Pathology Flashcards
Apoptosis
Programmed cell death (requires ATP) that utilizes caspases to mediate cellular breakdown. No inflammation. Characterized by eosinophilic cytoplasm, cell shrinkage, PKK, membrane blebbing, and consumption by macrophages.
DNA Laddering to detect apoptosis
DNA laddering detects apoptosis because during karyorrhexis, endonucleases cleave to yield 180 BP fragments.
Intrinsic pathway
Involved in tissue remodeling during embryogenesis and occurs when a regulatory factor is withdrawn or exposure to toxin. Increased mitochondrial permeability and cytochrome c release. BAX and BAK are pro-apoptotic. BCL2 is anti-apoptotic.
How does BCL-2 Work?
Stabilizes mitochondrial membrane by inhibiting APAF1 (which induces caspase activation). BCL2 is overexpressed in follicular lymphoma.
Extrinsic pathway
Fas ligand and FAS death receptor (CD95). This occurs in thymic t-cell selection. Binding of FasL to Fas causes death domain induction.
How do CD8 T cells induce response?
They release perforin which cuts holes in cells, and granzyme which activates caspases.
Coagulative necrosis
During ischemia (except in brain). Tissue is firm with structure preserved.
Liquefactive necrosis
Occurs in pancreas, brain, and abscesses. Enzymes dissolve tissue leading to liquification.
Caseous necrosis
Seen in TB and fungal infections (like liquefactive + coagulative)
Fibrinoid Necrosis
Happens in blood vessels due to protein deposition in the wall. Occurs during malignant hypertension and vasculitides and preeclampsia. Highlighter pink appearance on histology
Gangrenous necrosis
Happens in patients with diabetes (looks like mummified foot), or can be wet if superimposed infection. Common in limbs or GI tract.
Hallmark of reversible injury
Cell swelling (due to decreased Na-K ATPase)
Hallmark of irreversible injury
Pyknosis (nuclear shrinking), karyorrhexis (breaking up), karyolysis (dissolving).
Hallmark of reversible injury
Cell swelling (due to decreased Na-K ATPase). Ribosomes pop off and protein synthesis is down.
Hallmark of irreversible injury
Membrane damage. Pyknosis (nuclear shrinking), karyorrhexis (breaking up), karyolysis (dissolving). Amorphous densities in mitochondria, leakage of cyt c, and activation of caspases.
Red infarcts
Received dual blood flow and are loosely organized (testicle, lung, liver, intestine)
White infarcts
Receive single blood flow and are dense (spleen, heart, kidney).
Distributive shock
High output cardiac failure (increased co increased venous return, decreased resistance). Decreased PCWP, vasodilation, failure to increase BP with fluids.
SEPSIS, anaphylaxis
Hypovolemic/cardiogenic shock
Low output failure (decreased CO, increased TPR) increased PCWP in cardiogenic, decreased PCWP in hypovolemic. Blood pressure restored with fluids
Where does increased vascular permeability happen in acute inflammation
In post capillary venule.
Chromatolysis
A process that can be seen in a damaged neuron that increases protein synthesis in order to heal. Marked by cellular swelling, displacement of the nucleus to the periphery, and dispersion of nissl substance.
How do free-radicals damage cells?
Via lipid peroxidation (membranes) and oxidation of DNA.
How is O2- neutralized?
How about H2O2?
How about OH-?
SOD to H2O2
H2O2 via catalase, to h2o and o2
Via glutathione peroxidase.
Fenton reaction
Fe3+ creates OH-