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Haematology > Physiology and Biochemistry Basics > Flashcards

Physiology and Biochemistry Basics Flashcards

1
Q

why does a rbc not have a nucleus

A

makes it more deformable (needs to be flexible to go through capillaries) and more room for Hb

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2
Q

what cellular organelles do RBCs lack

A

nucleus

mitochondria

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3
Q

how does the high Hb concentration in RBCs affect them

A

gives them high oncotic pressure (Hb a protein) - makes them want to swell
creates an oxygen rich environment= oxidative damage risk

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4
Q

how do RBCs make energy

A

glycolysis (no mitochondrian so cant do krebs cycle)

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5
Q

describe the rbc membrane

A

has protein spars (e.g. ankyrin) that anchor it an make it flexible

has sodium potassium pumps (Na+ x 3 out, K+ x 2 in), prevents swelling of cell with water

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6
Q

what is the structure of haemoglobin

A

a tetrameric globular protein
adult= 2 alpha and 2 beta chains
heme group is Fe2+ in a flat porphyrin ring (one haem per sub group)

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7
Q

what form does the haem group have to be in to carry oxygen

A

Fe2+ (if Fe3+ (e.g. oxidative damage from free radicals) cannot bind to oxygen)

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8
Q

what are the roles of haemoglobin

A

delivers oxygen to the tissues
acts as a buffer for H+
CO2 transport

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9
Q

what regulates red cell production

A

hypoxia sensed by kidneys (juxtoglomerular apparatus)
erythopoietin produced
red cell production stimulated

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10
Q

where does red cell destruction occur

A

in the spleen and liver (old rbc taken up by macrophages)

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11
Q

what is the lifespan of a rbc

A

~120

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12
Q

what is recycled in rbc destruction

A

globin chains -> amino acids (used for globin synthesis)

heme group -> iron (goes into iron stores then turned into haem)

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13
Q

what is the haem group broken down into

A

iron and bilirubin (heme->porphyrin->biliverdin->bilirubin)

bilirubin taken to liver and conjugated then excreted in bile (colours faeces and urine

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14
Q

via what pathway do rbcs make energy

IN EXAM

A

anaerobic glycolysis or embden meyehof pathway

glucose-> glucose-6-phosphate ->… pyruvate -> lactate

net generation of ATP and NADH

ATP for energy for cell, NADH for prevention of oxidation of Fe2+ to Fe3+

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15
Q

what is the role of glutathione (GSH)

A

protects rbcs from hydrogen peroxide by reacting with it form water and GSSG

it is replenished by NADPH

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16
Q

what is the rate limiting enzyme in the glutathione/ NADPH/ hexose monophosphate shunt

A

glucose - 6 - phosphate dehydrogenase (G6PD)

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17
Q

what is the hexose monophosphate shunt

A

pathway that generates NADPH which maintains GSH (glutathione) levels preventing oxidative damage (limited by G6PD activity)

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18
Q

how does CO2 get from the tissues to the lungs

A

10% dissolves in plasma
30% bound directly to Hb as carbamino-Hb
60% converts to bicarbonate (generated by RBC) which then floats in blood (equilibrium reaction, high CO2 environment= made into bicarbonate, low CO2 environment (e.g. lungs) converted back to CO2 and released)

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19
Q

how does Hb buffer CO2 for transport

A

when Hb is deoxygenated it binds with H+ in acidic environments (acidosis, high CO2) to make HHb

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20
Q

how many O2 molecules per Hb

A

4

21
Q

what are the subunits in fetal haemoglobin

A

two alpha, two gamma

22
Q

what is the shape of the oxygen dissociation curve

A

michaelis menten kinetics- sigmoidal

23
Q

what is the allosteric effect

A

when one oxygen binds to Hb it changes shape making it easier for O2 to bind to the next subunit
(important as Hb needs to bind a lot of O2 where O2 is high in conc e.g. lungs and conversly allows us to tolerate a high level of anaemia or bodily stress as have spare capacity)

24
Q

how do the dissociation curves differ across the types of Hb molecules

A

fetal Hb saturates more at the same PO2 as adult (so can effectively get O2 from maternal circulation)

monomeric myoglobin (in muscles) saturates easier than even fetal Hb as takes its O2 from red cells

25
Q

what molecules shift the oxygen desaturation curve to the right

A

H+
CO2
2,3 BPG

26
Q

what does the oxygen desaturation curve shifting to the right mean

A

more O2 is delivered to tissues by making it harder for O2 to bind to Hb

27
Q

what is 2,3, BPG

A

made during glycolysis
can be raised in chronic anaemia
(aka 2,3 DPG)

28
Q

what is the rapapoport-lubering shunt

A

generates 2,3 DBG that right shifts the oxygen dissociation curve and allows more oxygen to be released

29
Q

why might rbc be low

A 
increased destruction (haemolysis) 
reduced production (e.g. chemotherapy) 
redistribution (e.g. portal hypertension causing splenomegaly- rbc trapped in spleen)
30
Q

why might blood cell count be high

A

increased production due to stimulus (high altitude, COPD, infection) or no stimulus (malignancy)
redistribution (neutrophils raised in those taking steroids as moved from margin to centre of vessel and easier to sample)

31
Q

what does -cytosis or -philia mean

A

an excess (neutrophilia, thrombocytosis)

32
Q

what does thrombophilia mean

A

excess clotting

33
Q

what does -penia mean

A

a shortage of (e.g. lymphopenia)

34
Q

what does anaemia mean

A

lack of RBC or Hb

35
Q

what does bone marrow hyperplasia mean

A

increase blood cell production

36
Q

what does bone marrow dysplasia mean

A

disordered blood cell production

37
Q

what does bone marrow hypoplasia mean

A

low blood cell production

38
Q

what does bone marrow aplasia mean

A

no blood cell production

39
Q

what can RBCs be identified as during the first few days after production

A

reticulocytes

40
Q

why are folate and B2 important in RBC production

A

catalyze steps allowing cell division

41
Q

where in kidneys detects hypoxia

A

interstitial fibroblasts near to the peritubular capillaries and the proximal convoluted tubule

42
Q

what does erythropoietin cause

A

stimulates cell division of red cell precursors and recruits more cells to red cell production in the marrow = erythroid hyperplasia

43
Q

where are the macrophages that engulf RBC

A

mostly in spleen

44
Q

what would low levels of raw material e.g. iron cause

A

low output of rbcs = low reticulocyte count
Hb will gradually drop = anaemia
no change in breakdown products e.g. bilirubin as rate same

45
Q

what might be a liminting factor in resolving homeostasis after a big haemorrhage

A

will need erythoid hyperplasia, this may quickly deplete iron stores

46
Q

what is a glucose-6-phosphate dehydrogenase deficiency cause

A

inability to withstand oxidative stress- reduced rbc life span = increased production needed, will have increased breakdown products
increased breakdown of rbc will cause anaemia then hypoxia

47
Q

how does chronic renal failure affect rbc count

A

will fall as kidneys no longer able to make erythropoietin

48
Q

how is rbc count affected by COPD

A

slowly increased over years due to chronic hypoxia

49
Q

what is transient erythropenia of childhood

A

rare condition where red cell production stops for a variable number of weeks because the virus has infected red cell precursors

Haematology (27 decks)

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