BRIEF DETAILS ABOUT TYPES OF ANEMIA IN LARGE & SMALL ANIMALS AND ANTI-ANEMIC DRUGS

1. Dr SINDHU KDr SINDHU K
MVSc SCHOLAR,MVSc SCHOLAR,
DEPT OF VPT,POOKODEDEPT OF VPT,POOKODE
ANTIANEMIC DRUGSANTIANEMIC DRUGS
IN VETERINARYIN VETERINARY
PRACTICEPRACTICE

2. AnemiaAnemia
Inadequate red blood mass usually is a secondaryInadequate red blood mass usually is a secondary
condition rather than representing a primarycondition rather than representing a primary
disease of the ERYTHRONdisease of the ERYTHRON
Deficiency of erythrocytes per unit volume ofDeficiency of erythrocytes per unit volume of
bloodblood
In simple words anemia = low hemoglobin, lowIn simple words anemia = low hemoglobin, low
RBC count and low RBC mass.RBC count and low RBC mass.

3. types of Anemiatypes of Anemia
Primary anemia = occurs due toPrimary anemia = occurs due to
excessive loss of bloodexcessive loss of blood
eg: hemolysis , hemorrhageeg: hemolysis , hemorrhage
Secondary anemia = impaired cellSecondary anemia = impaired cell
formationformation
eg: hypothyroidism , arsenic toxicityeg: hypothyroidism , arsenic toxicity
etcetc

4. MACROCYTIC NORMOCHROMICMACROCYTIC NORMOCHROMIC
Cobalt or vitamin b12 deficiencyCobalt or vitamin b12 deficiency
Folic acid deficiencyFolic acid deficiency
FeLV associated myelodysplasiaFeLV associated myelodysplasia
Congenital erythropoieticCongenital erythropoietic
porphyriaporphyria

5. MACROCYTICMACROCYTIC
HYPOCHROMICHYPOCHROMIC
 It is a transient condition occurring duringIt is a transient condition occurring during
the active phase of erythroid regenerationthe active phase of erythroid regeneration
following erythrocyte destruction or acutefollowing erythrocyte destruction or acute
blood lossblood loss
 HemolysisHemolysis
 Blood parasites, rickettsial agentsBlood parasites, rickettsial agents
 Ba, viral infectionsBa, viral infections
 Intrinsic erythrocyte defectsIntrinsic erythrocyte defects

6. NORMOCYTICNORMOCYTIC
NORMOCHROMICNORMOCHROMIC
 Acute blood loss prior to onset ofAcute blood loss prior to onset of
regenerative responseregenerative response
 Anemia of chronic inflammatory diseases ,Anemia of chronic inflammatory diseases ,
chronic renal failurechronic renal failure
 Hypoadrenocortisism, hypothyroidism,Hypoadrenocortisism, hypothyroidism,
lead poisoning,bracken fern poisoninglead poisoning,bracken fern poisoning
 Cytotoxic marrow damage-radiations &Cytotoxic marrow damage-radiations &
chemicalschemicals

7. NORMOCYTICNORMOCYTIC
HYPOCHROMICHYPOCHROMIC
 Early iron deficiencyEarly iron deficiency
MICROCYTIC NORMOCHROMICMICROCYTIC NORMOCHROMIC
 Iron deficiency in progression,NormalIron deficiency in progression,Normal
asymptomatic characteristic of Japaneseasymptomatic characteristic of Japanese
akitasakitas

8. MICROCYTIC HYPOCHROMICMICROCYTIC HYPOCHROMIC
 Iron deficiencyIron deficiency
 congenital anemia of neonatescongenital anemia of neonates
 Chronic gastro intestinal blood lossChronic gastro intestinal blood loss
 Infestation with hematophagous parasitesInfestation with hematophagous parasites
 Copper deficiencyCopper deficiency
 Molybdenum toxicityMolybdenum toxicity
 Pyridoxine toxicityPyridoxine toxicity

9. BLOOD LOSS ANEMIABLOOD LOSS ANEMIA
 Loss of blood from vascular space ,Loss of blood from vascular space ,
whether to the exterior of the body or towhether to the exterior of the body or to
extravascular regions with in the tissuesextravascular regions with in the tissues
 Acute or chronicAcute or chronic
 Principal pathophysiological effect isPrincipal pathophysiological effect is
HYPOVOLUMIAHYPOVOLUMIA
 Patient with acute blood los die ofPatient with acute blood los die of
hemorrhagic shock before anemia ishemorrhagic shock before anemia is
manifestedmanifested

10. TreatmentTreatment
 Life threatening problem -> hypovolemiaLife threatening problem -> hypovolemia
-->hemorrhagic shock-->hemorrhagic shock
 Therapeutic goal = Blood volume repletionTherapeutic goal = Blood volume repletion
 A balance crystalloid solutionA balance crystalloid solution
 ~7.2% sodium chloride to promote fluid~7.2% sodium chloride to promote fluid
redistribution from extravascular tissues toredistribution from extravascular tissues to
vascular compartment & positivevascular compartment & positive
ionotropic effects on heartionotropic effects on heart

11. TreatmentTreatment
 Synthetic colloids{ hypoproteinemia}Synthetic colloids{ hypoproteinemia}
 ~0.9%saline solutions with 6-10% dextran-~0.9%saline solutions with 6-10% dextran-
40, dextran-70, pentastarch or hetastarch40, dextran-70, pentastarch or hetastarch
 Plasma transfusionPlasma transfusion
 ACUTE BLEEDING – whole bloodACUTE BLEEDING – whole blood
transfusion , packed red blood celltransfusion , packed red blood cell
transfusion.transfusion.

12. IRON DEFICIENCY ANEMIAIRON DEFICIENCY ANEMIA
 If blood loss continues, sufficient IRONIf blood loss continues, sufficient IRON
eventually will be lost producing ironeventually will be lost producing iron
depleted state even with continueddepleted state even with continued
ingestion of dietary ironingestion of dietary iron
 Rate of hemoglobin lost exceeds that ofRate of hemoglobin lost exceeds that of
iron absorption=animal experiencesiron absorption=animal experiences
NEGATIVE IRON BALANCE resulting inNEGATIVE IRON BALANCE resulting in
typical MICROCYTIC HYPOCHROMICtypical MICROCYTIC HYPOCHROMIC
ANEMIAANEMIA

13. treatmenttreatment
 Transfusion of whole blood or bloodTransfusion of whole blood or blood
productsproducts
 Dogs <15% PCVDogs <15% PCV
 Cats < 12% PCVCats < 12% PCV
 Blood volume expansion - whole blood orBlood volume expansion - whole blood or
cell-free, polymerized hemoglobin,cell-free, polymerized hemoglobin,
crystalloids or colloid solutioncrystalloids or colloid solution

14. Blood transfusionBlood transfusion

15. HEMOLYTIC ANEMIAHEMOLYTIC ANEMIA
 Destruction of erythrocytes{oxidative orDestruction of erythrocytes{oxidative or
immunological damage}immunological damage}
 Blood parasites – anaplasma , babesia ,Blood parasites – anaplasma , babesia ,
hemobartonella , eperythrozoon.hemobartonella , eperythrozoon.
 Rickettsial - erlichiaRickettsial - erlichia
 Bacterial – leptospirosis , clostridium.Bacterial – leptospirosis , clostridium.
 Virus – feline leukemia virus, equineVirus – feline leukemia virus, equine
infectious anemia.infectious anemia.

16. TreatmentTreatment
 Supportive therapy – transfusion of wholeSupportive therapy – transfusion of whole
bloodblood
 Specific treatmentSpecific treatment
glutathione precursor in subduing the actionglutathione precursor in subduing the action
of oxidative drugsof oxidative drugs
Eg: N acetyl cysteineEg: N acetyl cysteine
Antioxidants {vitamin A ,E, C }Antioxidants {vitamin A ,E, C }
ANTIMICROBIALSANTIMICROBIALS

17. NONNON
REGENERATIVE/HYPOPLASTREGENERATIVE/HYPOPLAST
ICIC ANEMIA associated with bone marrowANEMIA associated with bone marrow
dysfunctiondysfunction
 Suppressive chemicals- pesticides ,Suppressive chemicals- pesticides ,
insecticides , antineoplastic agents.insecticides , antineoplastic agents.
 Endocrine failure affecting cell division &Endocrine failure affecting cell division &
erythropoiesis(EPO, insulin, thyroiderythropoiesis(EPO, insulin, thyroid
hormone)hormone)
 Chronic inflammationsChronic inflammations

18. TreatmentTreatment
 Characterized by erythroid precursorCharacterized by erythroid precursor
phagocytosis – responds tophagocytosis – responds to
immunosuppressive drugs or Humanimmunosuppressive drugs or Human
gamma globulingamma globulin
 Dogs – estrogen induced bone marrowDogs – estrogen induced bone marrow
suppressionsuppression
 Lithium carbonate 11mg/kg os BIDLithium carbonate 11mg/kg os BID

19. Primary dietary iron deficiencyPrimary dietary iron deficiency
anemiaanemia
 Iron responsiveness, microcytic,Iron responsiveness, microcytic,
hypochromic anemia relatively common inhypochromic anemia relatively common in
neonates especially pigletsneonates especially piglets
 ~300mg of iron required in first 3 weeks~300mg of iron required in first 3 weeks
but sow milk ~21 mgbut sow milk ~21 mg
 Poor growth rate, rough hair coat, pale &Poor growth rate, rough hair coat, pale &
wrinkled skin, dyspnea, fatigue,wrinkled skin, dyspnea, fatigue,
 very high mortality ratevery high mortality rate

20. TreatmentTreatment
 Iron dextran 100-150 mg IM on 2Iron dextran 100-150 mg IM on 2ndnd
or 3or 3rdrd
day to pigletsday to piglets
Absorbed in to lymphatic system with in 3Absorbed in to lymphatic system with in 3
days of administration & enters cells ofdays of administration & enters cells of
mononuclear phagocytes throughmononuclear phagocytes through
circulating blood & combines withcirculating blood & combines with
TRANSFERRINTRANSFERRIN
 Copper deficiency also participates inCopper deficiency also participates in
pathogenesis of baby pig anemia –pathogenesis of baby pig anemia –
application of iron copper preparation toapplication of iron copper preparation to

21. POLYCYTHEMIAPOLYCYTHEMIA
 A relative or absolute increase inA relative or absolute increase in
concentration of circulating erythrocytesconcentration of circulating erythrocytes
 Increase in erythrocytic no = increase inIncrease in erythrocytic no = increase in
hemoglobin concentration of the bloodhemoglobin concentration of the blood
 RELATIVE POLYCYTHEMIA results fromRELATIVE POLYCYTHEMIA results from
loss of fluid component of blood orloss of fluid component of blood or
hemoconcentrationhemoconcentration
 Transient state secondary to dehydrationTransient state secondary to dehydration

22. Polycythemia contd.,Polycythemia contd.,
 ABSOLUTE POLYCYTHEMIAABSOLUTE POLYCYTHEMIA
characterized by increase in the totalcharacterized by increase in the total
erythonerython
 Usually associated with hyperplasia ofUsually associated with hyperplasia of
erythropoietic elements of bone marrowerythropoietic elements of bone marrow
 Idiopathic=polycythemia veraIdiopathic=polycythemia vera
 dogs ~ carcinoma, fibrosarcoma,dogs ~ carcinoma, fibrosarcoma,
lymphosarcoma of kidneyslymphosarcoma of kidneys
 Right to left circulatory shunts-chronicRight to left circulatory shunts-chronic
hypoxia stimulating EPO release from

23. treatmenttreatment
 Directed at the primary disease &Directed at the primary disease &
improvement of oxygen delivery to tissuesimprovement of oxygen delivery to tissues
 Paraneoplastic syndrome of absoluteParaneoplastic syndrome of absolute
polycythemia = surgical removal of tumorpolycythemia = surgical removal of tumor
 PhlebotomyPhlebotomy
 Myelosuppressive agents = chlorambucil ,Myelosuppressive agents = chlorambucil ,
hydroxyurea , busulfan ,hydroxyurea , busulfan ,
radiophospherousradiophospherous

24. ANAEMIA OF CHRONICANAEMIA OF CHRONIC
RENAL FAILURERENAL FAILURE
 Loss of endogenous EPO resulting fromLoss of endogenous EPO resulting from
chronic renal failure culminates in non-chronic renal failure culminates in non-
regenerative anemiaregenerative anemia
 UREMIA ~ reduced erythrocyte survivalUREMIA ~ reduced erythrocyte survival
~ platelet dysfunction~ platelet dysfunction
~ gastrointestinal bleeding~ gastrointestinal bleeding
~uremic inhibitors of~uremic inhibitors of
erythropoiesiserythropoiesis

25. treatmenttreatment
 Therapy directed at slowing theTherapy directed at slowing the
progression of chronic renal failureprogression of chronic renal failure
 Ameliorating the adverse consequencesAmeliorating the adverse consequences
of uremiaof uremia
 Modifications of dietary intake of water, phModifications of dietary intake of water, ph
, na , trace minerals iron , water soluble, na , trace minerals iron , water soluble
vitamins , antioxidants.vitamins , antioxidants.

26. Iron deficiencyIron deficiency
 Gastrointestinal hemorrhage = frequentGastrointestinal hemorrhage = frequent
complication of anemiacomplication of anemia
 H2-receptor antagonist ~ cimetidine,H2-receptor antagonist ~ cimetidine,
ranitidineranitidine
 Mucosal protectants ~ sucralfateMucosal protectants ~ sucralfate

27. .

28. Iron PreparationsIron Preparations
 Oral IronOral Iron
– Ferrous SulfateFerrous Sulfate (Feosol) – 300 mg tid(Feosol) – 300 mg tid
– Side Effects are extremely mild:Side Effects are extremely mild:
 Nausea, upper abdominal pain, constipation or diarrhea.Nausea, upper abdominal pain, constipation or diarrhea.
– CheapestCheapest form of Iron and one of the mostform of Iron and one of the most widelywidely
usedused
 ParenteralParenteral
– Iron DextranIron Dextran (Imferon) – IM or IV(Imferon) – IM or IV
– IndicatedIndicated for patients who cannot tolerate or absorbfor patients who cannot tolerate or absorb
oral ironoral iron or where oral iron is insufficient to treat theor where oral iron is insufficient to treat the
condition ie. Malabsorption syndrome, prolongedcondition ie. Malabsorption syndrome, prolonged
salicylate therapy, dialysis patientssalicylate therapy, dialysis patients

29. ..

30. Dosing regimenDosing regimen

31. CLASSIFICATION OFCLASSIFICATION OF
ANTI-ANAEMIC DRUGSANTI-ANAEMIC DRUGS
 1. HEMATOPOIETIC GROWTH1. HEMATOPOIETIC GROWTH
FACTORSFACTORS
 2.NUTRITIONAL AGENTS2.NUTRITIONAL AGENTS

32. Haematopoietic growth factorsHaematopoietic growth factors
 1. erythroid growth factors1. erythroid growth factors
Eg: erythropoietinEg: erythropoietin
( epoetin alpha , epoetin beta )( epoetin alpha , epoetin beta )
Darbepoetin alfaDarbepoetin alfa

34. Sites of action for EPOSites of action for EPO

35. Therapeutic Uses of EPOTherapeutic Uses of EPO
 Anemia of end stage renal diseaseAnemia of end stage renal disease
 To treat AIDS anemia caused by AZT’sTo treat AIDS anemia caused by AZT’s
suppression of bone marrowsuppression of bone marrow
 Anemia related to cancer chemotherapyAnemia related to cancer chemotherapy
 OthersOthers
– To increase RBC levels for autologous blood donationTo increase RBC levels for autologous blood donation
– Anemia associated with rheumatoid arthritisAnemia associated with rheumatoid arthritis

36. ERYTHROPOIETINERYTHROPOIETIN
 Replacement therapy of endogenousReplacement therapy of endogenous
erythropoietin with a recombinant humanerythropoietin with a recombinant human
erythropoietin rhEPOerythropoietin rhEPO
 Recommended in anemia~ dogs PCVRecommended in anemia~ dogs PCV
<30% & CATS PCV < 25%<30% & CATS PCV < 25%
 DOSE- 100 units/kg BW s/c 3 times perDOSE- 100 units/kg BW s/c 3 times per
weekweek
 Regenerative response = appearance ofRegenerative response = appearance of
reticulocytes in peripheral bloodreticulocytes in peripheral blood

37. Hematopoietic Growth FactorsHematopoietic Growth Factors
 1. Granulocyte/Macrophage Colony Stimulating Factor1. Granulocyte/Macrophage Colony Stimulating Factor
((GM-CSFGM-CSF)-)- Sargramostim , molgramostim.Sargramostim , molgramostim.
 Acts synergistically with IL-3 to stimulate the formation andActs synergistically with IL-3 to stimulate the formation and
proliferation ofproliferation of colony forming cellscolony forming cells: CFU-GEMM, BFU-E,: CFU-GEMM, BFU-E,
CFU-Meg, CFU-GM, CFU-M, CFU-ECFU-Meg, CFU-GM, CFU-M, CFU-E
 Increases cytotoxicIncreases cytotoxic phagocytic activityphagocytic activity of matureof mature
granulocytesgranulocytes
 2. Interleukin 32. Interleukin 3 (IL-3) – oprelvekin(IL-3) – oprelvekin
 ActsActs synergistically with GM-CSFsynergistically with GM-CSF to stimulate the formationto stimulate the formation
of granulocytes, macrophages, eosinophils andof granulocytes, macrophages, eosinophils and
megakaryocytes.megakaryocytes.
 ActsActs synergistically with EPOsynergistically with EPO to stimulate formation ofto stimulate formation of BFU-EBFU-E
coloniescolonies
 Induces CFU-S and leukemic blast cells into cell cycleInduces CFU-S and leukemic blast cells into cell cycle

38. MoreMore Hematopoietic Growth FactorsHematopoietic Growth Factors
 3. Colony stimulating Factor-1 (3. Colony stimulating Factor-1 (CSF-1 or M-CSF-1 or M-
CSFCSF))
 Acts synergistically with GM-CSF and IL-3 to stimulateActs synergistically with GM-CSF and IL-3 to stimulate
monocyte/macrophage colony formation and functionmonocyte/macrophage colony formation and function
 4. Granulocyte Colony Stimulating Factor4. Granulocyte Colony Stimulating Factor
((G-CSFG-CSF) –) – filgrastimfilgrastim ,, pegfilgrastim , lenograstimpegfilgrastim , lenograstim
 ActsActs synergisticallysynergistically withwith IL-3, GM-CSF and CSF-1IL-3, GM-CSF and CSF-1 toto
stimulate formation of megakaryocytes, granulocyte-stimulate formation of megakaryocytes, granulocyte-
macrophage and high proliferative potential (HPP) coloniesmacrophage and high proliferative potential (HPP) colonies
 Induces release of granulocytes from marrowInduces release of granulocytes from marrow

39. MoreMore Hematopoietic Growth FactorsHematopoietic Growth Factors
 5. Thrombopoietin5. Thrombopoietin (TSF)(TSF)
 Increases the size and number of megakaryocytes.Increases the size and number of megakaryocytes.
(IL-11 also useful in stimulating production)(IL-11 also useful in stimulating production)
 Increases the concentration of earlyIncreases the concentration of early megakaryocytes cellsmegakaryocytes cells
(SACHE+cells) in bone marrow.(SACHE+cells) in bone marrow.
 Produces an increase in megakaryocytes endomitosis.Produces an increase in megakaryocytes endomitosis.
 Increases platelet size and number in plasma.Increases platelet size and number in plasma.

40. NUTRITIONAL AGENTSNUTRITIONAL AGENTS
 1. MINERALS1. MINERALS
Iron, cobolt, copper.Iron, cobolt, copper.
 2. VITAMINS2. VITAMINS
Vitamin B12, folic acid, pyridoxine,Vitamin B12, folic acid, pyridoxine,
riboflavin, ascorbic acid`riboflavin, ascorbic acid`

41. Iron CycleIron Cycle
 5 - 10%5 - 10% of ingested ironof ingested iron
isis absorbedabsorbed
 Once ingested theOnce ingested the acidacid
in thein the stomachstomach::
– 1. Aids in1. Aids in ionizationionization
of ironof iron
– 2.2. Splits chelatedSplits chelated
foodfood ironiron fromfrom
chelatorchelator
– 3. Maintains3. Maintains ironiron inin
solublesoluble formform
– 4. Allows iron to4. Allows iron to
remain in theremain in the
absorbable formabsorbable form FeFe3+3+

42. Mechanism of Iron AbsorptionMechanism of Iron Absorption

43. Therapeutic uses of IronTherapeutic uses of Iron
 Iron Deficient AnemiaIron Deficient Anemia
 PregnancyPregnancy
 Premature BabiesPremature Babies
 Blood lossBlood loss
 Hookworn infestationHookworn infestation
 MalabsorptionMalabsorption
SyndromeSyndrome
 GI Bleeding due to:GI Bleeding due to:
 UlcersUlcers
 AspirinAspirin
 Excess consumption ofExcess consumption of
coffeecoffee

44. Iron PreparationsIron Preparations
 Oral IronOral Iron
– Ferrous SulfateFerrous Sulfate (Feosol) – 300 mg tid(Feosol) – 300 mg tid
– Side Effects are extremely mild:Side Effects are extremely mild:
 Nausea, upper abdominal pain, constipation or diarrhea.Nausea, upper abdominal pain, constipation or diarrhea.
– CheapestCheapest form of Iron and one of the mostform of Iron and one of the most widelywidely
usedused
 ParenteralParenteral
– Iron DextranIron Dextran (Imferon) – IM or IV(Imferon) – IM or IV
– IndicatedIndicated for patients who cannot tolerate or absorbfor patients who cannot tolerate or absorb
oral ironoral iron or where oral iron is insufficient to treat theor where oral iron is insufficient to treat the
condition ie. Malabsorption syndrome, prolongedcondition ie. Malabsorption syndrome, prolonged
salicylate therapy, dialysis patientssalicylate therapy, dialysis patients

45. Ferrous sulphateFerrous sulphate
 Dogs: 100-300 mg total dose PO onceDogs: 100-300 mg total dose PO once
daily for 14 daysdaily for 14 days
 Cats: 50-100 mg total dose PO once dailyCats: 50-100 mg total dose PO once daily
for 14 daysfor 14 days
 Cattle: 8-15 g total PO once daily for 14Cattle: 8-15 g total PO once daily for 14
daysdays
 Horses: 2-8 g total dose PO daily for 14Horses: 2-8 g total dose PO daily for 14
daysdays
 Sheep & goat: 0.5-2 g PO daily 14 daysSheep & goat: 0.5-2 g PO daily 14 days

46. IRON DEXTRANIRON DEXTRAN
 FOR TREATMENT OF IRONFOR TREATMENT OF IRON
DEFICIENCY ANEMIADEFICIENCY ANEMIA
 Dogs: 10-20 mg/kg IM once daily followedDogs: 10-20 mg/kg IM once daily followed
by oral therapy with ferrous sulphateby oral therapy with ferrous sulphate
 Piglets: 100-200 mg of elemental iron totalPiglets: 100-200 mg of elemental iron total
dose IM on 2dose IM on 2ndnd
or 3or 3rdrd
dayday
repeated on 10repeated on 10thth
to 40to 40thth
dayday
depending on the requirement of pigletdepending on the requirement of piglet

47. Toxicity of Iron OverdoseToxicity of Iron Overdose
 5000 deaths/year5000 deaths/year in the US, usually in childrenin the US, usually in children
 20% of children presenting with iron toxicity will20% of children presenting with iron toxicity will
diedie
 1 to 2 grams are sufficient to cause death1 to 2 grams are sufficient to cause death
 At high doses, Iron is absorbed through passiveAt high doses, Iron is absorbed through passive
diffusion with no regulationdiffusion with no regulation

48. Iron – Clinical EffectsIron – Clinical Effects
 Early changesEarly changes
– Vomiting, diarrhea Blood Volume HR TPR (reflex)Vomiting, diarrhea Blood Volume HR TPR (reflex)
– Acidosis from Iron oxidation, Krebs cycle andAcidosis from Iron oxidation, Krebs cycle and
anaerobic metabolism citric acid and lactic acidanaerobic metabolism citric acid and lactic acid
 Intermediate changesIntermediate changes
 Improvement (short lived) profound shock and CVImprovement (short lived) profound shock and CV
Collapse Hepatic Failure, jaundice, pulmonaryCollapse Hepatic Failure, jaundice, pulmonary
edema and deathedema and death
 Late StageLate Stage
 Intestinal scarring, fatty acid degeneration of liver,Intestinal scarring, fatty acid degeneration of liver,
cirrhosis and death.cirrhosis and death.

49. Treatment of Iron OverdoseTreatment of Iron Overdose
 Toxic levelsToxic levels
 ALD – 200-300mgkg, plasma iron > 300ug/dlALD – 200-300mgkg, plasma iron > 300ug/dl
 ABC’s supportive careABC’s supportive care
 Bicarbonate for acidosisBicarbonate for acidosis
 FluidsFluids for blood lossfor blood loss
 Ipecac or lavageIpecac or lavage
 Chelation withChelation with DeferoxamineDeferoxamine

50. COBOLTCOBOLT
 ESSENTIAL TRACE ELEMENT & keyESSENTIAL TRACE ELEMENT & key
component of COBOLAMIN / vitamin B-12component of COBOLAMIN / vitamin B-12
 Synthesized by rumen microflora & COSynthesized by rumen microflora & CO
supplementations are necessary forsupplementations are necessary for
erythropoiesis in ruminantserythropoiesis in ruminants
 MOA: enhances synthesis of vitamin B 12MOA: enhances synthesis of vitamin B 12
by rumen microflora & increasesby rumen microflora & increases
production of erythropoietin in kidneyproduction of erythropoietin in kidney

51. Cobolt cont..,Cobolt cont..,
 Deficiency of cobolt- marked anemia ,Deficiency of cobolt- marked anemia ,
decrease in blood volume , loss of bodydecrease in blood volume , loss of body
weight emaciation , failure to thriveweight emaciation , failure to thrive
 Predominant in young growing ruminantsPredominant in young growing ruminants
& sheep reared on pasture where soil is& sheep reared on pasture where soil is
CO deficientCO deficient
 Topical dressing of soil 100-150 g cobaltTopical dressing of soil 100-150 g cobalt
sulphate per acresulphate per acre

52. COPPERCOPPER
 Essential component required forEssential component required for
formation of hemoglobin, bone, melanin &formation of hemoglobin, bone, melanin &
keratin.keratin.
 Integral component of certain enzymesIntegral component of certain enzymes
-ascorbic acid oxidases-ascorbic acid oxidases
-polyphenol oxidases-polyphenol oxidases
-cytochrome oxidases-cytochrome oxidases
-monoamine oxidases-monoamine oxidases

53. Cu cont..,Cu cont..,
 As hematinic necessary for normalAs hematinic necessary for normal
utilization of iron in hemoglobin &utilization of iron in hemoglobin &
absorption & increasing outflow of ironabsorption & increasing outflow of iron
from reticulo-endothelial cellsfrom reticulo-endothelial cells
 Copper deficiency= High level of dietaryCopper deficiency= High level of dietary
molybdenum , iron or sulphurmolybdenum , iron or sulphur
 Unthriftiness, anemia , loss of coat color &Unthriftiness, anemia , loss of coat color &
temporary sterilitytemporary sterility

54. DosesDoses
Copper sulphateCopper sulphate
Cattle:1-2g PO once daily 7 days, break of 5Cattle:1-2g PO once daily 7 days, break of 5
days & again treatment for 7 daysdays & again treatment for 7 days
Sheep:0.25g/45kg PO once dailySheep:0.25g/45kg PO once daily
Copper glycinate ( depot preparation )Copper glycinate ( depot preparation )
Cattle: 120mg IMCattle: 120mg IM
Sheep: 40mg IMSheep: 40mg IM

55. Vitamin BVitamin B1212
 Source: In food, especially in liver and kidneys. GISource: In food, especially in liver and kidneys. GI
Microorganism synthesis, Vitamin SupplementsMicroorganism synthesis, Vitamin Supplements
(Cyanocobalamin)(Cyanocobalamin)
 Necessary for normal DNA synthesisNecessary for normal DNA synthesis
 Absorption of BAbsorption of B1212
 1.1. Intrinsic FactorIntrinsic Factor (low dose): a protein made by stomach(low dose): a protein made by stomach
parietal cells that binds to Bparietal cells that binds to B1212 and delivers it from the ileum viaand delivers it from the ileum via
a calcium mediated event.a calcium mediated event.
 2.2. Mass ActionMass Action (High dose): 1000mg/day, absorbed via(High dose): 1000mg/day, absorbed via
passive diffusionpassive diffusion

56. BB1212 DeficiencyDeficiency
 AA BB1212 deficiencydeficiency will cause peripheral neuropathywill cause peripheral neuropathy
and aand a macrocytic anemiamacrocytic anemia, a pernicious anemia., a pernicious anemia.
 Folic AcidFolic Acid administration can correct theadministration can correct the
macrocytic anemia but willmacrocytic anemia but will fail to correctfail to correct thethe
peripheral neuropathyperipheral neuropathy..
 To treat theTo treat the neuropathy, Vit Bneuropathy, Vit B1212 must be utilized.must be utilized.

57. Mechanism for PeripheralMechanism for Peripheral
NeuropathyNeuropathy
 Cobalamin is a cofactor for the enzymeCobalamin is a cofactor for the enzyme
Methylmalonyl-CoA mutase which convertsMethylmalonyl-CoA mutase which converts
methylmalonyl-CoA to succinyl-CoAmethylmalonyl-CoA to succinyl-CoA..
 Succinyl-CoA enters the Krebs cycles and goesSuccinyl-CoA enters the Krebs cycles and goes
into nerves to make myelin.into nerves to make myelin.
 If no Vitamin BIf no Vitamin B1212, methylmalonyl-CoA goes on to, methylmalonyl-CoA goes on to
formform abnormal fatty acidsabnormal fatty acids and causes subacuteand causes subacute
degeneration of the nerves. Only Bdegeneration of the nerves. Only B1212 can correctcan correct
this problem.this problem.

58. Therapeutic Uses of BTherapeutic Uses of B1212
 Daily Requirements - 0.6-1.0mh/day; TDaily Requirements - 0.6-1.0mh/day; T1/21/2 ~ 1 year~ 1 year
 Pernicious AnemiaPernicious Anemia
 Impaired GI absorption of BImpaired GI absorption of B1212
 GastrectomyGastrectomy
 Corrosive InjuryCorrosive Injury of GI mucosaof GI mucosa
 Fish tape wormFish tape worm: worm siphons off B: worm siphons off B1212
 Placebo abuse with BPlacebo abuse with B12,12, especially in elderly patients.especially in elderly patients.

59. Other vitaminsOther vitamins
 Vitamin B 5 – pyridoxineVitamin B 5 – pyridoxine
Promotes RBC production & aids inPromotes RBC production & aids in
biosynthesis of monoaminobiosynthesis of monoamino
neurotransmitters serotonin, dopamine,neurotransmitters serotonin, dopamine,
norepinephrine.norepinephrine.
Used in dogs cats for treating microcyticUsed in dogs cats for treating microcytic
hypochromic anemia but of Lesshypochromic anemia but of Less
significantsignificant

60. Vit cont..,Vit cont..,
 Riboflavin { vitamin B 2} - required for wideRiboflavin { vitamin B 2} - required for wide
variety of cellular processvariety of cellular process
 Ascorbic acid { vitamin C } – water solubleAscorbic acid { vitamin C } – water soluble
vitamin which facilitates iron absorptionvitamin which facilitates iron absorption

61. Folic AcidFolic Acid
 SourceSource in food – yeast, egg yolk, liver and leafyin food – yeast, egg yolk, liver and leafy
vegetablesvegetables
 Folic Acid (F.A.) is absorbed in theFolic Acid (F.A.) is absorbed in the small intestines.small intestines.
 F.A. is converted toF.A. is converted to tetrahydrofolatetetrahydrofolate byby dihydrofolatedihydrofolate
reductase.reductase.
 Folic Acid deficiency (F.A. Deficiency) is also calledFolic Acid deficiency (F.A. Deficiency) is also called
Will’s Disease.Will’s Disease.
 Deficiency may produce megaloblastic anemia;Deficiency may produce megaloblastic anemia; neuralneural
tube defect in fetus.tube defect in fetus.

62. Therapeutic Uses of Folic AcidTherapeutic Uses of Folic Acid
 1.1. Megaloblastic AnemiaMegaloblastic Anemia due to inadequatedue to inadequate
dietary intake of folic aciddietary intake of folic acid
 Can be due to chronic alcoholism, pregnancy, infancy,Can be due to chronic alcoholism, pregnancy, infancy,
impaired utilization: uremia, cancer or hepatic disease.impaired utilization: uremia, cancer or hepatic disease.
 2. To alleviate2. To alleviate anemiaanemia that isthat is associatedassociated withwith
dihydrofolate reductase inhibitorsdihydrofolate reductase inhibitors..
 i.ei.e. Methotrexate. Methotrexate (Cancer chemotherapy),(Cancer chemotherapy),
PyrimethaminePyrimethamine (Antimalarial)(Antimalarial)
 Administration ofAdministration of citrovorum factorcitrovorum factor (methylated folic(methylated folic
acid) alleviates the anemia.acid) alleviates the anemia.

63. Therapeutic Uses of Folic Acid (cont)Therapeutic Uses of Folic Acid (cont)
 3. Ingestion of3. Ingestion of drugs that interfere with intestinaldrugs that interfere with intestinal
absorptionabsorption and storage of folic acid.and storage of folic acid.
 Mechanism- inhibition of the conjugases that break offMechanism- inhibition of the conjugases that break off
folic acid from its food chelators.folic acid from its food chelators.
 Ex. –Ex. – phenytoinphenytoin, progestin/estrogens (, progestin/estrogens (oral contraceptivesoral contraceptives))
 4. Malabsorption – Sprue, Celiac disease, partial4. Malabsorption – Sprue, Celiac disease, partial
gastrectomy.gastrectomy.
 5.5. Rheumatoid arthritisRheumatoid arthritis – increased folic acid– increased folic acid
demand or utilization.demand or utilization.

64. MISCELLANEOUS DRUGSMISCELLANEOUS DRUGS
 ANDROGENIC steroidsANDROGENIC steroids
Structurally related to testosteroneStructurally related to testosterone
Stimulates erythropoiesisStimulates erythropoiesis
Anabolic steroids increases intracellularAnabolic steroids increases intracellular
concentration of 2,3-bisphosphoglycerateconcentration of 2,3-bisphosphoglycerate
in erythrocytes thereby enhancing oxygenin erythrocytes thereby enhancing oxygen
release into tissuesrelease into tissues

65. Clinical useClinical use
 To stimulate erythropoiesis in anemiaTo stimulate erythropoiesis in anemia
particularly those associated with renalparticularly those associated with renal
disease accompanied by low EPO levels.disease accompanied by low EPO levels.

66. REFERENCESREFERENCES
 RICHARD ADAMSRICHARD ADAMS veterinary
pharmacology and therapeutics. 8th
edition
 Sandhu HS Essentials of veterinary
pharmacology and therapeutics. 2nd
edition
 Google images
 Online links

67. ThankThank
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