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Pathophysiology > Exam 1: Ch 2 > Flashcards

Exam 1: Ch 2 Flashcards

1
Q

atrophy

A

cells decrease in size and activity in response to decreased workload or poor environmental conditions

generally reversible

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2
Q

atrophy in muscle

A

decrease in oxygen consumption, # of mitochondria, and # of myofilaments

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3
Q

causes of atrophy

A

disease

denervation

poor nutrition

ischemia

decreased endocrine stimulation (IGF 1)

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4
Q

hypertrophy definition and 2 types

A

cells increase in size in response to increased workload

physiologic or pathologic

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5
Q

physiologic hypertrophy

A

increased muscle size with exercise

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6
Q

pathologic hypertrophy

A

response to disease

Hypertension

Valvular heart disease

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7
Q

excessive hypertrophy is _____

A

counterproductive

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8
Q

signals for hypertrophy

A

hormonal (IGF1, EGF, growth factors)

mechanical (HTN)

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9
Q

hyperplasia

A

increase in the number of cells (usually epithelial or connective tissue)

Tissues with cells capable of mitotic division

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10
Q

3 examples/types of hyperplasia

A

hormonal: breast enlargement with pregnancy
compensatory: liver cell division after partial hepatectomy

wound healing

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11
Q

metaplasia

A

change in cell type

results from chronic inflammation/irritation (if untreated can turn into dysplasia)

ex. cilliated columnar epithelium –> stratified squamous in airways of smokers

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12
Q

dysplasia

A

higher deranged cell growth (usually from inflammation)

precursor to cancer

ex. abnormal pap smear of cervix

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13
Q

intracellular accumulations

A

cells build up substances they cannot eliminate

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14
Q

categories of substances in intracellular accumulations

A

normal substances present in excess (jaundice, lipofuscin)

products of abnormal metabolism (lipids in brain –> Tay-Sachs, glycogen in liver —> Von Gierke)

exogenous substances (blue line in gum tissue from lead poisoning)

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15
Q

dystrophic calcification

A

deposits of calcium phosphate crystals in injured tissue

calcium found in atheroscletotic lesions or heart valves

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16
Q

metastatic calcification

A

deposits of Ca in normal tissues when serum Ca is high

occurs in lungs, blood vessels, and kidneys

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17
Q

3 causes of metastatic calcification

A

Paget’s disease (excessive osteoclast activity)

renal failure (phosphate retention)

cancer

Hyperparathyroidism

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18
Q

what can cause cell injury

A

physical agents

radiation

chemicals

biological agents

nutritional imbalances

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19
Q

cell injury: physical agents

A

mechanical trauma: damages tissues/blood vessels

temperature: burns, frostbite–destroy blood flow
electrical: disrupt cardiac and nervous system, burn

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20
Q

3 types of radiation

A

ionizing

nonionizing – thermal damage

UV

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21
Q

ionizing radiation

A

kills immediately/causes genetic damage

endothelium most vulnerable –> blood vessel damage, burns, enteritis

chronic damage –> fibrosis/scarring

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22
Q

UV radiation

A

sunburn

increased skin cancer risk (DNA damage)

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23
Q

cell injury: chemicals

A

drugs: directly toxic/toxic metabolites
lead: paint, old pipes, air, industrial exposure
mercury: industrial/medical sources

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24
Q

lead toxicity

A

absorbed through GI & respiratory tract

stored in bones and teeth

blocks brain development (demyelization) and is toxic to RBS (anemia)

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25
Q

lead is particularly toxic to _______

A

children

CDC says blood lead [ ] > 5 micrograms/dL is dangerous

26
Q

mercury toxicity

A

interferes with brain development

children/pregnant women at risk

predator fish contain mercury

27
Q

cell injury: biological agents

A

viruses

bacteria

parasites

28
Q

cell injury: nutritional imbalance

A

excesses or deficiencies

29
Q

what is a free radical (ROS–reactive oxygen species)

A

chemical with unpaired electron in outer shell– highly
unstable

product of normal metabolism (convert O2 to ROS)

product of increased reperfusion –> overwhelm protective mechanisms

30
Q

free radical injury

A

damages organelles (mitochondria) and DNA

may contribute to ALS, aging, other diseases

31
Q

which vitamins are free radical scavengers?

A

C & E

32
Q

hypoxia

A

oxygen deprivation

induction of genes for hypoxia inducible factors (HIF) –> increased RBC & angiogenesis

if severe, ATP production is interrupted

33
Q

hypoxic cell injury

A

time until damage depends on cell’s energy requirement

permanent damage in 4-6 min for brain

pH falls, Na/K pump fails

34
Q

hypoxia in rats

A

epithelial cells of kidney tubules can survive 20-30 min

anything greater than that decreases O2 delivery to tissues and produces hypoxic damage

35
Q

_____ is important as a 2nd messenger

A

calcium

36
Q

impaired calcium movement

A

levels must be kept very low

ischemia and toxins disrupt the ability of cells to exclude calcium

intracellular enzymes are released/activated and cell destroys itself

37
Q

reversible cell injury

A

Na/K pump fails and causes swelling (hypoxic damage)

intracellular fat accumulations: associated with high serum fat

38
Q

2 types of lethal cell injury

A

necrosis

apoptosis

39
Q

apoptosis

A

programmed cell death

eliminates excess and damaged cells

eventually membrane is disrupted and debris consumed by phagocytes

40
Q

apoptosis and cancer

A

important in normal development and destruction of cancer cells

cancer cells learn to escape apoptotic signals

p53 gene inactivated —> cancer

41
Q

diseases involving overstimulation of apoptosis

A

ALS

Parkinson’s

Alzheimer’s

42
Q

2 types of apoptosis pathways

A

extrinsic

intrinsic

both activate endonucleases –> DNA fragments

43
Q

extrinsic apoptosis

A

activation of death receptors like TNF or Fas ligand receptor

death domain activated

procaspases –> caspases (activated form) in cascade

44
Q

intrinsic apoptosis

A

multiple inputs damage mitochondria

caspase cascade activated

45
Q

necrosis

A

uncontrolled cell death that is not pre-programmed

46
Q

types of necrosis

A

liquefaction

coagulation

caseous (form of coagulation)

47
Q

liquefaction necrosis

A

cells die but enzymes remain active

dead tissue is soft

seen in infection

ex. flesh eating bacteria (meningococcemia)

48
Q

coagulation necrosis

A

area becomes hard

acidosis destroys enzymes

seen in ischemia/infarction

ex. dry gangrene, avascular necrosis

49
Q

caseous necrosis

A

fatty infiltrates

seen in interior of TB lesions

50
Q

gangrene

A

large mass of necrotic tissue

51
Q

3 types of gangrene

A

dry

wet

gas (type of wet)

52
Q

dry gangrene

A

type of coagulation necrosis

caused by interruption of arterial blood flow

line of inflammation between healthy/dead tissue

can progress to wet gangrene with infection

53
Q

wet gangrene

A

type of liquefaction necrosis from infection

caused by venous obstruction or infection

area cold, swollen, pulseless

rapid spread

54
Q

gas gangrene

A

type of wet gangrene (which is a type of liquefaction necrosis)

wound infection from Clodtridium bacteria

commonly following dirty trauma, bowel obstruction/rupture

bacteria product hydrogen sulfide gas –> tissue death

debridement, antibiotics, maybe amputation

55
Q

cellular aging

A

normal process that decreases organ system function over time

may reflect accumulation of environmental and genetic damage

56
Q

replicative senescence

A

cells can divide a fixed number of times (Hayflick limit)

involves shortening of telomeres

telomerase is active in germ cells/cancer cells

57
Q

genetic influences on cellular aging

A

some gene alleles protect against chronic disease (increases longevity)

58
Q

progeria

A

genetic defect that causes premature aging

59
Q

gene

A

DNA that codes for a protein

60
Q

cellular adaptation

A

how cells respond to persistent stress by activating gene pathways

61
Q

ARDS

A

acute respiratory distress syndrome

systemic infection

62
Q

DIC

A

disseminated intravascular coagulation

systemic infection

clotting factors/platelets get used up – excessive bleeding

Pathophysiology (24 decks)

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