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Physiology Kerry > 7. Blood + Immunology > Flashcards

7. Blood + Immunology Flashcards

1
Q

How long can blood be stored before expiry

A

depends soln CPDA1 -35 days

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2
Q

What determines length time

A

Survival rate tfused RCC after 24 tfusion

Crite min accept surval 70%

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3
Q

Preserve?

A

Preservative

Storage cond - low temp
- inhib red cell metab
1/30 gylcoysis
inhib bact

ASeptic tech - streilise equp - min bact contam

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4
Q

CPDA1

is this used in Ireland?

A

Citrate - anticoag - bind Ca

Phos - buffer - phos 4 metab

Dextrose - ocntin glycoysis + energy

Adnin - sub atp synth

Maint 2 3 dpg better

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5
Q

Storage lesion

A

Loss plt granulo

loss coag fact

decrease 2 3 dpg odc left

haemolysis

FOrmat microagreg

biochem change K, Na Fall Ph

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6
Q

What happens coag factors

A

V VIII - labile factors decrease quick

Normal haemostasis - VOOO 35% normal
acute phase protein - endog prod increase - decrease risk inadeq post tufsion

Other levels not signif until 21 days after stor

Packed cells - not plasma - diliton all coag factors
when just RCC + Crystalloid

Plt fuc lost stog 4’C
24-36h - most non functional

mass tfisoon - coag diln tycopenia b4 coag def

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7
Q

Why hyperkalaemia not commoner following tfusion

A

blood bank blood has a high [K] 12mmol/l @ 7d
despite hyperK not comon cause

Restoration RCC metab act = K reuptake by RCC
Na K Atpse

Elevated catehcol - cell uptake K

Dilutional effect distrib Excell space

Slow tfusion min risk

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8
Q

Compatability testing blood

Why need x match blood

A

b4 tufsion donor test recp blood - avoid tfusion rxn
blood group imcompat

reacting anbtiobdy

Main point = haemolysis prevention

3 diff procedures

1 Blood typing ABO + Rh

2 Abody screen

3 X match

Two comp - x match
Saline test check abo group
Indir Coombs test - det haemolytic IgG abod

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9
Q

What is indir coombs

A

presence IgG abod dir against rcc membrane antigens - cause haemolysis

Abod not cause aggult - during other test
Det incomplete abod - margin safet

Incubation
washing
Testing coomb reagent
Coombs control test

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10
Q

What is risk reaction ABO rh Compat donor tfused w/out abod / xmatch

How much reduced

A

Admin aboRh compat safe addit proced add addit maragin

Abo 99.4

Abo Rh 99.8

Abi rh + neg abod screen 99.94

Abdo Rh compat
neg abod
coombs 99.95

Coombs adds so little - removed routine testing

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11
Q

Plasma proteins

A

Ablumin
globulin
fibrogen

Glob a1 a2 b g glob
Gama - almost completely composed Ig

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12
Q

What normal conc plasma prot

A

50-80g L

Alb 45
Glo 25
Fib 3 (acute phase_

IG - 10-15

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13
Q

List fxn plasma protein

A

Oncotic pressure

transport / carrier fxn

Role a-b balance

Protelyti csystem - complement kinin coag fibrinolytic

Immune resp

Enzyme act

Metab

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14
Q

Albumin

A

highest concentration 35-55g l

Liver -> circ

12-15g day
25 total proti

Only pl prote not glyco

SStruct
Single polpept chain 585 AA
mol wt 69000
IV half life - circ 20d

5% exchange into ISF /hr
- retunr circ via lymph

Some taken tissue cell - metab aa for intracell use

Present blood 50% and rest 50% exvasc

Main fxn
Oncotic pressure
tport /carrier

Taken up tissue brogken to AA
syhtn protein / energy

Co2 tpor - carbimno n term (hb more)

High conc and Low mol wt 65-80% plasma oncotic pressure
capillary fluid dynamic
main IV volume

Lig bind
ffa
bili
calcium
hormone
cu
drugs
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15
Q

Is alb essential life

A

no
rar e- no albumin other healthy
other protein increase

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16
Q

Which plasma protein major inbolved bind basic drugs

A

A1 acid glycoprotein

Alb - binds acidic

retinol bind prot - 1/2 at 10-12h
acute starvation

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17
Q

Immune system

What are the major components

A

Host defence

Recog

Effector activity

1 Natural / inate
not dep prior exposure
primitive part

a barrier function

b Macrophage

c NK cell

d Complement

e other antibact protein

2 Acquire immunity

Lympohcytes

Powerul spec system
delayed onset - esp new antigen

a Humoral
B lympho - prod spec abod v antigen (can recog more than 2 epitope on invading)
prev exposed
each b can diff plasma - prod 1 type abod

Ig G A M E D
class type heavy chain
some stim b cell - memory cell - faster / larger response

b Cell immunity
T lymph - cell med immunity
T - kill ifncet / for cell

prod Lymphkine
amplify response immune cell
memory T prod

Essential role interaction

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18
Q

What type T lymph present

A

Cytotoxic

Helper

Suppresor

Memory

TCR - recog spec pep antigen bound to MHC in membrane - prlof activated cytotox T + Memory

Memory persist - futue exposure same antigen
- rapidly prolif

Cytotoxic Have CD8 membrane protein

Helper T cell - dont attack / destroy

regulation other aspect
CD4 on membrane

TCR of cells - recog spec pep antigen when bound to MHC II - knwon as Antigen preseting cell (maco / dendritic)

T cell stim - prolif prod mature help T + Memory helper T
T chemical factor - large amt lymphokines IL2,6 y interfon gran monocyte col stim

lymphokine cause cause
Stim phagocytic activity macropahe
Stim prolif cytotocix T lympho
Stim b lymp - prolif + diffnt into plassma cell
pos feedback - further activation helper T

Helper - Amplification - response

Suppresor - neg feedback control act cyototox t and helper

CD4 - recetpr used HIV virus into help celler

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19
Q

What is a killer cell

A

Activated cytotox T lympho

Nat killer cell - plasma

Cytotox T lmyph - 
maut cyto t
TCR- membrane cell - bind spec shoty pept antigen MHC1 prot membrane
infected cell have spec pept
how they are ID
perforin inserted membrane attack cell
cytotox sub injejct
swell and die - killer search new target

NK cel

Lymphocytic lineage
Nk Not b - not T
Lack antigen recgo mol
10% mononeculear cell - lymphoctes in blood NK
attack ill invading
body cell mailg
ciruses coat abod

not req sensitatisation
no mem or amplif with repeat exposure
innate

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20
Q

What is role MHC In immune rxn

MHC1 v MHC 2

A

Cell membrane protein
bind short pept antigen
present cells immune sys

2 gene MHC - loc chromo 6

1- two prote
b2 microglob three class a b c
indidiv six mhc 1
all cell mhc 1 on surface

pept bound to MHC class 1 molecule cell
display membrane - MHC complex recog - spec abd displayed B or by TCR rec on cytoi - lymp prolif
Class 2
Two membrane span prot
II - prd cetrain cell body
macro
dendrit b cell

Antigen presenting cell

Prtein degraed - external source
TCR helper T Cell - bind class II pept complex on APC
Act helper T cell prolif
prod lymphkine
stim rest cells
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21
Q

What are cytokine and lymphokines

A

Cells immune system secrete various polpetide chemical mediatior

Ig

Cytokine - ptent polypetitde act other cell
cell membrane receports

prod diff body cell
each cytokin
fel cell type predom precuros
production response to spec stimuli

Lymhpokine are cytokine prod lymphocytes

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22
Q

What are groups of cytokines

A 
IL
Interferon
Chemokin
heamatopeitc colony stim facto
TNF
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23
Q

What are Chemokines

A

Chemtatct cytokine attarct chem variy immun reaction

each - prod certain cell attract sepc cell

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24
Q

How are cytokine diff hormones

A

Not prod sepcial gland

most paracrine / autocrinme action

conc - small =bt extremely potent

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25
Q

Haemostasis

Coag system

A

Intrinsic + Extrinsic path - join final common fath firbrin clot

Intrinsic
activate contact cert surfaces
Act factor Xii-> Act XI
XIa act IC
Ca +Factor VII - Ixa convert X->Xa

Extrinsic pathway
Tissue injury expose thromboplastin

Combin + act VII
Complex act X

Final common path

Xa - Prothrombin-> thrombin (Ca, FV, Plt F 3)

Xa extemly important

Insol fibrin end reslt of 3 steps
Prrteolsyis
Pomyersaion 1
Polmresastion 2

Contract clot - decrease defect vessel wall

plt req cotnract

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26
Q

Role platelets in haemostasis

A

3 mains tage haemo stasis
vascon damage
form plt plu
blood clot

plt - partic all 3 satge
local vasocon - involved activation coag
sertonin + vasoctive txa2 adp rel act plt - vcon at site

plt adhesion
vWF bind - expos mult bind site on vWF mol
plt glycoprot mech plt adhere site inj

Plt activate
med - activate

Plt aggreg
Fibronge gpIIbIIIa complex plt - plt choesion
txa2 stim plt agreggotion vasocn

opposite prstacyclin

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27
Q

Preventing coagulation

A 
1 Thromboresistant endothel 
Abense damge - prevent collagin
gloycclayx repep plt coag
pgi2 - inhib plt agreg
no - inhib plt - 
thrombomodulin - act pro c
endothel - heparan sulp = act circ at III
smooth - prvent activation

2 Blood washes away mediator

Plasma prot - inhib / lim spread coag
ATIII (inc heparin)
Pro C Pro S thrombodulin
Extrenisc path inhb

fribonoyltic syst

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28
Q

vWF role haemostasis

A

Role plt adhesion to damage subendothkium

Role plt to plt bind

Bind Factor VIIIplasma - prevent degradation
ppl def vWF - prolong bleeding normal plt count

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29
Q

Citrate toxicity

A

Adverse effx hypoCa - massive tufsion

normal metab rapidly liver - imparid hypothermia decrease flow

myocardial depression

Ca cant get low enough to cause coag probs before it would cause arrest

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30
Q

Iron

what are major forms dietary iron

A

Bound haem - myoglob /red cells red meats

organic lgiands most ferric form

some food high iron
oxalate spinach prevent abosiprtion

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31
Q

Absorption Iron

A

Entercyte duodenum + upper jej

Firstly - Iron ferrous and ferric

Ferric convert to ferrous in stomach
promoted H+ andascrob avid

advant conersion
easily release ligand bound - soluble
Ferric precip >3
not avail abs

Ferrous sol up pH 7.5
avail absorption

Addit low gastric ph some sub - AA
bind ferric form sol chelate form - absorb in duo

Ideallly
1 Reduction of Ferric iron to ferrous - remain solbue at phys ph in do

Formation so chelate ferric release apical membrane

BOth facil low gastric pH

Ferriductase
DMT1

Haem abosorption
Diet Hb and my - degrad rel haem
haem soluble - alkaline duo contn
insol<6
Read abs intact - haem receptor

Indepp dmt1

Haem broken down rel ferrous

Transferrin bind Fe3 on 1 site
normal don tferrin 1/3 saturated

32
Q

How much iron absorbed day

A

Balance in = out

Typically .6-1mg dat male
2.1 mg female

Femal - menstrul loss
only 5-10% of whats in diet
Can increase during preg -

33
Q

How much iron is in the body

A

Tot body store70kg 3500-3700mg

NEarl all bound protein

Functional pool
Hb 65-70% 2500
Myo 5% 130
other prot 0.2% 8

Tport pool

Tferrin .1% 4mg

Storage pool
Ferritin (liver mostly) 25% 1000mg

34
Q

Why is always present bound

A

Chem active
potentially toxic sub
Bind non spec - many prot and impair func

Catalyst many ox reaction - lipid prex cell membrane

AVoid - always bound

No phys control mech - excretion
Control solely - regulation absorption

mense loss - other losses cell slouhgly
amt small
proess uncontrol

35
Q

Mucosal block

A 
COntrol store - small bowel mucosal cell
control absorption - prevent excess entering
enterocytes
overload - mech malfxn - haemochroma
cant excrete excess

If iron low plasma level tferrin high
iron sat low
more iron passes ferritin to mucosal cell to tferrin blood

Iron adequate - sat tferrin higher - iron remin entercote
turonver freq - iron loss cell shed

Mucosal block can be overwhelmed

36
Q

What is absorbed iron used for

How iron enter cell

A

Haem bound prot

Hb most imp prot
myoglob cycto catalases oxidase

25mg haem used in hb syhtn
recycle store

All cell req Iron cytochromes for ox phosp w mitochond

tferrin tport iron to membrane
tferrin rec - endocyosis
Release returned intact to ISF

37
Q

Ferritin

A

storage iron
entercyte and liver prod apoferr which bind iron
apoferr and iron - ferritn

1 ferritin can have 4000 molecules of Fe3

Cell iron increase bind mRNA - increase tranlsation prot
Increased storage

Liver - stored major
many cell spleen b,m contrain

REtendomacrophage stoarge

Demand = tferr sat fall and increase tferrin sythn

Iron release and conv to Fe++

Ferrous form bind tport - cross membrane

Caerolupasmin convert ferric form can bind tferrin in blood

if irons tore high cell accum hemosiderin- insol cell iron

38
Q

How is Iron carried blood

A

Fe++ cnc to Fe+++ carry transferrin

b2 glob

39
Q

How haem sythn

A

Iron contain tetraoyike 4 ring join methenyl bridges

Sythn series reaction
first step - condens sucily coa and glyine

40
Q

How much iron reqd preg

A

Adult femal store 2-2.5g

Iron req increase 1g
20 weeks takes up 6-mg iron day

Late trimester
foetus taking up 4mg da

Sythn foetal hb
necc other essent haem prot

41
Q

How iron cross plaental

A

Against conc grad

tferrin rec trophblast
rel umbil cap
com foetal tferring

effecient

42
Q

Reduced hb

A

generally deoxy hb
fe in both form

Oxidation - loss é Fe2 fe3
Methaem prod haem iron hb ox to ferric

43
Q

Blood groups

What are the major blood groups

A

Various group genet determine antigen present membrane

Divided based presence / absence

Importane - antigenicity

Most antigenic - ABO
Next Rh

44
Q

Tell me about ABO - what antigens involved

A

A
B
H

Gene H - tferase enz - gene involveddoes not directly code antigen - enzyme places fucose reside on end membrane

A - tfrease - NAcetlyglacatosamine end fucose reside - alter A Antigen

B - tfrese - galacctose reside end near fucose - does not code direct

Indi only have H - no A / B - in rCC call O
Have circulating Anti A + B abody
present w/out previous exposure

Also found salivar, kidney, liverlung
Rh only RCC

45
Q

What Ig class Anti A and Anti B -

A

Nat occuring - ant a + b - IgM

Some people devlop - igG

46
Q

Rhesus

A

Two close releated located on chr 1

each person up to 4 Rh gene

D + CcEe - D or Dand C or C&E or E or e

D antigen - means absence of d antigen

Rh status test
Rh antigen
Rh+ or Rh - based on D antigen sat

Have D - Rh +
85% Cascausian

No naturally occuring abod to Rh (req exposure)

47
Q

Rh + foetus - Rh - mother affect 1 st preg

A

Moth not have Rh abod (anti D)
Unless prev exposed Rh +

Previous preg Rh + foetus
Use anti D passive immunisation + Avoid RH+ child bearing age
RH sens during deliver - rare

48
Q

Other that can cause rxn

A

Kell Duffy Kidd - also cause haemolytic rxn

49
Q

Complement

A

Proteolytic system - present in plasma
aPart innate non spec

> 25 pl prot

Classical / alternative

Come together coomon final pathy
Combine C3

Classical - activated antigen-abod complex

alternative - can be active in absense abod

50
Q

Classical pathway

A

11 enzymes - circ inact preuros

11 enz C1 to C9

init - antig-abod complex iMg or igG
end formaing lytic complex
insert cell membrane - pores - cell lysis

C3B - opsonin
coats targets - site phagocyte bind

c3a c5a - anaphylatoxin
mast and baso bind- degran w. rel His

Can be comenced by alternate pathyway also

51
Q

Reaction known complement activation

What does lead to

A 
Cell lysis
Rel mediate - his mast (c3a c5a)
Local vdiln
Neutrophil aggregation
chemotaxis attract pahgo leuco - c5a
opsonisation c3b
52
Q

What antigen abod complex- can activate complement via classical pathway

A

Single Mol IgM - bound antigen bind act c1 + start complement cascade

some IgG can also activate

Nat AntiA + B abod - IgM - potent activators complmen - causes haemolysis

53
Q

Signif 1 esterase inhibitor defic to anaes practice

A

Reg several plasma protease systems

Inher Ad
Hered angioedma

Episodic attcak s- airway
may precip minor trauma

Danazol - induce sytn c1 esterase inhib from normal gene - usual effective preventing attacks

54
Q

Vitamin K what is diff hormone and vit

A

Vita org sub

Not prod body
must obt exog sub

req small amt

essential to survial

affects spec biochem rxn

not use caloric source

Vs Hormone
secrete ductless gland
combine sepc rec change metab distant cell

55
Q

Is vitk essential - where absorbed

A

Diet Vit K - ecc

some terminal ileum - bile salt
fat sol  -req bile
 sol micelle 
poor - obstructive jaund - absence bile salts
cylmicron to lymph
56
Q

MOA vit K

A

Vit K - post tranlastion modif - clotting
II VII IX X Pro C+S
Some bone proteins osteocalcin

Modif secon carbox - glut reside

two neg charge - chleation w/ Ca

carboxyase - catalyses rxn vit K cofactor - oxidised during reaction requires reduced active cofacor

1 ezyme inhb coumarin type anticoag - warfarin

57
Q

Vit K + newborn

A

Haemoorhage dis nebowrn
prev rout vit K - all infants

Defic - 
not x placenta 
clot facto low
bact prod vit k colonc not occur - bowel sterile
diet intake poor

Some maternal drugs exacerb
pehyntoin - conc liver - inhib vi K

58
Q

Spec conc Vit K injections

A

Care - avoid unnec large dose
1-2mg ncc - anticoag required post op
not desired
10mg dose given - large diffic reest anticoag post op

Crempophol EL - solub agent - can cause anaphylactoid

not immed
req snth new cloth fctor

FFP required if immed

59
Q

Erhythropoetin

what is it

Where is it produced

A

Glycoprotein - principle factor controll RCC prod

arg term AA removed = 165 aa active hormoe
reg prod control RCC mass - blood oxy carry capactiy

Kidney
Liver foetus (10% adult)
60
Q

Hw controled

A

Hypoxia - intracel - act tcript factors - bind dna mRNA - epo chr 7

Prod by interstitial fibroblasts peritubular capillary -

61
Q

What are its actions

A

EPO - rel kidney circulates BStream - act immature erhytoid cell in BM -

Action solely bind and activate spec cell mbrane EPO rec

=> Differentiation and proliferation to mature Red cell

Interaction - membrane rec - activation knases -
activate cytoplasmic tcription factor
move nucles - act new mrna sytn

62
Q

How commerc - majr clin use

A

mamm cell culture

ESRF + Anaemia

63
Q

What happens to EPO levels bab post birth

A

day 1 - undet
not found up 12weeks after

phys anaemi newborn

64
Q

Platelets

A

small 2-4um cell grafm - budding megakaryocte in BM

CIrc stream life span 8-12 dys
old - remoced macrophage in spleen

priamry hameostats - firstpahses - plt adhes to subend = plt plug

release vcon txa2 + serotonin

essential contraction final clot

65
Q

normal count

A

Count 150-300
50 min abnormal bleed surg

spont haem @5

assumin fuction

66
Q

Produ controlled

A

Thrombopoeitn
-term diff megakary -
act bind spec rec mega

expected feedback control

67
Q

How plt conc stored

A

1 temp 20-24

2agigation-contin platform agitator
-assists gas exhange - min diff dist

3 ph balc 6.2-7.8
special plastic - allow gas exchange

68
Q

Major disadv store room temp

A

spesis trsnfion - bacteria multy rapidly

lmits storage durn 5 days

69
Q

What is the plt count incremenet per bag

A

5000 to 10000 - lower in conumpstion

70
Q

TXA2

A

produciton increase in plt act

decrease camp level

prom rel sub - adp - promote adhesion

71
Q

Death of a red cell

Life span rbc

how muhc hb breakdown / day

A

120 days

Hb 150 g /l blood vol 5l
tot hb body 750 g

pred daily braeakd 750/120
~~ 6g day .08%

72
Q

How are old RCC removed

A

Spleen bone marrow
abrnomral - recog macophage and removed

10% occurs in blood

hb diss ab dimer - bind haptoglob
haemopexi bind haem

prevention excretio - red loss iron

73
Q

What happens to hb in macrophage

What components can be recyle

A

Msot Hb broken macrophage of RES

Globin metab - aa reutilised

haem not reutil - degrded rel iron
iorn back to pool

  1. Macrophage - haem oxygenase
    biliverdin
    fe++
    CO

Biliverdin to bili (bilv red)

3 BIli -> plasma (alb bound)

4 hepatocyte take bili (fac diff)

5 bili udp gluc - bili mono gluc bili dig

6 conj bili secre bile

74
Q

Direct v indirect bili

A

conj bili - direct react directly van de burg rx used to assay

unconj lip sol - req tx mentahol b4 van de rxn - indir bili

75
Q

Obstructive jaundice - predom form bili blood

A

Prevent excretion conj bili - spill blood causing conjugate or direct hyperbili (jaund)

Physiology Kerry (17 decks)

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