Path Flashcards
Karyorrhexis
Nuclear fragmentation
Pyknosis
Nuclear shrinkage
Role of Apaf-1
Apaf-1 induces caspases, but Bcl-2 prevents cytochrome c release by binding and inhibiting Apaf-1
Role of FADD
After Fas-FasL crosslink, multiple Fas molecules coalesce, forming a binding site for a death domain containing adaptor protein, FADD. FADD binds inactive caspaces, activating them
Karyolysis
Dissolution
30 year old female presents with fibrinoid necrosis reasoning?
Commonly seen in preeclampsia where very high BP can cause fibrinoid necrosis of the placenta
Areas suceptible to hypoxia/ischemia and infarction Brain Heart Kidney Liver Colon
ACA/MCA/PCA boundary areas
Subendocardium of LV
Straight segment of proximal tubule (medulla) and thick ascending limb (medulla)
Around the central vein (zone III)
Splenic flexure, rectum (watershed areas that receive dual blood supply from most distal branches of 2 arteries, which protects these areas from single-focal blockage). However, these areas are suceptible to ischemia from systemic hypoperfusion.
Likelihood of cell injury based on what 3 factors?
1) Type of stress
2) Severity
3) Type of cell affected
Final electron acceptor in ETC
O2
Areas suceptible to ischemia from systemic hypoperfusion (eg. cardiac arrest, shock)
ACA/MCA/PCA boundary areas, splenic flexure, rectum
Hypoic ischemic encephalopathy affects what two cells
Pyramidal cells of hippocampus and purkinje cells of cerebellum
Organ suceptibility to infarction after occlusion of feeding artery is ranked greatest to least as follows:
CNS>Myocardium>Kidney>Spleen>Liver
3 organs suceptible to hemorrhagic infarction
Lung, liver, intestine
3 organs suceptible to pale infarction
Spleen, heart, kidney
Chromatolysis in 3 steps
Axonal injury causes
1) cellular body swelling
2) movement of nuclei to periphery
3) dispersion of nissl substance to increase protein synthesis to help with regeneration of axon
Dystrophic calcification
Normocalcemic deposition of calcium into abnormal tissues secondary to necrosis/injury
Metastatic calcification
Hypercalcemic (secondary to disorder that increases calcium) deposition of tissues into normal tissue
3 common tissues of metastatic calcification?
Kidney, lung, gastric mucosa b/c these tissues lose acid quickly. Increase in pH favors deposition
Mechanism of cytoskeleton degradation?
Ubiquitin proteosome degradation by intermediate filaments of cytoskeleton are “tagged” with ubiquitin and destroyed by proteosomes
Two mechanisms by decrease in cell size
Ubiquitin proteosome degradation of cytokskeleton and autophagy of cellular components
Most dangerous free radical
*OH (hydroxyl free radical)
3 scenarios where you would see exudate
Lymphatic obstruction, malignancy, inflammation/infection
3 scenarios where you would see transudate
Increase Na+ absorption, Increased hydrostatic pressure (HF), decreased oncotic pressure (nephrotic syndrome, cirrhosis)
Granuloma formation
1) MHC Class II presenting macrophages present antigen to CD4+ t cells
2) Secrete IL-12 to differentiate CD4+t cells into Th1 cells
3) TH1 cells secrete interferon gamma to activate macrophages
4) Macrophages secrete TNF alpha to maintain/induce granuloma formation
