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Week 2 Reading Flashcards

1
Q

How is Thrombocytopenia treated

A

Administration of platelets or oprelvekin (megakaryocyte growth factor IL-11)

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2
Q

What type of solubility does Vitamin K have

A

Fat-soluble

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3
Q

What population is deficiency of vitamin K most commonly seen in

A

Older persons with abnormalities of fat absorption and newborns who are at risk of bleeding due to vitamin K deficiency

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4
Q

How is vitamin K deficiency treated

A

Vitamin K1 (phytonadione)

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5
Q

What is used to reverse the anticoagulent effect of excess warfarin

A

Vitamin K1 (phytonadione)

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6
Q

Which factors are used to treat hemophilia

A

Factor 8 for hemophilia A and factor 9 for hemophilia B (from fresh plasma or purified human blood)

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7
Q

What are the risks of factor 8 and 9 to treat hemophilia?

A

-Expensive
- Risk of infection
- Risk of immunologic reaction

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8
Q

What is the alternative to using factor 8 and 9 to treat hemophilia?

A

Vasopressin V2 (Desmopressin acetate) increases plasma concentration of vWF and Factor 8. Helps for patients with hemophilia A or vW disease

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9
Q

What is the function of desmopressin

A

increase plasma concentration of von Willebrand factor and factor 8 (increase clotting)

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10
Q

What is the purpose of antiplasmin agents

A

Prevent or manage acute bleeding episodes in patients with hemophilia

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11
Q

What are 2 antiplasmin agents

A

Aminocaproic acid and tranexamic acid

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12
Q

What class of drugs do aminocaproic acid and tranexamic acid fall into

A

antiplasmin agents
Inhibit fibrinolysis by inhibiting plasminogen activation

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13
Q

Which drug inhibits fibrinolysis by inhibiting plasminogen activation

A

Aminocaproic acid and tranexamic acid

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14
Q

Which drug increases the plasma concentration of vWF and factor 8

A

desmopressin

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15
Q

What is the essential metalic component of heme

A

Iron

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16
Q

What molecule is responsible for oxygen transport in the blood

A

heme

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17
Q

What does iron do

A

essential metallic component of heme, and heme does the bulk of o2 transport in the blood

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18
Q

Most of the iron in the body is contained in hemoglobin, but there are 2 other places it occurs. what are these?

A

Transferrin- a transport protein
Ferritin- a storage protein

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19
Q

Which individuals have an increased demand for iron

A

children and pregnant women

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20
Q

Which groups of people is iron deficiency most commonly found in

A
  • Vegetarians
  • Malnourished people
  • Women d/t menstrual blood loss
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21
Q

What are the 2 ways iron crosses the luminal membrane of intestinal mucosa

A
  1. active transport of ferrous iron (Fe 2+)
  2. Absorption of iron complexed with heme
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22
Q

Fe3+ is transported in a complex with which protein

A

transferrin

23
Q

What cell size change is consistant with iron deficiency

A

Microcytic RBCs due to decreased hemoglobin content

24
Q

How is iron deficiency anemia treated

A

ferrous sulfate
ferrous gluconate
ferrous fumerate

25
Iron should NOT be given in which type of anemia
hemolytic anemia (iron stores are elevated, not depressed)
26
Which drug do you want to give After an MRI and not before?
Ferumoxytol- iron oxide, give after MRI.
27
What are the common symptoms of iron overdose
Gastroenteritis Shock Metabolic acidosis coma death
28
What is chronic iron overload called
hemochromatosis Damage to organs that store excess iron (heart, liver, pancreas)
29
Who does hemochromatosis occur most often in
- Transfusion recipients for hemolytic disorders (thalassemia major) - inherited abnormality of iron absorption
30
Treatment of acute iron toxicity
Correct acid base talets, deferoxamine (chelator), NOT activated charcol (does not bind in gut to iron)
31
Treatment of chronic iron toxicity
Phlebotomy. deferoxamine or deferasirox (chelator)
32
What is vitamin B12 required for
cofactor for synthesis of DNA
33
What deficits does B12 deficency cause
Neurological also manifests first as anemia
34
How is vitamin B12 produced
by bacteria
35
B12 is absorbed in the GI tract as long as what product is also in the GI tract
Intrensic factor has to be in the GI tract for B12 absorption
36
Where is vitamin B12 stored and how long does its storage last there?
Stored in the liver, every person has enough to last 5 years
37
What are the 2 forms of vitamin B12
Cyanocobalmin and hydroxocobalmin (hydroxocobalmin is longer circulating)
38
Vitamin B12 is essential in which 2 reactions
converting mmcoa to succinyl coa and homocysteine to methionine. The second is needed in folic acid metabolism and dTMP, which is required for DNA synthesis
39
How does folic acid administration help patients with B12 deficiency
Giving folic acid helps refil tetrahydrofolate pool and corrects the anemia, but does not correct for vitamin B12 neurological deficits
40
Deficiency of Folic acid usually presents as which type of anemia
megaloblastic
41
Deficiency of which factor increases the risk of neural tube defects in fetuses
Folic acid deficiency
42
How long after dietary intake of folic acid is corrected do anemias resolve
A few months
43
What are the toxic effects of folic acid
No recognized toxicity
44
How was EPO purified
from the urine of patients with severe anemia
45
How long is the half life of EPO
4-13 hours
46
What does EPO stimulate
Erythroid proliferation and differentiation
47
Where is endogenous EPO produced
in the kidney
48
What stimulates epo release
tissue hypoxia
49
What kind of relationship exists between hematocrit or hemoglobin and EPO serum leel
Inverse relationship
50
What is the exception with the inverse relationship between EPO and hematocrit levels
Patients in kidney failure-- low EPO levels because kidneys can't produce EOI
51
How far after ESA administration does a AKI patient's reticulocyte count and hemoglobin level rise
Retics rise in 10 days, hct and hgb rise in 2-6 weeks
52
Which alternative approach to ckd anemia is now in clinical trials and what does it do
Roxadustat is a small molecule PHD inhibitor to increase hemoglobin. A DNA regulating factor called HIF (hypoxia inducing factor) inactivates normal O2 levels using PHDs, and during hypoxia, increase EPO. So, inhibiting PHDs makes the body think its in a hypoxic state, thus increasing EPO.
53
What are the most common adverse affects of EPO
HTN and Thrombotic complicatoins

Pharmacology (12 decks)

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