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Med 2 > Coagulation Disorders > Flashcards

Coagulation Disorders Flashcards

1
Q

What are the different stages of haemostasis?

A
  1. constriction of blood vessels
  2. Temp platelet plug =primary haemostasis
  3. Activation og coagulation cascade
  4. Formation of ‘fibrin plug’ =secondary haemostasis
  5. Clot resolution - tertiary haemostasis.
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2
Q

What is the process of vasoconstriction in coagulation?

A

Within 30 minutes of trauma to bv
ECM/collagen exposed to blood components
Release of clotting factors and platelets
Altered substances released by endo cells - dec NO, increase endothelin and thromboxane

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3
Q

What happens during formation of a primary platelet plug?

A

Cytokines and inflammatory markers lead to adhesion of platelets and aggregation
vWF helps platelets adhere to site on injury
Activates platelets release granules - positive feedback for process

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4
Q

What is the role of the coagulation cascade in blood clots?

A

Extrinsic and intrisncie pathway
Occr spontaneous and result in activation of factor X.
Continues as the common pathway.
Each step involves various coagulation factors
End goal - fibrinogen-> fibrin to form a stable clot and mesh formation (secondary haemostasis)

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5
Q

What coagulation factors are Vitamin K dependent?

A

1972
10, 9, 7, 2

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6
Q

How does clot resolution occur?

A

Tertiary haemostasis - activated platelets contract, leading to shrinkage of the clot volume.
Plasminogen is activates to plasmin = lysis of the fibrin clot
Restores blood flow in the damaged vessels.

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7
Q

What are the different indications for a coagulation screen?

A
  1. Confirm a suspected coagulopathy
  2. Acute blood loss
  3. Monitor a patient on anti-coagulant drugs
  4. Assess coagulation status prior to surgery
  5. Assess the synthetic function of the liver
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8
Q

What investigations are commonly ordered alongside a coagulation screen?

A

FBC for platelets
LFTs for general liver function
Albumin - liver synthetic function/malnutrition
D-dimer (if clinically indicated)
Cross match and group and save - if requiring blood transfusion.

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9
Q

How should a prothrombin time (PT) be interpreted?

A

Extrinsic pathway
It can be standardised as the INR for monitoring warfarin
Mainly focuses on factor 7
Higher time indicates higher bleeding risk.

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10
Q

What can cause a deranged PT test result?

A

Overall clotting factor synthesis - liver disease, DIC, Vitamin K deficiency and warfarin.

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11
Q

How should an activated partial thromboplastin time (aPTT) be interpreted?

A

Intrinsic pathway
Normally focus on VIII, IX, XI
High time = increased risk of bleeding.

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12
Q

What can cause an abnormal aPTT?

A

Overall cloting factor synthesis/consumption - DIC, liver failure, VitK defieicny
Von Willebrands disease
Haemophilias

Note anti-phospholipid syndrome can cause a high aPTT despite being a clotting disorder as it inactivates phospholipid in test.

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13
Q

What is the genetics of Haemophilia?

A

X-linked recessive condition (primarily affects males)
Haemophilia A - factor 8 deficiency - more common
Haemophilia B - factor 9 deficiency - Christmas disease

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14
Q

How does Haemophilia tend to present?

A

Severe bleeding disorders with a risk of excessive bleeding in response to minor trauma or even spontaneously.
Neonates - IC haemorrhage, haematoma, cord bleeding
Spontaneous haemarthrosis (ankle, knee, elbow).
May bleed from oral mucosa, epistaxis, GIT, UT.

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15
Q

What is the common management of Haemophilia?

A

IV infusion of affected clotting factors.
(beware of formation of inhibitor antibodies against these)

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16
Q

What is the most common inherited bleeding disorder?

A

Von Willebrand’s disease

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17
Q

What is the genetics behind Von Willebrands disease?

A

Autosomal dominant
Deficient, absence of malfunctioning of vWF - reduces platelet adhesion, aggregation.

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18
Q

What are the three different types of von Willebrand disease?

A

type 1 - partial deficiency of vWF (most common
type 2 - reduced function of vWF
type 3 - complete deficiency of vWF (rare and severe)

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19
Q

What is the common presentation of von Willebrands disease?

A

Unusually easy, prolonged/heavy bleeding - gums, nosebleeds, menorrhagia, surgical operation sites
FH very important.

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20
Q

How is von Willebrands disease often diagnosed?

A

History - inc FH
Bleeding scores
Lab investigation - coag screen
Genetic testing
Common have a low F8 as vWF transports this.

21
Q

What is the management for von Willebrands disease?

A

Only in response to significant bleeding/trauma:
1. Desmopressin (mimics ADH) - stimulates vWF release from endothelial cells
2. Tranexamic acid (anti-fibrinolytic)/mefenamic acid (NSAID)
3. vWF infusion +/- factor 8
4. Mirena coli, norehisterone, hysterctomy

22
Q

What is disseminated intravascular coagulation?

A

Rare but lifethreatening - abnormal blood clotting throughout the body.
Two stages:
1. Overactive clotting -> blood clotes throughout vessels = organ damage
2. Platelets and clotting factors run out -> uncontrolled bleeding

23
Q

What commonly causes DIC?

A

Inflammation - sepsis or malignancy

24
Q

What is the common treatment for DIC?

A

Manage underlying cause +/- blood products.

25
Q

What makes up Virchow’s triad?

A

Hemodynamic changes/stasis
Endothelial injury/dysfunction
Hypercoagulability

26
Q

What are some specific hyper-coagulable conditions?

A

Antiphospholipid antibody syndrome
Factor 5 Leiden mutation
Protein C deficiency
Protein S deficiency
Prothrombin gene mutation

27
Q

What is the typical question stem for antiphospholipid syndrome?

A

Young female - recurrent miscarriages and personal/family history of VTE

28
Q

What is the relevant risk of a DVT when a patient has a septal defect in their heart?

A

Thrombus can pass into left side heart and into systemic circulation
Travels to brain and may cause a stroke.

29
Q

What inpatient prophylaxis may be offered for a VTE?

A

LMWH - enoxaparin injections
Anti-embolic stokcings - not in PAD

30
Q

What is the PERC rule?

A

Used when physician concern over a DVT/PE is low - may justify not performing a D-dimer

31
Q

When might thrombolysis be indicated for a PE?

A

If PE confirmed and haemodynamically stable.

32
Q

What is the first line anti-coagulant for DVT/PE in pregnancy?

A

LMWH

33
Q

What is Budd-Chiari syndrome?

A

An obstruction to the outflow of blood from the liver due to thrombosis in the hepatic veins or inferior vena cava
Associated with hyper-coagulable states
Present: abdominal pain, hepatomegaly, ascites.

34
Q

What is the common treatment for Budd-Chiari syndrome?

A

Confirm with doppler ultrasonography
Anticoagulation (LMWH)
Endovascular procedure (thrombolysis or angioplasty)
Trans-jugular intrahepatic portosystemic shunt.
Liver transplant.

35
Q

What are the most common anti-platelets?

A

Aspirin = COX inhibitor
Clopidogrel and Aspirin = platelet aggregation inhibitors

36
Q

What are some common indications of anti-platelet medications?

A

ACS
post-PCI/CABG
Mechanical heart valves
Acute ischemic stroke
Essential thrombocytosis
Primary prevention of VTE

37
Q

What are some adverse effects of anti-platelets?

A

Upper GI bleed
Easy bruising
Haematuria
Epistaxis
Thrombocytopaenia

38
Q

What are some contraindications for anti-platelets?

A

Oesophageal varices
Recent stroke (<2yrs)
History of ICH/sig bleed
Major surgery - clopidogrel/tricagerlor stopped 5days prior to major surgery

39
Q

What are the key indications of anti-coagulants?

A

Atrial fibrillation
VTE
Heart valve replacements
VTE prevention in high-risk patients

40
Q

What are the common contraindications for anti-coagulants?

A

Active bleeding
Coagulopathy
Recent major surgery
History of ICH
GI bleed
Aortic dissection
Geriatrics (patient case be case)

41
Q

How does kidney disease affect anti-coagulation choice?

A

Stage 1-3 DOACs are preferred
Stage 4 - DOAC or warfarin
End-stage renal disease - warfarin.

42
Q

Compare the use of unfractionated and LMW heparin?

A

Unfractionated - prevention and treatment of VTE, rapid onset, short half life
LMW - longer duration of action, longer half life
Both are complex with AT-3 to inhibit various clotting factors.
Monitored with anti-factor Xa assay.

43
Q

What is the key clinical knowledge of warfarin?

A

Inhibits VitK (affects clotting factors 10,9,7,2)
Narrow therapeutic window - requires frequent monitoring with INR
Affect altered by diet, other drugs, genetic mutations

44
Q

What is the main mechanism of action of direct thrombin inhibitors?

A

Dabigatran
Inhibit the cleavage of fibrinogen to fibrin by thrombin (factor 2a)

45
Q

What is the key clinical knowledge of a DOAC?

A

Inhibit 2a or Xa
Less suspectible to interaction and rarely require monitoring
Apixaban - oral only, non-valvular AF, prevent/treat VTE.

46
Q

How can anti-coagulants be reversed?

A

Activated charcoal if within 2hrs of last ingestion
Haemodialysis
Blood transfusion for anaemia
Platelet transfusion for thrombocytopenia
Surgical or endoscopic intervention
Warfarin = Vit K

47
Q

What is meant by bridging with anti-coagulants?
When should it be used?

A

Used for patients with consideral risk of thrombotic events
DOACs - takes 2-3hrs
Warfari - 4 to 5 days

The use of a short acting anti-coag (LMWH?UFH) when a normal anti-coagulat must be stopped for a short period of time.

48
Q
A

Med 2 (22 decks)

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