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Adv. Pharm > Final Quiz Material > Flashcards

Final Quiz Material Flashcards

1
Q

Equation for BP

A

BP = CO x SVR

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2
Q

Equation for CO

A

CO = SV x HR

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3
Q

3 things that contribute to stroke volume

A
  • preload
  • afterload
  • contractility
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4
Q

2 centrally acting antihypertensive agents

A

1) a-Methyldopa
2) Clonidine/Dex

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5
Q

Clonidine shares a structure-activity relationship with which catecholamine

A

Norepi

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6
Q

MOA of Methyldopa and Clonidine

A

decreases SVR and CO 2* to decreased sympathetic outflow

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7
Q

SE of Methyldopa

A
  • CNS effects
  • hyperprolactinemia
    • Coombs test w/ or w/o hemolytic anemia
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8
Q

Which centrally acting antihypertensive can be given transdermally? Why?

A

Clonidine - highly lipid soluble

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9
Q

Problems with centrally acting antihypertensives:

A
  • sedation
  • orthostatic hypotension
  • endocrine problems
  • Na+ and H2O retention
  • rebound HTN with abrupt withdrawal
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10
Q

2 peripherally acting adrenergic agents

A
  • Guanethidine
  • Reserpine
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11
Q

MOA of peripheral acting adrenergic agents in genreal

A
  • catecholamine depleters
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12
Q

MOA of Guanethidine

A
  • replacement and gradual depletion of NE
  • transported across symp membrane by same mech as NE
    similar to Guanadrel
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13
Q

SE of Guanethidine

A
  • profound postural hypotension
  • drug interactions
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14
Q

MOA of Reserpine

A
  • blocks ability of adrenergic vesicles to take up and store NE, DA, and serotonin
  • results in central and peripheral depletion
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15
Q

SE of Reserpine

A
  • depression
  • EPS
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16
Q

Problems associated with blocking NE release and storage

A
  • orthostatic hypotension
  • nasal stuffiness
  • impairment of ejaculation
  • increased GI activity
  • EPS
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17
Q

2 mixed beta antagonists and their receptor selectivity

A
  • Labetalol and Carvedilol
    B1=B2>A1>A2
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18
Q

Problems with B-adrenergic receptor blockers

A
  • HF in pts with cardiac disease
  • increased airway resistance
  • fatigue
  • depression
  • rebound HTN
  • masking hypoglycemia
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19
Q

Prazosin, Terazosin, Doxazosin receptor selectivity

A

A1»»A2
A1-selective blockers

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20
Q

Phenoxybenzamine receptor selectivity

A

A1>A1
irreversible

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21
Q

Phentolamine receptor selectivity

A

A1=A2

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22
Q

Problems with A-adrenergic receptor blockers

A
  • orthostatic hypotension
  • tachycardia w/ non-selectives
  • nasal stuffiness
  • ejaculation impairment
  • Na+ and H2O retention (blocked renin release)
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23
Q

List 3 ACE inhibitors

A
  • Captopril
  • Enalapril
  • Lisinopril
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24
Q

Most favored ACE inhibitor and why

A

Lisinopril - pharmacokinetics means it is dosed once daily

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25
Q

Mechanism for why some patients get a cough with ACE inhibitors:

A

accumulation of bradykinin

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26
Q

MOA of ACE inhibitors

A
  • decreased conversion of AT1 to ATII
  • decreased aldosterone
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27
Q

SE of ACE inhibitors

A
  • pregnancy category D
  • hyperkalemia
  • cough
  • caution with renal patients (accumulation, renal artery stenosis, GFR alteration)
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28
Q

SE of ACE inhibitors are worsened with what condition

A

hypovolemia

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29
Q

MOA of ARBs

A
  • block ATII from binding to ATI receptors
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30
Q

SE of ARBs

A
  • pregnancy category D
  • hyperkalemia
  • renal effects
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31
Q

Antihypertensive class that can increase SVR

A

B-blockers

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32
Q

Most reabsorption of water and ions in the renal system occurs in the _______

A

proximal tubule

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33
Q

Class of diuretics that are most effective at excreting Na+

A

loop diuretics > metolazone = thiazides > K+ sparing

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34
Q

Class of diuretics working on the proximal tubule

A

carbonic anhydrase inhibitors

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35
Q

MOA of Acetazolamide

A
  • carbonic anhydrase inhibitor
  • causes excretion of bicarb
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36
Q

Uses for carbonic anhydrase inhibitors

A
  • metabolic alkalosis
  • urinary alkalization
  • glaucoma
  • altitude sickness
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37
Q

Problems with carbonic anhydrase inhibitors

A
  • hyperchloremic metabolic acidosis
  • ammonia toxicity
  • sulfa allergy
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38
Q

Drugs used in open-angle glaucoma therapy:

A
  • pilocarpine
  • carbachol
  • physostigmine
  • echothiophate
  • timolol
  • acetazolamide
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39
Q

Diuretics that work on the ascending loop of Henle are most effective at doing what?

A

moving fluid

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40
Q

List 3 loop duretics

A
  • furosemide
  • bumetanide
  • ethacrynic acid
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41
Q

MOA of Furosemide

A
  • works on inhibition of Na/K/Cl co-transport in in the ascending LoH
  • direct vasodilating effect
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42
Q

Uses of Furosemide

A
  • edema
  • CHF
  • HTN
  • hypercalcemia
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43
Q

Problems with Furosemide

A
  • ototoxicity
  • hypokalemia/mag/natremia
  • hypovolemia
  • hyperuricemia
  • interstitial nephritis
  • hypokalemic metabolic acidosis
  • sulfa allergies?
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44
Q

MOA of Ethacrynic acid

A
  • works on inhibition of Na/K/Cl co-transport in in the ascending LoH
    NOT a sulfonamide
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45
Q

Uses of Ethacrynic acid

A

diuretic for patients with sulfa allergy (cannot get Lasix)

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46
Q

Problems with Ethacrynic acid

A
  • ototoxicity
  • hypokalemia/mag/natremia
  • hypovolemia
  • interstitial nephritis
  • hypokalemic metabolic acidosis
    NO hyperuricemia, NO sulfa allergy
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47
Q

MOA of hydrochlorothiazide

A
  • inhibits NaCl reabsorption in the early distal tubule
  • direct vascular effects
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48
Q

Uses of HCTZ

A
  • HTN
  • CHF
  • nephrogenic DI
  • renal calcium stone formation
  • osteoporosis
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49
Q

Problems with HCTZ

A
  • hypokalemic metabolic alkalosis
  • hyponatremia
  • hyperglycemia
  • hyperlipidemia
  • hyperuricemia
  • hypercalcemia
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50
Q

Mechanism for how thiazide diuretics cause hypokalemia

A

inhibition of the NaCl pump dumps extra Na+ into the lumen; Na+ is later exchanged for K+, so the excess Na+ causes excess K+ to be kicked out

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51
Q

Where do potassium sparing diuretics work?

A

collecting tubule

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52
Q

MOA of Spironolactone

A

competitive aldosterone antagonist
(4-ring structure)

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53
Q

MOA of Triamterene and Amiloride

A

block Na+ channels in collecting tubule

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54
Q

List 3 potassium sparing diuretics

A
  • Spironolactone
  • Triamterene
  • Amiloride
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55
Q

Uses for potassium sparing diuretics

A
  • hyperaldosteronism (cirrhosis & ascites)
  • CHF
  • often added to non-K-sparing agents
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56
Q

Problems with potassium sparing diuretics

A
  • hyperkalemia
  • endocrine effects (Spironolactone)
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57
Q

Where do osmotic diuretics work?

A
  • proximal convoluted tubule
  • descending LoH
  • collecting duct
    attract water in areas of tubule that are freely permeable to H2O
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58
Q

Mannitol is a…..

A

osmotic diuretic

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59
Q

Uses for mannitol

A
  • increase urine volume
  • prevent anuria in hemolysis or rhabdo
  • reduce ICP or IOP
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60
Q

Problems with osmotic diuretics

A
  • extracellular volume expansion
  • dehydration
  • hypernatremia
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61
Q

List 2 ADH antagonists

A
  • Lithium
  • Demeclocycline
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62
Q

MOA of ADH antagonists

A

inhibit the effects of ADH on the collecting tubule (thought to decrease cAMP response to ADH)

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63
Q

Uses of ADH antagonists

A

SIADH when water restriction failed

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64
Q

Problems with ADH antagonists

A
  • nephrogenic DI
  • hypernatremia
  • acute renal failure
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65
Q

Which diuretics have the greatest impact on HCO3-

A

carbonic anhydrase inhibitors

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66
Q

BB can interact with which class of diuretics? to create what problem?

A
  • interact with thiazides
  • problem: increase in blood glucose, urates, lipids
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67
Q

Digitalis glycosides can interact with which class of diuretics? to create what problem?

A
  • interact with thiazides and loop diuretics
  • problem: hypokalemia –> dig toxicity
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68
Q

ACE inhibitors can interact with which class of diuretics? to create what problem?

A
  • interact with K-sparing
  • problem: hyperkalemia, cardiac effects
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69
Q

Aminoglycosides can interact with which class of diuretics? to create what problem?

A
  • interact with loop diuretics
  • problem: ototoxicity, nephrotoxicity
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70
Q

Adrenal steroids can interact with which class of diuretics? to create what problem?

A
  • interact with thiazides and loop diuretics
  • problem: enhanced hypokalemia
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71
Q

Chlorpropamide can interact with which class of diuretics? to create what problem?

A
  • interact with thiazides
  • problem: hyponatremia
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72
Q

Formula and normal value for cardiac output

A

CO = HR x SV

4-8L/min

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73
Q

Formula and normal value for cardiac index

A

CI = CO / BSA

2.5-4 L/min/m2

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74
Q

Normal value for MAP

A

70-90 mmHg

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75
Q

Formula and normal value for coronary perfusion pressure

A

CPP = DBP - PAWP

60-70 mmHg

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76
Q

Formula and normal value for rate pressure product

A

RPP = HR x SBP

<12,000

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77
Q

MOA of nitrates (in general)

A
  • nitric oxide activates guanylyl cyclase
  • increased cGMP
  • sarcoplasmic reticulum sequesters Ca2+
  • decreased smooth muscle contraction
  • vasodilation
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78
Q

MOA of Nitroglycerin

A

increased NO production –> increased cGMP

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79
Q

Effects of Nitroglycerin

A
  • primarily preload reduction
  • afterload effects @ higher doses
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80
Q

Advantages of Nitroglycerin

A
  • very titratable
  • more specific for preload
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81
Q

Disadvantages of Nitroglycerin

A
  • HA
  • nitrate tolerance
  • withdrawal
  • special tubing & glass vials d/t diffuses into plastic
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82
Q

MOA of Isosorbide Dinitrate

A
  • increased NO production –> increased cGMP
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83
Q

Advantages of Isosorbide Dinitrate

A

oral form available

84
Q

Effects of Isosorbide Dinitrate

A
  • reduces preload
  • some reduction of afterload @ higher doses
85
Q

Disadvantages of Isosorbide Dinitrate

A
  • HA
  • nitrate tolerance
  • withdrawal reactions
86
Q

MOA of Sodium Nitroprusside

A

increased NO production –> increased cGMP

87
Q

Effects of Sodium Nitroprusside

A

decreases BOTH preload and afterload

88
Q

Advantages of Sodium Nitroprusside

A
  • extremely titratable
  • inexpensive
  • familiar to staff
89
Q

Disadvantages of Sodium Nitroprusside

A
  • cyanide toxicity
  • pulmonary shunt
  • coronary steal
90
Q

Nitroprusside must be converted to which metabolite for excretion?

A

Thiocyanate

91
Q

Describe the metabolism of Nitroprusside

A

-

92
Q

Describe the metabolism of Nitroprusside

A
  • rapidly metabolized by RBCs
  • methemoglobin and cyanide released
  • cyanide converted to thiocyanate by rhondase (sulfur donor - Thiosulfate - required)
  • thiocyanate distributed in ECF and renally eliminated
93
Q

3 treatments for cyanide toxicity and how they work

A

1) sodium nitrite - increases MetHgb which can then be treated with methylene blue
2) sodium thiosulfate - acts as sulfur donor so rhondase system can convert cyanide to thiocyanate for renal elimination
3) hydroxocobalamin - converted to cyanocobalamin (Vit B12) needed for metabolism

94
Q

3 non-nitrate vasodilators

A
  • Hydralazine
  • Diazoxide
  • Minoxidil
95
Q

MOA of Hydralazine

A
  • increased NO production
  • increased cGMP
96
Q

Effects of Hydralazine

A

reduces afterload

97
Q

Advantage of Hydralazine

A

may be given as a bolus

98
Q

Disadvantages of Hydralazine

A
  • increases RAAS system
  • not very titratable
  • drug-induced lupus-like syndrome
99
Q

MOA of Minoxidil

A

facilitates opening of K+ channels in smooth muscle

100
Q

Effects of Minoxidil

A

reduces afterload

101
Q

Advantages of Minoxidil

A
  • oral form
  • hair growth
102
Q

Disadvantages of Minoxidil

A
  • increases in RAAS system
  • not titratable
103
Q

MOA of Diazoxide

A

facilitates opening of K+ channels in smooth muscle

104
Q

Effects of Diazoxide

A

reduces afterload

105
Q

Advantages of Diazoxide

A

used in HTN emergency

106
Q

Disadvantages of Diazoxide

A
  • increases RAAS system
  • not very titratable
  • hyperglycemia from inhibited insulin release
107
Q

MOA of Enalaprilat

A

ACE inhibitor; decreases ATII and aldosterone
IV form of Enalapril

108
Q

Effects of Enalaprilat

A

afterload reduction

109
Q

Advantages of Enalaprilat

A
  • can be converted to oral
  • may be bolused
110
Q

Disadvantages of Enalaprilat

A
  • not titratable
  • may worsen renal clearance
  • Pregnancy cat. D
111
Q

MOA of Fenoldepam

A

direct D1 agonist

112
Q

Effects of Fenoldepam

A
  • specific for afterload
  • acts on D1 receptors only
113
Q

Advantages of Fenoldepam

A
  • titratable
  • improved renal BF
114
Q

Disadvantages of Fenoldepam

A
  • expensive
  • increased IOP
  • hyperkalemia
115
Q

MOA of CCBs

A
  • modify Ca2+ channel to inhibit inward movement of Ca2+
  • reduce afterload
  • little effect on preload
116
Q

3 chemical classes of CCB for IV use:

A
  • Phenylalkylamine = Verapamil
  • Benzothiazepine = Diltiazem
  • Dihydropyridine = Nicardipine
117
Q

CCB with greatest effect on conduction and contractility

A

Verapamil (decreases both)

118
Q

CCB with limited effect on HR, conduction, & contractility

A

Nicardipine

119
Q

CCB with greatest effect on PVR

A

Nicardipine

120
Q

CCB that may increase HR

A

Nicardipine (reflex increase d/t significant effect on PVR)

121
Q

Med class of Clevidipine

A

3rd gen dihydropyridine CCB

122
Q

Advantage of Clevidipine

A
  • more rapid onset than Nicardipine
  • ultra-shirt half life
  • very titratable
123
Q

Vasodilator that can cause coronary steal

A

Nitroprusside

124
Q

Vasodilators that can cause methemoglobinemia

A
  • Nitroglycerin
  • Nitroprusside
125
Q

Describe systolic HF

A

(HFrEF)
- accounts for 70% of CHF
- LV dilation
- wall thinning
- decreased EF

126
Q

Describe diastolic HF

A

(HFpEF)
- hypertrophic myocardium
- normal EF

127
Q

Causes of systolic dysfxn

A
  • CAD (myocardial ischemia)
  • HTN
  • valvular dz
  • COPD
  • thyroid dz
  • decreased CO (^catecholamines & RAAS)
128
Q

Causes of diastolic dysfxn

A
  • HTN
  • aortic stenosis
  • ischemic heart disease
129
Q

Patients with ___ dysfxn have better outcomes because…

A

diastolic because LV fxn is usually maintained

130
Q

Long-term sympathetic stimulation has what effect on the myocardium

A
  • downregulation of B1 receptors
  • shift in B receptor density (B1/B2 ratio 80/20 to 60/40)
  • uncoupling of receptors 2* to BARK-1
131
Q

Substances involved in HF

A
  • catecholamines
  • ATII
  • aldosterone
  • neurohormones (endothelin, vasopressin)
  • cytokines (TNF, IL-6)
  • counterregulatory hormones (ANP, BNP)
132
Q

Drug class of Digoxin

A

cardiac glycoside

133
Q

MOA of Digoxin

A

increases intracellular Ca2+ by inhibiting Na-K-ATPase pump

134
Q

Uses of Digoxin

A
  • inotrope
  • antiarrhythmic
135
Q

Digoxin toxicity s/s:

A
  • CNS (visual problems, fatigue, stupor)
  • GI (anorexia, N/V)
  • cardiac (atrial and vent arrhythmias, AV block)
136
Q

Treatment for Digoxin toxicity

A

Digoxin Fab (digibind)

137
Q

You should monitor which electrolyte in patients receiving Digoxin

A

K+
- Digoxin binds to K+ site on Na-K-ATPas pump, can lead to hyperkalemia
- hypokalemia makes Digoxin toxicity more likely

138
Q

MOA of Milrinone

A
  • inhibition of phosphodiesterase
  • inhibits breakdown of cAMP
139
Q

Actions of Milrinone

A
  • vasodilator
  • inotrope
140
Q

Problems with Milrinone

A
  • arrhythmias
  • hypotension
  • long half-life
  • thrombocytopenia (Amrinone)
141
Q

Effect that inotropic agents and arterial vasodilators have on cardiac index

A

increase

142
Q

Effect that diuretics and venous vasodilators have on cardiac index

A

decrease

143
Q

Effect of Dopamine on SVR at low doses? High doses?

A
  • decrease slightly at low doses
  • increase at moderate to high doses
144
Q

Effect of Dobutamine on SVR

A

decrease

145
Q

3 types of shock

A
  • hypovolemic (d/t loss of blood volume, loss of plasma volume)
  • cardiogenic (MI, arrhythmias, compression/obstruction, valve disorder)
  • distributive (septic, anaphylaxis, neurogenic, ODs)
146
Q

Primary antimicrobial utilized in the OR

A

Cefazolin / Ancef

147
Q

Selection of the appropriate antimicrobial depends on 4 things:

A

1) selective toxicity
2) type of organism
3) anatomical location
4) host status

148
Q

Antibiotic:

A

substance produced by microorganisms that suppress the growth of other microorganisms

149
Q

Bacteriostatic drugs should not be given to what patient population? Why?

A

immunocompromised

bacteriostatic drugs stop growth/proliferation and allow the host’s immune system to take over. In an immunocompromised patient, no host system will take over.

150
Q

Compare bacteriostatic versus bacteriocidal

A

-static = stops growth but does not kill the microorganism
-cidal = kills the microorganism

151
Q

-cidal drugs must be used for what 5 conditions

A

1) immunocompromised host
2) meningitis
3) endocarditis
4) deep bone infxn
5) artificial device implants

152
Q

2 antimicrobial types that target cell wall:

A

1) b-lactams (PCN, cephalosporins)
2) b-lactamase inhibitors (vanco, bacitracin)

153
Q

Penicillin spectrum of effectiveness:

A
  • most anaerobes
  • G+
  • spirochetes
154
Q

What type of penicillin is the best option to treat B-lactamase+ staph?

A

-oxacillin

155
Q

Describe the targets of the 4 generations of Cephalosporins:

A

1st gen: G+
2nd gen: some G+, more G-
3rd gen: even less G+, mostly G-
*Ceftazidime = anti-pseudomonal
4th gen: like 3rd gen but also B-lactamases

156
Q

Vancomycin target organisms:

A

G+ only

157
Q

Vanco should be given IV only except for what illness?

A

can be given orally to treat C. Difficile

158
Q

Drugs associated with nephrotoxicity and ototoxicity:

A
  • Vanco
  • Aminoglycosides
159
Q

List 3 quinolones (antimicrobials)

A
  • Cipro
  • Rifampin
  • Metronidazole
160
Q

Quinolones MOA

A

inhibit DNA/RNA synthesis

161
Q

Major SE of quinolones

A

QTc prolongation

162
Q

Patients on Metronidazole should avoid…

A

EtOH d/t disulfiram reaction –> N/V

163
Q

Use of Tetracyclines

A

preferred agents for oddball drugs

164
Q

Chloramphenicol major SE

A

1) bone marrow depression
2) grey baby syndrome
3) optic neuritis & blindness

165
Q

Spectrum of action of macrolides

A

Azithro > Clarithro > Erythro

166
Q

SE of Erythromycin

A
  • N/V
  • potent inhibitor of CYP3A4
  • cardiac arrest ESP when on other drugs that inhibit 3A4 metab of Erythro
167
Q

SE of Linezolid

A
  • inhibits MAO
  • N/V/D, GI superinfxn
  • HA
168
Q

Abx to avoid when on Meperidine

A

Linezolid (inhibits MAO, r/f serotonin syndrome)

169
Q

Type of effect when trimethoprim and sulfamethoxazole are given together

A

synergistic effect

170
Q

3 known synergistic combinations in antimicrobial therapy

A

1) TMP/SMX
2) B-lactam + B-lactamase inhibitor
3) aminoglycoside + cell wall inhibitor

171
Q

4 antimicrobials that prolong the NM blockade

A
  • polymyxin B
  • aminoglycosides
  • clindamycin
  • tetracycline
172
Q

Class 1A antiarrythmics

A
  • Quinidine
  • Procainamide
  • Disopyramide
173
Q

Class 1A drugs can be used for (atrial/ventricular) arrhythmias

A

BOTH

174
Q

SE of Class 1As

A
  • hypotension
  • prolong QT
  • antimuscarinic
175
Q

Antiarrhythmic associated with lupus-like syndrome

A

Procainamide

176
Q

Class 1A effects on electrophysiology

A
  • decrease ectopic PM
  • slow conduction velocity
  • lengthen refractory period
177
Q

Class 1A effects on EKG

A

prolong QT interval

178
Q

Class 1A target channel(s)

A

Na+ and K+

179
Q

Class 1B antiarrhythmics:

A
  • Lidocaine
  • Phenytoin
  • Mexiletine
  • Tocainide
180
Q

Class 1B used for (atrial/ventricular)

A

ventricular

181
Q

Class 1B have a greater effect on what kind of tissue

A

depolarized

182
Q

First sign of Class 1B antiarrhythmic toxicity

A
  • circumoral numbness
  • tinnitis & lightheadedness
183
Q

Class 1Bs resistant to 1st pass effect

A
  • Tocainide
  • Mexilitine
184
Q

Phenytoin undergoes (first/zero) order kinetics

A

zero - high r/f toxicity

185
Q

Class 1C antiarrhythmics

A
  • Propafanone
  • Flecaniade
  • Encainide
186
Q

Class 1C agents used for (atrial/ventricular) arrhythmias

A

ventricular & supraventricular

187
Q

SE of Class 1Cs

A

arrhythmogenic
(Flecainide & Encainide not used anymore)

188
Q

Class 1C effects on electrophysiology

A
  • decrease ectopic PM
  • large decrease in conduction velocity
  • increase refractory preiod
189
Q

Class 1C EKG changes

A
  • prolong PR
  • prolong QRS
  • prolong QT
190
Q

Class 2 antiarrhymics

A

BB
- Propranolol
- Esmolol
- Acebutolol

191
Q

MOA of Class 2 agents

A

slow conduction through the AV node

192
Q

Class 3 antiarrhythmics

A
  • Amiodarone
  • Sotalol
193
Q

Amiodarone target channels

A
  • K+ channel blocker
  • Na+ channel blocker
  • weak Ca2+ channel blocker
  • noncompetitive BB
194
Q

Amiodarone used to treat (atrial/ventricular) arrhythmias

A

ventricular & supraventricular

195
Q

Cardiac SE of Amiodarone

A
  • hypotension
  • bradycardia
  • heart block
  • prolonged QT
196
Q

Other SE of Amiodarone

A
  • pulmonary fibrosis
  • corneal deposits
  • skin deposits
  • constipation
  • hypo & hyperthyroidism
  • drug interactions
197
Q

Sotalol target channels

A
  • K+
  • BB
198
Q

Class 4 antiarrhythmics

A
  • Diltiazem
  • Verapamil
  • Nifedipine
199
Q

Digoxin goals

A

slow conduction velocity & increase refractory period

200
Q

Digoxin used for what arrhythmias

A

supraventricular (A-Fib/Flutter)

201
Q

Adenosine MOA

A
  • decrease cAMP
  • decrease Ca2+
  • decrease SA firing & AV conduction
202
Q

SE of Adenosine

A
  • transient CP
  • flushing
  • dyspnea
203
Q

Tx for AFib/Flutter

A

Verapamil / Diltiazem / BB

204
Q

Tx for SVT

A

Adenosine / Verapamil / Diltiazem

205
Q

Tx for sustained VT

A

Lidocaine

206
Q

Tx for VFib

A

Lidocaine for prevention of recurrence

207
Q

Uses for mannitol

A
  • increase urine volume
  • prevent anuria in hemolysis or rhabdo
  • reduce ICP or IOP

Adv. Pharm (5 decks)

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