Revision lecture II Flashcards

1
Q

What measures the extrinsic pathway?

A

INR and PT

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2
Q

What is INR?

A

INR is ratio between the patients PT and the normal PT

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3
Q

What measures the intrinsic pathway?

A

aPTT

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4
Q

What part of the clotting cascade is affected by haemophilia?

A

Factor VIII (intrinsic)

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5
Q

What part of the clotting cascade is affected Liver disease?

A

Everything! Clotting factors are made in the liver.

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6
Q

What part of the clotting cascade is affected in DIC?

A

I, II, V, VIII, XI (intrinsic and common)

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7
Q

What part of the clotting cascade is affected by warfarin/vitamin K deficiency?

A

Synthesis of VII, IX, X

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8
Q

What part of the clotting cascade is affected by dabigatran?

A

Thrombin

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9
Q

Warfarin

A
  • Oral anticoagulant
  • Vitamin K antagonist –> responsible for II (prothrombin), VII, IX, X
    Affects VII - extrinsic pathways therefore monitored by INR
  • p450 enzyme inhibitors/inducers need to be careful of as that can increase clotting/bleeding
  • affects extrinsic and common
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10
Q

What part of the clotting cascade is affected by other DOACs (X)

A

Xa (common)

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11
Q

What part of the clotting cascade is affected by von willebrand disease?

A

vWF - primary haemostasis

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12
Q

Haemophilia

A
X linked recessive disease 
Haemophilia A = VIII 
Haemophilia B = IX (Christmas disease) 
Intrinsic pathway = increased aPTT 
haemarthroses --> leading to joint complications 
prolonged bleeding
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13
Q

Bleeding + Warfarin - what do you do when there is a major bleed?

A

Stop warfarin
Give IV vitamin K
Consider PCC or FFP

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14
Q

Bleeding + Warfarin - what do you do when there is an INR >8 and minor bleeding?

A

Stop Warfarin

Give IV vitamin K

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15
Q

Bleeding + Warfarin - what do you do when there is an INR >8 and no bleeding?

A

Stop warfarin

Give oral vitamin K

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16
Q

Why not use DOAC in metallic heart valve?

A

Not used for metallic heart valve as you cant deffo get an INR of 3 on DOACs which is the aim - so use warfarin

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17
Q

Why are DOACs not used in malignancy?

A

Not used in malignancy as you are in hyper coagulable state so give LMWH as you can control better

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18
Q

LMWH

A
  • Often used in hospital as VTE prophylaxis

* Used in pregnancy

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19
Q

Unfractionated heparin

A
  • Can be used in renal failure
  • Shorter on/off
  • Has antidote
  • Used if patient is high risk for bleeding and clotting e.g. metallic heart valve patient needing surgery.
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20
Q

Bleeding + Warfarin - what do you do when there is an INR 5-8 and minor bleeding?

A

Stop warfarin

Give IV vitamin K

21
Q

Bleeding + Warfarin - what do you do when there is an INR 5-8 and No bleeding?

A

Withhold 1-2doses.

22
Q

Von Willebrand disease?

A
  • Most common inherited bleeding disorder
  • vWF promotes platelet adhesion to damaged endothelium (primary haemostasis)
  • vRF also responsible as carrier for factor VIII (secondary haemostasis)
23
Q

Treatment of Von willebrand disease?

A

Supportive treatment

  • Tranexamic acid
  • Desmopressin
  • Factor VII concentrate
24
Q

DOACs

A
  • Dabigatran -> Thrombin inhibitor and has a licensed antidote
  • Rivaroxaban -> factor Xa inhibitor
  • Apixaban -> factor Xa inhibitor
  • Endoxaban -> factor Xa inhibitor

The Xa inhibitors not currently have a licensed for metallic heart valve or malignancy related issues.

25
Hodgkins Lymphoma
* Malignant proliferation of lymphocytes * Bimodal distribution (3rd and 7th decades) * Reed-Sternberg cells (owls eyes) on histology * B symptoms: night sweats, fever, weight loss * CT staging * Chemotherapy + radiotherapy
26
Myeloma
* Plasma cell proliferation * HyperCalcaemia (Constipation, bone pain, kidney stones, confusion) * Renal impairment (immunoglobulin deposition in renal tubules, amyloid deposition, hypercalcaemia) * Anaemia/pancytopenia/bleeding/infection --> bone marrow suppression * Bone -> lytic lesions * Rouleux cells on blood film (think about Rolo chocolate) * Urine bence jones proteins * IgA or IgG - monoclonal band on electrophoresis * Chemotherapy +/- autologous stem cell transplant
27
What is the mnemonic for Myeloma?
``` CRAB: C = HyperCalcaemia R = Renal impairment A = Anaemia B = Bone ```
28
What is the mnemonic for Antiphospholipid syndrome?
``` CLOT C= Coagulation defect L = Livedo reticularis O = Obstetric complications T = Thrombocytopenia ```
29
Antiphospholipid syndrome
* Coagulation defect (prolonged aPTT, arterial/venous thrombosis) * Livedo reticularis * Obstetric complications (fetal loss, pre-eclampsia
30
Transfusion reactions
Basic principles are to stop the transfusion, confirm the correct product and assess the patient.
31
What are the non-life threatening transfusion reactions?
* Urticarial: Hives only, common, use antihistamines | * Febrile non-haemolytic: Fever and chills in absence of systemic compromise
32
What are the life threatening transfusion reactions?
* TA cardiac overload: Pulmonary oedema - have history of cardiac abnormality. will improve with diuretics * TRA Lung injury: Fevers, chills, hypotension and resp distress - CXR appears overload * Acute haemolytic: ABO incompatibility, clercical errors, Rx = fluids and diuresis ++ * Sepsis * Anaphylaxis
33
DVT/PE
* Venous thromboembolism * Virchow's triad: haemostasis, hypercoagulability + endothelial change * Wells score -> d-dimer/imaging * Unprovoked = treat for 6 months --> always look for underlying cause (>40yrs should have CT CAP) * Provoked = treat for 3 months * 2+ events = lifelong treatment
34
Factor V Leiden
* Most common thrombotic disorder * Activated protein C resistance * Heterozygous = 4x increased risk of VTE event (DVT/PE) * Homozygous = 10x increased risk
35
Myeloproliferative Disorders
JAK 2 mutation Thrombocythaemia - Raised platelets - Livedo reticularis - Thrombosis - Nail fold infarcts Polycythaemia rubra vera - Raised Hb/HCT - thrombosis - prurigo after hot bath Myelofibrosis - Progressive fibrosis of bone marrow - Abnormal megakaryocytic - Splenomegaly
36
Polycythaemia vera
``` Raised Hb Raised hematocrit WCC normal Platelets normal Previous DVT is a risk factor Intense itching after bath ```
37
Acute lymphoblastic leukaemia
* Most common malignancy in children * Bone marrow failure * Classification with microscopy - FAB criteria based on morphology * Treated with chemotherapy + stem cell transplant after remission * Cure rates in children 70-90% * Poor prognostic factors (Philadelphia chromosome, male, age <1 or >10 worse prognosis, CNS involvement).
38
What Cell progenitor causes AML and CML?
Common myeloid progenitor and myeloblasts
39
What Cell progenitor causes ALL?
Common lymphoid progenitor and small lymphocytes
40
What Cell progenitor causes CLL?
B lymphocytes (95%)
41
What Cell progenitor causes myeloma?
Plasma cells
42
What Cell progenitor causes lymphoma?
Can be mixed. Lymphoid lineage. But mostly B cells.
43
ALL
Children age 2-6yrs Good prognosis Lymphocytes
44
AML
``` Adults Poor prognosis Secondary to myeloproliferative disorder auer rods neutrophils ```
45
CLL
``` Adults smudge/smear cells transform into high grade lymphoma lymphocytes ```
46
CML
Adults/elderly 60-70yrs philadelphia chromosome may undergo blast transformation neutrophils.
47
DIC
* In DIC, the processes of coagulation and fibrinolysis are dysregulated * Widespread clotting with resultant bleeding * Low platelets, prolonged aPPT + PT, increased fibrin degradation products * Tissue factor activation * Main causes: sepsis, trauma, malignancy, HELLP syndrome
48
Imatinib
Tyrosine kinase inhibitor | - related to the Philadelphia chromosome which affects the tyrosine kinase enzyme in CML