Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
43 Cards in this Set
- Front
- Back
hyperplasia: definition
|
increase in cell number
|
|
increase in cell number
|
hyperplasia
|
|
increase in cell size
|
hypertrophy
|
|
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
irreversible |
|
liquefactive necrosis
|
enzymatic disgestion of the cell, e.g. in bacterial infection
irreversible |
|
2 examples of atrophy
|
atrophy of the uterus shortly after parturition
nerve damage causes atrophy of the muscles supplied by the nerves |
|
anasarca
|
severe, generalized edema with profound subcutaneous tissue swelling
|
|
severe, generalized edema with profound subcutaneous tissue swelling
|
anasarca
|
|
causes of increased hydrostatic pressure
|
hydrostatic pressure can be increased:
locally, e.g. impaired venous outflow or 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
|
neutrophils
|
|
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
|
neutrophils
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 |
|
diapedesis
|
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 |
|
NO
|
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 |