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Z2F/Comprehensive Flashcards > Haematology > Flashcards

Haematology Flashcards

1
Q

lifespan of RBCs

A

120 days

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2
Q

lifespan of platelets

A

10 days

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3
Q

blood films: what is anisocytosis? associated condition?

A

RBCs which are unequal size
seen in Myelodysplastic syndrome (cancer where there is insufficient number of mature RBCs)

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4
Q

blood films: what are target cells? associated conditions?

A

RBCs which look like bullseyes
associated with iron deficiency anaemia or post-splenectomy

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5
Q

blood films: what are Howell-Jolly bodies? associated conditions?

A

nuclear remnants found in RBCs of patients with reduced or absent splenic function
Seen in severe anaemia or post splenectomy

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6
Q

blood films: what are reticulocytes? Associated condition ?

A

immature RBCs (still developing)
Haemolytic anaemia

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7
Q

blood films: what are smudge cells? associated condition?

A

ruptured CLL cells
Chronic Lymphocytic Leukaemia

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8
Q

causes of microcytic anaemia (5)

A

TAILS:
Thalassaemia
Anaemia of chronic disease
Iron deficiency
Lead poisoning
Sideroblastic anaemia

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9
Q

causes of normocytic anaemia (5)

A
  1. Haemolytic anaemia
  2. Hypothyroidism
  3. Acute blood loss
  4. aplastic anaemia
  5. anaemia of chronic disease
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10
Q

causes of megaloblastic macrocytic anaemia (2)

A
  1. B12 deficiency
  2. Folate deficiency
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11
Q

causes of normoblastic macrocytic anaemia (5)

A
  1. Alcohol abuse
  2. Hypothyroidism
  3. liver disease
  4. drugs e.g. Azathioprine
  5. reticulocytosis e.g. due to haemolysis
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12
Q

Iron deficiency anaemia:
1. features (4)
2. initial diagnostic test
3. possible underlying causes (4)
4. management when cause is unclear
5. treatment options

A
  1. features:
    - angular cholitis
    - tiredness
    - hair loss
    - koilonychia
  2. Initial diagnostic test= serum ferritin
  3. possible underlying causes:
    1- diet
    2- reduced absorption e.g. Coeliac
    3 - increased iron requirements e.g. pregnancy
    4- bleeding e.g. cancer or menorrhagia
  4. If cause unclear, refer for urgent OGD and colonoscopy to rule out GI cancer
  5. Tx options:
    - oral iron e.g. ferrous sulphate
    - iron infusion
    - blood transfusion if very low Hb
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13
Q

Pernicious anaemia:
1. What is it?
2. key symptom?
3. treatment?
4. should you treat B12 or folate deficiency first, and why?

A
  1. autoimmune condition where the immune system attacks the parietal cells of the stomach, which produce intrinsic factor which normally helps absorb B12. this leads to B12 deficiency
  2. Key symptom= peripheral neuropathy
  3. Tx: IM hydroxocobalamin injection
  4. treat B12 deficiency before folate deficiency, because treating folate deficiency can cause subacute combined degeneration of the spinal cord
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14
Q

Autoimmune Haemolytic Anaemia:
1. 2 types? which is more common?
2. management (4)
3. Blood film findings (2)
4. is it acquired or inherited?
5. inherited haemolytic anaemia examples? (4)

A
  1. Warm and Cold. Warm is more common
  2. Management:
    1- blood transfusions
    2- steroids (e.g. prednisolone)
    3- rituximab
    4- splenectomy
  3. blood film shows
    1- raised reticulocytes
    2- schistocytes
  4. Autoimmune haemolytic anaemia is ACQUIRED
  5. Examples of inherited haemolytic anaemias:
    - sickle cell anaemia
    - G6PD deficiency
    - thalassaemia
    - hereditary spherocytosis
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15
Q

Thalassaemia
1. main issue in thalassaemia
2. types
3. Inheritance pattern
4. diagnostic test
5. potential cure

A
  1. Main issue in thalassaemia= defective globulin chains
  2. types= alpha and beta, depending on which chains are affected
  3. Inheritance is autosomal recessive
  4. Diagnostic test= haemoglobin electrophoresis
  5. Bone marrow transplant
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16
Q

Thalassaemia features:
1. inspection
2. abdo
3. sclera
4. FBC

A
  1. pronounced forehead and malar eminences
  2. abdo- splenomegaly
  3. scleral jaundice
  4. FBC: microcytic anaemia
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17
Q
  1. Thalassaemia management if required? (2)
  2. why should serum ferritin be monitored in thalassaemia treatment?
A
  1. management if needed:
    - blood transfusions
    - splenectomy
  2. there is a risk of iron overload
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18
Q

Sickle cell anaemia:
1. inheritance pattern
2. One gene copy =?
3. antibiotic prophylaxis in children?
4. medication to stimulate HbF production?
5. Potential cure?

A
  1. Autosomal recessive
  2. sickle cell trait
  3. Penicillin V
  4. Hydroxycarbamide
  5. Bone marrow transplant
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19
Q
  1. Examples of acute diagnoses associated with sickle cell anaemia? (4)
  2. Management of acute sickle crises? (4)
A
  1. acute diagnoses:
    (1) acute chest syndrome
    (2) vaso-occlusive crisis
    (3) splenic sequestration crisis
    (4) aplastic crisis
  2. Sickle crises management:
    1- analgesia e.g. Morphine
    2- IV fluids
    3- Oxygen
    (4) if needed, give blood transfusion or exchange transfusion
20
Q

Leukaemia:
1. typical presentation of AML? (3)
2. cause of bruising in Acute Leukaemia?
3. definitive diagnostic tests for leukaemia (all types)?
4. other types of leukaemia?
5. main treatment of leukaemia?
6. Cause of increased uric acid in leukaemia?

A
  1. AML:
    (1) fatigue
    (2) pallor
    (3) abnormal bruising
  2. Abnormal bruising is caused by thrombocytopenia (low platelets)
  3. bone marrow biopsy= definitive diagnostic test
  4. CML, ALL, CLL
  5. chemotherapy and steroids are the main tx
  6. Tumor lysis syndrome
21
Q

condition associated with smudge cells

A

chronic lymphocytic leukaemia (CLL)

22
Q

conditions associated with philadelphia chromosome

A

CML + ALL

23
Q

condition associated with myelofibrosis

A

AML

24
Q

condition associated with richter’s transformation

A

CLL

25
Q

middle aged presenting with bruising, rash, nosebleeds and low platelets
1. diagnosis
2. treatment (4)

A
  1. Immune Thrombocytic Purpura(ITP): an autoimmune bleeding disorder
  2. Tx;
    1- steroids
    2- IV immunoglobulins
    3- Rituximab \
    4- Splenectomy
26
Q

causes of low platelets associated with
a. vitamin deficiency
b. lifestyle
c. drug induced antibodies
d. deficiency of ADAMST13

A

a. B12 or folate deficiency

b. Alcohol

c. Heparin induced Thrombocytopenia

d. Thrombotic Thrombocytopaenic purpura

27
Q

presentation: recurrent miscarriages and DVT
1. Diagnosis
2. investigation
3. Management + management in pregnancy

A
  1. Antiphospholipid syndrome
  2. Antiphospholipid antibodies:
    - anticardiolipin antibodies
    - lupus anticoagulant
    - anti-beta-2-glycoprotein antibodies
  3. Management= long term warfarin
    Management in pregnancy= LMWH + Aspirin
28
Q

presentation: Hx of heavy periods + nosebleeds, mother also had heavy periods
1. Diagnosis
2. Defective/deficient glycoprotein
3. Management (3)
4. Most common inheritance pattern

A
  1. Von Willebrand’s disease
  2. Affected glycoprotein= von willebrand factor
  3. Management:
29
Q

presentation: Hx of heavy periods + nosebleeds, mother also had heavy periods
1. Diagnosis
2. Defective/deficient glycoprotein
3. Management (3)
4. Most common inheritance pattern

A
  1. Von Willebrand’s disease
  2. Affected glycoprotein= von willebrand factor
  3. Management:
    1- Desmopression
    2- von willebrand factor infusion
    3- factor VIII infusion
  4. Most commonly Autosomal Dominant
30
Q

Haemophilia A and B
1. Inheritance pattern
2. Underlying pathologies?

A
  1. X-linked recessive (so males more likely to be affected because they only have one X)
  2. Haemophilia A: deficiency in factor VIII
    Haemophilia B: deficiency in factor IX
31
Q

4 causes of abnormal or prolonged bleeding

A

1- thrombocytopenia
2- von willebrands disease
3- Haemophilia A + B
4- disseminated intravascular coagulopathy

32
Q

‘ruddy complexion, conjunctival plethora and splenomegaly’
1. Diagnosis
2. Proliferating cell line?
3. key gene mutation
4. diagnostic test
5. management (3)
6. potential malignant transformation
7. Other myeloproliferative disorders

A
  1. Polycythaemia vera
  2. Erythroid cells
  3. JAK-2 mutation
  4. Bone marrow biopsy is diagnostic
  5. Management:
    - venesection
    - aspirin
    - chemotherapy
  6. Acute lymphocytic leukaemia (ALL)
  7. primary myelofibrosis
    essential thrombocythaemia
33
Q

Multiple Myeloma
1. Affected cells
2. Key features
3. specific initial lab tests (3)
4. test to confirm diagnosis
5. Description of skull on x ray
6. first line chemo options

A
  1. Affected cells= plasma cells
  2. CRAB:
    Calcium increased
    Renal failure
    Anaemia
    Bone pain/ lesions
  3. specific initial lab tests:
    1- serum protein electrophoresis
    2- serum light chain assay
    3- urine Bence-Jones protein
  4. confirm Dx by bone marrow biopsy
  5. ‘raindrop skull’ on XR
  6. Bortezomib, Thalidomide, Dexamethasone
34
Q

Multiple Myeloma
1. Affected cells
2. Key features
3. specific initial lab tests (3)
4. test to confirm diagnosis
5. Description of skull on x ray
6. first line chemo options

A
  1. Affected cells= plasma cells
  2. CRAB:
    Calcium increased
    Renal failure
    Anaemia
    Bone pain/ lesions
  3. specific initial lab tests:
    1- serum protein electrophoresis
    2- serum light chain assay
    3- urine Bence-Jones protein
  4. confirm Dx by bone marrow biopsy
  5. ‘raindrop skull’ on XR
  6. Bortezomib, Thalidomide, Dexamethasone
35
Q

Lymphoma:
1. Features of Hodgkin’s lymphoma
2. Associated viruses
3. Diagnostic tests + histology result for Hodgkin’s lymphoma
4. Staging system used
5. management

A
  1. 75% have lymphadenopathy (rubbery, painful with alcohol). 25% have B symptoms: fever, night sweats, weight loss
  2. Associated viruses= EBV and HIV
  3. Diagnosis is by lymph node biopsy. Histology shows Reed-Sternberg cells
  4. Ann Arbor staging system is used
  5. Management= chemotherapy + radiotherapy
36
Q

lymphoma type associated with EBV

A

Burkitt’s lymphoma

37
Q

lymphoma type associated with H.Pylori in the stomach

A

MALT Lymphoma

38
Q

lymphoma type associated with a rapidly progressing, painless mass

A

diffuse large B-cell lymphoma

39
Q

condition associated with Auer rods

A

AML

40
Q
  1. what is the difference between ITP and TTP?
  2. TTP management
  3. ITP management
A
  1. TTP is where there is a deficiency of enzyme ADAMTS13, which cleaves von willebrand factor, causing platelets to clump in the vessels. This usually presents with neuro signs and fever along with easy bleeding/bruising.
    ITP is where there is an immune-mediated reduction in the platelet count, leading to epistaxis/bruising/petechiae without any neuro signs.
  2. TTP is managed with blood replacement therapy
  3. ITP is managed with oral prednisolone
41
Q
  1. What is DIC?
  2. Risk factors for DIC
  3. Lab results for acute DIC (platelets, fibrinogen, PT, PTT, D- Dimer)
  4. Management of DIC (3)
A
  1. Dysregulation of coagulation and haemostasis, leading to the formation of clots throughout the body.
  2. May be seen after severe obstetric complications, severe burns or trauma, sepsis/infection or malignancy
  3. Platelets decreased, (due to use in clotting), fibrinogen decreased (less clots broken down), PT and PTT elevated (paradoxical rise in PTT), D Dimer elevated (produced when fibrin clots are broken down)
  4. Management:
    1- Fresh frozen plasma
    2- Cryoprecipitate to replace fibrinogen
    3- if bleeding or pre-op, give platelets
42
Q

management of INR on warfarin: major bleeding

A

stop warfarin, give IV vit K + prothrombin complex concentrate (if no prothrombin complex available, give fresh frozen plasma)

43
Q

management of INR on warfarin: INR <8 and minor bleeding

A

stop warfarin, give IV vit K -3mg, repeat dose if INR still high after 24hrs, restart warfarin when INR <5

44
Q

management of INR on Warfarin: INR >8 and no bleeding

A

stop warfarin, give IV vit K 1-5mg orally (using IV prep by mouth) , repeat vit K if INR still too high after 24hrs, restart when INR <5

45
Q

management of INR on warfarin: 5-8 and minor bleeding

A

stop warfarin, give IV vit K 1-3mg, restart when INR<5

46
Q

management of INR on warfarin: INR 5-8 and no bleeding

A

withhold 1-2 doses of Warfarin, reduce subsequent maintenance dose

Z2F/Comprehensive Flashcards (7 decks)

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