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Long Case > Haematology > Flashcards

Haematology Flashcards

1
Q

What are your differentials for a platelet disorder?

A 
Viral infection
Drugs
ITP
DIC
TTP
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2
Q

What are your differentials for coagulation disorders?

A 
Haemophilia Type A=factor 8 Type B=factor 9
Von willebrands
Warfarin
Vitamin K deficiency
Liver disease
DIC
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3
Q

Which factors does APTT assess?

A

Intrinsic and common pathways

All factors apart from 7 but especially Factors 8, 9, 11 and 12

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4
Q

Which factors does Prothrombin ratio assess?

A

Extrinsic and common pathways

Factors 2, 5, 7 , 10, fibrinogen and prothrombin

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5
Q

How does chronic immune thrombocytopenic purpura present?

A

Bleeding, purpura, epistaxis, menorrhagia without splenomegaly

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6
Q

Management of ITP

A 
If mild, just supportive
Prednisolone
Splenectomy cures 80% of relapses
IV IG
TPO-RAs
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7
Q

What is ALL associated with?

A

Children between 2 and 10.

Associated with Down’s Syndrome

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8
Q

Presentation of ALL

A

Marrow failure, bleeding, infection, lymphadenopathy, hepatosplenomegaly

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9
Q

Management of ALL

A 
Blood/platelet transfusion
Allopurinol (prevents tumour lysis syndrome)
IV antibiotics if febrile neutropenia
Chemotherapy
Bone marrow transplant
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10
Q

Prognosis of ALL

A

90% cure rate in children

40% in adults

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11
Q

What is AML associated with?

A

Complication of radiotherapy/chemo

Commonest acute leukaemia in adults

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12
Q

What is CML associated with?

A

Philadelphia chromosome in 80% of cases-better prognosis

Splenomegaly

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13
Q

Investigations for CML

A

FBC
Bone marrow aspirate
Check for Philadelphia chromosome

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14
Q

Management of CML

A

Chemotherapy: imatinib

Stem cell transplant

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15
Q

How does CLL present?

A

Most common leukaemia
Often incidental finding on bloods
Painless lymphadenopathy

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16
Q

Investigations for CLL

A

FBC
Blood film
Bone marrow aspirate
Direct coomb’s test

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17
Q

Management of CLL

A 
Watchful waiting if mild
Steroids
IVIG
Transfusions
Allogenic stem cell transplantation
Fludarabine, cyclophosphamide and rituximab
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18
Q

Complications of CLL

A

Autoimmune haemolysis
Infections
Marrow failure

19
Q

Key features of Hodgkin’s lymphoma

A

Reed-sternberg cells
FhX, EBV, sle
Young adults and elderly

20
Q

Symptoms of lymphoma

A 
Rubbery painless nodes
fever, weight loss, fatigue
Mediastinal involvement
Extranodal disease
Infection
21
Q

Investigations for lymphoma

A

Lymph node biopsy
Bone marrow aspirate
CXR/CT/MRI
Bloods

22
Q

Differentials for cervical lymph node enlargement

A

Infection: CMV,TB, EBV, HIV
Autoimmune: rheumatoid arthritis
Malignancy: Lymphoma, CLL, ALL, melanoma, thyroid cancer, stomach cancer, breast cancer

23
Q

What is the staging for lymphoma?

A

Ann Arbor Staging System
I-confined to single lymph node
II-> 2 nodal areas, same side of the diaphragm
III-> 2 nodal areas, both sides of diaphragm
IV- spread beyond lymph nodes

24
Q

Management for hodgkins lymphoma

A

80% 5 year survival
Radiotherapy and chemotherapy
ABVD chemo (adriamycin, bleomycin, vinblastine, decarbazine)

25
Q

Management for non-hodgkin’s lymphoma

A

40% 5 year survival
Low grade-just radiotherapy
High grade- RCHOP: rituximab, cyclophosphamide, hydroxydaunorubicin, oncovin, prednisolone

26
Q

What is the pathogenesis of multiple myeloma?

A

The malignant proliferation of plasma cells producing identical immunoglobulins

27
Q

Presentation of multiple myeloma

A 
CRAB
hyperCalcemia
Renal involvement
Anemia
Bone lesions/Back pain
Plus increased infections
28
Q

How to diagnose multiple myeloma

A

Monoclonal protein band on serum electrophoresis
Increased plasma cells on bone marrow biopsy
Evidence of end organ damage
Bence jones protein in urine

29
Q

Investigations for multiple myeloma

A

Bloods: anemia, hypercalcemia, rouleaux formation
Electrophoresis
Skeletal survey
Bone marrow

30
Q

Management of multiple myeloma

A 
Analgesia
Bisphosphonates
Transfusions and erythropoietin
IV immunoglobulin
Chemotherapy
3-4 year survival
31
Q

What is virchow’s triad

A

Hypercoagulability
Stasis of blood flow
Changes to blood flow wall

32
Q

Pathogenesis of Factor V Leiden

A

Protein C cleaves Factor V molecule

Factor V Leiden is resistant to cleavage and so protein C cannot act as an anticoagulant

33
Q

Causes of microcytic anaemia

A

Iron deficiency
Thalassemia
Sideroblastic anaemia
Iron deficiency: Serum ferritin is low, TIBC is up and iron is low

34
Q

Causes of normocytic anaemia

A 
Acute blood loss
Anaemia of chronic disease
Renal failure
Pregnancy
Bone marrow failure
Hypothyroidism
35
Q

Causes of macrocytic anaemia

A

B12/folate deficiency
Liver failure
Alcohol
Cytotoxic drugs

36
Q

Lab results in anaemia of chronic disease

A

Serum ferritin: high
TIBC: low
Iron: low

37
Q

What are the four myeloproliferative disorders?

A

Polycythaemia (RBC increased)
Chronic myeloid leukaemia (WBC increased)
Essential thrombocythaemia (platelets increased)
Myelofibrosis (fibroblasts increased)

38
Q

Presentation of polycythemia rubra vera

A 
Itch after bath/shower
Facial redness
Headaches
DVT
PVD
JAK2 positive
Massive splenomegaly
39
Q

Management of polycythemia rubra vera

A

Venesection
Hydroxyurea/interferon
Low dose aspirin

40
Q

Presentation of essential thrombocythaemia

A

Abnormal bleeding
Thromboembolism
Headaches
JAK2 -50%

41
Q

Management of thrombocythaemia

A

Don’t treat if asymptomatic
Transexamic acid
Aspirin
Hydroxyurea/interferon

42
Q

Presentation of myelofibrosis

A

Lethargy, weakness, weight loss, fever, easy bleeding

43
Q

Investigations for myelofibrosis

A

Tear drop cells on blood film
Nucleated RBCs
Fibrosis on bone marrow trephine

44
Q

Management of myelofibrosis

A

Bone marrow support-RBC and platelet transfusion

Long Case (11 decks)

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