Pathophysiology Midterm
| Complete Exam Study
Guide, Practice Questions,
Answers & ATI Review
Material
,pathologic stressors
HTN
pathologic cell stressors
ischemia/hypoxia, toxins, injury to cellular organelles, trauma, aging
toxins
free radicals, intracellular accumulations, autoimmune reactions
injury to cellular organelles
radiation, genetic defects
ischemia
decreased arterial or venous blood flow → DVT/PE, trauma
hypoxemia
decrease in PaO2 → CO poisoning, hypoventilation and CO2 retention
hypoxia
inadequate oxygenation of tissues
tissues susceptible to hypoxia
watershed areas between 2 blood supplies: like subendocardial tissue → layer of
tissue that contains electrical conduction system of the heart
free radicals
compounds with a single unpaired electron in an outer orbital → can degrade nucleic
acids and membrane structure destabilizing cells and organelles
,neutralization of free radicals in vivo (in body)
superoxide dismutase (in WBCs), glutathione peroxidase, catalase, vitamins
intracellular accumulations
excess accumulations of substances in cells leads to cellular injury due to toxicity,
immune response, and/or taking up cellular space
4 main pathways of intracellular accumulations
1. inadequate removal of normal substances
2. accumulation of an abnormal endogenous substance
3. deposition and accumulation of an abnormal exogenous substance → ex: carbon,
silica → what gives coal miners "black lung"
4. failure to degrade a metabolite due to inherited enzyme deficiencies
accumulation of an abnormal endogenous substance
substance made in body but is foreign to that specific cell
cholesterol (atherosclerosis)
endogenous intracellular accumulation / cholesterol laden smooth muscle cells and
macrophages → foam cells
melanin (Addisons)
endogenous intracellular accumulation / increased ACTH causing excess synthesis of
melanin and diffuse pigmentation
coal workers
exogenous intracellular accumulation / phagocytosis of black pigment by alveolar
macrophages "black lung"
, dystrophic calcification
calcification of dead or dying tissues in the presence of normal calcium levels, usually
occurs in necrosis → can be deposited in heart tissue, muscle tissue, etc
- calcium metabolism and serum calcium level is normal
- generally irreversible
lithopedion
type of dystrophic calcification of implanted fetus that has died and calcified "stone
babies"
dystrophic calcification etiology
necrosis (caseous, liquefactive, fat), infarcts, thrombi, hematomas, dead parasites, old
scars, atheroma, Monckenberg's sclerosis, certain tumors, cysts, calcified cysts
dystrophic calcification pathogenesis
increased binding of phosphates with necrotic and degenerative tissue → binds to
calcium → forms calcium phosphate precipitates (insoluble solid in liquid as result of
chemical reaction)
metastatic calcification
occurs in normal tissue when there is hypercalcemia
metastatic calcification etiology
increased secretion of parathyroid hormone, excessive bone destruction, vitamin D
intoxication, sarcoidosis (macrophages activate a vitamin D precursor), renal failure
leading to secondary hyperparathyroidism
metastatic calcification example
story about patient on dialysis with hypercalcemia that had painful lumps between his
thighs
| Complete Exam Study
Guide, Practice Questions,
Answers & ATI Review
Material
,pathologic stressors
HTN
pathologic cell stressors
ischemia/hypoxia, toxins, injury to cellular organelles, trauma, aging
toxins
free radicals, intracellular accumulations, autoimmune reactions
injury to cellular organelles
radiation, genetic defects
ischemia
decreased arterial or venous blood flow → DVT/PE, trauma
hypoxemia
decrease in PaO2 → CO poisoning, hypoventilation and CO2 retention
hypoxia
inadequate oxygenation of tissues
tissues susceptible to hypoxia
watershed areas between 2 blood supplies: like subendocardial tissue → layer of
tissue that contains electrical conduction system of the heart
free radicals
compounds with a single unpaired electron in an outer orbital → can degrade nucleic
acids and membrane structure destabilizing cells and organelles
,neutralization of free radicals in vivo (in body)
superoxide dismutase (in WBCs), glutathione peroxidase, catalase, vitamins
intracellular accumulations
excess accumulations of substances in cells leads to cellular injury due to toxicity,
immune response, and/or taking up cellular space
4 main pathways of intracellular accumulations
1. inadequate removal of normal substances
2. accumulation of an abnormal endogenous substance
3. deposition and accumulation of an abnormal exogenous substance → ex: carbon,
silica → what gives coal miners "black lung"
4. failure to degrade a metabolite due to inherited enzyme deficiencies
accumulation of an abnormal endogenous substance
substance made in body but is foreign to that specific cell
cholesterol (atherosclerosis)
endogenous intracellular accumulation / cholesterol laden smooth muscle cells and
macrophages → foam cells
melanin (Addisons)
endogenous intracellular accumulation / increased ACTH causing excess synthesis of
melanin and diffuse pigmentation
coal workers
exogenous intracellular accumulation / phagocytosis of black pigment by alveolar
macrophages "black lung"
, dystrophic calcification
calcification of dead or dying tissues in the presence of normal calcium levels, usually
occurs in necrosis → can be deposited in heart tissue, muscle tissue, etc
- calcium metabolism and serum calcium level is normal
- generally irreversible
lithopedion
type of dystrophic calcification of implanted fetus that has died and calcified "stone
babies"
dystrophic calcification etiology
necrosis (caseous, liquefactive, fat), infarcts, thrombi, hematomas, dead parasites, old
scars, atheroma, Monckenberg's sclerosis, certain tumors, cysts, calcified cysts
dystrophic calcification pathogenesis
increased binding of phosphates with necrotic and degenerative tissue → binds to
calcium → forms calcium phosphate precipitates (insoluble solid in liquid as result of
chemical reaction)
metastatic calcification
occurs in normal tissue when there is hypercalcemia
metastatic calcification etiology
increased secretion of parathyroid hormone, excessive bone destruction, vitamin D
intoxication, sarcoidosis (macrophages activate a vitamin D precursor), renal failure
leading to secondary hyperparathyroidism
metastatic calcification example
story about patient on dialysis with hypercalcemia that had painful lumps between his
thighs
