Haematology 2 Flashcards

1
Q

bone lesions in multiple myeloma

A

osteolytic

  • pathological fractures
  • vertebral collapse
  • punched out pepper pot skull
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

plasma hyperviscosity symptoms in multiple myeloma

A

headache
vision changes
tinnitus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what causes AKI in multiple myeloma

A

deposition of light chains in the tubules, hypercalcaemia, hyperuricaemia, amyloid deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what causes renal failure in multiple myeloma

A

CAST NEPHROPATHY

- light chains combine with Tamm Horsfall protein producing insoluble casts that block the nephron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

treatment of bone pain in multiple myeloma

A

biphosphonates – stop progression of bone disease e.g. zoledronate inhibits osteoclast activity
analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

treatment of hyperviscosity

A

plasmapheresis – removes light chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

treatment of multiple myeloma young/fit patients

A

lenlidomide + dexamethasone

allogenic bone marrow transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

treatment of multiple myeloma in old/unfit patients

A

lenlidomide + melphalan + prednisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

treatment of relapsed multiple myeloma

A

bortezomib + lenalidomide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is bortezomib

A

a proteome inhibitor used in relapsed myeloma treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ESR in multiple myeloma

A

almost always ELEVATED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

features of monoclonal gammopathy of uncertain significance

A

paraprotein <30g/L

no end organ damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

waldenstroms macroglobulinaemia

A

IgM paraprotein – hyperviscosity + neuropathy

tumour effects – lymphadenopathy, splenomegaly, marrow failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

treatment of waldenstroms macroglobulinaemia

A

plasmapheresis / chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is amyloidosis

A

accumulation of protein in abnormal fibrillar form - insoluble beta pleated sheet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

effects of amyloidosis

A

nephrotic syndrome
cardiomyopathy
carpal tunnel
periorbital pupura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

diagnosis of amyloidosis

A

congo red staining

apple green birefringence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

+ve direct Coombs test

A

autoimmune haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

antibody in warm autoimmune haemolysis

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

antibody in cold autoimmune haemolysis

A

IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

cause of warm autoimmune haemolysis

A

Idiopathic
SLE
Chronic lymphocytic leumaeimia
Penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

causes of cold autoimmune haemolysis

A

EBV
Mycoplasma
idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is seen in the blood if haemolysis is mechanical in nature

A

red cell fragmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

red blood cells that have lost their central pallor

A

spherocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Heinz bodies

A

G6PD deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

intermittent jaundice + gall stones

A

hereditary spherocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

inheritance of G6PD

A

X linked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

presentation of sickle cell disease in children

A

acute pain in hands + feet – occlusion of small vessels + avascular necrosis of bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

presentation of sickle cell disease in adults

A

pain in long bones, spine + pelvis

30
Q

presentation of HbH

A

intermittent jaundice when ill, asian ethnicity

31
Q

where are RBCs destroyed in extravascular haemolysis

A

Liver/spleen

32
Q

effects of extravascular haemolysis

A

release of protoporphyrin – unconjugated bilirubinaemia

  • jaundice + gall stones
  • splenomegaly
33
Q

where are RBCs broken down in intravascular haemolysis

A

circulation

34
Q

causes of intravascular haemolysis

A

ABO transfusion reaction
G6PD deficiency
paroxsysmal nocturnal haemoglobinuria
malaria

35
Q

effects of intravascular haemolysis

A

haemoglobinuria – dark urine
haemosiderinuria
+ve shumms test – methaemalbumin

36
Q

what are pappenheimer bodies and what are they seen in

A

abnormal iron granules

beta thalassaemia

37
Q

polychromasia

A

reticulocytosis = increased number of reticulocytes in the blood
blue staining ribosomal RNA

38
Q

inclusion bodies

A

HbH (severe alpha thalassaemia)

39
Q

Zieve’s syndrome

A

haemolysis, hyperlipidaemia, alcoholic liver

acquired cell membrane defect causing haemolysis

40
Q

what vitamin deficiency can cause haemolysis by RBC membrane defect

A

Vitamin E

41
Q

mutation in polycythaemia rubra vera

A

JAK2

42
Q

itchy after a hot shower/bath

A

aquagenic pruritus – polycythaemia rubra

- due to histamine release

43
Q

blood results in primary polycythaemia rubra

A

Increased RBC, Haematocrit, WBC, platelets
Increased blood viscosity
decreased EPO

44
Q

symptoms of primary polcythaemia rubra

A

splenomegaly - extra medullary haemopoiesis
gout- increase cell turnover + uric acid production
vision disturbance/headhace/tinnitus – increased blood viscosity
aquagenic pruritis
thrombosis

45
Q

tx of primary polcythaemia rubra

A
  1. venesection
  2. aspirin to prevent thrombosis
  3. hydroxycarbamide to decrease platelet count
46
Q

what can cause secondary polycythaemia

A

HYPOXIA - appropriate increased EPO

  • COPD
  • altitude

EPO secreting tumours - inappropriate EPO release

  • liver
  • renal
  • cerebellar
47
Q

what is pseudo polycythaemia

A

decreased plasma volume therefore relative increase in RBCs
acute- dehydration, shock, burns
chronic - smoking, diuretics

48
Q

difference in presentation of primary and secondary polycythaemia

A

no splenomegaly in secondary

platelet count normal in secondary

49
Q

what is essential thrombocytosis

A

clonal proliferation of megakaryocytes in the bone marrow

- increased platelet count, normal Hb/wbc

50
Q

symptoms of essential thrombocytosis

A

thrombosis

  • arterial - stroke/TIA
  • venous - DVT/PE
  • erythromelagia - thrombosis in hands/feet
51
Q

tx essential thrombocytosis

A

anti platelet e.g. aspirin

hydorxycarbamide - chemo agent that decreases platelets

52
Q

what is reactive thrombocytosis

A

more common cause of increased platelet count

due to infection /chronic inflammation / anaemia / haemorrhage / hyposplenism

53
Q

hypersegmented neutrophils

A

megaloblastic anaemia

54
Q

shistocytes

A

intravascular haemolysis

55
Q

tear drop RBCs

A

myelofibrosis

56
Q

Howell jolly bodies

A

hyposplenism

57
Q

pencil RBCs

A

iron deficiency anaemia

58
Q

sudden anaemia + low reticulocyte count

A

parvovirus

59
Q

how does acute sequestration affect reticulocyte count

A

increased reticulocytes

60
Q

duration of treatment for DVT

  • provoked
  • unprovoked
A

warfarin 3 months

warfarin 6 months

61
Q

if a patient has combined B12 + folic acid deficiency, which must you treat first and why

A

B12

- prevents sub acute degeneration of spinal cord

62
Q

starry sky on lymph node biopsy

A

burrkits lymphoma

63
Q

what is given for emergency reversal of anticoagulation in patients with severe bleeds

A

prothrombin concentrate

64
Q

patients with HIV get what type of lymphoma

A

non-hodgkin

65
Q

what drug can precipitate renal failure in multiple myeloma

A

NSAIDS

66
Q

what kind of abdomen pain do patients with hereditary spherocytosis get

A

biliary colic due to gall stones

67
Q

presentation of CLL

A

generalised lymphadenopathy
weight loss
bleeding, infections

often asymptomatic

68
Q

what is tumour lysis syndrome

A

cell breakdown following chemo
release of potassium, phosphate, uric acid
– confusion, muscle spasms

69
Q

what is activated protein C resistance also known as

A

factor V leiden (most common thrombophilia)

70
Q

why is ASCG better than karyotyping

A

higher resolution

71
Q

heterozygous sickle cell

A

in adults

commonly occurs in plane i.e. low oxygen

72
Q

what type of leukaemia can cause autoimmune haemolysis

A

CLL