basic pathology Flashcards
what is pyknosis?
nuclear shrinkage in apoptosis
what is karyorrhexis
nuclear fragmentation
what are two pathways of extrinsic apoptosi?
- ligand recpetor ineractions (Fas ligand binds to Fas = CD95)
- immune cell (cytotoxic release of performin and granzyme B)
name 6 types of necrosis
coagulative
liquefactive
caseous
fatty
fibrinoid
gangrenous
3 organs coag necrosis
heart
liver
kidney
3 examples of liquefactive necrosis
brain
bacterial abscess
pleural effusion
2 examples of caseous necrosis
TB
systemic fungi
fatty necrosis
perinpancreatic fat (saponification via lipase)
fibrinoid necrosis
blood vessels
gangrenous necrosis example
dry (ischemic coagulative) or wet (with bacteria); common in limbs and GI tract
what types of cell injury are reverisble with O2 (6)
decreased ATP synthesis
cellular swelling (no ATP –> impaired Na+/K+ ATPase)
nuclear chromatin clumping
decreased glycogen
fatty change
ribosomal detachment
what 5 changes are seen in irreversible cell injury?
think: membran damage
- nuclear pyknosis, karyolysis, karyorrhexis
- ca2+ influx–>caspase activation
- plasma membrane damage
- lysosomal rupture
- mitochondrial permeability
what areas are susceptible to hypoxia in:
brain -
heart -
kidney (2)
liver -1
colon -
brain - watershed areas of ACA/MCA/PCA/boundary - pyramidal cells of hippocampus and purkinje cells
heart - subendocardium (LV)
kidney: straight segment of proximal tubule(medulla) + thick ascending limb (medulla)
liver = area around central vein
colon - splenic flexure and rectum
where do red infarcts occur(3)?
damage of reperfusion
hemorhagic infarcts occur in **loose tissue ** with collaterals : liver, lung, intestine following **reperfusion **
reperfusion –>damage by free radicals
pale infarcts - 3 organs w/one blood supply
heart
kidney
spleen
hypovolemic/cardiogenic shock
type of output
tpr?
cardiac output
skin
Low-output failure
increased TPR
low cardiac output
cold, clammy pt (vasoconstriction)
septic shock
type of output
tpr?
cardiac output
skin
high-output failure
decreased TPR
dilated arterioles, high venous return
hot patient (vasodilation)
what are 6 causes of atrophy?
decreased hormones
decreased: innervation (motor neuron damage), blood flow, nutrients
increased pressure: nephrolithiasis
occlusion of secretory ducts: ie cystic fibrosis.
5 cardinal signs of inflammation
rubor -redness
dolor -pain
calor -heat
tumor -swelling
function laesa-loss of function
3 vascular components of acute inflammation
increased vascular permeability
vasodilation
endothelial injury
what are vascular components of inflammation
- increased vascular permeability (post cap venules)
- vasodilation of arterolies
- endothelial injury
3 things that mediate acute inflammation
neutrophil
eosinophil
antibody
what type of inflammation if a granuloma
chronic = nodular collections of epitheliod macrophages and giant cells
what are two outcomes of chronic inflammation?
scarring and amyloidosis
mononuclear cell mediated: charaterized by destruction and repair
associated with blood vessel proliferation, fibrosis
chronic inflammation
what are the four steps of leukocyte extravasation
note location: post capillary venules
- rolling (leukocyte: siall-lewis X; endothelial cell: e-selectin(induced by TNF-1 and IL-2), P-selectin(from weibel paladie bodies and mediated by histamine)
- tight binding: leukocyte: ICAM-1 (upregulated by TNF and IL-1) neutrophil - has LFA-1 = integrin upregulated by C5a, LTB4
3. diapedesis - PECAM-1
**4. migration - guided by chemotactic singals: C5a IL-8, LTB4, Kallikrein (CILK) **
what type of drug metabolism –> free radical injury?
phase I
which 3 enzymes can neutralize free radicals
which vitamins?
enzymes: H2O2: catalase +glutathione, peroxidase superoxide: superoxide dismutase,
vitamins: ACE
- retinopathy of prematurity
- bronchopulmonary dysplasia
- CCL4 —> liver necrosis(fatty change)
- acetaminophen OD
- iron overload (hemochromatosis)
- reperfusion after anoxia(superoxide)
are all examples of:
free radical injury
how do free radicals damage cells: 3 ways here
membrane lipid peroxidation
protein modification
DNA breakage