Robbins Chapter One
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- how does carbon tetrachloride kill you?
- in the liver, it is metabolized to free radical metabolites, which fuck your liver.
- which 2 phenomena are always associated with irreversible damage?
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1. loss of cell membrane integrity
2. inability to reverse mitochondrial damage - where is a temperature resistant isoform of AP found?
- biliary epithelium
- what color is eosinophilic?
- pink
- what color is basophilic?
- blue / purple
- what is fragmented nucleus?
- karyorrhexis
- what is faint dissolved nucleus?
- karyloysis
- how can proteases decrease cell membrane integrity?
- by cleaving cytoskeletal elements and making the cell membrane vulnerable to stretching and rupture
- why does hypoxia cause inflammation?
- because hypoxic parenchymal and endothelial cells release cytokines and upregulated cell adhesion molecules
- why can complement be involved in reperfusion injury?
- IgM deposit in ischemic tissues, and complement proteins can bind to the se immune complexes, and this can cause damage
- how do parenchymal cells die in pancreatic duct obstruction?
- apoptosis
- what phospholipid flips from inner to outer leaf to signal for phagocytosis?
- phosphotidylserine
- what determines whether TNF will activate apoptosis or survival?
- which adaptor protein binds to the TNF receptor
- what is NF-kB
-
a prosurvival transcription factor
TNF stimulates the degredation of the inhibitor of NF-kB resulting in survival
TNF can also causes apoptosis via a TNF receptor if the right adaptor protein binds - how do CTLs kill cells?
-
CTLs secrete perforin and granzyme B and also express FasL.
perforin allows entry of granzyme B
granzyme B can activate caspases and trigger apoptosis - megamitochondria
- in alcoholic liver disease and also nutrition deficiencies, mitochondria in liver cells become enormous and oddly shaped
- muscular disease and mitochondria?
- mitochondrial myopathy -hereditary myopathy with abnormal mitochondria
- oncocytoma
- benign tumor full of cells with huge mitochondria
- Mallory bodies
-
intracellular aggregates of IFs seen in the hepatocytes of chronic alcoholics.
Mallory, you are such a fucking drunk - alpha 1 antripsin disease
-
alpha 1 antitripsin doesnt fold right and accumulates in the ER of liver cells that produce it.
elastases in the lungs run wild and fuck everything up - where is fatty change most common?
- liver (and heart=2nd)
- what change can DM cause in liver?
- fatty change (abnormal lipid metabolism)
- how are lipids stored in cells with fatty change?
- small cytoplasmic droplets or big vacuoles
- why does corticosteroid cause fatty change in liver
- increases fatty acid entry into liver
- why does anoxia cause fatty change in the liver?
- decreased ability to utilize fatty acids
- why does CCl4 cause fatty change in liver?
- free radicals damage cell and lead to decreased apoprotein synthesis. (protein, not lipoprotein synth)
- how does alcohol cause fatty change?
-
1. more alpha-glycerophosphate around, and more triglyceride synthesis
2. impaired lipoprotein secretion - Niemann-Pick Disease, type C
- lysosomal storage disease - mutation of nzm in cholesterol catabolism. cholesterol accumulates in lysosomes
- cholesterolosis
-
GALLBLADDER
focal accumulations of cholesterol laden macrophages accumulate in the lamina propria of GB - what do protein inclusions look like?
- round eosinophilic (pink) droplets. think of how exudate is pinker than transudate
- amyloidosis
-
proteins accumulate in EXTRACELLULAR space.
think amyloid bodies in AD in the EXTRACELLULAR spae - Russell Bodies
- flamboyant production of IgG in plasma cells
- cystic fibrosis
- mutant CFTP doesnt fold right and is degraded
- what change occurs in damaged arterioles due to chronic HTN?
- extracellular hyaline change
- pigment derived from cell membrane lipid peroxidation
- lipofuscin
- pigment composed of aggregated ferritin
- hemosiderin
- what can cause systemic hemosiderin accumulation?
-
1 increased iron intake (primary hemochromatosis)
2 impaired iron utilization (thalassemia)
3 hemolysis
4 chronic transfusion - 2 types of calcification?
-
dystrophic (due to cell necrosis, atherosclerosis, or damaged heart valve)
metastatic (due to hypercalcemia) - how does dystrophic calcification begin?
-
extracellular
in dead or dying cells, small vesicles containing many negative charged phospholipids concentrate calcium. membrane bound phosphatases cleave phosphate. calcium + phosphate = crystals
intracellular
in dying mitochondria - 4 causes of metastatic calcification
-
all 4 causes cause hypercalcemia:
1. increased PTH
2. hyperparathyroidism secondary to hyperphosphatemia in renal failure
3. vitamin D toxicity or systemic sarcoidosis
4. destruction of bone tissue - Paget's disease and calcification?
- increased bone turnover can result in metastatic calcification
- reduction in vitamin E could cause ___???
- reduction in life span
- werner syndrome
-
defective dna helicase involved in dna repair
rapid accumultaion of chromosomal damage and rapid aging