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~ ~ ,~ ~ · ~ E 0 u lfl lfl Q.) \._ Q l) \._ 0 3 0 # a 11 a 1 •••a Ul!l•f ,,.a S · \\) :I •• . \._ 0 u 0 sdno.1fi poozg ~ 1J!tuauy: l) .. d Q I

~ ; .I!fo"~ -~ L21 c.~:~!~":"!i:~-:-:·~-~·- it»i 4'4ikb .:.;. L :.u.:.:_,.~ ~ .,.-_ .t .t _:~.:-"~ dilate~ "!-~ ~ z .,._ '!' - - • -· ildliJA+ Ji&4iJ ~+-:. '" fal~ m w ~ low ~ ~ EFFECTS OF ANEMIA ON THE CIRCULATORY SYSTEM 1 • In severe anemia the blood ~fcl~=may to · as as 1.5 times that of water rather than the normal value of approximately 3 times the viscosity of water. 2: The greatly decreased viscosity decreases the resistance to blood flow in the peripheral vessels ....:mu ft::S .. • --• so that far greater than normal quantities of blood return to the heart. 3. Moreover, hypoxia due to diminished transport of oxygen by the blood causes the tissue vessels to ......._ - -----"- .. -c. M!1 - _......._ allowing further increase in the return of .......... -?- ... _, ... ,r;- ... • ·- -- ·- .... blood to the . heart, increasing the cardiac output -· - - . - -- . ~ .. I to a still higher level. it-- Thus, one pf the major effects of anemia is greatly ·-: increased work load on the heart. 5. Consequently, during exercise, which greatly increasesthe ti~sue demand for oxygen, extreme tissue hypoxia results, and acute cardiac failure often ensues.

·-e:,: ,;~: ·~-~-;?~ , ·:~ ~- - ~- . :-~ ,'~ ~{ ; ,\~t1 diameter ~;: : b~ J\,\1' ~J ·:~ ~·~ ... . :lJ}ii!:t -· · -- . . - - ------ --- -- ----- - --------- --- ---- . . . . .. '-~;:,~t ·· · ) .. ·, ·~:~.1; ... . : :! .. . ..... '; Table 2.2. Classification of anaetnias ··. . .. .:. '; . MCJ<(fl) lr:/ A101plw/ogical MCJ/C{%) 32-36 -· 1. Nonnochromic normocytic ·. 2. llypochrornic norrnocytic 32 3. Hypochromic rnicrocytic <32 . >' 96 ·-:·· ... :~·; 4. Macrocytic Usually normal Normal 5. Microspherocytic Usually normal ~ reducet - . .. A('fiologiral ([;) Increased blood loss (i) Acute (a) Haemorrhage (ii) Chronic (h) llacmolysis (i) Corpuscular defects (ii) Extracorp_ uscular defects (2) Decreased blood production (i) Iron ·- (o) Nutritional deficiency (ii) Folic acid, cobalan1in (iii) Pyridoxine (iv) Ascorbic acid (v) Protein (i) Primary (idiopathic) (h) llonc marrow failure (ii) Secondary to drugs, chemicals, irradiation (iii) Other

· ~ bl~e -~ ~ l:..f- i· LC l 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 :.; l ll ;; . · 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 colour of this deoxygenated hemoglobin masks the red color of the oxygenated hemoglobin. Therefore, a person with polycythemia ordinarily has a ruddy complexion but often with a bluish (cyanotic) tjnt to the skin.

(H~po)(ia) Ctassiffc:at io/1 01 eryt n rocyto s1 ~ 1 . r <elati'fe ery th' ocytosis . Deny dration tf.. ;· "" fue f rythr oeyfos; J /- \. With incre«sed E-P l~vtL .. 1 Ph-ysiolo9ical- high alt1tude. . 1,. Drugs (a) Cobalt i hyro xifle (b) An dYo~et"s~ 1:3 . Ulith low or ilormal Sp. { Q.vt/ :::: P olycythaernia veva I

·. )· R~d ~ ~ - ,~ '-~·-_:.:- :, ~ o,; group~. · ~. ('•:l~ \,~1) ~> ~- ~i.j · :~ l~er!on .~:~:·', ·~;i~:< ~,., _~ !.~·r\:_• ·; - ·: . ~ '-\~ •,.·;,.~, -~-; ~/.Q;:'J'1 ~, ~"'· :~·-~: ~ · -:i~· -_-.-:~(;9:~ : ~1 · ·.'~' \~( - ~,: ~f '{'t.i.:;' "-·\·'1!<' ·~ ~-:F - \~. -~ ~:· 1-,\~ .~: , , ;~ -~.:.J-:. · ~,., -~- ~;.,~· ,.J ~'.,.:;_-~ . Cj-%·-·:·- - :; ' · · \'.: ~ - :~>i~{ - ~:~:\:·-Y:fl:.~p:~ · ~-c~:L · ,·".!:~-1'·~ ~:~;-h - ·~\ ;~ : · ~\-.: ,~} · · . .... -. ...... -1:..:-- ·- . .. . · :'" :-. . .... r. :- --·: '"'/0' ,_, ... 'Clr:.;. :· : '" -;;:; ·: ·.•. :- ':'. ·:· -- ..• . ~ '. ":.'' ·- '.: - . .. . ' .· ·,•; ~ .. . .... .. , ... !..l Ut S i' a ... .. •; · P , :/. ' :· . -~- . -;-. .- · ~- .. . . .- . : .· . / .. : > : . .. -;: ---- ... · ., .. -,. ,., ;-;: .... ~ . =,, ·. ,:! ·· .· .• ~· ·.r · I A ·.:.-,. 1' .': _· :. Aglutl~ogon b!tJOd C!>!! ., . ., _ ·.::_: : · F- .. . •'' -i ,:.\t.:ll . ·, • ! · • . ·. \~-~ . . ·'• · .· • I -. Agglutinogen s.. · : ; .· _ :. . _,. - :· . ·. . • l ' : 1_ •; '; ~ • I : • • • . : .•. , . A II. ·. ,. ' .... ,: .. · ::. , Red blood .. cell . ·:·:; .... 't- :,-t .r : i: .... , . , • \ • ., ,-.. • . , .•••• . \ ,., .. '\1'1,\4, o f I I r: •\, • t ,!\, '• ~ '• , , ' '4\ I , "fj •1 • Agglutinin anti-A '· · · ·.•-:;\;1_:.-:,! • I I •' • "\ I .• > ~:~ '\· ~H:, ' - · · ... - ,. 1 ~ .. _ ... . .. ·z. !'t p~ r. f)' . •t . r' J.,. .~ 1 i· _.ti'!. .. >:-'~-; 7 ) . ,, '· . ,. . . . .. · ': t w , /F :.:~·~·':·~!:)·;: · ·:~). r;:!, .. ) . . '..i: :: .. _ . -~ ... . '-/··-" , , .' :\ ': :<· I \. . . . ' . _ Rei? biC:OO. ·,· · :. ·. P.glutln~n antl: B. · : · ce . . ' Type 0 blood J FIGURE 21.16 . The antigens and antibodies present in lYP '" /\,B. 1\B, and 0 blood ,, I / .._i

~ ·~· li:~.·, :\~ ~)1P,~/):I!-I (; p~ ;( , ap : : -· · _; .?~ :- ~ . ' ' ' ~ · ~. ·I · '/ · · ·' . :;·'.:,:~ : - 1/:, - ': ;,;if?:·t:~,:;. ,\~': ~! ':~ lt "-~- ~ · · ;.'Jl (;\~ 1 ~ . i h . ~ f ·, 'J•', · Jr · , ·' ,'r',r,t · ' · .l · f'~'·~ \. · :. :r H · ·!r:, .· ·. . ' - -~-· -.- ~ · -·- · - · - · - ~ ~ - - · ~ ·.-:· - ·:, - ~; - ~-{~;~ : :'.:~ : i:~)~.:·-:.· - ., ' , ... ' . A· .. '": .J '· ,\/ .... .. .. / / ' ...... .. / 'lOU •• ,.,,.I' . •' .. · .' f t' . !.'r., ·,· ,.a I 0 • •• • , : ',: .:'},,!;<<·; ,~: ' I : Anit-A ·· ' !.o,_ · 1 ,; !.·! . ·f ·:· .:•i JUU ( I) 0 . I J.' ' '11 1 1: : · I 0 I L ngglutmtns . :.: ... . , . •' . ;· 1.:, : _ _ L • I ·' ,, ' I' 111 qroups :, :· · 1.·, I :; _ , .' .•,' ·:: ,· - ··:·· .. ·.-_ - , • I • ) I :.:l · : _;:;-;_:,i . ;.:'(;·:::/ - ,!. ·.,.: : ·u, B and 0 blood t : Ul Anti-B . · .· . .. ..r. : . :/ r\l flgg/utinins 0 . ' .. i t a. l , . . ' ' ·; ~ ' I ' .- '-. · r, . ~ ' ... ' ' in groups - !!-I '- · .' >.: · ·_ ;:.:: ;:; .. \ :: .:~; .)i, • . • • . J A and 0 blood 1 •l ,. [..: 1 ': ,·.I I • • " ', ; : ( ' • • ··; ,, ,f I :. l! }( . : I . • • ( ~ ;; } \ ~ 100 · h·Jt ' 1\ ~r: • J· , : .'; , · '· . , ., ,. "' · r .t ·.' ) . l :.~ Jl !I i: ;.: J I ! I ,. • ',·•, ,I ; ,·· \', \ ·. · ." · ' · ····lV";l l. ';t. ; (l:; , . . ;,·.( ·· •" -li -·( . 'I ; I ; .• . ,_II; I .. -:- . --:' . :: .. · - ,·:· "• I ; • ,, ·: ,r . 1, ,., ,-;.· t·. I I t ' , 1 0 - . ·,: 'f 0 ' 40 · so o o 20 1 30 GO Ago (years) 1 •1'' : \•)d·•·· · ,, ··, r ;• ·1 1 •' .. . I • , ·. •. ' · '( .. , "}(~':r,· Average titers of anti-A · and · anti-8 i ·agglutinlns Fiyute 35-1. in tl1e LJ/ooc..J of people in group D and group A. at - djfferent :; · 1 . :. ·, ... · ' '· . !, •, ·1 \ l • I' ' I I 1 • 1 tJ .. 1 I dCjl!S . I 1 I o 0 o'; I · : / · ; j/':/: ': fol ·\ 1 \'l,;l(b 1 1 o ./ ~, ' :( ~· 1 • , . : ·' • ·. ti ,· .' ,·. - :,; .1 ·: !,~!.' o I ·, :· o • •• , • • ; \. --c-·-.. . . ~/ . !j -£,., ! ~:- .., . ... -· . ,·.

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~ ~ "! \_~ ~ ~ · · 1 ,- ~: . ~ .. r .• - ' ;" ,. . ,; · -- - . .. ~ ::).. (' ,f:.\ I '\:'· t: • •• • (.''-:- -' Fortunately, this diseuse can he l)rcvciJlcd l)v givi11g a11 I, I (' j 11- \ · · Rh-negative rnother human gun1n1a glol.n1lin ugainsl H 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 antibod y synthesis by the 1nother. The administered untibodies are eventually catabolized.

- ~-: !:_~;-~ ·-. .· ~ ~ ~-~7·~ . ., -;:: : ".,(. ,. : .. , ·- ~ ~ .. ~3~-~ -. '• - ':\, \ I I . --.. ..__ . ()< :-: .10 ·you inay be wondering vvhether ABO inco- mpatibilities --.,·r- .. t· r. ) 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 'f c G- not readily cross t~r~;a. --- ) - - ,. ' ·•. T -- ' _, ..