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

Pathoma Growth adaptation, cellular injury, cell death Flashcards

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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
Injury occurs when stress exceed cell's ability to ____
adapt
26
What does injury depend on?
Depends on type of stress, severity, and type of cell affected
27
What does slow developing ischemia result in
Atrophy
28
What does acute ischemia result in
injury
29
What are common causes of injury
``` inflammation nutriitional deficiency or excess hypoxia trauma genetic mutations ```
30
Hypoxia
low oxygen delivery to tissue - so low ATP (impaired oxidative phosphorylation)
31
3 causes of hypoxia
Ischemia - decreased blood flow thru the organ Hypoxemia - Decreased O2 carrying capacity of the blood
32
How does ischemia occur?
Decreased arterial perfusion Decreased venous drainage (budd chairi - thrombosis of hepatic veins) Shock (hypoperfusion)
33
What is most common cause of Budd Chiari?
polycythemia vera - in hepatic vein
34
Hypoxemia
Low partial pressure in O2 in blood (PaO2PAO2 -> PaO2 -> SaO2 High altitude Diffusion defect Hypoventilation V/Q mismatch
35
Decreased O2 carrying capacity arises with?
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
What happens to PaO2 and SaO2 in anemia?
They are normal
37
What happens to PaO2 and SaO2 in CO poisoning?
PaO2 is normal | SaO2 is decreased
38
What is early sign of CO poisoning?
Headache
39
What form of iron binds O2?
Fe2+
40
What happens to PaO2 and SaO2 with methemoglobinemia
PaO2 normal | SaO2 decreased
41
What is classic finding in methemoglobinemia
Cyanosis and chocolate colored blood
42
TX for methemoglboinemia
IV METHYLENE BLUE
43
Low ATP disrupts key cellular functions
``` Na+/K+ pump (water build up in cell) Ca2+ pump (calcium into cell) Aerobic glycolysis (lactic acid lowering pH in cell) ```
44
What is hallmark of reversible injury?
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
What is hallmark of irreversible damage?
Membrane damage
46
3 membranes damaged in irreversible damage
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
What does cytochrome C activate?
apoptosis
48
What is morphologic hallmark of cell death?
Loss of nucleus Pyknosis, Karyohhrexis, Karyolysis
49
Pyknosis
Nuclear condensation
50
Karyohhrexis
Fragmentation
51
Karyolysis
Dissolution
52
2 mechanism of cell death
necrosis and apoptosis
53
Necrosis
death of large group of cells followed by acute inflammation Pathologic process
54
What are the types of necrosis?
Liquefactive (brain, abscess, pancreatitis) Coagulative necrosis - remains firm - cells retain shape but nuclei disappear (ischemic infarction) Gangrenous necrosis - mummified tissue Caseous necrosis
55
What process causes coagulative necrosis?
Ischemic infarct - except in the brain
56
What is the shape of area of infarcted tissue?
Wedged and pale
57
Red infarction must have what to happen?
Blood re-enters and tissue is loosely organized
58
Where do you see liquefactive necrosis
Brain infarction (microglial cells that destroy tissue) Abscess (neutrophils destroy tissues) Pancreatitis (proteolytic enzymes digest parenchyma - so liquefies pancreas itself)
59
Gangrenous necrosis
Ischemia of lower limb (also GI tract) if superimposed infection occurs, then liquefactive necrosis ensues (wet gangrene)
60
Caseous necrosis
Coagulative + Liquefactive necrosis Granulomatous inflammation d/t TB or fungal infection
61
Fat necrosis
necrotic adipose tissue w/ chalky white appearance d/t deposition of calcium
62
What 2 cases do you see fat necrosis?
Trauma to fat (breast) Pancreatitis mediated damage of peripancreatic fat
63
saponifiaction
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
What are the levels of calcium (& phosphate) in dystrophic calcification vs metastatic calcification
Dystrophic: normal Metastatic: high
65
Fibrinoid necrosis
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
Fibrinoid necrosis of placenta consequence of what?
Pre-eclampsia
67
Apoptosis morphology
Dying cell shrinks (eosinophilic) Nucleus condenses and fragments Apoptotic bodies fall from cell and are removed by MACROPHAGES
68
Is there inflammation with apoptosis?
NO - apoptotic bodies removed by macrophages
69
What mediates apoptosis?
Capsases - activate proteases Activate endonucleases
70
What activates caspases?
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
What free radical does ionizing radiation create?
OH - most damaging
72
Elimination of free radicals
Antioxidants Enzymes Metal carrier proteins (like transferrin)
73
SOD
Superoxide (O2.-) to H202
74
Glutathione peroxidase
2GSH + free radical -> GS-SG and H2O
75
Catalase
H2O2 -> O2 + H2O
76
Carbon tetrachloride
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
Reprofusion injury
Production of O2- derived free radicals which further damages tissue Leads to continued rise in cardiac enzymes after reperfusion of infarcted myocardial tissue
78
Amyloid
misfolded protein deposited in extracellular space
79
What is typical configuration of amyloid? What stain do you use and what do you see?
Beta pleated sheets and stain with congo red and have apple green birefringence
80
Where does amyloid deposit?
Around the blood vessels
81
Primary amyloidosis
Systemic - AL amyloid from Ig light chain
82
What is primary amyloidosis associated with?
Plasma cell dyscrasia - abnormality of plasma cell and can have over production of light chain
83
Secondary amyloidosis
AA amyloid from SAA (from acute phase reactant) - chronic inflammatory states
84
What is most common involved organ with amylodosis?
Kidney - causes nephrotic syndrome
85
Organs involved with amyloidosis
Kidney, restrictive cardiomyopathy, arrythmia, tongue enlargement, malabsorption, HSM

pathoma (12 decks)

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