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Pathological Processes > S1) Cell Injury > Flashcards

S1) Cell Injury Flashcards

1
Q

What are the 4 stages of response to cell injury?

A

Homeostasis, cellular adaption, cellular injury, cell death

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2
Q

Causes of cell injury (5)

A
  • Hypoxia/ ischaemia
  • Toxins
  • Physical agents eg direct trauma, extremes of temperature, changes in pressure and electric currents
  • Radiation
  • Micro-organisms
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3
Q

Name and describe the 4 types of hypoxia

A

1) Hypoxaemic hypoxia: arterial content of O2 is low
- Altitude and lung disease malabsorption

2) Anaemic hypoxia: decreased ability of haemoglobin to carry oxygen
- anaemia and CO poising

3) Ischaemic hypoxia: interruption to blood supply

4) Histiocytic hypoxia: inability to utilise oxygen
- Cyanide poisoning

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4
Q

Reversible hypoxia: What is the primary effect?

A

Decrease in oxidative phosphorylation, so decrease in ATP levels

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5
Q

What is the effect of decreased ATP levels? (3)

A

1) NaK ATPase
2) Increase in glycolysis
3) Detachment of ribosomes from RER

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6
Q

How does reduction of NaK ATPase activity effect the cell?

A

Cell swelling

ER swelling

Blebs

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7
Q

How does an increase in glycolysis affect the cell?

A

Lowered pH - chromatin clumps

Lowered glycogen

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8
Q

How does the detachment of ribosomes affect the cell?

A

Decreased protein synthesis, causing lipid deposition

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9
Q

What is the primary effect of irreversible hypoxia?

A

Increase in intracellular calcium (from mitochondria and ER)

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10
Q

What is the affect of increased intracellular calcium? (4)

A

Activation of 4 enzymes

  • ATPase (decreased ATP)
  • Phospholipase (decreased phospholipids)
  • Protease (disruption to membrane and cytoskeletal proteins)
  • Endonuclease (nuclear chromatin damage)
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11
Q

How does the immune system cause damage to cells? (2)

A

Hypersensitivity reactions

Autoimmune reactions

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12
Q

3 types of free radical

A

Hydrogen peroxide

Superoxide

Hydroxyl

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13
Q

How are free radicals produced? (5)

A

Oxidative phosphorylation

Inflammation

Radiation

Unbound metals in the body

Drugs and chemicals

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14
Q

How are free radicals suppressed? (3)

A
  • Anti-oxidant scavengers - vitamins A, C and E and glutathione
  • Metal carrier and storage proteins (transferrin for iron and ceruloplasmin for copper)
  • Enzymes which neutralise free radicals
    • Catalase converts hydrogen peroxide to water and oxygen
    • Superoxide dismutase turns superoxide to hydrogen peroxide
    • Glutathione peroxidase
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15
Q

What do free radicals do in the body? (3)

A

Oxidative imbalance:

1) Lipid peroxidation - creates even more free radicals by autocatalysis
2) Oxidised proteins, carbs and DNA, changing their conformation
3) Mutagenic and carcinogenic

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16
Q

How do cells protect themselves?

A

Heat shock proteins - these mend misfolded proteins

Unfoldases and chaperonins eg ubiquitin

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17
Q

Which 4 sites are most susceptible to injury?

A

Cell membranes, nucleus, proteins and mitochondria

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18
Q

How does the cell look during reversible injury?

A

Blebs

Clumping of chromatin

Autophagy by lysosomes

ER/ mitochondrial swelling

Dispersion of ribosomes

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19
Q

How does the cell look during irreversible injury?

A

Rupture of lysosomes and autolysis

Myelin figures / defects in cell membrane

Lysis of ER

Nuclear pyknosis (dark) or karyolysis (clear) or karyorrhexis (fragmented)

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20
Q

What is oncosis?

A

Cell death with swelling

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21
Q

What is necrosis?

A

The changes that occur after a cell has been dead for some time

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22
Q

What are the 4 types of necrosis?

A

Coagulative
Liquefactive (colliquitive)
Caseous
Fat necrosis

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23
Q

Coagulative necrosis:

Where does it occur?

What does it do?

What does it look like?

A

Ischaemia of solid organs eg the heart

Denaturation of proteins

White - cell architecture maintained (ghost cells)

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24
Q

Liquefactive necrosis:

Where does it occur?

What does it do?

What does it look like?

A

Ischaemia of loose tissues eg brain

Enzyme activation

Red - cell debris remains - lots of neutrophils

25
Q

Caseous necrosis:

Why does it occur?

What does it look like?

A

Infection eg TB

Cheese like appearance - structureless debris

26
Q

3 types of gangrene + types of necrosis which accompany them

A

Dry - modified by exposure to air - coag necrosis

Wet - modified by infection - liquefactive

Gas - wet gangrene with anaerobic bacteria which produce gas

27
Q

How can infarction be caused?

A

Thrombosis (clot)

Embolism (moving clot)

Hernia and twisting of vessels

28
Q

What causes white infarcts?

A

Occlusion of end arteries

29
Q

Where do red infarcts occur and why are they red?

A

They occur in loose tissue

Red because dual blood supply and raised venous pressure cause reperfusion

30
Q

Why is reperfusion after ischaemia sometimes more harmful? (3)

A

More oxygen free radicals

More neutrophils

Complement proteins activate complement pathway

31
Q

How does DNA breakdown in apoptosis differ to oncosis?

A

Apoptosis - controlled degradation

Oncosis - DNA is chopped randomly

32
Q

When does physiological apoptosis occur? (3)

A

Maintaining a steady state

Hormone controlled involution

Embryogenesis

33
Q

When does pathological apoptosis occur? (3)

A

Cytotoxic T cell killing of virus infected/neoplastic cells

Damaged cells (especially DNA defects)

Treatment of leukaemias

34
Q

Describe intrinsic intiation

A

Signal comes from within the cell

Triggered by 1) Irreparable DNA damage 2) Withdrawal of growth factors or hormones

P53 activated - makes outer mitochondrial membrane leaky

Cytochrome C released - activates caspases

35
Q

Describe extrinsic initation

A

Triggered by tumour / virus infected cells

TNFa released by cytotoxic cells - binds to cell surface activating caspases

36
Q

Budding or blebbing?

A

Apoptosis - budding

Necrosis - blebbing

37
Q

How does the nucleus differ in apoptosis / necrosis?

A

Apoptosis - cut into nucleosome sized fragments

Necrosis - pkynosis (shrinkage), karyolysis (fading) or karyorrhexis (fragmentation)

38
Q

Name 4 cell accumulations

A

Water - common with ischaemia

Lipids

Proteins

Pigments

39
Q

What is the name given to accumulation of triglycerides?

A

Steatosis

40
Q

What causes steatosis?

A

Alcohol, diabetes, obesity, toxins eg CCl4

Mainly in liver

41
Q

Why is cholesterol accumulation damaging?

Where can cholesterol be eliminated from?

A

Accumulates in smooth muscle and macrophages forming foam cells

The liver

42
Q

Where is cholesterol present in people with hereditary hyperlipidaemias and what does this cause?

A

Macrophages in skin and tendons

Causes xanthomas

43
Q

What does alcoholic liver disease cause?

A

Mallory’s hyaline (damaged keratin filaments)

44
Q

What cells remove carbon/soot and what can this cause in large quantities?

A

Alveolar macrophages

Fibrosis and emphysema

45
Q

What is haemosiderin/ when is it formed?

What causes haemosiderosis?

A

An iron storage molecule formed during systemic or local overload of iron eg in a bruise

Deposition of haemosiderin into organs

46
Q

What causes hereditary haemochromatosis and what does it cause?

How is it treated?

A

Increased intestinal absorption of iron - deposited into skin, liver, pancreas, heart and endocrine organs - causes liver cirrhosis and pancreatic scarring

Repeated bleeding

47
Q

What causes jaundice?

A

Accumulation of bilirubin

48
Q

How is bilirubin formed?

How is it carried to the liver?

How is it excreted?

A

Breakdown product of heme

Albumin

Bile

49
Q

Where does dystrophic calcification occur?

A

Areas of dying tissue

Tuberculous lymph nodes

50
Q

Causes of hypercalcaemia (2)

A
  • Increased PTH secretion causing bone resorption

- Destruction of bone tissue

51
Q

Describe the three types of increased PTH secretion

A

Primary - parathyroid hyperplasia / tumour

Secondary - renal failure and retention of phosphate

Ectopic - secretion of PTH related protein by malignant tumours

52
Q

What causes destruction of bone tissue? (4)

A

Primary tumours of bone marrow

Diffuse skeletal metastasis

Paget’s disease - accelerated bone turnover

Immobilisation

53
Q

What controls replicative senescence?

A

Length of telomeres

54
Q

How do cells respond to the heat shock response?

A

Decrease usual protein synthesis

Increase synthesis of HSPs

55
Q

Fat necrosis:

What occurs?

How does it appear?

Where does it occur?

A

Lipase releases fatty acids which complex with calcium to form soaps

Soaps appear as white chalky deposits

Pancreas, breast and salivary glands

56
Q

Differences between apoptosis and necrosis:

Number of cells?

Membrane integrity?

A

Apoptosis - single cells, membrane intact

Necrosis - group of cells, membrane lysed early

57
Q

Clinical signs of chronic hepatitis (5)

A

Raised ALT, AST and LDH

Raised bilirubin

Decreased albumin

Raised PT (prothrombin)

Raised ammonia

58
Q

Clinical signs of alcoholic liver disease (3)

A

Raised bilirubin

Raised alkaline phosphatase

Raised gamma GT

59
Q

Clinical signs of acute pancreatitis? (4)

A

Raised serum amylase within 24 hours

Raised serum lipase from 72-96 hours

Glycosuria

Possible hypocalcaemia

Pathological Processes (5 decks)

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