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ICC1 > Haematology > Flashcards

Haematology Flashcards

1
Q

Ischameia vs infarction?

A

Ischaemia: narrowing of blood vessels
Infarction: cutting off of the blood supply

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2
Q

What condition causes pain that radiates to left jaw, left arm and maybe the right shoulder?

A

Myocardial infarction

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3
Q

What are the contents of a blood clot

A

RBCs, fibrin, platelets, other constitutivents.

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4
Q

Main complication of DVT?

A

PE

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5
Q

Why do we mainly give arterial thrombosis patients anti platelets ?

A

The main content of an arterial blood clot are platelets. This clot usually occurs because an arterial plaque ruptures, and platelets go to occlude them.

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6
Q

Why do we gave patients of venous thrombosis anticoagulants?

A

The main content of a venous clot is usually the fibrin mesh network. Happens due to vessel damage or blood that moves slowly.

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7
Q

State virchow’s triad.

A

TRIAD OF THROMBOSIS:

  1. Hyper coagulable sate (pregnancy, previous thrombosis, oral contraceptives)
  2. Endothelial damage/ vessel wall injury
  3. Stasis of blood
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8
Q

Risk factors for arterial thrombosis

A 
Positive family history 
Male sex 
Hyperlipidaemia 
Hypertension 
Diabetes mellitus 
Hyperhomocysteinaemia 
cigarette smoking
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9
Q

Give the two biggest examples of venous thromboembolism

A

DVT and PE

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10
Q

What are the 2 main factors of virchow’s triad causing venous thrombosis?

A

Stasis: immobility, stroke
systemic hyper coagulability due to:
- reduced anticoagulants (protein C, S, antithrombin III)
- clotting factor mutations (factor V Leiden, prothrombin G20210 mutation
increased procoagulants (clotting factors, lupus anticoagulant, homocysteine tissue factors)

VESSEL INJURY IS MORE OF AN IMPORTANT FACTOR IN ARTERIAL THROMBOSIS

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11
Q

What is factor v Leiden?

A

a mutation of factor 5 (labile factor) . This mutation can increase your chance of developing abnormal blood clots, most commonly in your legs or lungs.

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12
Q

What is a lupus anticoagulant

A

Lupus anticoagulant (LA) is an antiphospholipid antibody found in many people with lupus. LA increases your blood’s ability to clot. Therefore, if you have this antibody, you have a greater risk of experiencing a blood clot.

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13
Q

What is prothrombin G202010 mutation?

A

An inherited condition that increases your predisposition to develop abnormal blood clots in the veins (deep vein thrombosis or DVT) and lungs (pulmonary embolism or PE).

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14
Q

Define thrombophilia

A

This term thrombophilia describes an inherited or acquired tendency for venous thrombosis
INHERITED:
Prothrombin mutation, hyperhomocysteinemia, deficiency of normal anticoagulants
ACQUIRED:
Lupus anticoagulant, polycythemia, HIIT (heparin induced thrombocytopenia and thrombosis)

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15
Q

What is heparin and what is its mechanism of action

A

The most important anti coagulant, works by activating anti thrombin III, a very important natural anticoagulant.

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16
Q

When to suspect inherited thrombophilia?

A

Thrombosis at a REALLY young age (25)

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17
Q

What is the inheritance pattern of antithrombin III deficiency?

A

AUTOSOMAL DOMINANT.

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18
Q

What are the consequences of antithrombin III deficiency

A

Recurrent venous thrombosis, may have arterial thrombosis, at young age (25)

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19
Q

Why does the PTT not increase in patients with antithrombin III deficiency that are on heparin?

A

The main mechanism of action of heparin is to increase the action of antithrombin III. Therefore, with no antithrombin III, there is nothing for heparin to work on, therefore there is no increase in clotting time.

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20
Q

Why does the PTT not increase in patients that DO NOT HAVE antithrombin III deficiency that are on heparin?

A

maybe this patient doesn’t have a heparin deficiency, but instead has a mutation in the heparin binding site of the antithrombin III (therefore not activated). OR a mutation in the thrombin binding site (therefore incapable to inhibit thrombin)

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21
Q

Why is nephrotic syndrome thought of as a hypercoagulable state?

A

Loss of proteins in urine = loss of natural anticoagulants = loss of antithrombin III

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22
Q

What is disseminated intra vascular coagulation (DIC)?

A

Disseminated intravascular coagulation (DIC) is a serious disorder in which the proteins that control blood clotting become overactive.Sep

23
Q

Why should we never antithrombin III level when on heparin?

A

Heparin uses up and consumes thrombin so will alter antithrombin level.

24
Q

Which coagulation factors do protein c and S work on?

A

5 and 8

25
Q

Normal levels of protein C?

A

65-135IU/dl

26
Q

Inheritance pattern of protein C deficiency?

A

Autosomal dominant

27
Q

Main functions of protein C?

A

The he main function of protein C is the protelytic cleavage of FVa and FVIIIa (HAS TO BE ACTIVATED)

•  It inhibits PAI-­‐3 (plasminogen activator inhibitor). activity leading to increasing the fibrinolytic activity

28
Q

What natural anticoagulants are vitamin K dependent?

A

Protein C and S

29
Q

What is the difference between PT and PTT?

A

PT: extrinsic pathway
PTT: intrinsic pathway

30
Q

How are PT and PTT affected in protein C deficiency?

A

Heterozygous PC deficiency: normal PT and aPTT Homozygous PC deficiency: abnormal basic coagulaCon tesCng consistent with DIC

31
Q

How does homozygous protein C deficiency present?

A

Purpura fulminans in infancy (black, gangrenous lesions due to thrombosis and necrosis)

32
Q

What is the most common reason for activated protein C resistance?

A

Factor 5 Leiden mutation. Makes activated factor V less susceptible to cleavage by activated protein C.

33
Q

How can we detected factor 5 Leiden gene?

A

PCR

34
Q

What are the consequences of factor 5 Leiden?

A

Increased tendency to venous thromboembolism due to:

  • resistance of factor 5 Leiden to protein C
  • continuous generation of thrombin, activating factor 5 and 7.
35
Q

What activates factor 5?

A

Thrombin.

36
Q

What is the name of the prothrombin mutation causing thrombophilia?

A

Prothrombin G20210A

37
Q

Function of plasminogen?

A

Plasminogen is the inactive precursor of plasmin, a potent serine protease involved in the dissolution of fibrin blood clots.

38
Q

Why is pregnancy associated with a hyper coagulable state?

A

Increase in plasminogen activator inhibitor-II

39
Q

What is lipoprotein a associated with? What effect does it have on the fibrinolytic system?

A

Associated with LDL and artherosclerosis.
INHIBITS PLASMIN AND THEREFORE INHIBITS FIBRINOLYSIS:
- decreases tPA, increases PAI, therefore causing fibrin accumulation
- main component of atherosclerosis

40
Q

Myeloproloferative diseases leading to thrombophilia?

A

Polycythemia

Essential thrombocythemia

41
Q

Why does hyper homocysteinemia cause thrombophilia

A

Endothelial dysfunction (one of virchow’s triad!) smooth endothelium is a natural anticoagulant

42
Q

Risk factors for hyperhomocysteinemia?

A
  1. B12 AND FOLIC ACID DEFICIENCY (they are needed to prevent accumulation of homocysteine)
  2. RENAL DAMAGE (homocysteine is partly excreted by the liver)
  3. Smoking
  4. Age
  5. Men, post menopausal women.
43
Q

If we have a woman who got a stroke at a very young age, what is a VERY important question to ask?

A

Ask about CHILDREN!!!

If she’s has abortions or miscarriages, then she probably has antiphoshpolipid syndrome which explains the blood clots

44
Q

What do we need to diagnose antiphospholipid syndrome?

A
45
Q

What type of heparin causes HITT?

A

Unfractionated and high molecular weight heparin.

46
Q

How can we diagnose HITT

A

Before heparin therapy perform APTT to know the baseline

 Before heparin therapy perform platelet count to be able to diagnose HI-­‐thrombocytopenia

47
Q

What are the 4 THINGS you need to ask to diagnose thrombophilia?

A
  1. Age: (young age indicates inherited thrombophilia)
  2. Medical history :
    - drugs: HITT?
    - any medical condition causing thrombophilia
  3. Past history: recurrent VTE?
    • in women: you MUST ask about oral contraceptives and miscarriages**
      4. Family history: hereditary thrombophilia
48
Q

Normal level of d dimer?

A

Less than 200mg/dl

49
Q

What are conditions that may raise d dimer?

A

DIC, DVT, PE

Pregnancy, malignancy

50
Q

Lab testing to diagnose thrombophilia?

A 
Complete blood picture
•  ESR
•  CRP
•  Prothrombin time
•APTT
•  Thrombin time
•  Fibrinogen
•  FDPs/D-­‐dimer:
51
Q

Why is there prolonged PTT in anti phospholipid syndrome?

A

The APS ABs react with the phospholipid reagent of the APTT test, therefore interfering with clot formation.

52
Q

How do we treat pregnant women with antiphospholid syndrome?

A

Heparin (anticoagulant). Must be stopped 24 hours before delivery.

53
Q

What is the molecular method we use to identify inherited thrombophilia

A

Real time pcr

54
Q

When to collect blood samples for thrombophilia testing?

A

Tests for thrombophilia are affected by the acute post-­‐thrombotic state and by anticoagulant therapy. Therefore, thrombophilia tests are usually best delayed until at least 1 month acer completion of a course of anticoagulant therapy since diagnosis of a thrombophilic disorder does not influence the management of the acute thromboembolic event.

ICC1 (4 decks)

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