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FINALS - HAEM > physiology blood > Flashcards

physiology blood Flashcards

1
Q

where does haematopoesis largely occur and from what cells

A

pluripotent stem cells in bone

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2
Q

precursor of red blood cells

A

reticulocyte

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3
Q

precursor platelet

A

megakaryocyte

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4
Q

structure + function eosinophil

A

bilobed, red granules // fight parasites + hypersensitivity

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5
Q

structure + function basophil

A

very rare, deep purple, unsudre function

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6
Q

structure + function neutrophil

A

multilobed // first defence cell // infection, trauma, infection

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7
Q

types of agranulocytes

A

monocyte (macrophage) + lymphocyte

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8
Q

where is bone marrow extracted

A

posterior iliac crest (trabecular bone)

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9
Q

Hb structure

A

2 alhpa and 2 betas subunit // iron binds with O2 at centre of haem group

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10
Q

what type of iron does o2 bind too

A

Fe2 not Fe3

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11
Q

how is erythropoesis stimulated

A

kidney senses hypoxia –> EPO –> Bone marrow

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12
Q

where are RBCs broken down

A

spleen (and liver)

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13
Q

what is blood broken down too

A

bilirubin + iron (bili excreted in bile)

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14
Q

what transports CO2

A

10% undissolved // 30% bound to Hb or carbamino Hb // 60% HCO3

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15
Q

how many molecules of O2 can 1 Hb carry

A

4

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16
Q

subunits foetal Hb

A

2 alpha 2 gamma

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17
Q

function foetal Hb

A

saturates O2 at similar O2 (can take blood from maternal circulation)

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18
Q

what does a curve shift to the right shift

A

more O2 released // high [H+] // high DPG // high temp // high CO2

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19
Q

what does a curve shift to the left shift

A

less O2 released // low [H] // low DPG // low temp // HbF, methaglobin, carboxyhaemoglobin

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20
Q

how is Hb synthesised

A

mitochondrion: make porphin ring + Fe2+ –> cytoplasm: they bind to make haem + join with subunits –> Hb

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21
Q

what is primary haemostasis

A

platelet plug

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22
Q

what is secondary haemostasis

A

fibrin clot

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23
Q

how long do platelets live

A

7-10 days

24
Q

what is exposed + released when endothelium is damaged (ie bleeding) that causes platelets to bind to site of injuery

A

collagen –> von willibrand factor (+ other proteins)

25
Q

once platelets have bound to endothelium, what do they release to aggregate more platelets

A

thromboxin A2 // ADP // glocoprotein II + III

26
Q

what can cause failure of platelet plug (broadly)

A

vascular weakness + lacking collagen eg old age // rediced platelets eg thrombocytopenia // VWF deficient

27
Q

what tests indicate failure or platelet plug formation

A

platelet count

28
Q

what do platelets release to attract clotting factors

A

phospholipids

29
Q

what is the initiation phase/ extrinsic pathway of fibrin clot

A

TF is released from epithelium which activates VII

30
Q

what is the propagation phase/ intrinsic pathway of fibrin clot

A

TF/ VII activate –> factor V + X which convert: prothrombin (IIa) –> thrombin (II)

31
Q

what blood marker shows intrinsic pathway function

A

prothrombin time (PT)

32
Q

what blood marker shows extrinsic pathway function

A

APTT

33
Q

what is the amplification phase of fibrin clot

A

thrombin coverts: fibrinogen –> fibrin // thrombin also activates VIII + IX // VIII + IX then also activate more V + X

34
Q

what breaks down the fibrin clot

A

plasmin

35
Q

how is plasmin activated

A

tPA converts plasminogen –> plasmin

36
Q

what is the breakdown product of fibrin clots

A

D-Dimer

37
Q

what causes failure of fibrin clot (broadly)

A

haemophillia // DIC

38
Q

how do serine protease inhibitors act as natural anticoags

A

produce antithrombin (AT III) which inhibits thrombin // inihibts fibringinogen –> fibrin // inhibits VIII + IX –> X + V

39
Q

how do protein C+S anticoag

A

released by thrombin at end of bleeding –> reduce clotting factors

40
Q

where are clotting factors made

A

liver (except VIII)

41
Q

function of Vit K in fibrin clot

A

carboxylates factor II (prothrombin), VII, IX, X, (and protein C)

42
Q

how is vit K absorbed

A

bile salts

43
Q

what are myloid cells

A

precursors of all RBCs, platelets, and myloblasts (basophil, neutrophil, eisonhil, monocyte (–>macrophage)

44
Q

what are lymphoid cells

A

precurors of NKs, T lymphoctes, B lymphoctes

45
Q

what are prescursors of plasma cells

A

B lymphoctes

46
Q

what organs are involved in the secondary lymphoid system

A

spleen and lymph

47
Q

what does the TIBC look at

A

transferrin levels

48
Q

when is TIBC raised

A

iron deficiency + pregnancy

49
Q

how is transferrin saturation calculated

A

serum iron / TIBC

50
Q

when is ferritin raised or lowered

A

(iron stores) raised in inflammation disorders eg RA // low in iron deficiency

51
Q

bloods, TIBC, ferritin in anaemia chronic disease

A

normo or hypochromic, normocytic anaemia // reduced TIBC // normal ferritin

52
Q

what is ferritin

A

protein that binds to iron and stores it

53
Q

causes raised ferritin without iron overload

A

inflammation // alcohol // liver disease // CKD // malignancy

54
Q

causes raised ferritin with iron overload

A

primary iron overload (haemochromatosis) // secondary iron overload (repeat transfusions)

55
Q

what test determines if iron overload is present

A

transferrin saturation (>45% females and >50% males)

56
Q

cause reduced ferritin

A

iron deficiency

FINALS - HAEM (18 decks)

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