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J Term 2 mix > MOD1 > Flashcards

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
Q

Characteristics of fat necrosis and what can it mimic?

A

Adipocyte damage due to…
1. lipases released from damaged pancreatic tissue
2. trauma
A breast tumour as it’s seen in breast tissue

26
Q

Characteristics of fibrinoid necrosis?

What would you see histologically

A

Associated with blood vessels and immune reactions

Fibrinoid - bright pink and amorphous fibrin and immune complexes that have leaked out of vessels

27
Q

4 Aetiology’s of infarction

A
  1. thrombosis
  2. embolism
  3. compression of vessels
  4. twisting of blood supply
28
Q

3 characteristics of a white infarct plus 3 vulnerable organs

A
  • organs with a strong stroma
  • single blood supply
  • arterial insufficiency

spleen, kidney and heart

29
Q

3 characteristics of a red infarct plus 3 vulnerable organs

A

-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
Q

What causes wet gangrene

A

necrosis modified by bacteria

31
Q

What types of necrosis can infarction be?

A

Coagulative and liquefactive

32
Q

What causes air gangrene

A

necrosis modified by air

33
Q

What causes gas gangrene

A

necrosis modified by gas-forming/anaerobic bacteria

34
Q

4 Physiological reasons for apoptosis

A
  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
Q

How does apoptosis occur?

A

Energy-dependent cell-mediated death, non-random internucleosomal cleavage

36
Q

3 pathological reasons for apoptosis

A
  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
Q

Some inducers of apoptosis

A

Withdrawal of growth factor and ECM, viral proteins, glucocorticoids, free radicals, ionizing radiation

38
Q

Some inhibitors of apoptosis

A

GF, ECM, sex steroids and some viral proteins

39
Q

What is the activation of caspases in apoptosis referred to?

A

cysteine dependent aspartate directed proteases

40
Q

What is the extrinsic pathway of apoptosis modulated by

A

TNF DEATH RECEPTORS, activated by a ligand

41
Q

What is the intrinsic pathway of apoptosis modulated by

A

removal of hormones and growth factors causing molecules to be released from the mitochondria, e.g; Bcl2, Bax, P53

42
Q

Where do the two pathways of apoptosis converge and what does this do?

A

Caspase 3 which cleaves proteins, causing chromatin condensation, nuclear fragmentation and blebbing

43
Q

What is the eventual fate of an apoptosed cell?

A

Eaten by macrophages, neighbouring cells or histiocytes

44
Q

Compare and contrast apoptosis and necrosis

Pounds can never prove care and patience

A

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
Q

What can high levels of myoglobin be a sign of

A

Rhabdomyolysis - muscle fibres dying, presents as myoglobinuria and can progress into renal failure

46
Q

What 3 things (in order of highest to lowest) would you test for in an MI

A
  1. Troponin
  2. Creatine Kinase
  3. Myoglobin
47
Q

Name 3 biochemical findings in cell death and injury

A

K+, myoglobin, enzymes

48
Q

What is the biggest irreversible point in cell damage/injury

A

Large intracellular calcium concentration

49
Q

Name 4 mechanisms for intracellular accumulations

A
  1. deranged metabolic processes
  2. deficiency in critical enzymes
  3. dysfunctional protein transport/folding
  4. inability to degrade phagocytose particles
50
Q

Name 5 intracellular accumulations that can occur

A
  1. pigments (exogenous and endogenous)
  2. water and electrolytes: hydropic swell
  3. proteins
  4. carbohydrates
  5. fat
51
Q

Name 4 exogenous pigments

A

Tattoos, coal, soot, carbon

52
Q

What are Mallory hyaline bodies and when would you see them?

A

Accumulation of damaged keratin filaments, in acute hepatitis (reversible)

53
Q

Why do we need alpha 1 antitrypsin globules

What things are associated with a deficiency?

A

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
Q

What is lipofuscin

A

Wear and tear old age pigment, and a sign of free radicals

Comprised of lipid-containing residues of lysosomal digestion

55
Q

What is hemosiderin

A

Iron storage complex

56
Q

What is hemosiderosis?

A

Iron overload resulting in too much hemosiderin

57
Q

What is hereditary hemochromatosis

A

Absorbing too much iron from the diet

58
Q

Why would you get a xanthelasma

A

Iron in the body overloads the transferrin system so it deposits under the skin, causing a local breakdown of blood vessels and tissues

59
Q

Where does bilirubin accumulate? What can this cause

A

In the liver, jaundice and an ichterus eye (yellow looking eye)

60
Q

Name 5 causes for a pathological calcification

A
  1. Vit D overdose
  2. Paget’s disease: abnormal bone turnover
  3. Parathyroid overactivity
  4. Malignant tumours
  5. Prolonged immobilization
61
Q

What causes cellular ageing

A

Telomerase lengthens the telomeres, as you get older telomerase activity decreases and your telomere length shortens

J Term 2 mix (8 decks)

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