5-4

Front 1

How much can the marrow compensate for increased hemolysis?

Back 1

5-8 times

Front 2

3 signs of increased RBC production?

Back 2

Increased reticulocyte count
Polychromasia
Erythroid hyperplasia in the marrow

Front 3

3 signs of increased RBC destruction?

Back 3

Increased LDH
Increased uncogugated bilirubin
Decreased hepatoglobin

Front 4

How long does it take for the marrow to compensate for decreased RBCs?

Back 4

4-7 days for retic count to go up

Front 5

One intrinsic anemia that IS NOT inherited is?

Back 5

Paroxysmal Nocturnal Hemoglobinuria (PNH)

Front 6

Intravascular hemolysis can kill you by? (3)

Back 6

Shock, DIC, renal failure

Front 7

Cold agglutinin disease?

Back 7

IgM attacks RBCs in cold tempuratures after an infection usually pneumonia.

Front 8

Donath-Landerstieiner Antibodies?

Back 8

IgG abs that bind RBCs in colder tempuratures and fix complement in warmer tempuratures. causes paroxysmal cold hemoglobinuria (PCH)

Front 9

4 signs or intravascular hemolysis?

Back 9

Hemoglobinemia
hemoglobinuria
hemosiderinuria
decreased haptoglobin

Front 10

Direct antiglobulin (coomb's test) looks for?

Back 10

immunoglobulin binding. autoimmuno hemolysis

Front 11

Osmotic fragility test looks for?

Back 11

hereditary spherocytosis

Front 12

Sickle cell disease?

Back 12

Sickle cell anemia with clinicl compliations

Front 13

What is the main complication of sicklers?

Back 13

Infarcts. lung, spleen brain and kidney

Front 14

What are pts with no spleen more suseptable to?

Back 14

encapulated organisms like Strep pneumoniae and hemophilius

Front 15

What are the main crises of sicklers? (4)

Back 15

Acute vasooccusive
sequestrian
acute hemolytic
acute aplasic

Front 16

Diagnosis?

Back 16

Hemoglobin CC disease

Front 17

Diagnosis?

Back 17

Hemoglobin SC disease

Front 18

Most common RBC enzyme defect?

Back 18

G6PD deficincy

Front 19

Role of G6PD?

Back 19

regenerates NADPH used to reduce back gluthathione after it detoxifies hydrogen peroixide

Front 20

Inheretance pattern for G6PD?

Back 20

X linked

Front 21

Mechanism of anemia for G6PD deficincy?

Back 21

increased sensitivity to oxidative stress

Front 22

Heinz bodies?

Back 22

aggregates of denatured hemoglobin seen with G6PD deficincy

Front 23

What are these?

diagnosis?

Back 23

Bite and Blister cells

G6PD deficency

Front 24

Characterisitics of the african varient of G6PD?

Back 24

mild activity G6PD activity decliens faster

Front 25

charactersitics of mediteranian varient of G6PD?

Back 25

reduced activity of G6PD even in retics. usually no helolysis at baseline and sensitivity of flava beans

Front 26

Why might you get an normal value for G6PD during an attack?

Back 26

The older cells that have the decreased activity are lyced leaving the normal younger cells

Front 27

Spectrin?

Back 27

Forms the skeleton of the RBC

Front 28

Ankyrin?

Back 28

Anchors the lipid bilayer to the spectrin sytoskeleton

Front 29

What are these?

Back 29

Spherocytes

Front 30

How can spherocytosis be treated? (3)

Back 30

RBC transfusion
Cholecystectomy
Splenectomy

Front 31

Elliptocytosis is inhereted how?

Back 31

Autosomal dominant

Front 32

elliptocytosis Is usually caused by?

Back 32

defects in spectin

Front 33

what are these?

diagnosis?

Back 33

elliptocytes

ellipocytosis

Front 34

Hereditary pyropokilocytosis is caused by?

Back 34

Autosomal recessive inheritance of ellipotocysosis gene

Front 35

which antibodies usually bind at colder tempuratures?

Back 35

IgM

Front 36

Cold reacting hemolysis is usually secondary to?

Back 36

infection

Front 37

Acrocyanosis?

Back 37

When fringers, tips of ears and toes turn blue due to RBC agglutination that plugs up capillaries.

Front 38

Paroxysmal cold hemoglobinuria? (PCN)

Back 38

IgG Ab (Donath-Lansteriner) bind RBC at colder tempuratures and then lyce at warmer tempuratures

Front 39

Most warm-reactive hemolysis occures?

Back 39

extravasularly, most often the spleen

Front 40

What is the antigen target usually assosiated with warm autoimmune hemolysis?

Back 40

RH

Front 41

Who usually gets idiopathic warm autoimmune hemolytic anemia?

Back 41

women

Front 42

treatment for idiopathic warm autoimmune hemolytic anemia?

Back 42

Prednisone but problems with tappering. avoid transfusions

Front 43

Mechanism of drug absorption type anemia?

Back 43

usually penicillin, binds to RBCs. Ab binds to penicillin and is taken in by macrophages.

Front 44

Neoantigen type anemia?

Back 44

drug binds to the RBC and forms and antigen that is able to fix complement. intravascular