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Hi Yield goljan

PO2 driving force for diffusion of O2 into tissue
SaO2 percent heme groups occupied by O2
Cyanosis decreased O2 saturation (SaO2); O2 content
Oxygen electron acceptor in oxidative pathway
Hypoxia inadequate O2 leads to ATP depletion
Ischemia decreased arterial (or venous) blood flow
Respiratory acidosis retention of CO, always decreases PaO2
Ventilation defect impaired delivery of O2 to alveoli; intrapulmonary shunting of blood (e.g., RDS)
Perfusion defect absent blood flow to alveoli; increased alveolar dead space (e.g., pulmonary embolus)
Diffusion defect O2 cannot cross alveolar-capillary interface; interstitial lung disease (e.g., sarcoidosis)
Methemoglobin ↓ SaO2; heme Fe+3; oxidizing agents (sulfur/nitro drugs); Rx with IV methylene blue
Clinical methemoglobinemia cyanosis not corrected by O2; chocolate colored blood
Carbon monoxide ↓ SaO2; left-shift O2 binding curve; inhibits cytochrome oxidase
Causes carbon monoxide poisoning car exhaust, space heaters, smoke inhalation
S/S carbon monoxide poisoning headache; cherry red color skin
Cyanide inhibits cytochrome oxidase; systemic asphyxiant
Carbon monoxide + cyanide poisoning house fires
Left-shifted O2 curve ↓ 2, 3 BPG, carbon monoxide, alkalosis, HbF, methemoglobin, hypothermia
Right-shifted O2 curve ↑ 2, 3 BPG, high altitude, acidosis, fever
High altitude respiratory alkalosis enhances glycolysis; ↑ synthesis 2,3 BPG
Mitochondrial poisons damages membrane and drains off protons; alcohol, salicylates
Uncoupling agents in mitochondria drain off protons; dinitrophenol, thermogenin (brown fat)
Complication mitochondrial poisons/uncoupling agents hyperthermia
Decreased ATP impaired Na+/K+ ATPase pump (cellular swelling); reversible
Anaerobic glycolysis ATP synthesis in hypoxia; lactate ↓ intracellular pH, denatures proteins
Irreversible injury hypoxia membrane/mitochondrial damage
Mitochondrial damage release cytochrome c activates apoptosis
Irreversible injury hypoxia ↑ cytosolic Ca2+ activates phospholipase, proteases, endonuclease
Free radicals unpaired electron in outer orbit; damage cell membranes and DNA
Free radicals superoxide, hydroxyl, peroxide, drugs (acetaminophen)
Superoxide dismutase neutralizes superoxide
Glutathione neutralizes peroxide, drug FRs
Catalase neutralizes peroxide
Lipofuscin indigestible lipid of lipid peroxidation; brown pigment increased in atrophy and FR damage
Reperfusion injury in heart superoxide FRs + calcium
Mitochondrial injury cytochrome c in cytosol initiates apoptosis
SER hyperplasia alcohol, barbiturates, phenytoin
Complications SER hyperplasia increases drug metabolism (e.g., oral contraceptives); low vitamin D
Chediak-Higashi membrane protein defect in transferring lysosomal enzymes to phagocytic vacuoles
Chediak-Higashi AR; giant lysosomes
I cell disease absent enzyme marker in Golgi apparatus (mannose 6-phosphate); empty lysosomes
Rigor mortis stiff muscles after death due to ATP depletion
Fatty change in liver MCC alcohol (increase in NADH); DHAP → G3P → TG
Fatty change in liver VLDL pushes nucleus to side
Causes fatty change ↑ synthesis TG/FAs, beta-oxidation of FAs, synthesis apoproteins/release VLDL
Fatty change in kwashiorkor ↓ synthesis of apoproteins
Ferritin primary iron storage protein; soluble in blood; serum level reflects marrow storage iron
Hemosiderin insoluble ferritin degradation product visible with Prussian blue stain
Atrophy reduction in cell/tissue mass by either loss or cell shrinkage
Created by: mcafej02



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