Summary of entire pathophysiology course (masterdoc)

Inflammation/hypersensitivity
Hypersensitivity I – immediate (onset 15-30 min)
Affects
- skin (urticaria and eczema, angioedema)
- eyes (conjunctivitis)
- nasopharynx (rhinorrhea, rhinitis),
- bronchopulmonary tissues (asthma)
- gastrointestinal tract (gastroenteritis)
- Anaphylaxis
Histology
- Extrinsic/exogenous antigen
- Antibody IgE
- Mediated by mast cell and basophil
- Lesion: mainly mast cell and eosinophil (also basophil, neutrophil)
- Appearance: red, swollen
Hypersensitivity II – cytotoxic (minutes-hours)
Symptoms
- Own tissues and cells
- Erythroblastosis fetalis
- Goodpasture’s nephritis
- Cytopenia
- Also: diabetes I, acute transplant rejection, pernicious anemia, Hashimoto’s thyroiditis, systemic
lupus erythematosus
Histology
- Endogenous (body’s own cell-surface antigens)
- Exogenous chemicals (haptens): drug-induced hemolytic anemia, granulocytopenia,
thrombocytopenia
- IgM, IgG, complement
- Phagocytes, NK cells (ADCC)
- Lesion: antibodies, complement, neutrophils
- Appearance: lysis, necrosis
Treatment
- Anti-inflammatory
- Immunosuppressants


Hypersensitivity III – Immune complex (3-10 hrs)
Symptoms

, - General (serum sickness)
- Skin (systemic lupus erythematosus, arthus reaction)
- Kidney (lupus nephritis)
- Lungs (aspergillosis, Farmer’s lung disease, hypersensitivity pneumonitis)
- Vessels (polyarteritis)
- Joints (rheumatoid arthritis)
-
Histology
- Soluble antibody complexes
- IgG, IgM
- Exogenous (bacterial, parasitic, viral)
- Endogenous (non-organ specific)
- Mediated by: platelets and neutrophils
- Lesion: neutrophils, immune complex deposits, complement
- Appearance: erythema, edema, necrosis
Hypersensitivity IV – cell mediated/delayed (48-72h+)
Types
- Tuberculin (antigen: tuberculin)
- Contact dermatitis (antigen: nickel, rubber, poison ivy)
- Granulomatous (21-28 days)
Affects
- Tuberculosis
- Leprosy
- Blastomycosis
- Histoplasmosis
- Toxoplasmosis
- Leishmaniasis
- Granulomas
- Also: diabetes I, acute transplant rejection, pernicious anemia, Hashimoto’s thyroiditis,
rheumatoid arthritis, hypersensitivity pneumonitis
Histology
- No antibody (cell mediated)
- T1 helper/ CD4+ recognize intracellular pathogenic antigen
- Appearance: erythema, eczema, local induration, hardening (granuloma)



Blood disorders and anemias
Hematopoiesis
Anemia

,Heart failure and circulatory pathology
Atherosclerosis can lead to:

 CAD
 Atherosclerotic stroke related to plaque
 Abdominal aneurysm due to weakening of the vessel
 Nontraumatic amputation of lower extremity
 Mesenteric angina
 Small bowel infarction
 Renovascular atherosclerosis of renal arteries
Hyaline arteriosclerosis
A. Diabetes
- Non-enzymatic glycosylation of small blood vessels, HBA 1C (protein acc. in vessel wall)
- Osmotic damage in tissues containing aldose reductase (converts glucose >> sorbitol, attracts
water until cell bursts), causing:
 Lens cataract
 Microaneurysms in retina
 Peripheral neuropathy
 Microalbuminuria (in diabetic nephropathy)
B. Hypertension
- Proteins forced in bm by increased diastolic pressure
- Kidney – shrunken, cobblestone appearance
- Lacunar strokes – tiny infarctions in internal capsule
Aneurysm – outpuching of vessel wall due to weakness
Law of Laplace – increased radius  increased stress on wall, therefore all aneurysms will rupture
Possible risk factor:
- Atherosclerosis


Abdominal aortic aneurysm
- Diameter >3cm or >50% larger than normal size
- Most common area of aneurysm
- Lacks blood supply (vasa vasorum) below renal arteries  high risk of hypoxia
- Symptoms of rupture:
 Severe left flank pain
 Hypotension
 Pulsatile mass on physical examination
 If larger than 5 cm  surgery
 Visualize with US

, Dissecting aortic aneurysm
Main risk factor:
- Hypertension
 Tear in aorta  blood runs to pericardial sac  cardiac tamponade (proximal dissection,
most common type)
Symptoms:
- Chest pain - TEARING pain radiates to back, retrosternal pain
- Absent/diminished pulse on left side due to subclavian closure
- X-ray – widening of proximal aortic knob
 Confirm with transesophageal US or
 Angiography
Aneurysm of arch of aorta
- Most common complication – tertiary syphilis (treponema)  leads to vasculitis of vasa vasorum
 Consequences:
 Endarteritis obliterans (obliteration of lumen)
 Ischemia
 Weakening under systolic pressure  depression of arch  stretching of aortic
valve ring  aortic regurgitation murmur


Heart failure (congestive)
Frank-Starling law works in pathologic conditions– in aortic regurgitation, incomplete aortic closure 
blood drips back  decreased stroke volume  more blood in left ventricle EDV (pathologic)
Concentric hypertrophy – increased afterload (pressure) due to aortic stenosis or chronic HTN
Eccentric hypertrophy – increased preload (vol)
Left heart failure – forward failure
- Left ventricle failure  ↑ EDV  blood flow back to atrium  pulmonary vessels  ↑
hydrostatic pressure  pulmonary edema
- Chronic LHF  hemorrhage  phagocytosis of RBC  rusty sputum/spit
 Cytology – hemosiderin (phagocytosed RBC)
Main symptom
- Dyspnea
- Paroxysmal nocturnal dyspnea – blood returns to lungs during sleep
- Pillow orthopnea – putting pillow under head decreases venous return to heart  decreases
dyspnea
Right heart failure – backward failure
- Right side cannot pump blood to left side  blood returns to veins  ↑ Hydrostatic pressure in
veins