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Normocytic Anemia Flashcards

1
Q

two different subtypes of anemia

A

normocytic w/ low reticulocyte count

normocytic wth high reticulocyte cout

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2
Q

anemias w/ low reticulocyte count

A

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

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3
Q

ACD is typically ___, but can also be ___

A

normochromic
normocytic
hypoproliferative

hypochromic
microcytic

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4
Q

ACD presents with

A

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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5
Q

treatment ACD

A

underlying disorder

transfusions, epo –>if necessary

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6
Q

aplastic anemia

A

pancytopenia (w/ empty bone marrow)

  • leukopenia (low WBC)
  • thrombocytopenia (low platelets)
  • anemia
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7
Q

primary causes aplastic anemia and prognosis

A

idiopathic, fanconi anemia

–poor

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8
Q

secondary aplastic anemia and prognosis

A

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

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9
Q

treatments of aplastic anemia include

A

G-CSF

GM-CSF

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10
Q

anemia of chronic kidney disease can be due to

A
  • decreased epo (due to decreased renal cortical cells)
  • blood loss
  • shortened RBC survival
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11
Q

why do RBCs have shortened survival?

A

uremic RBCs are less deformable and more prone to mechanical destruction

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12
Q

treatment of anemia of chronic kidney disease

A

epo

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13
Q

4 types of normocytic anemia w/ increased reticulocyte countjjjj

A

hemolysis
membranopathies
enzymopathies
hemoglobinopathies

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14
Q

hemolysis

A

anemia due to destruction of RBC before usual 120 days lifespan

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15
Q

normal RBC lifecycle

A

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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16
Q

Haptoglobin and intravascular hemolysis

A

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

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17
Q

what does intravascular hemolysis have that extravascular hemolysis does not

A

hemoglobinemia
hemoglobinuria
blood-tinged plasma
blood-tined urine

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18
Q

seen in both intravascular hemolysis and extravascular hemolysis

A

decrease RBC
increase indirect bilirubin
increase haptoglobin, LDH
increase reticulocyte

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19
Q

spherocytes

A

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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20
Q

schistocytes

A

fragment of RBC

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21
Q

immune hemolytic anemias

A

caused by antibodies directed aganst RBC antigens

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22
Q

what do you use to distinguish immune hemo anemia

A

Coombs test

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23
Q

warm antibodies bind to red cells at ___ and produce ___

A

37 degrees

IgG

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24
Q

what are warm hemolytic anmias due to

A

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

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25
Q

spleens role

A

destroys cells coated with IgG

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26
Q

treatment of warm antibodies

A

underlying disease
steroids
immunosuppression if those fail
splenectomy can be curative

27
Q

formation of spherocyte

A

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

28
Q

cold anemia

A

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

29
Q

Raynaud’s phenomenom

A

fingers turn white then red and painful on exposure to cold

30
Q

cold anemia occurs most frequently after

A

viral and mycoplastic infection

31
Q

three drugs that induce drug-induce hemoyltic anemia

A

penicilin
quinidine
methyldopa

32
Q

how does penicilin cause it?

A

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

33
Q

Quinidine drug induced hemolytic anemia mech

A

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

34
Q

methyldopa mech

A

drug incoporated into RBC membranej

35
Q

microangiopathic hemolytic anemia & three types

A

non-immune intravascular hemolytic processes with prominent red cell fragmentation (schstocytes)

  • TTP-HUS
  • DIC
  • malfunctioning heart valves
36
Q

thrombotic thrombocytopenia purpura-HUS

A

thrombocytopenia and RBC fragmentation

37
Q

TTP-HUS can be associated with

A

ADAMTS13 mutation, HIV, shiga toxin producing Ecoli infections

38
Q

treatment for TTP HUS

A

plasmarpheresis

39
Q

why do malfunctioning heart valves cause fragmentation?

A

turbulence and shearing forces from high pressure gradients

40
Q

membranopathies

A

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

41
Q

types of membranopathies

A

hereditary spherocytosis

paroxysmal nocturnal hemoglobinuria

42
Q

hereditary spherocytosis epi

A

congenital auto dominant

common in N europeans

43
Q

problem wth hereditary spherocytosis

A

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

MCHC elevated

44
Q

test for hereditary spherocytosis

A

osmotic fragility test (lysis of cells in hypotonic salt)

45
Q

if need to cure hereditary spherocytosis

A

splenectomy

46
Q

paroxysmal noctural hemoglobinuria is caused by

A

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

47
Q

PNH is an example of

A

intravascular hemolysis

48
Q

clinical signs PNH

A

dark urine
thrombocytopenia
anemia
DVT

49
Q

diagnosis of PNH

A

flow cytometry

50
Q

treatment of PNH

A

transfusion

anticomp drug Eculizumab, stem cell transplantation

51
Q

example of enzymopathy

A

G6PD de

52
Q

G6PD genetics

A

present on x chromosome

53
Q

what does G6PD

A

helps keep hemoglobin molecule intact when faced wth oxidant stressed

54
Q

2 syndromes associated with G6PD

A

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

55
Q

reticulocytes and G6PD

A

may possess higher levels of enzyme, obscuring diagnosis

56
Q

G6PD may cause

A

heinz bodies, bite cells

57
Q

hemoglobinopathies

A

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

58
Q

example of hemogloinopathy

A

sickle cell disease

59
Q

genetics of sickle cell disease

A

single AA sub on beta chain on chrom 16

if both chromosomes affected, sickle cell disease- if one affected, sickle cell disease

60
Q

Hb in SSD

A

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

61
Q

why is SC trait adaptive?

A

R against malara

62
Q

treatment SCD

A

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

63
Q

longterm treatment SCD

A

hydroxyurea–increases Hg F and decrease Hg S

stem cell transplant?

SBM (18 decks)

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