Key points Flashcards

1
Q

rbc lifespan?

A

120 days

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2
Q

neutrophil lifespan?

A

2-4 days

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3
Q

lymphocyte lifespan?

A

1 day to yrs

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4
Q

platelet lifespan, hence how many days prior to major surgery should antiplatelet drugs be stopped?

A

10 days

must stop at least 1 wk before surgery

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5
Q

what is the aa substitution that takes place in sickle cell disease?

A

glutamic acid to valine

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6
Q

what is the 1st recognisable cell that begins the process of granulopoiesis?

A

myeloblast

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7
Q

derivatives of the common myeloid progenitor cell?

A

megakaryocyte-platelet
proerythroblast-reticulocyte-erythrocyte
mast cell (from a mast cell progenitor)
myeloblast- neutrophil, basophil, eosinophil, monoblast-monocyte-macrophage

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8
Q

derivatives of common lymphoid progenitor cell?

A

B lymphocyte- plasma cell- cancer= multiple myeloma
T lymphocyte
natural killer cell= innate immune response

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9
Q

why is HbA1c diabetic monitoring inaccurate in a ptnt with a hameolytic anaemia?

A

hamolysis= shorter half life of rbc

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10
Q

up until 3 mnths gestation, where does haemopoiesis in the fetus take place?

A

yolk sac

begins in liver from 6 wks

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11
Q

where does hamopoiesis take place in fetus between 6 wks and 6 mnths gestatation?

A

liver and spleen

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12
Q

what would normal bone marrow cellularity be for a patient aged 30 years old?

A

100-30

=70% of active bone-producing cells

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13
Q

predominant location of bone marrow in adult?

A
pelvis
sternum
vertebrae
ribs
skull
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14
Q

why is hepatomegaly and splenomegaly seen in myeloproliferative disorders?

A

BM working overtime, hamopoiesis here therefore inadequate, so also occurs in liver and spleen

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15
Q

what can be given to ptnts receiving chemotherapy to shorten the duration of neutropenia which increases their infection risk?

A

recombinant granulocyte colony stimulating factor (GCSF)

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16
Q

how can Fe levels be regulated in the body?

A

only by absorption, to match losses from bleeding, sloughed mucosal epithelial cells and pregnancy.
excess Fe CANNOT be excreted by body

17
Q

what can free Fe2+ produce that is dangerous to the body?

A

OH and lipid free radicals which can damage lipid membranes, nucleic acids and proteins

18
Q

inheritence pattern of hereditary haemochromatosis- condition in which there is increased Fe absorption from the gut?

A

autosomal recessive

19
Q

how is hereditary haemochromatosis treated?

A

venesection- blood is drained off

20
Q

how can Fe overload be delayed in conditions requiring regular blood transfusions e.g. thalassaemia?

A

use Fe chelating agents e.g. desferrioxamine

21
Q

why does a macrocytosis (presence of abnormally large rbc in blood) occur with vit B12/folate deficiency?

A

these are required for DNA synthesis

without, rbc unable to progress from G2 to mitosis, so cells continue to grow without division.

22
Q

what is a megaloblast?

A

an abnormal form of any precursor cell to the rbc

23
Q

causes of macrocytic anaemias?

A
vit B12/folate deficiency
alcoholism
liver disease
hypothyroidism
Myelodysplastic syndromes
Marrow infiltration
Antifolate drugs e.g. Phenytoin
24
Q

Give 7 causes of a normocytic anaemia

A
Acute blood loss
Renal failure
BM failure
Anaemia of chronic disease
Hypothyroidism
Haemolysis
Pregnancy
25
Causes of a microcytic anaemia
Fe deficiency-most common cause of which is heavy periods Thalassaemia Sideroblastic anaemia
26
Based on FBC results, when should thalassaemia be suspected?
When MCV is too low for Hb level and red cell count is increased.
27
what is a paraprotein?
a monoclonal immunoglobulin
28
how does transfusion of 1 unit of blood affect Hb conc?
should increase it by 1g/dL