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1 Flashcards

1
Q

What are the 6 causes of cell injury

A 
Hypoxia
Toxins
Trauma
Microorganisms
Immune mech (reacting to self antigens)
Nutritional imbalance (obesity / diabetes)
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2
Q

What are the 4 reversible changes of cell injury? (General)

A
  1. Reduced ox phosp
  2. Reduced ATP
  3. Swollen cell bc reduced ATP causes Na to accum in cell
  4. Reduced prot synthesis bc of ribosome detachment
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3
Q

What are the irreversible changes of cell injury? (General)

A
  1. Cytosolic Ca accum

2. Cell death bc several enzymes activated

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4
Q

What are the 5 reversible changes of cell injury? (Structural)

A
  1. Swelling
  2. Chromatin clumping
  3. Autophagy
  4. Ribosome detachment
  5. Blebs
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5
Q

What are the 4 irreversible changes of cell injury? (Structural)

A
  1. Nuclear changes
  2. Lysosome rupture
  3. ER lysis
  4. Memb defects
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6
Q

What are Heat Shock Proteins?

A

Proteins that protect cell from injury
Not just heat but any injury

Recognise incorrectly folded protein ➡️ repair it
If can’t repair it ➡️ protein degen

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7
Q

What happens to the cell size in Oncosis?

A

Swells

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8
Q

What happens in Oncosis?

A

Hypoxia

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9
Q

What happens to the nucleus in Oncosis?

A

Karyolysis

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10
Q

What happens to the cell size in Apoptosis?

A

Shrinks

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11
Q

What happens in Apoptosis?

A

Cell activates enzymes that degrade own nucleus, DNA, and proteins

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12
Q

What are 3 examples of Physiological Apoptosis?

A
  1. X webbing of hands in fetal dev.
  2. Endometrium shedding @ menstruation
  3. Death of cells that have served function e.g neut
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13
Q

What are 2 examples of Pathological Apoptosis?

A
  1. AI conditions

2. AIDS

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14
Q

What 6 things induce Apoptosis?

A
  1. GF withdrawal
  2. No matrix
  3. Glucocorticoids
  4. Viruses
  5. Free radicals
  6. Ionising radiation
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15
Q

What 3 things inhibit Apoptosis?

A
  1. GF
  2. ECM
  3. Sex steroids
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16
Q

What caspase is activated in both Apoptosis pathways?

A

Caspase 3

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17
Q

What does caspase 3 activation cause in apoptosis?

A

Prot cleaved ➡️ chromatin condensation, nuclear fragmentation, blebbing

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18
Q

What happens in the Extrinsic Apoptosis Pathway?

A

Ligand activates external death receptor

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19
Q

What happens in the Intrinsic Apoptosis Pathway?

A

GF / Hormones withdrawal
Molecules released from Mt
Phagocytosis

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20
Q

What is necrosis?

A

Morphological changes after cell death

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21
Q

What happens in Coagulative Necrosis?

A

Protein denaturation > enzyme release

Cell architecture preserved ➡️ ghost outline left

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22
Q

What causes Coagulative Necrosis?

A

Infarcts

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23
Q

What happens in Liquefactive Necrosis?

A

Enzyme release > Protein denat

Tissue lysed ➡️ disappears

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24
Q

What causes Liquefactive Necrosis?

A

Infection

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25
Q

What is Caseous Necrosis?

A

Amorphous tissues (no defined shape)
Halfway between Coag n Liq
Caseous Nec in lungs is TB

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26
Q

What is Fat Necrosis?

A

Adipose tissue cell death

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27
Q

What is Gangrene?

A

Grossly visible necrosis

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28
Q

What is Dry Gangrene?

A

Coag

29
Q

What is Wet Gangrene?

A

Liq

Infection ➡️ Neut ➡️ Proteolytic enzymes

30
Q

What is a white infarct? (+where?)

A

End artery blockage ➡️ no blood in area

Kidney

31
Q

What is a red infarct? (+where?)

A

Blood vessel blockage ➡️ blood build up ➡️ haemorrhage ➡️ increased pressure ➡️ reduced blood flow ➡️ ischaemia + infarct

Bowel

32
Q

Does Necrosis happen to a group of cells or just single cells?

A

Group

33
Q

What happens to cell size in Necrosis?

A

Swells

34
Q

What happens to the plasma memb in Necrosis?

A

Lysis

35
Q

What happens to the cellular contents in Necrosis?

A

Enzyme digestion

36
Q

Is there adjacent inflamm in Necrosis?

A

Yes

37
Q

Does Apoptosis happen to a group of cells or just single cells?

A

Single cells

38
Q

What happens to cell size in apoptosis?

A

Shrinks

39
Q

What happens to the plasma memb in apoptosis?

A

Altered structure

40
Q

What happens to the cellular contents in apoptosis?

A

Released in apoptotic bodies

41
Q

Is there adjacent inflamm in apoptosis?

A

No

42
Q

What 3 molecules are releases as a result of Cell Death / Injury?

A

K
Enzymes
Myoglobin

43
Q

Whats the role of p53 in apoptosis?

A

It induces apoptosis @ DNA damage

44
Q

What 3 molecules make up the apoptosome?

A
  1. Cytochome C
  2. APAF1
  3. Caspase 9
45
Q

Whats the role of Bcl2 in apoptosis?

A

Prevents apoptosis by preventing cytochome C release from Mt

46
Q

What are caspases?

A

Effector molecules of apoptosis

47
Q

What happens when there is abn water accum in cells?

A

Cells enlarged
Cellular distress

If brain swells, vessels squeezed against skull ➡️ reduced brain blood flow

48
Q

What is steatosis?

A

Abn triglyceride accum in liver

49
Q

What causes steatosis?

A

Alcohol / diabetes

50
Q

What can steatosis cause?

A

Big greasy liver

51
Q

What happens when there is an abn cholesterol accum in cells?

A

Chol is insoluble and only removed thru liver
Excess chol stored in memb bound droplets
These droplets accum in SMC / MAC ➡️ Foam Cells

52
Q

Where does abn phospholipid accum come from?

A

Disrupted cell memb

53
Q

What does abn accum of phospholipids in cells cause?

A

Myelin figures in cell / tissue spaces

54
Q

What is Mallorys Hyaline?

A

Accum of damaged protein in hepatocytes

Accum of altered keratin filaments

55
Q

What causes Mallorys Hyaline

A

Alcohol liver disease

56
Q

What is alpha1-antitrypsin deficiency?

A

Liver prod incorrectly folded alpha1-antitrypsin
This isn’t packages by ER so accum in liver

Deficiency causes increase in lung proteases
This causes emphysema (lung tissue broken down)

57
Q

What happens when there is abn pigment accum in cells?

A

Discolour lung tissue
Can cause emphysema (lung tissue broken down)

E.g of exogenous pigments: C / soot

58
Q

What is Pathological Calcification and what are the 2 types?

A

Abn deposition of Ca in tissues

  1. Dystrophic (more common) (occurs in DYing tissue)
  2. Metastatic (body wide disturbance) (asymptomatic but can be lethal)
59
Q

What is replicative senescence?

A

When cells lose the ability to replicate due to cellular ageing

60
Q

How do cells reach replicative senescence?

A

End of cells called telomeres

@ every replication telomere shortened until it reaches critical length ➡️ X divide

61
Q

What are 3 effects on the liver from chronic excessive alcohol intake?

A
  1. Fatty change
  2. Acute alcohol hepatitis
  3. Cirrhosis
62
Q

Describe fatty change in the liver

A

Steatosis

Asymptomatic

63
Q

What causes Acute Alcohol Hepatitis?

A

Binge drinking

64
Q

What are the symptoms of Acute Alcohol Hepatitis?

A

Fever / Liver tenderness / Jaundice

65
Q

What happens in the liver @ Acute Alcohol Hepatitis?

A

Necrosis ➡️ Mallorys Hyaline formation

66
Q

Is Acute Alcohol Hepatitis reversible?

A

Yes

67
Q

What happens in Cirrhosis?

A

Shrunken hard liver

Irreversible + Fatal

68
Q

What is the histology of cirrhosis?

A

Micronodules of regen hepatocytes surrounded by bands of collagen

MOD (9 decks)

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