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103: Theme 2 > Haemostasis and Clotting > Flashcards

Haemostasis and Clotting Flashcards

1
Q

What is haemophilia C

A
  • Jewish populations - Autosomal recessive
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2
Q

What is deep vein thrombosis?

A
  • when there is a clot in the deep vein of your legs,
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3
Q

What are the compounds secreted by thrombocytes when they are activated, and what do each of them cause?

A
  • ADP: activate platelets further
  • Serotonin: vasoconstriction
  • Thromboxane A2 (TxA2): vasoconstriction and aggregation
  • Calcium and presence of phospholipids: allows coagulation reactions
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4
Q

What are the compounds that initiate the internal and external coagulation cascades?

A
  • Extrinsic (tissue factor) pathway: involves tissue factor
  • Intrinsic (contact activation) pathway: thrombin, factor XIIa, a nucleation site, glass in a laboratory
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5
Q

What are the enzymes directly responsible for transforming fibrinogen to a clot

A
  • Prothrombin –> Thrombin: converts fibrinogen into fibrin
  • Factor XIIIa, cross-links it into a clot
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6
Q

What are the enzymes that are only part of the intrinsic (contact activation) coagulation pathway?

A
  • factor XI
  • factotor XII
  • factor IXa
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7
Q

What is the role of vitamin K in haemostasis?

A
  • necessary for the production of Ca-dependent proteases in the liver - i.e factor II, VII, IX, X (extrinsic tissue factor pathway)
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8
Q

What physiological state might lead a patient to develop a vitamin K deficiency?

A
  • lack of bile salts, if exogenous lipids were not being properly digested
  • Warfarin toxicity: prevents recycling of vitK
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9
Q

What is the aetiology of haemophilia A

A
  • a mutation in the factor VIII gene
  • X-linked recessive disease
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10
Q

What is the aetiology of haemophilia B?

A
  • X-linked recessive - a mutation in the factor IX gene
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11
Q

GIve an overview of how the body responds to an injury in a blood vessel

A
  • formation of a haemostatic plug physically protects and coats the surface of the injury initially: platelet adhesion, activation and aggregation - coagulation - vasoconstriction: decreases local blood flow
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12
Q

Explain the role of platelets in haemostasis?

A
  • aggregate at the site of injury, over fibrinogen, forming a haemostatic plug - contribute to vasoconstriction by releasing vasoconstrictor compounds, serotonin TxA2 - secrete/provide compounds that encourage coagulation, including the phospholipids
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13
Q

List 4 differentiated cell types that develop from the lymphoid precursor cells

A
  • B cells - T helper cells - NK cells - Plasma cells
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14
Q

List 4 differentiated cell types that develop from the myeloid precursor cells

A
  • eosinophils - monocytes/macrophages - neutrophils - RBC
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15
Q

Explain platelet activation

A
  • change dramatically in response from ADP or exposed collagen
  • more spindly shape
  • metabolism goes up
  • exocytose many granules
  • their membranes gain proteins (GP2b/3a)
  • many reactions of the clotting cascade can only take place on the membrane of an activated platelet
  • platelet aggregation can only occur on the surface of already activated platelets
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16
Q

What prevents blood from clotting spontaneously and inappropriately?

A
  • Fibrinolysis.
  • Anticoagulation factors.
  • Maintaining platelets in the inactivated state.
  • Keeping coagulation initiation signals sequestered (eg Factor III/Tissue factor behind the endothelium).
  • Rapid blood flow
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17
Q

What is Factor X and Xa?

A
  • Factor Xa is an activated enzyme. It catalyses the conversion of prothrombin (factor II) to thrombin. Its activity is substantially increased when it combines with active factor five.
  • Factor X is the inactive form of Factor Xa
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18
Q

What is Xase?

A
  • converts Factor X to Xa
  • Intrinsic Xase is Factor IX + factor VIII,
  • Extrinsic Xase is Factor VII + tissue factor
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19
Q

What are the causes of bleeding?

A
  • Vascular disorders
  • Platelet disorders: thrombocytopenia, defective function
  • defective coagulation: inherited v acquired
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20
Q

where does the blood go

What are the different patterns of bleeding?

A

Vascular and platelet bleed cause:

  • bleeding into mucous membranes and skin

Coagulation disorders cause:

  • bleeding into joints and soft tissue
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21
Q

Give examples of Inherited and acquired vascular bleeding

A

Inherited:

  • Hereditary haemorrhagic telangiectasia (Oslo-Weber-Render syndrome), abnormal blood vessel formation, autosomal dominant
  • Ehlers-Danlos syndrome: affects connective tissue

Acquired:

  • Scurvy
  • Steriods: corticosteroids in GI bleeding
  • Senile
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22
Q

What is the normal platelet count range?

A
  • 150-400 x 109/L
  • below 150 is thrmobocytopenia
  • symptoms are seen when plts are <10
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23
Q

What are some symptoms of thrombocytopenia?

A
  • Aipistaxis
  • GI bleeds
  • menorrhagia
  • bruising
24
Q

What are some causes of thrombocytopenia?

A

failure to produce

  • selective megakaryocyte depression: drug toxixity or viral infection
  • General bone marrow failure

Increased consumption

  • immune and autoimmune
  • idiopathic
  • assoiciated ith systemic lupus erythematosus, CLL or lymphoma
  • infections: Helicobacter pylori, HIV, malaria drug induced = heparin
25
Q

What is ITP and what is its treatment?

A

Immune thrombocytopenia

  • treat with corticosteroids
  • intravenous immunoglobulins: rapid rise in platelet count
  • sometimes a splenectomy
26
Q

Explain Haemophilia A an B

A

Haemophilia A

  • sex linked chromosome
  • defect is in the absence of or low factor VII
  • largely caused by missense or frameshift mutaions or deletion in the factor VII gene

Haemophilia B

  • Christmas disease, incidence is 1/5 of Haem. A
  • Factor IX deficiency
27
Q

Haeme. A and B are the same

What are the clinical features of haemophilia

A
  • spontaneous bleeding into joints (haemarthrosis) and muscle
  • unexpected post-operative bleeding
  • chronic debilitating joint diseases
  • family history in the majority of cases
28
Q

Clinical diagnosis of haemophilia

A

Prolonged Activated Partial Thromboplastin Yome (APTT)

  • Factor VII, IX, XI, XII assay in the intrinsic pathway

Normal Prothrombin Time (PT)

  • testing factor II, V, VII, X in the intrinsic pathway
  • Low factor VII or IX levels: the lower the % the more severe
29
Q

What treatment is given for haemophilia?

A
  • Infusions of recombnant VIII or factor IX to 50-100% normal
  • if patients factor VIII is raised to 30-50% spontaneous bleeding should be controlled
  • 1-Diamino-8-D-arginine vasopressin (DDAVP); alternative for increasing plasma factor VIII level in milder hameophiliacs
30
Q

also what is VWF?

What is Von Willebrand disease?

A
  • reduced level or abnormal function of von Willebrand factor (VWF)
  • caused by a variety of missense mutations. autosomal dominant disease

VWF

  • produced in endothelial cells and megakaryocytes
  • large multimeric protein that carries factor VIII in the blood, prevents its premature destruction
  • promotes platelet adhesion
31
Q

What is the presentation of von Willebrand disease?

A
  • women are more badly to be affected than men at a given VWF level
  • mucous membrane bleeding: epistaxes, menhorrhagia
  • excessive blood loss from superficial cuts and abrasions
  • operative ad post-truamatic haemorrhage
32
Q

What are the lab tests for vWD?

A
  • prolonged APTT
  • normal PT
  • low vWF level/ function
  • low factor VIII level
  • prolonged bleeding time
  • defective platlet function
33
Q

What is the treatment for vWD?

A
  • antifibrinolytic agent: tranexamic acid for mild bleeding
  • DDAVP infusion for type 1 vWD: releases VWF from endothelial cells 30 minutes after infusion
  • high-purity VWF for patients with very low VWF levels
34
Q

What are Acquired disorders of coagulation?

A
  • Vitamin K deficiency
  • Liver disease
  • Disseminated intravascular coagulation
35
Q

How does Liver disease affect coagulation?

A
  • Biliary obstruction → impaired absorbiton of vitamin K. therefore decreased synthesis of clotting proteins
  • Decreased thrombopoeitin production from the liver contributes to thrombocytopenia
  • Impaired platlet function and fibrinolysis
36
Q

Explain Disseminated Intravscular Coagulation

A

This is the widespread intravascular deposition of fibrin with consumption of coagulation factors and platlets

  • occurs as a consquence of many disorders that release procoagulent material into the circulation or cause widespread endothelial damage or platelet agggregation
  • causes both bleeding and thrombosis to occur
37
Q

Disseminated intravascular Disease

What is the lab presentation of meningococcal DIC

A
  • Prolonged PT, APTT, TT
  • Low fibrinogen
  • low platelts
  • Raised D-dimers or FDPs
38
Q

What anticoagulent drugs are there?

A
  • Heparin: used to treat- MIs, PE, DVTs
  • Warfarin: used to treat- PEs, DVTs, AF, prothetic valves

Direct (novel) Oral anti-coagulants

  • Direct thrombin inhibitors: dabigatran, argatroban
  • Factor xa inhibitars: rivaroxaban, apixaban
39
Q

Explain Vitamin K deficency and its role in coagulation disorders

A
  • required for gamma-carboxylation of factors II, VII, IX, X
  • Inhibited by warfarin: interferes with the action of vitamin K epoxide reductase leading to functional vitamin K deficiency

Deficiency can be due to:

  • Malabsorption of vitamin K, or inadequete in the diet, or inhibited by drugs like warfarin
  • Biliary obstruction (jaundice)
  • Haemorrhagic disease of the newborn ( give 1mg at birth )
40
Q

What are characterised as deep veins?

A
  • Iliac Vein
  • Femoral Vein
  • Popilteal vein
  • Tibial Vein
41
Q

What would make a DVT more likely?

A
  • more risk if a lot is above the knee as there is more risk of embolism
  • occur in the deep veins where blood flow is slower
42
Q

Virchows Triad

What are risk factors for a DVT?

A
  • Hypercoagulable state: pregnancy, contraceptive pills,
  • Circulatory stasis: long periods of sitting/ inactivity
  • Epithelial injury: IV drug abuse, cancer, post operative
43
Q

What are the clinical presentations for DVTs, and possible differential diagnosis?

A
  • asymptomatic
  • unilateral calf swelling/heat/pain/redness/hardness

Differential

  • cellulitis
  • Baker’s cyst
  • muscular pain

Risk factors should be considered

44
Q

How is a DVT diagnosed?

A
  • a doppler ultrasound
  • shows a lack of blood flow in the leg
  • use a Wells score
  • use of a D-dimer test: indicates activation of the clotting cascade

raised score indicates a DVT has a high predictive negative value

45
Q

What is the initial treatment of a DVT?

A
  • Therapeutic anti-coagulation using sub-cut LMW heparin: tinzaparin or enoxaparin
  • Dosing is according to the patient’s weight, no monitoring required
  • if the patient has a renal impairment (creatinine clearances less than 30ml/min) anticoagulant with i.v. unfractionated heparin is used instead. This require monitoring
46
Q

What is the subsequent treatment for a patient with DVT?

A
  • oral warfarin for 3-5 days
  • stop LMW heparin when INR (International Normalised Ratio, based on the prothrombin time) > 2.0 for 2 days
  • if it’s there 1st DVT (femoral or iliac)- 6 months course of warfarin
  • if it’s there 2nd DVT/PE: lifelong warfarin
  • INR should be maintained between 2.0-3.0
47
Q

What are the classical symptoms of a Pulmonary embolism?

A
  • Pleuritic pain
  • acute dyspnoea
  • haemoptysis (coughing up of blood)
  • could cause syncope or death

On examination

  • tachycardic
  • tachypnoiec
  • hypotensive
48
Q

saddle embolism, pre and post embolysis

What investigations can be done to confirm a Pulmonary embolism?

A

CTPA scan

  • CT Pulmonary angiogram
49
Q

What is and what can be seen in a V/Q scan when investigating a PE?

A

a V/Q scan, uses a radioisotope to get images of the lung

  • under perfusion, even though ventilation is very good: V/Q mismatch
  • underlying lung disease

intermediate scans (rarely done)

50
Q

What can be seen on an ECG investigating a PE?

A
  • Sinus tachycardia: an increase in pulse rate
  • Atrial Fibrillation
  • Right Heart strain: right bundle branch block, struggle to get blood through the right lung
  • Classic: SI, QII, TIII pattern on the ECG (rare)
51
Q

What does a CXR when investigating a PE show?

A
  • usually normal
  • may see a small effusion
  • possibly linear atelectasis (shadowing)
52
Q

What are the outcomes for a PE?

A
  • 5% mortality with treatment: even with treatment
  • 4% develop pulmonary hypertension: clots in the pulmonary circulation
  • Cause of death in 10-30% of in-patient post mortems
  • Up to 60% have micro-emboli at post mortem
  • A leading cause of ‘preventable’ death in the western world (25,000 deaths/yr in England)
53
Q

What is the signs and treatment for a massive PE?

A
  • signs of shock, hypotension and acute SOB
  • Mx: thrombolysis and iv heparin
  • this presents with a 2-6% serious risk of bleeding
54
Q

What is the standard treatment for a PE?

A
  • LMW heparin injections – e.g. Tinzaparin
  • Warfarin (target INR 2.5) for 6 months
  • Consider underlying causes: possibly stop taking the pill
  • LMW heparin is better if underlying cancer
  • Inferior Vena Cava filters
  • Consider a DOAC (NOAC) as an alternative
  • Dabigatran p.o (direct thrombin inhibitor)
  • Rivaroxaban p.o (direct Xa inhibitor)
55
Q

What is a thrombophilia screen?

A
  • occasionally in younger patients with VTE (Venous thromboembolism)
  • Inherited risk factors
  • factor V Leiden
  • Prothrombin gene variant

- Anti-thrombin deficiency, rare

- Protein C deficiency, rare

- Protein S deficiency, rare

natural anticoagulant, more prone to clotting if you are deficient in these

  • Acquired risk: anti-phospholipid syndrome
  • increased risk of miscarriage
  • the phospholipid is required as part of the formation of prothrombinase

103: Theme 2 (8 decks)

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