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ESA 2 Brij > MOD Session 1 > Flashcards

MOD Session 1 Flashcards

1
Q

What is disease?

A

Consequence of failed homeostasis with consequent morphological and functional disturbances

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2
Q

What determines the degree of cellular injury?

A

1) Type of injury
2) Severity of injury
3) Type of tissue

More severe changes lead to cell adaptations, injury or death.

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3
Q

What is hypoxia?

A

Oxygen deprivation

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4
Q

What is hypoxaemic hypoxia and what are the consequences? Under what circumstances can this phenomenon happen?

A

Arterial oxygen content is low. Causes decreased ox phos and increases glycolysis (production of lactate). Can occur at high altitude due to decreased p02 and decreased absorption due to lung disease.

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5
Q

What is hypoxaemic hypoxia and what are the consequences? Under what circumstances can this phenomenon happen?

A

Decreased ability of Hb to carry oxygen. Caused by anaemia and CO poisoning.

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6
Q

What is ischaemic hypoxia and what are the consequences? Under what circumstances can this phenomenon happen?

A

Interruption to blood supply (more severe). This causes a reduced supply of oxygen and nutrients so cell injury occurs more rapidly. Caused by blockage of a vessel and heart failure.

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7
Q

What is histiocytic hypoxia and what are the consequences? Under what circumstances can this phenomenon happen?

A

Inability to utilise oxygen in cells due to disabled ox phos enzymes. e.g. Cyanide poisoning

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8
Q

List 8 examples of toxins that can cause cellular injury.

A 
Glucose and salt in hypertonic solutions
High [02]
Poisons
Alcohol
Drugs
Insecticides/Herbicides
Pollutants
Medicines
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9
Q

How do immune mechanisms cause cellular injury?

A

2 ways:

1) Hypersensitivity : host tissue is injured secondary to an overly vigorous immune reaction e.g. urticaria
2) Autoimmune reactions : immune system fails to distinguish self from non-self e.g. Grave’s

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10
Q

What physical agents can cause cell injury?

A

Direct trauma, extremes of temperature, electric currents, radiation

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11
Q

What micro-organisms can cause cell injury?

A

Viruses, bacteria, fungi, parasites

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12
Q

What two other ways can cause cell injury?

A

Dietary insufficiency/excess and genetic abnormalities.

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13
Q

What are the four principal targets for cell damage?

A

1) Cell membranes e.g. plasma and organelles (lysosomes)
2) Nuclues - DNA
3) Proteins - structural, enzymes
4) Mitochondria - Ox phos

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14
Q

Describe the pathogenesis of reversible hypoxia.

A

1) Cell becomes deprived of oxygen
2) Decreased production of ATP by ox phos
3) Loss of Na+/K+ pump
4) Na+ rises intracellularly which draws water in.
5) Oncosis (swelling of organelles)
6) Calcium influx causing damage
7) Decrease in pH and glycogen as lactate is produced (causes chromatin clumping)
8) Detachment of ribosomes (decrease in protein synthesis and increased fat deposition)

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15
Q

Describe the pathogensis of irreversible hypoxia.

A

1) Influx of Ca2+ due to increased membrane permeability
2) Ca2+ released from mitochondria and E.R increasing intracellular calcium
3) Causes acivation of ATPases, phospholipases, proteases and endonucleases.
4) Causes intracellular components to be damaged and degraded causing cell membrane damage and blebbing.

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16
Q

Describe the pathogenesis of ischemia-reperfusion injury.

A

If blood flow is returned to a damaged, but not yet necrotic tissue, damage sustained can be worse than if blood flow hadn’t returned.

May be due to:

1) Increased production of oxygen free radicals with reoxygenation
2) Increased neutrophil infiltrate resulting in more inflammation and increased tissue injury
3) Delivery of complement proteins and activation of the complement pathway.

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17
Q

What are the three free radicals that are of significance to cells?

A

1) Hydroxyl
2) Superoxide
3) Hydrogen peroxide

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18
Q

Under what circumstances are free radicals produced?

A

Produced in chemical and radiation injury, ischaemia-reperfusion injury, cellular aging, and at high oxygen concentrations.

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19
Q

Which two reactions produce hydroxyl radicals? What are two important substrates and importance of one of the reactions?

A

1) Fenton and Haber-Weiss reactions
2) The superoxide and hydrogen peroxide radicals are substrates causing more production of hydroxyl radicals.
3) Fenton reaction is important in bleeding as iron is freed and is a main substrate for the reaction

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20
Q

What pathological effects do free radicals have on cells?

A

1) Lipid peroxidation causing generation of more radicals
2) Attack proteins, carbs and DNA (these molecules can be bent out of shape, broken or crossed-linked and can be mutagenic.

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21
Q

What are the cellular defenses to free radicals?

A

1) Enzymes e.g. SOD, catalase
2) Free radical scavengers e.g. VIt A,C and E along with GSH.
3) Storage proteins e.g. transferrin and ceruloplasmin sequester iron and copper.

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22
Q

What do heat shock proteins do?

A

They respond to cell injury and are increased in their synthesis under stress. They aim to mend mis-folded proteins and maintain cell viability. Examples include chaperonins and ubiquitin.

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23
Q

Define oncosis.

A

Cell death with swelling, the spectrum of changes that occur prior to death in cells injured by hypoxia and some other agents.

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24
Q

Define necrosis.

A

In a living organism the morphologic changes that occur after a cell has been dead some time.

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25
Q

Define apoptosis

A

Cell death with shrinkage, cell death induced by a regulated intracellular program where a cell activates enzymes that degrade its own nuclear DNA and proteins.

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26
Q

What does the dye exclusion technique indicate and how?

A

Cell death. If the dye is absorbed a cell is dead as the membrane is leaky.

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27
Q

Under a light microscope what are the three main alterations seen when a cell undergoes oncosis and describe them.

A

1) Cytoplasmic changes - reduced pink staining of the cytoplasm due to accumulation of water (reversible change). This may be followed by increased pink staining due to detachment and loss of ribosomes from the endoplasmic reticulum and accumulation of denatured proteins (irreversible change).
2) Nuclear changes - chromatin is subtly clumped (reversible change). This may be followed by various combinations of pyknosis (shrinkage), karryohexis (fragmentation) and karryolysis (dissolution) of the nucleus (irreversible change).
3) Abnormal intracellular accumulations

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28
Q

Under an electron microscope what reversible changes can be identified when a cell undergoes oncosis?

A

1) Swelling – both of the cell and the organelles due to Na+/K+ pump failure
2) Cytoplasmic blebs, which are symptomatic of cell swelling
3) Clumped chromatin due to reduced pH
4) Ribosome separation from the endoplasmic reticulum due to failure of energy-dependant process of maintaining ribosomes in the correct location

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29
Q

Under an electron microscope what irreversible changes can be identified when a cell undergoes oncosis?

A

1) Increased cell swelling
2) Nuclear changes - pyknosis, karyolysis, or karyorrhexis
3) Swelling and rupture of lysosomes – reflects membrane damage
4) Membrane defects
5) The appearance of myelin figures (which are damaged membranes)
6) Lysis of the endoplasmic reticulum due to membrane defects
7) Amorphous densities in swollen mitochondria

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30
Q

What one feature differs oncosis/necrosis from apoptosis?

A

Apoptosis is ATP dependant

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31
Q

What are the two main types of necrosis?

A

1) Coagulative

2) Liquefactive

32
Q

Describe coagulative necrosis.

A

Denaturation of proteins dominates over release of active proteases. Cellular architecture is somewhat preserved “ghost outline”. Results in protein clumps. Intense pink staining along with karyolysis and neutrophil infiltrate.

33
Q

When does coagulative necrosis occur?

A

In ischaemia cell death e.g. MI

34
Q

Describe liquefactive necrosis.

A

Enzyme degradation is substantially greater than denaturation. Leads to enzymatic degradation of tissues. Massive neutrophil infiltrate,

35
Q

When and where is liquefactive necrosis seen?

A

Brain e.g. infarct. Bacterial infections. Tissue becomes viscous mass.

36
Q

What are the two special types of necrosis?

A

1) Caseous

2) Fat

37
Q

Describe caseous necrosis.

A

Contains amorphous (structureless) debris (no ghost outline).

38
Q

Where is caseous necrosis seen?

A

Associated with infections especially TB. Referred to as granulomatous.

39
Q

Describe fat necrosis and where it is seen. What does this cause?

A

Destruction of adipose tissue. Seen in acute pancreatitis from the release of lipases from acinar cells. Causes release of FFA which can react with calcium to form chalky deposits (calcium soaps).

Can also occur after direct trauma to fat tissue esp breast. After it heals, mimcs a nodule of breast cancer.

40
Q

Define gangrene.

A

Clinical term used to describe necrosis that is visible to the naked eye.

41
Q

What are the two subtypes of gangrene?

A

1) Dry

2) Wet

42
Q

Describe dry gangrene. What is the underlying process?

A

Necrosis that is modified by exposure to air. Drying occurs. Underying process is coagulative necrosis.

43
Q

Describe wet gangrene. What is the underlying process?

A

Infected tissue resulting in modification by bacterial infestation. Bacteria can get into the blood and cause septicaemia. Underlying process is liquefactive necrosis.

44
Q

What is gas gangrene? Describe a typical scenario.

A

Gas gangrene is wet gangrene where the tissue has become infected with anaerobic bacteria that produce visible and palpable bubbles of gas within the tissues. A typical scenario for gas gangrene is the crushing of a limb in a motorcycle accident. The injured tissue loses it blood supply and becomes necrotic resulting in the appearance of gangrene. The tissue is colonised by anaerobic bacteria picked up from the soil and gas gangrene develops.

45
Q

What is an infarction? What does it result in?

A

Cause of necrosis, namely ischaemia. It is an area of tissue death caused by the obstruction of a tissue’s blood supply (=ischaemic infarct). Results in gangrene.

46
Q

What are the most common way in which infarcts develop from? Occasionally from what else?

A

Thrombosis or embolism mainly.

Occasionally from external compression of a vessel e.g. tumour/hernia or twisted vessels e.g. volvulus of the bowel or testicular torsion.

47
Q

Describe a region that would have an infarct and undergo coagulative necrosis.

A

Myocardium e.g. MI

48
Q

Describe a region that would have an infarct and undergo liquefactive necrosis.

A

Brain e.g. cerebral infarction

49
Q

What does the colour of an infarct indicate?

A

Degree of haemorrhaging that has taken place.

50
Q

What is a white infarct?

A

A white (anaemic) infarct occurs in ‘solid’ organs (those with good stromal support) after occlusion of an “end” artery (i.e., any artery that is the sole source of arterial blood to a segment of an organ).

51
Q

What does the solid nature of the tissue limit?

A

The solid nature of the tissue limits the amount of haemorrhage that can occur into the infarct from adjacent capillaries.

52
Q

Why does the infarct appear white?

A

The tissue supplied by the end artery dies and appears pale/white because of a lack of blood in the tissue.

53
Q

Where do white infarcts usually occur. What shape do they appear to the eye and histologically?

A

White infarcts occur in the heart, spleen and kidneys. Most are wedge-shaped with the occluded artery at the apex of the wedge. Histologically white infarcts appear as coagulative necrosis

54
Q

What is a red infarct?

A

A red (haemorrhagic) infarct occurs where there is extensive haemorrhage into dead tissue.

55
Q

Under what circumstances does a red infarct occur?

A

Organs with a dual blood supply e.g. lung. (secondary artery allows blood to enter after main artery occlusion).
Venous insufficiency.
Numerous anastomoses e.g. intestine
Poor stromal support of capillaries e.g. lung
Previous congestion e.g. congestive heart failure
Raised venous pressure.

56
Q

What effects do infarcts have on tissues and what does it depend on?

A

1) None to death

2) Depends on:
- alternative blood supply
- speed of ischaemia
- tissue involved
- oxygen content of blood

57
Q

What do molecules released by injured/dying cells do?

A

1) Cause local inflammation
2) General toxic effects on body
3) Appear in high concentrations in blood and can aid in diagnosis.

58
Q

What is a potassium bomb? What does a high extracellular K+ concentration do to the heart? Where can K+ be released?

A

K+ is present in high concentrations in the cell. Heart stops with high [K+]. Can be released from MI or massive necrosis

59
Q

What can enzymes released from cells indicate?

A

Indicate organ involved, extent, timing and evolution of tissue damage.

60
Q

Where is myoglobin released from? What can occur if large amounts are released? Where can Mg release be seen?

A

Released from straited muscle and myocardium. Results in rhabdomyolysis which is a large amount of free Mg being released. Causes renal failure by blockage of renal tubules.

Seen in burns or trauma, strenuous exercise, potassium depletion

61
Q

What differs apoptosis from oncosis in relation to DNA breakdown.

A

Oncosis causes random degradation of DNA into random lengths.

Apoptosis is a non-random cleavage of internucleosomal DNA.

62
Q

Where can apoptosis be seen?

A

1) Physiological process
2) When cells are not needed
3) Tc killing
4) Embryogenesis
5) Disease

63
Q

Give 3 additional features of apoptosis.

A

1) Active process
2) Enzyme activation and degradation
3) Membrane integrity is maintained

64
Q

Describe the structural changes when a cell undergoes apoptosis.

A

1) Condensation of chromatin (pyknosis, karyorrhexis)
2) Fragmentation with budding
3) Apoptotic bodies

Intense pink staining, no inflammation as no leakage of cell contents

65
Q

What are the three phases of apoptosis?

A

1) Initiation
2) Execution
3) Degradation & Phagocytosis

66
Q

Describe the initiation and execution steps in apoptosis.

A

Either intrinsic (mitochondria, release of Cyt C, activates caspase-9) or extrinsic (receptor-mediated, external ligands e.g. TRAIL or Fas-L, caspase 8 activation)

Activated by DNA damage or loss of GFs

67
Q

Name the important molecules in apoptosis.

A

1) p53
2) Cyt , APAF 1, caspase 9 = apoptosome
3) Bcl-2 (inhibits cyt c release)
4) TRAIL, FAS
5) Caspases

68
Q

Why do molecules accumulate in cells?

A

Cell cannot metabolise the substance.

69
Q

What happens when fluid accumulates in cells? Why can this happen?

A

Appear as vacuoles or waterlogging of cell resulting in swelling by osmotic changes e.g. hydropic swelling.

Reduction in blood leading to Na+ and water influx. Bad for brain where this no space. Presses on foramen magnum.

70
Q

What happens when lipids accumulate in cells? Describe with examples of lipids.

A

TG accumulation - steatosis of liver

Cholesterol - accumulates in droplets in SMCs, marcophages&raquo_space;> atherosclerosis, (foam cells), hyperlipidaemias, tendon xanthoma, xanthelasma

PLs - form myelin figures in cells or tissue spaces

71
Q

What happens when proteins accumulate in cells?

A

Mallory’s hyaline - damaged protein in hepatocytes in ALD, accumulation of altered keratin filaments.

Alpha 1 ATD - liver produces incorrectly folded a1t protein which is stored in hepatocytes. Causes emphysema as proteases are not checked.

72
Q

What happens when exogenous pigments accumulate?

A

Soot/Air pollutants - ingested by macrophages and causes blackening of lung or LNs.

Tattoos- macrophages ingest pigment and remains there in the dermis.

73
Q

What happens when endogenous pigments accumulate?

A

Lipofuscin - brown pigment associated with wear and tear, sign of previous injury by FRs, seen in long lived cells e.g. neurones, myocardium, hepatocytes

Haemosiderin - iron storage molecule, deposited in organs (haemosiderosis) during tissue damage and iron release e.g. bleeding, anaemias, haemochromatosis, causes liver damage, pancreatic failure

Bilirubin - bile pigment, gallstones, cirrhosis, anaemia, jaundice, all cells can form bili.

74
Q

What is calcification?

A

Abnormal deposition of calcium salts.

75
Q

What are the two types of calcification?

A

1) Dystrophic

2) Metastatic

76
Q

Describe dystrophic calcification.

A

Localised calcification. More common.

Occurs in an area of dying tissue, in atherosclerotic plaques, in aging or damaged heart valves and in tuberculous lymph nodes. A local change or disturbance in the tissue favours the nucleation of hydroxyapatite crystals.

Normal calcium metabolism

77
Q

Describe metastatic calcification.

A

Systemic deposition of hydroxyapatite crystals when there is hypercalcaemia secondary to calcium metabolism disturbances.

ESA 2 Brij (47 decks)

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