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Pathophysiology > 4. Altered Cellular and Tissue Biology > Flashcards

4. Altered Cellular and Tissue Biology Flashcards

1
Q

Decrease or shrinkage of cell size

A

atrophy

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2
Q

Increase in size of cells

A

hypertrophy

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3
Q

Increase in the number of cells (from an increased rate of cellular division)

A

hyperplasia

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4
Q

Abnormal changes in size, shape, or organization of mature cells

A

dysplasia

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5
Q

Reversible replacement of one mature cell type by another

A

metaplasia

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6
Q

What 2 types of cellular adaptation occur in non dividing cells?

A

atrophy and hypertrophy

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7
Q

What types of body structures undergo atrophy?

A

skeletal muscles, heart, brain, and secondary sex organs

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8
Q

Physiologic vs Pathologic atrophy

A
  • Physiologic: normal process that usually occurs in early development (ex. thymus in children) - Pathologic: due to decreased pressure, use, blood, nutrition, hormones, or stimulation (ex. disuse atrophy in skeletal muscle)
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9
Q

Explain the ubiquitin-proteasome pathway

A

proteins conjugated to ubiquitin -> degraded by proteasomes (increased activity in atrophy)

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10
Q

chronic malnutrition atrophy is often accompanied by what?

A

autophagy -> autophagic vacuoles contain cellular debris and enzymes

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11
Q

What types of body structures undergo hypertrophy?

A

striated muscle (skeletal and cardiac) and kidneys

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12
Q

Physiologic vs Pathologic cardiac hypertrophy

A

Physiologic: temporary and preserves myocardial structure (ex. endurance training, postnatal development, and pregnancy) Pathologic: includes aging, strenuous exercise, sustained workload or stress

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13
Q

What is is called when cardiac hypertrophy is reversed?

A

regression

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14
Q

When does renal hypertrophy mainly occur

A

when 1 kidney is removed and the other one has to compensate for the loss

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15
Q

Explain compensatory hyperplasia. Where is it significant?

A

adaptive and allows for some organs to regenerate (epidermal and intestinal epithelia, hepatocytes, BM cells, and fibroblasts)

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16
Q

Explain hormonal hyperplasia

A

occurs in estrogen-dependent organs in response to hormonal stimulation (uterus and breast)

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17
Q

Explain pathologic hyperplasia

A

abnormal proliferation of normal cells (usually in response to excessive hormonal stimulation or GF on those cells)

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18
Q

2 most common examples of pathologic hyperplasia

A
  • hyperplasia of the endometrium (over secretion of estrogen) - BPH (due to changes in hormonal balance)
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19
Q

Dysplasia is also known as what?

A

atypical hyperplasia -> not a true adaptive change

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20
Q

Most common tissues to undergo dysplasia

A

epithelial tissue of the cervix (due to HPV) and respiratory tract

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21
Q

T/F: Dysplasia means the presence of cancer

A

False; dysplasia does NOT indicate cancer and may not progress to cancer if stimulus is removed early on

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22
Q

If metaplasia is not reversed, what can it advance to?

A

Dysplasia and possible cancerous transformations

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23
Q

Cellular injuries can be reversible or irreversible -> also know as what?

A

sublethal or lethal

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24
Q

Explain the general mechanisms of cellular injury (regardless of cause)

A
  • depletion of ATP - mitochondrial damage - O2 and O2-derived free radical membrane damage - protein folding defects - DNA damage - calcium level changes
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25
Q

Hypoxia vs Hypoxemia

A
  • Hypoxia: decreased O2 in tissues - Hypoxemia: decreased O2 in bloodstream (most likely to occur first)
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26
Q

Most common cause of hypoxia

A

ischemia (reduced blood supply)

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27
Q

What causes ischemia

A

narrowing of arteries (arteriosclerosis) or complete occlusion by clots (thrombosis)

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28
Q

Which is better tolerated - acute or progressive hypoxia? Why?

A

Progressive -> allows time for adaptive changes in cells

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29
Q

Explain what causes a cell to swell w/ hypoxic injury

A

decreased mitochondrial O2 -> decreased ATP -> Na/K pump failure -> increased intracellular Na -> increased intracellular H2O -> swelling

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30
Q

Explain what causes a decrease in protein synthesis w/ cellular hypoxic injury

A

increase intracellular H20 -> dilation of ER -> detachment of ribosomes

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31
Q

Explain what causes nuclear chromatin clumping w/ cellular hypoxic injury

A

decrease in O2 -> decrease in ATP -> increase anaerobic glycolysis -> decrease glycogen -> increase lactate -> decrease pH -> chromatin clumping & DNA damage

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32
Q

Explain changes to Na, K, and Ca during cellular hypoxic injury

A
  • increased intracellular Na - increased extracellular K - increased intracellular Ca
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33
Q

Where is intracellular Ca released from?

A

mitochondria and smooth ER

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34
Q

Name 4 mechanisms for ischemia-reperfusion injury

A
  • oxidative stress - increased intracellular Ca - inflammation - complement activation
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35
Q

Name 3 types of reactive oxygen species (ROS)

A
  • hydroxyl radical (OH-) - superoxide radical (O-) - hydrogen peroxide (H2O2)
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36
Q

How does cell structure change after reperfusion injury?

A

ischemic cell = swollen reperfusion injured cell = necrotic

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37
Q

electrically uncharged atom or group of atoms that has an unpaired electron -> capable of injuring chemical bonds

A

free radical

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38
Q

Effect of free radicals on lipids

A

lipid peroxidation (destruction of polyunsaturated lipids) -> increased membrane permeability

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39
Q

Effect of free radicals on proteins

A

fragmentation of polypeptide chains -> protein misfolding -> lose ion pumps and transport proteins

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40
Q

Effect of free radicals on DNA

A

causes mutations and decreased protein synthesis

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41
Q

List 5 mechanisms to classify chemical injuries by

A
  • direct damage (on-target toxicity) - exaggerated response (ex. OD) - biologic activation to toxic metabolites (includes free radicals) - hypersensitivities and other immune reactions - rare toxicities
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42
Q

main systems affected by lead (Pb)

A

nervous system and blood

43
Q

Lead toxicity is a primary hazard for who?

A

children and during pregnancy (can cause lower IQ, learning disorders, and ADHD)

44
Q

Blood lead level of intoxication

A

10 um/dL

45
Q

carbon tetrachloride (CCl4) affects what organ

A

liver

46
Q

Explain how CO causes hypoxic injury

A

has a higher affinity for hemoglobin than O2 -> carboxyhemoglobin

47
Q

Sxs of CO poisoning

A

dizziness, weakness, N/V, headache, tinnitus, confusion, and chest pain

48
Q

Primary systems affected by ethanol

A

brain and liver

49
Q

What nutrition deficiencies are associated w/ ethanol?

A

Mg, B6, thiamine, and phosphorus; folic acid is a problem for chronic drinkers

50
Q

Explain changes seen between acute and chronic alcoholism

A
  • Acute: depresses the CNS (sedation, loss of coordination, delirium) - Chronic: causes structural alterations in tissue that can metabolize ethanol -> mostly liver
51
Q

What is the spectrum of structural changes to the liver caused by ethanol?

A

fatty liver (steatosis) -> fatty w/ inflammation (steatohepatitis) -> cirrhosis

52
Q

Where is mercury commonly found?

A

human activity and silver fillings

53
Q

Active substance in marijuana

A

tetrahydrocannabinol (THC)

54
Q

How does methamphetamine affect the CNS?

A

CNS stimulant (produces euphoria)

55
Q

How does crack and cocaine affect the CNS?

A

potent CNS stimulate -> blocks reuptake of NE, dopamine, and serotonin

56
Q

What is heroin closely related to and what does it do to the CNS?

A
  • closely related to morphine, methadone, and codeine - high affinity for CNS; acts on receptors, enkephalins, and endorphins
57
Q

partial and total deprivation of oxygen

A

partial: hypoxia total: anoxia

58
Q

O2 fails to reach blood (occurs in entrapment)

A

suffocation

59
Q

obstruction of internal airways

A

choking asphyxiation

60
Q

compression/closure of blood vessels or air passages due to external neck pressure

A

strangulation

61
Q

compression of the neck by body weight due to a noose -> leaves an inverted V pattern on neck

A

hanging

62
Q

strangulation that leaves a horizontal pattern on the neck

A

ligature

63
Q

strangulation that leaves variable external trauma and internal damage (fx of the hyoid bone)

A

manual

64
Q

prevents delivery of O2 to tissues or blocks utilization of O2

A

chemical asphyxiants

65
Q

Name 3 types of chemical asphyxiants

A

CO, cyanide, and hydrogen sulfide

66
Q

alteration of O2 delivery to tissues due to inhalation of fluids (usually water)

A

drowning

67
Q

little/no water enters the lungs due to vagal-mediated laryngospasms

A

dry-lung drowning

68
Q

bleeding into skin or underlying tissues -> takes time to appear

A

contusion (bruise)

69
Q

collection of blood in soft tissue that appears quickly

A

hematoma

70
Q

superficial scrape/graze of the skin

A

abrasion

71
Q

tear or rip in skin

A

laceration

72
Q

extreme type of laceration where a wide area of skin is pulled away

A

avulsion

73
Q

wound is longer than it is deep -> usually has significant external bleeding w/ little internal bleeding

A

incised wound

74
Q

penetrating sharp-force injury deeper than it is long

A

stab wound

75
Q

produced by items w/ sharp points but dull edges (ex. stepping on a nail)

A

puncture wound

76
Q

heavy edged instruments that produce a combo of sharp and blunt force injuries

A

chopping wound

77
Q

What will affect the appearance of an entrance gunshot wound?

A

range of the gunshot

78
Q

What is seen w/ contact range entrance gunshot wound?

A
  • searing of the edges - blowback (gaping or jagged) - muzzle imprints
79
Q

What is seen w/ intermediate range entrance gunshot wound?

A
  • tattooing/stippling: fragments of gunpowder abrade but don’t enter the skin
80
Q

appearance is the same regardless of range

A

indeterminate range entrance wound AND exit wound

81
Q

Necrosis vs Apoptosis

A
  • Necrosis: unprogrammed death; cellular swelling -> lysis; inflammation; many cells affected - Apoptosis: programmed, organized disassembly; membrane bound shrinkage; no inflammation; one cell or small clusters
82
Q

nucleus gets smaller -> DNA condenses into shrunken particles

A

pyknosis

83
Q

fading away of nuclear envelope and nuclear material

A

karyolysis

84
Q

nuclear fragmentation

A

karyorrhexis

85
Q

Explain coagulative necrosis

A

ischemia -> decrease pH -> protein degeneration -> albumin becomes firm and opaque

86
Q

Where does coagulative necrosis occur?

A

kidneys, heart, adrenal glands

87
Q

Explain liquefaction necrosis

A

autolysis (hydrolytic enzymes) and heterolysis (bacterial infection) -> tissue becomes soft, liquefies, and segregates -> forms cysts

88
Q

Where does liquefaction necrosis occur?

A

neurons and glial cells of the brain

89
Q

Types of bacteria involved in liquefaction necrosis?

A
  • Staph - Strep - E. Coli
90
Q

Explain caseous necrosis?

A
  • mycobacterium is walled off in a granuloma -> cells disintegrate but not completely digested (combo of coagulative and liquefaction) - will resemble cottage cheese (soft and granular)
91
Q

Type of bacteria involved in caseous necrosis?

A

TB pulmonary infection (Mycobacterium tuberculosis)

92
Q

Explain fat necrosis

A
  • occurs by lipases -> break down triglycerides -> release FAs that combine w/ Ca, Mg, and Na (saponification) -> white and chalky
93
Q

Where does fat necrosis occur?

A

breast, pancreas, and other ABD organs

94
Q

Dry vs wet gangrene

A
  • Dry: poor perfusion (coagulative necrosis) - Wet: poor perfusion + pyogenic infection (liquefactive necrosis)
95
Q

Explain gas gangrene

A

caused by species of Clostridium -> produces hydrolytic enzymes and toxins -> destroy connective tissue and membranes -> gas bubble form in muscle cells -> death caused by shock

96
Q

List 4 cellular changes characteristic of aging

A
  • atrophy (decrease cell function) - lack of DNA repairs (possible mutations) - DNA, RNA, proteins, and membranes more susceptible to injury - compensatory hypertrophy and hyperplasia
97
Q

List 2 tissue/systemic changes characteristic of aging

A
  • progressive stiffness/rigidity - sarcopenia (loss of muscle mass/strength)
98
Q

List 4 common themes of mechanisms for sarcopenia

A
  • decrease MSK fibers and MSK protein synthesis - disregulation of anabolic hormones - cytokine production + inflammation - decrease nutrition and activity
99
Q

What occurs during algor mortis?

A
  • body temp decreases 1 degree per hour - by 24 hours -> body temp = environment
100
Q

What is the main event of livor mortis and how it is physically seen?

A
  • blood pools at the lowest point of the body (due to gravity) - purple discoloration where blood pools (line of demarcation) - can see pupils dilate and become nonreactive to light due to decreased retinal pressure (decrease muscle tension)
101
Q

What is the timeframe for rigor mortis?

A

starts within 6 hours after death and lasts for approximately 36 hours (then body becomes flaccid)

102
Q

What is the cause of rigor mortis?

A

acid builds up in muscles -> delete ATP -> myosin doesn’t work for relaxation -> rigid muscles (small muscles first)

103
Q

What is postmortem autolysis (putrefaction)?

A

breakdown of tissues that occurs between 24-48 hours (all cells start necrosing)

104
Q

What speeds up/slows down the process of postmortem autolysis?

A
  • warm environment speeds it up - cold slows it down

Pathophysiology (20 decks)

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