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SLIDE 1

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SLIDE 2

SLIDE 3

EFFECTS

OF

ANEMIA

ON

THE

CIRCULATORY SYSTEM

1 •

2:

In

severe anemia the blood ~fcl~=may

fal~

to · as

~

low

as 1.5 times that of water rather than the normal value of approximately 3 times the

viscosity of water.

~

'"

The greatly decreased viscosity decreases the

~

resistance to blood flow in the peripheral vessels

....:mu w

m ~+-:.

..

ft::S

.t ildliJA+ .I!fo"~ Ji&4iJ L21

• --•

so that far greater than normal quantities of blood

return to the heart.

3. Moreover, hypoxia due to diminished transport of

• xygen by the blood causes the tissue vessels to

it--

it»i 4'4ikb .:.;. L :.u.:.:_,.~

• _......._

M!1

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dilate~

allowing further increase in the return of

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blood to the . heart, increasing the cardiac output

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to a still higher level.

Thus, one pf the major effects of

increased work load on the heart.

anemia is greatly

c.~:~!~":"!i:~-:-:·~-~·-

·-:

5. Consequently, during exercise, which greatly

increasesthe ti~sue

demand for oxygen, extreme

tissue hypoxia results, and acute cardiac failure

• ften ensues.

SLIDE 4

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Table 2.2. Classification of anaetnias

';

; ,\~t1

A101plw/ogical

• ·1. Nonnochromic normocytic

·.

• 2. llypochrornic norrnocytic
• 3. Hypochromic rnicrocytic
• 4. Macrocytic
• 5. Microspherocytic

..

A('fiologiral

([;) Increased blood loss (a) Haemorrhage (h) llacmolysis

(2) Decreased blood production

·- (o) Nutritional deficiency

(h) llonc marrow failure

MCJ/C{%) 32-36 32 <32

Usually normal Usually normal (i) Acute

(ii) Chronic

··.

.

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·:~ ·-e:,:

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. MCJ<(fl)lr:/

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. >'96 ·-:··

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Normal

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diameter

~ reducet

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.

(i) Corpuscular defects

(ii) Extracorp_

uscular defects

(i) Iron

(ii) Folic acid, cobalan1in (iii) Pyridoxine

(iv) Ascorbic acid

(v) Protein (i) Primary (idiopathic) (ii) Secondary to drugs, chemicals, irradiation

(iii) Other

SLIDE 5

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Uf t.) U L 't L '( I I!

l M l A U f'l I l 1 L

L l l

( L U L A I U K y

·

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1.

The

greatly increased viscositX of the blood in

polycythemia, this increases the · heart work. 2.

The flow of blood through the vessels is often

very sluggish. 3.

It i s obvious that increasing the viscosity tends

• -------···--------

to decrease the rate of venous return to the heart.

q.

On the other hand, the blood volume is greatly

• ~

·

increased in polycythemia, which tends to increase the venous return.

5.

The blood passes sluggishly through the skin capillaries,

a

larger than normal proportion of the hemoglobin is

d e oxygenated . · ·The

bl~e

colour of this deoxygenated

hemoglobin masks the red color of the oxygenated hemoglobin.

Therefore, a person with polycythemia

• rdinarily has a ruddy complexion but often with a

bluish (cyanotic) tjnt to the skin.

SLIDE 6

Ctassiffc:at io/1 01 eryt n

rocyto

s1 ~

1 . r<elati'fe ery th'

• cytosis

. Deny dration

tf.. ;·""fue f rythr

• eyfos;

J

/- \. With incre«sed E-P l~vtL

..

1 Ph-ysiolo9ical- high alt1tude..

(H~po)(ia)

1,. Drugs

(a) Cobalt

(b) An dYo~et"s~

i hyro xifle

1:3. Ulith low or ilormal Sp. {

Q.vt/ :::: P

• lycythaernia veva

I

SLIDE 7

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Type 0 blood

FIGURE 21.16

.

The antigens and antibodies present in lYP'" /\,B. 1\B, and 0 blood

group~. .~:~:·',

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SLIDE 8

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Anti-B flgg/utinins in groups

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ngglutmtns . :.: ... . , . •'.;· 1.:, : _ _

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B and 0 blood t :

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A and 0 blood

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Fiyute 35-1.

in tl1e LJ/ooc..J

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Ago (years)

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Average titers of anti-A ·and ·anti-8 i·agglutinlns

~!

• f people in group D and group A.at -djfferent :;

· ' '· .!, •, · 1 . :.·, ...

, .· ·!r:, ·

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SLIDE 10

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Fortunately, this diseuse can he l)rcvciJlcd l)v givi11g a11

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j

\ · · Rh-negative rnother human gun1n1a glol.n1lin ugainsl H

11-

positive erythrocytes within 72 h after she has deliverec.l an Rh-positive infant. These antibodies bind to the antigenic sites on any Rh-positive erythrocytes that n1ight have en-

tered the 111other' s blood during delivery and prevent them fro111 inducing antibody synthesis by the 1nother. The administered untibodies are eventually catabolized.

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SLIDE 11

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·you inay be wondering vvhether ABO inco- mpatibilities are also a cause of hemolytic disease of the newbon1. For example, a woman witb type 0 blood has natural antibod- . ies to both the A and B antigens: If her fetus is type A or B, ·-this the~reticnily should cause a problen1. Forinnately, it usually does not; partly because the A and B antigens are not strongly e;me:s~d in fetal erythrocytes and parily be- cause the natural antibodies are of the Igivi type, \Vhich clo not readily cross t~r~;a.

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SLIDE 12 (

. . ( ~

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· · · ~Hemolytic

diseases of the newborn because the incompatibility ofRh blood groups: Three conditions in which the mother may develop antibodies:

• A. Blood transfusion before

marriage by blood from R1~­ person.

• B. leakage durir1g pregnancy of

small amount of fetal blood (Rh+) into maternal circulatio11 (placental he1norrhage ).

• C. during delivery, same bloocl

squeezed back to maternal blood.

(/ I i

,·;;

SLIDE 13

.. .. :J ..

y (

• 1

, i \

• .

,

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ln these conciltlOl1S

011e oi tne 1o11ow1r1gs

hemolytic diseases may occur:

• A. erythroblastosis fetalis (mild disease): small

amount of RBC,s leak into mother circulation, sotne mothers develop antibodies against D

• antigens. These antibodies pass to fetal blood ('?L

cause mild hemolysis of the RBC,s of the fetus. This newborn baby can be rescued by giving him (Rh-) blood, but not from his mother.

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....

!) (j

) ,,

SLIDE 14 ~ · · t

.. ·

\ · ' ' • .I

' ... :a

1

• ·

.b .

lcl~ru~

graves lleullaLurUlll

~Ker1c-te:rus)

(moderate disease): the infant is born at term, is jaundiced, or becomes so within 24 hours, there may be se,rere neurological lesions involving the basal ganglia in which th.e bile pigments deposited.

• C. Hydrops fetalis (severe disease). The hemolysis

is severe, the infant may die in uterus or may develop severe anemia, J au11dice & eden1a; dies within few hours.

. f? /. .•

SLIDE 15

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~-

~

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M \

• .
• Blood Transfusion

l11d1CallOllS 01 blOOd trailStUSlOil:

• 1. to restore the Blood Volume,

e.g. in haemorrhage.

• 2. to provide Red Blood Cells,

. e.g. anaemias.

• 3. to increase Blood Coagulability in

haem9rrhagic diseases, e.g. haemophilia & purpura.

• 4. to replace infant's blood with Rh.

~ ve

blood in erythroblastosis foetalis.

• 5. to supply a11tibodies to raise the

general resistance of the body.

• 6. to provide White Blood Cells, e.g. in

leucopenia(== decreased W.B.Cs).

• 7. to supply plasma proteins in

hypoproteinaemia.

• 0. 'l ~\

I)

~ ·

SLIDE 16

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.....

.

, ....

Complications of Blood Transfusion barly

Haemolytic reactions immediate delayed. Reactions due to infected blood Allergic reactions to white cells, Platelets or proteins Circulat(i<y :

• verload

Air embolism Citrate tox:icity H yperkalaemia Clotting abnonnalities (after 1nassive transfusion LaLe Transmission of disease e.g. hepatitis, malaria, syphilis, AIDS. Transfusional iron overload llnmune sensitisation, e.g. to rhesus D antigen (/ ~ g

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SLIDE 17

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Blood tran~fuslon

Blood for transfusion can be kept for several weeks if it

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• •.•

I.

_ . is ~1:5ted from

• ~o
• ~<?rs

un~:T ~_p~c

~on~ifu.~

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]

1

sterile plastic packs containing a suitable preservative .: -1 ,

' .

solution, and it is stored at 4°C. A commonly used

1

• ~

preservative, citrate-phosphate-<1extrose (CPO) solu- tion,· provides citrate as anticoagulant and glucose (dex- trose) as metabolic substrate for the red cells. Adequate numbers (i.e. not less than 70%) of red cells remain viable after transfusion when previously stored in CPO solution for 3-4 weeks at 4°C. Adding adenine to the solutlon can Increase this period to 5 weeks.

r· ~0

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SLIDE 18

~

·

( "Cl ., ... .

,,

... '

~urlng

storage at 4°C, the ~cd

• ~e~ls
• ~
• ~
• ~regresive

( decrease In content of adenosine triphosphate and 2,3-BPG, ' while with decreased activity of the Na+-K+ pump, the cells gradually lose K+ to the surrounding plasma and gain Na+- from

• it. The concentratlon of K+ in the plasma may reach values as

high as 30 mmol L

• I after storage of blood for 4 weeks.

The pH

• f the plasma also decreases with time of storage and its

concentration of ammonia rises. These changes can make stored blood dangerous for transfusion in certain patients, e.g. those with renal or hepatic failure. The decline in Na+-K+ pump actlvity makes some red cells spherocytic, with loss of

• deformability. These effects may be Irreversible and after

tran~fuslon

the abnormal red cells arc destroyed very rapidly

I

by macrophages in the spleen and elsewhere. Other con- stituents of blood do not withstand prolonged storage.

• 'tcGranulocytcs begin to lose their phagocytlc capacity within

6 h of collection and they are functlonally Inert after 24 h.

1" Platelets lose their haemostatlc effect (p. 3 I

0) within 48 h at 4 °C, while the labile coagulation factors, V and VIII (p. 3 14), also rapidly deteriorate in chilled blood .

....... :\ ,,

V\U I\

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SLIDE 19

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... 4

(?)

:;-B;fored~;dis

..

mad~

available for i~sue

f;~;-;:­

blood-bank. the ABO and rhesus groups of the cells are deter- mined.j_!}d commonly the serum is screened for atypical a~ti- bodies.'-serological tests are also done for syphilis, hepatitis and human immunodeficiency virus (HIY). Before transfu~ion, the ABO and rhesus groups of the patient's red cells are deter- mined, the serum is checked for unexpected antibodies and red cells from the donor arc tested against the patient's serum by cross-matching tests (compatibility tests). These cross- matching tests arc essential for checking that there has boon ·no error In ABO grouping of donor and recipient, and for ensuring that the recipient's serum docs not contain naturally \

• ccurring or immune antibodies active against the donor's

1 /'

cells.

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f/

SLIDE 20 ( ., .

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t

• v

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; ·~ ~i:~

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• ~
• T~sfusion
• f who!~-

blood ;~

· - -sometimes

necessary but,

I

• ver recent years, the use of cell-separator machines and

J ,

large-scale production of plcuma constituents hav~ . . made ;~

..

\ I ..

increcuingly possible to transfuse specific components c.l · blood which the patient lacks. Thus red-cell concentrates

I

• .

'

• ften resuspended 1n a small volume of electrolyte solution,
• ~!~
• -~d

to restore the haemoglobin concentration In an

~

• -
• ·
• · -

· · ·-

• -

· · ·

. . . .. . -- - .. --·--· -- -·····- - ···- . ··- --

• --....-

anaemic patlent in whom the plasma volume may already be

• expanded. Platelet concentrates are of use in patients with

severe· thrombocytopenia (p. 3 17). A variety of plasma frac-;- tions is also available to supply coagulation factors, e.g. cryo-:

precipitate, which is rich in factorYIII and fibrinogen, and for

J,.,_,.,

expanding plcuma volume, e.g. stable plasm_ a pr:-otein solu-

• tion. A useful source of antibodies against common viruses is

pooled normal immunoglobulin and ' various ·specific

Immunoglobulins are also avaiiablc, e.g. anti-0 ~nd antibodies

~lnst

tetanus, hopatltls ~

• ~n

_d diphtheria.

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SLIDE 21

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···- ····-

' ..........

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_.-----·- -·---·--···

...--r

• ~-
• :.:/ However much care Is taken in cross-matching and

administering blood, transfusion carries definite risks of unpleasant or even fatal complications. Major ,red-eel! incompatibility can lead to lethal intravascular haemo- lysis or delayed extravascular breakdown of donor cells. Transfusion of blood contaminated with bacteria can

.

'

cause profound shock with hyperpyrexia, while allergic

. • ' I . .

• reactions to transfused white cells
• . platelets and

plasma proteins can also be severe. Circulatory over- . load, air embolism and changes in plasma electrolyte concentrations (e.g. hypcrkalacmia) may occur and there may be direct transmission of disease, e.g. H!V. and cytomegalovirus infections, hepatitis and malaria.

·.

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SLIDE 22

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Relative Frequencies of the Different Blood Types.

The prevalence of the different blo?d types among one group of persons studied was approximately:

A B

AB 47% 41% 9% 3%

It is obvious from these percentages that the 0 and A genes occur frequently, whereas the B gene IS infrequent.

SLIDE 23

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Ganong's·

Review of

Medical Physiology

Twenty-Third Edition

TABLE 32-4 Summary·of ABO system.

Frequency in Plasma

Blood Agglutinins United States

Agglutinates Red Type in Plasma

(Ofo)

Cells of Type:

Anti-A, anti-B

45

A, B, AB

A

Anti-B

41

B, AB

B Anti-A

10

A, AB AB

None

4

None

SLIDE 24