent
o Restlessness – agitated
o Confusion
o Lethargy
o Obtunded
o Stupor
o Coma
Visual problem
o Blurring of vision
o Diplopia
Headache
Late sign:
Change in V/S
Cushing triad ( hyper – brady – brady )
o Increase BP ( systolic )
o Decrease RR
o Decrease HR
o Increased heart volume
Projectile vomiting
Pupil changes
Changes in motor function
o Spasm
o Paralysis ( transient )
Increase ICP
Increase temp.
Decrease RR
Decrease HR
Increase BP
Widened P.P
Nursing Management for increased ICP
Proper positioning
o Semi/ High Fowler ( neck properly
aligned )
Close monitoring ( GCS q1 – PERRLA papillary
reflex )
Promote oxygenation
Promote safety
Decrease environmental stimuli
Limit fluid intake
Prevent ICP
Instruct the patient to avoid this:
Valsalva maneuver
Excessive cough
Excessive vomiting
Lifting heavy object
Bleeding
Administer meds as ordered
Fast drip
Osmotic diuretic ( Mannitol )
o Cerebral decompression
Loop diuretic
o Onset 15 – 30 mins prior to
administration
Corticosteroid
Antipyretic
Anticonvulsant
Analgesic
PARKINSON DISEASE
Idiopathic
Chronic progressive disease by CNS
Predisposing factor
Poisoning ( lead monoxide )
Hypoxia
Encephalitis
Ss/Sx:
Resting tremor
Propulsive gait
Rigidity
Drooling
Shock
Decrease temp.
Increase RR
Increase HR
Decrease BP
Narrowed P.P
-
D
ysphagi
a
M
onotono
us
speech
Bradykinesia
o Micropphagia
o Hypomimia
o Hypophonia
Pharmacotherapy
Dopamine agonist
o Controls of voluntary movement
o Inhibits excitability of neuro
muscular junction
o Levodopa ( L –dopa )
o Carbedopa ( Sinemet ) inhibits
dopamine carboxillation
Artane ( minimize muscle rigidity )
Antihistamine ( decrease tremors )
Amantadine HCl ( symmetrel ) increase
availability of dopamine in the brain
Nursing management
Passive ROM exercise
Maintain good nutrition
o High protein
o High carbohydrates
o Increase oral fluid intake
o Increase fiber
Safety precaution
Promote ambulation
MULTIPLE SCLEROSIS
Demyelization of neuron
White matter
Ss/Sx:
Visual disturbances
o Blurring of vision
o Diplopia & nystagmus
o Scotoma
Impaired sensation
o Paresthesia
Impaired motor function
Urinary bowel disturbances
o Constipation
o Spastic bladder
o Flaccid bladder
Decrease sexual capacity
Late stage: ( psychiatric disturbance )
Depression
Apathy
Euphoria
Forgetfulness
Triad of M.S
I-ntentioanl tremors
N-ystagmus
A-taxia
DX:
CSF analysis
MRI
( + ) Lhermittes sign ( caudal portion)
Medication
Muscle relaxant
Immunosuppressive medication
Urinary cholinergics ( Bethanechol )
Urinary antispasmodic
Clonazepam ( reduce ataxia )
NI:
Promote safety
Provide eyepatch for diplopia
Establish regular exercise-rest pattern
Proper diet
Promote independence ( degree of flexion )
SPINAL CORD INJURY
Result from disruption of nerve tract and
neuron
May result to partial or complete loss of
motor sensation & reflex
Cause:
Contusion ( blunt )
Laceration ( penetrating )
Fracture of vertebrae
NI:
Enhance activity rest pattern
Facilitate normal nutrition
Facilitate spinal revery
Pharmacotherapy
Corticosteroid
Baclofen
Dantrolene sodium
Level of injuries
Cervical injury
o Respiratory difficulty
o Quadriplegia
Thoracic
o Paraplegia
o Bladder / Bowel dysfunction
Lumbar & Sacral
o Paraplegia
o Erectile dysfunction
Complication
Spinal Shock ( Neurogenic )
o Sudden onset
o Muscles are paralyzed
o Negative reflex
o Sign of shock
o Medical emergency
Autonomic dysreflexia / Hyperflexia
o Gradual onset (Hypertensive stroke)
o Caused by injured above T6
o Triggered by visceral distention (Full
bladder / Constipation)
o Sign of SNS stimulation
o Medical emergency
MYASTHENIA GRAVIS
Auto immune disorder
Low Acethylcholine ( Neurotransmitter )
o Excitability of NMJ
High production of Acethylcholinesterase
Decrease receptor site
Presence of resistance in receptor site
Ss/Sx:
Ptosis ( dropping of eyelid )
Diplopia
Dysphagia
Weakening of Laryngeal muscle
Muscle weakness
DX test for MG:
Edrophonium Chloride
o Tensilon Test ( Confirmatory )
o CSF Analysis

Increase Cholinesterase
Monitor for 2 types of crisis
Mysthenia Crisis
o Causes

Under Medication

Stress

Infection
o Management

Give Anticholinesterase
Cholinergic Crisis
o Over Medication
o Ss/Sx:

Salivation ( Thialism )




o
Lacrimation
Urination
Diarrhea
Body weakness

Evident Sign Depolarization
of Neuroplates
Management

Give Anticholinergic

Atropine
Sulfate
(Antidote)
TRIGEMINAL NEURALGIA ( Tic Douloureux )
Sensory disorder of the 5th cranial nerve
Assessment
Severe recurrent sharp pain along the tract
of the 5th CN
o Cheeks
o Superficial layer of the nose
o Lips
o Gums
Triggering factors
o Direct pressure
o Washing of the face
o Chewing
o Intake of foods or fluid ( Extreme
temperature )
o Exposure of cold environment
NI:
Diet modification
Avoid factor that triggers pain
Chew on the unaffected side
Pharmacotheraphy
Baclopen
Carbemazepine
o Relieves neuralgia
Surgical Intervention
Microvascular Decompression
o It relocates the artery that
compresses nerves & blood vessels
BELL’S PALSY
Facial Nerve ( CN7)
Cause
Lesion on lower motor neuron
Unilateral facial paralysis
Predisposing factors
Infection ( CNS )
Tumor
Trauma
Assessment
Facial Paralysis
o Unilateral ( 2 weeks )
Loss of taste
o anterior 2/3 of tongue
Intervention
Protect eyes from dryness
Instruct client to chew on affected side
GUILLAIN BARRE SYNDROME ( Spinal nerve )
Acute ( sudden onset ) -Post -Infection ( Resp.
GI infection ) –Polyneuritis
Form of an autoimmune disorder
o Damage Myelin Sheath
(Polyneuritis)
Ss/Sx:
Clumsiness ( Initial )
Paresthesia
Ascending muscle weakness
Dysphagia
Arrhythmic
Respiratory failure ( #1 complication )
DX:
CSF analysis
NI:
Maintain patient airway
Continuous monitoring
Promote safety
Plasmapherisis
o Extracorporeal treatment ( outside
the body – antecubital vein )

Cell separator
(Centrifugal force)
separates plasma
Pharmacotherapy
Corticosteroids ( SAWSO )
Anti arrhythmia
CVA ( Cerebro Vascular Accidents )
Disrupted cerebral blood flow
Common location
Middle Cerebral Artery ( MICA )
Internal Carotid Artery ( ICA )
Types:
Thrombolic ( Ischemic Stroke )
o Form inside the cerebral blood
vessel
Embolic ( Ischemic Stroke )

o
Form outside the cerebral blood
vessel
Hemorrhagic ( Hypertensive Stroke )
o Rupture of aneurysm
Risk Factors:
Atherosclerosis ( narrowing )
HPN, DM, MI
Valvular Heart Disease ( valvular stenosis )
Post Heart Surgery ( valvular replacement )
Lifestyle
o Smoking
o Sedentary Lifestyle
o Hyperlipidemic
o Prolonged use of Contraceptives

Abdominal pain

Chest pain

Headaches

Eye problem

Severe leg cramps
Stages of CVA
1. Transient Ischemic Attack
Reversible : Ss/Sx subside in 2hr
Same as CVA ( causes, effect, affectation )
o Headaches
o Dizziness
o Numbness
o Tinnitus
o Visual / Speech Disturbances
2. Stroke in evolution
o Progressive Ss/Sx of stroke
3. Complete stroke
o Paralysis
o Anorexia, Nausea & Vomiting
o Dysphagia
Late sign:
o Cheyne Stroke Respiration ( hyper
capnea with period of apnea )
Other Ss/Sx:
(+) Kernigs & Brudzinki ( hemorrhagic )
o Meningeal Irritation
Neurological Deficits
o Hemiplagia - Neglect Syndrome
( Unilateral Neglect )
o Homonyniuos Hemanopsia Neglect Syndrome
( Unilateral Neglect )

Approach on
intact vision
o
o
o
o
o
o
o
o
Encouraged
client to scan
environment
Aphaxia

Receptive

Expressive

Provide
alternative
ways for
expression

Put extra
patience

Simple phrases
Agraphia

Inability to write
Alexia

Inability to comprehend
Ataxia

Unsteady / Jerky
movements
Speech changes

Dyarthria
Decreased sensation
Bowel & Bladder dysfunction
Nuchal rigidity
DX procedure
CT scan
Angiography ( perfusion of blood vessel )
Management for CVA
Acute phase
Promote oxygenation
BP maintenance at 140/90mmHg
Suction secretion as needed
WOF increased ICP ( herniation of medulla
oblongata )
Proper positioning ( semifowlers )
Post Acute phase
Maintain patent airways
Elevate head of the bed
Monitor V/S, I&O, neurocheck
Prevent complication of immobility
Prevent aspiration ( thicken fluid )
Alternative means of complication
Maintain side rails
Pharmacotheraphy
Osmotic diuretic
Loop diuretic
Corticosteroid
-
o
Mild analgesic
Thrombolytics ( Ischemic stroke )
o Prevent blood clot
Anticoagulant
o Maintenance
Antiplatelet
o Prevent platelet adhesion &
aggregation
o Before meals
CONVULSIVE DISORDER
CONVULSION
Seizure – Abnormal excessive uncontrolled
electrical activity of the brain
Epilepsy – Characterized by chronic seizure
activity
Acute febrile seizure – ( Cytoplasmic
Reticulum Alteration ) Hyperpyrexia
Status Epilepticus - Epileptic spasm without
interval of consciousness
o Acute – Severe Exacerbation
(30mins of continuous episode of
epilepsy)
Drug Of Choice ( DIAZEPAM )
Predisposing factors
Head injury due to birth trauma
Carbon monoxide poisoning
Brain tumor
Genetics
Physical Stress
Sudden withdrawal of convulsant
Types of Seizures
Generalized
Tonic – Clonic Seizures
o With or without AURA

Epigastric pain

Halo vision

Burning sensation

Tactile aura

Ringing sensation

Epileptic cry
o Tonic phase ( 10 -20 sec )
o Stiffining or rigidity
o Clonic phase ( 30 sec )
o Jerking movement
o Hyperventilation
Absence Seizures ( Petit Mal )
o May or may not lose consciousness
-
-
Partial
-
-
Seizures may occur several times
during the day
o Blank stare
o Decreased blinking
Myoclonic
o Brief generalized seizures
o Clonic phase
Atonic / Akinetic ( drop attack )
o Sudden momentary loss of muscle
tone
Complex Partial ( Temporal damage )
o Psychomotor seizures
o Drastic change in behavior
Simple Partial
o Confined into a specific area
NI:
-
Note time and duration of seizures
Assess for AURA
If the client is standing, place client on the
floor
Support ABC
During Seizures:
Do not place anything in the client mouth
Do not restrain the client