Revision: Haemostasis and Thrombosis Flashcards

1
Q

Haemostasis definition

A

bodily response to stop bleeding and reduce blood loss

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2
Q

Vessel wall role in haemostasis

A

constrict to reduce blood flow, NSAbout mechanism

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3
Q

Platelets in haemostasis

A

adhere to the broken vessel wall and each other, form a platelet plug

the platelet release rxn uses ATP and involves aggregation then coagulation of platelets

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4
Q

coagulation in haemostasis

A

cascade, in which inactive components are transformed to active components, ending with: prothrombin->thrombin, thrombin catalyses fibrinogen->fibrin

Needs to be tightly regulated between anti- and pro-coagulent forces, as 1 ml of blood has enough thrombin to convert body’s supplies of fibrinogen to fibrin

-> thrombin inhibitors: alpha-1 antitrypsin, antithrombin III, prot. C and S -> prot. S and AThrom III can have inherited deficiencies -> easy thrombosis

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5
Q

fibrinoolytic system in haemostasis

A

plasminogen->plasmin, which breaks down fibrin in clots

plasminogen activators catalyse the rxn and are widely used in severe circumstances eg CAD, eg streptokinase, tPA/PLAT (tissue plasminogen activator)

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6
Q

Main components of haemostasis

A

1 vessel walls -> constrict to reduce blood flow

2 Platelets

3 coagulation system

4 fibrinolytic system

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7
Q

Thrombosis definition

A

formation of a thrombus (solid mass of blood) w/in circulatory system DURING LIFE

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8
Q

Risk factors of a thrombosis

A

Virchow’s triad - Changes in:

1) Blood flow eg turbulence, stagnation
2) vessel wall eg atheroma, injury, inflammation
3) Blood components eg due to smoking, pregnancy

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9
Q

Appearance of a thrombus

A

arterial: pale, granular, lines of Zahn, low cell content
venous: deep red, gelatinous, soft, high cell content

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10
Q

Effects of a thrombus

A

arterial: ischaemia -> infarction, overall effect depends on site and whether there is collateral circulation (ie whether or not it is an end artery)
venous: congestion, if venous press. > osmotic press. -> oedema, if hydrostatic/tissue pressure > arterial pressure -> ischaemia -> infarction

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11
Q

Outcomes of a thrombus

A

1 Lysis: thrombus is lysed by fibrinolytic system, esp. by plasmin, blood flow is reestablished, usually occurs w/ small thrombi

2 Propagation: Thrombus spreads steadily through vessel, distally w/ arteries and proximally w/ veins

3 Organisation: ‘repair’, similar to granulation tiss. as it contains capillaries and fibroblasts, but lumen is still obstructed

4 Recanalisation: Blood flow is allowed, though usually incompletely, one/more channels are usually formed thorugh organised thrombus

5 Embolism: bits of thrombus break off -> travel round in the blood -> lodges at a distal site

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12
Q

Definition of embolism and types

A

blockage of blood vessel by solid/liquid/gas at a site dital to its origin

90% of emboli are thrombo-emboli (discussed later), other types include air, nitrogen (‘bends’ when diving), medical equipment, tumour cells, amniotic fluid, fat

Iatrogenic: due to med. treatment eg air from injections

Nitrogen: N2 bubbles in blood w/ rapid decompression -> ‘the bends’

Fat: from long bone frx, laceration of adipose tiss., causing rashness, confusion, SOB

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13
Q

Thromboembolism

A

1 From systemic veins -> lungs, pulmonary embolism

2 From heart -> aorta -> mesenteric, renal or other arteries

3 From atheromatous carotid arteries -> cerebral

  • normally from atrial fibrillation on left side -> stasis -> thrombus -> goes to brain causing stroke/transient ischaemic attack

4 From atheromatous abdominal arteries -> arteries of leg

Also a deep vein thrombosis

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14
Q

Pulmonary embolism

A

From thromboemboli in systemic circulation -> lungs

Types - Massive: 60% reduction in blood flow -> rapidly fatal

Major: medium vessels blocked -> SOB, coughing, sputum stained w/ blood

Minor: small peripheral pulmonary arteries blocked -> asymptomatic/minor SOB

Recurrent minor PEs: pulmonary hypertension

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15
Q

Deep vein thrombosis

A

Risk factors: immobility, disseminating (spreading) cancer, pregnancy/postpartum, surgery, oral contraceptives, severe burns, cardiac failure

Prevention: Subcutaneous heparin, leg compression during surgery - these should be offered to patients thought to be at high risk of a DVT

Treatment: IV heparin, oral warfarin

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16
Q

Anti-coagulant therapy

A

heparin: cofactor for anti-thrombin III, an anticoagulant, administered subcutaneously for prevention and IV for treatment
warfarin: interferes w/ synth. of Vit K clotting factors, slow effect, given orally for treatment

leg compressions during surgery help to prevent a DVT

17
Q

Disseminated intravascular coagulation

A

variety of diseases trigger pathological activation of coagulation mechanisms

-recognised ones include endotoxins - widespread activation of coagulation system, amniotic fluid embolus (the fluid can enter the circulation during delivery)

small clots form around body, disrupting normal coagulation as clotting factors are used up, abnormal bleeding from skin

leads to dysfunction of major organs, septicaemia and inc. risk of serious bleeding

18
Q

Haemophilia

A

X-linked: A -> factor VIII, B -> factor IX

clotting is very slow and limited

in/external bleeding, former more likely, leads to joint pain and stiffness as bleed occurs around area, synovial hypertrophy, muscle bleeding -> press. and necrosis of nerves (v. painful)

19
Q

thrombocytopaemia

A

presence of low level of platelets and can be caused by variety of diseases eg leukaemia, vit. B12 deficiency

symptoms: abnormal bleeding, nosebleeds, petechiae
complications: GI bleeding - blood in faeces, intracerebral bleeding - blood in vomit

20
Q

thrombophilia

A

blood has an inc. tendency to clot, leading to an abnormal balance of coagulation system