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P2a - Haematology > mock questions > Flashcards

mock questions Flashcards

1
Q

what can malaria be caused by?

A

5 species of the same family
(plasmodium). Plasmodium falciparum = can cause most severe form of malaria
(complicated malaria) and has the highest mortality, it is most prevalent in Sub-Saharan
Africa. Others include: plasmodium ovale, plasmodium vivax, plasmodium malariae ,
plasmodium knowlesi

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2
Q

how is TTP treated?

A 
plasma exchange (replenishes ADAMTS13 and removes
antibody).
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3
Q

how is venous thromboembolism in post-hip replacement patients managed?

A

thromboprophylaxis with either a low molecular weight heparin administered for 10 days
followed by low-dose aspirin for a further 28 days, or a low molecular weight heparin
administered for 28 days in combination with anti-embolism stockings until discharge,
or rivaroxaban

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4
Q

what is the target for rituximab?

A

CD20, cancer drug used in CLL and NHL

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5
Q

what is the first line treatment for severe complicated malaria?

A

IV arthesunate

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6
Q

what is felty’s triad?

A

neutropenia, splenomegaly, RA

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7
Q

how would hereditary spherocytosis be treated?

A

splenectomy

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8
Q

what make malaria complicated?

A

characterised by vascular occlusion which can affect different organs therefore causing specific symptoms

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9
Q

what is TTP?

A

deficiency in ADAMTS13 enzyme causing vWF to thromboses, leads to raised bilirubin

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10
Q

what is secondary polycythaemia caused by?

A

Alcohol
Chronic hypoxia
Obstructive sleep apnoea
Living at altitude
Lung disease affecting oxygen transfer
Smoking (In hypoxic conditions, kidneys release high levels of EPO and hence more RBC are produced)
In abnormal conditions, it could be a tumour secreting EPO, GGWP.

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11
Q

what would be seen on the blood film of someone with multiple myeloma?

A

rouleaux formation

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12
Q

what would be seen in the urine of someone with multiple myeloma?

A

bence jones proteins

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13
Q

what cells are affected in multiple myeloma?

A

plasma cells

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14
Q

what type of crises can be suffered by patients with sickle cell?

A
  • vaso-occlusive - occlusion of vessles, swelling in hands and feet due to distal occlusion
  • Splenic sequestration crisis – where the blood flow in the spleen is compromised, resulting in acute splenomegaly and pain. This results in pooling of blood which can lead to severe anaemia and circulatory collapse  hypovolaemic shock
  • Aplastic crisis – temporary loss of the creation of new blood cells – commonly triggered by parvovirus B19 infection. Leads to significant anaemia – supportive management may require blood transfusions.
  • Acute chest syndrome – vasoocclusie crisis of pulmonary vasculature. diagnosed when there is fever or respiratory symptoms with new infiltrates seen on chest x-ray – may be due to infection such as pneumonia or bronchiolitis, or due to pulmonary vaso-occlusion. This is an emergency – high mortality rate. Requires prompt supportive management and treatment of underlying cause (antibiotics or antivirals, blood transfusion, incentive spirometry, intubation may be required).
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15
Q

how is a vasoocclusive sickle cell crisis managed in hospital?

A

Management is supportive: have a low threshold for hospital admission due to risks of complications.

  • Treat underlying infection
  • Keep warm
  • Maintain good hydration – IV fluids
  • Simple analgesia (paracetamol and ibuprofen if not contraindicated)
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16
Q

in which type of leukaemia would you fine auer rods on the blood smear?

A

AML

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17
Q

in vitamin B12 anaemia, what blood test would you carry out and what would be the results?

A 
- FBC 
↓Hb 
↑MCV (macrocytic anaemia) 
- Blood film 
Hypersegmented neutrophils (>5 lobes) and presence of oval macrocytes 
- Serum cobalamin ↓
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18
Q

what is the most common cause of B12 anaemia?

A

pernicious anaemia

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19
Q

what features in a history would point towards pernicious anemaia?

A

other autoimmune disease

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20
Q

what tests are needed to diagnose pernicious anaemia?

A

Test for antibodies: parietal cell and intrinsic factor (specific) antibodies

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21
Q

what is the most common cell of origin for NHL?

A

B lymphocytes

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22
Q

which autoantibody does warm autoimmune heamolytic anaemia involve?

A

IgG

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23
Q

what would be seen on a bold smear in both PBS and G6PD deficiency?

A

bite cells and heinz bodies

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24
Q

what is the direct antiglobulin test (Coombs’) used to distinguish?

A

autoimmune from non-immune aetiologies of haemolytic anaemia

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25
Q

what happens to hepatoglobulin levels in haemolytic anaemia?

A

decreased

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26
Q

what is haemolytic uraemic syndrome?

A

triad of microangiopathic haemolytic anaemia, thrombocytopenia and renal impairment.
Most are diarrhoea-associated (caused by Shiga-toxin producing E.coli) in children
Blood test results show:
FBC: anaemia and thrombocytopenia
Haemolysis: LDH, bilirubin
Peripheral blood smear: schistocytes
U&E: raised creatinine and electrolyte abnormalities
Management is mainly supportive

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27
Q

what is the trestment for mild uncomplicated malaria?

A

oral hydroxychloroquine

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28
Q

what changes would you see on the blood film of someone with iron deficiency anaemia?

A

hypochromic, poikilocytosis microcytic, anisocytosis

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29
Q

what causes microcytic anaemia?

A

iron deficiency, thalassaemia, chronic disease, sideroblastic

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30
Q

what are 4 signs of iron deficiency anaemia?

A

Koilonychia (spoon shaped nails), angular stomatitis, atrophic glossitis, pallor

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31
Q

what are the complications of PV?

A

dizziness, itching, haemorrhage and thrombosis

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32
Q

which plasmodium can cause relapses of malaria?

A

P. ovale and P. vivax

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33
Q

how is multiple myeloma characterised?

A

Monoclonal protein in serum or urine

  • Lytic bone lesions/ CRAB end organ damage
  • Excess plasma cells in bone marrow
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34
Q

what is the most common chromosomal abnormality in multiple myeloma?

A

t (11;14)

35
Q

You see a 50-year-old male in A&E who has presented with breathlessness, bone pain and a severe infection.
His temperature is 39.1, his heart rate is 110 and his blood pressure is 130/85. He tells you this is the 3rd
severe infection he has had in 6 months and thinks they are causing him to lose weight. On examination, you
note hepatosplenomegaly and see some gum hypertrophy.

A

AML

36
Q

what are 2 things associated with multiple myeloma?

A

downs syndrome, raditation

37
Q

what are the treatments fo multiple myeloma?

A 
Blood transfusion
Allopurinol (to prevent tumour lysis)
IV antibiotics
Chemotherapy
Steroids
Bone marrow transplant
38
Q

what age would you expect someone with CLL to be?

A

over 70

39
Q

what would you notice on examination of someone with CLL?

A

Enlarged, rubbery, non-tender lymph nodes
Sweating, anorexia
Commonly asymptomatic

40
Q

what would be seen on the blood smear of someone with CLL?

A

smudge cells

41
Q

how is CLL treated?

A

Chemotherapy
Monoclonal antibodies (rituximab)
Bruton kinase inhibitors (ibrutinib)

42
Q

what is a complication of CLL?

A

Richter’s syndrome – transformation of CLL to an aggressive lymphoma

43
Q

what does G6PD do?

A

It protects the RBCs against oxidative damage

44
Q

what are the common symptoms of G6PD deficiency?

A

Fatigue, palpitations, shortness of breath, pallor

45
Q

what would be seen on a blood smear of someone with G6PD deficiency?

A

bite cells, reticulocytes

46
Q

which antibiotic should be avoided in G6PD deficiency?

A

nitrofuratoin - can cause severe haemolytic anaemia

47
Q

what are the 6 Ps of critical limb ischaemia?

A

pain, pallor, perishingly cold, pulselessness, paralysis, paraesthesia

48
Q

what is the process of disseminated intravascular coagulation?

A

Tissue damage (from ARDS) will cause release and activation of tissue factor. This leads to
widespread clot formation and the consumption of platelets and coagulation factors (thrombosis
formation).A lso, the Tissue Plasminogen Activator is activated leading to increased fibrinolysis
hence clotting is removed but increased risk of bleeding.
Tissue Factor Release causes coagulation from both intrinsic & extrinsic pathways ➔ THROMBOSIS
Thrombus are broken down by Fibrinolysis ➔ BLEEDING

49
Q

what is the SEPSIS 6?

A

Give: Fluids, Broad spectrum Abx, Administer O2 if required Take: Bloods, Urine Output, Lactate
levels

50
Q

how are haemophilia A and B inherited?

A

X linked recessive

51
Q

how is haemophilia C inherited?

A

autosomal recessive

52
Q

what clotting factors are affected in haemophillia?

A

A=8, B=9, C=11

53
Q

what is platelet count?

A

level of platelets. A normal platelet count ranges from 150,000 to
450,000 platelets per microliter of blood.

54
Q

what is bleeding time?

A
  • Bleeding time is a laboratory test to assess platelet function and the body’s ability to
    form a clot.
55
Q

what is prothrombin time?

A

The prothrombin time is a measure of the integrity of the extrinsic and final common pathways of
the coagulation cascade. This consists of tissue factor and factors VII, II (prothrombin), V, X, and
fibrinogen.

56
Q

what is APTT?

A

– a measure of the functionality of the intrinsic and common pathways of the coagulation
cascade.

57
Q

what is thrombin time?

A

– Thrombin time is a screening coagulation test designed to assess fibrin formation
from fibrinogen in plasma.
The reference range for the thrombin time is usually less than 20 seconds

58
Q

what is fibrin degredation products testing for?

A

Fibrin and fibrinogen-degradation product (FDP) testing is commonly
used to diagnose disseminated intravascular coagulation (DIC).

59
Q

what is D-dimer?

A

D-dimer is the degradation product of crosslinked (by factor XIII) fibrin. It reflects ongoing
activation of the hemostatic system.

60
Q

which blood tests would be affected in haemophilia?

A

APTT and possibly TT would be increased

61
Q

what is spherocytosis?

A

caused by a defect in the red cell membrane, which causes them to lose part of their membrane as they pass through the spleen. This abnormality is then associated with an increased permeability to sodium ions

62
Q

how would you treat at DVT that was unprovoked and no cause was identified?

A

apixaban for 6 months

63
Q

what is the chance of a daughter inheriting an X-link recessive condition where the father has the disease and the mother is a carrier?

A

50%

64
Q

what would signify a poor prognosis in AML?

A

WCC>20 at time of diagnosis

65
Q

what is an anaemia with a low haemoglobulin but a high reticulocyte count?

A

sickle cell anaemia

66
Q

what is the gold standard treatment for haemochromatosis?

A

therapeutic phlebotomy

67
Q

what would the copper levels be in the serum of someone with wilson’s disease?

A

low

68
Q

what can be given to prevent sickle cell crisis?

A

hydroxycarbamide

69
Q

what are the symptoms of CLL?

A

bleeding, infection, abdo pain, fatigue, weight loss

70
Q

what is the gold standard investigation for diagnosing CLL?

A

immunophenotyping

71
Q

what are the treatment options for CLL?

A

chemo, radiotherapy, stem cell transplant, splenectomy

72
Q

what is it called when CLL turns into NHL?

A

richter’s transformation

73
Q

what is acute promyelocytic leukaemia?

A

APL is an aggressive form of AML - This build up of promyelocytes leads to a shortage of normal white and red blood cells and platelets in the body.

74
Q

how does von willebrand disease affect APTT?

A

prolonged, affects the intrinsic pathway

75
Q

what would a d-dimer score over over 2 indicate?

A

treat with compression ultrasound

76
Q

how is ITP treated?

A

prednisolone

77
Q

what is the mechanism of action of clopidogrel?

A

Clopidogrel is an antiplatelet medication like aspirin, but acts as an ADP-receptor antagonist by binding irreversibly to ADP receptors on the surface of platelets

78
Q

what are the risk factors for folate deficiency?

A

being elderly; malabsorption due to coeliac or Crohn’s disease; alcoholism; and low intake of green vegetable

79
Q

what is SEPSIS 6?

A

Blood cultures, Urine sample, Fluids, Antibiotics, blood Lactate, and Oxygen.

80
Q

what would a gram positive cocci with a positive catalase test suggest?

A

a staphlococcus?

81
Q

which staph would have a positive coagulase?

A

staph aureas

82
Q

what is DIC?

A

causes a systemic activation of coagulation, eventually leading to the consumption of platelets and clotting factors which results in bleeding. Patients are often acutely unwell (e.g. severe sepsis).

83
Q

what are the chances of being a carrier of sickle cell disease if a sibling has the disease but both parents don’t?

A

67%

50% of being a carrier but know NOT to have disease so 2/3 not 2/4

P2a - Haematology (18 decks)

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