Histopathology

Front 1

hyperplasia: definition

Back 1

increase in cell number

Front 2

increase in cell number

Back 2

hyperplasia

Front 3

increase in cell size

Back 3

hypertrophy

Front 4

hypertrophy: definition

Back 4

increase in cell size

Front 5

2 examples of hypertrophy

Back 5

muscle cell hypertrophy in response to increased workload

prolactin and estrogen cause breast hypertrophy

Front 6

2 examples of hyperplasia

Back 6

benign prostatic hyperplasia in response to androgens

increased estrogen causes hyperplasia of the endometrial glands

Front 7

2 examples of reversible cell injury

Back 7

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)

Front 8

2 examples of irreversible cell injury

Back 8

coagulative necrosis

liquefactive necrosis

Front 9

coagulative necrosis

Back 9

intracellular proteins denatured, e.g. in MI
irreversible

Front 10

liquefactive necrosis

Back 10

enzymatic disgestion of the cell, e.g. in bacterial infection
irreversible

Front 11

2 examples of atrophy

Back 11

atrophy of the uterus shortly after parturition

nerve damage causes atrophy of the muscles supplied by the nerves

Front 12

anasarca

Back 12

severe, generalized edema with profound subcutaneous tissue swelling

Front 13

severe, generalized edema with profound subcutaneous tissue swelling

Back 13

anasarca

Front 14

causes of increased hydrostatic pressure

Back 14

hydrostatic pressure can be increased:

locally, e.g. impaired venous outflow
or
systemically, e.g. CHF causes systemic edema

Front 15

pitting edema

Back 15

finger pressure over substantially edematous subcutaneous tissue displaces the interstitial fluid and leaves a finger-shaped depression

Front 16

when is centrilobular necrosis of the liver observed?

Back 16

in chronic passive liver congestion

Front 17

what are the features of centrilobular necrosis of the liver?

Back 17

central regions of hepatic lobules are red-brown and slightly depressed due to loss of cells
nutmeg liver = surrounding tan zones of uncongested liver

Front 18

nutmeg liver

Back 18

tan zones of uncongested liver that surround the reddish-brown congested central hepatic lobules in centrilobular necrosis of the liver

Front 19

lines of Zahn: definition

Back 19

alternating laminations in thrombi produced by lines of pale platelets and darker layers containing more RBCs

Front 20

what is the significance of lines of Zahn?

Back 20

imply that thrombus formed at a site of blood flow (during life)

Front 21

phlebothrombosis most commony occurs in

Back 21

veins and lower extremities

almost invariably occlusive

Front 22

phlebothrombosis =

Back 22

venous thrombosis

Front 23

disseminated intravascular coagulation

Back 23

sudden or insidious onset of widespread fibrin thrombi in the microcirculation

can cause diffuse circulatory insufficiency, esp. in brain lung heart kidneys

Front 24

what is incidence of pulmonary thromboembolism?

Back 24

20-25/100,000 hospitalized patients

Front 25

shape of kidney infarct?

Back 25

all infarcts tend to be wedge-shaped, with occluded vessel at tip and periphery of organ forming the base

Front 26

which 4 factors influence development of an infarct?

Back 26

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?)

Front 27

red infarct: characteristics

Back 27

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

Front 28

white infarct: characteristics

Back 28

arterial occlusions
solid organs: heart, spleen, kidney
solidity of tissue limits the amount of hemorrhange that can seep into area of necrosis

Front 29

virchow's triad

Back 29

for thrombus formation
1. endotheilal injury
2. abnormal bld flow: stasis or turbulence
3. hypercoagulability

Front 30

what is virchow's triad for?

Back 30

thrombus formation

Front 31

hallmark cells of acute inflammation

Back 31

neutrophils

Front 32

cardinal signs of inflammation

Back 32

tumor rubor calor dolor
swelling redness heat pain

Front 33

chemokines: function

Back 33

chemokines act as attractans for specific types of leukocytes

Front 34

cytokines: function

Back 34

cytokines are molecules that mediate inflammation

Front 35

how does aspirin affect the inflammatory response

Back 35

aspirin acetylates and inhibits the cyclooxygenase enzyme in prostaglandin synthesis

Front 36

serous inflammation

Back 36

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

Front 37

suppurative inflammation

Back 37

= purulent inflammation
large amounts of pus

Front 38

components of pus

Back 38

neutrophils
necrotic cells
edema fluid

large amounts seen in suppurative inflammation

Front 39

steps in leukocyte extravasation from vessel lumen to interstitial tissue

Back 39

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

Front 40

diapedesis

Back 40

leukocyte transmigration across vessel endothelium (2nd step in leukocyte extravasation)

Front 41

steps in phagocytosis

Back 41

1. recognition and attachment of foreign particle
2. particle engulfed; phagocytic vacuole formed
3. killing/degradation of ingested particle

Front 42

NO

Back 42

inflammation mediator
EDRF: relaxes vascular smooth muscle to cause vasodilation
derived from endothelium, macrophages, some neurons

Front 43

reactive oxygen intermediates

Back 43

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