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Mechanisms of Disease > Haemostasis, Thrombosis & Embolism > Flashcards

Haemostasis, Thrombosis & Embolism Flashcards

0
Q

What are the functions of platelets?

A

Adhere to damaged vessel wall and each other. They form a platelet plug. This is energy dependent.

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1
Q

What does successful haemostasis depend on?

A

Vessel wall
Platelets
Coagulation system
Fibrinolytic system

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2
Q

What does PF3 do?

A

Acts to convert prothrombin to thrombin

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3
Q

Describe the coagulation cascade

A

Prothrombin –> thrombin –> fibrinogen –> fibrin

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4
Q

What is the coagulation cascade?

A

A series of inactive components converted to active components.

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5
Q

List some thrombin inhibitors

A

Anti-thrombin III
Alpha 1 anti-trypsin
Alpha 2 macroglobulin
Proteins C & S

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6
Q

How is plasminogen converted to plasmin?

What is the function of plasmin?

A

By plasminogen activators.

Plasmin is a serine protease and therefore it is used in fibrinolysis

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7
Q

Define thrombosis

A

Formation of a solid mass of blood within the circulatory system

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8
Q

What does Virchow’s triad consist of?

A

Abnormalities in vessel walls, abnormalities of blood flow and abnormalities in blood components

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9
Q

How do arterial thrombi appear?

A

Pale, granular, lines of Zahn (pale = platelet rich, dark = RBC), lower cell content, generally have less RBCs than venous thrombi

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10
Q

How do venous thrombi appear?

A

Soft, gelatinous, deep red and they have a higher cell content than arterial thrombi

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11
Q

What are the four main outcomes of thrombi?

A

Lysis, propagation, organisation and recanalisation

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12
Q

What happens during lysis of thrombi?

A

Complete dissolution of thrombus. Fibrinolytic system is active, allowing for re-established blood flow. Usually occurs with small thrombi

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13
Q

What happens during propagation of thrombi?

A

Progressive spread of thrombosis (due to stagnation and tributaries being formed), gets bigger. Occurs distally in arteries and proximally in veins.

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14
Q

What happens during organisation of thrombi?

A

Ingrowth of fibroblasts and capillaries (similar to granulation tissue). Lumen remains obstructed. Reparative process.

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15
Q

What happens during recanalisation of thrombi?

A

Blood flow is re-established with one or more channels formed through ongoing thrombus.

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16
Q

Define embolism

A

Part of thrombus breaks off, travels through bloodstream, lodging at a distant site

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17
Q

What are the effects of arterial emboli?

A

Ischaemia, infarction, collateral circulation. Worse in end arteries e.g. retina

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18
Q

What are the effects of venous emboli?

A

Congestion, oedema, ischaemia and infarct

19
Q

What types of emboli are there?

A

Air, amniotic fluid, nitrogen, medical equipment and tumour cells

20
Q

Where to thrombo-emboli from systemic veins pass to and what are they called?

A

Lungs. Pulmonary embolus

21
Q

Where do thrombo-emboli from heart pass to?

A

Pass via aorta to renal, mesenteric and other arteries

22
Q

Where do thrombo-emboli from atheromatous carotid arteries end up?

A

Brain

23
Q

Where do thrombo-emboli from atheromatous abdominal aorta end up?

A

Arteries of legs

24
Q

What are the pre-disposing factors for DVT?

A

Immobility/bed rest, post-op, post-partum/pregnancy, oral contraceptives, severe burns, cardiac failure, disseminated cancers

25
Q

If a patient has a high risk of developing DVT how do you treat them?

A

Give them prophylaxis –> heparin given sub-cutaneously, leg compression during surgery, TED stocking

26
Q

What medication is given to treat DVT?

A

Anti-coagulants e.g. IV heparin or oral warfarin

27
Q

What are the effects of pulmonary emboli?

A

Massive PE - >60% reduced blood flow (no flow to the lungs)
Major PE - medium sized vessels blocked - patients short of breath and may have a cough with blood stained sputum
Minor PE - small peripheral pulmonary arteries blocked. Asymptomatic or minor shortness of breath

28
Q

What are the four main types of embolism?

A

Pulmonary, cerebral, iatrogenic and fat

29
Q

Define haemostasis

A

Maintaining blood in a fluid, clot-free environment. Maintenance of balance between anti-coagulant and procoagulant factors

30
Q

What does a full blood count contain?

A

Number of RBD, WBC & platelets per ml of blood
Calculates proportion of blood made up from RBC
Measures amount of Hb in RBC

31
Q

What does bleeding time tell us?

A

How long it takes for clotting to occur

32
Q

What does INR tell us?

A

Measures how much medicine (usually warfarin) to take

33
Q

What is a platelet aggregation test?

A

Rate at which (and extent to which) platelets form clumps (aggregate) after a chemical is added which stimulates aggregation.

34
Q

What drugs are used to treat coagulation disorders?

A

Desmopressin nasl/inj, stimate nasl, DDAVP inj, humate-P IV, antihemophilic factor vWF IV, alphanate IV and wilate IV

35
Q

How do heparin and warfarin work?

A

Heparin is an anti-coagulant thus it reduces the chances of a further thrombus forming or the clot growing. Heparin also activates anti-thrombin 3 which prevents the clot growing. Warfarin does the same thing but for the long term (inhibits vit K dependance). Need to measure INR before giving warfarin (takes a few days to measure thus you give people heparin until INR is back). Normal INR is 1, someone who has warfarin will need a higher INR

36
Q

How does cartilage heal?

A

Separation from their blood supply therefore they cannot heal well.

37
Q

How are thrombi treated?

A

Clot busters e.g. streptokinase and tPA (tissue prothrombin activator) and fibrinolytic agents
NO, angioplasty, percutaneous coronary intervention (stenting).

38
Q

How are thrombi detected?

A

Venogram, ultrasound (doppler), d dimer (marker for embulism which measures a fibrin degradation product) - non specific and can be raised in any infection.
Wells score - to show if its DVT or PE

39
Q

How can DVT be prevented?

A

Leg compressions during surgery/TED stockings
Filter in inferior vena cava (if recurrent/ongoing risk factor eg cancer)
Heparin
Early mobilisation
Hydration

40
Q

What is disseminated intravascular coagulation?

A

DIC is a condition which causes excessive clotting and eventually leads to haemorrhage. The patient has high prothrombin time, activated partial thromboplastin time and thrombin clotting time. Plasma fibrinogen, and platelets are low whereas FDPs are very high.

41
Q

What is the common clinical presentation of haemophilia a?

A

General - Weakness and orthostasis
Musculoskeletal (joints) - Tingling, cracking, warmth, pain, stiffness, and refusal to use joint (children)
CNS - Headache, stiff neck, vomiting, lethargy, irritability, and spinal cord syndromes
GI - Hematemesis and abdominal pain
Genitourinary - Hematuria, renal colic, and post circumcision bleeding
Other - Epistaxis, oral mucosal hemorrhage, hemoptysis, dyspnea (hematoma leading to airway obstruction), compartment syndrome symptoms, and contusions; excessive bleeding with routine dental procedures

42
Q

What are the lab findings of haemophilia a?

A

Hemoglobin/hematocrit: Normal or low
Platelet count: Normal
Bleeding time and prothrombin time: Normal
Activated partial thromboplastin time (aPTT): Significantly prolonged in severe hemophilia, but may be normal in mild or even moderate hemophilia

43
Q

What are the preventative measures that can be taken for haemophilia a?
What are possible side effects?

A

Regular injections of octocog alfa (an engineered version of clotting factor VIII). Injections every 48 hours are often recommended.
Common side effects of octocog alfa include an itchy skin rash and redness and soreness at the site of the injection.

44
Q

What are on demand treatments for haemophilia a?

What are possible side effects of this treatment?

A

Injections of octocog alfa or called desmopressin. Desmopressin is a synthetic hormone. Desmopressin works by stimulating the production of clotting factor VIII and is usually given by injection.
Possible side effects of desmopressin include headache, stomach pain and nausea.

45
Q

What are the possible complications of an MI?

A

Pain, ventricular fibrillation, shortness of breath, cardiogenic shock
Rupturing, heart block
Reduced cardiac output (heart failure), thrombi in the heart (mural thrombus), aneurysm, dressler’s syndrome, pericarditis, stretched atria - atrial fibrillation

Mechanisms of Disease (8 decks)

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