Transcript File - Shabeer Dawar

 Deficiency
of hemoglobin in the blood.
 Causes:
Too few RBCs.
 Too little hemoglobin in cells
 Decreased packed cell volume.
This may be due to:
 decreased production of RBCs.
 increased destruction.
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 Morphological
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1. normocytic normochromic anemia.
2. macrocytic normochromic anemia.
3. macrocytic hypochromic anemia.
4. Microcytic hypochromic anemia.
 Etiological
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classification.
classification.
1. hemorrhagic anemia.
2. hemolytic anemia.
3. nutritional deficiency anemia.
4. aplastic anemia.
5. anemia of chronic disease.
Depending upon size, color volume and number
of cells.
 1.Normocytic normochromic anemia:
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Size and colour are normal.
 Less in number.
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2. Macrocytic normochromic anemia:
Larger in size. Normal color.
 RBC count is less
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3. Macrocytic hypochromic anemia:
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Larger pale RBCs.
4. Microcytic hypochromic anemia:
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Smaller pale RBCs.
 Occurs
in both acute and chronic hemorrhagic
conditions.
 After acute hemorrhage:
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Plasma replaced in 24 hours.
Low concentration of RBCs.
RBC concentration return to normal in 4-6 weeks.
Less RBCs -> hemodilution.
Normochromic normocytic RBCs.
Hypoxia stimulates RBCs production.
 Chronic
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hemorrhage:
Loss of blood by internal/ external bleeding.
Enough iron can not be absorbed from intestines.
Small RBCs with little hemoglobin.
Microcytic hypochromic RBCs.
Fragile cells rupture easily while passing through
spleen and capillaries.
 Number of cells might be normal or greater than
normal but short life span.
 Destruction faster than formation.
 Classification:
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A. extrinsic hemolytic anemia.
B. intrinsic hemolytic anemia.
Types:
 Hereditary spherocytosis.
 Sickle cell anemia.
 Erythroblastosis fetalis.
 Thalassemia.
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 A:
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Destruction of RBCs by external factors.
Antibodies, chemicals and drugs.
Autoimmune hemolytic anemia.
Hereditary spherocytosis and Erythroblastosis
fetalis.
 B:
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Extrinsic hemolytic anemia.
Intrinsic hemolytic anemia.
Destruction due to defective RBCs.
Unhealthy short lived RBCs
Often inherited
E.g sickle cell anemia, thalassemia.
Cells are fragile and susceptible for hemolysis.
 Have
abnormal Hb S. with faulty beta chains.
 Inherited blood disorder.
 Exposure to low oxygen precipitates it into crystals.
 They elongate the cells into sickle.
 Damage cell membrane and cause serious anemia.
 In children, sickled cells block blood vessels and
cause infarction.
 Hand and foot syndrome.
 Sickle cell disease crisis:
 Low oxygen tension in tissues causes sickling
rupturing RBCs and further causing oxygen tension.
 Serious decrease in RBCs and eventually death.
 Inherited
disorder characterised by abnormal
hemoglobin.
 Types:
 Alpha thalassemia
 Beta thalassemia. (commom)
 Defective globin gene with imbalanced chains.
 Disturbed erythropoisis.
 Alpha
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Fetal life or infancy.
Alpha chains are less, absent or abnormal.
Children= gama chains excess.
Adults= beta chains are in excess.
Defective erythropoiesis and haemolysis.
Infants are stillborn or die immediately.
 Beta
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thalassemia:
thalassemia:
Beta chains are less, absent or abnormal.
Excess alpha chains.
Defective erythropoiesis and hemolysis.
 Small,
spherical cells lacking normal, loose
baglike cell membrane.
 Ruptured while passing through sphlenic pulp
and tight vascular beds.
 Rh-positive
RBCs of fetus attacked by Rhnegative antibodies of mother.
 Rh-positive cells become fragile and rupture
making child seriously anaemic.
 Substances
necessary for erythropoiesis are deficient.
 Iron, proteins, vitamins c and B12 and folic acid.
 Types:
 A: Protein deficiency anemia:
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Synthesis of hemoglobin is reduced.
Macrocytic hypochromic RBCs.
 B:
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Iron deficiency anemia.
Microcytic hypochromic RBCs.
Symptoms:
Brittle nails, atrophy of papillas in tongue and dysphagia.
 C:
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pernicious anemia/ Addison's disease
Deficiency of Vit B 12.
Atrophy of gastric mucosa due to autoimmune destruction of
parietal cells.
Decreased production of intrinsic factor and poor absorption
of Vit B12.
Macrocytic normochromic/ hypochromic RBCs.
Associated with Addison's disease or thyroid disorders.
 Symptoms:
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Paresthesia
Progressive weakness.
Ataxia.
Lemon yellow color of skin.
Red sore tongue.
Folic acid.
 Slow reproduction of erythroblasts in bone
marrow.
 Defective DNA synthesis.
 Large, odd shaped cells.
 Megaloblastic hypochromic RBCs.
 Neurological disorders are not present.
Bone marrow aplasia means lack of functioning
bone marrow.
 Bone marrow reduced and replaced by fatty
tissues.
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Gama ray radiation after nuclear blast can cause
complete destruction of bone marrow.
X-ray treatment.
Industrial chemicals.
Drugs.
Lethal anemia.
Tuberculosis.
Viral infections like hepatitis and HIV infections.
Normocytic normochromic RBCs.
 Second
most common type.
 Disturbed iron metabolism or resistance to
erythropoietin action.
 Develops after few months of sustained disease.
 Normocytic normochromic RBCs.
 Causes:
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Non infectious inflammatory diseases e.g rheumatoid
arthritis.
Tuberculosis.
Renal failure.
Neoplastic disorders.
 Viscosity
of blood falls to 1.5 times that of water
in severe anemia.
 Blood flow through the capillaries and heart
increases thus increasing cardiac output.
 Hypoxia due to diminished transport of oxygen
causes dilation of peripheral vessels.
 Increase in blood return to heart and cardiac
output and increased pumping workload on heart.
 Increased cardiac output overcomes reduced
oxygen supply.
 Exercise-> extreme hypoxia -> acute cardiac
failure.
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Skin and mucous membrane.
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Cardiovascular system.
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Albuminuria.
Reproductive system
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Rate is increased.
Kidney
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Anorexia, nausea, vomiting, abnormal discomfort, constipation.
Metabolism
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Increased ratee and flow of respiration.SOB and dyspnea.
Digestion
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Tachcardia, heart is hypertrophied,velocity of blood flow is increased.
Respiration.
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Pale thin and dry skin. Early greyness of hair. Brittle easily breakable
nails.
Menstural cycle s distured.
Neuromuscular system.
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Increased sensitivity to cold, headache, lack of concentration,
Restlessness, irritability, dizziness and vertigo. Weakness and fatigue