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EOY3 > Haematology > Flashcards

Haematology Flashcards

1
Q

normal Hb for males?

A

130-180g/L

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2
Q

what is the mean corpuscular volume (MCV)

A

the average volume of the erythrocytes

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3
Q

what is the mean corpuscular haemoglobin (MCH)

A

average mass of Hb per RBC

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4
Q

what is the mean corpuscular haemoglobin concentration (MCHC)

A

average conc of Hb in a given volume of blood

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5
Q

definition of red cell distribution width

A

measurement of the variability of the RBC size

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6
Q

what is the reticulocyte count

A

number of immature RBC in circulation - normally ~1%

a rise indicates rapid RBC production

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7
Q

what is the mean platelet volume (PMV)

A

average platelet size

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8
Q

what is a tear drop elliptocyte?

A

oval and elongated - associated with beta-thalassaemia

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9
Q

what is a pencil cell?

A

pencil shaped - associated with hereditary elliptocytosis

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10
Q

what is a hypochromic cell?

A

RBC is paler than normal - associated with iron deficiency anaemia

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11
Q

define normocytic normochromic

A

RBCs are average size and Hb is within normal limits

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12
Q

define anisocytosis

A

RBCs are unequal in size

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13
Q

define poikilocytosis

A

RBCs are unequal in shape

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14
Q

define microcytosis

A

RBCs are abnormally small

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15
Q

causes of normocytic normochromic anaemia

A 
acute blood loss
haemolytic anaemia 
aplastic anaemia 
G6PD deficiency 
HbS
hereditary spherocytosis 
acute bood loss
CKD
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16
Q

causes of microcytic hypochromic anaemia

A 
"TAILS"
thalassemia 
anaemia of chronic disease
iron deficiency anaemia
lead poisoning 
sideroblastic
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17
Q

causes of macrocytic normochromic anaemia

A 
"FAT RBC"
folate deficiency  
alcohol 
thyroid (hypothyroid) 
reticulocytosis 
B12 deficiency/ pernicious anaemia 
cytotoxic drugs - methotrexate, azathioprine
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18
Q

where in the fetus are RBCs produced?

A

initially the yolk sac
then the liver and spleen
and finally the bone marrow

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19
Q

where are RBCs produced in a healthy adult?

A

the bone marrow in the vertebra, ribs, sternum, sacrum, pelvis and proximal ends of the femur

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20
Q

common symptoms of anaemia

A

breathlessness
chest pain/ angina like symptoms
fatigue

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21
Q

physiological adaptations to anaemia

A

increased CO
reduced Hb O2 affinity due to increased 2,3 DPG
redistribution of blood flow

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22
Q

what may cause a raised reticulocyte count?

A 
autoimmune haemolysis 
acute leukaemia 
folate deficiency 
anaemia of chronic disease
acute blood loss
HbS
splenic sequestration
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23
Q

name some immune haemolytic anaemias

A 
autoimmune haemolytic anaemia
haemolytic disease of the newborn 
thrombotic thrombocytopenia purpura
anaemia associated with pre-eclampsia 
drug associated anaemia
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24
Q

what is seen on a post-splenectomy blood film?

A

Howell-Jolly bodies
Pappenheimer bodies
Target cells
Irregular contacted erythrocytes

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25
Q

Sickle cell crises

A
  • thrombotic, ‘painful crises’
  • sequestration
  • aplastic
  • haemolytic
    Rx: hydroxycarbamide if frequent crises
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26
Q

Thrombotic crises

A

also known as painful crises or vaso-occlusive crises
precipitated by infection, dehydration, deoxygenation
infarcts occur in various organs including the bones (e.g. avascular necrosis of hip, hand-foot syndrome in children, lungs, spleen and brain

27
Q

Sequestration crises

A

sickling within organs such as the spleen or lungs causes pooling of blood with worsening of the anaemia
acute chest syndrome: dyspnoea, chest pain, pulmonary infiltrates, low pO2 - the most common cause of death after childhood

28
Q

Aplastic crises

A

caused by infection with parvovirus

sudden fall in haemoglobin

29
Q

Haemolytic crises

A

rare

fall in haemoglobin due an increased rate of haemolysis

30
Q

Sickle cell anaemia

A

HbS
autosomal recessive common in Afro-Caribbean populations
A–>T base mutation causing a polar glutamate to a non-polar valine substitution in beta chains of Hb
deOHb polymerise, become fragile and haemolyse, sickle shaped RBC get stuck in small vessels and cause an infarction
heterozygous state is protective against malaria

31
Q

pernicious anaemia

A

anti-intrinsic factor antibodies bind to intrinsic factor of gastric parietal cells in gastric fundus - leads to poor vitamin B12 absorption and hence deficiency

32
Q

where is iron, folate and B12 absorbed in the GIT?

A

“dude is just feeling ill, bro”
Duodenum - iron
Jejunum - folate
Ileum - vitamin B12

33
Q

glucose-6-phosphate dehydrogenase deficiency

A

is the commonest RBC defect
X-recessive
many drugs can precipitate a crisis as well as infection and fava beans

deficiency of G6PD = low glutathione = increased cell susceptibility to oxidative stress

HEINZ BODIES ON BLOOD FILM

34
Q

types of polycythaemia

A

apparent or relative - due to decreased plasma volume (dehydration/burns/stress)
absolute polycythaemia - polycythaemia (rubra) vera or secondary polycythaemia

35
Q

polycythaemia rubra vera

A

is a myeloproliferative disorder caused by clonal proliferation of a marrow stem cell leading to an increase in red cell volume and overproduction of neutrophils and platelets
JAK2 mutation in 95% of patients
peak incidence in 6th decade

features: headache, dyspnoea, blurred vision, night sweats, pruritis (worse after a hot bath), hyper-viscosity, haemorrhage (due to abnormal platelet production), plethoric appearance (ruddy cyanosis)
treatment: aspirin, venesection (1st line - iron deficiency may limit erythropoiesis, doesn’t control the platelets), daily hydroxyurea (increases risk of leukaemia) or phosphorous-32 therapy (a single dose causes remission for two years)

prognosis - 5-15% myelofibrosis, 5-15% acute leukaemia

36
Q

secondary polycythaemia

A
  • caused by compensatory increase in EPO; high altitudes, respiratory diseases (COPD, obstructive sleep apnoea), CVS disease (especially congenital with cyanosis), increased Hb affinity, heavy cigarette smoking
  • caused by inappropriate EPO increase: renal disease or tumours
37
Q

Haemophilia A

A

factor VIII deficiency
X-linked recessive
(Ix: increase APTT and reduced factor VIII assay)
Rx: avoid NSAIDs and IM injections
minor bleeds - desmopressin (increases factor VIII)
if bleeding use recombinant factor VIII to increase levels to a % of normal (50% if major bleed, 100% if life-threatening)

38
Q

Haemophilia B

A

factor IX deficiency
X-linked recessive inheritance
Rx: recombinant factor IX

39
Q

von Willebrand’s disease

A

most common inherited bleeding disorder
autosomal dominant
lack of von Willebrand factor (which promotes platelet adhesion and is a carrier molecule for factor VIII)
Ix: increased APTT, increased bleeding time, reduced factor VIIIc, defective platelet aggregation with ristocetin
Rx: avoid NSAIDS, use tranexamic acid for mild bleeds, desmopressin (induces release of vWF), if major bleeds or surgery - vWF-containing factor VIII concentrate

40
Q

disseminated intravascular coagulation (DIC)

A

release of procoagulants into circulation causes widespread activation of coagulation, consuming clotting factors and platelets and hence increasing risk of bleeding
Ix: reduced fibrinogen (correlates with severity), raised d-dimer
blood film: schistocytes
Rx: FFP (to replace coagulation factors), cryoprecipitate (replace fibrinogen)

41
Q

Multiple myeloma

A

neoplasm of the bone marrow plasma cell
features: CRABS –> calcium high, renal insufficiency, anaemia (normocytic normochromic), bone pain and pathological fractures (especially of the vertebrae)
bence-jones proteins in urine
blood film - rouleaux
rX: analgesia, bisphosphonates, orthopathic procedures, transfusions or EPO, fluids, ABx if infection, regular IV immunoglobulin infusions if recurrent

42
Q

hypercalcaemia in myeloma pathophysiology

A

primarily due to increased osteoclastic bone reabsorption due to local cytokines (IL-1 and TNF) released by myeloma cells
also contributing is the impaired renal function, increased renal tubular calcium reabsorption and increased PTH-rP levels

43
Q

acute lymphoblastic leukaemia

A

most common malignancy in children (2-5y/o) 70-90% cure rate in children
immature cells of B or T cell lineages
blast cells on blood film and in bone marrow
lumbar puncture required to look for CNS involvement
Rx: blood/platelet transfusion, allopurinol (prevents tumour lysis syndrome), IV ABx for infections

44
Q

acute myeloid leukaemia

A

most common acute leukaemia in adults
death in 2 months if untreated as is rapidly progressive
has Auer rods and immature cells

45
Q

chronic myeloid leukaemia

A

Philadelphia chromosome is found in 95% of patients
proliferation of myeloid cells
causes splenomegaly and subsequent abdominal discomfort
median survival is 5-6 years
Rx: imatinib, hydroxyurea, interferon-alpha, allogenic bone marrow transplant

46
Q

chronic lymphoblastic leukaemia

A

proliferation well-differentiated (B) lymphocytes
often an incidental finding
blood film: smudge/smear cells
2/3 undergo Richter’s transformation - become high-grade fast growing non-Hodgkin’s lymphoma when reaches the lymph nodes

47
Q

Hodgkin’s lymphoma

A

Reed-Sternberg cell
alcohol consumption can cause severe pain
nodular sclerosing is the most common type ~70%
“B” symptoms predict a poor prognosis - weight loss (>10% in 6 months), fever >38, night sweats, lymphocyte depleted type also worsens prognosis

Rx: chemotherapy and radiotherapy –> one of the most treatable cancers (lymphocyte predominant improves prognosis)

48
Q

Non-Hodgkin’s lymphoma

A

can be a result of Richter’s transformation

Rx: rituximab, stem cell transplantation, multiple nodal group resection

49
Q

modifiable VTE risk factors

A 
smoking
immobility 
dehydration 
hyperlipidaemia
COCP, HRT (stop OCP 4 weeks prior to surgery) 
olanzapine
50
Q

non-modifiable VTE risk factors

A 
increasing age
femal 
trauma/surgery (the stress response)
AF
blood abnormalities 
malignancy 
thrombophilia
51
Q

what is the most common thrombophilia in the UK?

A

Factor V Leiden (activated protein C resistance) is the most common inherited thrombophilia, being present in around 5% of the UK population.

52
Q

LMWH MOA

A

e.g. dalteparin/enoxaparin

inactivates factor Xa

53
Q

unfractionated heparin MOA

A

binds to antithrombin, increasing its ability to inhibit thrombin, factor Xa and IXa

54
Q

warfarin MOA

A

inhibits the reductase enzyme responsible fore regenerating active vitamin K

reversed by vitamin K

55
Q

dabigatran MOA

A

direct thrombin inhibitor
mainly renally excreted

can be reversed by idarucizumab (praxabind)

56
Q

rivaroxaban MOA

A

direct factor Xa inhibitor

mainly hepatic excretion

57
Q

apixaban MOA

A

direct factor Xa inhibitor

mainly faecal excretion

58
Q

aspirin MOA

A

irreversible, non-selective COX-(1) inhibitor

stop 7 days pre-op

59
Q

clopidogrel MOA

A

blocks P2Y1Z so increases cAMP which prevents platelet aggregation
stop 5 days pre-op

60
Q

dipyridamole MOA

A

phosphodiesterase inhibitor, increases cAMP so inhibits platelet aggregation

61
Q

why are transfusions sometimes irradiated?

A

to get rid of T-cells to prevent GvHD e.g. if pt has Hodgkin’s lymphoma

62
Q

consequences of a transfusion reaction

A 
"GOT A BAD UNIT"
Graft vs Host disease
Overload 
Thrombocytopenia
Alloimmunization 
Blood Pressure unstable 
Acute haemolytic reaction (Rx: immediate transfusion termination, fluid resus and inform lab)
Delayed haemolytic reaction
Urticaria (Rx: temporarily discontinue transfusion and give antihistamines)
Neutrophilia
Infection 
Transfusion associated lung injury

Rx: for severe allergic reaction/anaphylaxis: permanent discontinuation of transfusion, IM adrenaline, supportive care, antihistamines, corticosteroids and bronchodilators

63
Q

post thrombotic syndrome

A

painful heavy calves, pruritus, swelling, varicose veins, venous ulceration
–> compression stockings

EOY3 (20 decks)

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