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Pharmacology > Chapter 9: Blood disorders > Flashcards

Chapter 9: Blood disorders Flashcards

1
Q

What drugs are used to treat anemia?

A

Iron

Folic acid

B6

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2
Q

Anemia: HGB levels

A

<13 in men

<12 on period

<11 if pregnant

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3
Q

How does Iron prevent/treat anemia

A

Help with production of HGB

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4
Q

when should iron supplements be avoided?

A

iron overload syndromes:

hemosiderosis

hemochromotosis

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5
Q

what patients often become anemic?

A

chronic renal failure

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6
Q

Iron mechanism of action

A

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

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7
Q

Iron: Absorption

A

the major control point

mainly in jejunum

5-10% of oral intake

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8
Q

Iron: distribution

A

remains in the body for many months

will ceoss placenta and enter breast milk

90%protein bound

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9
Q

Iron: metabolism

A

recycled daily

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10
Q

iron: excretion

A

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

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11
Q

how long is therapy needed to replace depleted stores of iron

A

3-6 months

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12
Q

Iron Side effects: DERM

A

flushing, uticaria

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13
Q

Iron sifeeffects: GI

A

heartburn

nausea

diarrhea/constipation

abdominal cramps

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14
Q

what can help ease GI side effects of iron?

A

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

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15
Q

iron side effects: MISC

A

pan at IM site

phlebitis at IV site

metallic taste

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16
Q

Iron side effects: NEURO

A

seizures, dizziness, syncope, headache

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17
Q

delayed side effects of iron

A

hemosiderosis

lymphadenopathy

myalgia, fatigue,

arthralgia and fever

anaphylactoid reaction

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18
Q

What medications decrease iron’s effect

A

Thyroxine

any drug that changes gastric pH

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19
Q

what other substances decrease iron’s effectiveness

A

coffee, tea, fiber/bran

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20
Q

Iron increases the absorption of what?

A

tetracyclines, OCN, quinolones

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21
Q

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

A

eval for GI cancers

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22
Q

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

A

incorrect diagnosis

complicating illness

non-compliance

inadequate dose

continuing iron loss

iron malabsorption

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23
Q

What enhances the absorption of iron?

A

Vitamin C

meat

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24
Q

what hinders absorption of iron?

A

calcium

fiber

tea

coffee

wine

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25
Q

Typical causes of iron deficiency

A

poor dietary intake

loss of blood

poor absorption

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26
Q

Risk factors for iron deficiency anemia

A

African American or Mexican

blood donation

poor

pregnant and post patum

child/adolescent obestity

vegetarian diet

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27
Q

what lab should be drawn before begining iron therapy?

A

serum ferritin

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28
Q

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

A

Iron sucrose

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29
Q

Serum ferritin level in iron deficiency anemia

A

<25mcg/L

>100mcg/L rules it out

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30
Q

Patient education for iron therapy

A

encourage compliance

possible black stools

avoid foods that reduce iron absorption

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31
Q

What does folic acid stimulate?

A

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

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32
Q

What is folic acid used for?

A

prevent or treat folate deficiency

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33
Q

Why is folic acid recommended for pregnant women?

A

reduces the incidence of neural tube defects in the offspring

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34
Q

dietary sources of folate

A

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

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35
Q

serum levels to indicate folate deficiency

A

< 2.5 mcg/L

< 5mcg/L in older adults

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36
Q

Folic acid: absorption

A

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

(oral)

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37
Q

folic acid: distribution

A

1/2 circulates through enterohepatic circulation

other 1/2 circulates bound to protein

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38
Q

folic acid: metabolism

A

converted by the liver to an active metabolite

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39
Q

folic acid: excretion

A

excess amounts excreted unchanged by kidney

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40
Q

folic acid: half-life

A

unknown

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41
Q

Folic acid side effects: DERM

A

rashes

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42
Q

folic acid side effects: MISC

A

fevers

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43
Q

which medication does folate interact with?

A

phenytoin

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

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44
Q

Folic acid contraindications

A

No known

make sure there are adequate B12 strores before prescribing

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45
Q

Folic acid: patient education

A

may turn urine yellow

report any rash

eat a balanced diet

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46
Q

What is vitamin B12?

A

coenzyme for many metabolic processes

not produced by the body so it must be supplemented

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47
Q

what is required for GI absorption of B12?

A

intrinsic factor and calcium

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48
Q

most common cause of B12 deficiency

A

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

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49
Q

Risk factors for B12 deficiency

A

those taking medications that alkalize stomach pH

surgical resection of the stomach or ileum

vegan diet

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50
Q

Clinical uses for B12

A

B12 deficiency anemia

neurologic complications

demetia

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51
Q

B12: distribution

A

stored in the liver

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52
Q

B12: metabolism/excretion

A

any excess is excreted unchanged in the urine

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53
Q

B12: half-life

A

6 days

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54
Q

B12 side effects: CV

A

peripheral vascular thrombosis

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55
Q

B12 side effects: DERM

A

itching, urticaria, swelling

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56
Q

B12 side effects: GI

A

diarrhea, N/V

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57
Q

B12 side effects: META

A

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

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58
Q

B12 side effects: MISC

A

pain at injection site, hypersensitivity reactions

(including anaphylaxis)

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59
Q

B12 side effects: NEURO

A

headache, anxiety

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60
Q

B12 contraindications

A

Those with Leber’s optic nerve atrophy

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61
Q

What if vitamin B12 deficiency goes undiagnosed?

A

can lead to irreversible neurological damage

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62
Q

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

A

HCT

reticulocyte count

folate/iron levels

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63
Q

How does erythropoietin induce RBC production?

A

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

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64
Q

what does erythropoietin do?

A

induces RBC production

Induces release of reticulocytes from marrow into bloodstream

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65
Q

erythropoietin contraindications

A

nonspecific anemia, uncontrolled HTN. albumin allery

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66
Q

Normal levels of erythropoietin

A

5-30 mU/mL

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67
Q

erythropoietin: absorption

A

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

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68
Q

Erythropoietin: distribution

A

unknown

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69
Q

Erythropoietin: metabolism/excretion

A

metabolized by liver to inactive metabolites

small amounts excreted unchanged into urine

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70
Q

eruthropoietin: half-life

A

4-13 hours

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71
Q

erythropoietin’s effect is dependent on what?

A

its dose

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72
Q

erythropoietin side effects: CV

A

can precipitate hypertensive crisis (id BP poorly controlled)

HTN/seizures (if HCT rises too rapidly)

MI, chest pain, vascular thrombosis (hemodialysis patients)

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73
Q

erythropoietin clinical uses

A

anemia associated with renal failure

(HCT should be 100ng/dL

and transferrin saturation should be >20-30%)

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74
Q

erythropoietin sidef effects: DERM

A

transient rashes

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75
Q

erythropoietin sidef effects: ENDO

A

restored fertility, resumption of menses

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76
Q

erythropoietin sidef effects: GI

A

diarrhea, nausea

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77
Q

erythropoietin sidef effects: HEM

A

thromboembolism

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78
Q

erythropoietin sidef effects: ONCOLOGY

A

lower survival rates

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79
Q

erythropoietin sidef effects: MS

A

paresthesias

80
Q

erythropoietin sidef effects: NEURO

A

seizures, headache

81
Q

erythropoietin sidef effects: PULM

A

upper respiratory infection

82
Q

erythropoietin interacts with which drugs

A

None

83
Q

erythropoietin: conscientious prescribing

A

Page 142 in text

84
Q

heparin: mechanism of action

A

binds to antithrombin converting it to a powerful anticoagulant

85
Q

Heparin: absorption

A

Not absorbed orally

must be given IV or SQ

86
Q

heparin: clinical uses

A

prevention of venous thromboembolism

treatment of venous or arterial thromboembolism

87
Q

unfractionate heparin v. low molecular weight heparins

A

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
Q

Things to watch for in patients taking heparin

A

hepatitis

bleeding

heparin-induced thrombocytopenia (HIT)

89
Q

heparin induced thrombocytopenia

A

serious and potentially life threatening condition caused by antibodies to platelets

90
Q

labs used to monitor Heparin

A

aPTT

ACT

91
Q

heparin contraindications

A

history of peptic ulcer disease

poorly controlled HTN

diabetic retinopathy

if patient has ever experienced heparin induced thombocytopenia

92
Q

NSAIDs and heparin

A

Increased bleeding risk

93
Q

When is INR needed with heparin

A

If coadministered with coumadin

94
Q

OTC products to avoid while on heparin

A

ginko, garlic, gimseng, vitamin E, fish oil

95
Q

Baseline labs for heparin

A

PT/PTT

HGB/HCT

platelets

96
Q

labs to monitor during heparin therapy

A

PTT

periodic platelet count

monitor for signs of bleeding

97
Q

Patient education: heparin

A

signs of bleeding

use soft toothbrush and electric razors

wear a medical alert bracelet

98
Q

LMW heparin drug names

A

danaparoi (Orgaran)

enoxaparin (Lovenox)

dalteparin (Fragmin)

fondaparinux (Arixtra)

tinzaparin (Innohep)

99
Q

LMW heparin: mechanism of action

A

inhibits factor Xa more that it does thrombin

100
Q

LMW heparin: absorption

A

parenteral administration as they are destroyed by enzymes in the bowel

101
Q

LMW heparin: metabolism/excretion

A

some ar artially metabolized or not at all, excreted renally

102
Q

LMW heparin: half lives

A

enoxaparin: 3-6hrs
dalteparin: 2hr
danaparoid: 24hrs
tinzaparin: 4hrs
fondaparinux: 17hr (21hrs in elderly)

103
Q

LMW heparin: clinical uses

A

prevention/treatment of DVT/PE

acute coronary syndrome

(more effective and safe than heparin for this)

104
Q

LMW heparin side effects: DERM

A

local skin reactions

105
Q

LMW heparin side effects: GI

A

diarrhe, nausea

106
Q

LMW heparin side effects: HEM

A

bleeding

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

107
Q

LMW heparin side effects: META

A

elevated tranaminases

108
Q

LMW heparin side effects: MS

A

long term use may cause osteoporosis

109
Q

LMW heparin contraindications

A

spinal or epidural catheters

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

110
Q

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

A

at least 4 hours

111
Q

how is LMW heparin administered

A

SQ not IM

112
Q

Are heparin, LMW heparins, and fondaparinux interchangeable?

A

NO

113
Q

herbals to avoid while on heparin

A

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

114
Q

Coumadin mechanism of action

A

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

115
Q

vitamin K-depedent clotting factors

A

2, 7, 9, 10

116
Q

How is coumadin administered

A

Oral only

117
Q

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

A

5-6 days

118
Q

coumadin: clinical uses

A

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
Q

therapeutic range for coumadin

A

2-3

120
Q

coumadin: absorption

A

nearly 100% bioavailability orally

121
Q

coumadin: distribution

A

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

122
Q

coumadin: metabolism/excretion

A

hepatic metabolism

123
Q

coumadin: half-life

A

1/2 day - 3 days

124
Q

what dose should you start coumadin at

A

5mg if also on heparin, otherwise 2.5mg

125
Q

Coumadin side effects: DERM

A

skin necrosis and gangrene d/t paradoxical local thrombosis

rare

often shows in limbs, penis, or breast

126
Q

Coumadin side effects: HEM

A

bleeding

127
Q

Coumadin side effects: MS

A

long term use associated with osteoporosis

128
Q

drugs that decrease effectiveness of coumadin

A

antithyroid drugs

barbituates

carbamazepine

phenytoin

rifampin

cholestyramine

129
Q

Coumadin: conscientious considerations

A

Page 147-148 of the text

130
Q

Pradaxa: clinical use

A

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

131
Q

pradaxa mechanism of action

A

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

132
Q

Pradaxa comes in what forms

A

PO and IM

133
Q

How long does it take for PO Pradaxa to reach peak

serum concentration

A

2 hours

134
Q

Pradaxa: absorption/distribution

A

3-7% is rapidly absorbed

135
Q

Pradaxa: metabolism/excretion

A

metabolized to active metabolite in the liver with elimination by kidneys

136
Q

converting from coumadin to pradaxa

A

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

137
Q

converting from pradaxa to coumadin

CrCl >50 mL/min

A

start coumadin 3 days before stopping pradaxa

138
Q

converting from pradaxa to coumdain

CrCl 31-50mL/min

A

start coumadin 2 days before stopping pradaxa

139
Q

converting from pradaxa to coumdain

CrCl 15-30 mL/min

A

start coumadin 1 day before stopping pradaxa

140
Q

converting from heparin to pradaxa

A

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

141
Q

discontinuing pradaxa prior to surgery

A

CrCl >50 = 1-2 days prior

CrCl <50 = 3-5 days prior

142
Q

Pradaxa side effects: GI

A

dyspepsia, abdominal pain

143
Q

Pradaxa side effects: HEM

A

bleeding

144
Q

what drug does pradaxa interact with

A

rifampin

(reduces the concentration of pradaxa)

145
Q

when is anti-platelet therapy indicated

A

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
Q

anti-platelet: aspirin

mechanism of action

A

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

147
Q

Aspirin: absorption

A

rapidly absorbed in stomach and upper bowel

148
Q

how long does it take for platelet inhibition

by aspirin to be detectable?

A

1 hour

149
Q

optimal aspirin dose for prevention of MI/stroke

A

50-100mg daily

150
Q

optimal aspirin dosage for acute conditions

(acute coronary syndrome, stroke)

A

160-325mg

151
Q

aspirin dsage for chronic use

A

no reason to exceed 81mg

152
Q

aspirin side effects: GI

A

dose related bleeding

153
Q

aspirin side effects: HEM

A

low risk of intracranial bleeding

154
Q

aspirin side effects: EENT

A

tinnitus

155
Q

aspirin interactions

A

coadministration with traditional NSAIDs can negate cardioprotective effect

156
Q

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

A

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

157
Q

clopidogrel (Plavix)

mechanism of action

A

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
Q

Plavix: absorption

A

well absobed orally

159
Q

Plavix: metabolism

A

quickly metabolized by the liver into an active metabolite

160
Q

Plavix: excretion

A

50% in urine

45% in feces

161
Q

Plavix: half-life

A

Active metabolite 8hrs

162
Q

When should plavix be used along with aspirin?

A

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

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

163
Q

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

A

indefinite if treated with stents

after 1 year if treated without stents

164
Q

When should aspirin alone be used

A

vascular disease without prior MI or stents

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

165
Q

when should aspirin be used prophylactically

A

no established heart disease but lots of risk factors

166
Q

Plavix side effects: CV

A

chest pain, edema, HTN

167
Q

Plavix side effects: DERM

A

pruritis, purpurea, rash

168
Q

Plavix side effects: HEM

A

bleeding

thrombotic thrombocytopenic purpura (rare)

169
Q

Plavix side effects: GI

A

abdominal pain, N/V, constipation

170
Q

Plavix side effects: NEURO

A

headache, dizziness, depression, fatigue, generalized pain

171
Q

Which drugs decrease effectiveness of plavix

A

atorvastatin, clarithromycin, erythromycin

172
Q

which drugs increase effect of plavix

A

rifampin and other antiplatelets and anticoagulants

173
Q

plavix contraindications

A

prior/active bleeding events

174
Q

prasugrel (Effient)

A

second thienopyridine approved as an antiplatelt drug

175
Q

effient mechanism of action

A

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

176
Q

why is effient a “pro-drug”

A

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

177
Q

when is effient indicated?

A

acute coronary syndromes who are undergoing primary coronary interventions

178
Q

effient contraindications

A

patients older than 75 or those weighing less than 60kg

patients with history of stroke

179
Q

why should effient not be routinely used

A

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

180
Q

effient: absorption

A

rapid within 30 minutes of oral administration

181
Q

effient: distribution

A

plasma proteins

182
Q

effient: metabolism

A

hepatic cytochrome P450 isoenzymes

(CYP3A4, CYP2C9. CYP2C19, CYP2B6)

183
Q

effient: excretion

A

mostly in urine, some in feces

184
Q

effient: half-life

A

7 hours

onset of platelet activity 30 minutes

steady state reached in 3 days

185
Q

effient dosage and administration

A

page 153

186
Q

Aggrenox

A

50mg of aspirin with 200mg ER dipyridamole

187
Q

Aggrenox: clinical use

A

prevention of vascular events

(most commonly used to prevent strokes)

188
Q

IV Aggrenox

A

used by cardiologists to cause maximal coronary vasodilation

189
Q

Aggrenox contraindications

A

patients with bronchospasm

190
Q

when is aspirin preferable to aggrenox

A

patients with establish CAD or PAD

191
Q

fibrinolytic (thrombolytic) agents

A

drugs that lyse blood clots

(all are forms of tissue plasminogen activator tPA)

192
Q

fibrinolytic agents: mechanism of action

A

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

193
Q

how are fibrinolytics administered

A

IV only

194
Q

fibrinolytics: clinical uses

A

treatment of ST-segment elevation MI

acute massive PE, acute ischemic stroke

to open clotted central venous access devices (alteplase only)

195
Q

Fribrinolytic drug names

A

Alteplase (Activase, cathflo activase)

reteplase (Retavase)

tenecteplase (TNKase)

196
Q
A

Pharmacology (28 decks)

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