Cell injury Flashcards
SaO2
Percent heme groups occupied by O2
PO2
Driving force for diffusion of O2 into tissue
Cyanosis
Decr O2 saturation (SaO2)
Oxygen
Electron acceptor in oxidative pathway
Hypoxia
Inadequate O2 leads to ATP depletion
Ischaemia
Decreased arterial (or venous) blood flow
Respiratory acidosis
Retention of CO2 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; incr alveolar dead space (e.g. PE)
Diffusion defect
O2 canot cross alveolar-capillary interface; interstitial lung disease (e.g. sarcoidosis)
Methemoglobin
decr SaO2; heme iron +3; oxidising agents (sulfur/nitro drugs)
Rx with IV methylene blue
Clinical findings of methemoglobinaemia
Cyanosis not corrected by O2, chocolate coloured blood
Carbon monoxide
Decr SaO2, left shift O2 binding curve
inhibits cytochrome oxidase
Causes of carbon monoxide poisoning
Car exhaust, space heaters, smoke inhalation
Signs + symptoms of CO poisoning
Headache, cherry red skin colour
Cyanide action
Inhibits cytochrome oxidase, systemic asphyxiant
CO + cyanide poisoning occurs in:
house fires
Left shifted O2 dissociation curve causes
Decr 2,3 BPG CO Alkalosis HbF Methemoglobin Hypothermia
Right shift O2 dissociation curve
Incr 2,3 BPG
high altitude
acidosis
fever
Mitochondrial poisons
Damages membrane and drains off protons
alcohol, salicylates
Uncoupling agents in mitochondria
Drain off protons
Dinitrophenol
Thermogenin (brown fat)
Decreased ATP
Impaired Na+/K+ ATPase pump (cellular swelling); reversible
SIDE note: Digitalis acts on this pump to INCR activity for incr INOTROPY
Anaerobic glycolysis
ATP synthesis in hypoxia
lactate decr intracellular pH
Denatures proteins and enzymes
Irreversible injury hypoxia
- what structures are damaged?
- How?
Membrane or mitochondrial damage
Incr cytosolic Ca2+ activates phospholipase, proteases, endonuclease