Term
|
Definition
| increased number of cells => increased tissue volume |
|
|
Term
| What 3 stimuli can cause hyperplasia? |
|
Definition
1) hormones
2) GF
3) cytokines |
|
|
Term
| What is the mechanism of cell proliferation in hyperplasia? |
|
Definition
| usually increased transcription of genes encoding GF & receptors and cell cycle promotors. Also, there's occasional recruitment of stem cells. |
|
|
Term
| What induces glandular epithelial cell proliferation in female breast in puberty & pregnancy? |
|
Definition
|
|
Term
| What induces smooth muscle cell proliferation in uterus in pregnancy? |
|
Definition
|
|
Term
| When might hyperplasia be compensatory? |
|
Definition
Partial hepatectomy (regeneration of liver needed)
unilateral nephrectomy (enlargement of contralateral kidney) |
|
|
Term
| What causes the endometrium in the uterus undergo hyperplasia? |
|
Definition
| prolonged unopposed estrogen stimulation |
|
|
Term
| Where is hyperplasia seen in wound healing & repair? |
|
Definition
|
|
Term
| Where does HPV cause hyperplasia? |
|
Definition
|
|
Term
|
Definition
| increased cell size due to increased synthesis of cellular components => increased tissue volume |
|
|
Term
| Can hypertrophy or hyperplasia been seen in non-mitotic cells? |
|
Definition
hypertrophy only.
hyperplasia can only been seen in cells with mitotic capability. |
|
|
Term
| What 2 stimuli can cause hypertrophy? |
|
Definition
1) hormones
2) increased workload |
|
|
Term
| Where is hypertrophy seen in pregnancy? |
|
Definition
| increased uterine smooth muscle cell size |
|
|
Term
| What causes hypertophy in skeletal muscle cells of weightlifters? |
|
Definition
|
|
Term
| When is hypertrophy seen in cardiac myocytes? |
|
Definition
| increased workload due to hypertension or stenotic outflow valve |
|
|
Term
| What 2 signals cause hypertrophy in cardiac myocytes? |
|
Definition
|
|
Term
| What does the heart do in response to increased workload? |
|
Definition
| increase transcription or re-express fetal genes to increase synthesis of proteins to increase cardiac function & decrease workload |
|
|
Term
|
Definition
| decreased cell size due to decreased cellular components => decreased tissue volume |
|
|
Term
| What 8 stimuli can cause atrophy? |
|
Definition
1) decreased workload
2) denervation
3) decreased vascular supply
4) malnutrition
5) decreased hormonal stimuli
6) aging
7) compression
8) cytokines
note: some of these can occur simulaneously |
|
|
Term
| Why do we not have some of our embryologic structures as adults? |
|
Definition
|
|
Term
| What in the postpartum mother atrophies? |
|
Definition
|
|
Term
| What in the postmenopausal female atrophies? |
|
Definition
|
|
Term
| What can atrophy after a spinal cord trauma? |
|
Definition
|
|
Term
| What can cause cerebral atrophy? |
|
Definition
| decreased blood flow & aging |
|
|
Term
| What atrophies due to starvation (malnutrition)? |
|
Definition
|
|
Term
|
Definition
| increased destruction of cellular components by lysosomes & proteasomes => incrased autophagic vacuoles |
|
|
Term
| What may atrophy be accompanying? |
|
Definition
| apoptosis/necrosis => fatty infiltration |
|
|
Term
|
Definition
| replacement of one mature cell type by another |
|
|
Term
| What stimuli initiates metaplasia? |
|
Definition
| chronic tissue trauma/irritation |
|
|
Term
| How does chronic tissue trauma/irritation cause metaplasia? |
|
Definition
| leads to signals by cytokines, GF & ECM components => transcriptional change => differentiation towards a new cell |
|
|
Term
| What epithelial metaplasia does cigarette smoke cause to the epithelium of the RT? |
|
Definition
| pseudostratified, ciliated, columnar epi => stratified squamous |
|
|
Term
| What epithelial metaplasia does gastroesophageal reflux cause to the epithelium of the lower esophagus? |
|
Definition
| stratified squamous => gastric & intestinal-type glandular epi. |
|
|
Term
| What CT metaplasia can be seen after trauma to skeletal muscle? |
|
Definition
myosis ossificans
(skeletal muscle => bone) |
|
|
Term
| What are the 2 normal functions of lysosomes? |
|
Definition
|
|
Term
| Which cells do most of the lysosomal heterophagy? |
|
Definition
| neutrophils & macrophages |
|
|
Term
|
Definition
| endocytosis of extracellular maerial => fusion of lysosome to form phagolysosome => enzymatic degradation |
|
|
Term
|
Definition
| collection of injured or unnecessary intracellular material to vacuoles => fusion with lysosomes to form autophagolysosomes => enzymatic digestion |
|
|
Term
| What happens when a lysosome is functioning abnormally? |
|
Definition
| enzymatic dysfunction => excess accumulation of lysosomal contents & potential cellular injury |
|
|
Term
| What can lead to enhanced smooth ER metabolism? |
|
Definition
| chronic exposure to certain agents metabolized by smooth ER => increased smooth ER synthesis => enhanced metabolism |
|
|
Term
| What alterations can cellular mitochondria see? |
|
Definition
Hypertrophy (increased #)
Atrophy (decreased #)
Genetic metabolic disease
Aquired disorder |
|
|
Term
| What 3 cellular components can have alterations in the cytoskeleton? |
|
Definition
Microtubules
Thin Filaments
Intermediate Filaments |
|
|
Term
| Which of the cytoskeleton cellular components that can have alterations, which can occur both genetically or aquired? |
|
Definition
Mirotubules & Intermediate filaments
(thin filament alterations are due to aquired alterations secondary to toxins) |
|
|
Term
| In what cellular reaction rate imbalances will there be an accumulation of normal endogenous substances? |
|
Definition
| if production/absorption rate > metabolic/removal rate |
|
|
Term
| In what cellular reaction defects will there be an accumulation of normal or abnormal endogenous substances? |
|
Definition
| alterted synthesis/metabolism/transport |
|
|
Term
| When what in the cell is lacking will there be an accumulation of abnormal exogenous substances? |
|
Definition
| lack of cellular metabolic/secretory pathways |
|
|
Term
|
Definition
|
|
Term
| What causes fatty deposits in the liver? |
|
Definition
| 1) stravation => fatty acid uptake from adipose 2) protein malnutrition & CCl4 toxicity => decreased apoprotein synthesis => decreased lipoprotein export
3) damage due to alcholism, DM, obesity, hypoxia => triglyceride production/removal alterations |
|
|
Term
| How are triglycerides removed from the liver? |
|
Definition
| Added to apoproteins to form lipoproteins |
|
|
Term
| How are trigylcerides formed in the liver? |
|
Definition
| from a fatty acid precursor |
|
|
Term
| What are the 2 fates of fatty acids in the liver? |
|
Definition
| become triglycerides or catabolism (to ketones, phospholipids, or cholesterol) |
|
|
Term
| What gross changes are seen in a fatty liver(steatosis)? |
|
Definition
| enlarged, greasy & yellow |
|
|
Term
| Microscopically, what is seen in a steatotic liver in an H&E stain? |
|
Definition
| clear vesicular cytoplasmic vacuoles in the parenchymal cells |
|
|
Term
| Microscopically, what is seen in a steatotic liver in an oil red-O stain? |
|
Definition
|
|
Term
| What gross change is seen in tissue with high cholesterol content? |
|
Definition
|
|
Term
| What microscopic change is seen in a tissue with excess cholesterol & cholesterol esters? |
|
Definition
| foam cells (round with clear bubbly cytoplasm) |
|
|
Term
| How do atherosclerotic plaques look microscopically? |
|
Definition
|
|
Term
| How do xanthomas due to hyperlipidemia look? |
|
Definition
| Masses that are often subcutaneous |
|
|
Term
| When is cholesterolosis in the subepithelium of the gallbladder seen? |
|
Definition
| with cholesterol-predominant gallstones |
|
|
Term
| How do protein deposits look microscopically? |
|
Definition
| variably-sized, pink, cytoplasmic globules |
|
|
Term
|
Definition
| increased protein reabsorption by the proximal renal tubular epithelial cells |
|
|
Term
| What causes Russell bodies is plasma? |
|
Definition
|
|
Term
| What causes α1-antitrypsin protein in ER of hepatocytes? |
|
Definition
| mutations in the α1-antitrypsin gene => abnormal protein => decreased intracellular transport & secretion |
|
|
Term
| How does glycogen accumulation look microscopically in an H&E stain? |
|
Definition
| small, clear, cytoplasmic vacuoles |
|
|
Term
| How does glycogen accumulation look microscopically in a PAS stain? |
|
Definition
|
|
Term
| Why does glycogen accumulate in DM? |
|
Definition
| abnormal glucose metabolism |
|
|
Term
| What inherited enzyme deficiencies can lead to glycogen accumulation? |
|
Definition
| glycogen storage diseases due to abnormal glycogen metabolism |
|
|
Term
| What type of pigments are unable to be degraded and persist in phagolysosomes? |
|
Definition
|
|
Term
| What 2 exogenous pigments can persist? |
|
Definition
|
|
Term
| What permanant pigment is seen due to carbon? |
|
Definition
| black granular pigment in the cytoplasm of macrophages |
|
|
Term
|
Definition
| black granular pigment caused by carbon in the cytoplasm of macrophages in lungs & hilar lymph nodes |
|
|
Term
| How can carbon cause anthracosis? |
|
Definition
| inhalation of carbon dust => phagocytosis of alveolar macrophages |
|
|
Term
| How does tattoo pigment become permanent? |
|
Definition
| phagocytosis by dermal macrophages |
|
|
Term
| What are the 4 endogenous pigments that can accumulate? |
|
Definition
lipofuscin
melanin
bilirubin
hemosiderin |
|
|
Term
|
Definition
"wear & tear pigment"
indigestible phospholipis/protein remnant within autophagolysosomes |
|
|
Term
|
Definition
| free radical injury => subcellular membrane lipid peroxidation |
|
|
Term
| What does lipofuscin look like microscopically? |
|
Definition
| perinuclear, finely granular, yellow-brown pigment with long-lived cells |
|
|
Term
| Where is lipofuscin especially prominent? |
|
Definition
|
|
Term
| What produces the brown-black pigment of melanin? |
|
Definition
|
|
Term
| How is bilirubin derived? |
|
Definition
| from the porphyrin ring of hemoglobin |
|
|
Term
| What are the 2 components that hemoglobin is broken down into? |
|
Definition
|
|
Term
| What are the 2 components that heme is broken down into? |
|
Definition
|
|
Term
| What does the porphyrin ring break down into? |
|
Definition
| biliverdin (open chain) => unconjugated bilirubin |
|
|
Term
| Where is unconjugated bilirubin found? |
|
Definition
| blood plasma - tightly bound to albumin |
|
|
Term
| How do hepatocytes remove unconjugated bilirubin? |
|
Definition
| conjugate it to bilirubin glucuronides |
|
|
Term
| Where is unconjugated bilirubin excreted from? |
|
Definition
|
|
Term
| Where is hemoglobin broken down into unconjugated bilirubin? |
|
Definition
|
|
Term
| What happens to the aa of globin? |
|
Definition
|
|
Term
| What happens to the Fe of heme? |
|
Definition
| transported to the bone marrow by transferrin & recycled |
|
|
Term
| Why must bilirubin be conjugated? |
|
Definition
| To become water-soluble for excretion |
|
|
Term
| How do serum unconjugated bilirubin levels increase? |
|
Definition
1) increased RBS destruction => increased production
2) hepatocyte dysfunction => decreased bilirubin conjugation |
|
|
Term
| How does hepatocyte dysfunction occur? |
|
Definition
|
|
Term
| How do serum conjugated bilirubin levels increase? |
|
Definition
1) hepatocyte dysfunction => decreased bilirubin secretion
2) cholestasis (biliary tract obstruction) => decrased excretion |
|
|
Term
| What can cause intrahepatic choestasis? |
|
Definition
| space-occupying leisons in the liver, destruction of intrahepatic bile ducts, cirrhosis, hepatic injury/swelling, medication |
|
|
Term
| What can cause extrahepatic cholestasis? |
|
Definition
| gallstones in biliary tract, internal compromise or external compression of common bile duct |
|
|
Term
| How do we test for cholestasis? |
|
Definition
| test for increased alkaline phosphatase (though conjugated bilirubin is also increased, it's a much less sensitive test) |
|
|
Term
| What does cholestasis look like mircoscopically? |
|
Definition
| smooth, green to golden-brown, globular pigment most commonly found in the liver |
|
|
Term
|
Definition
| intracellular, end-stage storage form of excess iron |
|
|
Term
| What are the 2 fates of intracellular iron? |
|
Definition
|
|
Term
| What does iron combine with prior to storage? |
|
Definition
|
|
Term
| What does iron combined with apoferritin form? |
|
Definition
|
|
Term
| How is hemosiderin formed? |
|
Definition
| Excess ferritin aggregates to form clusters & are engulfed by lysosomes & degraded |
|
|
Term
| What causes excess hemosiderin formation? |
|
Definition
1) increased absorption of dietary iron
2) increased degredation of hemoglobin
3) parenteral iron excess |
|
|
Term
| Where does increased absorption of dietary iron accumulate? |
|
Definition
| parenchymal cells (esp. pancreas, liver, and heart) |
|
|
Term
| Where does increased degradation of hemoglobin accumulate? |
|
Definition
| mononuclear phagocytes (macrophages) |
|
|
Term
| What can cause increased degradation of hemoglobin? |
|
Definition
localized breakdown of RBCs (hemorrhage)
systemic RBC destruction (hemolytic anemia) |
|
|
Term
| Where does parenteral iron excess accumulate? |
|
Definition
|
|
Term
| What is seen microscopically in hemosiderin accumulation in an H&E stain? |
|
Definition
| coarsely granular, rusty-orange/brown, refractile, sytoplasmic pigment |
|
|
Term
| What is seen microscopically in hemosiderin accumulation in a Prussian Blue stain? |
|
Definition
|
|
Term
| What 4 serum lab tests are there to assess iron status? |
|
Definition
1) ferritin
2) iron
3) transferrin - iron-bindind capacity
4) % transferrin saturation |
|
|
Term
| Where is transferrin synthesized? |
|
Definition
|
|
Term
|
Definition
| binds/transports all plasma iron |
|
|
Term
| How do you calculate % trasnferrin saturation? |
|
Definition
| serum iron/IBC (iron-binding capacity) |
|
|
Term
| What % of the transferrin iron-binding sites are normally filled? |
|
Definition
|
|
Term
|
Definition
| There is no physiological excretion mechanism |
|
|
Term
| Where does the majority (75%) of all iron absorbed per day go to? |
|
Definition
| bone marrow for RBC/hemoglobin synthesis |
|
|
