W1: Red Blood Cells Flashcards

1
Q

3 features or rbcs (erythrocytes)

A

*biconcave disc shape
*no nuc/ cytoplasmic organelles in mature rbcs
*contain Hb

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2
Q

what stops rbcs from aggregating?

A

neg charge of outer surface of rbc membranes

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3
Q

why do rbcs have transmembrane proteins?

A

to give shape + some rigidity

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4
Q

function of band 3 protein

A

anion transport e.g chloride + bicarbonate

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5
Q

function of glycophorin A

A

maintenance of neg charge – electrostatic repulsion to prevent aggregation, sugar transport

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6
Q

function of glycophorin C

A

regs cell shape, mem
deformability + mem mechanical stability

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7
Q

function of ankyrin

A

links lipid bilayer to spectrin

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8
Q

function of spectrin

A

maintenance of bioconcave disc

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9
Q

function of “actin complex”

A

links lipid bilayer to spectrin

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10
Q

most abundant rbc cytoskeletal protein

A

spectrin

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11
Q

how do rbcs obtain ATP + why

A

anaerobic glycolysis bc they do not contain mito

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12
Q

what is MetHb?

A

a form of haemoglobin that cannot carry oxygen to deliver to tissues, inoperative O2 carrier

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13
Q

what product of glycolysis regulates O2 affinity of Hb?

A

2,3 DPG (= 2,3 BPG)

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14
Q

define erythropoiesis

A

prod of new rbcs

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15
Q

what regs rbc prod?

A

erythropoetin (epo), prod in kidneys

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16
Q

how does no. of rbcs incr?

A

epo acts on committed erythroid precursors to incr cell division

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17
Q

what’s renal hypoxia + how does it affect epo prod?

A

low O2 levels (in kidneys)
incr epo prod

18
Q

what makes rbcs flexible to fit through capillaries?

A

bc nucleus is extruded + phagocytosed before release from marrow

19
Q

what’s a reticulocyte?

A

immature rbc

20
Q

important role of cytoplasmic organelles of reticulocytes

A

they continue to synthesise Hb for 1-2d after release into circ

21
Q

what does a high reticulocyte count indicate?

A

incr rate of rbc prod - acute bone marrow stress/ malignancy

22
Q

what organ is described as the rbc quality control organ

A

spleen

23
Q

how are rbcs destroyed?

A

by macrophages in spleen if senescent/ defective

24
Q

what incr rate of destruction by splenic macrophages in red pulp?

A

loss of mem pliability
antibody coating

25
Q

what is recycled by splenic macrophages?

A

Fe

26
Q

function of Hb

A

transportation of:
*O2 from lungs to respiring tissue
*CO2 from respiring tissue to lungs

27
Q

oxyhaemoglobin vs deoxyhaemoglobin

A

oxyhaemoglobin - oxygenated state – bright red colour
Deoxyhaemoglobin - deoxygenated state – dark red

28
Q

what is the main catalysing enzyme for CO2 transportation?

A

mem-associated carbonic anhydrase

29
Q

what does mem-associated carbonic anhydrase catalyse?

A

*CO2 + H2O → H2CO3- (= carbonic acid), rapidly dissociates to H+ & HCO3-
*HCO3- diffuses back into the plasma, (~70% of transported CO2)
*HCO3- dissociates back into CO2 + H2O in alveoli, CO2 released to air

30
Q

how does Hb act as a buffer?

A

H+ ions left from dissociation of carbonic acid to bicarbonate bind to globin chains of Hb

maintains stable plasma pH + protects against respiratory acidosis

31
Q

structure of Hb

A

terametric molecule
4 globin chains - 2 alpha, 2 beta
4 haem groups

32
Q

what does a haem group consist of?

A

an Fe atom in a porphyrin ring (physical not chem interaction)

33
Q

what’s O2 affinity?

A

relationship btwn Hb O2 saturation + partial pressure of O2

34
Q

why is O2 dissociation a curve shaped graph?

A

bc binding of 1st O2 is difficult but 2nd + 3rd easier
want to conserve O2 in arteries + give it up easily in tissues

35
Q

what specifically adjusts O2 affinity?

A

conformational change varies access to/ from haem groups

36
Q

what does 2,3DPG bind to + cause?

A

to deoxyHb + reduces O2 affinity further

37
Q

how does acidosis affect O2 affinity + O2 supply

A

reduces O2 affinity (Bohr effect) + incr O2 supply

38
Q

what is increased affinity of HbF due to?

A

less active binding (by y chains) to 2,3DPG
essential for developing foetus

39
Q

6 advs of artificial rbcs vs transfused human rbcs

A

*storage temp + shelf-life
*immediate, universal administration
*no lag in effectiveness unlike natural blood (due to 2,3-DPG (metabolite) + nitric oxide depletion during storage)
*no risk of disease transmission e.g HIV
*not dependant on donors
*avoid religious/ cultural issues e.g. Jehovah’s Witnesses

40
Q

why can’t Hb transfused in solution?

A

bc free globin chains are toxic to kidneys, scavenge nitrous oxide - leads to vasoconstriction + hypertension
unfavourable, fixed O2 affinity, short half life (30mins)