anaemia (1)
TRANSCRIPT
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Presenting
Symposium Medicus- Batch roll nos. 120 to 140
MANAGEMENT OF
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Decrease in oxygen carrying capacity of blood
characterized by number of RBCs below 4million/cubic mm or content of haemoglobinless than 12gm/dL
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ANAEMIA
HAEMORRHAGIC DIETARY
DEFICIANCY
IRON DEFICIENCY MEGALOBLASTIC
APLASTIC HEMOLYTIC
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IRON PHYSIOLOGY
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CAUSES OF IRON DEFICIENCY
ANAEMIA
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LOW DIETARY INTAKE
IMPAIRED ABSORPTION
INCREASED REQUIREMENT
CHRONIC BLOOD LOSS
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SIGNS AND SYMPTOMS
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Signs and Symptoms
No symptoms if the anemia is mild.
Most of the time, symptoms are mild at first and
develop slowly. Symptoms may include:
Irritability Fatigue
Dyspnea during exercise
Headaches
Problems concentrating or thinking
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As the anemia gets
worse, symptoms may
include:Blue color to the whites
of the eyes
Brittle nails
Light-headedness
when one stands up
Pale skin color
Shortness of breathSore tongue
Symptoms of the
conditions that cause
iron deficiency anemiainclude:
Dark, tar-colored stools
or blood
Heavy menstrualbleeding (women)
Pain in the upper belly
(from ulcers)
Weight loss (in people
with cancer)
http://www.nlm.nih.gov/medlineplus/ency/article/003247.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003244.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003075.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003075.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003244.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003247.htm -
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LABORATORY INVESTIGATIONS OF
ANAEMIA
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1.INITIAL INVESTIGATIONS
HEMATOLOGY PROFILE (Complete blood count) MCV,MCH,MCHC are decreased
MICROSCOPY
Blood picture reveals microcytosis, hypochromia,anisocytosis, poikilocytosis, pencil cells and target cells
Bone marrow findings show high cellularity, poorly
haemoglobinised normoblast and absence of stainable
iron
SERUM FERRITIN levels are decreased(normal levels-30 to
400ng/ml in males and 15 to 200 ng/ml in females)
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2.ADDITIONAL INVESTIGATIONS
SERUM IRON levels are decreased
(normal levels 65-176micrograms/dl in men,50-
170micrograms/dl in women,100-250micrograms/dl in
newborns and 50-120micrograms/dl in children)
TIBC (Total Iron Binding Capacity) is increased (normal-240 to
450micrograms/dl)
TRANSFERRIN SATURATION is decreased (normal-20 to 50%)
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NON PHARMACOLOGICAL
TREATMENT
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Dietary advice
To both anaemic and non-anaemic women.
Vitamin C significantly enhances iron absorption from
non-haem foods, the size of this effect increasing with
the quantity of vitamin C in the meal. Germination and fermentation of cereals and legumes
improve the bioavailability of non-haem iron by
reducing the content of phytate.
Tannins in tea and coffee inhibit iron absorption whenconsumed with a meal or shortly after.
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Oral iron therapy
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Oral iron therapy
Indication- women with mild to moderate deficiency withno absorption or compliance (or both) limiting factors
Ferrous iron salts are the preparation of choice. Oral dosein case anaemia due to iron deficiency should be 100-200mg of elemental iron daily. Doses not to be increasedto avoid saturation of absorption and dose related sideeffects.
Women should be counselled as to how to take oral ironsupplements correctly. This should be with a source ofvitamin C such as orange juice to maximise absorption.Consumption with meals may be necessary to avoid sideeffects. Other medications or antacids should not betaken at the same time.
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When side effects appear affecting compliance, titration of
dose to a level where side effects are acceptable or a trialof an alternative preparation may be necessary.Preparations with lower iron content should be tried.
Enteric coated or sustained release preparations should beavoided as the majority of the iron is carried past the
duodenum, limiting absorption. A repeat Hb at two weeks is required to assess response to
treatment.
The haemoglobin concentration should rise by
approximately 20 g/l over 3-4 weeks. Once the Hb is in the normal range, treatment should be
continued for a further 3 months and at least until 6 weekspostpartum to replenish iron stores.
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Parenteral Iron Therapy
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Parenteral Iron Therapy
Indications :
Deficiency is severe
Along with erythropoietin
Failure to tolerate oral iron
Failure to absorb oral iron
Non-compliance to oral therapy
Iron requirement = 4.4 x body weight (kg) x Hb deficit (g/dl)
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Parenteral Iron Therapy Preparations available for IM use:
Iron-dextran (Imferon): 1.5 ml vial, 50 mg of elemental
iron/ml
Iron-sorbitol-citric acid complex (Jectocos):1.5 ml vial,50 mg
of iron/ml
IM injection :
Common site : Gluteal region
Technique: Z track Dose: After an initial test dose of 25 mg,100 mg is
administered daily till calculated dose is attained.
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Iron-dextran Iron-sorbitol-citric acid
High molecular weight Low molecular weight
Can be given i.m or i.v Can be given only i.m.
Not bound to transferrin Tends to saturate transferrin
Given i.m. 10-30% is locally bound Not locally bound
Not excreted About 30% excreted in urine
Given i.m. absorbed via lymphatics Absorbed directly into circulation
Taken up by macrophages Directly available
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Parenteral Iron Therapy
Preparations available for IV use:
High molecular weight iron dextran (Imferon):
1-2 ml vial,50 mg iron/ml
Low molecular weight iron dextran (Cosmofer):
2 ml vial,50 mg iron/ml
Iron saccharate: 5 ml vial,20 mg of iron/ml
Ferric gluconate: 5 ml vial,12.5 mg iron/ml
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Parenteral Iron Therapy
IV injection:
After an initial dose of 0.5 ml given over a a period of 5-10
mins, 2 ml can be injected over 10 mins every day.
Alternatively the total calculated dose is diluted in 500 ml of
glucose/saline solution & infused slowly over 6-8 hours.
Ferric gluconate or iron saccharose may be used in repeated
boluses in the dose of 100-200 mg of elemental iron.
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Management in
pregnancy
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Full blood count taken at the booking appointment and at 28 weeks.
Prophylaxis starting in 2nd trimester for all pregnant women with 30
mg oral elemental iron daily.
Hb < 11g/dl up until 2 months or
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IRON TOXICITY
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ADVERSE EFFECT OF ORAL IRON THERAPY
BLACKENING OF TEETH AND FAECES DUE TOFORMATION OF
IRON SULPHIDE
SEVERE VOMITING
ABDOMINAL PAIN
HEMATEMESIS
DIARRHOEA
CARDIOVASCULAR COLLAPSE AND SHOCK
SOME MAY DEVELOP JAUNDICE,HYPOGLYCEMIAAND CONVULSIONS
SYMPTOMS BECOME EVIDENT AFTER 6HRS OF
CONSUMPTIONDOSES OF 1gm OR MORE OF FERROUS SULPHATE ARE
CONSIDERED TOXIC IN CHILDREN
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ADVERSE REACTION TO IM PREPARATION
LOCAL PAIN
PERMANENT SKIN DISCOLOURATIONREGIONAL LYMPHADENOPATHY
MYALGIA
ATHRALGIA
TACHYCARDIAFLUSHING
CIRCULATORY COLLAPSE
HAEMOLYSIS
SYSTEMIC TOXICITY MAY DEVELOP WITHIN
10MINS OF INJECTION
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ADVERSE EFFECT OF I.V IRON THERAPY
SYSTEMIC REACTIONS SIMILAR TO IM iron
SEVERE CHEST PAINRESPIRATORY DISTRESS
CIRCULATORY COLLAPSE
EXTRAVASATION INTO SUBCUTANEOUS TISSUE CAN
CAUSE ABSCESS FORMATION
ANAPHYLACTOID REACTIONCAN OCCUR WITHIN FIRST
FEW MINUTES OF ADMINISTRATION. THEREFORE TEST
DOSE MUST BE GIVEN PRIOR TO STARTING THE
TREATMENT
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Toxic dosage
The amount of iron ingested may give a clue to
potential toxicity. The therapeutic dose for irondeficiency anemia is 36 mg/kg/day. Toxic effects begin
to occur at doses above 1020 mg/kg of elemental iron
IRON POISONING MAY BE-
1]ACUTE IRON POISONING
2]CHRONIC IRON OVERLOAD
ADVERSE EFFECTS OF EXCESSIVE IRON
SUPPLEMENTS
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CAUSES-
ACCIDENTAL CONSUMPTION BY
CHILDREN
INTENTIONAL INGESTION BY ADULTS
SYMPTOMS BECOME EVIDENT AFTER
6HRS OF CONSUMPTION
DOSES OF 1gm OR MORE OF FERROUS
SULPHATE ARE CONSIDERED TOXIC IN
CHILDREN
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CHRONIC IRON OVERLOAD
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Iron is an extremely corrosive substance to the. It acts on the and canmanifest with nausea, vomiting, abdominal pain,hematemesis, and diarrhea; patients may becomehypovolemic because of significant fluid and bloodloss
Severe overdose causes
, which can result in .METABOLIC ACIDOSIS
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TREATMENT OF IRON POISONING
MILK AND EGG YOLK MIXTURE-TO BIND IRON
Gastric lavage with water containing desferroxamine or if not available then
with calcium disodium edetate
DESFERRIOXAMINE 1-2gm IM IS ADMINISTERED
DOC for iron intoxication.
Approximately 8 mg of iron is bound by 100 mg of
deferoxamine.
Readily chelates iron from ferritin and hemosiderin but nottransferrin
Most effective when administered continuously by infusion
Iv infusion 10-15mg/kg/hr to a maximum of of 80mg/kg in
24hr
Early replacement of body fluids and electrolytes using
isotonic saline,correction of metabolic acidosis and
hypotension by using ringer lactate and vasopressor
diazepam
DESFERRIOXAMINE
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VITAMIN B12
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HISTORY
Addison described anaemia not responding to Fe as
PERNICIOUS ANAEMIA (PERNICIOUS for INCURABLE
and DEADLY) and also its relation to atrophy of gastric
mucosa.
Minot and Murphy-included liver in diet of such
patients-received Nobel prize.
Castles hypothesis-an extrinsic factor(in diet)
combines with intrinsic factor(produced by stomach)-gives rise to haemopoietic principle.
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Vitamin B12
Water soluble,thermostable,red crystals.
Synthesized in nature only by microorganisms; plants
and animals get from them.
DIETARY SOURCES-Liver,egg yolk,kidney,cheese. *ONLY vegetable source-LEGUMES(pulses).
*Vit. B12- synthesized by colonic microflora but not
available for absorption in man.
COMMERCIAL SOURCE- Strep. Griseus.
Daily req.-1 -3 micro gm. In pregnancy and lactation-3-
5 micro gm.
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Active coenzyme forms-deoxyadenosylcobalamin(DAB12) and Methylcobalamin(methyl B12).
1.
Conversion of homocysteine to methionine.2. Purine and pyrimidine synthesis.
3. Propionic acid metabolism.
4. Synthesis of phospholipid and myelin.
5. Essential for cell growth and multiplication.
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Methionine S-adenosyl methionate
Malonic acid Succinic acid
DAB12
DAB12
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UTILISATION 0F VIT.B12
TRANSPORTED-In combination with transcobalamin II.
Congenital absence or abnormal proteins(like TCI and
TCIII)-interfere with delivery of vit.B12 to tissues.
Not degraded in body. Excreted in bile.Significant Enterohepatic circulation
takes place.
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CAUSES OF DEFICIENCY
1. Addisonian pernicious anaemia- Auto Immune
disorder
2. Gastric mucosal damage
3. Malabsorption4. Blind loop syndrome
5. Nutritional deficiency
6. Increase in demand in pregnancy and infancy
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MANIFESTATIONS OF DEFICIENCY
1. MEGALOBLASTIC ANAEMIA- First manifestation-with
hypersegmented neutrophil,giant platelets.
2. Glossitis and G.I. disturbances: damage to epithelial
structures.3. Neurological:
a) Subacute Combined Degeneration of Spinal Cord
b) Peripheral neuritis
c) Mental changes
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PREPARATIONS DOSE ANDADMINISTRATION
1. CYANACOBALAMIN.
2. HYDROXOCOBALAMIN.
3. METHYLCOBALAMIN.
4. METHYL B12- Required for integrity of myelin.Dose
1.5mg/day.5. When deficiency due to decrease in Intrinsic factor-i.m.
or s.c. but not i.v.
6. Initially- 30-100 micro gm/ day for 10 days,then 100 micro
gm weekly then monthly.7. Neuro complications 500-1000micro gm/ day.
8. Prophylactic-3-10 micro gm/day.
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USES OF VIT. B12
1. TREATMENT of VIT. B12 DEFICIENCY.
2. PROPHYLAXIS of VIT. B12 DEFICIENCY.
3. Neuropathies and psychiatric disorders.
4. Tobacco amblyopiaADVERSE EFFECTS-
a) Large doses are also safe.
b) Allergic reactions due to injection.
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FOLIC ACID DEFICIENCY ANAEMIA
FOLIC ACID : PTERIDINE + PABA + GLUTAMATE
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DIETARY SOURCES :
yeast, liver, kidney, green
leafy vegetables ( spinach ),
egg, meat, milk
DAILY REQUIREMENT : 150-200 microgram in children
400 microgram in adults
600 microgram or greater in pregnancy
500 microgram in lactation
Hepatic stores of folate contain 15-20 mg of folate, which is very less and can be
easily exhausted within 3-4 months of stopping oral folate administration
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NORMAL SERUM FOLATE LEVELS : 2.7-17 ng/ml
UTILISATION : Present in foods as polyglutamates of n5 methyl THFA
Absorbed in upper part of jejunum after convertingpolyglutamate residues to monoglutamate residues
Absorbed in this form by active and passive transportprocesses and demethylated in the cells to THFA by vitb12
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METABOLIC FUNCTIONS : active form : THFA
1. Conversion of homocysteine to methionine
2. Conversion of d ump to d TMP
3. Conversion of serine to glycine4. Purine synthesis which requires formyl and methenyl THFA histidine
metabolism for mediating formimino group transfer
FOLIC ACID DEFICIENCY IS SEEN IN :
Chronic alcoholic patients Liver disease
Pregnant women Hemolytic anaemia
Malabsorbtion syndrome Renal dialysis patients
Drugs likemethotrexate, trimethoprim, pyrimethamine, phenytoin
PREPARATIONS AND DOSE ti f 2 d
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PREPARATIONS AND DOSE : preparations of 2 compoundsavailable:
FOLIC ACID : FOLVITE , FOLITAB 5mg TABS
FOLINIC ACID : CALCIUMLEUCOVORIN, FASTOVORIN, RECOVORIN
PARENTERAL ADM IS RARELY NECESSARY AS ORAL FOLIC ACID ID=S WELLABSORBED EVEN IN PATIENTS WITH MALABSORBTION SYNDROMES
DOSE OF 1mg ORAL FOLIC ACID DAILY IS SUFFICIENT TO REVERSEMEGALOBLASTIC ANAEMIA, RESTORE NORMAL SERUM FOLATE LEVELSAND REPLENISH THE FOLATE STORES
THERAPY SHOULD BE CONTINUED TILL UNDERLYING CAUSE OFDEFICIENCY IS REMOVED OR CORRECTED
SHOTGUN ANTI ANAEMIA PREPARATIONS
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USES :
MEGALOBLASTICANAEMIAS DUE TO NUTRITIONAL FOLATE DEFICIENCY,
PERNICIOUS ANAEMIA, PREGNANCY, LACTATION, HEMOLYTIC ANAEMIA,MALABSORBTION SYNDROME, PROLONGED ANTIEPILEPTIC THERAPY
WITH PHENYTOIN
FOLATE ADM WILL REVERSE HEMATOLOGICAL CHANGES OF FOLATE AND
VIT B12 DEFICIENCY ANAEMIA, BUT NUEROLOGICAL DEFICIT OF VIT B12DEF ANAEMIA CANNOT BE REVERSED WITH FOLATE ADM
THE USA FDA HAD INTRODUCED GRAINS RICH IN FOLIC RICH
SUPPLEMENTATION TO ALL ITS CITIZENS TO REDUCE FOLATE DEFICIENCY.
INCIDENCES OF NTDS REDUCED BY 30% BUT THIS WAS FINALLY STOPPEDAS IT WAS THOUGHT IT WOULD MASK VIT B12 DEFICIENCY
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PROPHYLAXIS : 1mg/day IN PREGNANCY TO REDUCE NTDs
METHOTREXATETOXICITY : FOLINIC ACID IS USED AS
TREATMENT AS IT DOES NOT REQUIRE DHFRase TOCONVERT TO ACTIVE FORM
CITROVORUM FACTOR RESCUE
ADVERSE EFFECTS : ORAL FOLIC ACID IS ENTIRELY NONTOXIC, SENSITIVITY REACTIONS MAY OCCUR ONPARENTERAL ADM
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ERYTHROPOIETIN
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Sialoglycoprotein hormome (MW 34000) produced byperitubular cells of the Kidney.
Anaemia and hypoxia sensed by Kidney cells
Kidney cells
Rapid secretion of EPO
Acts on erythroid marrow
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ACTIONS
1. Stimulates proliferation of colony forming cells of the
erythroid series.
2. Induces haemoglobin formation and erythroid blast
maturation.
3. Releases reticulocytes in circulation
EPO binds to specific receptors that alters phosphorylation
of intracellular proteins and activates transcription factors to regulate
Gene expression.
Erythropoiesis is directly proportion to dose and has no effect on
Lifespan of RBC
USES
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US S
1. Anaemia of chronic renal failure due to low EPO
25-100 U/Kg s.c. or i.v. 3 times a week (600 U/kg max)
Raises Haematocrit and HBReduces need for transfusion
Improves quality of life
Start with low dose and titre upwards; Haematocrit between
30-36%, Hb 10-12g/dl
2. Anaemia in AIDs patients treated with zidovudine
3. Cancer chemotherapy induced anaemia
4. Preoperative increased blood production for autologous
transfusion during surgery
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ADVERSE EFFECTS
EPO is nonimmunogenic
Sudden increase in Haematocrit, blood viscosity and
peripheral vascular resistance
Increased clot formation in the A-V shunts
Hypertensive episodes
Seizures
Flu like symptoms lasting 2-4 hrs in some patients
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