Anemia

1. RATHEESH R.L

2.  Deficiency in the number of erythrocytes(RBC),
the quantity of hemoglobin and/or the volume
of packed RBCs

3.  Etiologic (underlying cause)
 Morphologic (cellular characteristic)
 Classification based on signs and symptoms

4.  Decreased erythrocyte production
 Blood loss
 Increased erythrocyte destruction

5.  Decreased hemoglobin synthesis
* Iron deficiency
* Thalassemia(decreased globin synthesis)
 Defective DNA synthesis
* Cobalamin deficiency
* Folic acid deficiency
 Decreased number of erythrocyte precursors
* Aplastic anemia
* Anemia of myeloproliferative
diseases(leukemia)

6.  Acute
* Trauma
* Blood vessel rupture
 Chronic
* Gastritis
* Hemorrhoids
* Menstrual flow

7.  Abnormal hemoglobin( Sickle cell anemia)
 Infectious agents
 Physical trauma

8.  Normocytic normochromic
 Macrocytic normochromic
 Microcytic hypochromic

9.  Mild
 Moderate
 severe

10.  Normal size and colour
 Causes include acute blood loss, chronic
kidney disease, aplastic anemia, sickle cell
anemia

11.  Large size normal colour
 Causes include cobalamin deficiency, folic
acid deficiency, liver disease, post
splenectomy

12.  Small size pale colour
 Causes include iron deficiency anemia,
Thalassemia

13.  Mild(Hb- 10-14gm/dl)
* cardiovascular: palpitations
* Pulmonary : Exertional dyspnea
 Moderate (Hb- 6- 10 gm/dl)
* Cardiovascular: Increased palpitations
* Pulmonary: Dyspnea
* General: Fatigue

14.  Severe(Hb- less than 6gm/dl)
* Integumentary: Pallor, pruitus
* Eyes: Icteric conjuctiva and sclera,
blurred vision
* Mouth: Glossitis, Smooth tongue
* Cardiovascular: Tachycardia,
increased pulse pressure, murmurs
* Pulmonary: tachypnea, orthopnea,
dyspnea at rest

15. * Neurologic: Headache, Vertigo,
irritability, depression, impaired thought
process
* Gastro intestinal: Anorexia,
hepatomegaly, splenomegaly, difficulty in
swallowing, sore mouth
* Musculo skeletal: Bone pain
* General : sensitivity to cold, weight loss
and lethargy

16.  Decreased Hb synthesis Iron deficiency anemia,
Thalassemia
 Defective DNA synthesis in RBC megaloblastic
anemia
 Diminished availability of erythrocyte precursors
Aplastic anemia, anemia of chronic disease

18.  Normal iron metabolism
 Obtained from food and dietary supplements
 Ingested iron absorbed in the duodenum and
upper jejunum
 Iron present in all RBC as heme in
hemoglobin and in a stored form(ferritin and
hemosiderin) in the bone marrow, spleen,
liver and macrophages

19.  Male 1 mg
 Adolesc. 2-3 mg
 Women in repr.age 2-3 mg
 Pregnant 3-4 mg

20.  Small loss of iron each day in urine, faeces, skin
and in menstruating females as blood (1-2 mg
daily)
 Normal diet contains about 15 mg of
iron/day
 6mg elemental iron/1000 cal
 1/10 of ingested iron is absorbed
 Gastric acid releases iron from food

21.  Iron deficiency anemia is defined as anemia
associated with either inadequate absorption
or excessive loss of iron from the body.

22.  Inadequate dietary intake
 Malabsorption
* After certain types of gastro intestinal
surgery(removal of bypass of duodenum)
* Malabsorption syndromes(diesases of the
duodenum)

23.  Blood loss
* sources of chronic blood loss are from GI
and GU systems
* Causes of GI blood loss – peptic ulcer,
gastritis, esophagitis, hemorrhoids and
neoplasms
* causes of GU blood loss – menstrual
bleeding
* At the time of delivery and lactation

24.  Pregnancy
- Diversion of iron to the fetus for
erythropoiesis
 Dialysis treatment
- blood lost in the dialysis equipment and
frequent blood sampling

25.  Fatigability
 Dizziness
 Headache
 Irritability
 palpitation
 Glossitis
 Stomatitis
 Dry pale skin
 Spoon shaped nails, koilonychia
 Hair loss
 Splenomegaly

26.  Hb,Hct,RBC:Low
 Plt:Normal/Low/High
 WBC:Normal/Low
 S iron: Decreased

27.  History collection and physical examination
 Stool routine: to identify the presence of
blood
 Endoscopy or colonoscopy: used to detect GI
bleeding

28.  Replace iron and folic acid and treat
underlying disease.
 Oral route is preferred for replacement.
 Intake of liver and muscle meats, eggs, dried
fruits, legumes, dark green leafy vegetables,
bread and cereals and potatoes
 If iron deficiency from acute blood loss require
transfusion of packed RBC

29.  Response can be followed by retic.
increase in 1-2 weeks (5-7 days)
 Hb response to treatment
 half normal by a month
 returns to normal by 2-4 months
 Replacement therapy is prolonged by 6-12
months to replenish stores of iron.
 Ongoing bleeding may cause indefinite
therapy.

30. DRUG THERAPY
 Oral iron is usually prescribed
 Total daily dose:150-200 mg elemental iron
 Give in 3-4 divided doses(each tablet contains 50
to100mg of iron)
 Each one hour before meals.
 Taking iron with Vit C enhances iron
absorbtion

31.  Undiluted liquid iron may stain patients
teeth, therefore diluted and ingested
through a straw
 Iron preparations cause the stools to become
black(GI tract excretes excess iron)
 Constipation is common, therefore started on
stool softeners

32.  Parenteral iron therapy:
Indications
 Malabsorbtion
 Intolerance to oral replacement
 Colitis/enteritis
 Needs in excess of amount that can be given
orally
 Patient uncooperative/poor compliance
 Hemodialysis

33. Parenteral iron therapy:
 Given intramuscularly or intravenously
 Iron dextran complex contains 50mg/ml of
elemental iron in 2ml
 Test dose of parenteral iron is often done to
assess for allergic reaction
 Given deep IM in the outer quadrant of the
buttocks with a 18 to 20 gauze needle

34.  Group of diseases that have an autosomal
recessive genetic basis involving inadequate
production of normal hemoglobin
 Normal hemoglobin is composed of 2 alpha and 2
beta globins
 Mutations in a given globin gene can cause a
decrease in production of that globin, resulting
in deficiency
 Absence of alpha globin chain alpha
thalassemia
 Absence of beta globin chain beta thalassemia

35.  Growth both physical and mental is retarded
Person with thalassemia major is pale and
displays other symptoms of anemia( Inadequate
production + ineffective erythropoiesis + haemolysis
Anaemia)
 Symptoms develop in childhood by 2 years of age
 Pronounced hepatosplenomegaly
(↑Haemolysis ↑demands of phagocytic function
 hyperplasia of phagocytes 
Hepatosplenomegaly )

36.  To compensate anaemia extramedullary
haemopoiesis in liver, spleen & brain
Organomegaly
 ↑Erythropoiesis marrow expansion & thinning of
cortex of skull bone Thalassaemia facies
 Jaundice from RBC hemolysis

37.  Hb concentration – Decreased
 ESR – Mild increase
 RBC count – Markedly decreased
 Reticulocyte count – Increased

38.  Thalassemia minor requires no treatment
 Treatment of thassemia major includes
 Chronic Transfusion Therapy
 Maximizes growth and development
 Suppresses the patient’s own ineffective
erythropoiesis and excessive dietary iron absorption
 RBC transfusions often monthly to maintain Hgb 10-
12

39.  Chelation Therapy
 Binds free iron and reduces hemosiderin
deposits
 8-hour subcutaneous infusion of deferoxamine,
5 nights/week
 Start after 1year of chronic transfusions
 Splenectomy--indications
 Trasfusion requirements increase 50% in
6months
 Severe leukopenia or thrombocytopenia

41.  Group of disorders caused by impaired DNA
synthesis and characterized by the presence of
large RBC
 Impaired DNA synthesis defective RBC
maturation
 Large (macrocytic) and abnormal RBC
megaloblasts

42.  Result from cobalamin (Vit B12) and folic
acid deficiencies
 Supression of DNA synthesis by
* drugs
* inborn errors of cobalamin and folic
acid metabolism
* erythroleukemia( malignanat blood
disorder characterized by proliferation of
erythropoietic cells in bone marrow)

43.  Vitamin B12
 Sources : Meat, fish
 Daily requirement : 2-5 micro gram
 Body stores : 3-5 mg( liver)
 Places of absorption: distal ileum

45. 1.Malabsorption
a) Inadequate production of intrinsic factor
- pernicious anemia
- gastrectomy, partial or total
b) Inadequate releasing vit. B12 from food
(partial gastrectomy, abnormality of
stomach function, chronic pancreatic
insufficiency)

46. c) Terminal ileum disease (celiac disease, ileal
resection, Crohn disease)
d) Competition for intestinal B12 :
- bacterial overgrowth: jejunal diverticula,
intestinal stasis and obstruction due to strictures
- Fish tapeworm

47. 2. Inadequate intake
- vegetarians
3. Inadequate utilisation
Drugs: Neomycin, Colchicin, Nitrous oxide ,long
term use of H2 receptor blockers

48.  Atrophic glossitis (shiny tongue)
 Abnormal gait
 Anemia related manifestations
 Personality changes
 Anorexia
 Nausea, vomiting
 Abdominal pain

49. Neurologic manifestations
 Paresthesias
 Memory loss
 Numbness
 Weakness
 Symmetric neuropathy legs>arms
 Severe weakness, spasticity, paraplegia and
incontinence
 Subacute combined degeneration of the dorsal
(posterior) and lateral spinal columns

50. 1. Blood cell count:
macrocytic anemia
Thrombocytopenia
leucopenia (granulocytopenia)
low reticulocyte count
2. Blood smear:
Hypersegmentation of granulocytes

51. 3. Bone marrow smear
Hypercellular
Erythroid cell changes (megaloblasts,
RBC precursor a abnormally large with
nuclear- cytoplasmic asynchrony)
Megakaryocytes are decreased and show
abnormal morphology

52.  If the patient has
dietary deficiency
of cobalamin
dietary sources
rich in cobalamin
should be provided

53. 1. Vitamin B12 administration intramuscular in dose
1000 μg per day for a week , then 100 μg 2x per
week for 2 weeks, 1 x per week 100μg for month
2. Reticulocytosis begins 2 or 3 days after therapy
started and maximal number reached on day 5 to 8.
* Serum iron monitoring, after 7-10 days of vit.B12
treatment,
* if Fe deficiency is diagnosed, start iron
substitution
3. 100 ug vit.B12 i.m. every month, regimen that must
be mainted for the rest on the patients life.

54.  Folic acid deficiency Megaloblastic
anemia
 Folic acid is required for DNA synthesis,
leading to RBC formation and maturation

55. Sources : Green vegetables, yeast
Daily requirement :50-100 ug
Body stores :10-12mg (liver)
Places of absorption : duodenum and proxymal
segment of small intestine

56. 1. Inadequate intake
- diet lacking leafy green vegetables, liver,
citrus fruits, dried beans, nuts and grains;
chronic alcoholism, total parenteral nutrition
2. Malabsorption
- small bowel disease ( celiac disease)
- alcoholism

57. 3. Increased requirements:
- pregnancy and lactation
- infancy
- chronic hemolysis
- malignancy
- hemodialysis
4. Defective utilisation
Drugs:folate antagonists(methotrexate,
trimethoprim), purine analogs (azathioprine),
primidine analogs (zidovudine), RNA reductase
inhibitor (hydroxyurea), miscellaneous
(phenytoin)

58.  Clinical features similar to those of
cobalamin deficiency
 GI disturbances include dyspepsia and a
smooth red tongue
 Absence of neurologic problem

59.  Hemoglobin – Decreased
 S. Folate level - Low

60.  Treated by replacement therapy
1. Oral administration of folate 1 (5) mg per
day, for 3 months, and maintance therapy if
it’s necessary.
2. Reticulocytosis after 5-7 days
3. Correction of anemia is over after 1-2
months of therapy

61.  Eat foods
containing large
amounts of folic
acid

63.  Chronic inflammatory, autoimmune,
infectious, or malignant diseases can lead to
anemia and it is known as anemia of chronic
disease
 Associated with under production of RBC and
shortening of RBC survival

64. Chronic conditions leading to anemia
 Renal diseases
 Autoimmune hemolysis
 Chemotherapy and radiation therapy
 Infections
 Hypopitutirism & Hypothyroidism

65.  Findings of elevated serum ferritin and
increased iron stores distinguish it from iron
deficiency anemia.
 Normal folate and cobalamin blood levels
distinguish it from those types of anemias.

66.  Correction of the underlying disorder
 Blood transfusions
 Erythropoetin therapy(Epogen, Procit)

67.  Rare disease caused by a decrease in or
damage to marrow stem cells, damage to
the microenvironment within the marrow,
and replacement of the marrow with fat.
It results in bone marrow aplasia
(markedly reduced hematopoiesis).

68.  Characterized by peripheral blood
pancytopenia( decrease of all blood types-
RBCs, white blood cells and platelets)

69. Congenital causes
 Fanconi syndrome( disease of the proximal renal
tubules in which glucose, uric acid and amino acids
are not absorbed properly)
 Congenital dyskeratosis( abnormal pigmentation of
the skin will occur)
 Amegakaryocytic thrombocytopenia( it’s a
hematological disease characterized by severe
thrombocytopenia due to altered immunological
status)

70. Acquired causes
 Exposure to ionizing radiation
 Chemotherapy
 Chemical agents( benzene, arsenic, alcohol)
 Viral and bacterial infections
 Medications( Anti seizure agents, anti
microbials)

71.  General manifestations of anemia( fatigue,
dyspnea along with cardiovascular and
neurologic responses)
 Patient with neutropenia susceptible to
infection and may be febrile
 Thrombocytopenia is manifested by a
predisposition to bleeding( petechiae,
epistaxis)

72.  Decreased Hb, WBC, and platelet values
 Normocytic, normochromic anemia.
 Low reticulocyte count.
 Prolonged Bleeding time .
 Elevated serum iron and total iron-binding
capacity (TIBC)
 Bone marrow biopsy - hypocellular with
increased yellow marrow (fat content).

73.  Identify and remove the causative agent
 Hematopoietic stem cell transplant and
immuno suppressive therapy with anti
thymocyte globulin(ATG) and cyclosporine or
high dose cyclo phosphamide

75.  Acute blood loss
 Chronic blood loss

76.  Trauma
 Complications of surgery
 Conditions or diseases that disrupt vascular
integrity.

77. Volume lost 10 %
None
Volume lost20%
No detectable signs or symptoms at rest,
tachycardia with exercise and slight
postural hypotension
Volume lost30%
Normal supine blood pressure and pulse rate at
rest ,postural hypotension and tachycardia with
exercise.

78. Volume lost 40%
Blood pressure,central venous pressure,and
cardiac output below normal at rest,
rapid,thread pulse and cold clamy skin.
Volume lost 50%
Shock and potential death

79.  Alert to patients expression of pain
 Internal hemorrhage cause pain
 Retro peritoneal bleed- may not experience
abdominal pain

80.  IV fluids - dextran, hetastarch, albumin, and/or
crystalloid electrolyte solutions such as lactated
Ringer's.
 Blood transfusions (packed RBCs) may be
needed if the blood loss is significant.
 If the bleeding is related to a platelet or
clotting disorder, replacement of that deficiency
is addressed.
 supplemental iron

81.  Bleeding ulcer
 Hemorrhoids
 menstrual and postmenopausal blood loss
etc.

82.  Condition caused by destruction or hemolyis
of RBCs at a rate that exceeds production.
 Occur because of problems intrinsic or
extrinsic to the RBC

83.  Intrinsic hemolytic anemia( heriditary)
*Abnormal hemoglobin
Sickle cell anemia
Thalassemia
*Red blood cell membrane abnormality
Heriditory spherocytosis
*Enzyme deficiencies
G6 PD deficiency

84.  Extrinsic hemolytic anemia( Acquired)
* damage is caused by external factors
such as trapping of cells within the sinuses of
the liver or spleen
* Antibody mediated destruction(Auto
immune hemolytic anemia)

85.  General symptoms of anemia
 Jaundice
 Enlarged liver and spleen

86.  Focus of treatment is to maintain renal
function

87.  Group of inherited, autosomal
recessive disorders characterized
by the presence of an abnormal
form of Hb in the erythrocyte.
 This abnormal Hb, hemoglobin S (Hb S),
causes the erythrocyte to stiffen and
elongate taking on a sickle shape in response
to low oxygen levels.

88.  Sickle cell anemia
 Sickle cell thalassemia
 Sickle cell Hb C disease
 Sickle cell trait

89.  Occurs when is homozygous for hemoglobin
S; the person has inherited Hb S from both
parents

90.  Occurs when a person inherits Hb S from one
parent and another type of abnormal
hemoglobin( thalassemia or Hb C) from other
parent

91.  Occurs when a person is heterozygous for Hb
S; the person inherits hemoglobin S from one
parent and normal hemoglobin(Hb A) from
another parent

92.  Triggered by low oxygen tension in the blood
 Hypoxia can be caused by
* viral or bacterial infection
* high altitude
* emotional or physical stress
* blood loss

93. Sickled RBC become rigid and take an
elongated cresent shape
Cannot easily pass through capillaries
Cause vascular occlusion
Acute or chronic tissue injury

95. Blood flow is impaired by sickled cells
Vasospasm occurs
Severe capillary hypoxia
Changes in membrane permeability
Plasma loss
Hemo-concentration and development of thrombi
Further circulatory stagnation

96.  Tissue ischemia, infarction and necrosis
occurs from lack of oxygen
 Shock can occur (life threatening consequence)

97.  Features of anemia( pallor of mucous
membranes, decreased exercise tolerance)
 Jaundice
 Primary symptom associated with sickling is
pain
- pain is severe
- affect an area of the body with the
back, chest, extremities and abdomen being
mostly affected

98.  Damaged vision: The sickled blood
cells, often clog the blood vessels that
connect to the retina, causing optical
damage.
 Limited Growth: The scarcity of
oxygen caused by sickle-cell anemia is
detrimental to healthy human growth.

99.  Peripheral blood smear
 Sickling test
 Electrophoresis of hemoglobin
 Jaundice
 Skeletal X- rays
 MRI scan
 Doppler studies

100.  Infections
 Pulmonary complications
Pneumonia
Acute chest syndrome
Pulmonary hypertension
 Cardiac complications
MI
HF
corpulmonale.

101.  Ophthalmic complications
Retinal vessel obstruction may result in
Hemorrhage
Scarring
retinal detachment
blindness.
 Renal complications
Renal failure.
 Neurologic complications
Stroke

102.  Musculoskeletal complications
Osteoporosis
Osteosclerosis
 Integumentory system complications
Chronic leg ulcers
 Genitourinary system complications
Priapism

103.  No specific treatment for the disease
 Focus on alleviating the symptoms and
minimizing end organ damage
 Instruct to avoid high altitude, maintain
adequate fluid intake and treat infections
promptly
 Chronic leg ulcers treated with bed rest,
antibiotics, warm saline soak, mechanical
debridement and grafting

104.  Oxygen administration
 Fluid administration
 Transfusion therapy
 Pain management
 Acute chest syndrome treated with broad
spectrum antibiotics, oxygen therapy and fluid
therapy
 Antisickling agents(Hydroxy urea)

105.  Hematopoietic stem cell transplantation
* Allogenic
* Syngenic
* Autologous

106.  High risk of infection related to an inadequate
secondary defenses (decreased hemoglobin
leucopenia, or a decrease in granulocytes
(inflammatory response depressed).
 Imbalanced nutrition less than body requirement
related to failure to digest or inability to digest the
food / nutrient absorption necessary for the
formation of red blood cells

107.  Activity intolerance related to imbalance
between oxygen supply (delivery) and
demand.
 Altered tissue perfusion related to decreased
cellular components required for the delivery
of oxygen / nutrients to the cells
 High risk of damage to skin integrity related
to circulatory and neurological changes

108.  Constipation or diarrhea related to
decreased dietary inputs; changes in the
digestive process; the side effects of drug
therapy.
 knowledge in relation to the lack of exposure
/ recall; incorrect interpretation of
information; do not know the source of
information