Drugs Used in Ttt of Anaemias Lec6

8/12/2019 Drugs Used in Ttt of Anaemias Lec6

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DRUGS ACTING ON BLOODDRUGS ACTING ON BLOOD

BYBY

Dr AliDr Ali

Professor ofProfessor of

pharmacology&Therapeuticspharmacology&Therapeutics


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DRUGS USED IN ttt OFDRUGS USED IN ttt OF

ANEMIASANEMIASDef.Def.anemia is the reduction belowanemia is the reduction below

normal range of RBCs number or Hbnormal range of RBCs number or Hbconc. r both.conc. r both.


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Classification Of anemiasClassification Of anemias

I.I.deficiency anemiadeficienc

y anemia!due to " of factors essential for normal!due to " of factors essential for normal

erythropoiesis#. erythropoiesis#.

1- i!n deficiency anemia1- i!n deficienc

y anemia!hypochromic microcytic anemia#!hypochromic microcytic anemia#

iron is re$uired for Hb prod% so absence of e ' small rediron is re$uired for Hb prod% so absence of e ' small red

cells ( insufficient Hb.cells ( insufficient Hb.Ca"#e#'' ) inade$uate inta*e) inade

$uate inta*e

+, -/ 012 +34 567 89: +;-?EFG2

IJ?3K42 L: M3, NO2*ecessiQe losses

+# ..... +?G,12 S +?+# ..... +?G,12 S +?YZTYZT!!

*ecessiQe demandse.g. low birthe.g. low birthweight% Pregnancy% lactationweight% Pregnancy% lactation..


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hypochromic microcytichypochromic microcytic


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[\ folic acid deficiency anemia !macrocytic anemia#

e.g. in pregnancye.g. in pregnancy

( some antiepileptic drugs !] malabsorption#( some antiepileptic drugs !] malabsorption# in infants fed ( goat^s mil*%in infants fed ( goat^s mil*%

Qitamin C "Qitamin C "

in malabsorption syndrome.in malabsorption syndrome.


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D"'# effecti(e in i!ndeficiency anemia

pharmacokineticspharmacokinetics

**normally \` . of e in diet is absorbed !but in e " anemia `\[normally \` . of e in diet is absorbed !but in e " anemia `\[absorbedabsorbed(.(.

*factors affecting absorb:*factors affecting absorb:11((Qalency of e e better than eQalency of e e better than e+++ .+++ .

[# acidity of stomach[# acidity of stomachreduction of e ' ereduction of e ' e++++

retard formation of insoluble Complees of e ( food constituentsretard formation of insoluble Complees of e ( food constituents..4? L: 2- Mj -;-V42 k?=2 444? L: 2- Mj -;-V42 k?=2 44achlorhydriaachlorhydria::>??


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) Site !f a*#!$ti!n +any part of YZT but it^s greatest in duodenum and proimal

qequnum

) I!n di#ti*"ti!n# in n!ma% ad"%t+ ' Hb in RBCs `\[ ' stored e as ferritin and hemosiderin

` ' myoglobin in muscles

less than ` ' cytochromes% enymes.% transferrin !transporte#

* iron absorption is regulated by:

\ leQel of serum e

\ saturation of transferrin !` globulin#


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* iron excretion:* iron excretion:there is no mechanism for iron ecretion.

nly small amounts are lost with epithelial cells which aredes$uamated from s*in and YZT !stool# traces are lost inurine% bile% sweat.

* iron requirements:* iron requirements:\ normal daily re$uirements for adult man \` mg.

\ re$uirements Qary with growth% pregnancy% menstruation.

*iron preparations:*ironpreparations:The only indication for the use of e preparation is treatment orThe only indication for the use of e preparation is treatment or

preQention of iron deficiency anemiapreQention of iron deficiency anemia


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)I,. !a% $e$aati!nI,. !a% $e$aati!n\ should be giQen after meals to aQoid YZT irritation.

\ for ~\E months to replenish e stores.

}amples errous sulphate ~ mg t.d.s ![ elemental#

errous gluconate E mg t.d.s !`[ elemental#

errous fumarate [ mg t.d.s !~ elemental#

542 ? L: ;F


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: }pigastric discomfort% colic*y pain% diarrhea or constipation

?34?(dose \ related. S time \ related)

: Abdominal pain% Qomiting% hematemesis% bloody diarrhea%

acidosis% cardioQascular collapse% coma% death.

J?42 >?@12 L: -V; ?34? U?V42 N


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Treatment of acute iron poisoning:Treatment of acute ironpoisoning:

`\ gastric aspiration followed by.

[\ gastric laQage ( ` aHC~ or phosphate !to form

insoluble e salts#.

~\ e chelating agents e.g. desferroamine !desferal# by

\ stomach tube !to bind gastric e#. \ Z._ or Z. drip !to bind absorbed e#.

\ symptomatic treatment for !dehydration.% conQulsions. #.

II,. $aentea% i!n $e$aati!n+II,. $aentea% i!n $e$aati!n+ indicati!n# \ in emergencies.

\ when oral is impractical !e.g. malabsorption orpost gastrectomy#.


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* preparations:*preparations:

** Fe dextran (imferon) = complex of Fe(OH)3 + dextranZ._ or Z. mgml !elemental#

542 ? L: ;F


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::C&!nic i!n T!icity!haemochromatosis and

haemosiderosis#\ when ecess e is deposited in heart% liQer%pancreas% other organs ' organ failure death.

\ occur in patients \with congenital disorder

characterised by ecessiQe e Absorption.

\who receiQe many bloodtransfusions.


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/enici!"# anemia and !t&e/enici!"# anemia and !t&eme'a%!*%a#tic anemia#me'a%!*%a#tic anemia#

5X ?5X ?

\\ pernicious anemiapernicious anemiaI failure of the stomachI failure of the stomachto secrete intrinsic factor ' B`[ " anemia.to secrete intrinsic factor ' B`[ " anemia.

5X ?5X ?

\\ megaloblastic anemiamegaloblastic anemiaI anemia withI anemia withmacrocytosismacrocytosis

!B`[ " \ folic "#!B`[ " \ folic "#


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- functions of !"# folic acid:- functions of !"# folic acid:) they are essential for DA synthesis.) they are essential for DA synthesis.) their " ' " DA synthesis ' " mitosis " maturation and function of) their " ' " DA synthesis ' " mitosis " maturation and function of

cells !speciallycells !specially cells with rapid diQision as YZT and B_ #cells with rapid diQision as YZT and B_ #

- c%inica% $ict"e !f B10 f!%ic acid deficiency +- c%inica% $ict"e !f B10 f!%ic acid deficiency +&- 'ematological%&- 'ematological%

macrocytic hyperchromic anemia !why megaloblastic anemia]#macrocytic hyperchromic anemia !why megaloblastic anemia]#

"" DA ' " diQision in the face of continued RA and Protein synthesis 'DA ' " diQision in the face of continued RA and Protein synthesis '

large RBCs.large RBCs.- !%- !%

\ glossitis.\ glossitis. \ diarrhea.\ diarrhea.

\ achlorhydria.\ achlorhydria.

3- nerological%3- nerological%\ peripheral neuritis.\ peripheral neuritis.

\ sub acute combined degeneration f spinal Cord !ataia .#.\ sub acute combined degeneration f spinal Cord !ataia .#. 89: 89:B`[B`[


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2intake of B12RARE

(

2intrini! fa!tor"erni!io# a.,-$#%eni&e3..

-after 'atre!to)

*i"+)&o,ot+A,nora&itie in

terina& i&e#

-- inf&ae. /eion.-after re'iona&

ree!tion.

0a&a,or".

-aetiology of anemia $!"(

B10 cyan!c!*a%amin.


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) #!"ce# !f B10+) #!"ce# !f B10+ 456789:;< => ? ?


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) $e$aati!n#+) $e$aati!n#+

`. cyanocobalamin inq ` or ` ugml Z_`. cyanocobalamin inq ` or ` ugml Z_

it^s the prep. f choice in ttt of pernicious anemia.it^s the prep. f choice in ttt of pernicious anemia.

BBhydroocobalamin is better than cyanocobalamin H]hydroocobalamin is better than cyanocobalamin H]because it has high protein binding ' retained in body forbecause it has high protein binding ' retained in body for

longer periods.longer periods.

[. Qit B`[ ( intrinsic factor concentrate orally[. Qit B`[ ( intrinsic factor concentrate orally

2?


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F!%ic acidF!%ic acid--water sol. it. f B comple gpwater sol. it. f B comple gp

aetiology of folic aaetiology of folic a. :. : 11. . dietary inta*e !nutrional megalobastic adietary inta*e !nutrional megalobastic a.(..(.22. . re$uirement e.g. in pregnancyre$uirement e.g. in pregnancy

megaloblastic. a. of pregnancymegaloblastic. a. of pregnancy..Recently ' foetal neural tube defect e.g. spinaRecently ' foetal neural tube defect e.g. spina

bifidabifida..33. . absorption e.g. malabsorp. yndromeabsorption e.g. malabsorp. yndrome..

44..drugs which interfere ( absorption of folic a. 'drugs which interfere ( absorption of folic a. 'anticonQulsant therapy e.g. hydantion anticonQulsant therapy e.g. hydantion..

55

.

.drugs interfere ( metabolism of folic adrugs interfere ( metabolism of folic a..

--trimethoprimtrimethoprim--methotreatemethotreate

--pyrimethaminepyrimethamineinhibit dihydrofolate red. }ninhibit dihydrofolate red. }n..

'ources:'ources:east% liQer% green Qeg.% fruitseast% liQer% green Qeg.% fruits..


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(etabolic functions:(etabolic functions:

\ folic a. is not actiQe as such.\ folic a. is not actiQe as such. \ it^s reduced in duodenum and qequnum to tetrahydrofolic\ it^s reduced in duodenum and qequnum to tetrahydrofolic

acid !folinic acid% THA# by tetrahydrofolate reductase en.acid !folinic acid% THA# by tetrahydrofolate reductase en.

\ THA is conQerted in liQer to methyl deriQatiQe\ THA is conQerted in liQer to methyl deriQatiQe

transported into bile ' undergo enterohepatic Circulationtransported into bile ' undergo enterohepatic Circulation..

%eq.:%eq.: ugday. ugday.

N@4?/N@4?/Dosage:Dosage:`\[ mgday`\[ mgday

toxicity:toxicity:oo

2- JU? 1? L: ,?#2- JU? 1? L: ,?#((


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A$%a#tic aA$%a#tic a

- ttt i# #"$$!ti(e+- ttt i# #"$$!ti(e+

O L4?


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em!%ytic aem!%ytic a

11--immediate withdrawal of causatiQe agent e.g.immediate withdrawal of causatiQe agent e.g.drugs as aspirin .. in YEPDdrugs as aspirin .. in YEPD..

+/6


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A'an"%!cyt!#i#A'an"%!cyt!#i#Def.Def.condition ch.ch. by mar*ed leucopenia and neutropeniacondition ch.ch. by mar*ed leucopenia and neutropenia..

)et.)et.ccurs as a hypersensitiQity reaction to many drugs asccurs as a hypersensitiQity reaction to many drugs as:: --analgesics \ aminopyrineanalgesics \ aminopyrine..

--phenyl butaonephenyl butaone.. --antithyroid as thiouracilantithyroid as thiouracil

>K@2J6 ?@642>K@2J6 ?@642--antibioticsantibiotics --goldgolddiagnosis:diagnosis:usually begins ( sore throat and feQerusually begins ( sore throat and feQer..;F, 0U -7


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Drugs Used in Ttt of Anaemias Lec6