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New: Medicine 5th year, 7th lecture/part one (Dr. Sabir)
 

New: Medicine 5th year, 7th lecture/part one (Dr. Sabir)

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The lecture has been given on Mar. 27th, 2011 by Dr. Sabir.

The lecture has been given on Mar. 27th, 2011 by Dr. Sabir.

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    New: Medicine 5th year, 7th lecture/part one (Dr. Sabir) New: Medicine 5th year, 7th lecture/part one (Dr. Sabir) Presentation Transcript

    • Iron-deficiency anemia By: Dr. Sabir M. Ameen
    • iron metabolism
      • Daily diet contain 15-20 mg of iron
      • Only 10% of this is absorbed
      • Absorption increases ( 20-30%) in iron-deficiency and pregnancy
      • Haem iron ( in meat) is better absorbed than non-haem iron ( in cereals, milk)
      • Absorption takes place in duodenum and jejunum
      • Absorption is favored by acidity of stomach keeping iron in ferrous rather than ferric form
    • Iron stores
      • 2/3 of total body iron is in circulation as Hb (2500-3000 mg)
      • Iron is stored in reticuloendothelial cells, hepatocytes, and skeletal muscles( 500-1500 mg)
      • 2/3 of stored iron is in form of ferritin and 1/3 in form of hemosiderin
      • About 4 mg is found in plasma bound to transferrin
    • requierments
      • Each day 0.5-1.0 mg of iron is lost in feces, urine, and sweat
      • Menstruating women lose 40 ml of blood per month ( 0.7 mg of iron/day)
      • Blood loss in excess of 100ml through menstruation will result in iron-deficiency
    • causes
      • Blood loss
      • Increased demands ( growth and pregnancy)
      • Decreased absorption ( e.g postgastrectomy)
      • Poor intake
      • Most common is blood loss usually from uterus or GIT
      • Iron-deficiency affects more than ¼ of world’s population
    • Clinical features
      • Symptoms ( non-specific):
      • Fatigue, headaches, faintness, breathlessness, angina of effort, intermittent claudication, palpitations
      • Signs: pallor, tachycardia, systolic flow murmur, heart failure,
      • Specific signs: brittle nails, koilonychia, atrophy of papillae of tongue, angular stomatitis, brittle hair, dysphagia( Plummer-Vinson or Paterson-Kelly syndrome)
    • Koilonychia
    • Koilonychia - spoon shaped nail
    • Nutritional deficiency anemia Angular stomatitis glossitis
    • investigations
      • Blood count and film:
      • RBCs are microcytic ( MCV < 80 fl) and hypochromic ( MCH < 27pg)
      • There is poikilocytosis ( variation in shape) and anisocytosis (variation in size)
      • Target cells are seen
      • Low serum ferritin
      • Low serum iron and high total iron binding capacity ( TIBC)
      • Transferrin saturation ( serum iron divided by TIBC ) is < 19%
      • BM: erythroid hyperplasia with ragged normoblasts ,but BM examination is not essential for diagnosis
    • Differential diagnosis of microcytic and hypochromic anemia
      • Thalassemia ( α or β ): s. Fe is↑/normal, and TIBC↓/ normal, also ferritin is ↑/normal
      • Sideroblastic anemia: s. Fe is raised, TIBC is ↓, serum ferritin raised
      • Anemia of chronic disease: s. Fe is reduced, TIBC is reduced, and serum ferritin raised
    • treatment
      • First find and treat the cause
      • Then give iron to correct anemia
      • Finally give iron to replace iron stores
      • Iron is best given orally as ferrous sulphate on empty stomach, if side effects develop such as nausea, diarrhea or constipation, tablets given with food or reducing dose with another preparation as ferrous gluconate
    • Treatment
      • ORAL
        • 200 mg of iron daily 1 hour before meal (e.g. 100 mg twice daily)
        • How long?
          • 14 days + (H b required level – H b current level) x 4
        • half of the dose 6 – 9 months to restore iron reserve
        • Absorption
          • is enhanced: vit C, meat, orange juice, fish
          • is inhibited: cereals, tea, milk
    • Treatment
      • PARENTERAL IRON SUBSTITUTION
        • Bad oral iron tolerance (nausea, diarrhoea)
        • Necessity of quick management (CHD, CHF)
        • 50 - 100 mg daily
        • I.v only in hospital (risk of anaph y lactic shock)
        • I.m in outpatient department
        • Total dose by iv infusion:
        • iron to be injected (mg) = (15 - Hb g ) x body weight (kg) x 3
    • Failure of response to oral iron
      • Lack of compliance
      • Continuing hemorrhage
      • Severe malabsorption
      • Another cause for the anemia
      • These possibilities should be considered before using parenteral iron
    • Normal Peripheral Smear
    • Iron Deficiency Anemia
    • Anemia of chronic disease (ACD) - definition ACD is a common type of anemia that occurs in patients with infectious, inflammatory, or neoplastic diseases that persist for more than 1 or 2 months. It does not include anemias caused by marrow replacement, blood loss, hemolysis, renal insufficiency, hepatic disease, or endocrinopathy, even when these dis o rders are chronic.
    • Anemia of chronic disease (ACD) -epidemiology
      • The ACD is extremely common
      • ACD is more common tha n any anemia syndrome other than blood loss with consequent iron deficiency
      • ACD is the most common cause of anemia in hospitalized patients
      • After patients with bleeding, hemolysis, or known hematologic malignancy were excluded, 52% of anemic patients met laboratory criteria for the anemia of chronic disorders
      • ACD is observed in 27% of outpatients with rheumatoid arthritis and in 58% of new admissions to hospital rheumatology units
    • Disorders Associated with the Anemia of Chronic Disease ACD(1)
      • Chronic infections
      • - Pulmonary infections: abscesses, tuberculosis
      • - Subacute bacterial endocarditis
      • - Pelvic inflammatory disease
      • - Chronic urinary tract infections
      • - Chronic fungal disease
      • - HIV infections
      • - Osteomyelitis
      • Chronic, noninfectious inflammations
      • - Rheumatoid arthritis
      • - SLE (Systemic lupus erythematosus)
      • - Sever e trauma, thermal injury
      • - Vasculitis
    • Disorders Associated with the Anemia of Chronic Disease ACD(2)
      • Malignant diseases
      • - Solid c ancer s
      • - Hodgkin’s and Non-Hodgkin’s Lympmhomas
      • - Leukemias
      • - Multiple myeloma
      • Miscellanous
      • - Alcoholic liver disease
      • Idiopathic ACD
    • Anemia of chronic disease (ACD) -laboratory features(1)
      • The anemia is usually mild or moderate ( Hb 7-11g/dl)
      • - lower values are observed in 20-30% of patients
      • The anemia is most often normochromic and normocytic (MCHC and MCV are normal)
      • ESR - usually rapid
      • Reti c ulocytes - most often normal or slightly decreased number, increased count is rare
    • Anemia of chronic disease (ACD) -laboratory features(2)
      • Iron metabolism
      • 1. Serum Iron - decreased (it is necessary for the diagnosis of ACD)
      • 2. TIBC - reduced
      • 3 . Serum Ferritin-increased
      • 4 . Sideroblasts in the bone marrow-reduced (5-20%)
    • Anemia of chronic disease (ACD) -therapy (1)
      • 1. Treatment of the underlying disorder
      • 2. Iron supplementation (IS)
      • - ACD with chronic infection or malignancy IS should be strictly avoided
      • - IS benefit patients with ACD associated with auto-immune or rheumatic disorders.
      • - when ACD is complicated by iron deficiency (about 27% patients)
    • Anemia of chronic disease (ACD) -therapy (2)
      • 3. Transfusion demand (about 30% )patients who have low Hb and are symptomatic
      • 4. Recombinant erythropoietin 10.000 units 3 times a week i.v. or s.c. 2-3 doses, in the absence of response 20000 u , If there is still no respose, the treatment should be discontinued. (in 40% of patients it reduces number of transfusions)
      • 5. Iron chelation with deferoxamine - in some patients therapy was associated with a rise in hemoglobin level
      • 6. In future anti-TNF-antibodies
    • Aplastic and Hypoplastic Anemias What happens when the bone marrow shuts down?
    • Aplastic anemia
      • is a severe, life-threatening syndrome in which production of erythrocytes, WBCs, and platelets have failed.
      • may occur in all age groups and both genders.
      • is characterized by peripheral pancytopenia and accompanied by a hypocellular bone marrow.
    • Hypocellular bone marrow in aplastic anemia
    • Aplastic anemia
      • Pathophysiology :
        • The primary defect is a reduction in or depletion of hematopoietic precursor stem cells with decreased production of all cell lines.
          • This may be due to quantitative or qualitative damage to the pluripotential stem cell.
          • In rare instances it is the result of abnormal hormonal stimulation of stem cell proliferation
          • or the result of a defective bone marrow microenvironment
          • or from cellular or humoral immunosuppression of hematopoiesis .
    • Aplastic anemia
          • Etiology
            • Acquired
              • Most cases are idiopathic
              • Exposure to ionizing radiation. Whole body radiation of 300-500 rads can completely wipe out the bone marrow. With sublethal doses, the bone marrow eventually recovers.
              • Chemical agents – with a benzene ring, chemotherapeutic agents, and certain insecticides.
              • Idiosyncratic reactions to some commonly used drugs such as chloramphenicol or quinacrine.
    • Aplastic anemia
              • Infections – viral and bacterial infections such as infectious mononucleosis, infectious hepatitis, CMV, and miliary TB occasionally
              • Pregnancy (rare)
              • Paroxysmal nocturnal hemoglobinuria – this is a stem cell disease in which the membranes of RBCs, WBCs and platelets have an abnormality making them susceptible to complement- mediated lysis.
              • Other diseases – preleukemia and carcinoma
    • Aplastic anemia
            • Congenital disorders
              • Fanconi’s anemia – the disorder usually becomes symptomatic ~ 5 years of age. Congenital defects such as skin hyperpigmentation and short stature are also seen in affected individuals.
              • Familial aplastic anemia – a subset of Fanconi’s anemia in which the congenital defects are absent.
            • Clinical manifestations
              • Fatigue
              • Heart palpitations
              • Pallor
              • Infections
              • Petechiae
              • Mucosal bleeding
    • Aplastic anemia
            • Lab findings
              • Severe pancytopenia with relative lymphocytosis (lymphocytes live a long time)
              • Normochromic, normocytic RBCs (may be slightly macrocytic)
              • Mild to moderate anisocytosis and poikilocytosis
              • Decreased reticulocyte count
              • Hypocellular bone marrow with > 70% yellow marrow
    • Treatment
            • in untreated cases the prognosis is poor
              • Remove causative agent, if known
              • Multiple transfusions
              • Bone marrow transplant
              • Immunosuppression
    • Treatment of aplastic anemia
      • Supportive care: transfusion of leucocyte-depleted red cells and platelets given to prevent HLA alloimmunisation to minimise the risk of rejection of a BM transplant and to prevent febrile transfusion reactions
      • BM transplantation: is the treatment of choice for pts < 20 yrs of age who have an HLA-identical sibling is available. Patients over 45 yrs are not eligible for BMT whether an HLA-identical donor is available or not, because of the high risk of GVHD
    • treatment
      • Immunosuppression: used for patients older than 45 and those in whom BMT is not available. Anti-lymphocyte globulin ( ALG) and cyclosporin are used alone or in combination
    • prognosis
      • A bad prognosis ( i.e: severe aplastic anemia) is associated with presence 2 of the following:
      • Absolute neutrophil count < 500
      • Platelet count < 20000
      • Reticulocyte count of 40000/mm3