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Heme > Anemia II > Flashcards

Anemia II Flashcards

1
Q

anemia of chronic disease/inflammation

A

normochronic, normocytic, hypoproliferative

can also by hypo chromic and microcytic

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2
Q

pathogenesis of anemia of chronic disease

A

autoimmune dysreg –> downstream effects

  • increased hepcidin –> less iron absorption
  • iron gets trapped in macrophages
  • direct inhibition of erythropoiesis

–> functional iron deficiency

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3
Q

labs in anemia of chronic disease

A 
ferritin normal-high
transferrin low to normal
T sat low-normal
iron low
marrow iron stores high
sed rate high
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4
Q

tx of ACD

A

transfusion if severe anemia

erythropoietin if nec

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5
Q

aplastic anemia

A

diminished or absent hematopoietic precursors due to injury to HSC –> pancytopenia and empty bone marrow

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6
Q

causes of aplastic anemia

A

primary: idiopathic, fanconi anemia (genetic)
secondary: radiation, chemo, other drugs, viruses (EBV)

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7
Q

anemia of chronic kidney disease

A

decreased erythropoietin production due to decreased renal cortical cells,
+ freq phlebotomy, shortened RBC life span –> normocytic anemia

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8
Q

other causes of hypoproliferative normocytic anemias

A

drugs (chemo)
infiltration of bone marrow (malignancy or infection)
endocrine: hypothyroidism, panhypopituitarism, low testosterone

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9
Q

intravascular hemolysis of RBCs

A

haptoglobin binds Hgb

HgB-haptoglobin removed by RES – prevents iron-utilizing bacteria from benefitting from hemolysis

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10
Q

extravascular hemolysis of RBCs

A

occurs in spleen and liver

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11
Q

lab findings in hemolysis (both intra- and extra-vascular)

A

anemia w/ increased reticulocytes
increased LDH
indirect bilirubin
decreased haptoglobin

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12
Q

lab findings specific to intravascular hemolysis

A

schistocytes
hemoglobinemia
hemoglobinuria

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13
Q

clinical findings differentiating extravascular hemolysis from intravascular

A

intravascular –> hemoglobinemia and -uria

extravascular –> NO hemoglobinemia or-uria

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14
Q

Immune hemolytic anemia

A

antibodies against RBCs

positive DAT or direct coombs

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15
Q

Direct coombs test

A

are RBCs in here already bound by antibodies?

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16
Q

tx for autoimmune hemolytic anemias

A 
address cause
steroids
immunosuppression
anti-CD20 therapy (rituximab)
splenectomy
17
Q

IHA due to warm antibodies

A

IgG - spleen destroys antibody coated RBCS

18
Q

IHA due to cold antibodies

A

IgM - bind in cold areas (extremities, face), pick up complement on way to body center –> RBCs lyse in circulation or in the liver
caused by virus and mycoplasma

19
Q

drug induced hemolytic anemia - 3 mech

A
  1. hapten (ex penicillin)
  2. innocent bystander (ex quinine)
  3. antigenic - drug incorporated into RBC membrane (ex methyldopa)
20
Q

microangiopathic hemolytic anemia

A

non-immune hemolytic process w/ prominent red cell fragmentation (schistocytes)

21
Q

causes of microangiopathic hemolytic anemia

A
  1. TTP-HUS
  2. DIC
  3. malfunctioning heart valves
22
Q

TTP - HUS

A

thrombocytopenia and RBC fragmentation
assoc w/ ADAMSTS mutations, HIV, shiga-toxin E coli
tx plasmapheresis

23
Q

membranopathies causing normocytic anemia

A
  1. hereditary sperocytosis

2. Paroxysmal nocturnal hemoglobinuria

24
Q

hereditary spherocytosis

A

autosomal dom inheritance, common in northern europeans
spectrin mutation –> decreasesd membrane mechanical stability –> RBCs can’t pass through splenic microcirculation, RBCs die prematurely
tx splenectomy

25
Q

paroxysmal nocturnal hemoglobinuria

A

acquired defect in cell membrane

missing GPI due to PIG-A gene defect –> RBCs vulnerable to complement –> intravascular hemolysis

26
Q

PNH s/sx

A

patient wakes up in morning w/ dark urine

significant risk of thrombosis

27
Q

PNH dx

A

flow cytometry - missing CD59 and CD55

28
Q

PNH tx

A

transfusions
fe and folate supplementation
eculizumab (anti-complement)
stem cell transplant

29
Q

G6PD deficiency

A

problems w/ maintaining Hgb in face of oxidative stress
dx: measure G6PD activity
path: Heinz bodies and best cells
x-linked

30
Q

what two infections cause hemolytic anemia?

A
  • malaria

- babeosis

31
Q

sickle cell mutation

A

single amino acid substitution in beta chain of chrome 16: valine for glutamic acid –> Hemoglobin S

32
Q

how long do sickle cells live?

A

10-20 days (most removed by spleen)

33
Q

clinical manifestations of sickle cell disease

A 
hemolysis
delayed growth
infection
vaso-occlusive
cerebrovascular events
retinopathy 
aplastic episodes (parvovirus)
34
Q

tx for sickle cell

A

supportive tx for pain crises
hydroxyurea - increases Hgb F, decreases Hgb S
Hematopoietic stem cell transplant

Heme (16 decks)

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