High-Yield Facts
in Pathology
1. CELL INJURY
a. Reversible Cell Injury
• swelling of cell organelles and entire cell
• dissociation of ribosomes from endoplasmic reticulum
• decreased energy production by mitochond
...
High-Yield Facts
in Pathology
1. CELL INJURY
a. Reversible Cell Injury
• swelling of cell organelles and entire cell
• dissociation of ribosomes from endoplasmic reticulum
• decreased energy production by mitochondria
• increased glycolysis decreased pH nuclear chromatin clumping
b. Irreversible Cell Injury
• irreversible damage to cell membranes and mitochondria
• influx of calcium into mitochondria; forms dense bodies (flocculent
densities in heart)
• release of cellular enzymes (e.g., SGOT, LDH, and CPK after MI)
• nuclear degeneration (pyknosis, karyolysis, karyorrhexis)
• cell death
2. FATTY CHANGE OF THE LIVER
(STEATOSIS; FATTY METAMORPHOSIS)
a. Mechanisms
1. Increased delivery of free fatty acids to liver
• starvation
• corticosteroids
• diabetes mellitus
2. Increased formation of triglycerides
• alcohol (note: NADH > NAD)
3. Decreased formation of apoproteins
• carbon tetrachloride
• protein malnutrition (kwashiorkor)
1
Copyright © 2007 by The McGraw-Hill Companies, Inc. Click here for terms of use.2 Pathology
3. CELL DEATH
a. Apoptosis
1. Characteristics
• “programmed” cell death
• single cells (not large groups of cells)
• cells shrink form apoptotic bodies
• gene activation forms endonucleases
• peripheral condensation of chromatin with DNA ladder
• no inflammatory response
2. Mechanisms/phases
a) initiation phase caspases are activated
b) execution phase cell death occurs
i. two distinct pathways
i) extrinsic receptor-mediated pathway
• mediated by cell surface death receptors type 1 TNF
receptor (TNFR1) and Fas (CD95)
ii) intrinsic (or mitochondrial) pathway
• increased permeability of mitochondria example is cytochrome c released into cytoplasm via bax channels
3. Examples of apoptosis:
a) physiologic
• involution of thymus
• cell death within germinal centers of lymph nodes
• fragmentation of endometrium during menses
• lactating breast during weaning
b) pathologic
• viral hepatitis
• cytotoxic T cell–mediated immune destruction (type IV hypersensitivity)
b. Necrosis
1. Characteristics
• cause hypoxia or toxins (irreversible injury)
• many cells or clusters of cells
• cells swell
• inflammation presentHigh-Yield Facts 3
2. Examples of necrosis:
• coagulative necrosis ischemia (especially of the heart and kidney but not the brain)
• liquefactive necrosis bacterial infection (and brain infarction)
• fat necrosis pancreatitis and trauma to the breast
• caseous necrosis tuberculosis
• fibrinoid necrosis autoimmune disease (type III hypersensitivity
reaction)
• gangrene ischemia to extremities dry (mainly coagulative
necrosis) or wet (mainly liquefactive necrosis due to bacterial
infection)
4. TERMS
a. Cellular Adaptation
• hypertrophy increase in the size of cells
• hyperplasia increase in the number of cells
• atrophy decrease in the size of an organ
• aplasia failure of cell production
• hypoplasia decrease in the number of cells
• metaplasia replacement of one cell type by another
• dysplasia abnormal cell growth
b. Abnormal Organ Development
• anlage primitive mass of cells
• aplasia complete failure of an organ to develop (anlage present)
• agenesis complete failure of an organ to develop (no anlage present)
• hypoplasia reduction in the size of an organ due to a decrease in
the number of cells
• atrophy decrease in the size of an organ due to a decrease in the
size or number of preexisting cells
5. STEM CELLS (LOCATIONS ARE CALLED NICHES)
• liver oval cells in the canals of Hering of the liver
• muscle satellite cells in the basal lamina of myotubules
• cornea limbus cells in the canals of Schlemm
• colon base of the crypts
• brain dentate gyrus of the hippocampus4 Pathology
6. CARDINAL SIGNS OF INFLAMMATION
• rubor red vasodilation)
• calor hot (increased blood flow)
• tumor swollen (fluid accumulation)
• dolor pain (bradykinin, and the like.)
7. COMPLEMENT CASCADE
a. Products
• C3b opsonin
• C5a chemotaxis and leukocyte activation
• C3a, C4a, C5a anaphylatoxins
• C5–9 membrane attack complex
b. Deficiencies
• deficiency of C3 and C5 recurrent pyogenic bacterial infections
• deficiency of C6, C7, and C8 recurrent infections with Neisseria
species
• deficiency of C1 esterase inhibitor hereditary angioedema
• deficiency of decay-accelerating factor paroxysmal nocturnal
hemoglobinuria
8. THROMBOXANE VS. PROSTACYCLIN
a. Thromboxane (TxA2)
• produced by platelets
• causes vasoconstriction
• stimulates platelet aggregation
b. Prostacyclin (PGI2)
• produced by endothelial cells
• causes vasodilation
• inhibits platelet aggregation
9. GRANULOMATOUS INFLAMMATION
a. Caseating Granulomas
• aggregates of activated macrophages(epithelioid cells)
• tuberculosis
b. Noncaseating Granulomas
• sarcoidosis
• fungal infections
• foreign-body reactionHigh-Yield Facts 5
10. COLLAGEN TYPES
a. Fibrillar Collagens
• type I skin, bones, tendons, mature scars
• type II cartilage
• type III embryonic tissue, blood vessels, pliable organs, immature
scars
b. Amorphous Collagens
• type IV basement membranes
• type VI connective tissue
11. EDEMA
a. Exudates
1. Composition
• increased protein
• increased cells
• specific gravity greater than 1.020
2. Cause
• inflammation
• increased blood vessel permeability
3. Examples
• inflammatory edema of lung bacterial pneumonia
• inflammatory edema of pleural cavity empyema
b. Transudates
1. Composition
• no increased protein
• no increased cells
• specific gravity less than 1.012
2. Cause abnormality of Starling forces
a) increased hydrostatic venous) pressure
• congestive heart failure
• portal hypertension
b) decreased oncotic pressure due to decreased albumin
• liver disease
• renal disease (nephrotic syndrome)6 Pathology
c) lymphatic obstruction
• tumors or surgery
• filaria
12. CARCINOMAS
a. Squamous Cell Carcinoma
• skin cancer
• lung cancer
• esophageal cancer
• cervical cancer
b. Adenocarcinoma
• lung cancer
• colon cancer
• stomach cancer
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