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Finals Studying - Condensed > Haem > Flashcards

Haem Flashcards

1
Q

presentation ALL

A 
CHILDREN
lymphadenopathy 
hepatosplenomegaly 
pallor
ecchymoses or petechiae 
fatigue 
dizziness
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2
Q

Ix for ALL

A

bone marrow aspirate - immunophenotyping

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3
Q

what is ALL

A

clonal malignancy of lymphoid precursors

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4
Q

what is AML

A

clonal malignancy of myeloid precursors

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5
Q

presentation AML

A 
ADULTS
hepatosplenomegaly 
pallor
ecchymoses or petechiae 
fatigue 
dizziness
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6
Q

Auer rods on peripheral blood smear

A

AML

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7
Q

CD24+ve on immunophenotyping

A

AML

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8
Q

smudge cells on peripheral blood smear

A

CLL

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9
Q

presentation CLL

A

often asymptomatic!!

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10
Q

common myeloid progenitor produces … what two further groups of progenitor cells?

A

megakaryocyte erythrocyte progenitor

myelocyte progenitor

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11
Q

megakaryocyte erythrocyte progenitor produces what cell types

A

erythrocytes (RBC) & platelets

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12
Q

myeloid progenitor produces what cell types?

A

Granulocytes

  • neutrophils
  • eosinophils
  • basophils

Macrophages

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13
Q

common lymphoid progenitor produces what cell types?

A

B cells
T cells
NK cells
Dendritic cells

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14
Q

RBC lifespan

A

120d

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15
Q

hormone regulating erythropoiesis

A

erythropoietin (from the kidneys) - detects reduced O2 and stimulates RBC production in the bone marrow

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16
Q

where does the nucleus of RBCs disintegrate

A

In the bone marrow

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17
Q

what is a reticulocyte

A

the earliest RBC in the blood stream - larger and blue appearance due to RNA

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18
Q

structure of Hb

A

4 globin subunits with a single haem molecule

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19
Q

what is a haem molecule composed of

A

single Fe2+ ion, surrounded by a porphyrin ring

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20
Q

breakdown products of RBC

A

amino acids
iron
unconjugated bilirubin (secreted into bile for conjugation in the liver to be excreted)

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21
Q

platelet lifespan

A

7-10 d

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22
Q

neutrophil appearance on blood film

A

segmented nucleus

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23
Q

eosinophil appearance on blood film

A

bi-lobed nucleus

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24
Q

basophil appearance on blood film

A

large granules that obscure nucleus

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25
Q

monocyte appearance blood film

A

kidney bean nucleus

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26
Q

lymphocyte appearance blood film

A

small spherical nucleus

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27
Q

cause of a microcytic anaemia

A

cytoplasmic defect (Hb is made in the cytoplasm)

therefore there is a problem with haemoglobinisation

lack of availability of:
haem (iron, porphyrin ring) or globin

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28
Q

causes of iron deficiency anaemia

A

diet deficiency
blood loss
malabsorption

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29
Q

presentation iron deficiency anaemia

A

fatigue
hair loss
nail changes (koilonychia)
pica (craving non food items)

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30
Q

koilonychia

A

spoon nails

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31
Q

blood results in iron deficiency

A

low Hb, low MCV (microcytic anaemia)
low ferritin
low retic count
low transferrin saturation

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32
Q

ferritin

A

measure of iron storage

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33
Q

Mx iron deficiency anaemia

A

ferrous fumarate for 3-6m (tds)

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34
Q

s/e of ferrous fumarate

A

black stools

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35
Q

causes of porphyrin ring synthesis problems

A

lead poisoning

v rare

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36
Q

causes of globin chain synthesis problems

A

thalassemia’s (reduced rate of production globin chain)

sickle cell anaemia (abnormal structure of globin chain)

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37
Q

inheritance of thalassaemia

A

autosomal recessive

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38
Q

HbA

A

2 alpha chains

2 beta chains

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39
Q

HbA2

A

2 alpha chains

2 delta chains

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40
Q

HbF

A

2 alpha chains

2 gamma chains

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41
Q

what forms of Hb are affected in alpha thal

A

all forms!

all contain alpha

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42
Q

alpha thal trait

A

1 or 2 genes missing

  • carrier state
  • no Tx needed
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43
Q

HbH disease (alpha thal)

A

only one gene left

  • mild anaemia
  • jaundice
  • splenomegaly
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44
Q

Hb Barts hydrops fetalis (alpha thal)

A

no functional genes

  • severe anaemia
  • growth retardation
  • most die in utero
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45
Q

what forms of Hb are affected in beta thal

A

only HbA

the only one to contain beta

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46
Q

forms of beta thal

A

beta thal trait
beta thal intermedia
beta thal major

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47
Q

beta thal trait presentation

A

asymptomatic

no/mild anaemia

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48
Q

beta thal intermedia presentation

A

requires occ transfusion

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49
Q

beta thal major presentation

A

present aged 6-24m (HbF stores have depleted)
failure to thrive
pallor
extramedullary haemopoeisis

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50
Q

Mx beta thal major

A

regular lifelong transfusions + iron chelation (desferrioxamine)

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51
Q

inheritance of sickle cell anaemia

A

autosomal recessive

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52
Q

forms of sickle cell anaemia

A

sickle cell trait

sickle cell anaemia

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53
Q

sickle cell trait presentation

A

HbAS (one normal beta gene, one abnormal)

  • asymptomatic carrier state
  • may sickle in severe hypoxia
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54
Q

sickle cell anaemia presentation

A

HbSS (both beta genes abnormal)

  • vascular occlusions and episodes of tissue infarct
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55
Q

Mx sickle cell anaemia

A

hydroxycarbamide (induces HbF)
penicillin
folic acid

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56
Q

Ix for thalassaemia

A

HPLC test

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57
Q

cause of a megaloblastic anaemia

A

nuclear defect - there is a problem with cell division

therefore there is abnormally large nucleated red cell precursors with an immature nucleus.

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58
Q

causes of a megaloblastic anaemia

A

B12 or folate deficiency

pernicious anaemia

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59
Q

vit B12 deficiency causes - what symp?

A

neurological problems

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60
Q

where is B12 absorbed

A

terminal ileum

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61
Q

what does B12 need to bind to for absorption

A

intrinsic factor (produced by gastric parietal cells)

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62
Q

where is folate absorbed

A

jejunum

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63
Q

blood film appearance in B12 or folate deficiency

A

hyper-segmented polymorphs

macro-ovalocytes

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64
Q

Mx B12 deficiency

A

IM hydroxocolbalamin (3xwk for 2w)

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65
Q

Mx folate deficiency

A

folic acid 5mg/day for 4m

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66
Q

why should you never give folic acid w/out checking B12 level

A

can induce subacute degeneration of the spinal cord

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67
Q

what is pernicious anaemia

A

autoimmune condition -

autoantibodies against gastric parietal cells, therefore no IF produced, therefore no B12 absorption

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68
Q

autoantibodies in pernicious anaemia

A

anti-intrinsic factor (specific, not sensitive)

anti-gastric parietal cells (sensitive, not specific)

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69
Q

Mx pernicious anaemia

A

B12 inj for life (hydroxocolbalamin)

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70
Q

causes of a non megalobastic macrocytic anaemia

A

alcohol
liver disease
marrow failure
hypothyroidism

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71
Q

cause of a false (spurious) macrocytic anaemia

A

cold agglutinins

haemolysis

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72
Q

when is haemolysis said to have progressed to haemolytic anaemia

A

when breakdown of RBCs exceeds response!

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73
Q

what are the normal responses to RBC breakdown

A

reticulocytosis and erythroid hyperplasia

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74
Q

what is extravascular haemolysis

A

excessive breakdown of RBC at the NORMAL site of destruction (spleen +/- liver)

therefore
you get the NORMAL breakdown products, but in excess:
- unconjugated bilirubinaemia
- urobilogenuria

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75
Q

causes of extravascular haemolysis

A

hereditary spherocytosis

sickle cell disease

autoimmune haemolysis

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76
Q

inheritance of hereditary spherocytosis

A

autosomal dominant

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77
Q

pathology of hereditary spherocytosis

A

RBCs are sphere shaped rather than biconcave disc, causing membrane disruption and destruction by the spleen.

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78
Q

blood film hereditary spherocytosis

A

spherocytes

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79
Q

Mx hereditary spherocytosis

A

RBC transfusions + folate replacement

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80
Q

autoimmune haemolysis

A

warm temperatures = IgG

cold temperatures = IgM

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81
Q

what is intravascular haemolysis

A

excessive breakdown of RBC within the circulation i.e. ABNORMAL site

therefore 
you get ABNORMAL breakdown products in excess:
- haemoglobinaemia 
- methylalbuminaemia 
- haemoglobinuria
- haemosiderinuria
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82
Q

causes of intravascular haemolysis

A

G6PD deficiency

ABO incompatability

DIC

HUS

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83
Q

inheritance of G6PD deficiency

A

X-linked

84
Q

pathology of G6PD deficiency

A

inborn error of metabolism, unable to deal with oxidative stress

85
Q

blood film G6PD deficiency

A

Heinz bodies

86
Q

Mx G6PD deficiency

A

supportive + folic acid

87
Q

what does FFP contain

A

all coagulation factors

88
Q

what is cryoprecipitate

A

blood component prepared from FFP

89
Q

indications for receiving FFP

A

bleeding

surgery in liver disease with impaired coag

DIC

90
Q

universal donor

A

group O

91
Q

universal recipient

A

group AB

92
Q

cause of an immediate haemolytic transfusion reaction

A

ABO incompatibility

93
Q

Mx of an immediate haemolytic transfusion reaction

A

discontinue transfusion, leave line in

flush saline 0.9%

94
Q

cause of a febrile non-haemolytic transfusion reaction

A

antibodies are contaminated with white cells

95
Q

presentation of a febrile non-haemolytic transfusion reaction

A

0/5 - 1 h after starting transfusion, get shivers and fever

96
Q

Mx of a febrile non-haemolytic transfusion reaction

A

slow or stop the transfusion

pcm

97
Q

Mx of an allergic/urticarial transfusion reaction

A

slow or stop the transfusion

chlorphenamine 10mg IV

98
Q

presentation of a delayed haemolytic transfusion reaction

A

5-10 d after transfusion, low Hb, fever, jaundice

99
Q

G+S

A

blood group is established and serum checked for Ab

this is a provision which allows rapid blood delivery in an emergency

100
Q

crossmatch

A

testing before a blood transfusion to determine if the donor’s blood is compatible with the blood of the intended recipient

101
Q

inheritance of hereditary haemochromatosis

A

autosomal recessive

102
Q

what gene is affected in hereditary haemochromatosis

A

HFE gene - affects hepcidin - can’t downregulate ferroportin

103
Q

pathology of hereditary haemochromatosis

A

iron is laid down in tissues rather than being stored in ferritin

104
Q

presentation of hereditary haemochromatosis

A 
"bronze diabetes" - from iron deposition in pancreas
weakness
fatigue
joint pains 
impotence
cirrhosis 
diabetes
cardiomyopathy
105
Q

Ix hereditary haemochromatosis

A
  1. serum transferrin saturation (raised)

2. serum ferritin (acute phase protein so is raised by other conditions, not specific)

106
Q

Mx hereditary haemochromatosis

A

venesection (exhaust iron stores)

107
Q

main cause of secondary iron overload

A

rptd red cell transfusions

108
Q

Mx of secondary iron overload

A

iron chelation Desferioxamine

109
Q

why is venesection not a Mx option for secondary iron overload

A

the pts are already anaemic, hence they are receiving transfusions

110
Q

Mx ALL

A

chemotherapy - long duration (2-3y)

111
Q

Mx AML

A

chemotherapy - intensive cycle

112
Q

what lineage does hodgkins lymphoma arise from

A

mature B cells

113
Q

presentation Hodgkin’s lymphoma

A

painless lymphadenopathy
itch without rash
alcohol-induced pain
‘B symptoms’ - wt loss, fever, night sweats

114
Q

Ix hodgkins lymphoma

A

lymph node biopsy

  • Reed Sternberg cells
  • Immunohistochemistry (CD 30 +ve)
115
Q

CD 30 +ve cells on immunohistochemistry

A

Hodgkin’s lymphoma

116
Q

reed Sternberg cells

A

hodgkins lymphoma

117
Q

Mx Hodgkin’s lymphoma

A

monoclonal Ab (brentuximab) + chemo

118
Q

what lineage does non hodgkins lymphoma arise from

A

90% - B cell lines

119
Q

presentation non hodgkins lymphoma

A

B symptoms - night sweats, fever, wt loss

120
Q

follicular lymphoma gene

A

non-hodgkins lymphoma -

t(14;18) between the bcl-2 gene

121
Q

Burkitts lymphoma

A

non-hodgkins lymphoma -

c-myc gene on (8;14)

122
Q

CD 20 +ve cells on immunohistochemistry

A

Burkitt’s lymphoma

123
Q

Mx non-Hodgkin’s lymphoma

A

monoclonal Ab (rituximab) + chemo

incurable apart from the early stage

124
Q

what is hyposplenism

A

reduced or absent splenic function

125
Q

causes of hyposplenism

A 
congenital absence
surgical removal 
trauma
immune 
infarction (sickle cell) 
infiltration (lymphoma, amyloid) 
drugs (methyldopa, chemo)
126
Q

blood film hyposplenism

A

Howell Jolly bodies

(inclusion of nuclear chromatin remnants)

127
Q

infection prophylaxis in hyposplenism

A

pneumoccal + HiB vaccines

long term oral penicillin

128
Q

what is hypersplenism

A

enhanced filtration, pathological pooling or shortening of RBC lifespan

129
Q

causes of hypersplenism

A

cirrhosis
lymphoma
TB
CTDs and inflammatory disease

130
Q

presentation of pancytopenia

A

anaemia - fatigue, SOB, CVS compromise

neutropenia - infection

thrombocytopenia - bleeding

131
Q

congenital cause of bone marrow failure

A

Fanconi’s anaemia

132
Q

inheritance of fanconis anaemia

A

autosomal recessive

133
Q

presentation fanconi’s anaemia

A

short stature
hyperpigmentation
skeletal abnormalities
increase in solid tumours + leukaemia

134
Q

acquired causes of primary bone marrow failure

A

aplastic anaemia

myelodysplastic syndromes

135
Q

what is aplastic anaemia

A

autoimmune attack against the haemopoietic stem cell

136
Q

bone marrow appearance aplastic anaemia

A

hypocellular

137
Q

what are myelodysplastic syndromes

A

a group of cancers, where there is apoptosis of the mature cells

138
Q

bone marrow appearance myelodysplastic syndromes

A

hypercellular - lots of immature cells due to ineffective erythropoiesis

139
Q

causes of secondary bone marrow failure

A

drugs - chemo, chloramphenicol, alcohol

B12/folate deficiency

lymphoma

HIV

140
Q

what is multiple myeloma

A

cancer of plasma cells

141
Q

the presence of ?-? characterizes multiple myeloma?

A

IgG monoclonal antibody (paraprotein)

142
Q

presentation multiple myeloma

A

Direct tumour effects:

  • bone lesions (punched out lytic lesions)
  • hypercalcaemia
  • bone pain
  • marrow failure

Paraprotein effects:

  • renal cast nephopathy
  • immune suppression
  • hyper viscosity
  • amyloid
143
Q

Ix multiple myeloma

A

serum/urine electrophoresis - bence jones proteins

144
Q

bence jones proteins

A

serum/urine electrophoresis

- multiple myeloma

145
Q

RBC appearance multiple myeloma

A

roleaux formation

146
Q

monoclonal gammopathy of uncertain significance (MGUS)

A 
high paraprotein (<30g/L)
NO clinical features of myeloma
147
Q

waldenstrom’s macroglobulinaemia

A

clonal disorder of intermediate cells between a lymphocyte and plasma cell

148
Q

paraprotein in waldenstrom’s macroglobulinaemia

A

IgM

149
Q

what is amyloidosis

A

mutation in the light chain of plasma,

leads to accumulation of the mutated protein in tissues - eventual organ failure & death

150
Q

Ix amyloidosis

A

organ biopsy

- Congo red stain with apple green birefringence under green light

151
Q

what is CML

A

a myeloproliferative disorder

clonal malignancy of myeloid precursors

152
Q

important mutation in CML

A

Philadelphia chromosome (9;22) translocation

BCR-ABL +ve

153
Q

presentation CML

A

splenomegaly
wt loss
excessive sweating
gout (due to purine breakdown)

154
Q

Mx CML

A

tyrosine-kinase inhibitor (imatinib)

155
Q

what is polycythaemia

A

a myeloproliferative disorder

a true increase in red cell mass

156
Q

causes of primary polycythaemia

A

polycythaemia rubra vera

157
Q

JAK 2 mutation

A

polycythaemia rubra vera

158
Q

causes of a secondary polycythaemia

A

smoking
COPD
altitude

159
Q

causes of a pseudo polycythaemia

A

dehydration
obesity
diuretic therapy

160
Q

presentation of polycythaemia

A

aquagenic pruritus
thrombosis
gout

161
Q

Mx polycythaemia rubra vera

A

hydroxycarbamide + aspirin

162
Q

what is essential thrombocythemia

A

a myeloproliferative disorder

a true increase in platelets

163
Q

Mx essential thrombocythaemia

A

if plt < 1500 x 10^9/L and no prev thrombosis - no Tx

low risk of thrombosis - aspirin

high risk of thrombosis - hydroxycarbamide

164
Q

what is myelofibrosis

A

reactive + reversible process
abnormal production of all 3 lineages due to marrow scarring
- therefore there is extramedullary haemopoiesis

165
Q

presentation myelofibrosis

A

massive splenomegaly

166
Q

blood film appearance myelofibrosis

A

leucoerythroblastic cells

teardrop RBCs

167
Q

Mx myelofibrosis

A

stem cell transplant

168
Q

what is responsible for primary haemostasis

A

platelets

169
Q

process of primary haemostasis

A

vessel wall damage
release of vWF from vessel wall
platelets have receptors to vWF

170
Q

screening test for primary haemostasis

A

platelet count

171
Q

what is responsible for secondary haemostasis

A

coagulation cascade

172
Q

explain process of coagulation cascade

A

INTRINSIC PATHWAY:
Tissue Factor (III) is released from damaged vessels.
Activates Factor VII (VIIa).
Activates Factors V and X (Va & Xa).
Activates prothrombin (II) to thrombin (IIa).
Activates fibrinogen (I) to fibrin (Ia).

EXTRINSIC PATHWAY:
Factors VIII and IX are activated (VIIIa & IXa).
Potentiates the activation of Va and Xa even more.

173
Q

screening test for the intrinsic coagulation pathway

A

prothrombin time (PT)

174
Q

screening test for the extrinsic coagulation pathway

A

activated partial thromboplastin time (aPTT)

175
Q

connection between vWF and Factor VIII

A

vWF has a role in binding to Factor VIII and protecting it

176
Q

what is responsible for the breakdown of fibrin clots

A

plasmin

(plasminogen produced by the liver,
converted to plasmin by tissue plasminogen activator)

177
Q

natural anticoagulants

A

anti thrombin

protein c and protein S

178
Q

role of anti thrombin

A

inhibits thrombin (IIa) and Factor Xa

179
Q

role of protein c and protein s

A

inhibits Factor Va and Factor VIIIa

180
Q

what activates protein c and protein s

A

the presence of thrombin

181
Q

disorders of primary haemostasis

A

VASCULAR PROBLEMS

  • inherited (marfans)
  • acquired (HSP)

PLATELET PROBLEMS

  • reduced number (thrombocytopenia)
  • reduced function (renal failure, nsaids, aspirin)

VON WILLEBRAND’S DISEASE

182
Q

inheritance of von willebrands

A

autosomal dominant

183
Q

presentation von willebrands

A

bruising
epistaxis
menorrhagia
increased bleeding post-tooth extraction

184
Q

Ix for von willebrands

A

APTT - prolonged

factor VIII has a protective factor on VIII

185
Q

causes of a prolonged APTT and PT

A

multiple clotting factor deficiency

liver failure, vit K deficiency, DIC

186
Q

inheritance of haemophilia

A

x-linked

187
Q

haemophilia A

A

factor VIII deficiency

188
Q

haemophilia B

A

factor IX deficiency

189
Q

presentation haemophilia

A

recurrent haemarthroses

recurrent soft tissue bleeds

190
Q

factor V leiden disease

A

inherited thrombophilia

point mutation in Factor V, so protein C can’t inhibit it

191
Q

anti phospholipid syndrome predisposes to what type of thrombosis?

A

both arterial and venous !

192
Q

heparin mode of action

A

potentiates anti-thrombin

193
Q

monitoring heparin

A

LMWH - anti Xa levels

unfractionated heparin - APTT

194
Q

Mx bleeding on heparin

A

stop heparin (has a short half life)

if bleeding severe - protamine sulphate

195
Q

mode of action of rivaroxaban

A

factor Xa inhibitor

196
Q

mode of action of apixaban

A

factor Xa inhibitor

197
Q

mode of action of dabigatran

A

direct thrombin inhibitor

198
Q

mode of act ion of warfarin

A

antagonizes vitamin K

199
Q

why does warfarin have a prothrombotic effect in the first few days

A

inhibits protein C

200
Q

monitoring warfarin

A

PT

201
Q

Mx bleeding on warfarin

A

stop warfarin
give Vit K (takes 6h to work)
give prothrombin complex concentrates (works immediately)

202
Q

aspirin mode of action

A

inhibit the COX pathway

- COX is needed to make thromboxane A2, which is released from platelets when they aggregate.

203
Q

s/e of aspirin

A

bleeding

blockage of prostaglandins - ulceration, bronchospasm

204
Q

mode of action of clopidogrel

A

ADP receptor antagonist

205
Q

mode of action of dipyradimole

A

phosphodiesterase inhibitor

206
Q

equations to work out cause of shock

A

MAP = CO x TPR

CO = HR x SV

Finals Studying - Condensed (22 decks)

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