Pathophysiology Final Study Guide
Patho Section 1
Cell & Tissue Function/Dysfunction
Atrophy: decrease in size of cells.
Hypertrophy: increase in cell size.
Hyperplasia: increase in number of cells.
Metaplasia: mature cell type is replaced by a different mature cell type.
Dysplasia: cells vary in size & shape within a tissue.
Anaplasia: undifferentiated cells with variable nuclear & cell structure.
Neoplasm: tumor.
Cell Damage
Ischemia: oxygen deficit due to respiratory or circulatory problems.
Hypoxia: reduced oxygen in tissue.
Oxygen Deficit: decreased energy production, loss of Na pump ↑ intracellular Na.
Temperature: inactivation of some enzymes, damages organelles, protein coagulation,
disruption of cell membrane.
Micro-organisms
Abnormal Metabolites: caused by genetic disorders or altered metabolism.
Nutritional Deficits
Cell Death
Apoptosis:programmed cell death controlled by genetics.
Necrosis:lysis of a cell, cell components leak into blood.
Liquification:dead cells liquefy due to release of enzymes.
Coagulation:cell proteins are altered or denatured causing coagulation.
Caseous:form of coagulation necrosis, thick, yellowish, cheesy.
Fat: fatty tissue is broken down into fatty acids.
Tissue Damage from Chemicals
Exogenous: from environment.
Endogenous: from inside the body,
Tissue Damage from Physical Agents
Hypothermia: vasoconstriction, ↑ blood viscosity, hypovolemic shock ↓ blood
pressure.
Hyperthermia: causes general vasodilatation, decrease in circulating blood
volume.
Radiation: primarily affects actively dividing cells
Biological Agents
Insects/Animals: direct injection of toxin, transmission of infectious agent,
allergic reaction to insect proteins.
Food Poisoning
Normal Defenses of the Body
1st Line Defense
Physical Barriers: unbroken skin, mucous membranes, nasal hair, clots.
Fluids: may contain enzymes or chemicals:saliva, tears, gastric, sweat.
2nd Line Defense-non-specific
Phagocytosis:neutrophils & macrophages engulf cells, debris, foreign mat.
Inflammation: automatic response to cell injury.
3rd Line Defense-specific defense produced by
Antibodies
Cell Mediated Immunity
Cellular Defenses
Mast Cells: located in tissue & release histamine & bradykinin.
Macrophages: monocytes that enter tissue & act as phagocytes.
Interferons: small proteins made by lymphocytes to prevent virus replication.
White Blood Cells
Granulocytes
Neutrophils: work by phagocytosis.
Basophils: release histamine leading to inflammation.
Eosinophils:combat the effects of histamine.
Agranulocytes
Monocytes:can enter tissue to become macrophages which
function as phagocyte.
Lymphocytes: B & T
Acute Inflammation
Vascular Response: vasodilatation & increased capillary permeability.
Cellular Response: migration of inflammatory cells through chemotaxis to injury site to
destroy ineffective organism, remove damaged cells, released inflammation
mediators.
Exudate
Serous: watery, mostly fluids, some proteins and WBC’s.
Fibrinous: thick, sticky, high fibrin content.
Purulent: thick, yellow-green, contains leukocytes, cell debris & microorganisms.
Abscess: Pocket of purulent exudates or pus in a solid tissue.
Local Effects of Inflammation-Cardinal Signs of Inflammation
Redness & Warmth: due to increased blood flow to area.
Swelling: shift of protein & fluid into interstitial space.
Pain: pressure on free nerve endings, chemical mediators irritate nerves.
Loss of Function: edema may restrict movement.
Systemic Effects of Inflammation
Mild Fever: due to resetting of hypothalamic thermoregulatory set point, release of
endogenous pyrogens.
Malaise
Fatigue
Headache
Anorexia
Treatment of Inflammation: drugs may decrease capillary permeability, reduce number of
leukocytes & mast cells.
Types of Healing
Resolution: minimal tissue damage, cells can repair themselves.
Regeneration: damaged tissue is replaced by identical tissue.
Replacement: functional tissue replaced by scar or fibrous tissue.
1st Intention: wound is clean, edges are close together with minimal gap.
2nd Intention: large break in tissue, longer healing process with more scar tissue.
Scar Formation: fibroblasts proliferate, abnormal amount of collagen.
Hypertrophic: overgrowth of fibrous tissue, keloid.
Ulceration: blood supply around scar is impaired resulting in tissue
breakdown.
Wound Staging
1. Partial thickness ulcer-red or pink ie. Sunburn.
2. Partial thickness ulcer-blister, scrape, abrasion.
3. Full thickness ulcer- through dermis.
4. Full thickness ulcer that includes muscle or bone.
Drainage
Transudate: clear & watery.
Serosanginous: clear w/ tinge of red/brown. Contains serum/blood thin & watery.
Exudate: creamy yellowish. Contains proteins & WBC’s Thick.
Purulent: yellowish. Contains leukocytes and necrotic debris, thick.
Infected Pus: hues of yellow, green or blue. Contains pathogens, thick.
Venous Insufficiency
Clinical Presentation
Incompetent Valves
medial leg area
Inefficient Calf Pump
edema
Distended Capillary Bed
wet wound
Decreased Fibrolysis
scaring, red base
Fibrin Leakage
hemosiderin deposits(purple/brown on leg)
Trauma
Ulcer
Documentation of Pulses
Normal: 2+
Diminished: 1+
Absent: 0
Arterial Insufficiency: decreased arterial blood supply.
Acute(thrombosis) vs Chronic(arteriosclerosis)
Characteristics
Dry Gangrene: nonviable dry tissue.
Wet Gangrene: tissue necrosis + bacterial infection. Drainage w/ odor.
Black Gangrene: gangrenous borders, mummified skin.
Pain w/ walking=Claudication
Skin is atrophic(no hair) slow nail growth & Diminished Pulse
Ankle Pressure Index: SBP LE/SBP UE
>1
no arterial occlusive disease
.9-1 min sx in LE
.5-.9 claudication pain(leg pain w/ walking)
.3-.5 ischemic rest pain
<.3
ischemic w/ tissue necrosis
Assessment of arterial flow, skin color w/ elevation/dependency
1. LE Elevation to 60º for 1 minute. Normal=no color change.
2. Lower the LE & record time for color to return.>30seconds
means arterial insufficiency. Will look hyperemic(bright red).
Immune Response-Third Body Defense
Humeral Immunity: antibodies are produced to protect body & stored in blood.
Cell Mediated Immunity:lymphocytes are programmed to attack non-self cells.
Antigens:immunogens, proteins, polysaccharides, glycoproteins on cell surface.
Cells
Macrophages:present throughout the body, derived from monocytes,
initiate immune response, engulf foreign materialprocess & display
foreign antigens & present them to lymphocytes, secrete monokines &
interleukins .
Lymphocytes:primary cell in immune response,
T: has 3 subgroups made in bone marrow & differentiate in
thymus, cell mediated immunity, can target certain cells.
1.Cytotoxic T:cells destroy cells bind to antigen & release enzymes
2.Helper T: facilitate immune response by activating & regulating
3.Memory T: remember antigens.
B:Made in bone marrow, located in spleen & lymphoid tissue,
produce antibodies.
Natural Killer:kill tumor or virus infected cells w/o prior exposure
Antibodies
IgG:most common, can activate compliment, cross placenta, primary &
secondary immune response.
IgM:can activate compliment, natural antibodies ie. Involved in blood type
IgA:not in blood, is in tears, saliva & colostrums.
IgE
IgD
Compliment System:antigen-antibody complex, activated during immune rxn w/ IgG or
IgM. Causes cell damage when activated, causes macrophages to release enzymes.
Immune Response
Primary: 1st exposure to antigen, 1-2 weeks needed for effective antibodies
Secondary:repeat exposure to same antigen, effective response in 1-3 days
Immunity: Innate-always present. Or acquired.
Hypersensitivity Reactions
Type 1 Hypersensitivity:allergic rxn, exposed to allergen causes development of
IgE’s,activate mast cells and causes inflammation. Ie. Hay fever, allergies, asthma
Type 2 Hypersensitivity:cytotoxic hypersensitivity. Antigen on cell membrane
reacts
w/ circulating IgG’s, activates compliment, cells w/ antigen destroyed. Ie incompatible blood
type exposure.
Type 3: Immune complex hypersensitivity-antigen & antibody combine forming
immune complexes that cause inflammation & tissue destruction.
Type 4:Cell Mediated or delayed response by T-lymphocytes. No antibodies
present. Ie. Tb test, contact dermatitis.
Immune System Malfunction
Hypersensitivity: full system immune response to non-noxious stimulus.
Asthma: central windpipe or airway disorder.
Interventions/Treatment:avoid triggers, medicate. Peak flow 50-80% of
person’s best signal moderate attack, >50% below best PF = major attack.
Autoimmune
Multiple Sclerosis: autoimmune demyelinization of nerves in brain &CNS
Classification
Clinically Isolated Syndrome-only suffer 1 attack.
MS-multiple attacks at least 1 month apart & damage to at
least 2 separate CNS areas & r/o all other possible causes.
Tests & Measures: MRI, visual evoked potentials, CSF analysis.
Interventions: modify disease course, treat attacks, manage sx.
Myasthenia Gravis: antibodies destroy Ach receptors at NM junction.
Guillen Barre Syndrome: demyelination of peripheral nerves.
Fibromyalgia: generalized musculoskeletal pain > 3 months, multiple
tender points affecting all 4 quadrants, 11/18 points, 4Kg force painful
Rheumatiod Arthritis:autoimmune destruction of joints affects multiple
joints in symmetrical pattern, inflammation can affect organs.
Scleroderma:affects microvessels causing hypoxia in all tissue. Skin &
organs commonly affected.
Sjogren’s Syndrome: autoimmune disease » loss of fluid for tears/saliva
Hashimoto’s Disease: autoimmune thyroid disease, causes hypothyroidism
Graves Disease: hyperthyroidism,
Type 1 Diabetes: autoimmune destruction of pancreas cells » no insulin.
Inflammatory Bowel Disease: group of disorders with inflammation of
intestines
Crohn’s: ulcers throughout intestines, except rectum.
Ulcerative Colitis: ulcers in lower intestines, may begin in rectum.
Immunosufficiency
HIV
Meningitis: photophobia is red flag.
Toxoplasmosis: parasitic infection. Contaminated cat feces in 1st trimester.
Histoplasmosis: fungal infection diagnoses based on organ involved
Micro-organisms
Bacteria-unicellular organisms, no nucleus, divide by binary fission.
Cocci-staph, strep, diplococci-pneumococcus
Bacilli-tetanus, botulinum.
Spirochetes-syphillis, cholerae.
Gram Positive: doesn’t retain crystal violet, has outer membrane layer.
Gram Negative: retains crystal violet, no outer layer, thick peptidoglycan layer
Toxins
Exotoxins: produced by gram+ bacteria.
Endotoxins: gram- bacteria. Released when bacteria die causing shock.
Virus
Active Viral Infection: virus attacks host cell injects genetic material, uses
host cell to produce viral proteins & nucleic acids. New viruses made in
cytoplasm & released by lysis or budding from host cell.
Latent Viral Infection: virus enters cell similar to active infection, replicates
slowly
or delays replication, viral proteins are inserted into cell
membrane of host cell causing
immune response. Ie. Herpes virus.
Fungi: eukaryotic organisms, primarily affect skin or mucous membranes.
Protozoa: eukaryotic organisms, usually parasites. Ie. Malaria, dysentary
Prions: protein like agent that can change shape of proteins in host cell. Mad Cow.
Modes of Transmission
Direct Contact
Indirect Contact
Droplet
Aerosol
Vector
Nosocomial Infections: infections that occur in healthcare setting.
Development/Stages of Infection
Incubation Period: time of organism entering body to appearance of clinical signs
Prodromal Period: infection is developing, nonspecific symptoms.
Acute Infection: fully developed infectious disease with peak clinical signs.
Chronic Infection: microorganism continues to replicate in body, sx milder.
Subclinical Infection: Microbe can reproduce in body but no signs present.
Septicemia: bacteria reproducing & circulating in bloodstream.
Complimentary Medicine
Red Flags: refer to Dr.
Chest pain/discomfort, unusual SOB w/ acute pain in chest, arm, throat or jaw,
unexplained dizziness, persistent hoarseness or cough, difficulty swallowing,
persistent abdominal pain/discomfort, coughing up blood, unexplained weight
gain/loss, persistent unexplained fatigue, changes in a mole, change in
bowel/bladder
habits, blood in stool, unexplained vaginal bleeding, lump in breast
or discharge or
change in size or shape, changes in testicles, severe HA, blurred vision, sores that don’t heal,
persistent unexplained lumps/swelling, persistent back pain even w/ rest, unexplained leg
swelling/pain.
Screening Lab
Fingernails
Absent Lunula: anemia, malnutrition.
Pyramidal Luluna: trauma or excessive manicures.
Red Luluna: cardiovascular disease, collagen disease of vessels, blood CA
Mee’s Lines: metal toxicity, chemotherapy exposure.
Longitudinal Lines: Addison’s disease, breast CA, melanoma, trauma.
Splinter Hemorrhages bacterial endocarditis, lupus, renal failure, psoriasis
Terry’s Nails:half& half appearance:edema & anemia »renal/liver disease.
Cancerous Moles-asymmetry, border, color, diameter
PATHO TEST 2 REVIEW
General Cancer Info
General Genetics Info
Cancer rundown
Bladder Cancer
:
-Early stages bleeding in urine but little no pain
-Hematuria 1st sign with changes in urination
Breast Cancer:
-New lump is most common symptom
-Manual palpation better catch than mammogram
Cervix cancer:
-often asymptomatic
-vaginal discharge, abnormal bleeding, pain during intercourse
Colorectal cancer:
-change in bowel habits most common
-Diarrhea, constipation, more narrow stools, blood in stool
-Bright blood-lower GI, Dark/black blood-Upper GI
Lung cancer:
-persistent cough with or w/o chest pain
-Feeling of an infection that just won’t go away
Prostate cancer:
-weak interrupted urine flow, frequent urination esp. @ night
Renal cancer:
-low back pain, especially if pain not assoc. w/ injury
Skin Cancer:
-Any new growth on skin should be examined
-Spot or bump that changes size, irregular borders
-Sore that will not heal
Change in bowel/other habits
A sore that does not heal
Unusual bleeding or discharge
Thickening or lump in breast
Indigestion or difficulty swallowing, unexplained weight loss
Obvious change in wart or mole
Nagging cough/hoarseness
Fluid/Electrolyte imbalance
Water -60% adult body wt, 70% infants, higher % in females
Fluid compartments
-Intracellular 2/3 water in body
-ECF 1/3
*Interstitial 3/4, Intravascular 1/4, Cerebro Spinal Fluid 1%
Control Fluid Balance->Thirst mechanism
-Antidiuretic Hormone (ADH): fluid output
-Aldosterone: Reabsorption of water and sodium
-Atrial Natriuretic Peptide (ANP): lowers BP by controlling blood volume
EDEMA: fluid excess in interstitial compartment
DEHYDRATION: Signs-decreased skin turgor, sunken eyes, low BP, rapid weak pulse, high temp
ELECTROLYTES
Intracellular electrolytes: potassium, phosphate, magnesium
Blood electrolytes: sodium, calcium, less extent bicarbonate
EXCESS/DEFICIENT ELECTROLYTE
CAUSES of
EFFECTS of
Excessive sweating, vomiting,
diarrhea, insufficient aldosteerone,
kidney failure, excessive waterintake
Insufficient ADH, loss of thirst
mechanism, watery diarrhea, rapid
respiration,
Diarrhea, diuresis, excessive
aldosterone, low dietary intake,
Insulin forces K+ into cell
Renal failure, deficit aldosterone,
leakage of K+ from ICF into ECF,
prolonged acidosis (H+ replaces)
Hypothyroidism, malabsorption
syndrome, deficient serum albumin,
increased serum pH
HypoMagnesmia
Malabsorption of assoc with
alcoholism, use of diuretics
Impaired nerve conduction, fatigue,
mm cramps, Abdom issues,
decreased Osmotic pressure in ECFTHUS fluid into cells
Fluid shift out of cells, weakness, dry
tongue mucous membranes,
increased BP
Cardiac Dysrythmias, interference
with neuromm junc, decreased dig.
Tract motility
Cardiac dysrythmias, mm weakness
common progressing to paralysis,
respiratory arrest
Increased permeability/ -excitability of nerve
membranes,spont stim of skeletal
mm, Tetany, weak Heart
contractions
Depressed neuromm activity
-interference with ADH function
-increased strength cardiac
contractions
Neuromuscular hyperirritability heart arrythmia
HyperMagnesmia
Renal failure
Depressed neuromm funct
HypoNatremia
HyperNatremia
HypoKalemia
HyperKalemia
HypoCalcemia
HyperCalcemia
Uncontrolled release from bones demineralization from immobil.
-increased intake
CAUSE(S)
GENETIC DISORDERS
Angelman syndrome
Cri du Chat
Downs syndrome
X-linked, lose “bit” of chromosome
Missing part chromosome 5,
mutation at
Trisomy 21
Fragile X syndrome
Fragile x retardation protein
Neurofibromatosis
Autosomal dominant,
CHARACTERISTICS
Flat head. PROTUDING TONGUES
odd bouts of Laughter, Balance
disorders
Hi “CAT-like” cry, webbed toes &
fingers, DOWNward slant to wide
set eyes, skin tags ant. ears
Flat face, Upward slanted eyes,
single DEEP crease palm of hand,
HYPOtonia (low muscle tone),
Large head w/ prominent forehead,
boys develop long face, tactile
defensiveness
Esp. effects nervous syst and skin,
birthmarks called café-au-lait,
freckles in armpits and groin,
purplish RUBBERY lesions on skin
GENETIC DISORDERS
CAUSE(S)
Prader Willi syndrome
Chromosome XV
Smith-Magenis Syndrome
Deletion @ XVII
Klinefelter’s Syndrome
Men w/ extra X chromosome
Turner Syndrome
Females w/ only 1 X chromosome
Triple X syndrome
Extra X chromosome
Williams syndrome
Random mutation chrom. 4
Cystic Fibrosis
Single point mutation CFTR
Muscular Dystrophy
Dystrophin-over 30 different genetic
diseases
CHARACTERISTICS
Extreme hunger/overeating,
obsessed w FOOD, temper
tantrums, violent outbursts, @ 1
Y.O. become ravenously hungry
Broad nasal bridge, PROTRUDING
jaw, ear anomalies, SPEECH &
middle ear problems, SLEEP
disturbances
Sudden Mood changes
Teenagers less developed,
prepubescent testosterone helps,
testosterone levels to diagnose,
infertility
WEBBED neck!! Underdeveloped
BREASTS
High BP, Type II diabetes
Girls TALL, often not diagnosed, no
long term problems
50% retardation, PUFFINESS around
eyes, long neck, sloping shoulders,
Poor DEPTH perception
Life limiting (30s), frequent
coughing w/ thick sputum, saltyskin, frequent lung infections,
-Duschenne most common (missing
dystrophin), affects skeletal &
cardiac Muscle
-Fascioscapulohumeral-faulty
dystrophin
-Myotonic; congenital, juvenile,
adult, late onset-over 50
ACID-BASE Imbalance -> Normal 7.4, ranges from 7.35 to 7.45
o
Enzymes act in narrow pH range
 20:1 base to acid ratio
 Respiratory system- alters carbonic acid levels Acidosis-> CO2 up
 Kidneys- modifies excretion rates of acids, Most effective control system
Acidosis: excess Hydrogen ions
Alkalosis: deficit in Hydrogen ions
Acidosis HCO3- down
Alkalosis HCO3- down
**compensation occurs to balance relative ratio (20:1), NOT total concentration
BLOOD DISORDERS
Hemocrit
- proportion of cells (RBC)
-indicates viscosity & inc or dec in hydration
Hemoglobin: Tetramer-> 4 hemes which carry 1 oxygen each
Hemostasis:
Hemophilia A: 90% of cases, deficit of clotting FACTOR III, an X-linked recessive trait
Hemophilia B: Xmas disease, deficit FACTOR IV
Hemophilia C: factor XI, milder form
Blood therapies:
o Whole blood: for severe anemia
o Artificial EPO (stimulates RBC production)
o Bone marrow Transplants: some cancers, immune deficiencies, blood cell disease
ANEMIAS- can lead to ANGINA or CHF
 Hemoglobin deficit= reduction in oxygen transport
 General signs
 Fatigue, pale face, dyspnea, tachycardia
 Causes
 Nutrient deficiency
 Impaired bone marrow
 Blood loss or excessive destruction of RBCs
Iron deficiency: impairs hemoglobin, very common, usually underlying CAUSE
Pernicious Anemia
o Large, immature, nucleated erythrocytes(RBCs)
o SYMPTOMS-> Tongue large, RED, sore, shiny
o
 Aplastic Anemia
o Temporary or permanent impairment or failure of bone marrow
o Bone marrow cells replaced by FAT
o Cause must be ID’d for prompt treatment & marrow recover or is LIFE threatening

Hemolytic anemia
o CAUSE: excessive destruction of RBCs via many causes

Sickle Cell Anemia-> abnormal hemoglobin
o Genetic condition; autosomal rec., heterozygous R carrier
 More common n AFRICAN ancestry
o Sickle cell crisis occurs when LOW O2 levels
 When deoxygenated HbS is unstable and crystallizes=sickle shape
Thalassemia
o Most common blood disorder in world
o Abnormal hemoglobin due to missing genes

ANEMIAS CONT.

Polycythemia
o Primary polycythemia->Increased rate of RBC production
o
 Secondary polycythemia-> Increased RBC production due to prolonged Hypoxia
Concerns for both:
Category


Sytemic disease
Musculoskeletal
Sluggish blood flow
Increased BP & hypertrophied heart

Indications of Blood clotting Disorders
o Persistent bleeding in gums & nose bleeds, bleeding into joint, coughing up/vomiting blood,
blood in feces, vomiting, low BP

Causes of clotting disorders
o Defective platelet function
o Long term use of warfarin

Hemophilia A (classic)
o Most common inherited clotting disorder
o Varying severity
o Spontaneous bleeding into joints

Disseminated Intravsascular Coagulation
o Excessive clotting & excessive bleeding in circulation
o Clotting factors reduced to dangerous level
o Widespread uncontrollable bleeding
o HIGH fatality rate
THE LEUKEMIAS
Acute High proportion of IMMATURE, nonfunctional cells in marrow and circulation
Onset is abrupt
SIGNS: Frequent uncontrolled infections ,BONE PAIN, Weight loss, fatigue, drowsiness, vomiting
Chronic Higher proportion of MATURE cells
Insidious onset
Mild signs & better prognosis
Diagnostics for all leukemias
Peripheral blood smears
Bone marrow biopsy confirmation
Treatment-> Chemo, Biologic therapy using INTERFERONS, Can stimulate immune system
Histology:
Differential diagnosis of Systemic Pain versus Musculoskeletal
Course/duration
Relieving Factors
Aggravating Factors
Quality
Intensity
Location
Associated signs & symptoms
Cyclic, progressive symptoms
Constant or may come & go
Usually NONE : if relieved by rest
or position, there is typically cyclic
progression of increasing frequency,
intensity, or duration until
rest/position doesn’t work
None specific
DEEP, ACHING, throbbing
DIFFUSE or waves/spasm
Severe if cancer spread to nerves
surrounding a visceral organ
From Upper back, middle to low
back regions. May also be in front
of trunk frequently in abdomen over
affected organ
Jaundice, skin rash, weight loss,
fatigue, low-grade fever, muscular
weakness, frequent infections
Sudden (gradual when related to
overuse)
Decrease with Rest
Increase with use affected region
SHARP
Depends on if acute, subacute, or
chronic
Located over injury sight.
If severe may also refer proximal
and distal to injury sight
Usually none- trigger pts may be
accompanied by nausea/sweat
Patho 3
Cardiovascular Disorders - Gould Ch. 18
-general treatment
-Low Na+, fat ->Decrease weight
-exercise – Increase HDL, decrease LDL (high and low density lipoproteins)
-smoking cessation
-Vasodilators, (e.g. nitroglycerin for coronary a.’s)
-Beta-blockers – prevent CNS stimulation of heart
-Ca2+ channel blockers – decrease contractility of heart
- anti-hypertensives – ACE inhibitors (angiotensin converting enzyme – work via renal
system), diuretics, cholesterol decreasing drugs, anticoagulates to prevent clots
Arteriosclerosis – hardening, narrowing of arteries – fibrous tissue formation (tunica adventicia
grows)  constriction
-caused by hypertension
Atherosclerosis – plaque buildup in arteries, “atheromas”
-coronary occlusion angina, MI
-clot to brain TIA or stroke
-clot in periphery  can lead to aneurysm
Cholesterol
-HDL – mostly protein, little fat – carries lipids to liver for excretion
-LDL – mostly fat, little protein – carries lipids to cells of body
-largely responsible for atheroma formation
Risk factors for cardiovasc problems – age, heredity, obesity, sedentary lifestyle, smoking,
glycemic control, serum lipids
Angina Pectoris – O2 low in heart muscle  severe, crushing chest pain, “angere”= “to choke”
Myocardial infarction – cell death from O2 deprivation  replaced with fibrous tissue
-majority occur in left ventricle
Congestive Heart Failure
-Forward effect – Not enough blood going out, pump FAILURE
-Backward effect – CONGESTION of blood behind failing ventricle
-One side fails first, ultimately leads to failure of other side
-Decreased CO (cardiac output) one side compensation mechanisms –
vasoconstriction, water & sodium retention, increased blood volume increased
work for the heart
-Eventually muscles of affected side weaken congestion behind affected side 
unaffected side pumps against increased resistance  Previously unaffected side
weakens
Right side failure – systemic congestion
Left side failure – pulmonary congestion
-pericarditis  effusion  fibrous adhesions
-myocarditis  arrhythmias
-endocarditis  infection of heart valves can lead to fibrosis
Dx tests for heart diseases
-auscultation – listen to valves
-exercise stress test
-imaging
-doppler blood flow
-blood test – can detect enzymes release from infracted myocytes
-EKG
EKG – usually 12 leads – at least 3
The basics –
-P wave – depolarization of atria
-QRS complex – depolarization of ventricles
-T wave – Repolarization of ventricles
EKG Abnormalities
-PAC –premature atrial contrx – slight flutter, benign
-PVC – premature ventricular contrx – many times benign, can lead to ventricular fib
(life threat)
-atrial flutter – atria contract quickly, but in rhythm – P waves not always followed by
QRS
-atrial fibrillation – atria quiver ineffectually (can live without coordinated atrial
contraction)
-ventricular tachycardia
-ventricular fibrillation – will die without swift intervention
Heart block – problem with SA node communication with AV node
-1st degree AV block – long PR interval – slow communication
-2nd – Missing QRS after P wave
-3rd – 2 consecutive missing QRS after P waves
Auscultation
-Sound 1 = tricuspid and mitral valves
-Sound 2 = semilunar valves
Nervous control of heart
-medulla of brain stem – control center of heart
-baroreceptors in aorta and internal carotid (peripheral a’s - stretch recepts for BP
monitoring)
-Autonomic system – increase and decrease HR
Vasculature
Artery layers
-tunica intima –endothelial cells
-endothelial cells respond to hormones, signal smooth muscle to contract, relax
-tunica media – muscle cells
-tunica externa (adventicia) – connective tissue
Venous return – thinner walls, valves prevent backflow
Hypertension
-95% idiopathic
-can cause endothelial cells to shear off
-epinephrine in blood stream = inhibitory for endothelial cells, excitatory for
smooth muscle underneath  vasoconstriction and incr. BP
-fat deposits in hole in intima atheroma
-blood can begin running between tunica intima and media dissecting aneurysm
Angiotensin Renin complex
-angiotensinogen
+renin
-Angiotensin I
+ACE (angiotensin converting enzyme)
-Angiotensin II
**ACTION = angiotensin II  receptor  vasoconstriction, incr. BP
Aneurysms
-fusiform – bulge in all directions
-saccular – sac forms on one side – pooling of blood causing clotting thrombus formed
-dissecting – most dangerous – blood runs between tunica intima and media – dissecting
aortic aneurysm =ticking time bomb
Circulatory shock – severe hypotension
-causes = hypovolemic, cardiogenic, septic, distributive (vasogenic, neurogenic,
anaphylactic)
-compensations – SNS incr. HR, force of heart contraction; kidneys release renin,
aldosterone, ADH
Diff Dx
Kawasaki’s Disease
-antibod’s produced against endothelial cells and smooth mm
-Presentation – red tongue, rash @ distal extremity, skin sloughing, edema
-recovery usually spontaneous
Raynaud’s Disease
-insufficient blood supplied to distal phalanges – Women>men
-prolonged ischemia can  gangrene.
Venous insufficiency
-valves fail due to age, injury, sendentary life, obesity
-chronic pooling of blood in LE
-brown, blue, purple skin in feet and toes – waste accumulation!
-minor trauma  large wound! Hard to treat
Lymphomas – cancer of T-cells and B-cells
-Hodgkins – Tcell; Non-Hodgkins- B-cell
-large lymph nodes and spleen
-good prognosis if tx’d before metastasis
Respiratory Disorders – Gould Ch. 19
How to Breathe – the basics
-respiratory muscles contract & thoracic cage expands, creating negative pressure in
lungs
-air goes in
-elastic fibers around alveoli passively contract
-air goes out
-Sympathetic activation  smooth mm relaxation, bronchodilation
-alveoli = squamous epithelium – maximizes gas exchange
-covered with surfactant – reduce surface tension of fluid, prevent collapse
-macrophages!
-intrapleural pressure a shade under atmospheric pressure
-feeling when you hold breath due to chemoreceptors for CO2.
Hypercapnia – Increased CO2 in blood – compensate with hyperventilation
Hypocapnia – decr. CO2 – compensate with hypoventilation
Hyper/hypoxemia – O2 sats
-As more O2 binds to hemoglobin, affinity for O2 rises – aids in acquisition and release
of O2.
Pneumonia
-viral, bacterial, or fungal; 1 lobe or both lungs
Tuberculosis
-spread by oral droplet, can survive in dry sputum
-TB takes root in primary infection stage, symptoms present in reinfection stage
-can go dormant for long periods, bacilli walled off in localized area of lung
- resurfaces when immune compromised
-tissues of lung die in active infection
-dx with skin test, chest x-ray, sputum culture
-Long multidrug treatment, 6 mos- 1 yr.
-grown more resistant to drugs in recent years.
Obstructive Pulmonary Disorders – impaired ability to push air out of lungs
-Cystic Fibrosis
-Single gene mutation
-increased mucus in the lungs, increased risk of infections
-Lung Cancer
-90% smoking related, 3rd most common cancer
-can be result of metastasis
-Lung Tumor
-inflammation and bleeding in lungs cough blood
-pleural effusion, pneumothorax
-can secrete hormones –“paraneoplastic syndrome”
-Asthma
-Type 1 hypersensitivity – IgE formed in response to allergen
-inflammation of mucosa  bronchoconstriction, obstructive mucus
-can cause atelectasis –collapse of lung because of airway blockage
(-pneumothorax involves a collapsed lung caused by mechanical damage or a
rupture of a small airsac or “bleb” on outside of lung)
-presents with hypoxia, respiratory alkalosis (initially due to hyperventilation), cyanosis,
cough, tightness in chest, thick mucus, tachycardia
-treat with inhalers and glucocorticoids
COPDs –progressive degeneration
-Emphysema –“pink puffers” – red face, overinflation
-destruction of alveolar walls permanent inflation
-smoking eliminates anti-trypsin that inhibits enzyme that destroys elastin elastin of
alveoli destroyedloss of septae between alveolar sacs decreased surface area for gas
exchange
-presents with “barrel chest” – ribs fixed in inspiration position
-Chronic Bronchitis – “blue bloater”
-inflammatory obstruction repeat infections, progressive, irreversible damage of
bronchioles
-hypertrophy, hyperplasia of mucus glands, fibrosis
-Present with constant cough, SOB, cyanosis
-treat by Stopping Smoking, O2 supplementation, available vaccinations for at risk
infections
Emphysema
Chronic Bronchitis
Alveoli affected
Bronchioles affected
Septae walls destroyed
Increased secretions
Some cough
Lots of coughing
Little sputum
Lots of sputum
No cyanosis
Cyanosis
Some infections
Frequent infections
-Bronchiectasis
-permanent dilation of medium-to-large-sized bronchi
-caused by recurrent inflammation
Restrictive Pulmonary Disorders – impaired lung expansion
-often abnormal chest wall or lung inself
-Pneumoconiosis
-exposure to irritants – coal workers
-inflammationfibrosis, “stiff lung”
- insidious onset
-Vascular Disorders
-Fluid collects in alveoli and interstitial fluid
-lung expansion decr, O2 in blood decr,
-leads to pulmonary hypertension and edema
-Pulmonary embolism
-blood clot from veins pumped to lungs – deadly
-Atelectasis
-collapse of lung caused by: obstructed airway, compression (tumor), increased surface
tension preventing expansion
-small areas asymptomatic, large areas –dyspnea and chest pain
-Pleural effusion – “hydrothorax”
-fluid in pleural cavity protiens and WBCs follow, respond to inflammation
-Incr pressue in pleural cavity, layers separate, prevent expansion
-presents with incr RR and HR, cyclic chest pain
-Pneumothorax
-air in chest cavity, lung collapse
-open – air enters through hole in chest cavity;
-closed – air in chest cavity from rupture on inside
-tension – air allowed to enter cavity, no natural way to remove it
-Adult Respiratory Distress Syndrome
-rapid, shallow resp, incr HR, confusion
-caused by shock, sepsis, burns, multiorgan failure
Diff Dx
- Sputum
-yellow-green = infection
-rusty-dark = pneumonia
-purulent and foul odor = bronchiectasis
-Breathing
-labored breathing – obstruction
-wheezing, whistling – obstruction of small airways
-stridor – high crowing noise – obstruction of small airways
Patho 4
Digestive Disorders
Digestive System Overview
5 layers of gut wall (inner to outer): mucosa, submucosa, circular muscle layer, longitudinal muscle layer, serosa
*Peristalsis (involuntary contractions) occurs in circular and longitudinal smooth muscle layers
Stomach
Gastrin cells (G cells): initiated by food entering stomach, stimulates chief and parietal cells
Intrinsic factor (parietal cells): needed for absorption of vitamin B12
HCL (parietal cells): activates pepsinogen, creates optimal pH ~2, denatures proteins
Pepsinogen (chief cells): pepsin not activated until pH of 6
Liver “Metabolic factory of the body”
1)Storage of nutrients 2) Maintains blood glucose 3) Blood reservoir 4) Produces bile, plasma proteins,
blood clotting factors, cholesterol/lipoproteins 5) Metabolic processes (detoxification, conversions)
Glucose -> Glycogen = Glycogenesis (when glycogen supply low)
Protein, Fat -> Glycogen = Glyconeogenesis
Glycogen -> Glucose = Glycogenolysis (maintains blood glucose levels)
Pancreas
Exocrine (secreting digestive enzymes and electrolytes) and endocrine organ
Trypsin, chymotrypsin, carboxypeptidase-break proteins
Ribonuclease-break nucleic acids
Pancreatic amylase-break starch
Lipase-break lipids
GI tract
Ileum=major site of nutrient absorption, villi (folds of mucosa)
Large intestine=fluid and electrolyte reabsorption, movement slow to allow absorption of water, vitamin K
synthesis (essential for blood clotting)
Neural and hormonal control
PNS (vagus mainly): increased motility and secretions, SNS: inhibits GI activity
Gastrin: increases gastric motility and promotes stomach entering, Secretin: decreases gastric secretions,
Cholecystokinin: inhibits gastric emptying
Upper GI Tract Disorders (includes differential diagnosis)
Disorder
Dysphagia
Description
Difficulty swallowing
Esophageal
Cancer
Squamous cells in distal esophagus,
poor prognosis
Hiatal hernia
Part of stomach protrudes into thoracic
cavity
Gastric substances reflux into distal
esophagus,often seen with hiatal
hernia
Stomach mucosa inflamed (either
acute or chronic)
*Helicobacter pylori infection typically
present w/ chronic
Inflammation of stomach AND
intestine
Erosion in mucosa
Common in proximal duodenum and
antrum of stomach (ulcers in general
rarely found in large intestine)
Gastroesophag
eal Reflux
Disease
Gastritis
Gastroenteritis
Peptic Ulcers
(gastric and
duodenal)
Stress Ulcers
Rapid onset, may form within hours of
precipitating event
Gastric Cancer
Primarily in mucous glands and in
antrum or pyloric area, poor prognosis
Narrowing and obstruction of pyloric
sphinctor
Pyloric Stenosis
Causes
1) Neurological deficit
2) Muscular disorder
3) Mechanical obstruction
-congenital atresia
-stenosis
-esophageal diverticulum
-tumors
Chronic irritation
-chronic esophagitis
-hiatal hernia
Decreased competence of lower
esophageal sphinctor
Acute: Infection, allergies to food,
spicy food, excessive alcohol,
ulgerogenic drugs
Chronic: Most idiopathic
Usually an infection
1) H. pylori infection
1) Increased acid-pepsin
secretions
2) Inadequate blood supply
3) Excessive glucocorticoid
secretion
4) Ulcerogenic subtances
Severe trauma: Burns (curling’s
ulcers), head injury (cushing’s
ulcers)
Systemic: hemorrage, sepsis
(ischemic ulcers)
Gone down bc we have
preservatives w/ food
May be developmental anomaly or
acquired later in life
Liver and Pancreas Disorders (includes differential diagnosis)
Gallbladder
Disorders
Cholelithiasis
Cholecystitis
Cholangitis
Choledocholithiasis
Description
Formation of gallstones*
Inflammation of gallbladder and cystic
duct
Inflammation related to infection of bile
ducts
Obstruction of biliary tract by
gallstones (due to larger stones)
*Risk factors for developing gallstones: Women (2x more likely), high cholesterol, obesity, multi parity (several
children), use of oral contraceptives or estrogen supplements, hemolytic anemia, alcoholic cirrhosis
Disorder
Jaundice
Description
Yellowish color of skin (not disease itself but
sign of other disorders)
Prehapatic: unconjugated bilirubin elevated
Intrahepatic: unconjugated and conjugated
bilirubin elevated
Posthepatic: conjugated bilirubin elevated
Hepatitis
Cirrhosis
Inflammation of liver
Mild: impaired hepatocyte function
Severe: necrosis and obstruction of blood/bile
flow along w/ impaired hepatocyte function
Progressive destruction of liver
Stage 1=fatty liver (asymptomatic & reversible)
Stage 2= alcoholic hepatitis (irreversible)
Stage 3=end stage cirrhosis (liver failure when
80-90% of liver destroyed)
Liver
Cancer
Initial signs mild, diagnosis occurs with
advanced stages
Acute
Pancreat
itis
Chronic or acute(medical emergency for acute)
Spreads to tissue surrounding the pancreas
Very painful (different than pancreatic cancer)
Chronic in 15% of cases
Pancreat
ic cancer
Adenocarcinoma-most common form
Asymptomatic until advanced (metastasizes
quickly)
Mortality=95%
Causes
Prehepatic: excessive
destruction of RBCs
Intrahepatic: disease or damage
to hepatocytes
Posthepatic: obstruction of bile
flow into gallbladder or
duodenum
1) Idiopathic (fatty liver)
2) Infection (viral or non-viral)*
1) alcohol (most common)
2) biliary: obstruction of bile flow
3) post-necrotic: linked w/
chronic hepatitis or long-term
toxic exposure
4) metabolic
Hepatocellular carcinoma (most
common primary tumor of liver)
Secondary/metastatic cancer
(arises from areas served by
hepatic vein)
Results from auto digestion of
the tissue (Premature activation
of pancreatic proenzymes)
Precipitating factors=alcohol
(most common), biliary tract
obstruction, gallstones, mumps
Risk factors=smoking,
pancreatitis, and dietary factors
*Viral Hepatitis
Hepatitis A: Infectious hepatitis, RNA virus, transmitted by fecal-oral route in areas of inadequate sanitation, no
carrier or chronic stage, vaccine available
Hepatitis B: Serum hepatitis, DNA virus, incubation period of 2 months, primarily transmitted by infectious blood
(may also be sexual transmission or from mother to fetus), carriers asymptomatic but contagious, vaccine available,
chronic hepatitis B (ascites) =engorgement of blood vessels, can’t filter toxins anymore
Hepatitis C: RNA virus, most common type transmitted by blood transfusion, has carrier state, increases risk of
hepatocellular carcinoma
Hepatitis D: Delta virus, incomplete RNA virus (needs hepatitis B to produce active infection), transmitted by blood
Hepatitis E: RNA virus, transmitted by oral-fecal route, no chronic or carrier state
Lower GI tract disorders (includes differential diagnosis)
Disorder
Celiac disease
Description
Malabsorption syndrome: prevents
further digestion of gliadin
(breakdown product of gluten)
Atrophy of villi
Primarily a childhood disorder
Progressive inflammation and fibrosis
cause obstructed areas
Normally affects small intestines (but
may affect any part of GI tract)
Inflammation occurs in “skip lesions”
Blood and mucous in stool
Inflammation starts in rectum and
progresses to colon
Obstruction of appendiceal lumen,
wall inflamed as fluid builds in
appendix
Occurs in 10% of population
Symptoms=LRQ rebound
tenderness, periumbilical pain
Diverticulum=outpouching of mucosa
through muscular layer of colon
Diverticulosis=asymptomatic
Diverticulitis=inflammation of
diverticula (very painful)
Symptoms=cramping, tenderness
nausea, fever, elevated WBC, do
NOT see blood in stool
Early diagnosis essential
Symptoms=alternating diarrhea and
constipation, bleeding,weight loss,
anemia, fatigue, red blood in stool,
pain doesn’t often occur
Most diagnosed cancer next to skin
cancer
Causes
Autoimmune disease (1% of
US population)
-defect in intestinal enzyme
Intestinal
Obstruction
Lack of movement of intestinal
contents (most common in small
intestine)
Peritonitis
Inflammation of peritoneal
membranes
Symptoms: sudden severe and
generalized abdominal pain,
abdominal distention, dehydration,
low blood pressure,tachycardia,
vomiting
Mechanical obstruc.
-tumors, adhesions, etc
Functional obstruc.
-impairment of peristalsis
-Ex: spinal cord injury
1) Chemical peritonitis: caused
by foreign chemical in
peritoneal (bile, chyme, etc)
2) Bacterial peritonitis: direct
trauma affecting intestines,
ruptured appendix
1) Abdominal surgery
(infection may develop)
2) Pelvic inflammatory disease
in women
Crohn’s disease
(included in
chronic
Inflammatory
Bowel Disease)
Ulcerative Colitis
(included in
chronic IBD)
Appendicitis
Diverticular
Disease
Colorectal Cancer
Genetic factor (often occurs
during adolescence)
Genetic factor (often occurs
during 2nd or 3rd decade)
Fecalith, gallstone, or foreign
object cause obstruction
May be genetic link
Most from adenomatous polyps
(polyp does not always mean
cancer!)
Risk factors: familial multiple
polyps, long-term ulcerative
colitis, diet low in fiber (why
susceptibility has increased)
Irritable Bowel
Syndrome
1) Change in bowel motility that is
associated with pain
2) Must be there 12 weeks out of the
year
3) Do NOT see blood in stool
Urinary Disorders
Urinary System Overview
Kidney
Nephron=functional unit of the kidney (>1 million), consists of renal corpuscle (filtration unit) and renal
tubule
ADH-prevents water loss (increases reabsorption of water in distal convoluted tubules and collect. duct)
Aldosterone-prevents water loss (increases sodium reabsorption in distal convoluted tubules)
ANP-allows water loss in response to high blood pressure
Glomerular rate: 1)afferent arteriole dilation=increased filtrate 2) efferent arteriole constriction=increased
filtrate 3) afferent arteriole constriction=decreased filtrate
Renin (kidney)
↓
ACE (lung)
↓
Angiotensinogen → Angiotensin I → Angiotensin II
(plasma)
vasoconstrictor
(Renin secreted in response to reduced afferent arteriole blood flow)
Urinalysis
Cloudy-presence of large amounts of protein, blood, bacteria, and pus
Blood: if large amount=increased glomerular permeability or hemorrhage, if small amount=infection,
inflammation or tumors in urinary tract
Dark color-hematuria, excessive bilirubin, highly concentrated urine
Unusual smell or odor-infection, diet, or medication
Elevated BUN and creatine=failure to excrete nitrogen waste
Metabolic acidosis (low pH, low bicarbonate)=failure of tubules to control acid/base balance
Urinary System Disorders (includes differential diagnosis)
Disorder
Urinary Tract Infection
Description
Lower=cystitis and urethritis
(hyperactive bladder and reduced
capacity), may have systemic signs
w/ painful urination
Upper=pyelonephritis (in one or both
kidneys: purulent exudate and
abscess block blood and urine flow),
Cause
E.coli
Predisposing
factors=incontinence,
retention of urine, direct
contact w/ fecal material
Glomerulonephritis
Nephrotic Syndrome
Bladder cancer
Vascular Disorders
Adult Polycystic kidney
disease
Polycystic disease in
children
Acute Renal Failure
Chronic Renal Failure
Kidney Stones
Wilms Tumor
Diabetic Neuropathy
Reflux Neuropathy
Incontinence
systemic sign of high fever *can lead
to renal failure*
Decreased GFR rate (decreased
urine output, elevated blood
pressure and edema)
Metabolic acidosis
Bloody, foamy urine and pain
Increased permeability in glomerular
capillaries
Hypoalbuminemia,increased
aldosetrone, severe edema
Often develops as multiple tumors
Early signs:hematuria and dysuria
Thickening/hardening of walls and
small arteries
Reduces blood to kidney-stimulation
of renin (increases blood pressure)
Manifests around 40
Multiple cysts in both kidneys-leads
to chronic renal failure
Manifested at birth, child dies in first
month or is stillborn
Rapid onset
Metabolic acidosis and
hyperkalemia
Ogliuria, increased serum urea
Gradual, irreversible destruction of
kidneys (<10%=end stage)
Asymptomatic w/ up to 40% left
Symptoms later on=polyuria with
dilute urine, anemia, fatigue
Axotemia=renal insufficiency<25%
Calcium (sharp),magneisum, uric
acid, cystine
1-5mm can be passed
Usually unilateral and gives purely
kidney symptoms
Leading cause of chronic renal
failure
1/3 ppl on dialysis have Type 1
diabetes, 2/3 have Type 2
Flow of urine from bladder to upper
tract
Can lead to end stage renal disease
1)Stress: most common Ex:sneeze
Acute poststreptococcal
glomerulonephritis caused by
presence of anti-streptococcal
antibodies
Predisposing factors: working
w/ chemicals (analine dyes,
rubber, aluminum), smoking,
recurrent infections, heavy
analgesics intake
Some normal w/ aging
Autosomal dominant gene on
chromosome 16
Autosomal recessive mutation
1) Acute bilateral kidney
diseases
1) Prolonged/severe
circulatory shock or heart
failure
2) Nephrotoxins
3) Mechanical obstruction
4) Burns
1) Chronic kidney disease
2) Polycystic disease
3) Systemic disorders
4) Low-level nephrotoxin
exposure over long time
Most common tumor in
children, defects in tumorsuppressor on chromosome
11
Primary (congenital)
Secondary (obstruction)
Associated with hypertension
Associated w/ aging, most
2)Urge: spasm
3)Overflow: can’t fully empty bladder
4)Functional: bladder normal,
something else keeps them from
going to bathroom Ex: spinal cord
injury
common in women
Dialysis-provides filtration and reabsorption (hemodialysis=blood moves from shunt into machine, 3x per week for
4 hours)(Peritonal dialysis= peritoneal membrane serves as semipermiable membrane, usually done at home
during night)
Endocrine System Differential Diagnosis
Gigantism
Acromagly- thicker skull and jaw (occurs after joint plates fuse)
Hyperthyroidism
Common cause=Grave’s disease
Common symptoms=exopthalmos, goiter, heat intolerance, and anxiety
Hypothyroidism
Very familial, 4X more likely in women
Common symptoms=weight gain, cold intolerance, fatigue
Myxedema- lots of fluid (would not pit), can look like fibromyalgia bc of muscle aches and trigger point
tenderness, sparse hair, brittle nails, may have buffalo hump
Thyroid storm-dumps T3 and T4 into system -> causes tachycardia, fever, and agitation
Thyroid cancer
Very treatable, most are benign (only 5% malignant and they normally dont metastasize)
Palpation will be painless, unilateral, and in one spot
Parathyroid glands
Maintain calcium levels between bone and blood
Parathyroid cancer=can’t easily be distinguished from thyroid cancer
Renal glands
Release epinephrine and aldosterone
Trousseau’s sign- positive sign would be tremors and twitching bc of nerve or muscle irritability (Non specific sign)
Chvostek’s sign-elicit this by having the patient relax face and then the therapist taps the facial nerve, watch for
twitch of mouth or side of face
Addison’s Diseases (hypoadrenal)- autoimmune, skin changes color to a slight grey
Cushing’s Syndrome (hyperadrenal)- too much glucocorticoids in system, can cause muscle wasting, bone
demineralization, and ligaments to be lax, might see buffalo hump on back (does NOT feel like fluid)
Diabetes (fasting plasma glucose >126mg/dL)
Action of insulin-when insulin gets to cell, it makes glucose transporters close to membrane (Below 100
mg/dL is normal for FPG)
Type 1=autoimmune (insulin producing B cell destruction), typically under age 20
Risk factors: sibling has Type 1, parents have type 1
Type 2=obesity (insulin resistance...receptor not binding to insulin as well, pancreas intact), hyperglycemia
develops slowly, may have genetic predisposition, 85-90% of all diabetes
Risk factors: overweight, over 45 yrs old, inactive, women who had a baby over 9ilbs, low HDL
Gestational=associated with type 2, glucose intolerance w/ pregnancy, increased risk of diabetes later on, if
continues >6 weeks after pregnancy...no longer GDM
Acute Hyperglycemia
Early signs: blood sugar >180mg/dL, blurred vision, thirsty, ketones,dry skin, increased urination, tired
Late signs: blood sugar >240mg/dL, nausea/vomiting, deep/rapid breathing, large ketones in urine, fruity
breath, some diabetes pts don’t sense changes bc of neuropathy
Acute Hypoglycemia
Caused by: over treatment w/ insulin, missed meal, exercising when insulin peaking, stress
Early signs: tachycardia, hunger, headache, dizziness, sweating, shaking, pale skin, tingling around mouth,
Late signs: slurred speech, confusion, sudden moodiness, clumsy or jerky movements, seizures, pass out
Treatment: Act quickly! Test blood sugar after attempting to raise it with 15 grams of fast acting sugar...if
<70 repeat, if >70 eat meal/snack (always assume they will drop 50 mg/dL while exercising)
Obesity **Nursing/Allied health professions have greater risk of injury due to rising obesity trends**
Underweight = <18.5 Normal weight = 18.5-24.9 Overweight = 25-29.9 Obesity = BMI of 30 or greater
Subcutaneous vs. Intra-abdominal fat
Subcutaneous fat needed for thermal control
Abdominal obesity=most important factor in determining pre-diabetic state (1 out of 5 US adults have
metabolic syndrome), want to avoid fat around organs (especially liver)
Hormone regulation
Fat=largest/most active endocrine organ, releases 50 hormones, Adiponectin=hormone that signals brain we
are full (as fat cell gets bigger, releases less of this)
More macrophages recruited with obesity, causing chronic inflammation
Lifestyle=big factor (obesity trends with US Pima Indians vs Mexican Pima Indians)
Epigenetics= We can change which genes we turn on and off by our activitity
Pathophysiology Exam 5 Review
Acute Neurologic Disorders
Neurons and Conduction of Impulses
 Neurons: highly specialized, non-mitotic cells which conduct impulses through the CNS and PNS
 Myelin sheath: insulates, speeds up conduction, formed by Schwann cells, Nodes of Ranvier
 Glial cells: astroglia, oligodendroglia, microglia, ependymal cells
 Regeneration of Neurons: neuronal cell body damaged = death of neuron; CNS = neurons do
NOT regenerate; PNS = neurons may be able to
 Conduction of impulses: depolarization (sodium influx)  generation of action potential 
repolarization (outward movement of potassium)  sodium – potassium pump moves ions into
their normal position; myelinated fibers: salutatory conduction = rapid conduction
 Chemical neurotransmitters: stimulated  released into synaptic cleft; inactivated by enzymes
or reuptake; postsynaptic neuron dendrites or cells body depolarizes depending on
neurotransmitters
 Neurotransmitters:
o Acetylcholine: (excitatory and inhibitory) located: neuromuscular junction, autonomic
nervous system (SNS and PNS), peripheral nervous system, CNS
o Catecholamines: (excitatory) present in the brain, norepinephrine: neuromuscular
junction and SNS, epinephrine: SNS, dopamine
o Seratonin: (excitatory) located in the CNS (brain) and GI; regulates behavior, attention,
digestive processes; implicated in mood changes
o Glutamate: (excitatory)
o Y-Aminobutyric acid (GABA): (inhibitory) located in brain
 Autonomic Nervous System:
o Involuntary, motor and sensory innervation: cardiac muscle, smooth muscle, glands,
sympathetic/parasympathetic, neural pathway: preganglionic fibers (in brain or spinal
cord)  postganglionic fibers (outside CNS)
 Sympathetic Nervous System:
o “Fight or flight”; stress response, increase general level of activity: cardio, respiratory,
neurologic, Neurotransmitters: preganglionic fibers release acetylcholine (cholinergic);
postganglionic fibers release norepinephrine (adrenergic)
 Parasympathetic Nervous System:
o Dominates digestive system, aids recovery after sympathetic activity, vagus N:
innervates heart and GI, neurotransmitter: acetylcholine; receptors (cholinergic):
nicotinic and muscarinic
Acute Neurologic Disorders
Problem/Disorder
Description
Treatment
Increased Intracranial Pressure
Expansion of fluids/tissue 
Increase in pressure
Ischemia and infarction
Herniation
Displacement of brain tissue
Brain Tumors
Vascular Disorders
Transient Ischemic Attacks
Cerebrovascular Accidents
Cerebral Aneurysms
Meningitis
Brain Abscess
Encephalitis
Rabies
Tetanus
Poliomylitis
Herpes – Zoster (shingles)
Post-polio syndrome
Reye Syndrome
Guillain – Barre syndrome
caused by large mass
(clot/tumor)
Lesions that cause increased ICP
Hemorrahagic (increased ICP) or
ischemic
Temporary reduction of blood
flow in the brain
Small mini-strokes occurring
continually
Connected to dementia
Infarction of the brain due to
lack of blood
Localized dilation in the wall of
an artery
Bacterial infection of the
meninges of the CNS
Localized infection; necrosis of
tissue
Infection of the parenchymal or
conn tissue in the brain and
spinal cord
Viral transmitted by bite of rabid
animal or transplantation of
contaminated tissues
Infection by puncture wound
Polio virus; attacks motor
neurons of the spinal cord and
medulla
Caused by varicella – zoster in
adults
Occurs 10 – 40 years after initial
infection
Viral infection linked to children
treated with aspirin
Inflammatory condition of the
PNS
If accessible then removal
Clot busting agents, surgery,
glucocorticoids, team approach
Surgery before rupture,
antihypertensive drugs
Antimicrobial therapy,
glucocorticoids, vaccines
Surgical drainage, antimicrobial
therapy
Antimicrobial therapy, antiviral
drugs (depends on the type of
encephalitis)
Prophylactic immunization
Immunizations advised
Immunization available
Vaccine available for ages 60+
No immediate cure
Recovery usually spontaneous;
supportive treatment
Chronic Neurologic Disorders
Problem/Disorder
Hydrocephalus
Spina Bifida
Description
Excess CSF within the skull
Non-communicating (flow of
CSF through ventricular
system is blocked)
Communicating: absorption of
CSF through subarachnoid
villi impaired
Failure of the posterior
Treatment
Diagnostic Tests: alpha –
spinous processes to fuse 
meninges and spinal cord
herniated
Cerebral Palsy
Multiple Sclerosis (MS)
Parkinson’s Disease
Amyotrophic Lateral Sclerosis
fetoprotein (AFP) elevated,
ultrasound
Surgical repair, OT/PT
afterwards
Motor impairment due to brain Speech, PT/OT, assistive
damage: intellectual function, devices, monitor
behavior, communication /
hearing/vision, alternate
speech, seizures, visual or
modes of communication
hearing deficits
Causes: genetic mutations,
abnormal fetal formation,
brain damage, difficult
delivery, hypoxia (ischemia)
Spastic paralysis:
hyperreflexia
Dyskinetic: loss of
coordination with fine
movement
Ataxic: loss of balance and
coordination
Progressive demyelination of
MRI for diagnosis and
neurons in brain, spinal cord,
monitoring
and cranial nerves
Research treatments:
Cause: unknown
interferon beta – 1b,
S&S: blurred vision, diplopia, glucocorticoids
scotoma, weakness in legs,
PT/OT
progressive weakness and
Muscle relaxants
paralysis, paresthesia,
dysarthria, loss of
coordination, bladder / bowel /
sexual dysfunction, chronic
fatigue
Progressive degeneration in
Removal of cause if known
basal nuclei; imbalance
Dopamine replacement
between excitation and
therapy
inhibition
Anticholinergic drugs
Excess stimulation affects
Speech/language, PT/OT
movement and posture
Treatment of respiratory or
S&S: resting tremors (“pill
urinary tract infections
rolling”), muscular rigidity,
difficulty initiating movement,
postural instability, decreased
flexibility, fatigue, lack of
facial expressions, propulsive
gait, bradykinesia
Muscle wasting, progressive
Stem cell therapy under
(ALS)
Myasthenia Gravis (MG)
Huntington’s Disease
Dementia
Alzheimer’s Disease
degenerative disease affecting
motor neurons
Cause: unknown
Cognition, sensory neurons,
neurons of eye are unaffected
Loss of upper motor neurons:
spastic paralysis and
hyperreflexia
Loss of lower motor neurons:
Flaccid paralysis, decreased
muscle tone and reflexes
Autoimmune disorder: autoantibodies to acetylcholine
receptors at NMJ
S&S: muscle weakness in
face/eyes, weakness in
arms/trunk, impaired vision
and speech, difficulty chewing
and swallowing, head droops,
upper respiratory infections
Rapid, jerky movements,
chronic progressive
neurodegenerative chorea,
hereditary, autosomal
dominant (~40 years of age)
Progressive atrophy of brain
S&S: mood swings,
personality changes,
restlessness, choreiform
movements in arms and face,
intellectual impairments
Intellectual deterioration that
interferes with occupational or
social function
S&S: impaired cognitive
skills, impaired thinking,
judgment, and learning,
memory loss, confusion,
behavioral and personality
changes
Causes: vascular disease,
infections, toxins, genetic
disorders
Progressive cortical atrophy:
neurofibrillary tangles and
amyloid plaques
investigation
Moderate exercise and rest
Electronic communication
devices
Team approach
No specific treatment to slow
degeneration
Diagnostic tests: EMG, serum
antibody test, acetylcholine
esterase inhibitor
Treatment: antiacetylcholine
esterase agents,
gludocorticoids,
plasmaphoresis, thymectomy
Diagnositc test: DNA analysis
Treatment: no therapy to slow
progress, only symptomatic
therapy
1st stage: short term memory
loss, social withdrawal, no
sense of humor
Creutzfeld – Jacob Disease
(Mad Cow Disease)
AIDS Dementia
Cause: unknown
S&S: onset insidious,
behavioral changes
(irritability, hostility, mood
swings), gradual loss of
memory and lack of
concentration, impaired
learning, poor judgment,
decline in cognitive function,
memory and language, change
in food intake, inability to
recognize family, environment
unawareness, incontinence
2nd stage: general confused
stage, wandering (sundown
syndrome)
3rd stage: terminal stage,
incontinent, apathetic,
institutionalized
No diagnostic tests available
Treatment: anti-acetylcholine
esterase drugs, OT/PT,
psychologists, speech
therapists, team approach
Rapidly progressive
Cause: prion ingested or
transmitted through
contaminated blood
S&S: memory loss, behavioral
changes, motor dysfunction,
progressive disorders,
dementia
Common in later stages of
AIDS, virus invades brain
tissue
Gradual loss of memory and
cognitive ability, impaired
motor function
Diagnosis: blood tests
Fatal: within 6 months = dead
Complex Regional Pain Syndrome (CRPS)
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Pathogenesis: abnormal activity of the SNS, gate control theory, reflexive muscle spasm
Stages of CRPS:
o Stage 1 (acute): right after injury, weeks to 3 mo., excess sympathetic activity, persistent
burning pain and swelling, hyperesthetic, hyperhidrosis, increased nail/hair growth, pain
will be severe
o Stage 2: dystrophic stage, 3 – 6 mo., persistent pain and stiffness, trophic skin changes,
muscle atrophy, flexion contractures, pain exacerbated by stimulus, limb: edematous,
cool, cyanotic, mottled, hair loss, cracked brittle nails, skin cool to touch
o Stage 3: atrophic stage, ~6 mo., pain can increase or decrease, progressive atrophy of
skin, subcutaneous tissue, muscle, and bone, bone demineralization, skin: cool, thin and
shiny
o Stage 4: existence of stage 4 is questionable, 2+ years, psychosocial level, swelling is
gone, atrophy is permanent (muscle, bone, skin), no NOC firing now
Definite CRPS: pain and tenderness in extremity, S&S of vasomotor instability, swelling,
dystrophic skin changes
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Probable CRPS: pain and tenderness OR swelling, dystrophic skin changes often present
Possible CRPS: vasomotor instability AND/OR swelling, NO pain but tenderness, dystrophic skin
changes occasional
Doubtful CRPS: unexplained pain and tenderness in an extremity
PAIN
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How we interpret pain: NOC  perception  interpretation  emotions  social
Pain: the perception of nociception that is not directly measurable
Pain behavior: the observed consequence of a painful experience (distress response); Pain
behaviors: verbal, vocal, facial expressions, physical actions, function, social actions
 Benign pain: not associated with terminal illness vs. Malignant: associated with terminal disease
Acute Pain
Chronic Pain
Recent onset (<3 mo.)
>3 mo.
Close link with pain generator
Loose link with pain generator
Not a learned response even though there will be
Learned behavior, positive reinforcement for pain
pain behavior
behavior
Objective findings coincide with generator
No lab or clinical findings to support pain
Unlikely to have errors in stimulus discrimination
Pt. may confuse pain with other forms of
distressful stimuli
Brief in nature
lengthy
Differential Diagnosis of Chronic Pain
Test
Wadell’s Signs
Mankopf’s Test
O’ Donoghue’s Maneuver
McBride’s Test
Hoover’s Test
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
Description
Distracted SLR, rotation of back, superficial
tenderness, regional pain, migrating trigger
points, sham axial loading of spine, regional
weakness
Pain should raise pulse rate of person by 5% +
AROM > PROM = + sign
Stand on one leg and raise other leg to chest =
should decrease LBP
Supine, hold pt.’s heels off table and have
them raise one leg, feel downward pressure if
they try to lift the leg
Symptom magnifier: magnifying their symptoms vs. Malingerer: knowingly manipulating the
system for their own gain, purposely deceiving the health care providers
Look at pt’s work history
SEIZURES
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Review types of seizure table
Seizure: abnormal discharge of a group of cortical or subcortical neurons
Epilepsy: syndrome characterized by experience of recurrent seizures
Aura: subjective sensation or motor phenomenon that precedes a seizure (pre-ictal/prodomal)
Ictal period: period of abnormal EEG activity; seizure S&S are evident
Post-ictal period: period following acute seizure, time of confusion, EEG activity = normal

Status epilepticus: series of rapidly repeated epileptic convulsions without any period of
consciousness between them
Seizures
Epilepsy
Inappropriate electrical activity
Recurrent seizures or neurological syndrome
associated with seizures
Transient neurological signs (seizure)
Seizures occurring with little or no provocation
Altered consciousness, involuntary movements,
Individual or multiple seizure types; characteristics
and disturbed perception often occur
may change with age
Defined by neurological S&S and EEG patterns
Spectrum of seizure types, EEG, clinical settings
 Etiology: genetic (inherited metabolic abnormalities, lowered threshold to electrical activity of
the brain), structural (disturbed cerebral flow, disorders of blood composition), environmental
(anoxia, toxins, drug withdrawal), head trauma, idiopathic causes
 Triggering mechanisms: visually induced, movement induced, hyperventilation, trauma,
emotions, hydration/electrolyte imbalance, fever, alcohol or drug withdrawal, premenstrual
period, lack of sleep, illness
 Diagnosis: medical history, diagnostic tests (lab studies, x-rays, lumbar puncture, CT, MRI, EEG),
clinical observation
 Treatment: drugs, surgery, diet, microcomputers, education
 Differentiate from: disorders of cerebral blood flow or blood constitution, structural, psychiatric
conditions, and migraine headaches
Mental Health Disorders of Children
Autism Spectrum Disorder
 Autistic disorder, pervasive developmental disorder, and Asperger’s disorder: differ in when the
symptoms start, how fast they appear, and severity
 Cause is unknown; genetic and environmental factors; structural brain abnormalities: larger
total brain mass, smaller frontal cortex, abnormal cerebellum
 S&S: lack of social skills, avoid eye contact and physical contact, echolalia, don’t listen,
aggressive or passive (may switch), inflict self injury, resistant to change, diff in expressing
needs, tantrums
 Early indications: no babbling or pointing, no single words, no response to name, loss of
language or social skills, poor eye contact, excessive lining of objects, no social responsiveness
 Later indicators: impaired ability to make friends or initiate conversation, impaired play,
echolalia, preoccupation with objects, inflexible adherence to routines and rituals
 Screening tests: Childhood Autism Rating Scale (CARS), Checklist for Autism in Toddlers (CHAT),
Autism screening questionnaire, screening test for autism in 2 year olds
 Treatment: intensive behavior therapy
Attention Deficit Hyperactivity Disorder (ADHD)
 Inability to focus on one thing in all aspects of life impairing function; diagnosis (must have all 3):
inattention, hyperactivity, and impulsivity
Tourettes Syndrome

Characterized by tics; tics: involuntary, rapid, repetitive, and stereotyped movements of
individual muscle groups
 Transient tic disorder: do not persist for more than 1 year vs. chronic tic disorder: duration over
many years (unchanging character) vs. chronic multiple tics: several chronic motor tics vs.
Tourettes: multiform frequently changing motor and phonic tics, unknown cause
Bipolar Disease
 Combination of euphoria and depression; in kids: continuous, rapid-cycling, irritable, and mixed
symptom state that may co-occur with disruptive behavior disorders
School Refusal/Avoidance
 Refuse to go to school on a regular basis or problem staying in school once there
Separation Anxiety Disorder
 Extreme anxiety when away from home or separated from parents
Selective Mutism
 Fail to speak in situation where speech is expected or necessary
Oppositional Defiant Disorder (ODD)
 Persistent / consistent pattern of defiance, disobedience, and hostility towards authority figures
Conduct Disorder
 Fighting, bullying, intimidating, physically assaulting, sexually coercing, cruel to people and
animals, vandalism, theft, truancy, drug and alcohol abuse, precocious sexual activity
Adult Mental Health Disorders
Dementia, Alzheimer’s, Vascular Dementia (TIAs), Creutzfeld – Jakob, Huntington’s refer to table
General Anxiety Disorder
 Excessive worry for 6+ mo., focus of worry will shift between things
Obsessive-Compulsive Disorder (OCD)
 Persistent, recurring thoughts and obsessions, obsessive behavior with repeated behavios
Panic Disorder
 3 types of attacks: unexpected, situational, and situationally predisposed
Post Traumatic Stress Disorder
 Follows exposure to a traumatic event; 3 symptoms: relive the disaster, avoidance behavior,
emotional detachment from others
Social Anxiety Disorder
 Extreme anxiety about being judged by others or being embarrassed, cause avoidance behavior
Specific Phobias
 Fear is at a level that is inappropriate and recognized as irrational
Major Depression
 Combination of symptoms that interfere with work, sleeping, eating, and social activities
Dysthymia
 Less severe form of depression, chronic, doesn’t interfere with everyday activities
Bipolar Disorder
 Cyclic mood swings with mania and depression
Paranoid Personality Disorder
 Continual mistrust, view everyone as an enemy, hypersensitive, defensive and antagonistic
Delusional Paranoid Disorder
 Persistent non-bizarre delusions without symptoms of any other mental disorder, delusions of
being persecuted
Schizophrenia
 Extremely bizarre delusions or hallucinations; hear voices or believe thoughts are controlled
Antisocial Personality Disorder
 Long-standing pattern of a disregard for other people’s rights, can only be diagnosed in ages 18+
Avoidant Personality Disorder
 Long-standing & complex pattern of feelings of inadequacy, extreme sensitivity, social inhibition
Borderline Personality Disorder
 Labile interpersonal relationships characterized by instability, shallow, impulsive behaviors
Narcissistic Personality Disorder
 Pervasive pattern of grandiosity, need for admiration, lack of empathy
Schizoid Personality Disorder
 Detachment from social relationships and a restricted range of expression of emotion in
interpersonal settings
Musculoskeletal Disorders
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Bones classified by shape: long, short, blat, irregular
Bone tissue: intercellular matrix (fibers, calcium phosphate, strong/rigid structure) and cells
-cytes (mature cells), -blasts (producing cells), -clasts (resorption cells)
Bone remodeling: regulated by stress (weight bearing, mm tension) & hormones (growth, PTH)
Osteoblasts: make collagen/proteins of matrix; osteoclasts: secrete collagenase/degrading
enzymes (regulated by PTH)
 Bone tissue: compact: outer covering of bone; cancellous (spongy) interior of bone
 Periosteum: fibrous conn tissue cover over bone; endosteum: osteoblast rich lining of medullary
cavity
 Functions: body movement, body position, stabilize joints, maintain body temp.
 Skeletal Muscle: bundles of protein fibers covered by conn tissue, striated, voluntary,
respiration: aerobic and anaerobic, glycogen for energy
 Joints: synarthroses (immovable), amphiarthroses (slightly moveable), diarthroses (freely
moving)
Disorder
Description
Treatment
Fracture
Bleeding, local inflammation,
necrosis of tissue at the end of
the broken bone
Osteoporosis
Decrease in bone mass and
Dietary supplements (calcium,
density, loss of bone matrix and
vitamin D), weight bearing
mineralization
activities, PT, fluoride,
Predisposing factors: 50+ yrs.,
bisphosphonates, calcitonin
sedentary, hormonal, low BMI,
diet, Asian/European ancestry
Rickets and Osteomalacia
Paget’s Disease
Tumors
Muscular Dystrophy (MD)
Osteoarthritis (OA)
Rheumatoid Arthritis
Gout
Deficit of vitamin D and
phosphates, kids = weak bones,
adults = soft bones
Excessive bone destruction with
replacement by fibrous tissue
and abnormal bone
Common site of secondary
tumors, majority of primary
tumors are malignant
Osteosarcoma: bone pain at rest
Chondrosarcoma: cartilage cells
(adults)
Ewing’s sarcoma: shaft of long
bones (adolescents)
Autosomal recessive disorders,
degeneration of skeletal mm,
Duchenne MD most common
(boys): deficit of dystrophin,
skeletal mm replaced by fat and
fibrous conn tissue
Degenerative, “wear and tear”,
result of increased weight
bearing or lifting, articular
cartilage damage, surface =
rough and worn, bone spurs,
narrow joint space,
inflammation, lack of ROM, pain,
predisposition of falls
Autoimmune, chronic systemic
inflammatory, rheumatoid factor
(RF), synovitis, red, swollen,
painful jt., pannus formation,
cartilage erosion, fibrosis,
ankylosis, atrophy of mm.,
muscle spasms, contractures,
bilateral joint involvement, jt.
Becomes fixed and deformed,
systemic: fatigue, anorexia, mild
fever, generalized aching
Unknown cause
Deposits of uric acid and crystals
in jt. Causing local inflammation,
affects single jt. (hallux), redness,
swelling, pain
Excision of tumor if possible
Surgical amputation
Chemotherapy
Diagnostic tests: ID genetic
abnormalities, elevated creatine
kinase levels, EMG, muscle
biopsy, blood test
Treatment: no curative
treatment, moderate exercise,
assistive devices, PT/OT,
massage, ventilator
Treatment: assistive devices,
mild exercise program, orthotics,
massage therapy, PT/OT,
acupuncture, glucosaminechondroitin suppletments,
injection of synthetic synovial
fluid, NSAIDS, analgesics,
arthrotomy, jt. replacement
Treatment: rest/moderate
activity, heat/cold, NSAIDS,
glucocorticoids, analgesics,
surgery, Drugs
Diagnosis: examination of
synovial fluid and blood tests
Treatment: reduce uric acid
levels by drugs and dietary
changes
Ankylosing Spondylitis
Joint fixation, inflammation of a
spinal joint, SI and
costovertebral joints and
intervertebral spaces of axial
skeleton, fibrosis and
calcification of jts., S&S: LBP,
pain when supine, rigid spine;
systemic: fatigue, fever, weight
loss, iritis
Treatment: relieve pain and
maintenance of mobility: antiinflammatory drugs, analgesics,
daily exercise, PT/OT
Patho Test 6 Review
Skin- body’s largest organ
*Thickest on scalp, palms soles and back (1.4 to 4mm)
*Function:barrier, temp regulation, secretion/excretion, vita D production, immunologic,
sensation
Burns:
Superficial burn- epidermis only
Partial thickness- papillary layer of dermis
Deep partial- damage to reticular layer of dermis
Full thickness- entire thickness to subcutaneous tissue
Subdermal- beyond skin to bone, fat of muscle
Histological Assesment of burn wound:
Zone of coagulation (necrosis)
Zone of stasis (injury)
Zone of hyperemia
Epidermal healing
Begin in 24-48 hours after burn
Epithelial cells detach from basale layer and migrate toward wound, proliferate by
mitosis and differentiate into mature epidermal cells
Contact guidance and contact inhibition
Dermal healing
Inflammatory phase
Hemostatic events
Vascular events
Cellular events
Fibroplastic stage
Fibroblasts
Ground substance
Tensile strength
Collagen synthesis
Granulation tissue
Wound contraction
Maturation phase
Hypertrophic scar
Keloid
Rule of nines: front of leg, front upper torso, front lower torso, entire head, entire arm, each are
9% of body when estimating burn coverage. (Genital area 1%)
Treatment of burns:
Silicone pressure garments
Grafts
Allograft, xenograft, cultured skin, dermal substitutes, synthetic skin
Splints
***Never put legs in dependent position without compression. Initially don’t move graft
site! Ambulation guided by physician.
Dermis: made of connective tissue (flexible/ strong), contains nerves(sensory receptors)
and blood vessels.
Skin accessory structures: hair follicles, sebaceous glands, sweat glands, nails.
Subcutanous tissue: below skin includes connective tissue, fat cells, macrophages,
fibroblasts, large blood vessels and nerves.
Inflammatory Disorders
Contact dermatitis: exposure to allergen (soap), sensitization on first exposure.
Chemical irritation: doesn’t involve immune response.
Urticara (Hives): Type 1 hypersensitivity. Ingestion of substance (shellfish). Lesion pruritic, part
of anaphylaxis (check airway for breathing).
Atopic dermatitis (eczema)- inherited allergy, moist pruritic rash on face/chest in infants. Dry,
scaly in adults. Type 1 hypersensitivity. Treatment: glucocorticoids
Psoriasis- chronic inflam. skin disorder, abnormal T- cell activation, excess keratinocytes.
Lesions on face scalp elbow and knees. Treatment: gluco. Anti-metabolites, UV light
Scleroderma: systemic skin disorder, increased collagen/ inflam. Shiny tight hard areas of skin.
May lead to renal failure, intestinal obstruction, respiratory failure.
Keratoses: Benign lesion assoc. w/ aging/ skin damage.
Seborrheic keratoses- proliferation of basal cells, painless, round, dark, elevated
Actinic keratoses- on UV exposed skin, common in fair skinned, looks scaly and may
develop into squamous cell carcinoma.
Squamous cell carcinoma- painless, malignant tumor of epidermis. From sun, smoking. Slow
growing. Good prognosis with early removal.
Malignant melanoma: highly metastic skin cancer, multicolored w/ irregular border, grows
quickly and changes in appearance.
ABC’s of melanoma: increase in Area. Change in Border. Change in Color. Increase in
Diameter.
Karposi’s sarcoma- occurs in AIDS and other immunocompromised pt.s Purple skin spots.
Senescence: biological processes that lead to aging, begins prior to birth. Also the period from
onset of old age to death.
Cardio changes w/ aging: size/ # of cardiac muscle fibers decrease. Fatty tissue and collagen
accumulate. Reduced strength in contraction. Heart valve thickens, less flexible. Less oxygen to
heart, cardiac reserve diminished.
Arteriosclerosis: loss of elasticity, accumulation of collagen, thickening of arteries
Atherosclerosis- hyperlipidemia, accumulation of cholesterol. Common cause of heart attack.
Osteoarthritis: degeneration of cartilage in joints. Associated with sports injury
Neuro changes with aging: reduction in neurons, lipid accumulation in neurons, loss of myelin,
slower response time.
Vision changes with aging: lens less flexible, yellow, night/ color vision reduced.
Falls account for 70% of all deaths in those over 75. 90% of hip fractures due to fall.
Fall intervention: exercise, decrease meds, pressure stockings, gait training, balance exe.
Geriatric physical exam should include: Up and Go Test, Tinetti gait and balance test.
Reproductive System
Menstrual abnormalities
Amenorrhea: no menstruation
Dysmenorrhea: painful menstruation due to excess release of prostaglandins.
PMS
Abnormal bleeding:
Menorrhagia: increase flow
Metrorrhagia: bleeding btwn cycles
Polymenorrhea: short cycles less than 3 wks
Oligomenorrhea: long cycle more than 6 wks.
Endometriosis: endometrial tissue occurs outside uterus. Bleeding/ pain
Candidiasis: not sexually transmitted. Caused by fungus. Opportunistic infection by normal flora
of vagina. White curdlike discharge. Antifungal treatment.
Pelvic Inflammatory disease: infection of uterus, fallopian tubes or ovaries. Originates from
lower reproductive tract. Arises from STD, non sterile abortion or postpartum. Potential
complications: peritonitis, pelvic abcesses, septic shock.
Signs: pain, high temp, guarding, nausea, leukocytosis, purulent discharge. Rx: antibiotic
therapy in hospital.
Leiomyoma: benign tumor of myometrium, well defined encapsulated masses. Surgery or
hormonal therapy for treatment.
Ovarian cysts: last 8-12 wks. Multiple small fluid filled sacs requiring surgical removal if
bleeding is present. ID with ultrasound.
Polycystic ovarian disease: fibrous capsule thickens around follicles of ovary. Hereditary,
absence of ovulation and infertility. Hormonal imbalance, amenorrhea, hirstuism. Rx: surgical
wedge resection of pharmacology.
Fibrocyctic breast disease: cyclic occurrence of nodules or masses in breast tissue
Carcinoma of breast: increase after age 20, usually unilateral, metastasis via lymph nodes.
Predisposing factors: family hx, BRACA gene, late 1st pregnancy, sedentary lifestyle,
smoking, high fat diet.
Cervical cancer: usually due to HPV, Pap Smear can ID early.
Carcinoma of uterus: vaginal bleeding early sign.
Risk factors: over 50 y.o., high dose estrogen without progesterone, obesity, diabetes.
Pap smear down not detect. Slow growing but invasive.
Ovarian Cancer: no reliable screening, detected by pelvic exam.
Risk factors: BRACA gene, early menarche, obesity, late first pregnancy, fertility drugs.
Oral contraceptives are protective.
Pregnancy terminology: number of term infants, pre- term, abortions, kids currently alive (3-0-03)
Avoid modalities on pregnant women.
Ectopic pregnancy: implantation outside the uterus
Prostatitis: inflammation of prostate.
Acute bacterial: gland swollen, tender, bacteria in urine.
Non-bacterial: urine has leukocytes
Chronic bacterial- gland slightly enlarged, dysuria, frequency/ urgency.
Bacterial infection- from e-coli
Occurs in: young men w UTI’s, old men w/ prostatic hypertrophy, w/ STD’s,
through a catheter and bacteria.
Signs: low back pain, decrease urinary stream, muscle aches, anorexia, fever etc.
Benign prostatic hypertrophy: signs- obstructed urinary flow, dribbling, nocturia etc.
Cancer of prostate: often androgen dependent. Hard nodule on periphery of gland, hesitancy in
urinating, recurrent UTI, etc. Diagnosis by serum marker: PSA, prostate specific antigen and
prostatic acid phosphatase.
Testicular cancer: most common solid tumor cancer in young men. Self exam preventative.
Biopsy not performed. Tumor markers: hCG and AFP. Ultrasound
Chlamydia: most common STD.
Males: itchy, white discharge, painful swollen scrotum.
Females: no symptoms until PID or infertility. May infect newborn.
Gonorrhea: males: inflammation of urethra
Females: asymptomatic until PID. May cause blindness in newborns.
Syphillis: chancre at site of infection. Painless firm ulcerated nodule, 3 wks after exposure. If
untreated flu like illness with rash. Tertiary stage: dementia blindness. Rx: antimicrobials.
Genital herpes: blisters on genitals, itching, painful. Antivirals.
Genital warts: HPV, incubation up to 6 months, asymptomatic, may predispose to cervical or
vulvar cancer.