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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
liver **diffuse hepatic lipidosis** diffuse, enlarged, yellow, soft, friable liver with rounded edges (reticular pattern)
26
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)
27
glycogen accumulation from too much steroids cytoplasmic swelling and clearing of hepatocytes
28
Some cells may retain evidence of previous injury in the form of ___ accumulation after autophagocytosis of damaged organelles.
lipofuscin
29
necrosis vs apoptosis
necrosis→ what happens to a cell after death → messy (inflammation) apoptosis → programed cell death → highly regulated, doesn't really cause a fuss
30
nuclear shrinkage and increased basophilic
pyknosis
31
pyknosis step of necrosis→ nucleus shrinks and becomes more pink (basophilic)
32
\_\_\_ is nuclear fragments
karyorrhexis step in necrosis that usually follows pyknosis (shrinkage and increased basophilic)
33
\_\_\_ is the fading of a nucleus
karyolysis last step in necrosis
34
what are three things that happen to the nucleus during necrosis
**Pyknosis:** nuclear shrinkage and increased basophilic **Karyorrhexis:** nucleus fragments (usually following pyknosis) **Karyolysis:** fading or disappearance of the nucleus
35
what happens to mitochondria during necrosis
get big with little cristae
36
calcification is a step in necrosis or apoptosis
necrosis
37
karyorrhexis → nuclear fragments
38
if necrosis is multifocal it is usually caused by \_\_\_
infections
39
if necrosis is massive it is usually caused by \_\_\_
toxic or nutritional cause
40
if necrosis is zonal or regional it is usually caused by \_\_\_
usually toxic, hypoxic or metabolic
41
multifocal-random distribution of necrosis in the liver severe tan necrosis with black rim hemorrhagic tissue
42
\_\_\_ necrosis preserves the cell outline and is usually caused by \_\_\_
coagulative ischemia
43
\_\_\_ necrosis breaksdown the cell outline and is usually caused by \_\_\_
liquefactive bacteria
44
\_\_\_ is cheeselike
caseous
45
\_\_\_ is an example of fat necrosis
pancreatitis- enzymatic destruction of fat
46
coagulative necrosis still have cell outline but no nucleus
47
gangrene is a type of ___ necrosis caused by \_\_\_
coagulative (dead- no nucleus but still has outline) ischemia
48
liquefactive necrosis liver- no cell wall→ necrotic wave→ bacterial
49
fat necrosis due to acute necrotizing pancreatitis
50
Fa t necrosis with mineralization (saponification→ make soap)
51
\_\_\_(heat, cold, radiation, electric shock) may directly rupture cells, damage their blood supply, denature cell proteins, create free radicals, or damage DNA.
Physical agents
52
\_\_\_ (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.
Infectious agents
53
\_\_\_\_failure to respond to infectious agents and other antigens as a result of congenital or acquired immunodeficiencies; autoimmune diseases; hypersensitivity reactions.
Immunologic dysfunction
54
\_\_\_ (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).
Genetic derangements
55
\_\_\_ include decreased food intake (starvation), excessive ingestion of calories leading to obesity, and deficiencies or excessive intake (toxicity) of vitamins and minerals.
Nutritional imbalances i
56
Normally free radicals are scavenged, but when there is an excess of production or decreased removal then \_\_\_occurs.
oxidative stress
57
Once formed, free radicals damage tissues by: ___ of membranes (this can be autocatalytic or self-perpetuating); Oxidative modification of proteins; DNA damage.
Lipid peroxidation
58
\_\_\_that scavenge free radicals
Antioxidants
59
Free radical-scavenging enzyme systems including catalase, superoxide dismutases, and \_\_\_peroxidase
glutathione
60
what are some ultrastructural changes during hydropic degeneration
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
\_\_\_ is the accumulation of fat in hepatocytes
hepatic lipidosis
62
\_\_\_ refers to the spectrum of morphologic changes (gross, histologic, and ultrastructural) that follow cell death in a living tissue
Necrosis
63
\_\_\_\_ 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.
Apoptosis
64
Coagulative necrosis occurs most often with ____ and for a few days the cells maintain their basic outline.
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
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 \_\_\_
**dry gangrene.** **wet gangrene.**
66
Liquefactive necrosis occurs most commonly with ___ and the cells are digested by their own enzymes, bacterial toxins, or the enzymes of leukocytes.
bacterial, fungal, or lytic viral infections ## Footnote Cells are replaced by neutrophils and macrophages. Focal collections of white blood cells (pus) and cellular debris are termed **abscesses.**
67
during liquefactive necrosis, Cells are replaced by neutrophils and macrophages. Focal collections of white blood cells (pus) and cellular debris are termed \_\_\_
abscesses.
68
mineralization of fat
saponification
69
Mycobacterium tuberculosis in humans and Corynebacterium in sheep are examples of \_\_\_
caseous necrosis
70
4 steps of apoptosis
Cell shrinkage Chromatin condensation Membrane blebs and apoptotic bodies Phagocytosis of apoptotic cells
71
apoptosis→ shrunking cell
72
autolysis
when tissue is not preserved and starts to breakdown **after death**
73
autoysis→ softening of tissues after death→ melting apart
74
autolysis → lungs, happened after death
75
rigor mortis
contraction of muscle
76
\_\_\_ is the contraction of muscle
rigor mortis
77
livor mortis
gravational pooling of blood in lung
78
gravational pooling of blood in lung
livor mortis
79
imbibition
when things next to each other color each other → bile from gallbladder
80
\_\_\_ is when bile changes the color of things near it
imbibition
81
\_\_\_ – blood pigment that is digested by bacteria
Pseudomelanosis
82
Pseudomelanosis
blood pigment that is digested by bacteria
83
during the initiation phase of apoptosis ___ become active
**. 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
execution phase of apoptosis
Caspases cleave cytoskeletal and nuclear membrane proteins, activate DNAase that induces internucleosomal cleavage of DNA
85
\_\_\_is the degradation of a cell by its own enzymes after it has died
Autolysis
86
the gradual cooling of the cadaver
algor mortis
87
hypostatic congestion or gravitational pooling of blood
livor mortis
88
pyknosis karyolysis karyorrhexis

22 fall: path (46 decks)

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