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Pathophysiology > Cellular Adaptation, Injury, Death > Flashcards

Cellular Adaptation, Injury, Death Flashcards

1
Q

atrophy

A

decrease in cell size

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2
Q

why does atrophy happen

A

disuse (ex: casts), denervation (ex: paralysis), loss of endocrine stimulation (ex: estrogen and menopause), inadequate nutrition (shrink for survival), ischemia (decreased blood flow)

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3
Q

hypertrophy

A

increase in cell size

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4
Q

why does hypertrophy happen

A

normal physiologic: exercise (more work)
abnormal pathologic conditions: disease
>adaptive (ex: hypertension [increased B.P. makes heart bigger to work harder])
>compensatory (ex: nephromegaly [larger remaining tissue/organ makes up for loss])

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5
Q

hypertension

A

high blood pressure, force of blood against arterial walls is too high

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6
Q

hypertrophic cardiomyopathy

A

enlarged for underlying diseases
>[usually left ventricle]becomes thick and stiff so less blood is pumped out

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7
Q

dilated cardiomyopathy

A

ventricle enlargement with thin ventricular walls

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8
Q

hyperplasia

A

increase in NUMBER of cells

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9
Q

why does hyperplasia happen

A

physiologic: hormonal (ex: breast and uterine enlargement during pregnancy), compensatory (ex: liver regeneration)
non-physiologic: (ex: endometrial hyperplasia-abnormal)

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10
Q

can more than one cell adaptation happen simultaneously

A

yes! with pregnant women the uterus goes under hypertrophy (enlargement) and hyperplasia (increased #) from estrogen stimulation

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11
Q

metaplasia

A

replacement of adult cells with other cells (only pathologic)

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12
Q

why does metaplasia happen

A

chronic irritation and inflammation (ex: smokers trachea tissue-SSE replaces CPCE for survival, acid reflux disease)

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13
Q

dysplasia

A

deranged cell growth of a specific tissue (size, shape, organization, only pathologic)

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14
Q

why does dysplasia happen

A

precursor of cancer (preneoplastic)

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15
Q

which of the following describes cellular adaptation seen in chronic cigarette smokers?
a) atrophy
b) hypertrophy
c) hyperplasia
d) metaplasia
e) dysplasia

A

D) metaplasia
in smokers, stratified squamous epithelium replaces ciliated pseudostratified columnar epithelium

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16
Q

3 sources of intracellular accumulations

A

1) normal body substances
2) abnormal endogenous products
3) exogenous products

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17
Q

intracellular accumulations

A

storage of products in abnormal amounts that are too fast for the cell to use right away or to get rid of-usually accumulate in lysosomes (digestive system) or cytosol

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18
Q

normal body substances (IA)

A

lipids, proteins, carbs, melanin, bilirubin (ex: jaundice-build up of bilirubin, yellow skin pigment)

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19
Q

abnormal endogenous products (IA)

A

resulting from inborn errors of metabolism

20
Q

exogenous products

A

environmental agents and pigments not broken down by the cell (ex: tattoo pigment, coal dust)

21
Q

pathologic calcifications

A

abnormal tissue deposition of calcium salts with smaller amounts of iron, magnesium and other minerals

22
Q

types of pathologic calcifications

A

dystrophic-occurs in dead or dying tissue following injury (ex: atherosclerosis, aortic stenosis [thin, injured aorta where blood does not flow normally])
metastatic-occurs in normal tissue from increased calcium (ex: hyperparathyroidism)

23
Q

true or false: dystrophic calcification can result from prolonged ischemia

A

true! ischemia is a decrease in blood flow which results in tissue damage/injury

24
Q

kinds of cellular adaptation

A

size (atrophy/hypertrophy), number (hyperplasia), type or form (metaplasia) and size/shape/organization (dysplasia)

25
Q

cell injury-physical agents

A

mechanical forces (ex: GSW), extreme temps (ex: hypoxic [decreased oxygen] cell injuries where cold increases blood thickness and constricts blood vessels), electrical injuries (usually localized burns)

26
Q

cell injury-radiation

A

ionizing radiation (ex: radiation dermatitis, [electrons/molecules knocked off] scarring of tissue/organs)
UV radiation (ex: melanoma, tanning salons [disrupt bonds]
nonionizing-least extreme, minor damage (causes vibrations)

27
Q

cell injury-chemical

A

drugs (ex: liver failure from overdosing on Tylenol), carbon monoxide (CO takes O2 out of RBC, hypoxic injury), lead toxicity (leading sign of anemia, competes with calcium, affects CNS and brain development)

28
Q

normal hemoglobin levels

A

men: 13-18
women: 12-16

29
Q

cell injury-biological agents

A

viruses (spread, multiply), parasites, bacteria

30
Q

cell injury-nutritional imbalances

A

excesses, deficiencies

31
Q

reversible cell injury

A

impairs function, does not result in cell death

32
Q

2 types of reversible cell injury

A

cellular swelling-impairment of Na+/K+ pump (usually from hypoxic injury since it needs ATP0
fatty changes-linked to intracellular accumulation of fat

33
Q

necrosis

A

cell death in organs and tissues of living people

34
Q

cell injury is…

A

REVERSIBLE

35
Q

metastatic calcification

A

increased serum calcium levels

36
Q

UV radiation

A

spectrum of radiation ABOVE visible range

37
Q

T/F pap smears detect atrophy

A

false! pap smears detect dysplasia

38
Q

apoptosis

A

programmed cell death

39
Q

what is caused by varieties of clostridium bacteria

A

gas gangere

40
Q

what moves into the cell when damage happens

A

sodium/water

41
Q

what happens with cellular hypoxia

A

failure of the Na+/K+ pump since O2 is needed for ATP which drives the pump

42
Q

dysplasia is adaptive or maladaptive

A

always maladaptive

43
Q

what happens to the cell membrane during cell death

A

disruption of permeability

44
Q

a client is weak in the legs after prolonged bed rest. what kind of cellular adaptation took place?

A

atrophy-decreased usage

45
Q

chronic ischemia will result in this adaptation

A

atrophy-cells shrink to take in less oxygen to survive

46
Q

what is the most concerning adaptation found in biopsy

A

dysplasia-precursor of cancer

Pathophysiology (15 decks)

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