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ANEMIA

Decrease in the level of Hemoglobin or RBC coount


General signs and symptoms:

Weakness and fatigue


Pale skin
Cold hand and feet
headache, lightheadedness, dizziness
Dyspnea

Microcytic Anemia Normocytic Anemia Macrocytic Anemia


MCV<80 fl MCV: 80-100 fl MCV: >100 fl

Hemolytic -↑ bilirubin
Ferriin ↓ Ferritin: Normal/↑ Ferritin ↑ Ferritin ↑ Ferritin Normal Non-hemolytic Reticulocyte Vitamin B12 deficiency or Vitamin B12 Normal
(Peripheral -↑ LDH
TIBC ↑ Iron: Normal/↑ TIBC ↓ TIBC ↓ TIBC Normal (Underproduction ) low count High folate deficiency Folate Normal
Serum Iron ↓ Serum Iron ↓ Serum Iron ↑ Serum Iron Normal destruction ) -↓ Haptoglobin
TIBC: Normal
Serum Lead>10mcg/dl
zinc protoporphyrin ↑ Megaloblastic Anemia Non-Megaloblastic Anemia
Intravascular Extravascular

Decreased DNA synthesis—>Impaired red cell


Iron Chronic Sideroblastic Lead Aplastic Paroxysmal nocturnal G6PD Autoimmune Sickle cell production or to a lesser degree destruction occurs Macrocytic anemia with no
Thalassemia Hereditary Hemglobin C in the bone marrow prior to release of mature DNA impairment
deficiency diseases anemia poisoning anemia hemoglobinuria deficiency hemolytic anemia
spherocytosis erythrocytes into the peripheral blood
anemia
Decreased production of
most common type of globin chains of hemoglobin.
This is the only hemolytic Vitamin B12 Myelodysplastic Diamond-
anemia, and it occurs when Iron being trapped in bone Anemia in which bone An acquired mutation X-linked recessive disorder Autosomal recessive mutation in Folate deficiency Liver dysfunction Alcoholism Hypothyroidism
your body doesn’t have anemia that is microcytic.
marrow macrophages, leading marrow produces
Anemia due to lead poisining Failure or damage to
leading to loss of CD55/59 resulting in reduced half-life Antibody-mediated (IgG or
Inherited defect of RBC the beta chain of hemoglobin Autosomal recessive mutation in deficiency Syndrome (MDS) blackfan anemia
enough of the mineral iron. that results from inhibition of hematopoietic stem cells cytoskeleton membrane A single aminoacid change => beta chain
to decreased utilization of sideroblasts instead of on RBC membrane of G6PD IgM) destruction of RBCs.
heme synthesis resulting in pancytopenia. tethering protein glutamate-> valine Glutamic acid -> lysine
endogenous iron stores healthy RBCs
-Severe dietary deprivation - Genetic factors predisposing HSCs to
-Pregnancy
- Macrocytosis occur due increased
- Lead inhibits enzymes in injury
α β - X-linked defect in ALA -Warm (IgG)is associated with Loss of membrane renders cells -Dilantin(phenytoin),oral contraceptives deposition of cholesterol or
Chronic consumption of more
- Heavy menstrual bleeding heme synthesis such as ALA - Radiation and drugs phospholipids on the membranes of - Environmental factors (example: - Decreased production of
thalassemia thalassemia Inflammation=> ↑ hepcidin=> synthase SLE and some drugs (alpha round instead of disc shaped -Folic acid antagonist chemotherapy for than 80 grams of alcohol per Congenital erythroid aplasia
before surgery or physical dehydratase - Viral agents Loss of CD55/59 on RBC - Rarely due to dietary deficiency cancer circulating red blood cells (RBCs) cytotoxic chemotherapy, radiation, erythropoietin
↓release of iron from - Myelodysplastic Reduced half-life of G6PD methyldopa) Spherocytes are less able to Mutation causes a change in the day and often due to direct due to mutation in ribosomal
trauma - Limits iron delivery to - Fanconi anemia membrane => complemet- Increase risk of sickling with - Decreased absorption of Vitamin -Relative folate deficiency - Chronic liver disease bleeding and viral infection and - BMS
macrophages syndromes leading to increase - Cold is acute associated with maneuver through splenic shape of the red blood toxicity of the alcohol on the gene (RPS genes)
- Gastrointestinal diseases ferrochelatase hypoxemia, dehydration and B12 due to a decrease in intrinsic -intestinal malabsorption caused by: - Jaundice benzene exposure)
- Alcohol - Idiopathic may follow mediated hemolysis susceptibility of RBCs to mycoplasma pneumonia & sinusoids and are consumed by
- Increase RBC acidosis factor 1)Sprue - Hepatitis marrow - Clonal mutation predominates in the
or blood loss - Vitamin B6 and copper acute hepatitis oxidative stress infectious mononucleosis
- Feeling tired or weak protoporphyrin splenic macrophages resulting 2)Giardia lamblia infection - Wilson disease bone marrow, suppressing healthy stem
- Diets lacking iron foods Gene deletion in chromosome 16: deficiency - Chronic lymphocytic leukemia - Cirrhosis
- Having pale skin - Inhibits rRNA degradation in anemia cells.
- Intravascular hemolysis - 1 gene deletion—> silent carier Point mutation in Beta - Isoniazid and linezolid
- 2 gene deletion—> alpha globin gene on - Having shortness of breath
- Depression -Short stature
thalassemia trait chromosome 11 - Sweating -Fatigue, malaise and -Early greying of the hair -Pale skin
- Pale - Abdominal colic and -Aplastic crisis - Psychosis -Weight gain -Craniofacial abnormalities
- 3 gene deletion—>HbH disease
- Minor:β0/β+ - Being dizzy or feeling faint pallor. - Painful blue fingers and -Weakness due to anemia -Decreased appetite - Hemorrage - Bleeding
- Unexplained fatigue and - 4 gene deletion—> hydrops - Palor sideroblastic anemia -Autosplenectomy - Splenomegaly -Fatigue -Upper extremities and
- Rapid heartbeat -Purpura -Venous thrombosis - Back pain -Lemon-yellow skin color -Lack of energy - Pallor - Petechia
weakness fetalis(incompatible with life) - Major:β0/β0 - Tachycardia - encephalopathy toes with cold exposure - Splenomegaly -Leg ulcers Mild anemia -Sluggish movements urogenital malformations
- Having headache - Increased bleeding -Hematuria - Hematuria -Stomatitis and glossitis -Diarrhea - Fatigue - Jaundice - Fever
- Shortness of breath or - Palpitations - lead lines on gingiva (IgM) - Jaundice with UCB -Severe pain attacks -Cold intolerance -Cleft palate
tendancy -Subacute degeneration of the -Smooth and tender tongue - Bacterial infections - Anxiety - Multiple infections
chest pain - Fatigue - Memory loss - Hematuria -Dactylitis -Dry skin -Cardiac defect
-Infection spinal cord -NO neurological symptoms - Vomiting
- Rapid heartbeat - Chest pain - Loss of apetite - Shortness of breath -Memory loss -Low birth weight and growth
- Headache - Silent carrier—>asymtomatic - Increased serum ferritin - Metallic taste in mouth -Myxedema delay
- Thalassemia trait—> mild - Minor—>mild anemia - Hypochromia and microcytosis
- Brittle nails or hair loss
anemia with fatigue and pallor - Major—>severe anemia - Voluminous cytoplasm of -Coombs -ve hemolytic - Low serum B12
- Picophagia - Increased serum homocysteine -Low serum folate levels -↑ liver enzymes specifically
- Hbh disease present 6 months after birth—> macrophages - Hypochromia anemia -Blood smear: RBCs with -Hb electrophoresis confirms - Increased methyl-malonic acid in Gamma-glutamyl transferase
—>splenomegaly, ineffective erythropoiesis, - Abundant iron in macrophages - Microcytosis - Basophilic stippling in RBCs -pancytopenia - Osmotic fragility test (spherocyte -Increased serum homocysteine - Elevation in liver enzymes - Pancytopenia - Elevated eADA levels (80-
- Hypochromic microcytic hepatomegaly,jaundice, iron - EPO ↑ Heinz bodies and bite cells. the presence and urine (GGT) - Macrocytic anemia
extravascular hemolysis and reduced to absent iron in red from peripheral blood smears -flow cytometry: CD55/59 -ve - Coombs test positive fragility in hypotonic solution) HbC crystals on blood Blood smear shows: - Pancytopenia - Ineffective hematopoiesis 85% of patients)
anemia overload(elderly) and growth - Ringed sideroblasts - Hypocellular bone marrow -↑: reticulocytes, indirect predominance of HbS - Anti-intrinsic factor antibodies -Phosphatidyl ethanol (PEth) - ↑serum TSH
,hepatosplenomegaly and cell precursors - Lead lines on metaphysis x- RBCs - Hematuria - Spherocytes with loss of central smear Blood smear pancytopenia and - Reticulocytopenia presence in blood - Dry tap upon bone marrow - Genetic testing for mutation
- MCH ↓ retardation(children) - Stained for iron (Prussian blue stained by prussian blue with fatty Infiltration. bilirubin and LDH -Target cell on blood smear - Abnormal schilling test - ↑ FT4.
extramedullary hematopoiesis ray -Hemoglobinuria, pallor hyper-segmented neutrophils, - Coagulopathies -Carbohydrate-deficient biopsy - Macrocytic anemia
- MCHC ↓ - Hyrops fetalis—> death in reaction) - Peripheral blood smear -Hematuria and -Crew cut appearance on xray Blood smear pancytopenia and hyper-
utero hemoglobinemia, - Increase RDW and MCHC (>36%) segmented neutrophils, anisocytosis, anisocytosis, macrocytes, transferrin (CDT)
- RDW ↑ shows basophilic stippling hemosiderinuria. -Chipmunk facies
hemosidenuria. macrocytes, ovalocytes, Howel-Jolly ovalocytes, Howel-Jolly bodies
- Smear shows occasionally Minor: of RBCs
elliptocytes and pencil cells bodies
- Inflammation treatment
- HbA2 >3.5% (normal=2.5%) -Withdrawal of offending - Steroid therapy – to
- Hbh disease—> Heinz - blood transfusion - Allogenic HSCs
- HbF=2% (normal=1%) - Vitamin B6 agent increase hemoglobin by
bodies after brilliant cresyl - HbA—> slightly - EPO - Avoid: drugs causing -Vitamin B12 injections - Hematopoietic cell transplantation if age <55
- Thiamine supplementation - Immunosuppressive - Corticosteroids Splenectomy -> anemia resolves -Eating a healthy diet - Anti-depressants stimulating the bone marrow
- Diet including: meat, blue staining+ Hbh 5% to decreased(normal=97-98%) - Dimercaprol and EDTA -Eculizumab oxidant stress, broad beans Hydroxyurea No treatment -In milder cases: diet changes and transplantation +high risk AML development Levothyroxine
- Iron chelation to prevent regimens - Transfusion but spherocytes persists and -Taking folic acid - Disulfiram, naltrexone, acamprosate to produce more red blood
poultry, fish, legumes and 30% - Lead chelation -Take folic acid supplement in vitamin B12 supplements in pill or - Immunosuppressive therapy - Supportive treatment
Major: hemochromatosis - Bone marrow allograft - Erythropoietin therapy Howell Jolly bodies emerge on supplements - Supportive therapy cells
cereals - Hydrops fetalis—> Hb chronic hemolysis. as a nasal spray (transfusion+ antibiotics) if
- RBC/platelet transfusion blood smear - Blood transfusion
- Medicinal iron(2-5 barts ~80% - HbF elevated at birth(97%) age>65 and low risk disease.
- Bone marrow stimulation - Iron chelation
mg/kg/day) - HbA2 variable - HSCT is the only cure.
- IV iron(iron dextran,iron - HbA little or absent
sucrose and ferric - Smear shows microcytic
hypochromic anemia, target cells,
gluconate) howell jolly bodies, nucleated RBCs
- Blood tranfusion - Xray shows crew cut skull and
chipmunk face due to expanded
HbH disease—> may
hematopoiesis
require occasional or
regular blood tranfusion
,splenectomy if severe Major : continuous transfusion Resources:
splenomegaly, iron and risk of secondary
Text
Names: Uptodate Legend: Definition Symptoms
chelation hemochromatosis Khaled Abou Dib First Aid
Yasmine Accad BRS Pathology
AbdelRahman Al Baba Kaplan Pathology
Aya AL Abdullah Pathoma
Fatima Banna Medscape Causes Investigation
Iman Al Khalaf
Lara Al Mais
Mohiedine Al Sayyed Aboul Joud

Treatment

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