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A short essay about 4 types of anemia
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Kalsoom SaleemCMS # 8107
Glucose-6-Phosphate Dehydrogenase Enzyme Deficiency• Pathophysiology
Glucose-6-Phosphate Dehydrogenase Enzyme Deficiency
Causative Agents• Food-Fava beans • Medications-Sulfasalazine
Reduced Glutathione• Consumed during oxidative
stress
Attack RBCs• Globin chain-denaturing
hemoglobin
Heinz Bodies• Precipitation of hemoglobin-
intracellular inclusions
Intravascular Hemolysis Extravascular Hemolysis• Phagocytosis of less
damaged RBCs
Bite Cells• Plucked out by phagocytes
Morphology
Microscopic
-Red Cells with precipitates of denatured globin (Heinz bodies)-Bite shape of cells (Bite Cells)
Morphology
Gross
Yellow coloration of cornea due to hemolysis of RBCs causing jaundice
Etiology
Drugs (Sulfonamides, Ciprofloxacin, Aspirin, Sulfonylureas)
GeneticKidney Failure
DiabetesFood (Fava Beans)
Symptoms
Rapid heart rateFast breathing
SplenomegalyPale Skin
Elevated Body TemperatureDark to yellow-orange urine
Complete Blood Count and Reticulocyte Count
Heptaglobin Test
Renal Function Test
Diagnosis
Avoiding specific medications, foods and environmental exposures
Dialysis-in kidney failure
SupplementsBlood transfusion
Treatment
Prognosis
• Patients with G6PD enzyme deficiency get fewer illnesses as compared to other people and the possible outcome is general recovery from disease.
Proxymal Nocturnal HemoglobinuriaPathogenesis
MorphologyMicroscopic
•Hypercellular marrow with erythroid hyperplasia.
Morphology Gross
Flushing of skin due to pancytonpenia
Etiology
•Somatic mutation in PIGA gene in stem cells (bone marrow)
Symptoms
Abdominal pain
Headaches
Back pain
Weakness/Fatigue
Splenomegaly
Recurrent infections
Dia
gnos
isFlow Cytometry (detection of mutant gene, percentage and degree of deficient RBCs)
Bone Marrow Analysis
Acid Hemolysis Test
•Corticosteroids•Iron Replacement Therapy
Treatment•Splenectomy•Folate Supplements
Treatment Stem Cell TransplantationTreatment
•Complement Inhibitors (Ecluzimab)
•Blood Transfusion
Treatment
Prognosis
Death results after 10-11 years of diagnosis with decreased cell number
Autoimmune Hemolytic Anemia• Some people develop antibodies -interact with determinants on RBCs - causing
hemolytic anemia.• Classified according to
• nature of the antibody • presence of predisposing conditions.
• Warm Antibody Immunohemolytic Anemia: • It is caused by the IgG or IgA (rarely) immunoglobulins which are active at room
temperature (370C) that attach to RBCs membranes making their Fc portion exposed which get attached to Fc receptors on monocytes and macrophages. This will allow them to phagocytize the RBC membranes changing them to spherocytes. Spherocytes are not flexible as normal RBCs and are, therefore, erythrophagocytosed in Spleen leading to hemolysis.
Autoimmune Hemolytic Anemia
• Cold Antibody Immunohemolytic Anemia:• Circulating antibodies esp. IgM causes the destruction of RBCs• Their concentration in normal being is too low to trigger disease • Patients with CAIA have higher concentrations of IgM• At low temperatures i.e. below 300C, IgM antibodies bind to glycoproteins on the
surface of RBCs activating the complement system which then damages the RBCs by forming Membrane Attack Complex injecting proteins into the RBCs forming pores leading to membrane instability causing intravascular hemolysis. If the complement response is insufficient, then extravascular hemolysis occurs due to deposition of MAC proteins viz. C3b and C4b on RBCs activating opsonization process and their destruction by phagocytosis in spleen.
Idiopathic
HIV infection
autoimmune diseases (e.g.systemic lupus erythematosus (SLE)
lymphoproliferative disorders (e.g. non-Hodgkin's lymphoma)
lymphoproliferative disorders
Mycoplasma pneumonia
Infections such as Epstein-Barr virus
Idiopathic
EtiologyWarm AIHA Cold AIHA
Fatigue
Fever
Splenomegaly
Symptoms
Symptoms
Breathing difficulty
Symptoms
JundiceDark UrineChest Pain
Com
plet
e Bl
ood
Coun
t
Bilir
ubin
Lact
ate
Dehy
drog
enas
e
Test Ur
ine
Hem
oglo
bin
Diagnosis
Treatment
Blood Transfusion
Corticosteroids
Immunosuppressants
Plasmapheresis
Bone Marrow Transplant
Life style changes
MalariaPathogenesis
Morphology Microscopic• Blood smear showing red blood cells that contain developing P.
vivax parasites
EtiologyFemale
Anopheles Mosquito
Infected blood
through Blood
Transfusion
Organ Transplant
SymptomsAbdominal
pain
Poor appetite
Muscle aches Orthostatic hypotension
High fevers
Headache Chills and sweats
Diarrhea, nausea, and
vomiting
Blood Test
Serological TestingDiagnosis
Treatment
Quinine followed by
doxycycline or clindamycin
Chloroquine tablets (eg
avloclor, malarivon or nivaquine)
Atovaquone with proguanil
(malarone)
Artemether with
lumefantrine (riamet)