Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MBBS Y5 > Medicine - Haematology > Flashcards

Medicine - Haematology Flashcards

1
Q

define anaemia

A

low Hb

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

TAILS: causes of microcytic anaemia?

A

NAME?

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

3As and 2Hs: causes of normocytic anaemia?

A

NAME?

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

how can macrocytic anaemia be classified?

A
  • megaloblastic| - normoblastic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

causes of megaloblastic anaemia?

A
  • B12 def| - folate def
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

causes of normoblastic, macrocytic anaemia?

A

NAME?

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

symptoms of anaemia?

A

NAME?

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

which conditions may worsen with anaemia?

A

NAME?

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

which 3 symptoms of anaemia are specific to iron deficiency anaemia?

A

NAME?

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

signs O/E of anaemia?

A

NAME?

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

which signs O/E are specific to iron deficiency anaemia?

A

NAME?

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

which type of anaemia is jaundice specific to?

A

haemolytic anaemia

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

which type of anaemia do bone deformities indicate?

A

thalassaemia

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

findings O/E of anaemia due to CKD?

A

NAME?

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

bloods done to investigate for anaemia?

A

NAME?

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

non-blood test investigations done in anaemia?

A
  • oesophageal-gastroduodenoscopy (OGD)| - bone marrow biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

causes of iron deficiency?

A

NAME?

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

where in the gut does iron get absorbed? what is the soluble form of iron?

A
  • duodenum and jejunum| - ferrous (Fe 2+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how is iron converted from the insoluble Fe3+ to the soluble Fe2+?

A

using stomach acid

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

how can PPIs cause an iron deficiency?

A
  • they reduce gastric acid secretion- stops iron being converted to the soluble form of Fe 2+- therefore not absorbed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

most common cause of iron deficiency in adults not menstruating?

A

blood loss in the GI tract

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

most common cause of iron deficiency in children?

A

dietary insufficiency

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

how can transferrin saturation be calculated?

A

serum iron / TIBC

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

what can cause a raised ferritin?

A

infection

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

how are TIBC and transferrin affected by iron deficiency?

A

both increase

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

how are TIBC and transferrin affected by iron overload?

A

both decrease

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

what could cause iron studies to give an iron overload impression?

A
  • iron supplements| - acute liver damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

3 management options for iron deficiency anaemia?

A
  1. blood transfusion2. iron infusion3. PO ferrous sulfate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how should Hb rise with oral iron supplements?

A

10g/L per week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the 2 causes of B12 deficiency?

A
  • insufficient dietary uptake| - pernicious anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is needed to absorb B12? where is this secreted?

A
  • intrinsic factor| - parietal cells of the stomach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

where in the gut does B12 get absorbed?

A

terminal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

neuro signs of B12 deficiency?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

pathophysiology of pernicious anaemia?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how is pernicious anaemia diagnosed?

A

test for the following antibodies:- intrinsic factor antibody (1st line)- gastric parietal cell antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

management of insufficient dietary B12?

A

PO cyanocobalamin supplements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

management of pernicious anaemia? hint: can’t be oral because won’t be absorbed

A

IM hydroxycobalamin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

why is it important to treat a B12 def before a folate def (in pts with both)?

A

giving folic acid to pt with B12 def can cause subacute combined degeneration of the spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

how can causes of haemolytic anaemia be classified?

A

inherited vs acquired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

inherited forms of haemolytic anaemia?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

acquired forms of haemolytic anaemia?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

signs O/E of haemolytic anaemia? (hint: all due to RBC destruction)

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

investigations for haemolytic anaemia?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is seen on the blood film in haemolytic anaemia?

A

schistocytes (fragments of RBCs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

when does the direct Coombs test give a positive result?

A

autoimmune haemolytic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

mode of inheritance of hereditary spherocytosis?

A

autosomal dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

presentation of hereditary spherocytosis?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

which organism can bring on an aplastic crisis in hereditary spherocytosis patients?

A

parvovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how is hereditary spherocytosis diagnosed?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

findings on blood film in hereditary spherocytosis?

A

spherocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

finding on FBC in hereditary spherocytosis? hint: it’s a rogue one

A

MCHC is raised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

treatment of hereditary spherocytosis?

A
  • folate supplements| - splenectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

key difference between hereditary spherocytosis and hereditary elliptocytosis?

A
  • in the second one, RBCs are ellipse shaped| - otherwise identical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

mode of inheritance for G6PD deficiency?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

G6PD deficiency is more common in patients of which descent?

A

Mediterranean / African

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what can trigger a G6PD deficiency crisis?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

drugs which cause G6PD deficiency crisis?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

how is G6PD deficiency diagnosed?

A

G6PD enzyme assay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

signs O/E of G6PD deficiency crisis?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what is seen on the blood film of someone in G6PD deficiency crisis?

A

Heinz bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

how can autoimmune haemolytic anaemia (AIHA) be classified?

A
  • warm type: haemolysis at normal or higher temperatures| - cold type: haemolysis at colder temps
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

causes of warm AIHA?

A

idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

causes of cold AIHA?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

management of AIHA?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what is alloimmune haemolytic anaemia? give 2 types

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what are the chains making up normal adult Hb?

A

2 alpha + 2 beta globin chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

pathophysiology of thalassaemia?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

potential signs and symptoms of thalassaemia?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

investigations in thalassaemia?

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

how can thalassaemia (and treatment) result in iron overload?

A
  • increased Fe absorption in response to anaemia| - recurrent blood transfusion therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what needs to be monitored in thalassaemia patients? why?

A
  • serum ferritin| - to check for iron overload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

presentation of iron overload in thalassaemia? hint: similar to haemachromatosis

A

NAME?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

where is the affected gene in alpha thalassaemia?

A

chromosome 16

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

where is the affected gene in beta thalassaemia?

A

chromosome 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

how is iron overload in thalassaemia managed?

A
  • limit blood transfusions| - iron chelation
76
Q

management of alpha thalassaemia?

A

NAME?

77
Q

what are the types of beta thalassaemia?

A
  • thalassaemia minor - “ “ intermedia - “ “ major
78
Q

presentation of thalassaemia minor?

A
  • mild microcytic anaemia| - only monitoring needed, no treatment
79
Q

presentation of thalassaemia minor? management?

A
  • mild microcytic anaemia| - only monitoring needed, no treatment
80
Q

presentation of thalassaemia major?

A

NAME?

81
Q

pathophysiology of sickle cell anaemia?

A
  • abnormal beta globin chain gene on chromosome 11 - this causes HbS to form instead of HbA - HbS causes RBCs to be sickle-shaped
82
Q

what is the relation between sickle cell trait and malaria?

A

having sickle cell trait reduces the severity of malaria infection

83
Q

how is sickle cell disease tested for in newborns?

A

part of the day 5 heel-prick test (Guthrie)

84
Q

complications of sickle cell anaemia?

A

NAME?

85
Q

general management principles of sickle cell anaemia?

A

NAME?

86
Q

potential triggers of a sickle cell crisis?

A

NAME?

87
Q

management of a sickle cell crisis?

A

all supportive:- low threshold for admission- treat underlying cause (e.g. ABx, keep warm, hydrated)- paracetamol / ibuprofen - penile aspiration if priapism

88
Q

pathophysiology of a vaso-occlusive crisis?

A
  • sickle-shaped RBCs clog up capillaries| - causes distal ischaemia
89
Q

presentation of vaso-occlusive crisis?

A

NAME?

90
Q

pathophysiology of splenic sequestration crisis? how does it present?

A

NAME?

91
Q

management of splenic sequestration crisis?

A

NAME?

92
Q

what is an aplastic crisis in sickle cell disease?

A

temporary cessation of erythropoiesis

93
Q

typical trigger of an aplastic crisis?

A

parvovirus B19 infection

94
Q

management of aplastic crisis?

A
  • blood transfusions if needed| - otherwise self-resolving within a week
95
Q

how is acute chest syndrome of sickle cell disease diagnosed?

A

both must be present:- fever / resp symptoms - new infiltrates seen on CXR

96
Q

infective causes of acute chest syndrome?

A
  • bronchiolitis| - pneumonia
97
Q

non-infective causes of acute chest syndrome?

A
  • pulmonary vaso-occlusion| - fat emboli
98
Q

management of acute chest syndrome?

A

NAME?

99
Q

age groups typically affected by ALL?

A

<5 years and >45 years

100
Q

age group typically affected by CLL?

A

> 55 years

101
Q

age group typically affected by CML?

A

> 65 years

102
Q

age group typically affected by AML?

A

> 75 years

103
Q

presentation of leukaemia? hint: pancytopenia

A

NAME?

104
Q

differentials for a non-blanching rash?

A
  • leukaemia- meningococcal septicaemia- vasculitis- HSP (lower limbs, buttocks)- ITP- NAI (children / vulnerable adults)
105
Q

initial investigation for leukaemia?

A

urgent FBC (<48h) for all with suspected leukaemia

106
Q

investigations for leukaemia?

A

NAME?

107
Q

what might the blood film show in leukaemia?

A
  • abnormal cells| - inclusions
108
Q

where is a bone marrow biopsy usually taken from?

A

iliac crest

109
Q

which cell type over-proliferates in ALL and CLL?

A

usually B-lymphocytes

110
Q

which genetic condition is ALL associated with?

A

downs syndrome

111
Q

blood film findings in ALL?

A

blast cells

112
Q

characteristic chromosomal change seen in CML in adults?

A

philadelphia chromosome

113
Q

what type of anaemia could CLL give?

A

warm autoimmune haemolytic anaemia

114
Q

which other cancer could CLL transform into?

A
  • high-grade lymphoma| - called richter’s transformation
115
Q

blood films findings in CLL?

A

“smudge” / “smear” cells (WBCs which ruptured in the process of preparing the film)

116
Q

3 phases of CML?

A

NAME?

117
Q

3 phases of CML?

A
  • chronic phase (asymptomatic, 5 years)- accelerate phase - blast phase
118
Q

what is seen in the blast cells on a blood film in AML?

A

auer rods

119
Q

which cancer could a myeloproliferative disorder (e.g. PRV) transform into?

A

AML

120
Q

management of leukaemia?

A

NAME?

121
Q

complications of chemotherapy for leukaemia?

A

NAME?

122
Q

pathophysiology of tumour lysis syndrome?

A

NAME?

123
Q

management of tumour lysis syndrome?

A

allopurinol and rasburicase to reduce uric acid levels

124
Q

how can lymphoma be categorised?

A
  • hodgkin’s| - non-hodgkin’s (all the other types)
125
Q

peak ages affected by hodgkin’s lymphoma? hint: bimodal

A

aged 20 and then aged 75

126
Q

risk factors for hodgkin’s lymphoma?

A

NAME?

127
Q

presentation of hodgkin’s lymphoma?

A

NAME?

128
Q

what are B symptoms? list them

A

NAME?

129
Q

investigations in hodgkin’s lymphoma

A

NAME?

130
Q

lymph node biopsy findings in hodgkin’s lymphoma?

A

reed-sternberg cells (large B cells with multiple nuclei)

131
Q

what is ann arbor staging used for? what does it take into account?

A

NAME?

132
Q

management of hodgkin’s lymphoma?

A
  • chemotherapy| - radiotherapy
133
Q

prognosis of hodgkin’s lymphoma?

A
  • chemo and radiotherapy are curative- they both carry own risk of secondary malignancy- B = BAD (B-symptoms have worse prognosis)
134
Q

types of non-hodgkin’s lymphoma?

A

NAME?

135
Q

key association with MALT lymphoma?

A

H. pylori infection

136
Q

which other conditions are associated with burkitt lymphoma? hint: all infections

A

NAME?

137
Q

risk factors for non-hodgkin’s lymphoma?

A
  • HIV- EBV - H. pylori (MALT)- hep B / C- exposure to pesticides- FHx
138
Q

management of non-hodgkin’s lymphoma?

A

NAME?

139
Q

pathophysiology of myeloma? what is multiple myeloma?

A

NAME?

140
Q

skin sign of pernicious anaemia?

A

gives “lemon tinged” skin

141
Q

most common immunoglobulin to be raised in myeloma?

A

IgG

142
Q

urinalysis finding in myeloma?

A

bence jones protein

143
Q

which bones are most commonly affected in myeloma?

A

NAME?

144
Q

effects of myeloma on bone turnover? result of this?

A

NAME?

145
Q

how does myeloma cause renal impairment? hint: multifactorial

A
  • lots of Igs block tubular flow- high Ca- dehydration - bisphosphonate therapy … all cause impairment
146
Q

how is plasma viscosity affected in myeloma?

A
  • increases| - due to increased Igs
147
Q

complications relating to increased plasma viscosity in myeloma?

A

NAME?

148
Q

what type of anaemia arises from myeloma?

A

normocytic, normochromic

149
Q

how does myeloma cause anaemia?

A

bone marrow being resorbed

150
Q

presentation of myeloma?

A

NAME?

151
Q

risk factors for myeloma?

A

NAME?

152
Q

what must be considered in anyone over 60 with bone pain? which investigation is key?

A
  • myeloma| - urgent FBC required
153
Q

findings on bloods for myeloma?

A

NAME?

154
Q

BLIPE: initial investigations for multiple myeloma?

A
  • Bence jones protein (urine electrophoresis)rest are all in blood: - Light-chain assay - Immunoglobulins - Protein Electrophoresis
155
Q

diagnostic investigation for multiple myeloma?

A

bone marrow biopsy

156
Q

pereferred investigation to stage multiple myeloma?

A

whole body MRI

157
Q

signs on X-ray in multiple myeloma?

A
  • punched out lesions - lytic lesions - “rain-drop skull” appearance
158
Q

management of myeloma?

A

NAME?

159
Q

management of bone disease secondary to myeloma?

A

NAME?

160
Q

complications associated with myeloma?

A

NAME?

161
Q

what are the 3 types of myeloproliferative disorder?

A

NAME?

162
Q

gene mutations associated with myeloproliferative disorders?

A

NAME?

163
Q

presentation of myeloproliferative disorders?

A

NAME?

164
Q

feautres of polycythaemia vera?

A
  • plethoric conjunctiva and face- “ruddy” complexion- splenomegaly- pruritis, worse after hot bath - HTN
165
Q

findings on FBC in polycythaemia vera?

A

isolated rise in Hb

166
Q

findings on FBC in essential thrombocythaemia?

A

raised platelets

167
Q

findings on FBC in myelofibrosis?

A

more variable: - anaemia (low Hb)- high OR low WCC- high OR low platelets

168
Q

findings on blood film in myelofibrosis?

A

NAME?

169
Q

diagnostic investigation and finding for myeloproliferative disorders?

A
  • bone marrow biopsy| - comes back “dry”
170
Q

management of myelofibrosis?

A
  • if mild, none needed- allogeneic stem cell transplant could be curative- chemotherapy- supportive (for anaemia / splenomegaly / portal HTN)
171
Q

management of polycythaemia vera?

A

NAME?

172
Q

management of essential thrombocythaemia?

A
  • aspirin| - chemotherapy
173
Q

findings on FBC in myelodysplastic syndrome?

A

NAME?

174
Q

risk factors for myelodysplastic syndrome?

A

NAME?

175
Q

which malignancy could myelodysplastic syndrome transform into?

A

AML

176
Q

presentation of myelodysplastic syndrome?

A

NAME?

177
Q

how can a diagnosis of myelodysplastic syndrome be confirmed?

A

on bone marrow aspiration and biopsy

178
Q

management of myelodysplastic syndrome?

A

NAME?

179
Q

causes of thrombocytopenia relating to reduced platelet production?

A

NAME?

180
Q

causes of thrombocytopenia relating to increased platelet destruction?

A

NAME?

181
Q

drugs which can cause thrombocytopenia?

A

NAME?

182
Q

presentation of thrombocytopenia?

A

NAME?

183
Q

differentials for prolonged bleeding?

A

NAME?

184
Q

pathophysiology of ITP?

A

antibodies made against platelets

185
Q

management of ITP?

A

NAME?

MBBS Y5 (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions