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IOD - Haematology > Revision lecture II > Flashcards

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
Q

Hodgkins Lymphoma

A
  • 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
Q

Myeloma

A
  • 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
Q

What is the mnemonic for Myeloma?

A 
CRAB: 
C = HyperCalcaemia 
R = Renal impairment 
A = Anaemia 
B = Bone
28
Q

What is the mnemonic for Antiphospholipid syndrome?

A 
CLOT
C= Coagulation defect 
L = Livedo reticularis 
O = Obstetric complications 
T = Thrombocytopenia
29
Q

Antiphospholipid syndrome

A
  • Coagulation defect (prolonged aPTT, arterial/venous thrombosis)
  • Livedo reticularis
  • Obstetric complications (fetal loss, pre-eclampsia
30
Q

Transfusion reactions

A

Basic principles are to stop the transfusion, confirm the correct product and assess the patient.

31
Q

What are the non-life threatening transfusion reactions?

A
  • Urticarial: Hives only, common, use antihistamines

* Febrile non-haemolytic: Fever and chills in absence of systemic compromise

32
Q

What are the life threatening transfusion reactions?

A
  • 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
Q

DVT/PE

A
  • 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
Q

Factor V Leiden

A
  • Most common thrombotic disorder
  • Activated protein C resistance
  • Heterozygous = 4x increased risk of VTE event (DVT/PE)
  • Homozygous = 10x increased risk
35
Q

Myeloproliferative Disorders

A

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
Q

Polycythaemia vera

A 
Raised Hb
Raised hematocrit 
WCC normal 
Platelets normal 
Previous DVT is a risk factor 
Intense itching after bath
37
Q

Acute lymphoblastic leukaemia

A
  • 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
Q

What Cell progenitor causes AML and CML?

A

Common myeloid progenitor and myeloblasts

39
Q

What Cell progenitor causes ALL?

A

Common lymphoid progenitor and small lymphocytes

40
Q

What Cell progenitor causes CLL?

A

B lymphocytes (95%)

41
Q

What Cell progenitor causes myeloma?

A

Plasma cells

42
Q

What Cell progenitor causes lymphoma?

A

Can be mixed. Lymphoid lineage. But mostly B cells.

43
Q

ALL

A

Children age 2-6yrs
Good prognosis
Lymphocytes

44
Q

AML

A 
Adults 
Poor prognosis 
Secondary to myeloproliferative disorder 
auer rods 
neutrophils
45
Q

CLL

A 
Adults 
smudge/smear cells 
transform into high grade 
lymphoma 
lymphocytes
46
Q

CML

A

Adults/elderly 60-70yrs
philadelphia chromosome
may undergo blast transformation
neutrophils.

47
Q

DIC

A
  • 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
Q

Imatinib

A

Tyrosine kinase inhibitor

- related to the Philadelphia chromosome which affects the tyrosine kinase enzyme in CML

IOD - Haematology (8 decks)

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