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PHASE 2A > ICS > Flashcards

ICS Flashcards

1
Q

2 types of autopsy

A

Hospital and Medico-legal - coronal and forensic

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2
Q

Types of deaths referred to coroners

A

Presumed natural - not know cod and not seen by doctor with recent illness in last 14 days
Presumed iatrogenic - Peri/post op, abortion, complications
Presumed unnatural - accidents, suicide, murder, neglect etc

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3
Q

What is a coronial autopsy?

A

a systematic scientific examination that helps the coroner determine who the deceased was, when and where they died and how they came about their death.

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4
Q

Who refers the autopsy?

A

Doctors
Registrar of BDM - statutory duty to refer
Others - relatives / police

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5
Q

Autopsy process

A

Identification
External Examination
Evisceration - y shaped incision
Internal Examination

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6
Q

What is inflammation

A

The local physiological response to tissue injury

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7
Q

What is acute inflammation

A

local physiological initial and transient series of tissue reactions to injury that lasts a few hours to a few days. It has a sudden onset, short duration and usually resolves.

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8
Q

Benefits of inflammation

A

Destruction of invading microorganisms
The walling off of an abscess cavity, thus preventing spread of infection

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9
Q

Problems with inflammation

A

An abscess in the brain would act as a space-occupying lesion compressing vital surrounding structures
Fibrosis resulting from chronic inflammation may distort the tissues and permanently alter their function

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10
Q

Cells involved in inflammation

A

Neutrophil polymorphs
Macrophages
Lymphocytes
Endothelial cells
Fibroblasts

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11
Q

What cell is first at the site of acute inflammation that is not present in chronic

A

Neutrophil polymorphs

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12
Q

Steps of acute inflammation

A

Vascular - dilation of vessels
Exudative - vascular leakage of protein rich fluid
Neutrophil polymorph recruitment

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13
Q

Outcomes of acute inflammation

A

Resolution
Suppuration - pus formation e.g. abscess
Organisation - fibrosis
Progression - chronic inflammation

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14
Q

What is organisation in acute inflammation

A

Healing by fibrosis where there is substantial damage to CT framework and lacks ability to regenerate.
Dead tissue + exudate removed by macrophages
Then filled with granulation tissue
Then produces collagen to form fibrous collagenous scar

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15
Q

Causes of acute inflammation

A

Microbial infections e.g. viruses
Hypersensitivity reactions e.g. parasites
Physical agents e.g. trauma/ radiation
Chemicals e.g. corrosives/ acids
Bacterial toxins
Tissue necrosis e.g. ischaemic infarction

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16
Q

3 responses of acute inflammation

A

Changes in vessel calibre and flow
Increased vascular permeability and formation of the fluid exudate
Formation of the cellular exudate – emigration of the neutrophil polymorphs into the extravascular space

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17
Q

Macroscopic appearances of acute inflammation and their causes

A

Rubor redness - dilation of small bv
Calor heat - hyperaemia
Tumor swelling - oedema
Dolor pain - chemical mediators
Loss of function - by pain or swelling

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18
Q

Causes of inc vascular permeability

A

Immediate transient - chemical mediators
Immediate sustained - severe direct vascular injury
Delayed prolonged - Endothelial cell injury

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19
Q

Stages of neutrophil polymorph emigration

A
  1. Margination - neutrophils flow into plasmatic zone due to loss of intravascular fluid and inc in plasma viscocity
  2. Adhesion - vascular endothelium at sites of damage become sticky and neutrophils adhere
  3. Neutrophil emigration - cells involved in inflammation create a gap between enodthelial cells and migrate to the vessel wall
  4. Diapedesis - Red blood cells leave vessels
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20
Q

How is histamine released

A

Mast cells degranulating due to C3a and C5a from lysosomal proteins released from neutrophils.

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21
Q

Role of tissue macrophages in acute inflammation

A

Secrete chemical mediators when stim by local infection or injury. Most important IL-1 and TNF-alpha which stimulate histamine and thrombin. Also cause cells to secrete MCP-1 to attract neutrophil polymorphs.

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22
Q

Process of vascular changes in acute inflammation

A

In acute inflammation, capillary hydrostatic pressure increased and there is escape of plasma proteins into the extravascular space (due to the increased pressure) thereby increasing osmotic pressure there - this results in much more fluid leaving the vessels than is returned to them - this results in increased vascular permeability

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23
Q

How can histamine act so quickly

A

it is stored in preformed granules and is thus instantly able to be released

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24
Q

4 enzymatic cascade systems

A
  1. Complement
  2. the Kinins
  3. Coagulation factors
  4. Fibrinolytic system
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25
Q

What is the complement system

A

to remove or destroy antigen, either by direct lysis or by opsonisation (the enhancement of phagocytosis by factors (opsonins) in plasma.

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26
Q

What is the kinin system

A

Activated factor XII and plasmin activate the conversion of prekallikin to kallikrein. This stimulates the conversion of kininogens to kinins, such as bradykinin (causes vasodilation). Prekallikrein can also be activated by leucocyte proteases e.g trypsin:

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27
Q

Role of lymphatics in acute inflammation

A

In acute inflammation the lymphatic channels become dilated as they drain away the oedema fluid of the inflammatory exudate
-
Antigens are carried to the regional lymph nodes for recognition by
lymphocytes

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28
Q

Role of mast cells in acute inflammation

A

On stimulation by the C3a/C5a complement components they release preformed inflammatory mediators (i.e. histamine) stored in their granules and metabolise arachidonic acid into newly synthesised inflammatory mediators such as leukotrienes, prostaglandins and thromboxanes

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29
Q

Benefits of fluid exudate

A

Dilution of toxins

Entry of antibodies

Transport of drugs to the site where bacteria are multiplying

Fibrin formation from exuded fibrinogen which may impede the movement of microorganisms thereby trapping them and thus facilitating phagocytosis.

Delivery of nutrients & oxygen

Stimulation of immune response

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30
Q

Harmful effects of fluid exudate

A

Digestion of normal tissues
Swelling
Inappropriate inflammatory response - IgE

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31
Q

Systemic effects of acute inflammation

A

Pyrexia - fever Neutrophil polymorphs & macrophages produce compounds known as endogenous pyrogens which act on the hypothalamus to set the thermoregulatory mechanisms at a higher temperature

Also anorexia, nausea and weight loss

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32
Q

What do Th1 cells do

A

Cytokine IFN-gamma
via classical pathway
activate macrophages

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33
Q

What do Th2 cells do

A

Secrete IL-4, 5 and 13
Via alternate pathway
Activate macrophages and eosinophils

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34
Q

What do Th17 cells do

A

Secrete IL-17
Recruit neutrophils and monocytes

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35
Q

What is chronic inflammation

A

The subsequent and prolonged tissue reactions to injury following the initial response OR
inflammatory process which lymphocytes, plasma cells and macrophages predominate

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36
Q

Causes of chronic inflammation

A
  • Resistance of infective agent to phagocytosis - tuberculosis, leprosy
  • Endogenous - necrotic adipose tissue bone

-Exogenous - Silica, asbestos

  • Autoimmune diseases e.g. rheumatoid arthritis or hashimotos thyroiditis
  • Specific diseases of unknown aetiology - chronic ibd
  • Primary granulomatous diseases - chrons
  • Transplant rejection

-Acute inflammation

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37
Q

Most common type of acute inflammation to develop to chronic

A

suppurative type - if the pus forms an abscess cavity that is deep-seated, and drainage is delayed or inadequate, then by the time that drainage occurs the abscess will have developed thick walls composed from granulation and fibrous tissues.

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38
Q

Macroscopic appearances of chronic inflammation

A
  • Chronic ulcer:
  • Such as a chronic peptic ulcer of the stomach with breach of the mucosa -

Chronic abscess cavity:
* For example osteomyelitis
- Thickening of the wall of a hollow organ -

Granulomatous inflammation:
* Occurs when the immune system attempts to wall off substance but is unable to eliminate it, this forms a granuloma (a collection of epithelioid histiocytes (a stationary phagocytic cell (macrophage) found in tissue)

  • Fibrosis:
  • Thickening or scarring of connective tissue
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39
Q

Microscopic features of chronic inflammation

A

The cellular infiltrate consists characteristically of lymphocytes, plasma cells & macrophages.

A few eosinophil polymorphs may be present but neutrophil polymorphs are
scarce

Some of the macrophages may form multinucleate giant cells

Exudation of fluid is not a prominent feature, but there may be production of new fibrous tissue from granulation tissue

There may be evidence of continuing destruction of tissue at the same time as tissue regeneration and repair

Tissue necrosis may be a prominent feature, especially in granulomatous conditions such as tuberculosis

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40
Q

Paracrine stimulation of connective tissue proliferation leads to..

A

angiogenesis (formation of new blood vessels) followed by fibroblast proliferation and collagen synthesis resulting in granulation tissue

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40
Q

Paracrine stimulation of connective tissue proliferation leads to..

A

angiogenesis (formation of new blood vessels) followed by fibroblast proliferation and collagen synthesis resulting in granulation tissue

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41
Q

What does growth factor EGF do

A

Regeneration of epithelial cells

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42
Q

What does growth factor TGF-alpha do

A

regeneration of epithelial cells

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43
Q

What does growth factor TGF-beta do

A

Stim fibroblast proliferation and collagen synthesis. Controls epithelial regeneration

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44
Q

What does growth factor PDGF do

A

Mitogenic and chemotactic for fibroblasts and smooth muscle cells

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45
Q

What does growth factor FGF do

A

Stim fibroblast proliferation, angiogenesis and epithelial cell regeneration

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46
Q

What does growth factor IGF-1 do

A

Synergistic effect with other growth factors

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47
Q

What does TNF do

A

Stim angiogenesis

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48
Q

Two types of lymphocyte in lymphatic tissue infiltrate and their function

A

B lymphocyte - Which on contact with antigen, become progressively transformed into plasma cells (cells specially adapts for the production of antibodies)

T lymphocyte - cell-mediated immunity
* On contact with antigen, produce a range of soluble factors called cytokines, with important activities, such as the recruitment & activation of other cell types e.g macrophages etc.

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49
Q

Role of macrophages in chronic inflammation

A

move by amoeboid motion through the tissues and respond to certain chemotactic stimuli.

Macrophages can ingest a wider range of materials then can polymorphs and, being long-lived, they can harbour viable organisms if they are unable to kill them by their lysosomal enzymes

When macrophages participate in the delayed-type hypersensitivity response to these types of organism, they often die in the process, contributing to the large areas of necrosis by release of their lysosomal enzymes

Macrophages in inflamed tissue are derived from blood monocytes that have migrated out of vessels and have become transformed in the tissues they are thus part of the mononuclear phagocyte system also known as the reticuloendothelial system.

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50
Q

What is a granuloma

A

an aggregate of epithelioid histiocytes

TUBERCULOSIS most common

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51
Q

How to identify granuloma histologically

A

Use Ziehl-neelson stain and will be bright red

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52
Q

Causes of granulomas

A

Specific infections - mycobacteria

Materials that resist digestion

Specific chemicals - beryllium

Drugs

Unknown - chrons and sarcoidosis

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53
Q

What are histolytic giant cells

A

form where particulate matter that is indigestible by macrophages accumulates when two or more macrophages attempt simultaneously to engulf the same particle; their cell membranes fuse and the cells unite

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54
Q

What are langerhans giant cells

A

horseshoe arrangement of peripheral nuclei at one pole of
the cell
- Characteristically seen in TUBERCULOSIS

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55
Q

What are foreign body giant cells

A

Large cells with nuclei randomly scattered throughout their cytoplasm
Characteristically seen in relation to particulate foreign body material

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56
Q

What are Toulon giant cells

A

Have a central ring of nuclei, peripheral to which there is lipid material

Seen when macrophages attempt to ingest lipids and in xanthomas (yellowy patch, can appear anywhere on skin e.g eyelids)/dermatofibromas (fibrous nodule) of the skin

57
Q

Role of acute and chronic inflammation in CV system

A

Acute in the response to acute myocardial infarction and the generation of some complication of MI such as cardiac rupture

Chronic involved in myocardial fibrosis after MI

58
Q

Role of chronic inflammation in cancer

A

Initiation and propagation and its progression e.g. ulcerative colitis

59
Q

Role of inflammation and atheroma

A

macrophages adhere to endothelium, migrate into the arterial intima and, with T lymphocytes, express cell adhesion molecules which recruit other cells into the area. The macrophages are involved in processing the lipids that accumulate in atheromatous plaques

60
Q

Role of chronic inflammation in tissue injury

A

Multiple sclerosis with chronic demyelinating neurodegenerative disorder in which chronic inflammation

61
Q

Difference between exudate and transudate

A

Exudate - high protein content due to being from increased vascular permeability

Transudate low protein content due to vessels having normal permeability characteristics.

62
Q

Cells involved in cell renewal

A

Labile cells
Stable cell populations
Permanent cells
Stem cells

63
Q

Where to find stem cells in the body

A

In the epidermis stem cells are found in the basal layer immediately adjacent to the basement membrane, in the hair follicles and sebaceous glands

In intestinal mucosa the stem cells are near the bottom of the crypts

In the liver they are found lying between hepatocytes and bile ducts

There is also a separate pool of stem cells available in the bone marrow; these haemopoietic stem cells are able to seed into other organs and differentiate locally into the appropriate tissue

64
Q

Process of complete restitution in a minor skin abrasion

A

The epidermis is lost over a limited area, but at the margins of the lesion there remain cells that can multiply to cover the defect
* At first, cells proliferate and spread out as a thin sheet until the defect is covered
* When a confluent layer has been formed, the stimulus to proliferate is switched off; this is known as contact inhibition, and controls both growth and movement
* Once in place, the epidermis is rebuilt from the base up until it is indistinguishable from normal - this whole process is called healing

65
Q

What is organisation

A

The repair of specialised tissues by the formation of a fibrous scar. It occurs by the production of granulation tissue and the removal of dead tissue by phagocytosis.

66
Q

What is granulation tissue

A

Loops of capillaries supported by myofibroblasts which actively contracts to reduce wound size; this may result in a structure later.

67
Q

How can we treat inflammation

A

NSAIDS, antibiotics, antifungal, aspirin etc

68
Q

Healing by 1st intention

A

1st detention – can suture up the cut
Incision -> exudation of fibrinogen -> weak fibrin join -> epidermal regrowth and collagen synthesis -> strong collagen join

69
Q

Healing by 2nd intention

A

Can’t bring the skin edges together the cut is too deep
Loss of tissue -> granulation tissue -> organisation -> early fibrous scar -> scar contraction
Phagocytosis to remove any debris
Granulation tissue to fill in defects and repair specialised tissues lost
Epithelial regeneration to cover the surface

70
Q

What is repair

A

Initiating factor still present
Tissue damaged and unable to regenerate
Replacement of damaged tissue by fibrous tissue
Collagen produced by fibroblasts

71
Q

Cells that can regenerate

A

Hepatocytes
Pneumocytes
All blood cells
Gut epithelium
Skin epithelium
Osteocytes – help remodel bone fractures

72
Q

Cells that cannot regenerate

A

Myocardial cells
Neurones

73
Q

Why is brain fibrosis called gliosis?

A

Glial cells instead of fibroblasts

74
Q

What is thrombosis

A

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

74
Q

What is thrombosis

A

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

75
Q

What is thrombosis

A

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

76
Q

What is a blood clot

A

Blood coagulated outside of the vascular system or after death

77
Q

What prevents a thrombus normally

A

Laminar flow - cells travel in centre of arterial vessels and don’t touch sides

Endothelial cells - are not “sticky” when healthy

78
Q

Origin and role of platelets

A

No nucleus and derived from megakaryocytes

Platelets are activated and the contents of their granules released when come into contact with collagen, found in damaged vessel walls

The platelets change shape and extend pseudopodia; their granules releases their contents and platelets form a mass that covers the vessel wall defect until the endothelial cells have regenerated

79
Q

What do platelets contain

A

Alpha granules:
* Contain several substances involved in the process of platelet
adhesion to damaged vessel walls
* Substances include; fibrinogen, fibronectin & platelet growth
factor

Dense granules:
* Contain substances such as; adenosine diphosphate (ADP) that cause platelets to aggregate

80
Q

Process of thrombus formation

A

Platelet aggregation -

Platelets release chemicals when the aggregate which cause other platelets to stick to them and also which start off the cascade of clotting proteins in the blood

Both these reactions involve positive
feedback loops so that once they have started they are difficult to stop

Once the clotting cascade has started there is formation of the large protein molecule fibrin which makes a mesh in which red blood cells can become entrapped

81
Q

Three factors that can cause thrombosis

A

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

Not all 3 are needed.

82
Q

How do cigarette smokers cause the risk factor for thrombosis

A

cigarette smoke damages endothelial cells resulting in both a change in vessel wall and blood flow over the injured/absent cells

83
Q

Arterial thrombosis process

A
  1. Raised fatty streak on intimal surface
  2. Plaque grows to protrude into lumen and turbulent blood flow
  3. Turbulance results in loss of intimal cells and exposed plaque is presented to blood cells.
  4. Results in fibrin deposits and platelet clumping and platelets adhere to exposed collagen
  5. Platelet0growth factor in alpha granules causes proliferation of arterial smooth muscle cells which add to plaque.
  6. Platelet layer and rbc become trapped in fibrin meshwork
  7. Build up protrudes even further into lumen more platelet deposition
  8. disrupts laminar flow and thrombi grow in direction of blood flow (propagation)
84
Q

Venous thrombosis process

A

Atheroma do not occur due to low bp but starts at valves

  1. valves disturb blood flow as protrude into vessel lumen especially if damaged by trauma, stasis or occlusion
  2. if bp falls flow is slower (stasis) and thrombosis more likely through successive deposition via propagation
85
Q

Risk factors for venous thrombosis

A

surgery when bp falls
After MI
elderly or those immobilised for long periods of time for DVT
any individual can get DVT

86
Q

What does arterial thrombosis result in

A
  • The loss of pulse distal to the thrombus
  • Area becomes cold, pale & painful
  • Eventually the tissue will die and gangrene results
87
Q

What does venous thrombosis result in

A

The area becoming tender due to developing ischaemia in the vein wall initially, but there is also general ischaemic pain as the circulation worsens
- Area becoming reddened - since blood is still carried to the site by the arteries but cannot be drained away by the veins)
- Area becoming swollen

88
Q

Outcomes of thrombi (4)

A

A - Resolves as body dissolves it

B - Organised into a scar by invasion of macrophages which clear away thrombus and fibroblasts replace it with collagen

C - intimal cells proliferate and small sprouts of capillaries grow into thrombus and fuse to larger vessels. Recanalised

D - Fragments of thrombus may break off resulting in embolism

89
Q

What does aspirin do to a thrombus

A

inhibits platelet aggregation and a low dose can help prevent it.

90
Q

What does warfarin do

A

Inhibits vitamin K to prevent clotting

91
Q

What is an embolus

A

An embolus is a mass of material in the vascular system able to lodge in a vessel and block its lumen

92
Q

Causes of embolus

A
  1. thrombus
  2. air
  3. Cholesterol crystals
  4. Tumour amniotic fluid
  5. Fat
93
Q

What happens during a venous embolism

A

If an embolus enters the venous system it will travel to the vena cava, through the right side of the heart and will lodge somewhere in the pulmonary arteries (depending on its size) - resulting in a PULMONARY EMBOLISM

94
Q

What happens during an arterial embolism

A

If an embolus enters the arterial system it can travel anywhere downstream of its entry point, for example:

  • A mural thrombus overlying a myocardial infarct in the left ventricle can go anywhere in the systemic circulation
  • Cholesterol crystals from an atheromatous plaque in the descending aorta can go to any of the lower limb and renal arteries
95
Q

Effects of a small pulmonary emboli

A

May occur unnoticed and be lysed within the lung
* May become organised and cause some permanent, though small, respiratory deficiency - the accumulation of such damage over a long period may be the cause of so-called ‘idiopathic pulmonary hypertension’

96
Q

Effects of a medium size pulmonary emboli

A

May be large enough to result in acute respiratory and cardiac
problems that may resolve slowly with or without treatment

  • The main symptoms are; chest pain and shortness of breath due to the effective loss of the area of lung supplied by the occluded vessel - the area may even become infarcted
  • Although many patients recover, their lung function is impaired and are at risk of further emboli in the future from the same source
97
Q

Effects of a large pulmonary emboli

A

These result in sudden death

  • They are usually long thrombi derived from the leg veins and are often impacted across the bifurcation of one of the major pulmonary arteries
98
Q

How does thrombosis occur after AF

A

ineffectual movement of the atria cause blood to stagnate in the atrial appendages and thrombosis to occur - when the normal heart rhythm is re-established the atrial thrombus may be fragmented and emboli broken off

99
Q

What is ischaemia

A

A reduction in blood flow to a tissue or part of the body caused by constriction or blockage of the blood vessels supplying it

100
Q

What is infarction

A

The necrosis / death of part or the whole of an organ that occurs when the artery supplying it has been obstructed

101
Q

Why are people susceptible to infarction

A

Most of the organs in the human body have only a single artery supplying them (end arterial supply) so they are very susceptible to infarction if this supply is interrupted

102
Q

Organs with dual arterial supply

A

Liver
Lung
Brain

103
Q

What is reperfusion injury

A

Damage when perfusion is resetablished as damage is oxygen dependent and the only way for oxygen to get to the site is by blood flow

When blood flow returns to an area of tissue that has been ischaemic, tissue where transport mechanisms across the cell membrane have been disrupted in particular where calcium transport out of the cell and from organelles such as mitochondria is impaired
*
This appears to be the trigger for the activation of oxygen-dependent free radical systems that begin the clearing away of dead cells - a hallmark of reperfusion injury
*
Neutrophil polymorphs and macrophages enter the area and begin to clear away debris and themselves import their own intrinsic oxygen free radicals into the area - resulting in more damage

104
Q

What is gangrene

A

When whole areas of a limb or a region of the gut have their arterial supply cut off and large areas of mixed tissue die in bulk.

105
Q

Two types of gangrene and their features

A

Dry gangrene:
* The tissue dies and become mummified and healing occurs above it
* So that eventually the dead area drops off - this is a sterile process, and is the common fate of gangrenous toes as a complication of diabetes

  • Wet gangrene:
  • Bacterial infection supervenes as a secondary complication; in this case the gangrene spreads proximally and the patient dies from overwhelming sepsis
106
Q

How does frostbite result in ischaemia

A

capillaries are damaged in exposed areas and thus construct severely so that the area they normally supply becomes ischaemic and infarcts

107
Q

Alternate causes of infarction

A

Spasm - decrease NO
External compression
Steal - diverted blood
Hyperviscosity - increased blood viscosity
Vasculitis - inflammation of vessel wall

108
Q

What is an atheroma

A

The fatty material which forms deposits in the arteries.

109
Q

What is an atheroma

A

The fatty material which forms deposits in the arteries.

110
Q

What is athersclerosis

A

Disease characterised by the formation of atherosclerotic plaques in the intima and degeneration of the walls of the arteries caused by accumulated fatty deposits and scar tissue, and leading to restriction of the circulation and a risk of thrombosis.

111
Q

Complications of atherosclerosis

A

Cerebral infarction
- Carotid atheroma - emboli causing transient
ischaemic attacks or cerebral infarcts
- Myocardial infarction
- Aortic aneurysm - rupture causes certain death
- Peripheral vascular disease
- Gangrene

112
Q

Characteristics of the plaque composition

A
  • central lipid core with fibrous tissue
  • Collagens and SMC
    Macrophages and lymphocytes and mast cells
  • Bordered by foam cells (macrophages that have phagocytksed oxidised lipoproteins with large amounts of cytoplasm)
    Calcifications in late stages
113
Q

Risk factors of atherosclerosis

A

Hypercholersterolaemia
Smoking
Hypertension
Diabetes
Male gender
Increasing age

114
Q

How do plaques develop

A
  1. Injured endothelial cells:
    * Enhanced expression of cell adhesion molecules for monocytes
    * High permeability for macromolecules such as low-density lipoprotein (LDL)
    * Increased thrombogenicity
  2. This allows inflammatory cells and lipids to enter the intimal layer and form plaques
  3. In more advanced stages of plaque formation large amounts of macrophages and T cells also accumulate in the plaque tissue
  4. Lipid-laden macrophages (foam cells) die, after phagocytosing LDL but eventually die
  5. Growth factors, particularly platelet-derived growth factor (PDGF), stimulate the proliferation of intimal smooth muscle cells and the subsequent synthesis of collagen, elastin and mucopolysaccharide by smooth muscle cells
  6. This results in the formation of a fibrous cap which encloses the lipid-rich core
  7. Growth factors are secreted by; platelets, injured endothelium, macrophages & smooth muscle cells themselves
  8. Another important mechanism of plaque growth is haemorrhage - this results from rupture/leakage of micro vessels within the plaque, especially fully developed plaques
  9. Large haemorrhage can cause rapid expansion of plaques and may produce clinical symptoms
115
Q

Clinical manifestations of atherosclerosis

A
  1. Progressive lumen narrowing due to plaque stenosis. When the stenosis is severe, ischaemic pain may develop even at rest
  2. Acute atherothrombotic occlusion leading to infarction
  3. Embolisation
  4. Ruptured abdominal atherosclerotic aneurysm leading to haemorrhage
116
Q

Preventative measures of atherosclerosis

A
  • Smoking cessation
  • Control of blood pressure
  • Weigh reduction
  • Low dose aspirin - inhibits the aggregation of platelets, advised for people with clinical evidence of atheromatous disease
  • Statins - cholesterol reducing drug
117
Q

What is an aneurysm

A

A localised permanent dilation of part of the vascular tree

118
Q

What is an atherosclerotic aneurysm

A

Commonly develop in elderly patients
- They may impair blood flow to the lower limbs and contribute to the development of peripheral vascular disease
- They may rupture into the retroperitoneal space

119
Q

What Is an aortic dissection aneurysm

A

Blood is forced through a tear in the aortic intima to create a blood-filled space in the aortic media
- This can track back into the pericardial cavity, causing a fatal haemopericardium (blood in pericardiac sac), or can rupture through the aortic adventitia

120
Q

What is a berry aneurysm

A

Occur in the circle of willis, the normal muscular arterial wall is replaced by fibrous tissue
- The lesions arise at points of branching, and are more common in young hypertensive patients
- Results in a subarachnoid haemorrhage if ruptured

121
Q

What is a stroke

A

A sudden event with disturbance of CNS functions due to vascular disease

122
Q

Types of stroke

A

Transient Ischaemic attack
Cerebral infarction
Intracranial haemorrhage
Subarachnoid haemorrhage

123
Q

What is a TIA

A

A stroke that lasts for less than 24hours and that is associated with complete clinical recovery
- Although they show complete resolution, they are risk markers for subsequent cerebral infarction

124
Q

What is a Cerebral infarction and its causes

A

Most occur within the internal carotid territory, particularly in the distribution of
the middle cerebral artery

Thrombosis
Emboli
Head injury
Occlusion
Reduction in blood flow, oxygen or infection

125
Q

What is an intracranial haemorrhage and where does it occur

A

Occurs 80% of the time in the basal ganglia

Other places include; brainstem, cerebellum and cerebral cortex
*
Most occur in hypertensive adults over 50
*
The haemotoma that forms as a result of the haemorrhage acts as a space-occupying lesion resulting in a rapid increase in intracranial pressure & herniation
* Most intracerebral haemorrhage occur following the rupture of the lenticulostriate branch of the MIDDLE CEREBRAL ARTERY

126
Q

What is a sub arachnoid haemorrhage and its causes

A

Occurs between the arachnoid and pia layers of the cranial meninges - haemorrhage here results in an increase in pressure between the layers which in turn puts pressure on the underlying brain and intracranial vessels
* Occurs usually due to the spontaneous rupture of a saccular aneurysm on the circle of willis

127
Q

What is apoptosis

A

A physiological cellular process in which a defined and programmed sequence of intracellular events leads to the removal of a cell WITHOUT the release of products harmful to surrounding cells

(programmed cell death)

128
Q

What is necrosis

A

traumatic cell death which induces inflammation and repair

129
Q

Purpose of apoptosis

A

ensures a continuous renewal of cells - enabling tissues to be more adaptable to environmental demands
act to suppress the inflammatory response triggered by necrosis

130
Q

How is HIV defective apoptosis

A

HIV proteins may activate CD4 on uninfected T-helper lymphocytes inducing apoptosis with resulting immunodepletion & dysfunction

131
Q

Apoptosis inhibitors

A
  • Growth factors
  • Extracellular cell matrix
  • Sex steroids
  • Some viral proteins
132
Q

Apoptosis inducers

A
  • Growth factor withdrawal
  • Loss of matrix attachment
  • Glucocorticoids
  • Some viruses
  • Free radicals
  • Ionising radiation
  • DNA damage
  • Ligand-binding at ‘death receptors’
133
Q

Intrinsic pathways of apoptosis

A

Bcl-2 can inhibit many factors that induce apoptosis
Bax forms Bax-Bax dimers which enhance apoptotic stimuli

intrinsic pathway responds to stimuli such as growth factors (or
their withdrawal) and biochemical stress

134
Q

How is the p53 involved in apoptosis?

A

p53 is a multifunctional protein which induces cell cycle arrest
and initiates DNA damage repair

When DNA damage occurs this leads to the stabilisation of the
protein product of the p53 gene

However if the damage is more difficult to repair then p53 can induce APOPTOSIS via activation of pro-apoptotic members of the Bcl-2 family

135
Q

Extrinsic pathway of apoptosis

A

Activation of apoptosis characterised by ligand-binding at death receptors on the cell surface tumour necrosis factor receptor
(TNFR) gene family e.g.: * TNFR1
* Fas (CD95)

Ligand binding at these receptors promotes clustering of receptor molecules on the cell surface, and the initiation of a signal transduction cascade resulting in the activation of CASPASES (cell death enzymes)

  • This pathway is the mechanism by which the immune system eliminates lymphocytes that would otherwise produce self-antigens
136
Q

Execution phase of apoptosis

A

Activation of apoptosis by either the intrinsic or extrinsic pathways results in a cascade of activation of caspases

  • Caspases are proteases, normally present as inactive pro-caspase molecules
  • Triggering of apoptosis first leads to the activation of initiator caspases to produce active caspases which cause the degradation of many targets including the cytoskeletal framework and nuclear proteins
  • Dead cells not phagocytosed fragment into smaller membrane-bound apoptotic bodies - these bodies do not trigger an inflammatory response and are eventually phagocytosed
137
Q

What is coagulative necrosis

A

Commonest form of necrosis
* Can occur in most organs
* Caused by ischaemia
* Following the lack of blood, the cells will retain their outline as their proteins coagulate and metabolic activity ceases

138
Q

What is liquefactive / colliquative necrosis

A

Occurs in the brain because of its lack of any substantial supporting
stroma; thus necrotic neural tissue may totally liquefy

139
Q

What is caseous necrosis

A

a pattern of necrosis in which the dead tissue is structureless almost like “soft cheese”
* Whenever caseous necrosis is seen in biopsy TUBERCULOSIS MUST be thought of

140
Q

What is gangrene necrosis

A

Type of necrosis with rotting of the tissues, sometimes as a result of certain bacteria particularly clostridia

  • The affected tissue appears black because of the deposition of iron sulphide from degraded haemoglobin

PHASE 2A (2 decks)

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