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Flashcards in Chapter 9: Blood disorders Deck (196):
1

 

 

What drugs are used to treat anemia?

 

 

Iron

Folic acid

B6

2

 

 

Anemia: HGB levels

 

<13 in men

<12 on period

<11 if pregnant

3

 

 

How does Iron prevent/treat anemia

 

 

Help with production of HGB

4

 

 

when should iron supplements be avoided?

 

 

iron overload syndromes:

hemosiderosis

hemochromotosis

5

 

 

what patients often become anemic?

 

 

chronic renal failure

6

 

 

Iron mechanism of action

 

 

molecule of iron becomes incorporated into a heme

one heme unit attaches to a globin protein

4 heme-globin subunits combine to make one unit of HGB

7

 

 

Iron: Absorption

 

 

the major control point

mainly in jejunum

5-10% of oral intake

8

 

 

Iron: distribution

 

 

remains in the body for many months

will ceoss placenta and enter breast milk

90%protein bound

9

 

 

Iron: metabolism

 

 

recycled daily

10

 

 

iron: excretion

 

 

small daily losses through sweat, desquamination, urine, and bile (unless there is a massive blood loss)

11

 

 

how long is therapy needed to replace depleted stores of iron

 

 

3-6 months

12

 

 

Iron Side effects: DERM

 

 

flushing, uticaria

13

 

 

Iron sifeeffects: GI

heartburn

nausea

diarrhea/constipation

abdominal cramps

14

 

 

what can help ease GI side effects of iron?

 

 

start with small dose and work up over several days or weeks

15

 

 

iron side effects: MISC

 

 

pan at IM site

phlebitis at IV site

metallic taste

16

 

 

Iron side effects: NEURO

 

 

seizures, dizziness, syncope, headache

17

 

 

delayed side effects of iron

 

 

hemosiderosis

lymphadenopathy

myalgia, fatigue, 

arthralgia and fever

anaphylactoid reaction

18

 

What medications decrease iron's effect

 

Thyroxine

any drug that changes gastric pH

19

 

 

what other substances decrease iron's effectiveness

 

 

coffee, tea, fiber/bran

20

 

 

Iron increases the absorption of what?

 

 

tetracyclines, OCN, quinolones

21

 

 

what should be considered with iron deficiency anemia past age 50?

 

 

eval for GI cancers

22

 

 

What should you consider if iron therapy does not resolve anemia?

 

incorrect diagnosis

complicating illness

non-compliance

inadequate dose

continuing iron loss

iron malabsorption 

23

 

 

What enhances the absorption of iron?

 

 

 

 

 

 

Vitamin C

meat

24

 

 

what hinders absorption of iron?

 

 

calcium

fiber

tea

coffee

wine

25

 

 

Typical causes of iron deficiency

 

 

poor dietary intake

loss of blood

poor absorption

26

 

 

Risk factors for iron deficiency anemia

 

African American or Mexican

blood donation

poor

pregnant and post patum

child/adolescent obestity

vegetarian diet

27

 

 

what lab should be drawn before begining iron therapy?

 

 

serum ferritin

28

 

 

What should be used for iron therapy in patients on dialysis?

 

 

Iron sucrose

29

 

 

Serum ferritin level in iron deficiency anemia

 

 

<25mcg/L

>100mcg/L rules it out

30

 

 

Patient education for iron therapy

 

encourage compliance

possible black stools

avoid foods that reduce iron absorption

31

 

 

What does folic acid stimulate?

 

 

production of protein synthesis needed for RBCs, WBCs, and platelet formation

32

 

 

What is folic acid used for?

 

 

prevent or treat folate deficiency

33

 

 

Why is folic acid recommended for pregnant women?

 

 

reduces the incidence of neural tube defects in the offspring

34

 

 

dietary sources of folate

 

green leafy vegetable, meats, yeasts, nuts, beans, organ juice, dairy products, grains, cereals

35

 

 

serum levels to indicate folate deficiency

 

< 2.5 mcg/L

< 5mcg/L in older adults

36

 

 

Folic acid: absorption

 

 

well absorbed within 30-60 minnutes in the proximal small intestine

(oral)

37

 

 

folic acid: distribution

 

 

1/2 circulates through enterohepatic circulation

other 1/2 circulates bound to protein

38

 

 

folic acid: metabolism

 

 

converted by the liver to an active metabolite

39

 

 

folic acid: excretion

 

 

excess amounts excreted unchanged by kidney

40

 

 

folic acid: half-life

 

 

unknown

41

 

 

Folic acid side effects: DERM

 

 

rashes

42

 

 

folic acid side effects: MISC

 

 

fevers

43

 

 

which medication does folate interact with?

 

 

phenytoin

(which is associated with folate deficiency in and of itself)

44

 

 

Folic acid contraindications

 

 

No known

make sure there are adequate B12 strores before prescribing

45

 

 

Folic acid: patient education

 

may turn urine yellow

report any rash

eat a balanced diet

46

 

 

What is vitamin B12?

 

 

coenzyme for many metabolic processes

not produced by the body so it must be supplemented

47

 

 

what is required for GI absorption of B12?

 

 

intrinsic factor and calcium

48

 

 

most common cause of B12 deficiency

 

 

inability of patient to split the R factor from B12 in foods

49

 

 

Risk factors for B12 deficiency

 

those taking medications that alkalize stomach pH

surgical resection of the stomach or ileum

vegan diet

50

 

 

Clinical uses for B12

 

 

B12 deficiency anemia

neurologic complications

demetia 

51

 

 

B12: distribution

 

 

stored in the liver

52

 

 

B12: metabolism/excretion

 

 

any excess is excreted unchanged in the urine

53

 

 

B12: half-life

 

 

6 days

54

 

 

B12 side effects: CV

 

 

peripheral vascular thrombosis

55

 

 

B12 side effects: DERM

 

 

itching, urticaria, swelling

56

 

 

B12 side effects: GI

 

 

diarrhea, N/V

57

 

 

B12 side effects: META

 

 

hypokalemia with heavy dosing d/t intracellular shift of the potassium ion

58

 

 

B12 side effects: MISC

 

 

pain at injection site, hypersensitivity reactions

(including anaphylaxis)

59

 

 

B12 side effects: NEURO

 

 

headache, anxiety

60

 

 

B12 contraindications

 

 

Those with Leber's optic nerve atrophy

61

 

 

What if vitamin B12 deficiency goes undiagnosed?

 

 

can lead to irreversible neurological damage

62

 

 

What other labs should be monitored when a patient is on B12

 

HCT

reticulocyte count

folate/iron levels

63

 

 

How does erythropoietin induce RBC production?

 

 

stimulating division and differentiation of erythroid precursor cells in the bone marrow

64

 

 

what does erythropoietin do?

 

 

induces RBC production

Induces release of reticulocytes from marrow into bloodstream

65

 

 

erythropoietin contraindications

 

 

nonspecific anemia, uncontrolled HTN. albumin allery

66

 

 

Normal levels of erythropoietin

 

 

5-30 mU/mL

67

 

 

erythropoietin: absorption

 

 

rapidly absorbed from subQ sitesand is taken up by bone marrow, liver, and kidneys

68

 

 

Erythropoietin: distribution

 

 

unknown

69

 

 

Erythropoietin: metabolism/excretion

 

 

metabolized by liver to inactive metabolites

small amounts excreted unchanged into urine

70

 

 

eruthropoietin: half-life

 

 

4-13 hours

71

 

 

erythropoietin's effect is dependent on what?

 

 

its dose

72

 

 

erythropoietin side effects: CV

 

can precipitate hypertensive crisis (id BP poorly controlled)

HTN/seizures (if HCT rises too rapidly)

MI, chest pain, vascular thrombosis (hemodialysis patients)

73

 

 

erythropoietin clinical uses

 

anemia associated with renal failure

(HCT should be 100ng/dL

and transferrin saturation should be >20-30%)

74

 

 

erythropoietin sidef effects: DERM

 

 

 

transient rashes

75

 

 

erythropoietin sidef effects: ENDO

 

 

restored fertility, resumption of menses

76

 

 

erythropoietin sidef effects:  GI

 

 

diarrhea, nausea

77

 

 

erythropoietin sidef effects:  HEM

 

 

thromboembolism

78

 

 

erythropoietin sidef effects:  ONCOLOGY

 

 

lower survival rates

79

 

 

erythropoietin sidef effects:  MS

 

 

paresthesias

80

 

 

erythropoietin sidef effects: NEURO

 

 

seizures, headache

81

 

 

erythropoietin sidef effects:  PULM

 

 

upper respiratory infection

82

 

 

erythropoietin interacts with which drugs

 

 

None

83

 

 

erythropoietin: conscientious prescribing

 

 

Page 142 in text

84

 

 

heparin: mechanism of action

 

 

binds to antithrombin converting it to a powerful anticoagulant

85

 

 

Heparin: absorption

 

 

Not absorbed orally

must be given IV or SQ

86

 

 

heparin: clinical uses

 

 

prevention of venous thromboembolism

treatment of venous or arterial thromboembolism

87

 

 

unfractionate heparin v. low molecular weight heparins

 

LMWHs have a longer half life and can be given 1-2 daily doses

UH mst be given as cont IV infusion or multiple daily SQ injections

88

 

 

Things to watch for in patients taking heparin

 

 

hepatitis

bleeding

heparin-induced thrombocytopenia (HIT)

89

 

 

heparin induced thrombocytopenia

 

 

serious and potentially life threatening condition caused by antibodies to platelets

 

90

 

 

labs used to monitor Heparin

 

 

aPTT

ACT

91

 

 

heparin contraindications

 

history of peptic ulcer disease

poorly controlled HTN

diabetic retinopathy

if patient has ever experienced heparin induced thombocytopenia

92

 

 

NSAIDs and heparin

 

 

Increased bleeding risk

93

 

 

When is INR needed with heparin

 

 

If coadministered with coumadin

94

 

 

OTC products to avoid while on heparin

 

 

 

ginko, garlic, gimseng, vitamin E, fish oil

95

 

 

Baseline labs for heparin

 

 

PT/PTT

HGB/HCT

platelets

96

 

 

labs to monitor during heparin therapy

 

 

PTT

periodic platelet count

monitor for signs of bleeding

97

 

 

Patient education: heparin

 

signs of bleeding

use soft toothbrush and electric razors

wear a medical alert bracelet

98

 

 

LMW heparin drug names

 

danaparoi (Orgaran)

enoxaparin (Lovenox)

dalteparin (Fragmin)

fondaparinux (Arixtra)

tinzaparin (Innohep)

99

 

 

LMW heparin: mechanism of action

 

 

inhibits factor Xa more that it does thrombin

100

 

 

LMW heparin: absorption

 

 

parenteral administration as they are destroyed by enzymes in the bowel

101

 

 

LMW heparin: metabolism/excretion

 

 

some ar artially metabolized or not at all, excreted renally

102

 

LMW heparin: half lives

enoxaparin: 3-6hrs

dalteparin: 2hr

danaparoid: 24hrs

tinzaparin: 4hrs

fondaparinux: 17hr (21hrs in elderly)

103

 

 

LMW heparin: clinical uses

 

 

prevention/treatment of DVT/PE

acute coronary syndrome

(more effective and safe than heparin for this)

104

 

 

LMW heparin side effects: DERM

 

local skin reactions

105

 

 

LMW heparin side effects: GI

 

 

diarrhe, nausea

106

 

 

LMW heparin side effects: HEM

 

 

bleeding

most serious sites are: CNS, GI tract, and retroperitoneal space

107

 

 

LMW heparin side effects: META

 

 

elevated tranaminases

108

 

 

LMW heparin side effects: MS

 

 

long term use may cause osteoporosis

109

 

 

LMW heparin contraindications

 

spinal or epidural catheters

(risk for spinal and epidural hematoma that can cause paralysis)

110

 

 

how long after removal of a spinal or epidural catheter must you wait before administering LMW heparin

 

 

at least 4 hours

111

 

 

how is LMW heparin administered

 

 

SQ not IM

112

 

 

Are heparin, LMW heparins, and fondaparinux interchangeable?

 

 

NO

113

 

 

herbals to avoid while on heparin

 

 

dong quai, evening primrose, garlic, ginger, ginko, ginseng, green tea

114

 

 

Coumadin mechanism of action

 

 

interferes with synthesis of vitamin K-dependent clotting factors by inhibiting vitamin K epoxide reductase

115

 

 

vitamin K-depedent clotting factors

 

 

2, 7, 9, 10

116

 

 

How is coumadin administered

 

 

Oral only

117

 

 

how long does it take for coumading to stabilize in the body?

 

 

5-6 days

118

 

 

coumadin: clinical uses

 

 

reduce risk of stroke or peripheral embolism in those with non-valvular a-fib

prevent/treat DVT/PE

patients with metal cardiac valves

short term use after placement of bioprosthetic cardiac valves

119

 

 

therapeutic range for coumadin

 

 

2-3

120

 

 

coumadin: absorption

 

 

nearly 100% bioavailability orally

121

 

 

coumadin: distribution

 

 

crosses placenta but does not enter breast milk because it is 99% protein bound

122

 

 

coumadin: metabolism/excretion

 

 

hepatic metabolism

123

 

 

coumadin: half-life

 

 

1/2 day - 3 days

124

 

 

what dose should you start coumadin at

 

5mg if also on heparin, otherwise 2.5mg

125

 

 

Coumadin side effects: DERM

 

skin necrosis and gangrene d/t paradoxical local thrombosis

rare

often shows in limbs, penis, or breast

126

 

 

Coumadin side effects: HEM

 

 

bleeding

127

 

 

Coumadin side effects: MS

 

 

long term use associated with osteoporosis

128

 

 

drugs that decrease effectiveness of coumadin

 

antithyroid drugs

barbituates

carbamazepine

phenytoin

rifampin

cholestyramine

129

 

 

Coumadin: conscientious considerations

 

 

Page 147-148 of the text

130

 

 

Pradaxa: clinical use

 

prevention of stroke or peripheral embolism in patients with a-fib

131

 

 

pradaxa mechanism of action

 

 

directly inhibts production of thrombin (Final step in the clotting cascade)

132

 

 

Pradaxa comes in what forms

 

 

PO and IM

133

 

 

How long does it take for PO Pradaxa to reach peak

serum concentration

 

 

2 hours

134

 

 

Pradaxa: absorption/distribution

 

3-7% is rapidly absorbed

135

 

 

Pradaxa: metabolism/excretion

 

 

metabolized to active metabolite in the liver with elimination by kidneys

136

 

 

converting from coumadin to pradaxa

 

 

d/c coumadin and start pradaxa when INR falls below 2

137

 

 

converting from pradaxa to coumadin

CrCl >50 mL/min

 

 

start coumadin 3 days before stopping pradaxa

138

 

 

converting from pradaxa to coumdain

CrCl  31-50mL/min

 

 

start coumadin 2 days before stopping pradaxa

139

 

 

converting from pradaxa to coumdain

CrCl  15-30 mL/min

 

 

start coumadin 1 day before stopping pradaxa

140

 

 

converting from heparin to pradaxa

 

 

start pradaxa 0-2 hours before next heparin dose is due

141

 

 

discontinuing pradaxa prior to surgery

 

CrCl >50 = 1-2 days prior

CrCl <50 = 3-5 days prior

142

 

 

Pradaxa side effects: GI

 

 

dyspepsia, abdominal pain

143

 

 

Pradaxa side effects: HEM

 

 

bleeding

144

 

 

what drug does pradaxa interact with

 

 

rifampin

(reduces the concentration of pradaxa)

145

 

 

when is anti-platelet therapy indicated

 

 

all acute coronary syndromes

after noncardioembolic stroke/TIA

patients with peripheral artery disease after CABG or carotid endarterectomy

primary prevention (if multiple risk factors)

146

 

 

anti-platelet: aspirin

mechanism of action

 

 

potent irreversible inhibitor of cyclo-oxygenase (COX-1)

147

 

 

Aspirin: absorption

 

 

rapidly absorbed in stomach and upper bowel

148

 

 

how long does it take for platelet inhibition

by aspirin to be detectable?

 

 

1 hour

149

 

 

optimal aspirin dose for prevention of MI/stroke

 

 

50-100mg daily

150

 

 

optimal aspirin dosage for acute conditions

(acute coronary syndrome, stroke)

 

 

 

 

160-325mg

151

 

 

aspirin dsage for chronic use

 

 

no reason to exceed 81mg

152

 

 

aspirin side effects: GI

 

 

dose related bleeding

153

 

 

aspirin side effects: HEM

 

 

low risk of intracranial bleeding

154

 

 

aspirin side effects: EENT

 

 

tinnitus

155

 

 

aspirin interactions

 

 

coadministration with traditional NSAIDs can negate cardioprotective effect

156

 

 

what if a patient has cardiovascular disease but gets GI bleeds with aspirin

 

 

combination therapy with esomeprazole 20mg and low dose aspirin 75mg

157

 

 

clopidogrel (Plavix)

mechanism of action

 

blocks platelet activation by selectively and irreversibly blockng the binding of ADP to the platelet

this prevents the ADP-dependent activation of Gp IIb-IIIa complex

158

 

 

Plavix: absorption

 

 

well absobed orally

159

 

 

Plavix: metabolism

 

 

quickly metabolized by the liver into an active metabolite

160

 

 

Plavix: excretion

 

 

50% in urine

45% in feces

161

 

 

Plavix: half-life

 

 

Active metabolite 8hrs

162

 

 

When should plavix be used along with aspirin?

 

management of acute coronary syndrome, including unstable angina and acute MI

in patients undergoing angioplasty with either bare metal or drug eluting stents

163

 

 

how long should you wait to d/c plavix after ACS is relieved?

 

indefinite if treated with stents

after 1 year if treated without stents

164

 

 

When should aspirin alone be used

 

 

vascular disease without prior MI or stents

(stable CAD, prior TIA or CVA, peripheral artery disease)

 

165

 

 

when should aspirin be used prophylactically

 

no established heart disease but lots of risk factors

166

 

 

Plavix side effects: CV

 

 

chest pain, edema, HTN

167

 

 

Plavix side effects: DERM

 

 

pruritis, purpurea, rash

168

 

 

Plavix side effects: HEM

 

 

bleeding

thrombotic thrombocytopenic purpura (rare)

169

 

 

Plavix side effects: GI

 

 

abdominal pain, N/V, constipation

170

 

 

Plavix side effects: NEURO

 

 

headache, dizziness, depression, fatigue, generalized pain

171

 

 

Which drugs decrease effectiveness of plavix

 

 

atorvastatin, clarithromycin, erythromycin

172

 

 

which drugs increase effect of plavix

 

 

rifampin and other antiplatelets and anticoagulants

173

 

 

plavix contraindications

 

 

prior/active bleeding events

174

 

 

prasugrel (Effient)

 

 

second thienopyridine approved as an antiplatelt drug

175

 

 

effient mechanism of action

 

 

binds to ADP receptor on platelet surface and irreversibly inhibits platelet activity

176

 

 

why is effient a "pro-drug"

 

 

it undergoes metabolic activation by intestinal esterases and then through liver's CYPA34 and 2B6 systems

177

 

 

when is effient indicated?

 

 

acute coronary syndromes who are undergoing primary coronary interventions

178

 

 

effient contraindications

 

 

patients older than 75 or those weighing less than 60kg

patients with history of stroke

179

 

 

why should effient not be routinely used

 

 

higher efficiency but also higher side effects (increased bleeding risk)

180

 

 

effient: absorption

 

 

rapid within 30 minutes of oral administration

181

 

 

effient: distribution

 

 

plasma proteins

182

 

 

effient: metabolism

 

 

hepatic cytochrome P450 isoenzymes

(CYP3A4, CYP2C9. CYP2C19, CYP2B6)

183

 

 

effient: excretion

 

 

mostly in urine, some in feces

184

 

 

effient: half-life

 

 

7 hours

onset of platelet activity 30 minutes

steady state reached in 3 days

185

 

 

effient dosage and administration

 

 

page 153

186

 

 

Aggrenox

 

 

 

 

 

 

50mg of aspirin with 200mg ER dipyridamole

187

 

 

Aggrenox: clinical use

 

 

prevention of vascular events

(most commonly used to prevent strokes)

188

 

 

IV Aggrenox

 

 

used by cardiologists to cause maximal coronary vasodilation

189

 

 

Aggrenox contraindications

 

 

patients with bronchospasm

190

 

 

when is aspirin preferable to aggrenox

 

 

patients with establish CAD or PAD

191

 

 

fibrinolytic (thrombolytic) agents

 

 

drugs that lyse blood clots

(all are forms of tissue plasminogen activator tPA)

192

 

 

fibrinolytic agents: mechanism of action

 

 

tPA binds to fibrin and convert plasminogen to plasmin which causes local fibrinolysis, dissolving clots

193

 

 

how are fibrinolytics administered

 

 

IV only

194

 

 

fibrinolytics: clinical uses

 

 

treatment of ST-segment elevation MI

acute massive PE, acute ischemic stroke

to open clotted central venous access devices (alteplase only)

195

 

 

Fribrinolytic drug names

 

 

Alteplase (Activase, cathflo activase)

reteplase (Retavase)

tenecteplase (TNKase)

196