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43 Cards in this Set

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  • Back
hyperplasia: definition
increase in cell number
increase in cell number
increase in cell size
hypertrophy: definition
increase in cell size
2 examples of hypertrophy
muscle cell hypertrophy in response to increased workload

prolactin and estrogen cause breast hypertrophy
2 examples of hyperplasia
benign prostatic hyperplasia in response to androgens

increased estrogen causes hyperplasia of the endometrial glands
2 examples of reversible cell injury
cellular swelling
(loss of ATP-dependent ion pumps causes loss of ion and fluid homeostasis causes cellular swelling)

fatty change
(hypoxic, toxic, or metabolic injury causes lipid vacuoles in cytoplasm of cells involved in fat metabolism)
2 examples of irreversible cell injury
coagulative necrosis

liquefactive necrosis
coagulative necrosis
intracellular proteins denatured, e.g. in MI
liquefactive necrosis
enzymatic disgestion of the cell, e.g. in bacterial infection
2 examples of atrophy
atrophy of the uterus shortly after parturition

nerve damage causes atrophy of the muscles supplied by the nerves
severe, generalized edema with profound subcutaneous tissue swelling
severe, generalized edema with profound subcutaneous tissue swelling
causes of increased hydrostatic pressure
hydrostatic pressure can be increased:

locally, e.g. impaired venous outflow
systemically, e.g. CHF causes systemic edema
pitting edema
finger pressure over substantially edematous subcutaneous tissue displaces the interstitial fluid and leaves a finger-shaped depression
when is centrilobular necrosis of the liver observed?
in chronic passive liver congestion
what are the features of centrilobular necrosis of the liver?
central regions of hepatic lobules are red-brown and slightly depressed due to loss of cells
nutmeg liver = surrounding tan zones of uncongested liver
nutmeg liver
tan zones of uncongested liver that surround the reddish-brown congested central hepatic lobules in centrilobular necrosis of the liver
lines of Zahn: definition
alternating laminations in thrombi produced by lines of pale platelets and darker layers containing more RBCs
what is the significance of lines of Zahn?
imply that thrombus formed at a site of blood flow (during life)
phlebothrombosis most commony occurs in
veins and lower extremities

almost invariably occlusive
phlebothrombosis =
venous thrombosis
disseminated intravascular coagulation
sudden or insidious onset of widespread fibrin thrombi in the microcirculation

can cause diffuse circulatory insufficiency, esp. in brain lung heart kidneys
what is incidence of pulmonary thromboembolism?
20-25/100,000 hospitalized patients
shape of kidney infarct?
all infarcts tend to be wedge-shaped, with occluded vessel at tip and periphery of organ forming the base
which 4 factors influence development of an infarct?
1. nature of vascular supply (dual vs. single)
2. rate of dvpt of occlusion (slow gives time for alternative perfusion pathways)
3. vulnerability of tissue to hypoxia (neurons 3-4 min; heart cells 20-30 min muscle cells hrs)
4. blood oxygen content (does patient already have compromised flow and ventilation, e.g. CHF?)
red infarct: characteristics
venous occlusions
loose tissue
tissue with dual circulation (lung, small intestine)
tissue previously congested
area where flow is re-established to an area of previous arterial occlusion and necrosis
white infarct: characteristics
arterial occlusions
solid organs: heart, spleen, kidney
solidity of tissue limits the amount of hemorrhange that can seep into area of necrosis
virchow's triad
for thrombus formation
1. endotheilal injury
2. abnormal bld flow: stasis or turbulence
3. hypercoagulability
what is virchow's triad for?
thrombus formation
hallmark cells of acute inflammation
cardinal signs of inflammation
tumor rubor calor dolor
swelling redness heat pain
chemokines: function
chemokines act as attractans for specific types of leukocytes
cytokines: function
cytokines are molecules that mediate inflammation
how does aspirin affect the inflammatory response
aspirin acetylates and inhibits the cyclooxygenase enzyme in prostaglandin synthesis
serous inflammation
outpouring of a thin fluid that, depending on the size of the injury, is derived from either plasma or secretions of mesothelial cells lining peritoneal, pericardial, or pleural cavities
suppurative inflammation
= purulent inflammation
large amounts of pus
components of pus
necrotic cells
edema fluid

large amounts seen in suppurative inflammation
steps in leukocyte extravasation from vessel lumen to interstitial tissue
1. in vessel lumen, leukocytes undergo margination, rolling, and adhesion to activated endothelium
2. transmigration across endothelium = diapedesis
3. migration in interstitial tissue toward chemotactic stimulus
leukocyte transmigration across vessel endothelium (2nd step in leukocyte extravasation)
steps in phagocytosis
1. recognition and attachment of foreign particle
2. particle engulfed; phagocytic vacuole formed
3. killing/degradation of ingested particle
inflammation mediator
EDRF: relaxes vascular smooth muscle to cause vasodilation
derived from endothelium, macrophages, some neurons
reactive oxygen intermediates
hydroxyl radical (OH); H2O2; superoxide anion (O2-)
function: destroy phagocytosed microbes
at higher levels, also results in damage to host endothelial cells, parenchymal cells, and RBCs