MOD1 Flashcards

1
Q

List the 7 causes of cell injury

A
  1. Hypoxia
  2. chemical agents
  3. physical agents
  4. nutrition
  5. genetics
  6. Immune-mediated
  7. Infections
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2
Q

List the 4 types of hypoxia and define each

A
  1. Histiocytic - the inability to use oxidative phosphorylation enzymes. Ex; cyanide and paracetamol poisoning
  2. Anemic - decreased O2 carrying capacity. e.g; anemia, CO poisoning
  3. Hypoxemic - low arterial O2. e.g; high altitudes, cardioresp. failure
  4. Ischemic - disturbance to blood flow, e.g; blocked blood vessel
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3
Q

List the 5 chemical agents and drugs

A
  1. O2 in high concentrations
  2. glucose and salt in hypotonic concentrations
  3. Trace amounts of poisons; cyanide and arsenic
  4. daily exposures; pollutants, asbestos
  5. Drugs and alcohol :)
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4
Q

List the 2 main consequences of immune-mediated responses

A
  1. hypersensitivity

2. autoimmune diseases

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5
Q

List 5 physical agents

A
  1. Mechanical trauma
  2. temp extremes
  3. extreme atmospheric pressure
  4. radiation
  5. electric shock
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6
Q

What is a hydropic change and what does it look like?

A

An accumulation of water in the cell, reversible

Swelling, dense nuclei, cytoplasm looks moth-eaten, disruption/loss of membrane

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7
Q

Name 4 reversible ultrastructural changes

A
  1. PM blebbing, loss of microvilli
  2. swelling of mitochondria and appearance of small densities
  3. dilation of ER and ribosome detachment
  4. Clumping of nuclear chromatin
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8
Q

4 irreversible ultrastructural changes

A
  1. Nucleus: Pyknosis, karyorrhexis and karyolysis
  2. Myelin figures formation; Fatty acids react with calcium
  3. Breakdown of PM
  4. Organelle degradation
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9
Q

4 reversible Light microscopic changes

A
  1. cell swelling
  2. vacuolar change
  3. fatty change
  4. surface blebs
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10
Q

3 irreversible microscopic changes

A
  1. Increased eosinophilia
  2. cytoplasm looks moth eaten
  3. nuclear dissolution
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11
Q

What are the consequences of ischemia causing low ATP and lowering the na+ pump

A

water, na+ and calcium influx, K+ efflux –> ER and cell swelling, loss of microvilli

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12
Q

What are the consequences of ischemia causing low ATP and detaching ribosomes from the ER

A

lower protein synthesis - more fat deposition

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13
Q

What are the consequences of ischemia causing low ATP and increasing anaerobic glycolysis

A

lower glycogen, more lactic acid, lower pH - clumps nuclear chromatin

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14
Q

What 4 enzymes does increased intracellular calcium activate and what are the consequences

A

Membrane damage:
Phospholipase - damages phospholipids
Protease - hurts cytoplasmic and PM proteins

Nuclear Damage: activation of endonuclease

lower ATP: ATPase

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15
Q

How does intracellular calcium affect the mitochondria

A

increases permeability, which lowers ATP production

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16
Q

What is the most dangerous free radical

A

Hydroxyl ion OH-

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17
Q

Why are free radicals present in low concentrations?

A
  1. cell signalling

2. used by phagocytes to aid degradation of pathogens

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18
Q

Name 5 things that increase free radical production

A
  1. chemical and radiation injury
  2. killing of pathogens by phagocytes
  3. cellular ageing
  4. High O2 concentrations
  5. Ischemia-reperfusion
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19
Q

What two enzymes and other factors scavenge free radicles?

A

Catalase and peroxidase

Vit A,C,E, glutathione and storage proteins

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20
Q

What do Heat shock proteins do and name 3 examples

A

Mend misfolded proteins and provide optimal conditions for protein folding

Chaperonins, unfoldidases and stress proteins. E.g; ubiquitin

  1. provide optimal conditions for protein folding
  2. prevent protein aggregation
  3. mark abnormal proteins for degradation
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21
Q

Name the 2 main processes of necrosis

A
  1. degradation of proteins
  2. enzyme digestion through lysosomes essential to the dying cell and lysosomes of leukocytes that are part of the inflammatory reaction
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22
Q

Characteristics of coagulative necrosis including microscopic and gross changes

A
  1. most common
  2. result of protein degradation
    Microscopic: Ghost cells (pale, cytoplasm and cell borders unrecognizable) and neutrophils
    Gross: a firm pale wedge of tissue that can become softer later
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23
Q

Characteristics of liquefactive necrosis including a common site

A

The brain, seen in infections and often involves abscess formation

  • degradation of tissues by enzymes
  • necrotic material often creamy yellow due to the presence of dead neutrophils
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24
Q

Characteristics of caseous necrosis and a common associated disease…

A

“Cheese-like”
Amorphous debris surrounded by histiocytes, resulting in granulomatous inflammation
TB!

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25
Characteristics of fat necrosis and what can it mimic?
Adipocyte damage due to... 1. lipases released from damaged pancreatic tissue 2. trauma A breast tumour as it's seen in breast tissue
26
Characteristics of fibrinoid necrosis? | What would you see histologically
Associated with blood vessels and immune reactions Fibrinoid - bright pink and amorphous fibrin and immune complexes that have leaked out of vessels
27
4 Aetiology's of infarction
1. thrombosis 2. embolism 3. compression of vessels 4. twisting of blood supply
28
3 characteristics of a white infarct plus 3 vulnerable organs
- organs with a strong stroma - single blood supply - arterial insufficiency spleen, kidney and heart
29
3 characteristics of a red infarct plus 3 vulnerable organs
-organs with a weak stroma - easier to hemorrhage -dual blood supply -arterial OR venous insufficiency: Secondary bleeding will occur as the hemorrhage floods into the veins and surrounding tissue Liver, lungs and intestine
30
What causes wet gangrene
necrosis modified by bacteria
31
What types of necrosis can infarction be?
Coagulative and liquefactive
32
What causes air gangrene
necrosis modified by air
33
What causes gas gangrene
necrosis modified by gas-forming/anaerobic bacteria
34
4 Physiological reasons for apoptosis
1. Embryological - apoptosis in the webbing of the hands 2. hormone-dependent involution - endometrial shedding 3. in already proliferating cell populations: bottom of crypts and regulation of the immune system 4. When cells have served their function, e.g; neutrophils
35
How does apoptosis occur?
Energy-dependent cell-mediated death, non-random internucleosomal cleavage
36
3 pathological reasons for apoptosis
1. AIDS: HIV proteins manipulate CD4 cells to target uninfected T lymphocytes - leading to depletion of the immune system 2. Autoimmune diseases: failure to apoptose host-directing antibodies 3. Neoplasm
37
Some inducers of apoptosis
Withdrawal of growth factor and ECM, viral proteins, glucocorticoids, free radicals, ionizing radiation
38
Some inhibitors of apoptosis
GF, ECM, sex steroids and some viral proteins
39
What is the activation of caspases in apoptosis referred to?
cysteine dependent aspartate directed proteases
40
What is the extrinsic pathway of apoptosis modulated by
TNF DEATH RECEPTORS, activated by a ligand
41
What is the intrinsic pathway of apoptosis modulated by
removal of hormones and growth factors causing molecules to be released from the mitochondria, e.g; Bcl2, Bax, P53
42
Where do the two pathways of apoptosis converge and what does this do?
Caspase 3 which cleaves proteins, causing chromatin condensation, nuclear fragmentation and blebbing
43
What is the eventual fate of an apoptosed cell?
Eaten by macrophages, neighbouring cells or histiocytes
44
Compare and contrast apoptosis and necrosis | Pounds can never prove care and patience
P-pattern: A- single, N- contiguous group Cell size - A - shrinks, N- swells Nucleus - A- fragmentation into nucleosome sized fragments PM - A- stays intact but phospholipids get fucked, N - degraded Cellular contents - A-remain intact but released into apoptotic bodies, N - degraded Acute inflammation: A - no, N - yes Pathological or physiological: A - can be both, N - pathological
45
What can high levels of myoglobin be a sign of
Rhabdomyolysis - muscle fibres dying, presents as myoglobinuria and can progress into renal failure
46
What 3 things (in order of highest to lowest) would you test for in an MI
1. Troponin 2. Creatine Kinase 3. Myoglobin
47
Name 3 biochemical findings in cell death and injury
K+, myoglobin, enzymes
48
What is the biggest irreversible point in cell damage/injury
Large intracellular calcium concentration
49
Name 4 mechanisms for intracellular accumulations
1. deranged metabolic processes 2. deficiency in critical enzymes 3. dysfunctional protein transport/folding 4. inability to degrade phagocytose particles
50
Name 5 intracellular accumulations that can occur
1. pigments (exogenous and endogenous) 2. water and electrolytes: hydropic swell 3. proteins 4. carbohydrates 5. fat
51
Name 4 exogenous pigments
Tattoos, coal, soot, carbon
52
What are Mallory hyaline bodies and when would you see them?
Accumulation of damaged keratin filaments, in acute hepatitis (reversible)
53
Why do we need alpha 1 antitrypsin globules | What things are associated with a deficiency?
Excreted by the liver to protect organs (e.g the lungs) from neutrophil elastase which breaks down ECM and collagen. A deficiency is associated with increased microvascular damage and permeability (edema)
54
What is lipofuscin
Wear and tear old age pigment, and a sign of free radicals | Comprised of lipid-containing residues of lysosomal digestion
55
What is hemosiderin
Iron storage complex
56
What is hemosiderosis?
Iron overload resulting in too much hemosiderin
57
What is hereditary hemochromatosis
Absorbing too much iron from the diet
58
Why would you get a xanthelasma
Iron in the body overloads the transferrin system so it deposits under the skin, causing a local breakdown of blood vessels and tissues
59
Where does bilirubin accumulate? What can this cause
In the liver, jaundice and an ichterus eye (yellow looking eye)
60
Name 5 causes for a pathological calcification
1. Vit D overdose 2. Paget's disease: abnormal bone turnover 3. Parathyroid overactivity 4. Malignant tumours 5. Prolonged immobilization
61
What causes cellular ageing
Telomerase lengthens the telomeres, as you get older telomerase activity decreases and your telomere length shortens