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PATH > Unit 1: cellular injury > Flashcards

Unit 1: cellular injury Flashcards

1
Q

normal cell function depends on 3 things…

A
  1. continuous supply of nutrients
  2. removal of waste products from metabolism
  3. a normal cell environment
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2
Q

stages of cell injury…

A
  1. cell is injured
  2. cells function is altered
  3. cell degeneration
  4. cell death
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3
Q

adaptive cell responses

A
  • atrophy
  • hypertrophy
  • hyperplasia
  • metaplasia
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4
Q

what is degeneration

A

abnormality in cell structure/function (non-lethal injury)
- potentially reversible
- cells may reach a static state, where they continue to function on a suboptimal level

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5
Q

what is necrosis

A

cell death resulting from a lethal injury to the cells or tissues of a living organism
- can only occur in living organisms
- LOCAL cell death

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6
Q

what are the mechanisms of cell degeneration

A
  1. depletion of ATP
  2. impaired cell membrane function
  3. intracellular accumulations
  4. genetic abnormalities
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7
Q

what conditions can we see impaired ATP production in

A
  • hypoxia
  • hypoglycemia
  • enzyme inhibition
  • uncoupling of oxidative phosphorylation
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8
Q

what is hypoxia

A

insufficient oxygen in cells

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9
Q

cause of hypoxia

A
  • caused by any disease or obstruction of the respiratory system
  • blood entering the lungs is not oxygenated enough
  • can include things such as asthmatic attacks
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10
Q

what is hypoxemia

A
  • the decreased ability of blood to carry oxygen
  • e.g. in anemia oxygen is not carried effectively by the blood to tissues
  • may still be a normal amount of hemoglobin, but it could be altered
  • can occur with local vessel obstruction or ischemia
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11
Q

what is hypoglycemia

A

low glucose levels in the blood

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12
Q

hypoglycemia and depletion of ATP

A
  • cells not getting enough nutrients (glucose) to generate ATP
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13
Q

enzyme inhibition and depletion of ATP

A
  • interference with enzymes is the respiratory chain
  • e.g. cyanide
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14
Q

uncoupling of oxidative phosphorylation and depletion of ATP

A
  • anything that alters how enzymes and chemical reactions are organized on the mitochondrial membrane leads to decreased ATP production
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15
Q

main effects of ATP depletion in cells

A

Have to do with pumping water and sodium out of the cell
1. Intracellular accumulation of water
2. swelling of cytoplasmic organelles
3. switch to anaerobic glycolysis

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16
Q

ATP depletion and intracellular accumulation of water

A
  • lack of ATP leads to dysfunction of the cell membrane energy-dependent sodium pump
  • leads to cloudy swelling due to accumulation of fluid and electrolytes
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17
Q

ATP depletion and swelling of cytoplasmic organelles

A
  • influx of sodium and water can lead to this swelling
  • Swelling of the mitochondria causes physical uncoupling of oxidative phosphorylation
  • Appears as vacuolated spaces around the nuclei and the cytoplasm
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18
Q

ATP depletion and the switch to anaerobic glycolysis

A
  • switch leads to lactic acid production, which causes intracellular pH to decrease
  • causes further disruption of organelle membranes - damage to lysosomal membranes leads to the release of lysosomal enzymes into the cytoplasm
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19
Q

first signs of hypoglycemia and hypoxia

A

loss of consciousness (because the effects of defective energy production will first affect those cells with the highest BMR such as brain cells)

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20
Q

what can cause cell membrane damage

A
  1. free radicals
  2. activation of the compliment system
  3. direct lysis of the cell membrane
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21
Q

free radicals and cell membrane damage

A

free radicals initiate a cascade or oxidative damage to lipids, proteins, DNA, etc. 3 reactions relevant to cell injury mediated by free radical…
1) lipid peroxidation
2)protein oxidation
3) DNA damage

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22
Q

activation of the compliment system and cell membrane damage

A
  • the final compounds of the activated complement cascade can damage cell membranes
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23
Q

direct lysis of the cell membrane can be induced by…

A
  1. enzymes with lipase-like activity
  2. certain viruses cause lysis by direct insertion into the cell membrane or by initiating an immune response against infected cells
  3. physical and chemical agents such as extreme cold or heat and chemical solvents
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24
Q

what are some effects of impaired cell membrane function…

A
  1. loss of structural integrity
  2. loss of function
  3. deposition of lipofuscin
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25
Q

loss of structural integrity due to impaired membrane function

A
  • less severe injury may allow the membrane to be repaired, though some membrane may be lost
  • e.g. RBCs: can assume a spheroidal shape - spherocytes can be diagnostic for immune medicated anemia
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26
Q

Deposition of Lipofuscin due to impaired cell membrane function

A
  • damaged bits of cell membrane are deposited into the cytoplasm - results in complexes of phospholipids and proteins from free-radical peroxidation of the lipids in sub-cellular membranes
  • “wear and tear”
  • No effect on cell function
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27
Q

Types of intracellular accumulation that can lead to cell degeneration

A
  1. Fatty degeneration (fatty change)
  2. Iron deposition
  3. Bilirubin accumulation
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28
Q

what is fatty degeneration

A

when triglycerides accumulate in the cytoplasm of parenchymal cells
- can result in fatty liver disease
- anything which disturbs the balance of fatty acid processing and exporting mechanism can lead to triglyceride accumulation in liver cells

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29
Q

the balance of fatty acid processing and exporting mechanisms can be upset and start favouring triglyceride accumulation in the liver due to…

A
  • increased mobilization of adipose tissue (increased FAs reach liver)
  • overactivity of enzyme systems (increased conversion of FAs to triglycerides
    -oxidation of triglycerides to other forms is decreased
  • Apoprotein synthesis is decreased
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30
Q

what happens if too much fat accumulates in the liver

A
  • would appear pale, beige and enlarges
  • would feel friable, fragile, softer and greasy
  • might float in water
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31
Q

Hepatic Lipidosis (fatty liver syndrome) in cats

A
  • caused when the cat starts eating considerably less
  • elevated plasma triglycerides, marked fat accumulation in hepatocytes, and accumulation of bile pigments - leading to jaundice
  • The ability of the liver to esterify fatty acids from adipose tissue is likely normal, until plasma transport mechanisms become saturated - triglycerides accumulate in hepatocytes
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32
Q

what is a bruise

A

an area of hemorrhage caused by blunt trauma which injures blood vessels in the tissues

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33
Q

how do bruises form

A

when the blood vessel is injured, RBCs are broken down within the tissue to their components - the breakdown of hemoglobin produces pigments responsible for colour changes as the bruise resolves

34
Q

what is hemosiderin

A
  • when excess iron is deposited in connective tissue
35
Q

example of local accumulation of iron

A

when hemoglobin is broken down at sights of hemorrhage - this is the cause of colour changes in bruises

36
Q

what is hemochromatosis

A

rare inherited defect where free ferric iron accumulates and is chemically reduced to produce toxic free radicals - harm the cells in tissues

37
Q

how does bilirubin accumulate in the cell

A
  • when hemoglobin is broken down, the porphyrin ring is further catabolized to become bilirubin
  • Bilirubin is carried in the plasma bound to albumin in its lipid-soluble form
  • Once it reaches the liver it is conjugated to glucuronide (becoming water soluble)
  • must be excreted into bile to be removed
38
Q

what is jaundice

A

a clinical SIGN of increased bilirubin secretion - characterized as yellow pigmentation of skin, eyes, internal fat and organs
- not a disease

39
Q

jaundice can result from 3 different mechanisms

A
  1. hemolysis
  2. hepatocellular dysfunction
  3. obstruction of bile flow (cholestasis)
40
Q

jaundice from hemolysis

A
  • when RBCs are broken down in large numbers bilirubin production increases and the liver can’t conjugate it fast enough
  • Unconjugated bilirubin accumulates and is lipid soluble, so not excreted in urine
41
Q

jaundice from hepatocellular dysfunction

A
  • if the liver is injured then uptake, conjugation and excretion of bilirubin is affected
  • both conjugated and unconjugated bilirubin levels increase
42
Q

jaundice from obstruction to bile flow (cholestasis)

A
  • if the bile tract or gall bladder is obstructed, then bilirubin can’t be excreted adequately
  • Conjugated bilirubin will reflux into the plasma causing jaundice
43
Q

functional significance of jaundice

A
  • deposition of bilirubin in connective tissue of the skin, scalar and internal organs = yellow discolouration but no functional abnormality
  • deposition of bilirubin in parenchymal cells = cellular injury
  • deposition of bilirubin in hepatocytes = toxic cell injury
  • deposition of bilirubin in brain cells = neuronal dysfunction (kernicterus) and cell death
44
Q

genetic abnormalities that can lead to cell degeneration

A
  • interference with mitosis: damage of RBC precursors lead to anemia, damage to intestinal mucosa leads to intestinal dysfunction, diarrhea or hemorrhage
  • Failure of synthesis of structural proteins
  • Failure of growth-regulating protein: can lead to cancer
  • Failure of enzyme synthesis
45
Q

ultra cellular changes of cells to recognize degeneration

A
  • dilation of the ER
  • mitochondrial changes
  • glycogen accumulation
  • loss of microvilli
  • membrane blebbing
46
Q

coagulation necrosis

A
  • cell death due to ischemia
  • proteins appear denatured
  • Nuclei is lost, demarcated areas
47
Q

Liquefaction necrosis

A
  • caused by infection or ischemic injury to the brain
  • Gross evidence: tissue is in a liquid form, sometimes creamy yellow
  • Microscopic evidence: inflammatory cells within numerous neutrophils
48
Q

caseous necrosis

A
  • caused by tuberculosis
  • Gross evidence: white, soft, cheesy looking
  • Microscopic evidence: uniformly eosinophilic center surrounded by a collar of lymphocytes and activated macrophages
49
Q

fat necrosis

A
  • caused by acute inflammation affecting tissues with numerous adipocytes (such as pancreas and breast tissue)
  • Damaged cells release digestive enzymes which break down lipids to generate free FAs
  • Usually not grossly discernible
  • Microscopic: deposition of fibrin within blood vessels
50
Q

2 subgroups of fat necrosis…

A
  1. enzymatic
    - associated with pancreatic injuries or acute pancreatitis
    - Causes the release of pancreatic enzymes into adjacent fat tissue in the abdominal mesentery and omentum
    - Chalky white appearance due to action of pancreatic lipase which breaks down triglycerides
  2. non-enzymatic
    - occurs in breasts and subcutaneous tissue, usually following trauma
    - Necrotic fat induces an inflammatory response which is typically granulomatous
51
Q

cytoplasmic evidence of necrosis

A
  1. cytoplasm becomes more homogenous and deeply staining
  2. The cytoplasm may have a vacuolated (bubbly) appearance: from sodium and water moving into the cel
  3. Dystrophic calcification: abnormal deposition of calcium salts in dead or dying tissues
52
Q

Why are lysosomal enzymes released in cell injury?

A
  • lack of oxygen causes cells to become anaerobic
  • Leads to lactic acid production - lowers the cells pH
  • Acidic environment damages lysosomal membranes, releasing their enzymes
  • The release of these enzymes is a result of cell death, NOT a cause
53
Q

dystrophic vs metastatic calcification

A

dystrophic: occurs in previously damaged tissues
metastatic: occurs in previously normal tissues

54
Q

nuclear evidence of necrosis

A
  • most definitive evidence of necrosis
  • Nuclear chromatin clumps in a dead cell, nucleus becomes smaller and dense, these nuclei are pyknotic
  • Pyknotic nucleus then breaks into fragments (process of kerrhyorhexis) or undergo complete lysis (karrhyolysis) - due to action of lysosomal enzymes
55
Q

what are some clinical problems associated with tissue necrosis

A
  1. altered function of organs
  2. loss of tissue
  3. secondary infection
  4. systemic effects
  5. local effects
  6. release of enzymes from necrotic cells
56
Q

altered function of organs due to tissue necrosis

A
  • results if sufficient number of cells become necrotic - depends on the tissue type
  • large functional reserve = liver
  • small functional reserve = motor cortex of the brain
57
Q

stroke

A

results in a weakness of one side of the body, loss of bladder control, dropping eyelids

58
Q

what is a heart attack

A

occluded blood supply to the myocardium and necrosis of the affected area

59
Q

what is gangrene

A

localized death and decomposition of body tissue resulting either from obstructed circulation or bacterial infection

60
Q

frost bite

A
  • and example or gangrene
  • typically affects areas furthest from the circulatory system - easiest to impair blood flow here
  • Dead tissue will likely appear darkly discoloured and clearly demarcated from normal adjacent tissue
61
Q

tissue necrosis and secondary tissue infection

A
  • since blood flow is needed to allow inflammatory cells to enter a tissue, they cannot enter necrotic tissue
  • Necrotic tissue is an ideal growth medium for infection (usually if moist) - beyond the reach of inflammatory cells
62
Q

systemic effects of tissue necrosis

A
  • fever and increased WBC count are seen in high degree necrosis
  • Fever is due to release of pyrogens from necrotic cells and WBCs
  • Increased WBC is due to inflammatory response
63
Q

local effects of tissue necrosis (ulcers)

A

Gastric ulceration: tissue lining the inner wall of the stomach has become necrotic - sloughed
Bleeding ulcer: when a blood vessel I’m the submucosa becomes injured, hemorrhage may occur - blood is lost into the stomach and intestinal tract

64
Q

effects of bleeding ulcers

A
  • digested blood in stools causes melena
  • blood loss can lead to anemia
  • abdominal pain may occur because nerve endings in the submucosa are affected by inflammation
  • Gastric irritation can lead to nausea - possibly account for vomiting and weight loss
65
Q

release of enzymes from necrotic cells (clinical effect)

A
  • cytoplasmic enzymes may be released into blood
  • the type of enzymes exerted are used to indicate the tissue with necrosis
66
Q

what is apoptosis

A

programmed cell death

67
Q

apoptosis can occur in situations of…

A
  • programmed cell death during embryogenesis
  • hormonal-driven regression of tissues
  • cell death in tissues with normal rapid turn-over
  • elimination of potentially harmful self-reactive lymphocytes during maturation
68
Q

All cells have internal mechanisms for inducing apoptosis when cells are damaged beyond repair, occurs when there is…

A
  • damage to DNA
  • accumulation of misfolded proteins
  • viral infections
  • pathogenic atrophy of organs
69
Q

action of cytotoxic T-cells

A

capable of inducing cell death through apoptosis in their neighbours if they detect abnormalities

70
Q

2 pathways of apoptosis

A
  1. mitochondria pathway: BH3-only proteins sense a lack of survival signals, they activate effector molecules that increase mitochondrial permeability - mitochondria becomes leaky and caspases are released
  2. Death receptor pathway: signals from plasma membrane receptors lead to the assembly of adaptor proteins into a “death-inducing signalling complex” which activate caspases
71
Q

how is apoptosis different from necrosis

A
  • programmed (not accidental)
  • active, organized and orderly
  • cell is enlarged (swelling)
  • cell membrane remains intact (organelles remain membrane bound)
  • produces neatly packaged fragments
  • no inflammation
72
Q

how are the 2 paths of apoptosis similar

A
  • both culminate in activation of caspases, even though they are induced differently
73
Q

apoptosis and the development of cancer

A

in order for an abnormal cell to produce a tumor it must induce apoptosis to avoid…
- Endogenous suicide signals as a result of DNA abnormalities
- Recognition and response from cytotoxic T-cells

74
Q

Diseases driven by apoptosis can exhibit altered function like necrosis BUT do not include…

A
  • loss of tissue in the same manner
  • predisposition of bacterial infection
  • local and systemic effects
  • release of cellular enzymes
75
Q

what is autophagy

A

Cell “eats” and recycles cytoplasmic organelles that are not essential for survival to provide energy
- can be caused due to starvation of cells
- A cytoplasmic lysosome will fuse with an autophagic vacuole containing the cytoplasmic organelle and digest the contents as a nutrient source
- leads to apoptosis

76
Q

what are post Morton changes

A

changed to cells that occur due to the continues action of cellular enzymes following death
- rigor mortis
- post mortem lividity
- post mortem blood clotting
- putrefaction
- autolysis

77
Q

what is rigorous mortis

A

stiffening of a dead body - due to reduction of ATP in muscles

78
Q

what is post mortem lividity

A

gravitational settling of the blood in dependent parts - breakdown of Hb produces green discolouration of skin

79
Q

what is post mortem blood clotting

A

results in formation of larger clots (e.g. in chambers of the heart)

80
Q

what is putrefaction

A

ermentation caused by saprophytic bacteria - may have rupture of the stomach or “foamy liver” which is full of gas bubbles

81
Q

what is autolysis

A

digestion of tissues or organs as a whole - due to action of their own enzymes
- difficult to distinguish from necrosis, but inflammatory cells are generally not seen with autolysis

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