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Pathoma > Growth Adaptations, Cell Injury, and Cell Death > Flashcards

Growth Adaptations, Cell Injury, and Cell Death Flashcards

1
Q

Hypertrophy

A

Increase in cell size- inc cytoplasm produc

- involves gene activation, protein synthesis, and production of organelles (ie: inc # of mitochondria)

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2
Q

Hyperplasia

A

Increase in number of cells

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3
Q

Hyperplasia

A

production of new cells from stem cells

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4
Q

Permanent cells that only undergo hypertrophy b/c cant undergo hyperplasia

A

Cardiac muscle
Skeletal muscle
Nerves

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5
Q

Pathologic hyperplasia can progress to

A

dysplasia and cancer

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6
Q

Endometrium grows w/ exposure to

A

Estrogen

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7
Q

Endometrium sheds w/ exposure to

A

Progesterone

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8
Q

Endometrium undergoes __ during pregnancy

A

hyperplasia

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9
Q

Benign prostatic hyperplasia

A

not cancerous

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10
Q

Decrease in cell number via

A

Apoptosis

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11
Q

Decrease in cell number via

A

Ubiquitin-proteosome degradation of cytoskeleton

Autophagy of cellular components

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12
Q

Change in cell type

A

Metaplasia

most often involves change in surface epithelium

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13
Q

Example of metaplasia

A

Barrett Esophagus

Due to acid reflux, will change from Squamous epi ==> Columnar nonciliated, mucinous epi (better suited to handle acid)

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14
Q

Metaplasia occurs via

A

reprogramming of stem cells

-Reversible w/ removal of the driving stressor

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15
Q

Metaplasia is

A

REVERSIBLE

-remove the key stress that led to the metaplasia will lead to reversal of metaplasia

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16
Q

Metaplasia can progress to

A

dysplasia and cancer

Exception: apocrine metaplasia (changes in assoc w/ fibrocystic changes in breast)

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17
Q

Exception of metaplasia that doesnt inc risk of cancer

A

Apocrine metaplasia

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18
Q

Vitamin A deficiency can result in

A

metaplasia

and Night Blindness

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19
Q

Night Blindness results due to deficiency in

A

Vitamin A
needed for maintenance of specialized epithelia of eye, like conjunctiva of eye
Keratomalacia = conjunctiva of eye thickens

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20
Q

15:17 translocation

A

Vit A receptor
needed for maturation of immune system
disrupts it; causes cells to remain trapped in the blast state, accumulae –> promylocytic leukemia
ATRA = tx- binds the mutated receptor

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21
Q

Mesenchymal tissues can undergo

A

metaplasia
bone, blood vessel, fat, cartilage - connective tissue
ie- myositis ossificans = inflam of skel muscle results in a meaplastic produc of bone w/in skel muscle - skel muscle converts into bone

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22
Q

Myositis ossificans *

A

inflam of skel muscle results in a meaplastic produc of bone w/in skel muscle - skel muscle converts into bone

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23
Q

Dysplasia

A

disordered cellular growth; due to pathologic hyperplasia or metaplasia
Refers to proliferation of cancerous cells
CIN- cervical cancer - actually dysplasia

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24
Q

Dysplasia is

A

reversible

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25
Q

Aplasia

A

failure of cell production during embryogenesis

ie- unilateral renal agenesis

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26
Q

Hypoplasia

A

decrease in cell production during embryogenesis

Results in a relatively small organ

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27
Q

Budd Chiari Syndrome

A

occlusion of hepatic veinsv–> ischemia
blood cant flow through hepatic parenchyma, leads to infarction
Polycythemia Vera is most common cause

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28
Q

Hypoxemia

A

low O2 partial pressure within the blood

PaO2 < 60 mmHg; SaO2 < 90% (O2 in Hg in RBC)

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29
Q

High altitude, partial pressure of O2

A

Lower atmospheric Partial Pressure of O2

- can get hypoxemia

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30
Q

Anything that increases the PACO2, will ___ PAO2

A

decreases PA O2 (Partial pressure of Alveolar O2)

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31
Q

CO2 would build up in lungs in under __ conditions

A

hypoventilation , bc it’s not being blown off

COPD- air trapped w/in lung- dec/ PAO2

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32
Q

SaO2 is

A

the % of Hg bound in RBC’s by O2

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33
Q

PA02 v. PaO2

A 
PAO2 = alveolar O2
PaO2= arteriolar O2
34
Q

Early sign of CO poisoning

A

headache

35
Q

Fe2+ binds O2

A

If oxidized to Fe3+ = methemoglobinemia - can’t carry O2 anymore –> SaO2 decreased
* Seen with oxidant stress- Sulfa and Nitrate drugs

36
Q

Tx for methemoglobinemia

A

IV methylene blue - reduces Fe3+ back to Fe2+ state

37
Q

Findings in initial phase of injury that are reversible

A 
Hallmark= cellular swelling **
(due to dec ATP pumps, more Na inside cell, H20 follows Na in)
- loss of microvilli
- membrane blebbing
- swelling of RER
38
Q

Cellular swelling

A

hallmark of REVERSIBLE injury

–> loss of micro villi + memb blebbing

39
Q

Membrane damage

A

hallmark of IRREVERSIBLE injury

40
Q

Cyanosis with chocolate colored blood

A

Methemoglobinemia

Tx= IV methylene blue

41
Q

Hypoxia decreases ___

A

ATP –> disrupts key cellular functions

  • Na/ K pump (more Na and H2O inside –> cell swelling)
  • Ca pump (more Ca in cytosol; dangerous- can activate more enzymes)
  • Aerobic glycolysis disrupted, swith co anaerobic glycolysis; lower cellular pH due to lactic acid
42
Q

Want to keep a ____ intracellular Ca concentration

A

low

43
Q

Cytochrome C is present inside the mitochondria

A

if Cytochrome C leaks out of mitochondria and into cytoskeleton, it can activate apoptosis

44
Q

Cytochrome C activates

A

apoptosis

45
Q

Morphologic hallmark of cell death is loss of nucleus

A

Occurs via:

pkynosis, karyorrhexis, and karyolysis

46
Q

pyknosis

A

nucleus shrinks down

47
Q

kayorrhexis

A

nucleus breaks up into pieces

48
Q

karyolysis

A

pieces of nucleus broken down into building blocks

49
Q

Necrosis

A

death of a large group of cells followed by acute inflammation
due to an underlying PATHOLOGIC process, never physiologic

50
Q

Necrosis is followed by

A

neutrophils come into the area
leads to acute inflammation

Necrosis is Always Pathologic

51
Q

Coagulative necrosis

A

necrotic tissue that remains firm
The tissue dies, but cells retain their shape and organ structure is preserved by coagulation of cellular proteins
Nucleus disappears

** characteristic of Ischemic Infarction of any organ except the brain

52
Q

Coagulative necrosis is characteristic of

A

Ischemic Infarction of any organ except the brain

53
Q

Ischemic infarction leads to what kind of necrosis?

A 
Coagulative Necrosis 
(for any organ except brain)
54
Q

Pale infarction

A

due to ischemic necrosis

55
Q

Red infarction

A

Hemorrhagic infarctions
Blood must reenter tissue after ischemia; tissue must be loosely organized
ie: testicle that has undergone hemorrhagic infarction (artery is open but the vein is blocked)

56
Q

Liquefactive necrosis

A

Necrotic tissue that becomes liquiefied- due to enzymatic lysis of cells

57
Q

If blood supply is cut to brain, it leads to

A

liquefactive necrosis
due to microglial cells that kill cells post necrosis
(all other tissues have coagulative necrosis)

58
Q

Liquefactive necrosis is seen in

A
  1. Brain infarction- via microglial cells
  2. Absecess- neutrophils have hydrolytic enzymes of neutrophils
  3. Pancreatitis - pancreas get autodigestion via pancreatic enzymes
59
Q

Gangrenous necrosis

A

coagulative necrosis that resembles mummified tissue- dry gangrene
CHARACTERISITIC of ischemia of lower limbs

60
Q

ischemia of lower limbs leads to

A

gangrenous necrosis

61
Q

wet gangrene

A

if superimposed infection occurs on gangrenous necrosis, leads to liquefactive necrosis

62
Q

Caseous necrosis

A

cottage cheese like appearance
** Characteristic of granulomatous inflammation due to TB or fungal infection

Combo of Coagulative and liquefactive necrosis

63
Q

Fat necrosis

A

Necrosis of fat tissue
ie- trauma to breast
Chalky white appearance due to deposition of calcium - saponification **

64
Q

Saponification

A

When fat is damaged, fatty acids are released by trauma or lipase, and join with calcium
Ex= dystrophic calcification

65
Q

metastatic calcification

A

serum Ca and K is high; so it can deposit in various tissues in the body

66
Q

dystrophic Caclification

A

serum Ca is normal, serum K is normal

67
Q

Fibrinoid necrosis

A 
necrotic damage to blood vessel wall
- leaking of proteins into vessel wall results in bright pink staining
Characteristic of:
1. malignant hypertension
2. vasculitis
68
Q

Fibrinoid necrosis is characteristic of:

A

Characteristic of:

  1. malignant hypertension
  2. vasculitis
69
Q

Consequence of pre-eclampsia leads to

A

fibrinoid necrosis of placenta

70
Q

Endometrial shedding during menstrual cycle sheds via

A

apoptosis

71
Q

Process of apoptosis

A

Dying cells shrink - become eosinophilic
Nucleus condenses and fragments
Apoptotic bodies fall from cell- are removed by Macrophages
** NO inflammation

72
Q

Apoptosis is mediated by

A

Caspases

  • activate proteases (breakdown cytoskeleton)
  • activate endonucleases (breakdown DNA)
73
Q

Caspases

A

mediate apoptosis

–> activate proteases and endonucleases

74
Q

Intrinsic mitochondrial pathway

A

Cellular injury (ie mitochondrial memb damage)
DNA damageBcl
Decreased hormonal stimulation inactivates Bcl2

75
Q

Intrinsic mitochondrial pathway is mediated by

A

cytrocrhome c

–> which activates caspases

76
Q

Bcl2

A

stabilizes mitochondrial membrane so that cytochrome c doesnt leak out

77
Q

If Bcl2 is knocked out..

A

allows cytochrome c to leave mitochondria and get into cytoplasm, where it activates caspases which leads to apoptosis

78
Q

Extrinsic receptor-ligand pathway

A

something from outside binds a receptor on cell and activates apoptosis
FAS ligand binds FAS death receptor (CD95) on target cell

TNF bings TNF receptor on target cell

79
Q

positive selection of T cell

A

can it bind self Ag + self MHC

if yes = survives

80
Q

Negative selection of T cell

A

can it bind self Ag too tightly?

yes = apoptosis - via FAS ligand pathway

81
Q

Negative selection of T cells in thymus

A

via Fas ligand - Fas death receptor

apoptosis

Pathoma (3 decks)

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