Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 6 > Hemolytic Anemia 1 > Flashcards

Hemolytic Anemia 1 Flashcards

1
Q

lifespan of RBC

A

120d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

sites of extra medullary hematopoiesis

A

spleen
liver
lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

hemoglobinopathy

A

genetic mutation for abnormal globins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

thalssemia

A

mutation decreasing globin synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

hemolysis

A

RBC destruction resulting in release of Hb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

signs of hemolytic anemia

A

elevated erythropoietin
increased erythropoiesis
increased Hb catabolites (bilirubin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

intravascular hemolysis

A

mechanical injury or toxic injury resulting in complement fixation from antibody/antigen reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

consequences of intravascular hemolysis

A 
anemia
hemoglo binemia
hemoglobinuria
hemosiderinuria
jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

anemia

A

reception in total RBC cells leading to tissue hypoxia and reduced oxygen caring capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

hemoglobinemia

A

free Hb in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

hemoglobinuria

A

free Hb in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

hemosiderinuria

A

hemosiderin binds iron from hemoglobin in urine and is excreted in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

best marker for intravascular hemolysis

A

hemosiderinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

jaundice

A

yellowing of skin from elevated bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

extravascular hemolysis

A

less severe, more common

less deformable RBCs that can’t get through spleen and get stuck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

consequences of extravascular hemolysis

A

anemia
splenomegaly
jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

cell counts/ indices that indicate hemolysis

A 
increased reticulocyte count
reduced MCV
elevated MCHC
increased free Hb
decreased haptoglobin
increased LDH
increased free Hb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

haptoglobin

A

binds free Hb

reduced in hemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

osmotic fragility test

A

expose abc to decreasing salt/increasing water concentration and watch when lysis occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

osmotic fragility test in hemolysis

A

decreased in membrane defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

conditions with membrane defects

A

hereditary spherocytosis

hereditary elliptocytosis

22
Q

protein electrophoresis

A

separating RBC membrane proteins by size with predictable migration pattern

23
Q

protein electrophoresis in hemolysis

A

different band patterns in membrane defects

24
Q

sickling test

A

used for sickle cell disease

mix blood with oxygen consuming agent and watch for sickling

25
Q

Hemoglobin electrophoresis

A

different band pattern from Hb with a change in the protein (sickle cell)

26
Q

hereditary spherocytosis genetics

A

autosomal dominant
heterogeneous
northern europeans
same mutations within familiese

27
Q

etiology of hereditary spherocytosis

A

membrane defect from reading frame shifts of stop codons resulting in mutated ankyrin, spectrum, band 4.2

28
Q

pathophysiology of hereditary spherocytosis

A

fragile less deformable RBC

little pieces of membrane are lost –> forms a sphere

29
Q

diagnostic findings associated with membrane defects

A

low/normal MCV
elevated MCHC
more sensitive to osmotic lysis
missing bands in protein electrophoresis

30
Q

complications of membrane defect

A

abc get trapped in the spleen

10-20d life

31
Q

treatment for membrane defects

A

splectomy

32
Q

hereditary elliptocytosis genetics

A 
autosomal dominant
equatorial africa (resistance to malaria)
33
Q

etiology of hereditary elliptocytosis

A

alpha spectrin mutation

34
Q

G6PD deficiency genetics

A

x linked recessive
G6PDa- blacks
G6PD mediterranean- middle east

35
Q

pathophysiology of G6PD deficiency

A

increased susceptibility to oxidative injury

missing G6PD needed to convert NADP to NADPH which reduces glutathione so it can remove H2O2

36
Q

diagnostics for G6PD deficiency

A

Heinz bodies

bite cells

37
Q

heinz bodies

A

denatured Hg clumps inside RBC

38
Q

bite cells

A

RBC with bites taken out by splenic macrophages

attempted removal of heinz bodies

39
Q

consequences of G6PD deficiency

A

acute hemolysis when exposed to oxidative compounds

40
Q

oxidative compounds

A

certain drugs (antimalarials, sulfonamides, nitrofurantoin)
fava beans
viral/bacterial infections

41
Q

treatment for g6PD deficiency

A

avoid oxidative stressses

42
Q

sickle cell disease genetics

A

8% of blacks

homozygous

43
Q

sickle cell disease etiology

A

point mutation in beta global gene that switches glutamate for valine

44
Q

sickle cell disease pathogenesis

A

deoxygenation triggers polymerization reaction that forms rigid polymers that damage the membrane
may be reversible with oxygenation

45
Q

sickle cell disease diagnosis

A 
clinical presentation
family history
blood smear- drepanocytes, anisocytosis, poikilocytosis
sickling test
hemoglobin electrophoresis
dna testing
46
Q

sickle cell disease acute complications

A

acute microvascular occlusion and tissue damage
bone, lung, spleen- infarction, sequestration, brain, penis
susceptibility to encapsulated organisms

47
Q

sickle cell disease chronic complications

A

anemia
cholelithiasis
aplastic crisis

48
Q

sickle cell treatment

A 
reduce HbS
blood transfusion
dehydration
increase HbF
reduce inflammation
maintain intracellular pH
49
Q

complications of hemolytic disorders

A

bone marrow expansion
iron overload with chronic transfusion
gallstones
aplastic crisis

50
Q

aplastic crisis

A

parvovirus infects erythroid precursor cells
low Hb and Hct
giant pronormoblasts in bone marrow

51
Q

infectious causes of hemolysis

A

parvovirus b19
babes microti
falciparum malaria
clostridium welchii

Block 6 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions