Pathophysiology

Question 1

Incidence

Answer 1

number of new cases per unit time

Question 2

Prevalence

Answer 2

number of cases at any one time

Question 3

ischemia

Answer 3

lack of arterial blood flow (arterial occlusion, venous occlusion); pump failure

Question 4

hypoxemia

Answer 4

failure of lungs to oxygenate blood flow, failure to ventilate or perfuse the lungs, inadequate RBC mass, inability of hemoglobin to carry or release oxygen

Question 5

failure of oxidative phosphorylation

Answer 5

cyanide, carbon monoxide, dinitophenol

Question 6

what happens with hypoxemia?

Answer 6

ETC stops, Na+/K+ATPase fails, Na+ and H20 enter cell, lactic acid accumulation and pH drop, Ca2+ATPase fails, Ca2+ enters

Question 7

free radical injury

Answer 7

radiation, poisons, normal metabolism

damage cell membranes, DNA mutations, aging?

Question 8

superoxide dismutase

Answer 8

turns free radicals into H2O3

Question 9

catalase

Answer 9

hydrogen peroxide to water and oxygen

Question 10

antioxidants

Answer 10

vitamin E and C

Question 11

chemical injury

Answer 11

acids/alkalis destroy membranes, formaldehyde crosslinks proteins and DNA

Question 12

cyanide

Answer 12

blocks ETC (e- adherers)

Question 13

mushrooms

Answer 13

destroy ribosomes

Question 14

chemotherapy

Answer 14

damages DNA

Question 15

strychnine

Answer 15

motor neuron synapses

Question 16

carbon monoxide

Answer 16

replaces O2 on hemoglobin, blocking ETC

Question 17

cellular accumulations

Answer 17

triglycerides, glycogen, complex lipids or carbs, pigments, calcium

Question 18

fatty change

Answer 18

involves heart or liver, marker for injury, closely linked to heavy drinking, NASH, malnutrition/hyperalimentation, outdated tetracycline, ill bypass

Question 19

mechanisms of fatty change

Answer 19

too much free fat coming from liver, too much fatty acid synthesis by liver, impaired fatty acid acid oxidation by liver, excess esterification of fatty acid to triglycerides by the liver, too little apoprotein synthesis by liver, failure of lipoprotein secretion by liver

Question 20

glycogen storage diseases

Answer 20

often pediatric problem; inborn errors of metabolism

Question 21

pigments

Answer 21

carbon (anthracosis in lungs), lipofuscion, melanin, bilrubin

Question 22

melanin

Answer 22

eumelanin: protects from UV light
pheomelanin: generates free radicals UV exposure (abnormal)
Hyperpigmentationincreased ACTH
hemochromatosis: decreased breakdown of melanin

Question 23

bilirubin

Answer 23

yellow/orange, product of hemoglobin breakdown, normally conjugated by the liver and excreted in bile

Question 24

jaundice

Answer 24

too many red blood cells being broken down(hemolytic processes) ; liver can’t conjugate bilirubin fast enough; biliary obstruction (gall stone, pancreatic cancer)

Question 25

calcium

Answer 25

calcium precipitates complexed w/ negative charged ions, producing salts, and if enough, crystals occur
normal dystrophic calcification happens in pineal gland, airway cartilages, mitral valve annulus, aortic valve sinuses

Question 26

abnormal dystrophic calcification

Answer 26

breast cancers, caseous necrosis, surgical scars, pancreatic necrosis, and retained abortions

Question 27

metastatic calcification

Answer 27

occurs with high calcium or phosphate levels

pH gradients more likely (small airway walls, gastric fungus epithelium, renal tubular walls)

Question 28

necrosis

Answer 28

gross and microscopic changes that indicate cell death

Question 29

types of necrosis

Answer 29

coagulation, liquefactive, caseous, apoptosis

Question 30

coagulation

Answer 30

usually due to ischemic hypoxia or free radicals except in brain; death of groups of cells; soft and pale; cytoplasm stays in tact and causes inflammatory response

Question 31

liquefaction

Answer 31

usually due to bacterial infections or poisons or ischemic hypoxia in CNS; death of groups of cells; hydrolysis via lysosomal or WBC enzymes cause pus; gelatinous mass or nothing there; cells disappear

Question 32

caseous necrosis

Answer 32

saponification/soap formation; usually due to immune injury in response to certain infections (TB and fungus); pale and cheesy; midpoint between coagulation and liquefaction

Question 33

apoptosis

Answer 33

programmed cell suicide due to mitochondrial death (capsizes) or death receptor (Fas or TNF);cell membrane remains intact but no inflammatory response; remains phagocytosed

Question 34

gangrene

Answer 34

advanced and visible necrosis; mostly coagulation is dry (no smell, no infection usually) and mostly liquefactive is wet (stinky, infected)

Question 35

atrophy

Answer 35

decrease in cell size, not number (loss of cellular organelles), usually reversible

Question 36

causes of atrophy

Answer 36

loss of motor innervation, decreased blood supply, loss of hormonal stimulation, malnutrition, again?

Question 37

hypertrophy

Answer 37

increase in cell size (increased protein synthesis, increased organelles
causes: adaptive response to increased workload, increased hormonal stimulation

Question 38

hyperplasia

Answer 38

increase in cell number, may result in increased organ size

causes: compensatory, hormonal, genetic mutations,

Question 39

metaplasia

Answer 39

adaptive? substitution of one cell for another, often response to a stimulus
ex. of Barett’s syndrome

Question 40

dysplasia

Answer 40

bad growth (atypical hyperplasia); loss of cell uniformity and orientation; resemble cancer cells but not invasive

Question 41

anaplasia

Answer 41

ugly cells, confined to epithelium (anaplasia) OR invading (cancer)

Question 42

proto-onco genes

Answer 42

normal genes that are potentially cancer genes

Question 43

neoplasm

Answer 43

abnormal growth