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Year 3 TCDs > Clotting Factors > Flashcards

Clotting Factors Flashcards

1
Q

What inhibits blood from clotting?

A

Natural inhibitors (i.e. Heparin)

  • Protein C + S
  • Antithrombin 3
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2
Q

What dissolves a blood clot?

A

Plasminogen/plasmin system (rTPA - increases plasmin activity)

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3
Q

What are 4 ways to assess a bleeding patient via their bloods?

A
  1. FBC with platelet count
  2. PT
  3. APTT (activated partial thromboplastin time)
  4. Fibrinogen
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4
Q

What is a 50/50 mixture study and what can it indicate?

A

If PT/APTT are abnormal a 50/50 mixture study compares the patient’s plasma with normal plasma

If there’s a correction = deficiency of coagulation factor
If no correction = inhibitor present

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5
Q

Name some common X-Linked recessive disorders

A
  1. Red-Green colour blindness
  2. Hemophilia A (factor 8 gene mutation + thus factor 8 deficiency)
  3. Hemophilia B (factor 9 deficiency)
  4. Duchenne Muscular Dystrophy (mutation in dystrophin gene: loss of skeletal muscle control -> respiratory failure -> death)
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6
Q

What blood tests would you order if you suspected a familial blood disorder?

A
  1. Full blood count

2. Clotting tests (PT, APTT)

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7
Q

What clotting factors are affected by APTT?

A

Factors 8, 9, 11, 12 and von Willebrand factor

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8
Q

What is the treatment for hemophilia A?

A
  1. Clotting factor products
    - Plasma-derived factor concentrates
    - Recombinant factor concentrates (no risk of other blood-borne viruses)
  2. Emicizumab
    - Replaces the function of factor 8
    - Used to either prevent or reduce the frequency of bleeding episodes in people with hemophilia A
    - Given as injection under the skin
  3. Desmopressin Acetate
    - Act to release factor 8 from where it is stored in the body tissues
    - Can be given thru vein or via nasal spray
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9
Q

What is the function of Von Willebrand factor?

A
  1. Binding to other proteins, in particular factor 8

2. Important in platelet adhesion to wound sites

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10
Q

What is an embolus?

A

An embolus is some material which is transported in the blood stream and lodges in a blood vessel at a different site. An embolus can be gaseous, e.g. an air bubble, or solid, e.g. part of a thrombus. When it impedes or blocks blood flow in the artery it causes an embolism, the consequences of which are infarction of the tissue supplied by the artery. The bigger the embolus the bigger the artery it blocks and the bigger the area of infarction.

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11
Q

What is a thrombus?

A

A blood clot within the body

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12
Q

What is a pulmonary embolism? Explain from the presentation of a DVT

A

A Deep Vein Thrombosis (DVT) is formation of a thrombus in the deep veins, usually of the leg.

When part of the thrombus break off, travels in the venous system to the heart and then into the right atrium, passes out of the right ventricle and into the pulmonary arteries, where it lodges and blocks the artery – this is called Pulmonary Embolism.

A “massive” pulmonary embolism can block the flow of blood in the right atrium and ventricle leading to a cardiac arrest.

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13
Q

How does lower limb DVT present?

A

An unilateral, swollen, painful leg

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14
Q

What else may present like a lower limb DVT? (3)

A
  1. Cellulitis (infection of the skin of the leg)
  2. A ruptured baker’s cyst
  3. Muscle haematoma
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15
Q

On examination, what signs would indicate a DVT?

A
  1. Warm, swollen leg.
  2. Tenderness in the calf – worse with dorsiflexion of the ankle (Homan’s sign).
  3. Calf circumference < 3 cm compared with unaffected leg.
    - To ensure you are comparing like for like – take a tape measure and make a mark at 10cm from tibial tuberosity on each leg. Then use this mark to measure circumference.
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16
Q

What are the main causes of DVT?

A
  1. Inactivity
  2. Hospital inpatient
  3. Blood vessel damage (i.e. vasculitis, varicose veins)
  4. Medical/genetic conditions (i.e. cancer, heart disease, thrombophilia)
  5. Pregnancy
  6. OCP/HRT
  7. Obesity, smoking, dehydration, elderly
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17
Q

What are typical symptoms of PE?

A
  1. Sudden onset of pleuritic chest pain;
  2. Shortness of breath
  3. Haemoptysis
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18
Q

What are the physical signs of PE?

A
  1. Increased respiratory rate
  2. tachyarrythmias (commonest sinus tachycardia but might be atrial fibrillation)
  3. Possibly signs of DVT
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19
Q

What might you see on ECG with PE?

A

The commonest abnormality of an ECG is sinus tachycardia. However you might see atrial fibrillation or evidence of right heart strain (i.e. right axis deviation and right bundle branch block) with the classical S1Q3T3 pattern

  • Deep S wave in lead 1
  • Deep Q wave in lead 3
  • T wave inversion in lead 3
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20
Q

What might you see on ABG with PE?

A

Hypoxia (low oxygen level) or type 1 respiratory failure

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21
Q

What is the scoring system for DVT and PE?

A

Wells Score
> 2 = DVT likely
> 4 = PE likely

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22
Q

If the Wells Score is “low clinical probability” what should you check next?

A

D-dimer (highly sensitive for VTE, DVT, PE)

If negative = VTE can be excluded
If positive = CTPA scan for PE, US doppler scan for DVT

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23
Q

How is a massive PE defined?

A

A massive pulmonary embolism is a large clot which lodges in the right side of the heart, or in both pulmonary arteries (saddle embolus) or 1 of the pulmonary arteries. It classically presents with syncope (loss of consciousness) as well as the other symptoms of PE. It is defined clinically as a massive PE by the presence of arterial hypotension (systolic blood pressure less than 100 mmHg) or cardiogenic shock / cardiac arrest. It is a medical emergency and requires urgent thrombolysis.

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24
Q

What factors are responsible for inhibiting the clotting of blood?

A

Protein C + S

Antithrombin 3

examples are heparins

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25
Q

What factor stabilizes the fibrin clot formation?

A

Factor 13

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26
Q

What system is responsible for dissolving clots? What is the agent that is commonly used in the medical environment?

A

Plasminogen/plasmin system

rTPA = tissue plasminogen activator - increases plasmin activity

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27
Q

How is the extrinsic coagulation cascade pathway initiated?

A

Tissue factor (TF) from damaged endothelial cells of vessel walls activates FACTOR 7 to initiate the EXTRINSIC PATHWAY

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28
Q

How is the intrinsic coagulation pathway initiated?

A

Pre-Kallikrein (PK) and HMWK (kininogen) activate FACTORS 11 + 12 to activate the INTRINSIC PATHWAY

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29
Q

How is Factor 10a activated?

A

It is the centre of the coagulation cascade and is activated by FACTOR 11, 12 + 7

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30
Q

What factor does heparin + DOACs work on?

A

10a

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31
Q

What is the function of factor 10a?

A

It forms thrombin which is then used to convert fibrinogen into fibrin

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32
Q

What are the 3 main concepts of the coagulation cascade?

A
  1. Coagulation cascade tries to form a clot
  2. Natural inhibitors prevent clot from forming
  3. If clot forms plasminogen/plasmin system can dissolve it
33
Q

Outline the factors involved in the extrinsic pathway and how this pathway is measured in bloods?

A

Tissue Factor (TF) -> Factor 7a -> Factor 10a

Measured by PT

34
Q

Outline the factors involved in the intrinsic pathway and how this pathway is measured in bloods?

A

Factor 9 -> Factor 12 -> Factor 8a -> Factor 10a

Measured by APTT

35
Q

Outline the factors involved in the common pathway and how this pathway is measured in bloods?

A

Factor 10a -> Thrombin

Measured by thrombin time. However, abnormality in the common value will increase both PT and APPT so normally measure FIBRINOGEN.

36
Q

What are causes of a prolonged PT?

A
  1. Warfarin
  2. Factor 7 deficiency
  3. Factor 2 deficiency
  4. Factor 5 deficiency
  5. Factor 10 deficiency
37
Q

What are causes of a prolonged APTT?

A
  1. Heparin
  2. Factor 8 deficiency
  3. Factor 9 deficiency
  4. Factor 11 deficiency
  5. Factor 12 deficiency (no bleeding/bruising)
  6. Von Willebrand’s disease
38
Q

What are 4 pathologies that could be causing a prolongation of both PT and APTT?

A
  1. Vitamin K deficiency + low fibrinogen -> liver disease/malabsorption
  2. DIC (disseminated intravascular coagulation) + low fibrinogen -> Fibrin degradation products, high D-dimer, low platelets, RBC fragments
  3. Heparin toxicity + normal fibrinogen
  4. Deficiency in factor 5 or 10 + normal fibrinogen
39
Q

What are the vitamin K dependent factors?

A

Factor 2, 7, 9, 10, Protein C + S

40
Q

What is the diagnostic triad for blood clotting disorders?

A
  1. Personal history of bleeding
  2. Family history of bleeding
  3. Supportive lab tests
41
Q

What should you ask in the personal history of bleeding?

A
  1. Bruising: no injury, lumpy
  2. Epistaxis: > 30min + frequency
  3. GI: mouth -> anus
  4. Menses: Duration, flooding/clots, # of pads
  5. Urine: Hematuria
  6. Surgical history, dental history, cuts/injuries
42
Q

Name 4 platelet tests

A
  1. FBC
  2. Microscopy
    - Large platelets: Bernard Soulier Syndrome
    - Small platelets: Wiskott Aldrich Syndrome
    - Neutrophil inclusions: May Hegglin Anomoly
    - Platelet inclusions: Paris Trousseau/Jacobsen’s
  3. PFA: screen of platelet function
    - Lab bleeding time
    - Insensitive
  4. Specialist tests
    - Aggregation + nucleotide inclusion
    - Glycoproteins
    - Molecular genetics (MYH9)
    - Bone marrow: consumption vs production
43
Q

What are 4 coagulation tests?

A
  1. PT
  2. APTT
  3. Fibrinogen
  4. Thrombin time (not used much anymore)
44
Q

Name 3 ways you can assess clot stability?

A
  1. Euglobin clot lysis (make clot on orange stick, is it still there 24h after refrigeration)
  2. Factor 13 assay
  3. PAI-D (Amish, Chinese)
45
Q

What should you do if there’s no abnormalities on coagulation/platelet tests but a good bleeding history?

A
  1. von Willebrand’s tests (factor 8, vWF antigen, vWF activity)
  2. Platelet aggregation + nucleotide release
46
Q

What is the treatment of hemophilia based on?

A
  1. Factor level (<1iu/dl; 1-5; >5)
  2. Bleeding (spontaneous, slight injury, trauma)
  3. Frequency (1-2wk, 1/mo, rare)
  4. Site (often joint, less often joint, rare)
47
Q

What is the normal range for factor 8?

A

50-150iu/dl

48
Q

What is the treatment of hemophilia A?

A
  • Avoid drugs like aspirin (can cause platelet dysfunction)
  • Give coagulation factor 8 IV immediately
  1. Factor 8: Recombinant, large molecule = decreased distribution in body
    - Amount needed: rise x weight (kg)/2
    - Half-life: 8h (1-3x/day)
  2. Desmoppressin (DDAVP)
    - Releases stored factor 8 so increases factor 8 two-three times its level. Test with a trial of the drug first so no hypotension
    - Given SC, IV, intranasal
49
Q

What is the treatment of hemophilia B?

A

Factor 9: Recombinant, small molecule = increased distribution in body

  • Amount needed = rise x weight (kg)
  • Half-life: 18-24h (1x/day)
50
Q

What is a drug that can be used in both hemophilia A and B?

A

Tranexamic acid

  • Anti-fibrinolytic
  • Oral
  • Decreases plasmin/plasminogen system
  • Increases time clot stays
51
Q

What does prophylaxis treatment for hemophilia involve?

A
  1. Primary prophylaxis - start between 18mo-3y
  2. Secondary prophylaxis - after 3 joint bleeds
  3. Give factor 9 -> 2x/week
  4. Give factor 8 -> 3x/week, alternate days
  5. Very effective + expensive
52
Q

What is von Willebrand’s Disease?

A
  • Commonest coagulopathy (0.5% of population)
  • Mucocutaneous bleeding
  • 15% menorrhagia
  • 3 types
  • > Type 1: decreased amount of normal vWF protein
  • > Type 2: abnormal vWF protein (IIb)
  • > Type 3: no vWF protein
53
Q

How do you test for von Willebrand disease?

A

von Willebrand screen:

  1. Factor 8 (normal 50-150iu/dl)
  2. vWF antigen
  3. vWF activity
54
Q

How do you differentiate between type 1 and type 2 von Willebrand disease?

A

Look at the vWF activity: vWF antigen ratio.

If activity:antigen > 0.6 = T1
If < 0.6 = T2

55
Q

Describe type 1 von Willebrand disease

A
  • mild disease
  • bruising/mucosal bleeding
  • menorrhagia
  • invasive procedures = increased bleeding
56
Q

Describe type 2 von Willebrand disease

A

Like type 1 except for type 2b:

  • Overactive protein
  • Can result in thrombocytopenia
  • Avoid desmoppressin -> will release vW from stores
  • Use vWF concentrate to treat
57
Q

Describe type 3 von Willebrand disease

A
  • Severe
  • Increased bleeding + joint bleeding
  • Operations without proper cover = life-threatening
58
Q

What is the treatment for each type of von Willebrand’s disease?

A

Type 1: desmopressin + tranexamic acid

Type 2: vWFactor/DDAVP (not for type IIb)

Type 3: vWFactor

  • Give iron b/c of increased bleeding
59
Q

What is Virchow’s triad?

A
  1. Stasis of blood flow (i.e. immobile)
  2. Hypercoagulability (reactant proteins = fibrinogen, factor 8, vWF)
  3. Endothelial injury
60
Q

What is the pharmacological management of a VTE?

A
  1. LMWH
  2. UFH (unfractioned heparin)
  3. DOAC
    - Risk of bleeding (use protamine to reverse effects)
    - Allergies/heparin induced thrombocytopenia + thrombosis
61
Q

Why is warfarin not used as much anymore?

A
  1. Intensity of anticoagulation is unpredictable

2. Increased bleeding risk

62
Q

What is acute VTE management?

A
  • Tender calf, groin over femoral vein, swollen, red/hot on examination
  • V/Q scan of lungs for PE
  • Wells Scores for DVT, PE
  • Start treatment before investigations
  • Use heparin/UFH
  • Give oral warfarin (takes 48-72h to have effect). Will be taken at home. When INR > 2 can stop heparin
63
Q

What are the 4 possible fates of a thrombus?

A
  1. Dissolution -> fibrinolysis
  2. Propagation -> gets bigger
  3. Recanalization -> adhesion of thrombus to vein wall, inflammatory response, revascularisation
  4. Embolization -> breaks off into bloodstream to other site in body
64
Q

What are 3 possible clinical consequences of VTE?

A
  1. DVT-PE -> venous
  2. MI + stroke -> arterial
  3. DIC -> widespread thrombi = concurrent widespread bleeding
65
Q

Name 3 common types of emboli

A
  1. Thromboembolis
  2. Fat -> common with broken bones
  3. Amniotic fluid -> trauma to womb
66
Q

What is the agent of choice for thrombolytic therapy?

A

tPA (tissue plasminogen activator) -> breaks down the clot

67
Q

What factor deficiency causes thrombophilia?

A

Factor 5 deficiency which is produced by protein C + S

68
Q

Maureen is 46year old chronic alcoholic.

When reviewed in OPD there were concerns that her liver function was deteriorating despite having been abstinent for over 4 years.

Maureen is brought in to have a liver biopsy but before having the procedure she undergoes blood tests.

Results of blood tests:

  • Haemoglobin: 115g/L (normal range 130-170
  • Platelets: 126x109/L (normal range 150-400)
  • PT: 27.2s (range 10.5-14.0)
  • APTT: 47.6s (range 24.0-32.0)
  • Fibrinogen: 0.7g/L (range 2.4-4.0)

What would you do next?

A

Administer fresh frozen plasma (FFP) and repeat tests pre-biopsy

69
Q

How many deaths/yr are caused by VTE?

A

25000 in the UK

- more than that of road traffic accidents/yr

70
Q

Why are anti-embolus stockings contraindicated in patients with intermittent claudication?

A

Anti-embolus stockings exacerbate pre-existing peripheral arterial disease

71
Q

A 55-year-old man attends the local anticoagulant clinic. He was initiated on enoxaparin 120mg daily SC two weeks ago for a recently diagnosed DVT. PMH. Cancer of the stomach, hypertension DH. Oramorph 10mg 4-hrly PRN, ramipril 10mg daily and omeprazole 20mg daily.

He reports feeling well and reports no episodes of unexplained bruising or bleeding.

The plan is to keep this gentleman on enoxaparin and not initiate warfarin due to his cancer diagnosis.

Only a full blood count has been requested for this gentleman and the results are as follows:

Yesterday - Hb 150 g/L (130–180), platelet count 250 × 109/L (150–400 x 109/L)

Last week - eGFR 50 mL/min (>90).

What is the most appropriate additional monitoring option for identifying potential adverse effects of this treatment?

A

Potassium levels should be monitored when patients take LMWH for longer than 7 days.

Those patients that have diabetes, chronic renal impairment and on medication that can increase potassium levels are more susceptible to hyperkalamia (This patient was taking ramipril)

72
Q

Practice prescribing a medical patient a regular dose of a low molecular weight heparin for the prophylaxis of a DVT. The patient has no known drug allergies. The patients eGFR >90mL/min.

A

Enoxaparin 40mg SC

73
Q

What factor does vWF carry? What process does this factor help in?

A

Factor 8

Helps in platelet adhesion. (von Willebrand’s disease causes mucocutaneous bleeding)

74
Q

What sex is more commonly affected by Von Willebrand’s Disease? Hemophilia?

A

vWD = females

Hemophilia = males

75
Q

Name 9 DVT risk factors

A
  1. Age > 60
  2. BMI > 30
  3. PMH/FH of VTE
  4. OCP/HRT
  5. Varicose veins
  6. Hx of cancer
  7. Known thrombophilia
  8. Inpatient stay > 3 days
  9. Anaesthesia > 90min
76
Q

What is the rule for investigating VTE?

A

Don’t investigate VTE unless this can be done within 1hr for PE or within 4hr for DVT
- Give HEPARIN immediately if Well’s Score > 2 (for DVT) or > 4 (for PE)

77
Q

What is the issue with giving macrolide antibiotics (i.e. clarithromycin) to a patient on warfarin?

A

Warfarin is metabolized by Cytochrome P450 and this enzyme is inhibited by macrolide antibiotics. Thus, the antibiotic must be switched as it will increase the anticoagulatory effects of warfarin (i.e. INR > 3).

78
Q

What is the treatment for Sickle Cell frequent crises?

A

Hydroxycarbamide

Year 3 TCDs (24 decks)

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