pancytopenia (w/ empty bone marrow) - leukopenia (low WBC) - thrombocytopenia (low platelets) - anemia

Normocytic Anemia Flashcards by Tina Jaramillo

two different subtypes of anemia

normocytic w/ low reticulocyte count

normocytic wth high reticulocyte cout

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anemias w/ low reticulocyte count

anemia of chronic disease
aplastic anemia
chronic kdney disease
hypoprolfeirative normocytic anemia

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ACD is typically ___, but can also be ___

normochromic
normocytic
hypoproliferative

hypochromic
microcytic

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ACD presents with

normal to inc ferritin (all Fe in MOs)
decreased to nm transferrin
inc sed rate
dec epo production and diirect inhibition of erythopoiesis in bone marrow

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treatment ACD

underlying disorder

transfusions, epo –>if necessary

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aplastic anemia

pancytopenia (w/ empty bone marrow)

leukopenia (low WBC)
thrombocytopenia (low platelets)
anemia

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primary causes aplastic anemia and prognosis

idiopathic, fanconi anemia

–poor

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secondary aplastic anemia and prognosis

radiation, chemotherapy, alkylating agents
drug- chloramphenicol, bezene
viruses-epstein-barr, parvo

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treatments of aplastic anemia include

G-CSF

GM-CSF

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anemia of chronic kidney disease can be due to

decreased epo (due to decreased renal cortical cells)
blood loss
shortened RBC survival

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why do RBCs have shortened survival?

uremic RBCs are less deformable and more prone to mechanical destruction

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treatment of anemia of chronic kidney disease

epo

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4 types of normocytic anemia w/ increased reticulocyte countjjjj

hemolysis
membranopathies
enzymopathies
hemoglobinopathies

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hemolysis

anemia due to destruction of RBC before usual 120 days lifespan

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normal RBC lifecycle

survival of the fittest–>weaklings engulfed by macrophages that line splenic sinusoids–>hemoglobin broken down–>Fe recovered and stored in macrophage ferritin or transported back to marrow & heme ring metabolized to bilirubin, transported to liver, and excreted into bile

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Haptoglobin and intravascular hemolysis

haptoglobin binds hemoglobin released into circulation–>complex removed by RES
–prevents Fe utilizing bacteria from benefiting from hemolysis

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what does intravascular hemolysis have that extravascular hemolysis does not

hemoglobinemia
hemoglobinuria
blood-tinged plasma
blood-tined urine

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seen in both intravascular hemolysis and extravascular hemolysis

decrease RBC
increase indirect bilirubin
increase haptoglobin, LDH
increase reticulocyte

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spherocytes

RBC that have part of their membrane removed by RES and as a result lose the donut shape and have no central pallor

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schistocytes

fragment of RBC

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immune hemolytic anemias

caused by antibodies directed aganst RBC antigens

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what do you use to distinguish immune hemo anemia

Coombs test

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warm antibodies bind to red cells at ___ and produce ___

37 degrees

IgG

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what are warm hemolytic anmias due to

1/3 lymphoproliferative diseases
1/3 CT diseases like lupus
1/3 idopathic

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spleens role

destroys cells coated with IgG

treatment of warm antibodies

underlying disease steroids immunosuppression if those fail splenectomy can be curative

formation of spherocyte

antibodies attach to RBC Fc R on splenic macrophage binds to antibody splenic macrophage pits antibody-antigen complex fragmenting RBC damaged RBC reseals

cold anemia

IgM antibodies bind in cold areas (nose, ears, finger tips etc)-->pick up C3b-->lyse in circulation or in liver

Raynaud's phenomenom

fingers turn white then red and painful on exposure to cold

cold anemia occurs most frequently after

viral and mycoplastic infection

three drugs that induce drug-induce hemoyltic anemia

penicilin quinidine methyldopa

how does penicilin cause it?

it is a hapten [[small molecule that can elicit an immune response only wen attached to larger carrer) --ab targeted against RBC+drug-->complement removes RBC via spleen

Quinidine drug induced hemolytic anemia mech

innocent bystander- drug combines with Ab that happens to land on RBCj

methyldopa mech

drug incoporated into RBC membranej

microangiopathic hemolytic anemia & three types

non-immune intravascular hemolytic processes with prominent red cell fragmentation (schstocytes) - TTP-HUS - DIC - malfunctioning heart valves

thrombotic thrombocytopenia purpura-HUS

thrombocytopenia and RBC fragmentation

TTP-HUS can be associated with

ADAMTS13 mutation, HIV, shiga toxin producing Ecoli infections

treatment for TTP HUS

plasmarpheresis

why do malfunctioning heart valves cause fragmentation?

turbulence and shearing forces from high pressure gradients

membranopathies

decreases in spectrin, ankyrin ,or cyto protein--> RBC fragility

types of membranopathies

hereditary spherocytosis | paroxysmal nocturnal hemoglobinuria

hereditary spherocytosis epi

congenital auto dominant | common in N europeans

problem wth hereditary spherocytosis

membrane defect so red cells processed by spleen form spears-->lyse--> inc bili, decreased haptoglobin, inc retculocytes MCHC elevated

test for hereditary spherocytosis

osmotic fragility test (lysis of cells in hypotonic salt)

if need to cure hereditary spherocytosis

splenectomy

paroxysmal noctural hemoglobinuria is caused by

acquired (rather than inherited) intrinsic defect in cell membrane defect in PIG-A gene-->missing membrane molecule GPI-->RBCS become vulnerable to complement medaited destruction

PNH is an example of

intravascular hemolysis

clinical signs PNH

dark urine thrombocytopenia anemia DVT

diagnosis of PNH

flow cytometry

treatment of PNH

transfusion | anticomp drug Eculizumab, stem cell transplantation

example of enzymopathy

G6PD de

G6PD genetics

present on x chromosome

what does G6PD

helps keep hemoglobin molecule intact when faced wth oxidant stressed

2 syndromes associated with G6PD

hemolysis AFTER oxidant stress (drugs, infection ,diabetic ketoacidosis, eating fava beans) chronic, on-going hemolysis w/o drug stress -drugs that induce sulfonamides, acetysalicylc iacd, vt K, nitrofuranotoin, prmaqune, qunne, chlorampehnicol

reticulocytes and G6PD

may possess higher levels of enzyme, obscuring diagnosis

G6PD may cause

heinz bodies, bite cells

hemoglobinopathies

qualitative disorders of hemoglobin caused by mutated (rather than deleted) globin genes

example of hemogloinopathy

sickle cell disease

genetics of sickle cell disease

single AA sub on beta chain on chrom 16 | if both chromosomes affected, sickle cell disease- if one affected, sickle cell disease

Hb in SSD

hemoglobin is poorly soluble when deoxygenated (Hemo S) and when polymerizes, RBCS form a sickle shape-->less deformable, vasooclussve plaques occur

why is SC trait adaptive?

R against malara

treatment SCD

propylaxis-hydration, oxygenation, warm temp, algesics--treat pain!

longterm treatment SCD

hydroxyurea--increases Hg F and decrease Hg S stem cell transplant?

Normocytic Anemia Flashcards

(63 cards)