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pathoma > Pathoma Growth adaptation, cellular injury, cell death > Flashcards

Pathoma Growth adaptation, cellular injury, cell death Flashcards

1
Q

Hypertrophy

A

Increase in organ size

Involves gene activation, protein synthesis, and production of organelles

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2
Q

Hyperplasia

A

Increase in cell number

Production of new cells from stem cells

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3
Q

Permanent tissues cannot under go?

A

Hyperplasia

ONLY UNDERGO HYPERTROPHY

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4
Q

What are permanent tissues? (3)

A

cardiac myocytes, skeletal muscle, nerves

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5
Q

Pathologic hyperplasia can progress to?

A

Dysplasia and cancer

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6
Q

What is a type of pathologic hyperplasia but doesn’t progress to cancer?

A

BPH

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7
Q

Atrophy

A

Decrease in stress so decrease in cell #/size

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8
Q

How does atrophy occur?

A

Decrease cell # = apoptosis

Decrease cell size = ubiquitin proteosome degredation of cytoskeleton & autophagy of cellular components

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9
Q

Metaplasia

A

Change in cell type - most commonly involves surface epithelium (one type to another)

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10
Q

Barrett’s esophagus change

A

From nonkeratinizing squamous epithelium to nonciliated, mucin producing columnar cells

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11
Q

How does metaplasia occur?

A

Reprogramming of stem cells

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12
Q

Is metaplasia reversible?

A

Yes - by removing stressor

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13
Q

Metaplasia under persistent stress turns to

A

Dysplasia and eventually cancer

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14
Q

Does apocrine metaplasia increase risk for future breast cancer?

A

No even though it is a metaplasia (in the breast)

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15
Q

What vitamin deficiency can result in metaplasia?

A

VIT A

EX: keratomalacia

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16
Q

Keratomalacia

A

Goblet cell/columnar epithelium of conjunctiva undergo metaplasia to keratinizing squamous epithelium

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17
Q

What is vitamin A necessary for in regards to epithelium

A

Maintaining specialized epithelium

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18
Q

What is an example of mesenchyma tissues undergoing metaplasia

A

Myositis ossificans - skeletal muscle trauma heals as bone

*THIS IS NOT AN OSTEOSARCOMA (which grows off the bone)

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19
Q

Dysplasia

A

Disordered cellular growth - proliferation of precancerous cells

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20
Q

How does dysplasia arise?

A

Longstanding pathologic hyperplasia or metaplasia

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21
Q

Is dysplasia reveresible?

A

Yes if stress removed but if stress not - it will become carcinoma

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22
Q

Is carcinoma reversible?

A

NO

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23
Q

Aplasia

A

failure of cell production during embryogenesis

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24
Q

Hypoplasia

A

Decrease in cell production during embryogenesis resulting in small organ

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25
Q

Injury occurs when stress exceed cell’s ability to ____

A

adapt

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26
Q

What does injury depend on?

A

Depends on type of stress, severity, and type of cell affected

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27
Q

What does slow developing ischemia result in

A

Atrophy

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28
Q

What does acute ischemia result in

A

injury

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29
Q

What are common causes of injury

A 
inflammation
nutriitional deficiency or excess
hypoxia
trauma
genetic mutations
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30
Q

Hypoxia

A

low oxygen delivery to tissue - so low ATP (impaired oxidative phosphorylation)

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31
Q

3 causes of hypoxia

A

Ischemia - decreased blood flow thru the organ

Hypoxemia -

Decreased O2 carrying capacity of the blood

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32
Q

How does ischemia occur?

A

Decreased arterial perfusion

Decreased venous drainage (budd chairi - thrombosis of hepatic veins)

Shock (hypoperfusion)

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33
Q

What is most common cause of Budd Chiari?

A

polycythemia vera - in hepatic vein

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34
Q

Hypoxemia

A

Low partial pressure in O2 in blood (PaO2PAO2 -> PaO2 -> SaO2

High altitude
Diffusion defect
Hypoventilation
V/Q mismatch

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35
Q

Decreased O2 carrying capacity arises with?

A

Hb loss or dysfunction

Anemia - decrease in RBC mass
PaO2 normal & SaO2 normal

CO poising - binds 100x compared to O2 affinity

Methemoglobinemia (Iron in heme oxidized to Fe3+)

36
Q

What happens to PaO2 and SaO2 in anemia?

A

They are normal

37
Q

What happens to PaO2 and SaO2 in CO poisoning?

A

PaO2 is normal

SaO2 is decreased

38
Q

What is early sign of CO poisoning?

A

Headache

39
Q

What form of iron binds O2?

A

Fe2+

40
Q

What happens to PaO2 and SaO2 with methemoglobinemia

A

PaO2 normal

SaO2 decreased

41
Q

What is classic finding in methemoglobinemia

A

Cyanosis and chocolate colored blood

42
Q

TX for methemoglboinemia

A

IV METHYLENE BLUE

43
Q

Low ATP disrupts key cellular functions

A 
Na+/K+ pump (water build up in cell) 
Ca2+ pump (calcium into cell) 
Aerobic glycolysis (lactic acid lowering pH in cell)
44
Q

What is hallmark of reversible injury?

A

CELLULAR SWELLING

sodium builds up in cell so water comes in and cell swells

loss of microvilli, membrane blebbing, swelling of ER (ribosomes pop off so decrease in protein synthesis)

45
Q

What is hallmark of irreversible damage?

A

Membrane damage

46
Q

3 membranes damaged in irreversible damage

A

Plasma membrane - enzyme leak out
Mitochondrial membrane - loss of ETC inner mito membrane & cytochrome C leaks into cytosol (activates apoptosis)

lysosomal membrane - hydrolytic enzymes leak into cytosol (activated by calcium)

47
Q

What does cytochrome C activate?

A

apoptosis

48
Q

What is morphologic hallmark of cell death?

A

Loss of nucleus

Pyknosis, Karyohhrexis, Karyolysis

49
Q

Pyknosis

A

Nuclear condensation

50
Q

Karyohhrexis

A

Fragmentation

51
Q

Karyolysis

A

Dissolution

52
Q

2 mechanism of cell death

A

necrosis and apoptosis

53
Q

Necrosis

A

death of large group of cells followed by acute inflammation

Pathologic process

54
Q

What are the types of necrosis?

A

Liquefactive (brain, abscess, pancreatitis)

Coagulative necrosis - remains firm - cells retain shape but nuclei disappear (ischemic infarction)

Gangrenous necrosis - mummified tissue

Caseous necrosis

55
Q

What process causes coagulative necrosis?

A

Ischemic infarct - except in the brain

56
Q

What is the shape of area of infarcted tissue?

A

Wedged and pale

57
Q

Red infarction must have what to happen?

A

Blood re-enters and tissue is loosely organized

58
Q

Where do you see liquefactive necrosis

A

Brain infarction (microglial cells that destroy tissue)
Abscess (neutrophils destroy tissues)
Pancreatitis (proteolytic enzymes digest parenchyma - so liquefies pancreas itself)

59
Q

Gangrenous necrosis

A

Ischemia of lower limb
(also GI tract)

if superimposed infection occurs, then liquefactive necrosis ensues (wet gangrene)

60
Q

Caseous necrosis

A

Coagulative + Liquefactive necrosis

Granulomatous inflammation d/t TB or fungal infection

61
Q

Fat necrosis

A

necrotic adipose tissue w/ chalky white appearance d/t deposition of calcium

62
Q

What 2 cases do you see fat necrosis?

A

Trauma to fat (breast)

Pancreatitis mediated damage of peripancreatic fat

63
Q

saponifiaction

A

fatty acids released by trauma/lipase and join with calcium

Is an example of dystrophic calcification (dead/dying tissue is a nidous for calcium)

64
Q

What are the levels of calcium (& phosphate) in dystrophic calcification vs metastatic calcification

A

Dystrophic: normal
Metastatic: high

65
Q

Fibrinoid necrosis

A

necrotic damage to blood vessel wall

leaking of proteins into vessel wall results in bright pink staining of wall

Characteristic of malignant HTN & vasculitis

66
Q

Fibrinoid necrosis of placenta consequence of what?

A

Pre-eclampsia

67
Q

Apoptosis morphology

A

Dying cell shrinks (eosinophilic)
Nucleus condenses and fragments

Apoptotic bodies fall from cell and are removed by MACROPHAGES

68
Q

Is there inflammation with apoptosis?

A

NO - apoptotic bodies removed by macrophages

69
Q

What mediates apoptosis?

A

Capsases - activate proteases

Activate endonucleases

70
Q

What activates caspases?

A

intrinsic mitochondiral pathway (BCL-2 prevents Cyto C from leaking)

Extrinsic receptor ligand pathway (ex: FAS death receptor)

cytotoxic CD8+ T cell pathway - perforins create pores in membranes and granyzmes enter pores activating caspases

71
Q

What free radical does ionizing radiation create?

A

OH - most damaging

72
Q

Elimination of free radicals

A

Antioxidants
Enzymes
Metal carrier proteins (like transferrin)

73
Q

SOD

A

Superoxide (O2.-) to H202

74
Q

Glutathione peroxidase

A

2GSH + free radical -> GS-SG and H2O

75
Q

Catalase

A

H2O2 -> O2 + H2O

76
Q

Carbon tetrachloride

A

converted to carbon trichloride in P450 system of liver and damages hepatocytes
Cellular swelling - RER swells so protein synthesis reduced

Fatty change in the liver d/t decreased apolipoproteins

77
Q

Reprofusion injury

A

Production of O2- derived free radicals which further damages tissue

Leads to continued rise in cardiac enzymes after reperfusion of infarcted myocardial tissue

78
Q

Amyloid

A

misfolded protein deposited in extracellular space

79
Q

What is typical configuration of amyloid? What stain do you use and what do you see?

A

Beta pleated sheets and stain with congo red and have apple green birefringence

80
Q

Where does amyloid deposit?

A

Around the blood vessels

81
Q

Primary amyloidosis

A

Systemic - AL amyloid from Ig light chain

82
Q

What is primary amyloidosis associated with?

A

Plasma cell dyscrasia - abnormality of plasma cell and can have over production of light chain

83
Q

Secondary amyloidosis

A

AA amyloid from SAA (from acute phase reactant) - chronic inflammatory states

84
Q

What is most common involved organ with amylodosis?

A

Kidney - causes nephrotic syndrome

85
Q

Organs involved with amyloidosis

A

Kidney, restrictive cardiomyopathy, arrythmia, tongue enlargement, malabsorption, HSM

pathoma (12 decks)

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