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Microspherocyte
- Hyperchromic and microcitic
- high Hb concentration
- found with hereditary spherocytosis (extra hemolytic)
- autoimmune hymolytic (extra hemolytic)
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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)
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Tear drop cells
- Myelofibrosis
- Bone marrow infiltration in neoplasia
-
Schistocyte
- Hemolytic anemia associated with mechanical stress
- Dissemenated intravascular coagulation
-
Target Cells
- Excess cell membrane
- Thalassemia
- iron deficiency
- alcoholic liver disease
-
Punctated Basophilia (Stippling
- Ribosomes remain on mature RBC
- Lead poisoning
- THalassemia
- Megaloblastic anemia
- Drugs and Alcohol abuse
-
Howell-Jolly bodies
- DNA ramenant
- Abscent spelln
- sickle cell induced spleen disfunction
-
Heinze Bodies
- Broken aggregated Hb
- G6PD deficiency
- alpha thalassemia
-
Siderocyte
- Iron overload
- Transfussion iron overload
- Lead poisoning
- B6 deficiency
- Thalassemia
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Macrocytic Anemia
Megaloblastic anemia
-
Microcytic Anemia
- Iron deficiency-decrease Iron
- Lead poisoning - decrease Hemecomplex (iron overload)
- Thalassemia- dcrease hemoglobin (normal iron)
-
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
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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-
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Chronic Granulomatous
- Knock out NADPH oxidase, no hydrogen peroxide in Neutrophils
- results in frequent infections
-
Eosinophil
- Kills parasite and participates in allergies
- Bi-lobular dna
- Specific - Internum major basic protein, denatures plasma membrane of eukaryotes
-
Crohn's disease
- Overactivation of eosinophils
- inflamation of the intestines
- Helminthic therapy introduce worms to fight eosinophils
-
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
-
Leukocytosis
- Increase in leukocytes
- Normal -babies to young children and prego
- Lots of pathologies
-
Neutropenia
- Aplastic Anemia (BM failure)
- Megaloblastic anemia
- Overwhelming infection
- Splenomegaly (especially when lymphocytes are increased)
-
Agranulocytosis
- Large decrease in neutrophils
- Drug toxicity (Ab mediated autoimmune)
- resultsin death within days from sever infection
-
Neutrophilia
- Acute appendicitus
- Abscess
- Leukemoid reaction (you think leukemia, actually infection... i don't know how that can happen)
-
Dohle bodies
rER inclusion bodies
-
Leukemoid Rxn
- large increase in leukocytes and granulocytes
- looks like its leukemia
- but is actually sever infection or mononucleosis
-
Eosinophilia
- Allergies
- Parasite
- Hodgkin's lymphoma
-
-
Monocytosis
- Macrophage increase
- Chronic infections (TB)
- Chronic inflammation (Lupus and colitus)
-
Lymphocytosis
- Increase in lymphocytes
- Viral infections (Mono, CMV, mumps)
- Whooping cough and T.B.
- Cancer
-
Typical presentation ofT-cell lymphocytosis
- Downy cells
- fever
- lymph and spleen englargment
-
Lymph Hyperplasia (chronic)
- Follicular - B-cell growth - HIV, Rhematoid arthritis
- Paracortical - T-cell growth - Chronic Mono
- Sinus - Carcinoma nearby
-
Hemoglobin development
- Embroynic = zeta/alpha - episolon/gamma
- Fetus = alpha - gamma
- adult = alpha - beta
some alpha gamma is still produced in adult (~3%)
-
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
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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)
-
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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