Chapter 9: Blood disorders Flashcards

(196 cards)

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
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