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Finals > Haematology > Flashcards

Haematology Flashcards

1
Q

How can you tell if an anaemia is caused by an issue with removal or production of RBCs

A

measure reticulocyte count

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2
Q

Causes of microcytic anaemia

A

iron deficiency
thalassaemia
anaemia of chronic disease
sideroblastic anaemia

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3
Q

causes of normocytic anaemia

A 
acute blood loss
anaemia of chronic disease
CKD
autoimmune rheumatic disease
Endocrine disease
haemolytic anaemia
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4
Q

Causes of macrocytic anaemia

A 
vitamin B12 or folate deficiency 
alcohol
liver disease
hypothyroidism 
drug therapy e.g. azathioprine
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5
Q

How is iron absorpbed

A

intestinal haem transporter HCP1 actively transports iron into the duodenal epithelial cells where some binds to ferritin (intracellular store) and the rest circulates in blood bound to transferrin.

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6
Q

How is iron used

A

majority in haemoglobin

the rest in reticuloendothelial cells, hepatocytes and skeletal muscle cells as ferritin or haemosiderin

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7
Q

Serum test results in iron deficiency

A

low serum iron
high total-iron binding capacity
increase in transferrin receptors
low reticulocyte count

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8
Q

Treatment of iron deficiency

A

usually find a cause first
ferrous sulphate oral
ferrous gluconate if bad SE
parenteral iron (IV iron or IM iron) only in extreme cases.

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9
Q

what is anaemia of chronic disease

A

bone marrow is sick
second most common cause of anaemia and common in hospitalised patients
usually normocytic

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10
Q

Common causes of anaemia of chronic disease

A 
tuberculosis
crohns
rheumatoid arthritis
SLE
malignant disease
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11
Q

what is pernicious anaemia

A

autoimmune disorder in which parietal cells of stomach are attacked resulting in atrophic gastritis and the loss of intrinsic factor production and hence b12 malabsorption

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12
Q

where is b12 absorped

A

terminal ileum using intrinsic factor (produced by parietal cells in stomach)

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13
Q

risk factors for pernicious anaemia

A

elderly
female
fair haired
autoimmune disease

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14
Q

Treatment for pernicious anemia

A

b12 injections (IM hydroxocobalamin)

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15
Q

how might you distinguish between a folate and b12 deficiency

A

no neuropathy in folate deficiency

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16
Q

treatment of folic acid deficiency

A

folic acid tablets WITH B12 unless known to be normal as can precipitate subacute combined degeneration of the cord

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17
Q

main causes of haemolytic anaemia

A

RBC membrane defects - hereditary spherocytosis

enzyme defects - glucose-6-phosphate dehydrogenase deficiency

haemoglobinopathies:
B thalassaemia
A thalassaemia
sickle cell disease

autoimmune haemolytic anaemia

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18
Q

features of haemolytic aneamia (bilirubin)

A 
high unconjugated bilirubin
high urobilinogen
high stercobilinogen (dark stool)
splenomegaly
bone marrow expansion
reticulocytosis
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19
Q

hereditary spherocytosis summary

A

autosomal dominant
deficiency in structural protein spectrum
sphere shaped RBC get stuck in spleen and cause premature haemolytic and splenomegaly

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20
Q

presentation of hereditary spherocytosis

A 
jaundice at birth
can have delayed jaundice
anaemia
splenomegaly
ulcers on leg
gall stones

aplastic anaemia after infections (particularly parvovirus)

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21
Q

treatment of hereditary spherocytosis

A

splenectomy delayed until after childhood (risk)

post-op life-long penicillin prophylaxis

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22
Q

G6PD deficiency summary

A

heterogenous x-linked (more common in males)
G6DP reduces NADP to NADPH which is essential for protecting RBCs from oxidative stress
Leads to reduced RBC lifespan

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23
Q

Presentation of G6PD deficiency

A

asymptomatic

drug-induced haemolytic:
aspirin
antimalarials (quinine, chloroquine)
nitrofuratonin
fava beans

In attacks:
rapid anaemia
jaundice

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24
Q

Results/treatment of G6DP attacks

A 
irregular cells on film
Bite cells (cells with indentation in)
reticulocytosis
G6PD enzyme levels will be low but can be falsely high
blood transfusion may be life saving
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25
Q

What are the types of haemoglobin

A 
HbA
foetal Hb (HbF)
Hb delta (HbA2)

In an adult
HbA - 97%
HbA2 - 2%
HbF - 1%

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26
Q

What is the normal production of alpha and beta chains

A

1:1 ratio

HbA has 2 alpha and 2 beta

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27
Q

Beta thalassaemia summary

A

reduced B chain production results in excessive alpha chains.
Excess alpha chains bind with any delta or gamma chains available and oriduce excess Hb delta and foetal Hb
IF HETEROZYGOUS THEN ASYMPTOMATIC OR MILD ANAEMIA

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28
Q

Mutations in beta thalassaemia

A

Point mutations

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29
Q

Mutations in alpha thalassaemia

A

gene deletions

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30
Q

summary of alpha thalassaemia

A

four gene deletion - no alpha chain synthesis
only Hb Parts (4 gamma chains) is present
incompatible with life
stillborn infant or die very shortly after birth - hydrops fetalis

three gene deletion - reduction in alpha synthesis, HbH has 4 beta-chains, moderate anaemia

two gene deletion - microcytosis mild anaemia

one gene deletion - normal

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31
Q

inheritance of sickle cell trait

A

autosomal recessive

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32
Q

when does sickle cell present

A

after 6 months as foetal haemoglobin is normal (no beta chains)

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33
Q

mutation of sickle cell

A

single base mutation on beta chain

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34
Q

complications of sickle cell disease

A

vaso-occlusive crises:
pain in hands/feet in chidlren
long bone pain in adults (femur, spine, ribs) due to avascular necrosis of bone marrow

acute chest syndrome
vaso-occlusive crisis of pulmonary vasculature
pulmonary hypertension and chronic lung disease are the most common cause of death in adults with sickle cell

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35
Q

Treatment for sickle cell

A

vaccinate - prevent infection
folic acid to all haemolytic patients
attacks - fluids, analgesia, oxygen, antibiotics
blood transfusion for acute chest syndrome, aplastic crisis
ORAL HYDROXYCARBAMIDE to increase HbF concentration

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36
Q

Aplastic anemia definition and causes

A

pancytopenia (all major blood cell lines)

Idiopathic
Fanconi's anaemia
benzene, toluene and glue sniffing
chemo drugs
antibiotics - carbamazepine, azathioprine and chloramphenicol
infections: EBV, HIV TB
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37
Q

clinical presentation of aplastic anaemia

A 
obvious:
anaemia
infections
bleeding
bleeding gums, bruising

DD: other causes of pancytopenia - drugs, lymphomas, myeloma, SLE

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38
Q

treatment of aplastic anaemia

A

broad spectrum antibiotics
red cell and platelet transfusion
bone marrow transplant

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39
Q

polycythemia vera

A

Janus kinase 2 mutation
clonal stem cell disorder causing excessive proliferation of RBCs, EBCs and platelets causing a raised haematocrit and viscosity

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40
Q

Clinical presentation

A 
vague hyper viscosity symptom
headache
itching
tiredness
dizziness
tinnitus
visual disturbance
severe itching when warm
gout
hypertension
hepatosplenomegaly
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41
Q

treatment of polycythemia vera

A

venesection weekly - 500ml
chemotherapy - hydroxycarbamide for those who don’t tolerate venesection
++ low dose aspirin

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42
Q

What is ITP

A

thrombocytopenia due to immune destruction

bruising
epistaxis
menorrhagia
purpura
gum bleeding
43
Q

What is primary ITP

A

acute in children (2-6)
recent viral infection. e.g. chickenpox
self limiting purport usually on legs

44
Q

What is secondary ITP

A

chronic in adults
women and often associated with autoimmune disorders such as SLE, thyroid disease
CLL and HIV infection.

45
Q

Treatment of ITP

A

prednisolone
IV IgG if going into surgery as this will raise the platelet count more rapidly
second line: splenectomy

46
Q

What is thrombotic thrombocytopenia purpura TTP

A

widespread adhesion and aggregation of platelets. due to a deficiency in a protease than breakdown vWF

47
Q

Causes of TTP

A 
idiopathic
autoimmune (SLE)
cancer
pregnancy
drug associated (quinine)
48
Q

Clinical presentation of TTP

A

florid (red) purpura
fever
fluctuating cerebral dysfunction
haemolytic anaemia

49
Q

Treatment for TTP

A

plasma exchange
IV methylprednisolone
IV rituximab

Low platelets but do not give as in hypercoaguable state!!!

50
Q

would you see schistocytes in ITP or TTP

A

TTP think clots tear apart RBCs causing fragmentation

51
Q

Which is more serious ITP or TTP

A

TTP! it is an emergency as blood is clotting! but do a plasma exchange.

Can leave ITP if asymptomatic

52
Q

How does DIC arise

A

systemic activation of coagulation either by release of procoagulant material such as tissue factor or via cytokine pathways as a part of the inflammatory response.

caused by extensive damage to vascular endothelium exposing tissue factor or enhanced expression of tissue factor by monocytes in response to cytokines

53
Q

Conditions associated with DIC

A 
sepsis
major trauma and tissue destruction
advanced cancer
obstetric complications
pancreatitis
54
Q

Clinical findings in DIC

A

severe thrombocytopenia
elevated fibrin degradation products - d-dimer
fragmented RBCs on film
prolonged PT

55
Q

Treatment for DIC

A

treat cause
platelet transfusion
FFP to replace coat factors

56
Q

What should you monitor after starting Heparin

A

platelet levels as can get heparin induced thrombocytopenia

57
Q

most common ages for ALL

A

2-4 years old

58
Q

which cells does ALL affects

A

T and B precursors
all B cells - children
all T cells - adult

59
Q

Diagnosis of ALL

A

high WCC
blast cells on film and in bone marrow
CXR/CT may show lymphadenopathy

60
Q

treatment for ALL

A 
blood transfusion
prophylactic antibac/fung
allopurinol prevents tumour lysis syndrome 
chemo
marrow transplant
61
Q

Symptoms of AML

A

anaemia - fatigue, claudication, breathlessness, pallor and cardiac flow murmur

infection - fever and mouth ulcers

low platelets - bleeding, bruising

gum hypertrophy
hepatomegaly/splenomegaly

62
Q

treatment for AML

A 
blood and platelet transfusion
infection prophylaxis
allopurinol to prevent tumour lysis syndrome
chemo
marrow transplant
63
Q

age group for CML

A

40-60 years, male predominance

more than 80% have the Philadelphia chromosome

64
Q

diagnosis for CML

A

very high WCC - whole spectrum of myeloid cells increased, neutrophils, basophils, eosinophils
low HB
low platelets
hypercellular bone marrow

65
Q

treatment for CML

A

IMATINIB

tyrosine kinase inhibitor (Philadelphia chromosome linked to increase TK activity which stimulates cell division)

66
Q

age range for CLL

A

the most common leukaemia

presents in later life - elderly

67
Q

CP of CLL

A

asymptomatic often an incidental finding

68
Q

diagnosis of CLL

A

normal/low hb
raised WCC w/ very high lymphocytes
smudge cells on blood film

69
Q

outlook for CLL

A

rule of 3s
1/3 never progress
1.3 slowly
1/3 quickly

70
Q

treatment for CLL

A

human IV immunoglobulins
chemo
blood transfusion

71
Q

Hodgkins lymphoma

A

Reed-Sternberg cells
male predominance
teenagers 13-19 and over 65s
EBV plays a role

72
Q

CP of Hodgkins lymphoma

A 
cervical lymphadenopathy (rubbery)
B symptoms

emergency presentation:
infection
SVC obstruction
blackouts

73
Q

diagnosis of Hodgkins lymphoma

A

CT/MRI for staging (Ann Arbor)
lymph node excision or bone marrow biopsy for Reed-Sternberg cells
PET scan

74
Q

Ann Arbor staging

A

I confined to single lymph node
II involvement of two or more lymph node regions on same side of diaphragm
III involvement of nodes on both sides of the diaphragm
IV spread beyond lymph to liver or bone

A: no systemic symptoms (other than itching)
B: B symtpoms

75
Q

Non-Hodgkin’s lymphoma

A

all lymphomas without reed-sternberg
80% is B cell origin
strong link with EBV and Burkitts lymphoma

76
Q

two grades of non-hodgkins

A

low grade - follicular lymphoma
(incurable, slow growing around 11 year survival)

high grade - diffuse large B-cell lymphoma

77
Q

treatment of non-hodgkins

A 
R-CHOP regimen
Rituximab
Cyclophosphamide
Hydroxy-daunorubicin
Oncovin
Prednisolone

May also use radiotherapy

78
Q

what is myeloma

A

cancer of differentiated B cells (PLASMA CELLS) which produce antibodies. accumulate in the bone marrow and cause failure
peak age 70

79
Q

presentation of myeloma

A 
OLD CRAB
OLD age
Calcium elevated
Renal failure
Anaemia
Bone lytic lesions (activate osteoclasts and inhibit osteoblasts)
80
Q

signs of myeloma

A 
normocytic normochromic anaemia
raised ESR
Rouleaux formation on blood film (RBC stack like coins)
hyperclacaemia
pepper-pot skull
vertebral collapse
81
Q

treatment of myeloma

A 
analgesia for bone pain (avoid NSAID renal)
bisphosphonates
transfusion/EPO injection
chemo
stem cell transplant
82
Q

what is febrile neutropenia

A

temp above 38 in a patient with neutrophils <1x10^9
life threatening emergency

basically infection in someone with neutropenia

83
Q

risk factors for febrile neutropenia

A 
chemo <6 weeks ago
aplastic anaemia
autoimmune disease
leukaemia
methotrexate
carbimazole
clozapine
84
Q

treatment of febrile neutropenia

A

broad spectrum antibiotics immediately

85
Q

which cancers most commonly cause malignant spinal cord compression

A

myeloma

lymphoma

86
Q

management of malignant spinal cord compression (caudal equine)

A

quick!
bed rest
dexamethasone
urgent MRI spine

87
Q

what is tumour lysis syndrome

A

malignant cells breakdown quickly:

high uric acid
hyperkalaemia
hyperphosphatemia
hypocalcaemia

88
Q

complications of tumour lysis syndrome

A

neuro (hypocalcaemia):
muscle cramps, seizure

cardiac (hyperkalaemia)
arrest

renal (uric acid crystals)
failure

89
Q

treatment of tumour lysis syndrome

A

allopurinol reduces uric acid levels to prevent kidney failure
monitor electrolytes
dialysis if needed

90
Q

clinical presentation of hypercalcaemia

A

bones moans stone psychiatric groans

confusion
boe pain
constipated
nausea
polyuria
renal stones
abdo pain
shortening of QT interval
91
Q

treatment of hypercalcaemia

A

hydration 3-4L/day

bisphosphionates (takes a few days to effect)

92
Q

how to reverse heparin

A

protamine

93
Q

reversal of warfarin

A

immediate - fresh frozen plasma FFP

vitamin K will reverse slowly

94
Q

when would heparin be used

A

bypass surgery

95
Q

when is LMW heparin used

A

SC injection

treatment and prophylaxis

96
Q

what is the normal target INR

A

2-3

97
Q

which clotting factors are vitamin K dependent

A

1972
II, VIII, IX and X

(1 is a 10)

98
Q

which clotting factors do NOACs affect

A

II or X

99
Q

when would NOACs be used

A

AF, DVT, PE

100
Q

when would warfarin be preferred over NOAC

A

mechanical heart valves as NOAC does not allow for exact control over INR

OR

pregnancy

101
Q

what is the action of rivaroxaban/apixaban

A

factor Xa inhibitor

102
Q

what is the antibiotic therapy of choice for neutropenic sepsis

A

piperacillin and tazobactam

103
Q

what is the most common thrombophilia

A

factor V Leiden - causes mutation in factor V resulting in resistance to inactivation by protein C.

104
Q

What does protein C do

A

negative feedback on clotting cascade

Finals (15 decks)

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