Pathoma Notes

Chapter 1 Growth Adaptations, Cellular Injury, & Cell Death

Growth Adaptations
- Permanent tissues (cardiac & skeletal muscle, & nerves) only undergo hypertrophy no stem cells
- Pathologic hyperplasia can progress to dysplasia then cancer
o Ex: Increased EST endometrial hyperplasia endometrial carcinoma
o Exception: BPH no increased risk for prostate cancer
- Atrophy Either decrease in cell number (apoptosis) OR cell size
o Cell size decrease due to ubiquitin-proteasome OR autophagy
Autophagy generation of autophagic vacuoles that fuse with lysosomes
enzymes break down cells
- Barretts esophagus: Squamous Columnar nonciliated mucinous epithelium (similar to stomach
epithelium)
o Can progress to adenocarcinoma of esophagus
- Metaplasia: reprogramming of stem cells produce new cells REVERSIBLY with removal of stress
- Vitamin A deficiency metaplasia: conjunctiva columnar epithelium squamous.
- Myositis ossificans CT w/in muscle changes to bones after healing from trauma
- Cervical intraepithelial neoplasia dysplasia that is precursor to cervical cancer
- Dysplasia is reversible but can progress to carcinoma
Cell Injury
- Neurons are highly susceptible to ischemic injury, skeletal muscle are more resistant
- Slowly developing ischemia atrophy. Ex: renal artery atherosclerosis
- Acute ischemia injury. Ex: renal artery embolus
- Low O2 impaired oxidative phosphorylation decreased ATP cell injury
- Hypoxia ischemia, hypoxemia, decreased oxygen-carrying capacity
o Ischemia
Decreased arterial perfusion, ex: atherosclerosis: blocks arterial flow
Decreased venous drainage
Budd-Chiari: thrombosis of hepatic vein infarction in liver parenchyma
o MCC Polycythemia vera
o SLE hypercoaguable state
Shock generalized hypotension poor tissue perfusion
o Hypoxemia: low partial P of oxygen in blood (PaO2 <60, SaO2 <90%)
High altitude decreased barometric P decreased PaO2
Hypoventilation Increased PaCO2 leads to decreased PaO2
Diffusion defect PaO2 cannot push O2 into blood due to thick diffusion barrier
Ex: Interstitial pulmonary fibrosis
V/Q mismatch
Blood bypasses oxygenated lung (circulation problem: R L shunt)
Or Oxygenated air cant reach blood (ventilation problem atelectasis)
o Decreased O2-carrying capacity Hb loss or dysfunction
Anemia (Normal PaO2; Normal SaO2)
CO poisoning (Normal PaO2; Decreased SaO2)
Methemoglobinemia Iron in heme is oxidized to Fe3+ Cant bind O2
Normal PaO2, Decreased SaO2
Seen with oxidant stress Sulfa/nitrate drugs, or in newborns
Cyanosis with chocolate-colored blood tx: IV methylene blue
- Hypoxia impairs oxidative phosphorylation decreased ATP disrupts cell functions:
o Na-K pump sodium/water buildup in cell Swelling
o Ca pump Ca buildup in cytosol activation of various enzymes
o Aerobic glycolysis Cell switches to anaerobic glycolysis Lactic acid buildup, decreased
pH denatures proteins & precipitates DNA
- Initial phase of injury reversible cellular swelling: loss of microvilli & membrane blebbing
o Swelling of RER dissociation of ribosomes & decreased protein synthesis
- Irreversible injury
o Membrane damage:
Cytosolic enzymes leaking into serum MI: cardiac troponin
Additional calcium enters cell
o Mitochondrial damage Loss of ETC & cytochrome c leaking into cell (apoptosis)

Lysosome membrane damage hydrolytic enzymes leak into cytosol (which are activated
by high Ca leaking in)

Cell Death
- Loss of nucleus via pyknosis, karyorrhexis, karyolysis
o AKA: nuclear condensation, fragmentation, dissolution
- Coagulative necrosis ischemic infarction of any organ except the brain
o Wedge-shape infarction
o Red infarction if blood re-enters loosely organized tissue: Pulmonary or testicular
infarction
Block of vein prevents blood from leaving
- Liquefactive necrosis enzymatic lysis of cells & protein
o Brain infarction proe