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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
Aplasia
failure of cell production during embryogenesis | ie- unilateral renal agenesis
26
Hypoplasia
decrease in cell production during embryogenesis | Results in a relatively small organ
27
Budd Chiari Syndrome
occlusion of hepatic veinsv--> ischemia blood cant flow through hepatic parenchyma, leads to infarction Polycythemia Vera is most common cause
28
Hypoxemia
low O2 partial pressure within the blood | PaO2 < 60 mmHg; SaO2 < 90% (O2 in Hg in RBC)
29
High altitude, partial pressure of O2
Lower atmospheric Partial Pressure of O2 | - can get hypoxemia
30
Anything that increases the PACO2, will ___ PAO2
decreases PA O2 (Partial pressure of Alveolar O2)
31
CO2 would build up in lungs in under __ conditions
hypoventilation , bc it's not being blown off | COPD- air trapped w/in lung- dec/ PAO2
32
SaO2 is
the % of Hg bound in RBC's by O2
33
PA02 v. PaO2
``` PAO2 = alveolar O2 PaO2= arteriolar O2 ```
34
Early sign of CO poisoning
headache
35
Fe2+ binds O2
If oxidized to Fe3+ = methemoglobinemia - can't carry O2 anymore --> SaO2 decreased * Seen with oxidant stress- Sulfa and Nitrate drugs
36
Tx for methemoglobinemia
IV methylene blue - reduces Fe3+ back to Fe2+ state
37
Findings in initial phase of injury that are reversible
``` 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
Cellular swelling
hallmark of REVERSIBLE injury | --> loss of micro villi + memb blebbing
39
Membrane damage
hallmark of IRREVERSIBLE injury
40
Cyanosis with chocolate colored blood
Methemoglobinemia | Tx= IV methylene blue
41
Hypoxia decreases ___
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
Want to keep a ____ intracellular Ca concentration
low
43
Cytochrome C is present inside the mitochondria
if Cytochrome C leaks out of mitochondria and into cytoskeleton, it can activate apoptosis
44
Cytochrome C activates
apoptosis
45
Morphologic hallmark of cell death is loss of nucleus
Occurs via: | pkynosis, karyorrhexis, and karyolysis
46
pyknosis
nucleus shrinks down
47
kayorrhexis
nucleus breaks up into pieces
48
karyolysis
pieces of nucleus broken down into building blocks
49
Necrosis
death of a large group of cells followed by acute inflammation due to an underlying PATHOLOGIC process, never physiologic
50
Necrosis is followed by
neutrophils come into the area leads to acute inflammation Necrosis is Always Pathologic
51
Coagulative necrosis
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
Coagulative necrosis is characteristic of
Ischemic Infarction of any organ except the brain
53
Ischemic infarction leads to what kind of necrosis?
``` Coagulative Necrosis (for any organ except brain) ```
54
Pale infarction
due to ischemic necrosis
55
Red infarction
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
Liquefactive necrosis
Necrotic tissue that becomes liquiefied- due to enzymatic lysis of cells
57
If blood supply is cut to brain, it leads to
liquefactive necrosis due to microglial cells that kill cells post necrosis (all other tissues have coagulative necrosis)
58
Liquefactive necrosis is seen in
1. Brain infarction- via microglial cells 2. Absecess- neutrophils have hydrolytic enzymes of neutrophils 3. Pancreatitis - pancreas get autodigestion via pancreatic enzymes
59
Gangrenous necrosis
coagulative necrosis that resembles mummified tissue- dry gangrene CHARACTERISITIC of ischemia of lower limbs
60
ischemia of lower limbs leads to
gangrenous necrosis
61
wet gangrene
if superimposed infection occurs on gangrenous necrosis, leads to liquefactive necrosis
62
Caseous necrosis
cottage cheese like appearance ** Characteristic of granulomatous inflammation due to TB or fungal infection Combo of Coagulative and liquefactive necrosis
63
Fat necrosis
Necrosis of fat tissue ie- trauma to breast Chalky white appearance due to deposition of calcium - saponification **
64
Saponification
When fat is damaged, fatty acids are released by trauma or lipase, and join with calcium Ex= dystrophic calcification
65
metastatic calcification
serum Ca and K is high; so it can deposit in various tissues in the body
66
dystrophic Caclification
serum Ca is normal, serum K is normal
67
Fibrinoid necrosis
``` 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
Fibrinoid necrosis is characteristic of:
Characteristic of: 1. malignant hypertension 2. vasculitis
69
Consequence of pre-eclampsia leads to
fibrinoid necrosis of placenta
70
Endometrial shedding during menstrual cycle sheds via
apoptosis
71
Process of apoptosis
Dying cells shrink - become eosinophilic Nucleus condenses and fragments Apoptotic bodies fall from cell- are removed by Macrophages ** NO inflammation
72
Apoptosis is mediated by
Caspases - activate proteases (breakdown cytoskeleton) - activate endonucleases (breakdown DNA)
73
Caspases
mediate apoptosis | --> activate proteases and endonucleases
74
Intrinsic mitochondrial pathway
Cellular injury (ie mitochondrial memb damage) DNA damageBcl Decreased hormonal stimulation inactivates Bcl2
75
Intrinsic mitochondrial pathway is mediated by
cytrocrhome c | --> which activates caspases
76
Bcl2
stabilizes mitochondrial membrane so that cytochrome c doesnt leak out
77
If Bcl2 is knocked out..
allows cytochrome c to leave mitochondria and get into cytoplasm, where it activates caspases which leads to apoptosis
78
Extrinsic receptor-ligand pathway
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
positive selection of T cell
can it bind self Ag + self MHC | if yes = survives
80
Negative selection of T cell
can it bind self Ag too tightly? | yes = apoptosis - via FAS ligand pathway
81
Negative selection of T cells in thymus
via Fas ligand - Fas death receptor | apoptosis

Pathoma (3 decks)

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