Week 2 Reading Flashcards

1
Q

How is Thrombocytopenia treated

A

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

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

What type of solubility does Vitamin K have

A

Fat-soluble

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

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

How is vitamin K deficiency treated

A

Vitamin K1 (phytonadione)

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

What is used to reverse the anticoagulent effect of excess warfarin

A

Vitamin K1 (phytonadione)

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

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

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

A

-Expensive
- Risk of infection
- Risk of immunologic reaction

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the function of desmopressin

A

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

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

What is the purpose of antiplasmin agents

A

Prevent or manage acute bleeding episodes in patients with hemophilia

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

What are 2 antiplasmin agents

A

Aminocaproic acid and tranexamic acid

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

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

A

antiplasmin agents
Inhibit fibrinolysis by inhibiting plasminogen activation

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

Which drug inhibits fibrinolysis by inhibiting plasminogen activation

A

Aminocaproic acid and tranexamic acid

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

Which drug increases the plasma concentration of vWF and factor 8

A

desmopressin

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

What is the essential metalic component of heme

A

Iron

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

What molecule is responsible for oxygen transport in the blood

A

heme

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

What does iron do

A

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

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

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

Which individuals have an increased demand for iron

A

children and pregnant women

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

Which groups of people is iron deficiency most commonly found in

A
  • Vegetarians
  • Malnourished people
  • Women d/t menstrual blood loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Iron should NOT be given in which type of anemia

A

hemolytic anemia (iron stores are elevated, not depressed)

26
Q

Which drug do you want to give After an MRI and not before?

A

Ferumoxytol- iron oxide, give after MRI.

27
Q

What are the common symptoms of iron overdose

A

Gastroenteritis
Shock
Metabolic acidosis
coma
death

28
Q

What is chronic iron overload called

A

hemochromatosis
Damage to organs that store excess iron (heart, liver, pancreas)

29
Q

Who does hemochromatosis occur most often in

A
  • Transfusion recipients for hemolytic disorders (thalassemia major)
  • inherited abnormality of iron absorption
30
Q

Treatment of acute iron toxicity

A

Correct acid base talets, deferoxamine (chelator), NOT activated charcol (does not bind in gut to iron)

31
Q

Treatment of chronic iron toxicity

A

Phlebotomy.
deferoxamine or deferasirox (chelator)

32
Q

What is vitamin B12 required for

A

cofactor for synthesis of DNA

33
Q

What deficits does B12 deficency cause

A

Neurological
also manifests first as anemia

34
Q

How is vitamin B12 produced

A

by bacteria

35
Q

B12 is absorbed in the GI tract as long as what product is also in the GI tract

A

Intrensic factor has to be in the GI tract for B12 absorption

36
Q

Where is vitamin B12 stored and how long does its storage last there?

A

Stored in the liver, every person has enough to last 5 years

37
Q

What are the 2 forms of vitamin B12

A

Cyanocobalmin and hydroxocobalmin (hydroxocobalmin is longer circulating)

38
Q

Vitamin B12 is essential in which 2 reactions

A

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
Q

How does folic acid administration help patients with B12 deficiency

A

Giving folic acid helps refil tetrahydrofolate pool and corrects the anemia, but does not correct for vitamin B12 neurological deficits

40
Q

Deficiency of Folic acid usually presents as which type of anemia

A

megaloblastic

41
Q

Deficiency of which factor increases the risk of neural tube defects in fetuses

A

Folic acid deficiency

42
Q

How long after dietary intake of folic acid is corrected do anemias resolve

A

A few months

43
Q

What are the toxic effects of folic acid

A

No recognized toxicity

44
Q

How was EPO purified

A

from the urine of patients with severe anemia

45
Q

How long is the half life of EPO

A

4-13 hours

46
Q

What does EPO stimulate

A

Erythroid proliferation and differentiation

47
Q

Where is endogenous EPO produced

A

in the kidney

48
Q

What stimulates epo release

A

tissue hypoxia

49
Q

What kind of relationship exists between hematocrit or hemoglobin and EPO serum leel

A

Inverse relationship

50
Q

What is the exception with the inverse relationship between EPO and hematocrit levels

A

Patients in kidney failure– low EPO levels because kidneys can’t produce EOI

51
Q

How far after ESA administration does a AKI patient’s reticulocyte count and hemoglobin level rise

A

Retics rise in 10 days, hct and hgb rise in 2-6 weeks

52
Q

Which alternative approach to ckd anemia is now in clinical trials and what does it do

A

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
Q

What are the most common adverse affects of EPO

A

HTN and Thrombotic complicatoins