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Bethany's Phase 2A > Introduction to Clinical Sciences > Flashcards

Introduction to Clinical Sciences Flashcards

1
Q

Define inflammation.

A

A reaction to injury or infection involving cells such as neutrophils and macrophages. Textbook: Initial reaction of tissue to injury.

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2
Q

Benefit of inflammation?

A

In infection and injury.

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3
Q

Disadvantages of inflammation?

A

Autoimmunity.

When it’s an over-reaction to the stimulus.

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4
Q

Define acute inflammation.

A

Sudden onset. Short duration. Usually resolves. (Involves neutrophil polymorphs)

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5
Q

Define chronic inflammation.

A

Slow onset or after acute. Long duration. May never resolve. (Involves lymphocytes and macrophages)

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6
Q

What cells are involved in inflammation?

A 
Neutrophils polymorphs.
Macrophages.
Lymphocytes.
Endothelial cells.
Fibroblasts.
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7
Q

What is the neutrophil polymorphs role in inflammation?

A
  1. Margination (central flow to peripheral)
  2. Pavementing (adhesion to endothelial cells)
  3. Pass between endothelial cells
  4. Pass through basal lamina and migrate into adventitia
  5. Engulf bacteria in vacuole.
  6. Lysosomes fuse with the vacuole and enzymes digest bacteria.
  7. Bacteria debris released.
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8
Q

What are the 2 components of acute inflammation?

A

Vascular component: dilation of vessels.

Exudative component: vascular leakage of protein-rich fluid.

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9
Q

Causes of acute inflammation?

A
  1. Microbial infections.
  2. Hypersensitivity reactions.
  3. Physical agents
  4. Chemicals
  5. Tissue necrosis
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10
Q

What are the 5 macroscopic appearances of acute inflammation?

A 
Redness (rubor)
Heat (calor)
Swelling (tumor)
Pain (dolor)
Loss of function
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11
Q

What’s the main cell in acute inflammation?

A

Neutrophil polymorph.

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12
Q

Role and life span of a macrophage in inflammation.

A 
Long lived cells (weeks to months).
Phagocytic properties.
Ingest bacteria and debris.
May carry debris away.
May present antigen to lymphocytes.
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13
Q

Role and life span of lymphocytes in inflammation.

A

Long lived cells (years). Produce chemicals which attract in other inflammatory cells.
Immunological memory for past infections and antigens.

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14
Q

Role of endothelial cells in inflammation.

A

Line capillary blood vessels in areas of inflammation. Become sticky in areas of inflammation so inflammatory cells adhere to them.
Become porous to allow inflammatory cells to pass into tissues.
Grow into areas of damage to form new capillary vessels.

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15
Q

Role and life span of fibroblasts in inflammation.

A

Long lived cells. Form collagen in areas of chronic inflammation and repair.

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16
Q

Example of acute inflammation.

A

Acute appendicitis:

Neutrophils, blood vessels dilate, inflammation of serosal surface, pain felt. Bursts/removed/ inflammation resolved.

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17
Q

Outcomes of acute inflammation?

A
  1. Resolution
  2. Suppuration (pus formed)
  3. Chronic inflammation
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18
Q

Example of chronic inflammation.

A

Tuberculosis:

No initial acute inflammation, mycobacteria ingested by macrophages, macrophages often fail to kill it, fibrosis occurs.

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19
Q

What are granulomas?

A

Particular sort of chronic inflammation. Group of (pale-ish) macrophages surrounded by lympocytes. Can point towards a cause of inflammation.

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20
Q

Which deaths are referred to the coroner?

A
  1. Presumed natural - unknown cause of death or has a chronic illness & not seen dr in last 14 days.
  2. Presumed iatrogenic - peri/postopertive/anaesthetic death, abortion, therapy complications.
  3. Presumed unnatural - accident, industrial, suicide, unlawful killing, neglect etc.
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21
Q

What is some legislation relevant to coronial autopsy practice?

A

Human Tissue Act 2004.

Family has more input in what happens to the ‘retained’ material.

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22
Q

Roles of the coronial autopsy?

A
  1. Who was the deceased?
  2. When did they die?
  3. Where did they die?
  4. How did they come about their death? (not why!)
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23
Q

Components of the autopsy?

A
  1. History/scene
  2. External examination -identification, injuries etc.
  3. Evisceration (or digital/CT examination instead) - Y-shaped incision.
  4. Internal examination
  5. Reconstruction
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24
Q

2 types of autopsy?

A 
Hospital = < 10% of all autopsies in the UK.
Medico-legal = >90%
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25
Q

What is resolution/healing/regeneration?

A

Initiating factor removed.

The tissue is undamaged or able to regenerate.

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26
Q

What is repair?

A

Initiating factor still present.
Tissue is damaged and UNABLE to regenerate. Replacement of damaged tissue by fibrous tissue, collagen produced by fibroblasts. (Fibrous scar formed)

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27
Q

Does the liver regenerate or repair?

A

Both. It can regenerate hepatocytes. However, repair takes place instead of regeneration if there is a lot of constant damage and the architecture is changed. = cirrhosis.

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28
Q

Does regeneration or repair occur in lobar pneumonia?

A

Regeneration. Pneumocytes can regenerate (cells that line alveoli) as long as you don’t damage structure of alveoli. (Lobar pneumonia = alveoli filled with neutrophil polymorphs instead of air due to bacteria).

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29
Q

What is the ideal: regeneration or repair?

A

Regeneration.

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30
Q

What are the 3 types of skin wounds?

A
  1. Abrasion
  2. Healing by 1st intention
  3. Healing by 2nd intention
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31
Q

Characteristics of an abrasive skin wound?

A
  1. Epidermis lost.
  2. Scab forms.
  3. Epidermis growing out from adnexa (from cut off gland necks),protected by scab.
  4. Epidermis grows back + scab falls off.
32
Q

What do fibroblasts produce?

A

Collagen (and extracellular matrix).

33
Q

Characteristics of healing by 1st intention?

A
  1. Cut goes right through skin, very little damage.
  2. Exudation of fibrinogen = weak fibrin join.
  3. Epidermal regrowth + collagen synthesis = strong collagen join.
  4. Small scar.
34
Q

Characteristics of healing by 2nd intention?

A
  1. Tissue is lost (edges of skin can’t be pulled together).
  2. Granulation tissue grows
  3. Organisation
  4. Early fibrous scar
  5. Scar contraction
35
Q

What is granulation tissue made of?

A

Capillary loops proliferate and arch into damaged areas. Supported by myofibroblasts (Fibroblasts acquire muscle filament bundles).

36
Q

What is granulation tissue an example of?

A

It’s a repair phenomenon.

37
Q

How does a scar contract?

A

Due to the presence of myofibroblasts. They pull the scar together.

38
Q

What is a scar?

A

Collagenous/fibrous REPAIR (not regeneration).

39
Q

What cell types can regenerate?

A

Hepatocytes. Pneumocytes. All blood cells. Gut epithelium. Skin epithelium. Osteocytes.

40
Q

What cell types can’t regenerate?

A

Myocardial cells. Neurons.

41
Q

What is the classification of cells according to their renewal potential?

A 
Labile = good.
Stable = slow.
Permanent = none.
42
Q

Define thrombosis.

A

Solid mass of blood constituents formed within an intact vascular system during life.

43
Q

What are the predisposing factors to thrombosis?

A 
Virchow's triangle.
Changes to:
-Vessel wall
-Blood flow
-Blood constituents
44
Q

What is an arterial thrombosis most commonly superimposed on?

A

Atheroma.

45
Q

What is venous thrombosis most commonly caused by?

A

Stasis (no/little blood movement)

46
Q

What should a thrombosis not be confused with?

A

A clot. Clots are due to damage to the vessel wall.

47
Q

Describe the formation of an arterial thrombus.

A
  1. Atheroma plaque present.
  2. Plaque grows + creates turbulent blood flow.
  3. Causes damage to endothelial cells - collagen exposed.
  4. Turbulence predisposes to fibrin deposition + platelet aggregation.
  5. Platelets bind to collagen.
  6. Platelets release chemicals + granules.
  7. Positive feedback. Activation + adhesion.
  8. Thrombus formed = alternating layers of platelets, fibrin and RBC.
48
Q

Describe normal blood flow in vessels.

A

Laminar. Cells flow in the centre (axial). Plasma flows along the periphery.

49
Q

What are alternating bands of white platelets and red blood cells in thrombi called?

A

Lines of Zahn.

50
Q

Describe the formation of venous thrombosis.

A
  1. Lower pressure than arteries, blood flow slower.
  2. Turbulence at valves.
  3. Causes damage to endothelial cells - collagen exposed.
  4. Turbulence predisposes to fibrin deposition + platelet aggregation.
  5. Platelets bind to collagen.
  6. Platelets release chemicals + granules.
  7. Positive feedback. Activation + adhesion.
  8. Thrombus formed = alternating layers of platelets, fibrin and RBC.
51
Q

Example of venous thrombosis?

A

95% of venous thrombosis occurs in deep leg vein thrombosis. Immobilised elderly patients are at risk (potential for blood stasis).

52
Q

What are the potential consequences/end results of thrombosis?

A
  1. Lysis and resolution.
  2. Organisation = scar tissue.
  3. Recanalisation = restore blood flow.
  4. Embolism = fragmentation of thrombus.
53
Q

Define embolism.

A

A mass of material in the vascular system able to become lodged within a vessel and block its lumen.

54
Q

What are most emboli derived from?

A

Thrombi.

55
Q

What can emboli be derived from?

A

Thrombi. Atheromatous plaque material. Tumour fragments. Amniotic fluid. Gas. Fat. Vegetations on heart valves (infection).

56
Q

What is pulmonary embolism?

A

An emboli getting lodged in a pulmonary vessel in the lung. Can arise from venous thrombosis. The lungs act as a filter for any venous emboli.

57
Q

What is systemic embolism?

A

Usually arise from thrombi formed in the heart or on an atheroma.

58
Q

Why can thrombi form in the heart after myocardial infarction?

A

Dead myocardium will be adynamic and disrupt normal blood flow within the heart = turbulence.

59
Q

Name 5 origins of systemic arterial emboli.

A
  1. Atheroma with thrombus.
  2. Atrial thrombus.
  3. Valve vegetation.
  4. Thrombus - old myocardial infarct (adynamic).
  5. Thrombus - recent myocardial infarct.
60
Q

What is embolic atheroma?

A

Fragments of atheroma embolising.

61
Q

What is platelet emboli?

A

Fragments of platelet deposition embolsing (very tiny, usually only significant in the brain).

62
Q

What is infective emboli?

A

Vegetations on the heart valves. Microorganisms can cause extremely friable (easily crumbled) vegetations.

63
Q

What is fat embolism?

A

Arises following fracture to long bones, extensive soft tissue injury or severe burns. fat is released.

64
Q

What is gas embolism?

A

Caisson disease experienced by divers = nitrogen bubbles appear in blood after rapid decompression from high pressure.
Or surgical - vessel open to air.

65
Q

What is repurfusion injury?

A
  1. Blood flow reenters after ischaemia.

2. Mechanisms that were once disrupted, trigger activation of oxygen-dependent free radical systems.

66
Q

Define infarction.

A

Reduced blood flow with subsequent tissue death (necrosis).

67
Q

What do infarctions cause?

A

An inflammatory reaction.

68
Q

What is the name of an infarction of mixed tissues in bulk?

A

Gangrene.

69
Q

Why don’t blood clots form all the time?

A
  1. Laminar flow - cells travel in the centre of arterial vessels and don’t touch the sides.
  2. Endothelial cells which line vessels are not ‘sticky’ when healthy.
70
Q

Define iscahemia.

A

Reduced blood flow to a tissue.

71
Q

What 3 organs are less susceptible to infarction and why?

A

Dual blood supply.

  1. Liver = portal venous + hepatic artery.
  2. Lung = pulmonary venous + bronchial artery.
  3. Brain = circle of Willis
72
Q

What tissues are vulnerable to infarction?

A
  1. Watershed areas.
  2. If perfused by portal vasculature.
  3. If distal to pathological arterial stenoses.
  4. Metabolically active tissues.
73
Q

What is a watershed area in relation to infarction?

A

Tissue situated precariously on the fringes of 2 arteries adjacent territories, with no collateral circulation to provide blood from alternative vessels. e.g. splenic flexure. If BP drops then an infarct can occur, not necessarily from a single blocked artery.

74
Q

What is portal vasculature?

A

Tissues perfused by blood that has already passed through one set of capillaries. e.g. anterior pituitary (via hypothalamus), renal tubular epithelium.

75
Q

What is ‘end artery supply’?

A

Only one blood supply to a particular tissue. If there’s a blockage, tissue will die.

Bethany's Phase 2A (1 decks)

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