Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Aaron-Exit: Championship Rounds > Pathoma Chapter 1C > Flashcards

Pathoma Chapter 1C Flashcards

1
Q

Anemia leading to decreased O2 carrying capacity.

A

(decrease in RBC mass) PaO2 normal; SaO2 normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Carbon monoxide poisoning

A

CO binds hemoglobin more avidly than oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the PaO2 and SaO2 for carbon monoxide poisoning?

A

PaO2 normal; SaO2 decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Exposures for Carbon monoxide poisoning

A

include smoke from fires and exhaust from cars or gas heaters.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Classic finding for Carbon monoxide poisoning

A

cherry-red appearance of skin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Early sign of exposure for Carbon monoxide poisoning

A

headache; significant exposure leads to coma and death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Methemoglobinemia?

A

Iron in heme is oxidized to Fe3+ which cannot bind oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

PaO2 and SaO2 for Methemoglobinemia?

A

PaO2 normal; SaO2 decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Methemoglobinemia is Seen with?

A

oxidant stress (eg sulfa and nitrate drugs) or in newborns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Classic finding for Methemoglobinemia?

A

cyanosis with chocolate-colored blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment for Methemoglobinemia?

A

intravenous methylene blue, which helps reduce Fe3+ back to Fe2+ state.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hypoxia results in low ATP how?

A

impairs oxidative phosphorylation resulting in decreased ATP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Low ATP disrupts what?

A

key cellular functions including 1. Na/K pump 2. Ca2+ pump 3. Aerobic glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Disruption of Na/K pump results in what?

A

sodium and water buildup in the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Disruption of Ca2+ pump results in what?

A

Ca2+ buildup in the cytosol of the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Disruption of Aerobic glycolysis results in what?

A

switch to anaerobic glycolysis. Lactic acid buildup results in low pH, which denatures proteins and precipitates DMA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

The hallmark of reversible injury is

A

cellular swelling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cytosol swelling results in

A

loss or microvilli and membrane blebbing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Swelling of the rough endoplasmic reticulum (RER) results in

A

dissociation of ribosomes and decreased protein synthesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

The hallmark of irreversible injury is

A

membrane damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Plasma membrane damage results in

A
  1. Cytosolic enzymes leaking into the serum {e.g cardiac troponin) 2. Additional calcium entering into the cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Mitochondrial membrane damage results in

A
  1. Loss of the electron transport chain (inner mitochondrial membrane) 2. Cytochrome c leaking into cytosol (activates apoptosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Lysosome membrane damage results in

A

hydrolytic enzymes leaking into the cytosol, which in turn, are activated by the high intracellular calcium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

The end result of irreversible injury is

A

cell death.

25
Q

The morphologic hallmark of cell death is

A

loss of the nucleus,

26
Q

loss of the nucleus occurs via

A

nuclear condensation (pyknosis), fragmentation (karyorrhexis), and dissolution (karyolysis)

27
Q

The two mechanisms of cell death are

A

necrosis and apoptosis.

28
Q

NECROSIS

A

A. Death of large groups of cells followed by acute inflammation B. Due to some underlying pathologic process; never physiologic C. Divided into several types based on gross features

29
Q

GROSS PATTERNS OF NECROSIS

A

A. Coagulative necrosis, B. liquefactive necrosis, C. Gangrenous necrosis D. Caseous necrosis E. Fat necrosis F. Fibrinoid necrosis

30
Q

What is Coagulative necrosis?

A

Necrotic tissue that remains firm, cell shape and organ structure are preserved by coagulation of proteins, but the nucleus disappears

31
Q

Coagulative necrosis is Characteristic of?

A

ischemic infarction of any organ except the brain

32
Q

Area of infarcted tissue for Coagulative necrosis?

A

It is often wedge-shaped (pointing to focus of vascular occlusion) and pale.

33
Q

What is Red infarction

A

arises if blood re-enters a loosely organized tissue (e.g. pulmonary or testicular infarction)

34
Q

What is Liquefactive necrosis?

A

Necrotic tissue that becomes liquefied; enzymatic lysis of cells and protein results in liquefaction.

35
Q

Liquefactive necrosis is Characteristic of?

A

Brain infarction, abscess, pancreatitis

36
Q

What type of necrosis for brain infarction?

A

Liquefactive necrosis - Proteolytic enzymes from microglial cells liquefy the brain.

37
Q

What type of necrosis for abscess?

A

Liquefactive necrosis - proteolytic enzymes from neutrophils liquefy tissue

38
Q

What type of necrosis for pancreatitis?

A

Liquefactive necrosis - Proteolytic enzymes from pancreas liquefy parenchyma.

39
Q

What is Gangrenous necrosis?

A

Coagulative necrosis that resembles mummified tissue (dry gangrene)

40
Q

Gangrenous necrosis is characteristic of?

A

ischemia of lower limb and GI tract

41
Q

What is wet gangrene?

A

superimposed infection of dead tissues occurs, then liquefactive necrosis ensues (wet gangrene).

42
Q

What is Caseous necrosis?

A

Soft and friable necrotic tissue with cottage cheese-like appearance. It’s a combination of coagulative and liquefactive necrosis

43
Q

What is caseous necrosis characteristic of?

A

granulomatous inflammation due to tuberculous or fungal infection

44
Q

What is fat necrosis?

A

Necrotic adipose tissue with chalky-white appearance due to deposition of calcium

45
Q

What is fat necrosis characteristic of?

A

trauma to fat (eg. breast) and pancreatitis-mediated damage of peripancreatic fat

46
Q

Fat necrosis and saponification

A

Fatty acids released by trauma (eg to breast) or lipase (eg pancreatitis) join with calcium via a process called saponification which is an example of dystrophic calcification in which calcium deposits on dead tissues.

47
Q

dystrophic calcification

A

the necrotic tissue acts as a nidus for calcification in the setting of normal serum calcium and phosphate

48
Q

Dystrophic calcification vs metastatic calcification

A

high serum calcium or phosphate levels lead to calcium deposition in normal tissues (eg. hyperparathyroidism leading to nephrocalcinosis)

49
Q

Fibrinoid necrosis

A

Necrotic damage to blood vessel wall, Leaking of proteins (including fibrin) into vessel wall results in bright pink staining of the wall microscopically

50
Q

What is fibrinoid necrosis characteristic of?

A

malignant hypertension and vasculitis

51
Q

What is apoptosis?

A

Energy (ATP)-dependent, genetically programmed cell death involving single cells or small groups of cells.

52
Q

Examples of apoptosis include

A
  1. Endometrial shedding during menstrual cycle 2. Removal of cells during embryogenesis 3. CD8+ T cell-mediated killing of virally infected cells
53
Q

Morphology of apoptosis

A
  1. Dying cell shrinks, leading cytoplasm to become more eosinophilic (pink) 2. Nucleus condenses (pyknosis) and fragments (karyorrhexis).
54
Q

Apoptotic bodies

A

fall from the cell and are removed by macrophages; apoptosis is not followed by inflammation

55
Q

Apoptosis is mediated by

A

caspases that activate proteases and endonucleases

56
Q

Proteases

A

break down the cytoskeleton.

57
Q

Endonucleases

A

break down DNA,

58
Q

How are caspases activated?

A
  1. Intrinsic mitochondrial pathway 2. Extrinsic receptor-ligand pathway 3. Cytotoxic CD8+ Tcell-mediated pathway
59
Q

What is the main molecule in the intrinsic mitochondrial pathway?

A

Bcl2

Aaron-Exit: Championship Rounds (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions