Heme Pathology Mini2

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Author:
pandachowmein
ID:
113006
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Heme Pathology Mini2
Updated:
2011-10-29 16:56:43
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Mini2 Blood
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Blood Mini 2
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  1. Microspherocyte
    • Hyperchromic and microcitic
    • high Hb concentration
    • found with hereditary spherocytosis (extra hemolytic)
    • autoimmune hymolytic (extra hemolytic)
  2. Sickle cell
    • Sickle shaped cells
    • Glu - Val on beta sub-HemeGlobin
    • Hbss and Hbsc genetic profile
    • percipitates in deoxygenated state
    • produces hemolysis, infarctions, and occlusions
    • clinically spleenomegli, bad circulation failure to thrive, repeated infections (from compliment deleption during hemolysis)
  3. Tear drop cells
    • Myelofibrosis
    • Bone marrow infiltration in neoplasia
  4. Schistocyte
    • Hemolytic anemia associated with mechanical stress
    • Dissemenated intravascular coagulation
  5. Target Cells
    • Excess cell membrane
    • Thalassemia
    • iron deficiency
    • alcoholic liver disease
  6. Punctated Basophilia (Stippling
    • Ribosomes remain on mature RBC
    • Lead poisoning
    • THalassemia
    • Megaloblastic anemia
    • Drugs and Alcohol abuse
  7. Howell-Jolly bodies
    • DNA ramenant
    • Abscent spelln
    • sickle cell induced spleen disfunction
  8. Heinze Bodies
    • Broken aggregated Hb
    • G6PD deficiency
    • alpha thalassemia
  9. Siderocyte
    • Iron overload
    • Transfussion iron overload
    • Lead poisoning
    • B6 deficiency
    • Thalassemia
  10. Macrocytic Anemia
    Megaloblastic anemia
  11. Microcytic Anemia
    • Iron deficiency-decrease Iron
    • Lead poisoning - decrease Hemecomplex (iron overload)
    • Thalassemia- dcrease hemoglobin (normal iron)
  12. Megaloblastic Anemia
    • Pernicious Anemia (Intrinsic factor deficiency)
    • B12 deficiency (ilieum absorption defect)
    • Drugs - oral contraceptive
    • Alcoholism
    • Presents with macrocytic RBC, leukopenia, hyersegmented neutrophils
    • Increase in serum methylmalonic acid points to B12
    • increase in homocysteine points to both B12 and Folate
  13. Neutrophils
    • highest percetage of leukocyte 60-70
    • Multisedgmented nucleus (3-5)
    • Specific granule - Lactoferrin (iron chelator Collagenase, enzymes, H2O2)
    • Azurophilic granule - myeloperoxidase lysosome , collagenase
    • Oxidative burst produces OCl- from H2O2 and Cl-
  14. Chronic Granulomatous
    • Knock out NADPH oxidase, no hydrogen peroxide in Neutrophils
    • results in frequent infections
  15. Eosinophil
    • Kills parasite and participates in allergies
    • Bi-lobular dna
    • Specific - Internum major basic protein, denatures plasma membrane of eukaryotes
  16. Crohn's disease
    • Overactivation of eosinophils
    • inflamation of the intestines
    • Helminthic therapy introduce worms to fight eosinophils
  17. Basophils
    • Rare with FcEpsilon receptor (IgE activated)
    • Specific - histamine and herpin granules
    • Similar to Mast cells and will produce alergies and anaphlaxis
    • Basophilic because its (neg basic) proteins will become basophilic in blood
  18. Leukocytosis
    • Increase in leukocytes
    • Normal -babies to young children and prego
    • Lots of pathologies
  19. Neutropenia
    • Aplastic Anemia (BM failure)
    • Megaloblastic anemia
    • Overwhelming infection
    • Splenomegaly (especially when lymphocytes are increased)
  20. Agranulocytosis
    • Large decrease in neutrophils
    • Drug toxicity (Ab mediated autoimmune)
    • resultsin death within days from sever infection
  21. Neutrophilia
    • Acute appendicitus
    • Abscess
    • Leukemoid reaction (you think leukemia, actually infection... i don't know how that can happen)
  22. Dohle bodies
    rER inclusion bodies
  23. Leukemoid Rxn
    • large increase in leukocytes and granulocytes
    • looks like its leukemia
    • but is actually sever infection or mononucleosis
  24. Eosinophilia
    • Allergies
    • Parasite
    • Hodgkin's lymphoma
  25. Basophilia
    • Rare
    • Myeloid leukemia
  26. Monocytosis
    • Macrophage increase
    • Chronic infections (TB)
    • Chronic inflammation (Lupus and colitus)
  27. Lymphocytosis
    • Increase in lymphocytes
    • Viral infections (Mono, CMV, mumps)
    • Whooping cough and T.B.
    • Cancer
  28. Typical presentation ofT-cell lymphocytosis
    • Downy cells
    • fever
    • lymph and spleen englargment
  29. Lymph Hyperplasia (chronic)
    • Follicular - B-cell growth - HIV, Rhematoid arthritis
    • Paracortical - T-cell growth - Chronic Mono
    • Sinus - Carcinoma nearby
  30. Hemoglobin development
    • Embroynic = zeta/alpha - episolon/gamma
    • Fetus = alpha - gamma
    • adult = alpha - beta
  31. some alpha gamma is still produced in adult (~3%)
  32. Alpha Thalassiemia
    • 3 alpha gene = silent carrier
    • 2 alpha gene = Not enough alpha/beta, makes beta tetromers to compenate (HbH) might have some residual HbBart at birth
    • 1 alpha gene = Sever anemia, lots of HbH compensation, hemolysis (jaundice, hepatosplenomegaly)
    • 0 alpha gene= hydrops fetalis, can't even make fetal alpha/gamma complex, need to make gamma tetromers (HbBarts) before expression of beta after birth
  33. Beta Thalassiemia beta(+)
    • Variable expression from defective beta production
    • Beta+ (intermediate) Reduced beta production, no transfusion needed but will have anemia from alpha deposites
    • avoid iron suppliment to avoid iron overload (ineffective Hb can't bind it anyways)
  34. Beta Thalassiemia beta(0)
    • No beta production at all (but since beta takes over at 6 month babies are born healthy)
    • Alpha/Gamma compensation with lots of alpha deposits
    • --microcytic iron overload
    • --anemia - jaundice splenomegaly
    • --transfusion required
    • --iron chealtion required to treat iron overload
    • --splenonectomy needed
    • -- death from anemia by age 6 or iron overload by age 30 unless chelation and transfusion is continued

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