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MOD > Haemostasis, Thrombosis And Atheroma > Flashcards

Haemostasis, Thrombosis And Atheroma Flashcards

0
Q

Define haemostasis

A

The body’s response to stop bleeding and loss of blood

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1
Q

What does successful haemostasis depend on?

A

Vessel walls
Platelets
Coagulation system
Fibrinolytic system

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2
Q

How do the blood vessels aid haemostasis?

A

They constrict to limit blood loss

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3
Q

How do platelets aid haemostasis?

A

They adhere to damaged vessel walls and to eachother to form a platelet plug

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4
Q

How does the coagulation system aid haemostasis?

A

The cascade reaction converts prothrombin to thrombin and fibrinogen to fibrin.
Requires tight regulation, maintained by balance of procoagulant and anticoagulant (eg thrombin inhibitors).

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5
Q

How does the fibrinolytic system aid haemostasis?

A

Breaks down clots by releasing anti-thrombotic factors from endothelium.
Plasminogen converted to plasmin to break down fibrin

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6
Q

How is the coagulation system regulated?

A

Thrombin positively feeds back on factors V, VIII, XI

Thrombin Inhibitors: anti-thrombin III, alpha 1 anti-trypsin, alpha 2 macroglobulin, protein C/S

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7
Q

What is thrombophilia?

A

Inherited deficiency of antithrombin III or protein C/S

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8
Q

Give 2 examples of fibrinolytic therapy

A

Streptokinase and Tissue plasminogen activators both activate plasminogen = ‘clot busters’.

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9
Q

Define thrombosis

A

The formation of a solid mass of blood within the circulatory system during life.

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10
Q

What three things lead to thrombosis formation and what is the collective name for these?

A

Vessel wall abnormalities
Blood flow abnormalities
Blood component abnormalities
= Virchow’s Triad

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11
Q

Give some examples of vessel wall abnormalities that can lead to thrombosis formation

A

Atherosclerosis
Direct injury
Inflammation

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12
Q

Give some examples of blood flow abnormalities that can lead to thrombosis formation

A

Turbulence

Stagnation

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13
Q

Give some examples of blood component abnormalities that can lead to thrombosis formation

A

In smokers
Pregnancy
Post-op, leads to hypercoaguable blood

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14
Q

How does the appearance of arterial and venous thrombi differ?

A

Arterial = pale, granular, lower cell content, show lines of Zahn (red and yellow lines of RBCs and fibrin)

Venous = deep red, soft, higher cell content, gelatinous

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15
Q

What are the possible effects of arterial thrombi?

A

Ischaemia
Infarction
(Depends on site and collateral circulation)

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16
Q

What are the possible effects of venous thrombi?

A

Congestion
Odema
Ischaemia (if tissue pressure > arterial pressure due to odema)
Infarction

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17
Q

What are the five possible outcomes of thrombosis?

A 
Lysis
Propagation
Organisation
Recanalisation
Thrombo-embolism
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18
Q

What occurs in lysis of a thrombus?

A

Complete dissolution of the thrombus, the fibrinolytic system activates and breaks down clot.
Blood flow is re-established.

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19
Q

What occurs in propagation of a thrombus?

A

Progressive spread of the thrombus (distally in arteries, proximal in veins)

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20
Q

What is organisation of a thrombus?

A

A reparative process with ingrowth of fibroblasts and capillaries into the thrombus.
Lumen remains obstructed.

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21
Q

What occurs in recanalisation of a thrombus?

A

One or more channels forms through organising thrombus.

Blood flow is re-established (usually incompletely).

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22
Q

How can a thrombus lead to an embolism?

A

Part of the thrombus breaks off, travels through the blood stream and lodges at a distant site eg. coronary artery

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23
Q

Define embolism

A

The blockage of a blood vessel by a solid, liquid or gas at a site distant from its origin.

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24
Q

List types of embolism

A 
Thrombi-embolism
Air
Amniotic fluid
Nitrogen
Medical equipment
Tumour cells
25
Q

Where do thromboembolisms from the heart pass to?

A

Pass via aorta to renal/mesenteric arteries etc

26
Q

Where do thromboembolisms from atheromatous carotid arteries pass to?

A

The brain (stroke)

27
Q

Where do thromboembolisms from an atheromatous abdominal aorta pass to?

A

To the arteries of the legs

28
Q

Where do thromboembolisms from the systemic veins pass to?

A

The lungs (pulmonary embolism) as they will not get stuck in the large veins near the heart.

29
Q

What’s the difference between massive, major and minor pulmonary emboli?

A

Massive PE = >60% reduction in blood flow, rapidly fatal

Major PE = blockage of medium sized vessels, leads to shortness of breath, cough, blood stained sputum.

Minor PE = blockage of small peripheral arteries, can be asymptomatic or cause shortness of breath.

30
Q

What do recurrent pulmonary emboli lead to?

A

Pulmonary hypertension

31
Q

List possible causes of a deep vein thrombosis

A 
Immobility/bed rest
Post-operative
Pregnancy and post-partum 
Oral contraceptives
Severe burns
Cardiac failure
Disseminated cancer
32
Q

How would you treat a DVT?

A

Intravenous heparin = an anticoagulant and a cofactor for anti-thrombin III

Oral warfarin = interferes with synthesis of vitamin K dependent clotting factors (slower effect)

33
Q

When might a fat embolism occur and what symptoms can it have?

A

After long bone fractures/ lacerations of adipose tissue.

Rash, shortness of breath, confusion

34
Q

When might a cerebral embolism occur and what symptoms can it have?

A

In atrial fibrillation (as this causes stasis of blood leading to thrombus formation, if this is in the left heart it goes to the brain)

Can cause stroke or transient ischaemic attack

35
Q

When might an iatrogenic embolism occur?

A

Due to medical treatment eg. an air embolism from an injection.

36
Q

How does a nitrogenic embolism occur?

A

Nitrogen bubbles form in the blood with rapid decompression. Commonly called “the bends”, common in divers due to rapid changes of pressure.

37
Q

What is Disseminated Intravascular Coagulation (DIC)?

A

Pathological activation of coagulation mechanisms in response to diseases.
Small clots form throughout the body, disrupt normal coagulation and use up clotting factors, so abnormal bleeding occurs from the skin.

38
Q

What can trigger Disseminated Intravascular Coagulation?

A

Infection
Trauma
Liver disease
Obstetric complications

39
Q

What’s the difference between haemophilia A and haemophilia B?

A 
A = deficiency of factor VIII
B = deficiency of factor IX
40
Q

What causes haemophilia?

A

Deficiency of clotting factor due to a nonsense point mutation.
X-linked recessive.

41
Q

What can haemophilia lead to?

A

Haemorrhage into major joints, synovial hypertrophy, pain
Haemorrhage into retroperitoneum/urinary tract
Muscle bleeding causes increased pressure/necrosis of nerves (painful)

42
Q

How do you treat haemophilia?

A

Factor replacement therapy (self-administered)

43
Q

What is thrombocytopenia?

A

Platelet count well below reference range, usually accompanied by a bone marrow dysfunction eg. leukaemia, anaemia.

44
Q

What can cause thrombocytopenia?

A

Failure of platelet production
Increased platelet destruction
Sequestering of platelets (cause may be DIC)

45
Q

Define atheroma

A

The accumulation of intracellular and extracellular lipid in the intima and media of large or medium sized arteries

46
Q

Define atherosclerosis

A

The thickening and hardening of arterial walls as a consequence of atheroma

47
Q

Define arteriosclerosis

A

The thickening and hardening of arteries and arterioles as a result of hypertension/diabetes mellitus.

48
Q

Describe the macroscopic appearance of an atheroma

A

Fatty streak: lipid deposits in the intima are yellow and slightly raised.

Simple plaque: raised, yellow/white, irregular, widely distributed, enlarge and coalesce.

Complicated plaque: leads too thrombus, haemorrhage into plaque, calcification and aneurysm formation.

49
Q

Describe the microscopic appearance of atheroma

A

Early changes: proliferation of SMCs, foam cells, extracellular lipid

Later changes: fibrosis, necrosis, cholesterol clefts, inflammatory cells.

50
Q

Summarise the unifying hypothesis of atherogenesis

A

Endothelial damage
Platelet adhesion: PDGF release, SMC proliferation & migration, insudation of lipids, uptake of lipids by SMCs & macrophages producing FOAM CELLS.
Stimulates SMCs produce matrix material.
Foam cells secrete cytokines causing further SMC stimulation & recruitment of other inflammatory cells.

51
Q

What can cause endothelial damage (leading to atheroma formation)?

A

Increased LDLs
Toxins eg. from smoking
Hypertension
Haemodynamic stress

52
Q

What are possible effects of severe atherosclerosis?

A

Ischaemic heart disease
Cerebral Ischaemia
Mesenteric Ischaemia
Peripheral vascular disease

53
Q

What can ischaemic heart disease lead to?

A

MI
Angina
Arrhythmias
Cardiac failure

54
Q

How can atherosclerosis lead to ischaemic heart disease?

A

If atheroma forms in a coronary artery and blocks it

55
Q

What can cerebral ischaemia lead to?

A

Cerebral infarction (stroke)
Transient ischaemic attack
Multi-infarct dementia

56
Q

What can mesenteric ischaemia lead to?

A

Ischaemia colitis
Malabsorption
Intestinal infarction
Aneurysm (due to increased pressure leading to hardening and weakening)

57
Q

What can peripheral vascular disease lead to?

A

Intermittent claudication
Leriche syndrome (atheroma in bifurcation of abdominal aorta), leading to ischaemic rest pain
Gangrene

58
Q

List some risk factors for atheroma

A 
Age
Gender (women have hormonal protection before menopause)
Hyperlipidaemia (familial lead ps to corneal arcus & xanthalasma)
Smoking
Hypertension
Diabetes
Alcohol
Infection
Obesity
Oral contraceptives
Stress
59
Q

How can you prevent atheroma formation?

A

Stop smoking
Modify diet
Treat hypertension & diabetes
Lipid lowering drugs

60
Q

What affects susceptibility to coronary heart disease?

A

Genetic eg. disorders such as familial hypercholesteraemia increase risk
Geographical, less common in the Mediterranean
Ethnicity, common in Asians

MOD (7 decks)

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