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Anaemia Tachypnea

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					Hematopoiesis Development
Sites of hematopoiesis
First Trimester - Yolk Sac
 Second Trimester -Liver and Spleen
Third Trimester - Central, Peripheral Skeleton
 Adulthood - Axial Skeleton , Vertebral Bodies ,
Sternum Ribs Pelvis
Hematopoiesis may re-xpand into fetal sites in
times of severe demand,
   e.g. thalassemia
Anemia :
Decrease in Hgb.
Decrease in rbc
decrease in hct
                    ANEMIA
                      Causes
* Blood loss
* Decreased production of red blood cells (Marrow
failure)

* Increased destruction of red blood cells
Hemolysis

* Distinguished by reticulocyte count
    Decreased in states of decreased production
     Increased in destruction of red blood cells
     Clinical picture of anemia

Symptoms of anemia
* pallor, fatigue, lethargy, dizziness, and
  anorexia.
 * Jaundice and, occasionally, dark urine
  may be present with significant hemolysis.
* Failure to thrive indicates a long-
standing condition
Physical signs :
 * tachycardia, tachypnea
 * pallor, jaundice, edema, and signs of
bleeding
 *systolic ejection murmur
 *signs of CHF (eg, tachycardia, gallop
rhythm, tachypnea, cardiomegaly,
hepatomegaly).
 *Splenomegaly
 *dysmorphic features and other
congenital anomalies
Different ways to classify anemias

* Size and hemoglobin content of rbc
* Mechanism of its production
    Classification according to
            mechanism
1- Blood loss acute and chronic
2- Excessive destruction of rbcs
3- Decreased production of rbcs
decreased red cell production
 1- Marrow failure
       *Diamond-Blackfan anemia
     * Aplastic crisis
     * Aplastic anemia

 2- Impaired erythropoietin production
     * Anemia of chronic disease in renal failure
      *Chronic inflammatory diseases
     *Hypothyroidism
    *Severe protein malnutrition

 3- Defect in red cell maturation
     *Nutritional anemia secondary to iron, folate, or vitamin B-12
deficiency
     * Sideroblastic anemias
   increased red cell destruction
            (hemolysis)
o**Intracellular causes :
1-Red cell membrane defects (eg, hereditary
spherocytosis, elliptocytosis)
o2-Enzyme defects (eg, G-6-PD deficiency, pyruvate
kinase deficiency)
3-Hemoglobinopathies (sickle cell , Thalassemias )

**Extracellular causes
1-Antibodies (autoimmune hemolytic anemia)
2-Infections, drugs, toxins
 3-Thermal injury to red blood cells (with severe burns)
4-Mechanical injury (hemolytic-uremic syndrome,
cardiac valvular defects)
Laboratory diagnosis of anemia
*CBC, reticulocyte count, and review of the peripheral
smear
*Bilirubin level, lactate dehydrogenase (LDH)
(hemolytic anemia)
*Direct antiglobulin or Coombs test (autoimmune
hemolytic anemia)
*Hemoglobin electrophoresis (hemoglobinopathies)
*Red cell enzyme studies (eg, G-6-PD, pyruvate kinase)
*Osmotic fragility (spherocytosis)
*Iron, TIBC, ferritin (iron deficiency anemia)
*Folate, vitamin B-12
(macrocytic/megaloblastic anemia)
*Bone marrow aspiration and biopsy
*Viral titers (eg, Epstein-Barr virus,
cytomegalovirus)
*BUN/creatinine levels to assess renal
function
*Thyroxine (T4)/thyroid-stimulating hormone
(TSH) to rule out hypothyroidism
         Treatment of anemia
1- Transfusion with packed RBCs (PRBC) is the
universal treatment

2-Medications for specific forms of anemia (eg,
corticosteroids for autoimmune hemolytic
anemia, iron therapy for iron deficiency anemia).

3-Recombinant erythropoietin (renal failure),
chemotherapy , prematurity )
•
         Hemolytic anemias

Hemolytic anemia is a disorder in which the
red blood cells are destroyed faster than
.the bone marrow can produce them
Clinical Features:

   Pallor
  Jaundice
   Splenomegaly
   No bile in urine
  Pigment gall stones – in chronic forms
  Crisis – aplastic, hemolytic, vascular
  Ankle ulcers
   Clinical
Features of
Sickle Cell
  Disease
Clinical picture of thalassemia
         Laboratory Evaluation:
Features of RBC breakdown:
   Hyperbilirubinemia
   Increased Urine UBG & Faecal stercobilinogen.
   Low or absent Haptoglobins
   Haemoglobinaemia, Haemoglobinuria, Haemosiderinuria
   Methhaemalbuminaemia
Features of increased RBC Production:
    Reticulocytosis
    Marrow erythroid hyperplasia – bone changes
Specific tests
   Morphology, Osmotic Fragility,coomb”s test
   Decreased RBC survival – 51Cr labelling.
   Hemoglobin electrophoresis, enzyme abnormality
    Treatment for hemolytic
           anemia
*blood transfusions
*corticosteroid medications
*surgical removal of the spleen
*immunosuppressive therapy
*Iron chelation therapy
     Structure & Synthesis of Haemoglobin:

Hb in adult     Hb A     Hb F      Hb A2

Structure       α2 ß 2    α2 γ2    α2δ2

Normal %         96-98   0.5-0.8   .5-3.2
Nutritional anemia
Nutritional anemia
*Iron deficiency
*Vit. B12 and folate deficiencies
*Vitamin-deficiency (vit.A, vit. B group, vit. C/scurvy,
vit.E)
*Mineral deficiencies other than iron (copper and zinc)
*Starvation (anorexia, war prisoners, conscientious
objector)
*Kwashiorkor (protein deficiency)
*Alcoholism in adolescent
     Mechanism of Nutritional
           Anaemias
Impaired dietary intake
   I intake or delivery to small intestine
Maldigestion
   inability to digest macronutrients
Malabsorption
  impaired nutrient transport across intestinal mucosa
Impaired metabolism
  altered metabolism of energy and nutrients
Nutrient excretion
  excessive loss of nutrients
Increased requirements
Iron Deficiency
    Anemia
Causes of Iron deficiency Anemia:
1-Iron store depletion
Inadequate intake-Rapid Growth- Blood
donation
 2-Abnormal Iron looses
menses in childbearing age women, iron
transfer to the fetus during pregnancy,
hookworm infestation or intake of
aspirin or other anti-inflammatory drug
Infants at High Risk for Iron Deficiency

•   Low birth weight
•   Perinatal bleeding
•   Low hemoglobin at birth
•   High growth rate
•   Low socioeconomic status
•   Chronic hypoxia- high altitude
•   Frequent infections
•   Early cow milk +/- solid food intake
•   Frequent tea intake
•   Low meat, Vit C intake
                 Clinical Presentation
Asymptomatic
Pallor
• Irritability, exercise intolerance,
  fatigue, and tachycardia
• Koilonychia
•  In severe Fe-deficient patients,
  fingernails become brittle and
  ridged, and eventually "spoon-
  shaped" or concave.
•Tongue may atropy("glossitis")
•Impaired neuromuscular response
(total exercise time and maximum
workload are all affected adversely).
•Behavioral studies report irritable,
disruptive, have short-attention
spans, and lack interest in their
surroundings.
Laboratory investigations

• Low hematocrit and hemoglobin
• Small red blood cells
• Low serum ferritin
• Low serum iron level
• High iron binding capacity (TIBC) in
  the blood
• Blood in stool (visible or microscopic)
Prevention of Iron Deficiency

*Improve Dietary intake of iron
*Breast feed to 1 yr (at least)
*Iron-fortified formula to 1 yr (if not
BF)
*No solid foods before 6 mo
*No cow's milk or tea before 1 yr
5- two months usually need to achieve
normal Hb and then 2 more months of
therapy for replenishing stores
6-maintenance afterwards if indicated at
2mg/kg/d
7-IM and IV iron ( iron dextran) available
but rarely indicated
8-Transfusion: rarely needed and if so
give slowly and small amount with
diuretic to avoid added strain to heart
  Treatment of iron deficiency
           Anemia
*-encourage iron rich foods and vit C
*-start iron therapy at 4-6 mg/kg/d 3-using
the ferrous sulfate ( fer in sol)
preferably ( up to 200mg/d max) or
ferrous gluconate
*-check retic count at 1 week and Hb at 2-
3 weeks ( should be reaching midway
level)
Megaloblastic
  Anemia
   Causes of Megaloblastic
          Anemia

        Vitamin B12 Deficiency:
*inadequate B12 intake
*malabsorption from the gut
*intestinal disease (fish tapeworms or
inflammation)
*lack of intrinsic factor or its receptor
*transcobalamin II (TCII) deficiency
       Folate Deficiency:
*inadequate folate intake
*increased folate loss of need
*malabsorption from the gut
*defective intracellular metabolism
(inherited defects)
*antimetabolites used in chemotherapy
Clinical Data
*Some patients can have GI symptoms –
such as loss of appetite, weight loss,
nausea, and constipation.
*Patients may have a sore tongue and –
canker sores.
*Patients may have symptoms of anemia. –
*Early neurological symptoms include –
paresthesias in the feet and fingers, poor
gait, and memory loss.
*At later stages, patients can have severe –
disturbances in gait, loss of position
sense, blindness due to optic atrophy, and
psychiatric disturbances. In some patients,
neurological impairment can occur without
anemia.
     Laboratory diagnosis
• Complete blood count (shows anemia with
  large red blood cells)
• Bone marrow examination
• Serum B-12
• Schilling test (may identify poor
  absorption as cause of vitamin B-12
  deficiency)
• Serum folate
  Treatment of Megaloblastic
          Anemias

•Due to folic acid deficiency
  --oral folate (5 mg per day for 4 months)
•Due to vitamin B12 deficiency
--parenteral (by shot NOT in ingestion)
  vitamin B12 (6 doses of 100 µg of vitamin
  B12 over a period of 2-3 weeks
  --pernicious anemia treatment is life-long
  administration of vitamin B12
Aplastic anemia
Defenition :
• aplastic anemia is a failure of the bone marrow
  to cells. Cells.properly form all types of blood

Causes :
• 70 % of aplastic anemia cases are idiopathic,
  but other known causes are :
 **Hereditary:
• Fanconi anemia
• Dyskeratosis congenital
• Schwachman-Diamond syndrome
• Amegakaryocytic thrombocytopenia
    **Acquired:
1-Direct stem cell destruction
2-Drugs (Chemotherapy-Chloramphenicol -
Sulfonamides - Phenytoin )
3-Toxic chemicals (Benzene – Toluene –
Insecticides)
4-Infection (viral hepatitis)
5-Immune disorders
6-Collagen vascular diseases (Systemic Lupus
Erythematosus )
7-Radiation therapy
          Clinical features

*Anemia: fatigue and pallor
*Thrombocytopenia: unexplained or
excessive bleeding, easy bruising
*Neutropenia: fever, mucosal ulcerations,
bacterial infection
    Clinical features of Fanconi
               anemia
- Short stature
- Anomalies of the thumb and arm
- skeletal abnormalities (hip abnormalities, spinal
malformations, scoliosis )
- Abnormalities of the gastrointestinal tract ,kidney
  and heart.
- Skin discoloration
- Small head or eyes
- Mental retardation
Laboratory diagnosis:

1- Complete blood count shows anemia,
decreased white blood cell count,
decreased platelets , low reticulocytic
counts.
2-Bone marrow biopsy shows few blood
3-Chromosome breakage and other tests
  for fanconi anemia
Treatment:
1- Transfusions(red blood and platelet
transfusions).
2- immunosuppressive drugs
    *antilymphocyte globulin (ALG)
    *cyclosporine
    *G-CSF & GM-CSF (stimulate white
   blood cell production)
    *Androgens
  3- Bone Marrow Transplantation
    MORPHOLOGICAL
CLASSIFICATION OF ANEMIA
      IN CHILDREN
   **Microcytic hypochromic
           anemia
    1-Iron deficiency
     2- Thalassemia syndrome
    3-Anemia of chronic infection and
inflammations
    4-Sideroblastic anemias
    5-Lead poisoning
  Normocytic, Normochromic
          anemia
 i) Post-hemorrhage - early stage
 ii) Hemolytic anemia,
 iii) IDA - early stage,
iv) Systemic diseases like endocrinal, renal
and hepatic diseases
 v) Bone marrow disorders like hypoplastic
anemia, myeloinfiltration,
dyserythropoiesis, myelodysplasia and
masked megaloblastosis.
       Macrocytic anemia
**Non-megaloblastic anemia like:
  Hemolytic anemia, Liver disorder,
obstructive jaundice , Post splenectomy,
Bone marrow disorders like hypoplastic
anemia , dyserythropoietic anemia
**Megaloblastic anemias like:
  Folate deficiency, B12 deficiency,
Congenital disorders of DNA synthesis like
Orotic aciduria

				
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