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22 fall: path > Test 1: lecture 3 cell injury > Flashcards

Test 1: lecture 3 cell injury Flashcards

1
Q

when can you detect biochemical changes

A

seconds to minutes

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2
Q

when can you detect ultrastructural changes?

A

mins-hours

changes seen by an electron microscope

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3
Q

when can you detect microscopic changes

A

6-12 hours

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4
Q

when can you see gross changes from cell injury

A

hours-days

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5
Q

how does decreased ATP effect cell

A

Na/K pump fails and Na floods cell, water follows salt and cell swells

Calcium pump fails, too much calcium in the cell caused increased enzyme activity

cells switch to using glucose for energy (glycolysis), this causes an increase in lactic acid which decreases intracellular pH, decreases enzyme activity

ribosomes fall off → protein misfolding

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6
Q

what happens to mitochondria with decreased ATP

A

breakdown in membrane means no oxidative phosphorylation (no new ATP is made)

this leads to the release of cytochrome C which leads to apoptosis

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7
Q

an increase in intracellular Ca leads to

A

PLA (phospholipase A) activation (breaks down phospholipids in membranes which damages mitochondrial membrane

amino acid generation

ATPases

Proteases

endonucleases

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8
Q

ATP loss, ROS, increased intracellular Ca and PLAs will recruit ___ and cause ___

A

T cells, viruses and complement factors

cell membrane to become leaky and cause the loss of AST,ALT and CK which can be seen on blood tests

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9
Q

5 mechanisms of cell injury

A

Decrease ATP

  • Mitochondrial damage
  • Calcium influx
  • ROS
  • Membrane permeability
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10
Q

Loss of ATP leads to:
Plasma membrane ___ pump fails → leads to increase of ___ in the cell

A

Na + K+ ATPase

Sodium, water follows and cell swells

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11
Q

Ca pump failure causes ___ which will ___ enzyme activity

A

increased intracellular Ca

increased (can damage stuff, too active)

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12
Q

if ATP not available, cells will switch to ___ for energy. This produces ___ as a waste product which causes a ___ in intracellular pH which causes ___

A

glycogen (glycolysis)

lactic acid and inorganic phosphate

decrease (more acidic)

decreased activity of some enzymes

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13
Q

protein misfolding will cause the activation of ___ factors

A

proapoptotic

(ribosomes detach form the RER, which decreases protein synthesis)

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14
Q

breakdown of the mitochondrial membrane will cause the loss of what function and will cause the release of ___

A

oxidative phosphorylation (making ATP)

release of cytochrome C → apoptosis

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15
Q

increased Ca inside cell activates ___ which will cause damage to ___

A

phospholipase A

membranes (mitochondrial and other cell membranes)

increased Ca will also activate proteases, ATPases and endonucleases

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16
Q

___ degrade chromatin

A

endonucleases

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17
Q

increased Ca generates ___ which is a mediator of inflammation

A

arachidonic acid

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18
Q

The cell membrane is damaged by the above insults and direct injury by infectious agents, complement, ____ and physical and chemical agents

A

killer T cells,

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19
Q

Membrane damage allows cell contents to leak into the plasma - these can be detected in ___

A

blood samples.

ALT, AST ect

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20
Q

another name for cell swelling

A

hydropic degeneration

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21
Q
A
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22
Q

what are some things that can happen to a cell during hydropic degeneration

A

swells

mitochondria (swollen with little cristae)

membrane blebs

loss of microvilli

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23
Q

lipidosis

A

accumulation of fat in a non-adipose cell

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24
Q

lipidosis can be caused by

excessive dietary intake of fat
• increased mobilization of fat (due to ___)
• excessive intake of carbohydrates
• decreased fatty acid oxidation due to hepatocyte dysfunction
• decreased apoprotein synthesis with subsequent decreased export of lipoproteins (protein malnutrition)

• impaired secretion of lipoproteins (toxins)

A

starvation

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25
Q
A

liver

diffuse hepatic lipidosis

diffuse, enlarged, yellow, soft, friable liver with rounded edges (reticular pattern)

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26
Q
A

glycogen accumulation in the liver

orangish, rounded

steroid hypertrophy

cytoplasmic swelling and clearing

reversible cell injury caused by the use of steroids (either exogenous- pred or endogenous-cushings- too much cortisol)

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27
Q
A

glycogen accumulation from too much steroids

cytoplasmic swelling and clearing of hepatocytes

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28
Q

Some cells may retain evidence of previous injury in the
form of ___ accumulation after autophagocytosis
of damaged organelles.

A

lipofuscin

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29
Q

necrosis vs apoptosis

A

necrosis→ what happens to a cell after death → messy (inflammation)

apoptosis → programed cell death → highly regulated, doesn’t really cause a fuss

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30
Q

nuclear shrinkage and increased basophilic

A

pyknosis

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31
Q
A

pyknosis

step of necrosis→ nucleus shrinks and becomes more pink (basophilic)

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32
Q

___ is nuclear fragments

A

karyorrhexis

step in necrosis that usually follows pyknosis (shrinkage and increased basophilic)

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33
Q

___ is the fading of a nucleus

A

karyolysis

last step in necrosis

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34
Q

what are three things that happen to the nucleus during necrosis

A

Pyknosis: nuclear shrinkage and increased basophilic

Karyorrhexis: nucleus fragments (usually following pyknosis)

Karyolysis: fading or disappearance of the nucleus

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35
Q

what happens to mitochondria during necrosis

A

get big with little cristae

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36
Q

calcification is a step in necrosis or apoptosis

A

necrosis

37
Q
A

karyorrhexis → nuclear fragments

38
Q

if necrosis is multifocal it is usually caused by ___

A

infections

39
Q

if necrosis is massive it is usually caused by ___

A

toxic or nutritional cause

40
Q

if necrosis is zonal or regional it is usually caused by ___

A

usually toxic, hypoxic or metabolic

41
Q
A

multifocal-random distribution of necrosis in the liver

severe

tan necrosis with black rim hemorrhagic tissue

42
Q

___ necrosis preserves the cell outline and is usually caused by ___

A

coagulative

ischemia

43
Q

___ necrosis breaksdown the cell outline and is usually caused by ___

A

liquefactive

bacteria

44
Q

___ is cheeselike

A

caseous

45
Q

___ is an example of fat necrosis

A

pancreatitis- enzymatic destruction of fat

46
Q
A

coagulative necrosis

still have cell outline but no nucleus

47
Q

gangrene is a type of ___ necrosis caused by ___

A

coagulative (dead- no nucleus but still has outline)

ischemia

48
Q
A

liquefactive necrosis

liver- no cell wall→ necrotic wave→ bacterial

49
Q
A

fat necrosis due to acute necrotizing pancreatitis

50
Q
A

Fa t necrosis with mineralization (saponification→ make soap)

51
Q

___(heat, cold, radiation, electric shock) may directly rupture cells, damage their blood supply, denature cell proteins, create free radicals, or damage DNA.

A

Physical agents

52
Q

___ (viruses, prions, bacteria, rickettsiae, protozoan and metazoan parasites) can damage cells directly by invading the cells or producing toxins, or the damage may be due to the inflammatory reaction they induce.

A

Infectious agents

53
Q

____failure to respond to infectious agents and other antigens as a result of congenital or acquired immunodeficiencies; autoimmune diseases; hypersensitivity reactions.

A

Immunologic dysfunction

54
Q

___ (mutations) cause a wide spectrum of abnormalities, from gross defects that are incompatible with life, to subtle variations in susceptibility to other diseases and include inborn errors of metabolism (storage diseases).

A

Genetic derangements

55
Q

___ include decreased food intake (starvation), excessive ingestion of calories leading to obesity, and deficiencies or excessive intake (toxicity) of vitamins and minerals.

A

Nutritional imbalances i

56
Q

Normally free radicals are scavenged, but when there is an excess of production or decreased removal
then ___occurs.

A

oxidative stress

57
Q

Once formed, free radicals damage tissues by: ___ of membranes (this can be autocatalytic or self-perpetuating); Oxidative modification of proteins; DNA damage.

A

Lipid peroxidation

58
Q

___that scavenge free radicals

A

Antioxidants

59
Q

Free radical-scavenging enzyme systems including catalase, superoxide dismutases, and ___peroxidase

A

glutathione

60
Q

what are some ultrastructural changes during hydropic degeneration

A

membrane alterations: blebs, blunting, and loss of microvilli, myelin figures (whorls of detached membranes), and loss of intercellular junctions

mitochondrial swelling, rarefaction, and small amorphous dense deposits

dilation of the endoplasmic reticulum with detachment of ribosomes

clumping of nuclear chromatin

61
Q

___ is the accumulation of fat in hepatocytes

A

hepatic lipidosis

62
Q

___ refers to the spectrum of morphologic changes (gross, histologic, and ultrastructural) that follow cell death in a living tissue

A

Necrosis

63
Q

____ refers to one group of pathways of cell death that are the result of a regulated intracellular program that activates intracellular enzymes to cause degradation of cell proteins and DNA, cell shrinkage, and death.

A

Apoptosis

64
Q

Coagulative necrosis occurs most often with ____ and for a few days the cells maintain their basic outline.

A

ischemia or toxins

Eventually enzymatic action and entering leukocytes leads to proteolysis and loss of the cell outline. Ischemic necrosis of an extremity with subsequent coagulation necrosis is called dry gangrene. When the action of bacteria causes liquefaction of the gangrenous tissue it is called wet gangrene.

65
Q

Eventually enzymatic action and entering leukocytes leads to proteolysis and loss of the cell outline. Ischemic necrosis of an extremity with subsequent coagulation necrosis is called ___ . When the action of bacteria causes liquefaction of the gangrenous tissue it is called ___

A

dry gangrene.

wet gangrene.

66
Q

Liquefactive necrosis occurs most commonly with ___ and the cells are digested by their own enzymes, bacterial toxins, or the enzymes of leukocytes.

A

bacterial, fungal, or lytic viral infections

Cells are replaced by neutrophils and macrophages. Focal collections of white blood cells (pus) and cellular debris are termed abscesses.

67
Q

during liquefactive necrosis, Cells are replaced by neutrophils and macrophages. Focal collections of white blood cells (pus) and cellular debris are termed ___

A

abscesses.

68
Q

mineralization of fat

A

saponification

69
Q

Mycobacterium tuberculosis in humans and Corynebacterium in sheep are examples of ___

A

caseous necrosis

70
Q

4 steps of apoptosis

A

Cell shrinkage

Chromatin condensation

Membrane blebs and apoptotic bodies

Phagocytosis of apoptotic cells

71
Q
A

apoptosis→ shrunking cell

72
Q

autolysis

A

when tissue is not preserved and starts to breakdown after death

73
Q
A

autoysis→ softening of tissues after death→ melting apart

74
Q
A

autolysis → lungs, happened after death

75
Q

rigor mortis

A

contraction of muscle

76
Q

___ is the contraction of muscle

A

rigor mortis

77
Q

livor mortis

A

gravational pooling of blood in lung

78
Q

gravational pooling of blood in lung

A

livor mortis

79
Q

imbibition

A

when things next to each other color each other → bile from gallbladder

80
Q

___ is when bile changes the color of things near it

A

imbibition

81
Q

___ – blood pigment that is digested by bacteria

A

Pseudomelanosis

82
Q

Pseudomelanosis

A

blood pigment that is digested by bacteria

83
Q

during the initiation phase of apoptosis ___ become active

A

. Caspases

Initiation Phase via either the extrinsic (death receptor-mediated) or intrinsic (mitochondrial) pathway

Caspases become catalytically active (caspases are a family of cysteine proteases that cleave the nuclear scaffold and cytoskeleton proteins)

84
Q

execution phase of apoptosis

A

Caspases cleave cytoskeletal and nuclear membrane proteins, activate DNAase that induces internucleosomal cleavage of DNA

85
Q

___is the degradation of a cell by its own enzymes after it has died

A

Autolysis

86
Q

the gradual cooling of the cadaver

A

algor mortis

87
Q

hypostatic congestion or gravitational pooling of blood

A

livor mortis

88
Q
A

pyknosis

karyolysis

karyorrhexis

22 fall: path (46 decks)

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