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Phase 2 > Pathology 2 > Flashcards

Pathology 2 Flashcards

1
Q

Define Acute Inflammation

A

Initial, transient series of tissue reactions to injury
Lasts hours to days

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2
Q

Example of acute inflammation

A

Appendicitis

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3
Q

State 2 benefits of inflammation

A

Destroys invading microorganisms
Walls off abscess cavity ∴ prevents spread of infection

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4
Q

State 2 disadvantages of inflammation

A

Fibrosis can distort tissue and alter function
Abscess (e.g. in brain) can act as space-occupying lesion ∴ compressing surrounding structures

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5
Q

List some examples of acute inflammation

A

Microbial infections (e.g. bacteria, viruses)

Hypersensitivity reactions (e.g. parasites)

Physical agents (e.g. trauma)

Chemicals (e.g. corrosives)

Bacterial toxins

Tissue necrosis (e.g. ischaemic infarction)

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6
Q

Describe the steps of acute inflammation

A
  1. Vascular changes - vasodilation! ∴ ↑ vessel flow
  2. ↑ Vessel permeability ∴ formation of fluid exudate
  3. Formation of cellular exudate - neutrophil polymorphs emigrate into extravascular space
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7
Q

What are the potential outcomes of acute inflammation?

A
  1. Resolution
  2. Suppuration - pus formation
  3. Organisation - healing via fibrosis
  4. Progression to chronic inflammation
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8
Q

5 Cardinal signs of inflammation

A
  1. Rubor (redness)
  2. Calor (heat)
  3. Tumor (swelling)
  4. Dolor (pain)
  5. Functio laesa (loss of function)
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9
Q

Rubor is due to

A

dilation of capillaries within damaged area

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10
Q

Calor is due to

A

Increased blood flow to damaged region

Results in vascular dilation
∴ more warm blood to region

Also, maybe systemic fever

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11
Q

Tumor is due to

A

Oedema!
(fluid accumulates in extravascular space)

+ formation of new connective tissue

Also, maybe mass of inflammatory cells migrating into region

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12
Q

Dolor is due to

A

Stretching of tissue due to inflammatory odema
+ pus under pressure in abscess cavity

Also, chemical mediators of acute inflammation are known to cause pain
e.g. bradykinin, prostaglandins, serotonin

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13
Q

Functio laesa (loss of function) due to

A

Conscious and reflexly inhibited by pain
+ severe swelling may immobilise tissue

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14
Q

What cellular component is essential for a histological diagnosis of acute inflammation?

A

ACCUMULATION of neutrophil polymorphs

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15
Q

How does organisation (healing by fibrosis) work in acute inflammation?

A

Dead tissue and inflammatory exudate first removed from damaged areas BY MACROPHAGES

Defect is then filled by specialised vascular connective tissue (aka GRANULATION TISSUE) - this is organisation

Then granulation tissue gradually produces collagen to form fibrous scar

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16
Q

How do microbial infections cause acute inflammation?

A

VIRUSES - cause death of cells via intracellular multiplication

BACTERIA - release specific eXotoxins, these make chemicals that initiate inflammation
+ release specific enDotoxins, associated w cell walls

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17
Q

How do hypersensitivity reactions cause acute inflammation?

A

Altered immunological response cause inappropriate/excess immune response - damages tissues

Cellular or chemical mediators

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18
Q

How do physical agents cause acute inflammation?

A

Tissue damage through -
e.g. physical trauma, burns,, radiation (UV), frostbite

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19
Q

How do irritant and corrosive chemicals cause acute inflammation?

A

Gross tissue damage (from acids, alkalis etc)

Infecting agents may release specific chemical irritants that cause inflammation directly

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20
Q

How does tissue necrosis result in acute inflammation?

A

Tissue death from lack of O2/nutrients
∴ infarction
^ potential inflammatory stimulus due to peptides released from dead tissue

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21
Q

What accumulates in the extracellular space of damaged tissue in the early stages of acute inflammation?

A

Oedema fluid
Fibrin
Neutrophil polymorphs

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22
Q

Smooth muscle of arteriolar walls form __________ to regulate blood flow through the capillary bed

A

Pre-capillary sphincters

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23
Q

What happens to the pre-capillary sphincters in arteriolar walls in acute inflammation?

A

Relax
∴ ↑ Blood flow through capillaries

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24
Q

How is capillary hydrostatic pressure and therefore, osmosis into the extravascular space changed during acute inflammation?
What happens to the vascular permeability?

A

Pressure increased
∴ increasing osmotic pressure
∴ more fluid leaving vessels than returned
∴ ↑ Vascular permeability

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25
Q

Net escape of protein-rich fluid from capillaries is called?
Hence, what is the fluid called?

A

Exudation
Fluid exudate

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26
Q

3 Types of causes of ↑ Vascular permeability?
Give examples

A
  1. Immediate transient - chemical mediators e.g. histamine, nitric oxide (vasodilator), platelet activating factor
  2. Immediate sustained - severe vascular injury i.e. trauma
  3. Delayed prolonged - endothelial cell injury e.g. X-rays, bacterial toxins
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27
Q

Name the 4 stages of neutrophil polymorph emigration

A
  1. Margination of neutrophils
  2. Adhesion of neutrophils
  3. Neutrophil emigration
  4. Diapedesis
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28
Q

Describe the 1st stage of neutrophil polymorph emigration

A

1. Margination of neutrophils
NORMALLY, cells confined to central (axial) stream

HOWEVER, in acute inflammation, ↓ intravascular fluid and ↑ plasma viscosity
∴ cells flow in plasmatic zone! (to the side)

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29
Q

Describe the 2nd stage of neutrophil polymorph emigration

A

2. Adhesion of neutrophils
NORMALLY, neutrophils randomly contact endothelium but do NOT adhere

HOWEVER, in acute inflammation, at sites of injury pavementing occurs early - ONLY IN VENULES.

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30
Q

What is pavementing?

A

Adhesion of neutrophils to the vascular endothelium

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31
Q

Describe the 3rd stage of neutrophil polymorph emigration

A

Neutrophil emigration
Leucocytes migrate through walls of venules/small veins
NOT usually through capillaries !

Neutrophils, eosinophil polymorphs and macrophages all insert pseudopodia between endothelial cells.
Then these cells migrate through created gap

Then through basal lamina into vessel wall.

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32
Q

Describe the 4th stage of neutrophil polymorph emigration

A

Diapedesis
RBCs also escape from vessel but this is PASSIVE
∴ depends on hydrostatic pressure forcing RBCs out = diapedesis

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33
Q

What does a large number of RBCs in the extracellular space indicate?

A

Severe vascular injury e.g. tear in vessel wall

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34
Q

How does the acute inflammation response spread?

A

Chemical substances from injured tissue spreads outwards into uninjured area

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35
Q

Early in response, what causes the up-regulation of adhesion molecules on endothelial cell surface?

A

Histamine and thrombin which is released by initial inflammatory response

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36
Q

What do endogenous chemical mediators cause?

A

Vasodilation
Emigration of neutrophils
Chemotaxis
↑ Vascular permeability
Itching & pain

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37
Q

What does histamine cause when released from cells during acute inflammation?

A

Vascular dilation
Immediate transient phase of ↑ vascular permeability

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38
Q

How does histamine have an immediate effect on vascular permeability?

A

Bc it is stored in preformed granules
∴ able to be instantly released

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39
Q

What is the key source of histamine?
What are other sources?

A

Mast cells
Basophils and eosinophil leucocytes, platelets

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40
Q

What stimulates the release of histamine from its sources?

A

C3a & C5a
Lysosomal proteins released from neutrophils

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41
Q

Name some chemical mediators, other than histamine

A

Lysosomal compounds
Eicosanoids
5-hydroxytryptamine (serotonin)
Chemokine

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42
Q

How many enzymatic cascade systems does plasma contain? Name them.

A
  1. Complement
  2. the Kinins
  3. Coagulation factors
  4. Fibrinolytic system

All interrelated

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43
Q

What is the main purpose of the complement system?
How does it carry this out?

A

Remove/destroy antigens
Via direct lysis or opsonisation

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44
Q

What is opsonisation?

A

Enhancement of phagocytosis by factors in plasma

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45
Q

Describe the kinin system pathway

A

Activated factor XII and plasmin (also maybe leucocyte protease) activates conversion of prekallikin to kallikrein

This activates conversion of kininogens to kinins e.g. bradykinin

DRAW PICTURE
PAY FOR BRAINSCAPE

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46
Q

How do neutrophil polymorphs stain under H&E?

A

Nucleus stains blue
Cytoplasm stains pink/purple

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47
Q

skipped from 15 - 19

A
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48
Q

What are the 4 main outcomes of acute inflammation?

A
  1. Resolution
  2. Suppuration
  3. Organisation
  4. Progression to chronic inflammation
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49
Q

What is resolution?

A

Complete restoration of tissues to normal after acute inflammation

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50
Q

What conditions favour resolution?

A

Minimal cell death/tissue damage

If it happens in an organ that is capable of regeneration e.g. liver

Causal agent is rapidly destroyed

Local vasculature rapidly removes fluid and debris

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51
Q

Give an example of an acute inflammatory response that completely resolves

A

Acute lobar pneumonia

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52
Q

What occurs in suppuration?

A

Formation of pus, cellular debris and lipid globules

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53
Q

What condition is necessary for acute inflammation to result in suppuration?

A

Causative stimulus is persistent and vv likely to be infectious, usually pyogenic bacteria

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54
Q

Give an example of pyogenic bacteria

A

Staph. aureus
Neisseria species

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55
Q

What happens in suppuration after pus accumulates in the tissue?

A

Pus becomes surrounded by ‘pyogenic membrane’
This consists of sprouting capillaries, neutrophils and fibroblasts

Start of healing - results in granulation tissue and scarring

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56
Q

What is a collection of pus known as?

A

An abscess

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57
Q

Why is an abscess a bit of a problem?

A

Bc bacteria within cavity is relatively inaccessible to antibodies and antibiotics

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58
Q

What is organisation?
Describe the process

A

Tissue being replaced by granulation tissue to repair them

New capillaries grow into inflammatory exudate
Macrophages emigrate into area and fibroblasts proliferate (by TGF-beta)
∴ fibrosis and scar formation

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59
Q

What conditions favour organisation?

A

When large amounts of fibrin produced - cannot all be removed by fibrinolytic enzymes from plasma/neutrophil polymorphs

Lots of tissue becomes necrotic or dead tissue cannot be digested

Exudate/debris cannot be removed

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60
Q

Why can acute inflammation sometimes progress to chronic?

A

if causing agent isn’t removed

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61
Q

What happens during the progression of acute to chronic inflammation?

A

Cellular exudate changes

Neutrophil polymorphs REPLACED by lymphocytes, plasma cells, macrophages, multinucleate giant cells and fibroblasts

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62
Q

Name a systemic effect of inflammation

A

Fever (Pyrexia)

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63
Q

What causes pyrexia during inflammation?

A

Endogenous pyrogens act on hypothalamus, causes higher temp

64
Q

Which endogenous pyrogen has the greatest effect on pyrexia?

A

Interleukin-2 (IL2)

65
Q

What produces pyrogens?
What stimulates their release?

A

Produces : Neutrophil polymorphs & macrophages

Stimulates release : Phagocytosis, endotoxins and immune complexes

66
Q

Why is weight loss a symptom of chronic inflammation?

A

negative nitrogen balance
bc lots of energy req to produce inflammatory mediators

67
Q

What is likely to be the cause of inflammation with an increased amount of eosinophils in the blood?

A

Allergies and parasitic infections

68
Q

What is likely to be the cause of inflammation with an increased amount of neutrophils in the blood?

A

pyogenic infections & tissue destruction

69
Q

What is likely to be the cause of inflammation with an increased amount of lymphcytes in the blood?

A

Chronic infection, viral infections and whooping cough

70
Q

What is likely to be the cause of inflammation with an increased amount of monocytes in the blood?

A

Bacterial infections e.g. TB, typhoid

71
Q

What is one potential result of long-standing chronic inflammation?

A

↑↑ SAA (serum amyloid A protein)
∴ ↑ amyloid deposit in tissue/organs
∴ secondary amyloidosis

72
Q

Define chronic inflammation

A

Prolonged tissue reaction to injury following initial response
Lymphocytes, plasma cells and macrophages predominate

73
Q

What’s an example of a chronic abscess?
Why is this difficult to get rid of?

A

Abscess in the bone
difficult because bone has poor access to macrophages

74
Q

*
The presence of what materials favours chronic inflammation with an abscess? Why?

A

Indigestible materials e.g. keratin or fragments of necrotic bone
Bc materials are resistant to lysosomal enzymes

75
Q

What causes granulomatous inflammation?
What further impact do they have on macrophages?

A

Foreign bodies e.g. wood, metal, glass etc
Cause macrophages to form multinucleate giant cells

76
Q

What is an example of recurrent episodes of acute inflammation resulting in chronic inflammation?

A

Chronic cholecystitis from gallstones

77
Q

Describe the macroscopic features in chronic inflammation

A

Chronic ulcer
Chronic abscess cavity
Thickened wall of hollow organ
Granulomatous inflammation
Fibrosis

78
Q

Describe the microscope features in chronic inflammation

A

Cellular infiltrate usually has lymphocytes, plasma cells & macrophages

NO neutrophil polymorphs, sometimes will have eosinophil polymorphs

Some macrophages may form multinucleate giant cells

Maybe new fibrous tissue

Tissue necrosis, esp in granulomatous conditions

79
Q

How do macrophages move through tissue?

A

Amoeboid motion

80
Q

go over page 26+27

A
81
Q

Name some important cytokines produced by macrophages

A

Interferon-alpha & -beta
Interleukin-1, 6 & 8
TNF-a

82
Q

What is a granuloma?

A

An aggregate of epithelioid histiocytes formed in response to chronic inflammation

83
Q

What is the most common cause of granulomas?

A

Tuberculosis

84
Q

Describe the features of epithelioid histiocytes

A

Large vesicular nuclei
Lots of eosinophilic cytoplasm
Elongated
Little phagocytic activity

85
Q

What aspect of epithelioid histiocytes can act as a marker for disease? What type of disease?

A

Secretes enzymes - one being angiotensin converting enzyme (ACE)
If measure ACE levels, can act as a marker for systemic granulomatous diseases
e.g. sarcoidosis

86
Q

skipped from 28 - 37

A

do all this but later

87
Q

Give examples of cells that DO regenerate

A

Hepatocytes
Pneumocytes
ALL blood cells
Gut epithelium
Skin epithelium
Osteocytes

88
Q

Give examples of cells that do NOT regenerate

A

Myocardial cells
Neurons

89
Q

Define thrombosis

A

When blood contents formed within vascular system during life solidify

90
Q

Define a clot

A

Blood coagulates outside of vascular system OR after death

91
Q

Why don’t thrombus’ form all the time?

A

Bc of laminar flow - cells travel in centre of vessels i.e. don’t touch the sides!

Also, bc endothelial cells are not sticky if healthy!

92
Q

Where are platelets derived from?

A

Bone marrow cells - megakaryocytes

93
Q

What’s a distinguishing feature of platelets?

A

NO nucleus

94
Q

State the types of granules platelets contain and their function

A

Alpha granules - contain substances that help platelets stick to damaged vessel wall
Dense granules - help platelets to aggregate

95
Q

When are the contents of platelet granules released?

A

When platelet comes into contact w/ collagen (which is found in vessel walls)

96
Q

Thrombosis is caused by which 3 factors?

A

Virchow’s triad
1. Changes in vessel wall
2. Changes in blood flow
3. Changes in blood constituents

All 3 not req, any one can result in thrombosis

97
Q

Describe the first stage of thrombosis

A

Platelet aggregation
this then starts clotting cascade

98
Q

Why is platelet aggregation and the clotting cascade difficult to stop?

A

Bc they are both positive feedback loops

99
Q

By what protein molecule are RBCs entrapped during thrombosis?

A

Fibrin

100
Q

Why does an atheromatous plaque result in a thrombus?

A

Bc change in vessel wall AND change in blood flow

101
Q

describe the process of arterial thrombus

A

fatty streak etc p38

102
Q

Where do most venous thrombi occur?
Why?

A

Usually begin at valves
Bc valves create turbulence bc protrude into vessel lumen
easily damaged by trauma, stasis or occlusion

103
Q

Which side of a venous thrombus is the turbulence greatest?

A

Upstream side

104
Q

What is venous return from the legs dependent on?
∴ what risk factor does this create?

A

Calf muscle contraction and relaxation
∴ if people are immobilised (esp elderly) creates a higher risk of formation of DVT

105
Q

How does arterial thrombosis present?

A

Loss of pulse distal to thrombus
Area becomes cold, pale and painful

Eventually, the tissue will die and gangrene occurs

106
Q

How does venous thrombosis present?

A

Area becomes tender & general ischaemic pain
Area becomes red and swollen

107
Q

What are the 4 potential outcomes of thrombosis? (& brief description)

A

PICTURE

1. Lysis and resolution - body dissolves it and clears it away

2. Organisation - may become organised into a scar. macrophages clear away thrombus and fibroblasts replace it with collagen ∴ vessel slightly narrows.

3. Recanalisation - Intimal cells of vessel proliferate. Small capillaries grow into thrombus and fuse, creates large vessels.
∴ OG occlusion is recanalised and vessel is functional again

4. Embolism

108
Q

What is the term for when RBCs flow in the middle of the arteries?

A

Laminar flow

109
Q

Why can aspirin prevent thrombosis?

A

It inhibits platelet aggregation
∴ low dose can be used to prevent thrombosis

110
Q

What can be used in severe cases to prevent thrombosis? Why?

A

Warfarin bc inhibits Vitamin K (clotting factor)

111
Q

What is an embolus?

A

Mass of material in vascular system able to lodge in a vessel and block its lumen
Usually broken off piece from thrombus

112
Q

Other than a thrombus, what are some less common causes of an embolus?

A

Air - IV fluids/bloods, esp in children

Cholesterol crystal - from atheromatous plaques

Tumour amniotic fluid - rare, pregnant women w rapid labour

Fat - severe trauma w multiple fractures

113
Q

How does a pulmonary embolism occur?

A

Embolus enters venous system -> vena cava -> R heart -> lodges in pulmonary arteries

114
Q

Why can’t a venous embolus enter the arterial circulation?

A

Bc capillaries in lungs too narrow for it to pass through
∴ lungs act as a filter

115
Q

If a venous embolus DOES enter the arterial circulation, what does this indicate?

A

Perforated septum in heart

116
Q

How do small emboli present?

A

Usually unnoticed and are lysed by lung

MIGHT become organised and cause permanent but small damage
Over time might cause idiopathic pulmonary hypertension

117
Q

How do mid-sized emboli present?

A

Chest pain, shortness of breath

MIGHT be large enough to cause actue resp and cardiac problems - could resolve with/without treatment slowly

Lung function is impaired and at higher risk of future emboli

118
Q

How do massive emboli present?

A

Result in sudden death

Often impacted at bifurcation of major pulmonary arteries

119
Q

When can a thrombus form on areas of cardiac muscle?

A

When muscle has died from MI
bc these areas have lost endothelial lining ∴ exposing collagen to circulating platelets

OR

AF - causes blood to stagnate ∴ thrombus
when normal heart rhythm is back, thrombus breaks off and forms embolus

120
Q

What does the reversibility of ischaemia on tissues depend on?

A

Duration of ischaemia - if brief, could be reversed

Metabolic demands of tissue - i.e. cardiac myocytes and cerebral neurones esp vulnerable

121
Q

Define ischaemia

A

Reduction in blood flow to tissue/part of body caused by constriction or blockage of blood vessels supplying it

122
Q

Define infarction

A

NECROSIS of part/whole organ when artery supplying it is obstructed

123
Q

Why are organs esp vulnerable to infarction?

A

Bc most organs have only one artery supplying them

124
Q

What organs have dual arterial supply?
Name the supply

A

Liver - portal venous and hepatic artery
Lung - Pulmonary venous and bronchial artery
Brain - circle of Willis

125
Q

What is reperfusion injury?

A

Very common

Tissue damage doesn’t occur until perfusion is re-established
bc damage is usually O2 dependent ∴ has to wait till blood flows back to organ.

Area of tissue that was ischaemic has been damaged - transport mechanisms across membrane disrupted - esp calcium out of cell
∴ mitochondria impaired

This triggers activation of O2-dependent free radical system to clear dead cells!
-> hallmark of reperfusion injury

ALSO, neutrophil polymorphs and macrophages enters area and clears away debris
imports own free-rads into area
∴ more damage

126
Q

Define Gangrene

A

Whole areas of limb/region of gut have arterial supply cut off
∴ Large areas of mixed tissues die in bulk

127
Q

Types of gangrene
Brief description

A

Dry gangrene - Tissue dies, healing occurs above. Eventually, dead area drops off.
Sterile process.
Commonly found in gangrenous toes as complication of diabetes.

Wet gangrene - Bacterial infection is a 2° complication. Gangrene spreads proximally, patient dies from sepsis

128
Q

Describe Disseminated Intravascular Coagulation (DIC)

A

Thrombosis without counterbalance
∴ small thrombi form throughout body
∴ bleeding occurs at multiple places bc these thrombi use all the clotting factors (consumption of clotting factors)

129
Q

What is a watershed area?

A

Tissue that is at the adjacent territory of 2 arteries (supplied by both)

130
Q

Why is a watershed area vulnerable to infarction during hypofusion?

A

Bc it’s supplied by distal end of arteries ∴ less likely to receive sufficient blood during hypofusion
However, not vulnerable during atherosclerosis bc 2 artery supply

131
Q

Give 3 examples of a watershed area

A
  1. Splenic flexure of colon
  2. Regions of cerebral hemispheres
  3. Myocardium between endocardium and myocardium perfused by coronary arteries
132
Q

Other than thrombi, state and describe some other causes of ischaemia/infarction

A

Spasms - spasm in smooth muscle in vessel wall.
Happens bc ↓ of nitric oxide by vascular endothelium bc cellular injury
Occurs in angina

External compression - Veins more susceptible to occlusion this way
Occurs in strangulated hernias, testicular torsion, torsion of ovaries

Steal syndromes - when blood is diverted from vital territory
Blood will divert away from atheromatous vessel ∴ territory supplied by that vessel becomes ischaemic

Hyperviscosity - Increased blood viscosity, most impact on small vessels
Occurs in myeloma

Vasculitis - Inflammation of vessel wall narrows lumen

PICTURES !!

133
Q

skipped from 49 - 56

A

Atherosclerosis - rlly cba
& Aneurysms/strokes etc
don’t want that right now

134
Q

What is Apoptosis?

A

Intended programmed cell death

135
Q

Where does apoptosis regularly occur in the body?

A

In the gut - duodenum
Individual cells of gut villi apoptose and are replaced

136
Q

What are some inhibitors of apoptosis?

A

Growth factors
Extracellular cell matrix
Sex steroids
Viral proteins

137
Q

What are some inducers of apoptosis?

A

WITHDRAWAL of growth factors
LOSS of matrix attachment
Glucocorticoids
Some viruses
Free radicals
DNA damage

138
Q

Describe the intrinsic and extrinsic pathway of Apoptosis

A

draw a diagram i think

139
Q

What factors influence tumour invasion?

A

↓ Cellular adhesion
Secretion of proteolytic enzymes
Abnormal or ↑ Cellular motility

140
Q

What does altered expression of adhesion molecules cause?

A

Decreased cell-cell adhesion in carcinomas
∴ allows them to escape from site of origin
i.e. metastasise

141
Q

How is the cellular motility of neoplasms abnormal?

A

More motile
Shows loss of normal mechanism that stops or reverses normal cellular migration

142
Q

What are the most important proteinases in neoplastic invasion?

A

Matrix metalloproteinases

143
Q

How are matrix metalloproteinases secreted?
How is this useful?

A

By malignant neoplastic cells, enables them to digest surrounding connective tissue

144
Q

What are the 2 types of Autopsy?

A

Hospital autopsies
Medico-legal autopsies

145
Q

Which is the most common type of autopsy?

A

Medico-legal

146
Q

When are hospital autopsies useful?

A

Audit
Teaching
Governance
Research

147
Q

What is the Human Tissue Act 2004?

A

Autopsies only happen on licensed premises
Consent from relative for use of tissue retained at autopsy if not subject to coronial legislation or retained for criminal justice purposes
Public display requires consent from deceased

If you don’t follow the Human Tissue Act, penalties include up to 3 years of imprisonment and/or fine

148
Q

What are the types of death referred to by coroners?

A

Presumed natural - cause of death not known, not seen by a doctor in the last 14 days for illness

Presumed iatrogenic - anaesthetic deaths, abortion, complications of therapy, peri/postoperative

Presumed unnatural - accidents, suicide, industrial death, unlawful killing, neglect, custody deaths

149
Q

What is the Coroners Act 1988?

A

Allows coroners to order autopsy when death is likely due to natural causes to obviate need for inquest.

Also allows coroners to order autopsy where death is unnatural and inquest is needed

150
Q

What is the Coroners Rules 1984?

A

Autopsy ASAP by pathologist of suitable qualification and experience
Report findings ONLY to coroner
Autopsy only on appropriate premises

151
Q

What is the Amendment Rules 2005?

A

Pathologist must tell coroner what materials have been retained
Coroner authorises retention and sets disposal date, also informs family of retention

& Family has choice of :
Return material to family
Retain for research/teaching
Respectful disposal

Coroner informs pathologist of family’s decision

152
Q

What is the Coroners and Justice Act 2009?

A

Coroner can now defer opening the inquest and launch an investigation instead
Inquests not have conclusions, not verdicts

153
Q

What does Virchow’s triad describe?

A

The factors contributing to thrombosis

154
Q

State the 3 factors in Virchow’s triad

A

Stasis of blood flow
Endothelial injury
Hypercoagulability

OR

Change in blood flow
Change in vessel wall
Change in blood constituents

155
Q
A

Phase 2 (24 decks)

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