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Test 4 Flashcards

1
Q

MOA of Beta-Adrenergic Receptor Agonists

A

Stimulate Beta 2 receptors in the lungs –> increased ATP –> increased cAMP –> Relaxation in the lungs

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2
Q

Therapeutic Effects of Beta Adrenergic Receptor Agonists

A

Bronchodilate, Inhibit bronchoconstricting mediators, increase mucus clearance

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3
Q

MOA of non-selective Beta Adrenergic Agonists

A

Act on both beta 1 and beta 2 receptors in heart and lungs

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4
Q

MOA of selective Beta Adrenergic Agonists

A

Act on just beta 2 receptors in lungs unless high doses

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5
Q

Non-Selective Beta-Adrenergic Receptor Agonist Drugs

A

Epinephrine (Adrenalin, Primatene)

Terbutaline (Brethine)

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6
Q

Epinephrine (Adrenalin, Primatine)

A

Non-Selective Beta-Adrenergic Receptor Agonist, SABA

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7
Q

Terbutaline (Brethine)

A

Non-Selective Beta-Adrenergic Receptor Agonist, SABA

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8
Q

Selective Beta-Adrenergic Receptor Agonist Drugs

A

Albuterol, Levalbuterol, Salmeterol, Formoteral

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9
Q

Albuterol (Proventil, Ventolin)

A

Selective Beta-Adrenergic Receptor Agonist Drugs, SABA

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10
Q

Levalbuterol (Xopenex)

A

Selective Beta-Adrenergic Receptor Agonist Drugs, SABA

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11
Q

Salmeterol (Serevent)

A

Selective Beta-Adrenergic Receptor Agonist Drugs, LABA

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12
Q

Formoterol (Foradil)

A

Selective Beta-Adrenergic Receptor Agonist Drugs, LABA

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13
Q

SABA MOA

A

Onset 5 min, Duration 4-6h, rescue inhaler

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14
Q

LABA MOA

A

Onset 30 min, Duration 12 h, maintenance inhaler, last choice

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15
Q

What must you prescribe with a Beta Adrenergic Receptor Agonist?

A

Corticosteroid, Contra Indicated without

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16
Q

Adverse effects of Beta-Adrenergic Receptor Agonists

A

Tachycardia, Decreased serum potassium, tremors, Tolerance

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17
Q

Beta-Adrenergic Receptor Agonists DDIs

A

Adrenergic, beta blockers

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18
Q

MOA Methalxanthines

A

Inhibit PDE which breaks down cAMP –> 5’-AMP. More cAMP leads to more relaxation in lungs. Increases mucus clearance.

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19
Q

Clinical use Methylxanthines

A

Limited because of narrow therapeutic index. Maintenance therapy if you’ve tried everything else.

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20
Q

Therapeutic Index of Methalxanthines

A

5-15

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21
Q

ADE of Methalxanthines

A

Happen at any concentration. CNS = seizures, insomnia. Tachycardia, N/V, Tremors. Lots of DDI.

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22
Q

Pharmokinetics of Methalxanthines

A

90% liver metabolism, 10% excreted unchanged by kidneys

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23
Q

Methylxanthines

A

Theophylline - PO, Aminophylline - IV.

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24
Q

Theophylline

A

PO. No mg to mg switching, Methylxanthine.

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25
Q

Aminophylline

A

IV, Methylxanthine

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26
Q

Anticholinergic Agents MOA

A

Compete with ACH at muscarinic receptor. Decrease vagal tone to airway which leads to bronchodilation.

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27
Q

Anticholinergic Uses

A

Inhalation only, treat acute asthma with a SABA because they have an additive effect.

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28
Q

What do you need to prescribe with an anticholinergic to treat acute asthma

A

SABA, additive effect

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29
Q

Corticosteroid MOA

A

Reduce markers of inflammation, decrease vascular congestion and cellular infiltration, improve beta 2 receptor sensitivity

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30
Q

Corticosteroid Therapeutic Effects

A

IV or PO (1-2 hrs vs 2wks), for acute use IV –> oral, for prevention use inhalation and dose based on severity.

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31
Q

Corticosteroid Inhallation ADE

A

Fungal infections in the mouth, wash mouth

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32
Q

Corticosteroid Systemic Short Term ADE

A

Hyperglycemic, Psychiatric

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33
Q

Corticosteroid Systemic Long Term ADE

A

Osteoporosis/fractures, HTN, poor wound healing, Adrenal suppression, myopathy, glaucoma

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34
Q

Corticosteroid DDI

A

Cushings and adrenal insufficiency reported with CYP inhibitors

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35
Q

What three classes/drugs lower seizure threshold?

A

Beta-Lactams (Imipenem), Buproprion, Meperidine

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36
Q

Sodium Channel Blockers MOA

A

Reduce Na+ influx which reduces neuron firing, prolongs the inactivation state of neurons and inhibits the release of excitatory amino acids

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37
Q

Class for Carbamazepine (Tegretol)

A

Sodium Channel Blocker

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38
Q

Carbamazepine Pharmicokinetics

A
  • Highly protein bound
  • Autoinduction
  • Hepatic Metabolism with active metabolites
  • Inducer of CYP34A
  • Monitor Serum levels
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39
Q

Carbamazepine Theraputic Uses

A

Generalized tonic-clonic and partial

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40
Q

Carbamazepine ADE

A

CNS: Blurred vision, unsteady, headache, sedation. Nausea. Hyponatremia (SIADH)

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41
Q

Carbamazepine BBW

A

Blood dyscrasia and Derm (Steven’s Johnson and TENS). Worse for Asians due to alleel.

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42
Q

Carbamazepine DDI

A

Inducer, displacement reactions

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43
Q

Oxcarbazepine (Trileptal) Class

A

Sodium Channel Blocker, analog of Carbamazepine

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44
Q

Oxcarbazepine (Trileptal) Pharmicokinetics

A
  • Highly protein bound
  • Not CYP450 Metabolized
  • Eliminated by kidneys
  • Inducer of CYP34A
  • Initiate dose at 1.5x > Carbamazepine
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45
Q

How many times higher is an Oxcarbazepine (Trileptal) dose than a Carbamazepine dose?

A

1.5 times higher for Oxcarbazepine (Trileptal)

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46
Q

Oxcarbazepine (Trileptal) Theraputic Uses

A

Generalized tonic-clonic, partial

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47
Q

Oxcarbazepine (Trileptal) ADE

A

No BBW, SIADH

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48
Q

Oxcarbazepine (Trileptal) DDI

A

Inducer of 34A, reduced oral contraception

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49
Q

Eslicarbazepine Class

A

Sodium Channel Blocker, analog of Carbamazepine

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50
Q

Eslicarbazepine Clinical Application

A

Partial onset seizures

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51
Q

Eslicarbazepine Pharmacokinetics

A
  • Highly protein bound
  • Adjust for renal dysfxn
  • Inhibits CYP 2C19, Induces CYP 34A
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52
Q

Eslicarbazepine ADE

A

No BBW, Derm rxn, hyponatremia, hepatotoxicity, reduces oral BC

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53
Q

Phenytoin (Dilatin) Class

A

Sodium Channel Blocker

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54
Q

Phenytoin (Dilantin) Types

A

Phenytoin Acid and Phenytoin Sodium - Sodium has 8% less phenytoin. NOT bioequivilent. Check levels when dosing

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55
Q

Phenytoin (Dilatin) Levels

A

Levels are given with bound + free. Free is usually 10% unless they have hypoalbumin (less is bound) or high urea and bilirubin which can knock it off. Can order “free” level

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56
Q

Phenytoin (Dilatin) Conditions that affect binding

A

Renal failure, liver failure, hypoalbuinemia (Major trauma, burns, nephrotic syndrome, malnutrition, surgery)

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57
Q

Phenytoin (Dilatin) Metabolism

A

Dose-dependent, Michaelis-Mentin or capacity limited metabolism. CYP450 interactions. 20% less clerance in the elderly

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58
Q

Phenytoin (Dilatin) Target concentrations

A

10-20 mcg (1-2 mcg free)

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59
Q

Phenytoin (Dilatin) Adjustments

A

Adjust for Albumin

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60
Q

Phenytoin (Dilatin) Treatment uses

A

Generalized tonic-clonic, partial

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61
Q

Phenytoin (Dilatin) Dose dependent ADE

A

> 20 –> nystagmus, >30 ataxia, seizures, >40 –> lethargy or coma

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62
Q

Phenytoin (Dilatin) Hypersensitivity ADE

A

Rash, increased LFT, Fever

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63
Q

Phenytoin (Dilatin) Long Term ADE

A

Gingival Hyperplasia, Hirsuitism

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64
Q

Phenytoin (Dilatin) IV ADE

A

CV problems from propolene glycol in IV, Purple glove syndrome from extravision

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65
Q

Phenytoin (Dilatin) ADE

A

N/V/C, Decreased cognitive ability, Leukopenia, Thromboytopenia, Anemia

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66
Q

Phenytoin (Dilatin) DDI

A

Inducer of 3A4, Metabolized by 2C9/2C19, protein bound, tube feedings and antacids reduce availability, separate by 2 hr

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67
Q

Phenytoin (Dilatin) vs Fosphenytoin

A

Max infusion of Phenytoin is 50 (25 in elderly) vs 150 because Fosphenytoin has no propylene glycol. Phenytoin cannot be given IM, Fosphenytoin can.

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68
Q

Fosphenytoin vs Phenytoin doses

A

1.5 mg of fosphenytoin = 1 mg of phenytoin

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69
Q

Fosphenytoin (Cerebyx) Pharmokinetics

A

Prodrug of Phenytoin, converts in the blood. Can be IM or IV. Same ADE as Phenytoin minus the IV ADE.

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70
Q

Zileuton (Zyflo)

A

Leukotriene Modifer

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71
Q

Zileuton (Zyflo) MOA/ADE

A

Prevent leukotriene formation, Hepatotoxicity

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72
Q

Zafirlukast (Accolate)

A

Leukotriene Modifier

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73
Q

Montelukast (Singular)

A

Leukotriene modifier

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74
Q

Leukotriene Modifier MOA

A

Affect Leukotrenes which are potent constrictors produced from arachidonic acid. Affect LTC and LTD4.

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75
Q

Zafirlukast and Montelukast MOA

A

Receptor antagonists for LTD4

76
Q

Leukotriene Modifier Uses

A

Maintenance therapy, alternative to corticosteroids, Prophylaxis and aspirin induced asthma

77
Q

Leukotriene Modifier ADE

A

Headache, GI upset, CYP 450 Interactions

78
Q

Monoclonal Antibody MOA

A

Inhibits IgE from binding to receptors on mast cells

79
Q

Monoclonal Antibody ADE

A

Injection site rxn

80
Q

Monoclonal Antibody Therapeutic uses

A

Moderate to severe allergy asthma not controlled by steroids

81
Q

What should every asthmatic have on hand?

A

SABA, Beta-2 Rescue inhaler

82
Q

What should every persistent asmathtic by eon?

A

Corticosteroid

83
Q

Goals of COPD Therapy

A

Prevent disease progression, relieve sxs, tx and prevent acute exacerbations, smoking cessation

84
Q

Long term management of COPD

A

Supplemental oxygen, regular tx with bronchodilators (Anticholinergics), inhaled corticosteroids

85
Q

Acute COPD Exacerbations

A

SABA, Antibiotics (if not viral infection)

86
Q

Most important part of smoking cessation

A

Set a quit date

87
Q

Nicotine Replacement MOA

A

Maintain levels of dopamine over time, can be slowly decreased

88
Q

Nicotine Replacement Cautions

A

Patients that are post MI, with arrhythmias or angina

89
Q

Bupropion SR (Zyban) Mechanism of Action

A

Blocks the reuptake of dopamine

90
Q

Bupropion SR (Zyban) Therapeutic Uses

A

Use with NR, first choice for depressed patients, well tolerated in patients with CV disease, delays weight gain, begin therapy 1-2 weeks before quit date

91
Q

Bupropion SR (Zyban) Caution

A

Seizure disorders

92
Q

Varenicline (Chantix) MOA

A

Selective for nicotine receptors, partial agonist, prevents full agoinst activity

93
Q

Varenicline (Chantix) ADE

A

Serious neuropsychaitric symptoms such as agitation, depression, suicial ideation

94
Q

Which Insulin should be cloudy

95
Q

What do you use Rapid/Short acting insulin for?

A

Meal intake, elevated glucose, IM or IV

96
Q

What do you use intermediate/long acting insulin for

A

Basal insulin needs, NOT to cover long meals, must be given IM

97
Q

How much does 1 unit of insulin lower blood glucose?

A

50-100 mg/dL

98
Q

How long do you wait before adjusting the dose?

A

24hr to prevent hypoglycemia

99
Q

Insulin injection sites

A

Abdomen > buttocks > arm/leg. Exercise/rubbing.heat accelerates absorbtion

100
Q

Treat Mild Hypoglycemia

A

Simple sugar (juice, candy, sugar_

101
Q

Treat Severe hypoglycemia (Unconscious)

A

20-50 mL of 50% dextrose by IV. 1mg glucoagon subq or IM

102
Q

Technosphere insulin

A

Dry, powder insulin. Dose at begining of meal. BBW for bronchoconstriction, not recommended for smokers

103
Q

Lispro (Humalog)

A

Rapid acting insulin

104
Q

Aspart (Novolog)

A

Rapid Acting insulin

105
Q

Glulisine (Adventis)

A

Rapid Acting insulin

106
Q

Rapid Acting Insulin

A

Onset 15-30min, Peak 1-2h, Duration 3-4h, Admin before meal, IV or SubQ, clear

107
Q

Regular (Humulin R)

A

Short Acting Insulin

108
Q

Short Acting Insulin

A

Onset 30 min, Peak 2-3h, Duration 4-6h, Admin 40-45min before meal, IV or SubQ, clear

109
Q

NPH (Humulin N) and NPH (Novolin N)

A

Intermediate Acting Insulin

110
Q

Intermediate Acting Insulin

A

Onset 2-4h, peak 4-8hr, duration 8-12hr, usually BID, Only SubQ, Cloudy

111
Q

Glargine (Lantus)

A

Long Acting Insulin

112
Q

Detemir (Levemir)

A

Long Acting Insulin

113
Q

Insulin ADE

A

Hypoglycemia, Insulin allergy, Insulin resistance (Animal), Lipohypertrophy –> reduced absorbtion

114
Q

Glipizide

A

Sulfonylurea

115
Q

Glimepiride

A

Sulfonylurea

116
Q

Glyburide

A

Sulfonylurea

117
Q

Sulfonylureas MOA

A

Target Sulfonylurea receptor on beta pancreatic cell to force insulin to be released without needing glucose to be present

118
Q

Sulfonylureas Use/Pharmikokinetics

A

Extended duration of action, DM 2, reduce dosing with hepatic impairtment

119
Q

Sulfonylurea ADE

A

Hypoglycemia, Sulfa moity –> Derm (rash, photosensitivity), GI: N/V/LFTs, weight gain

120
Q

Glipizide Preferred Use

A

Elderly, no renal excretion “Glip is Hip”

121
Q

Glyburide Risks

A

50/50 renal and hepatic excretion, accumulates in pts with CrCl

122
Q

Repaglinide (Prandin)

A

Meglitinide

123
Q

Nateglinide (Starlix)

A

Meglitinide

124
Q

Meglitinide MOA

A

Same as Sulfonylurea but no sulfa moity

125
Q

Meglitinide uses

A

Preferable for those who skip meals, shorter duration of action, preferable for those with renal dysfunction

126
Q

Meglitinide ADE

A

Hypoglycemia, weight gain, DDI: Inhibit CYP450

127
Q

Metformin (Glucophage)

128
Q

Biguanide MOA

A

Decrease hepatic glucose output, increase peripheral glucose utilization

129
Q

Biguanide Uses

130
Q

Biguanide Advantages

A

Cause weight loss, decreaes triglicerides

131
Q

Biguanide Contraindications

A

Men CrCL >1.5, Women >1.4, Hypoxia, Renal impairment, hepatic impairment, contrast materials all lead to lactic acidosis

132
Q

Biguanide ADE

A

GI upset, bloating and flatulance, lactic acidosis

133
Q

Acarbose (Pregose)

A

Alpha Glucosidase Inhibitor

134
Q

Miglitol (Glyset)

A

Alpha Glucosidase Inhibitor

135
Q

Alpha Glucosidase Inhibitor MOA

A

Inhibit brush border alphaglucosidases which slows down digestion of complex carbohydrates

136
Q

Alpha Glucosidase Inhibitor ADE

A

Flatulence, Abd pain, diarrhea, CI in pt with GI disorders

137
Q

Acarbose (Pregose) ADE

A

Increases LFTs

138
Q

Rosiglitazone (Avandia)

A

Thiazolidinedione

139
Q

Pioglitazone (Actose)

A

Thiazolidinedione

140
Q

Thiazolidinedione MOA

A

Promote uptake of glucose into muscle/adipose. Decrease insulin resistance, increase insulin sensitivity, no effect on insulin secretion

141
Q

Thiazolidinedione ADE

A

Hepatotoxicity and edema, fracture risk, caution in CHF patients and risk for ostoporosis

142
Q

Pioglitazone (Actose) ADE

A

Risk for bladder cancer, CI in bladder cancer

143
Q

Exenatide (Byetta), Ligalutide (Victoza), Albiglutide (Tanzeum), Dulaglutide (Trulicity)

A

GLP-1 Antagonists

144
Q

GLP-1 Antagnosts MOA

A

Mimic Action of GLP-1. Stimulate insulin release, delay gastric emptying, suppress glucagon release. Recombinant form.

145
Q

GLP-1 Antagonists Contraindications

146
Q

GLP-1 Antagonists ADE

A

N/V, Headache, **Pancreattitis

147
Q

Sitagliptin (Januvia), Saxagliptin (Onglyza) Alogliptin (Nesina), Lingagliptin (Tradjenta)

A

DPP-4 Inhibitors

148
Q

DPP-4 Inhibitors MOA

A

Inhibit DPP-4 Enzyme that breaks down GLP-1.

149
Q

DPP-4 Inhibitors ADE

A

Adjust for renal dysfunction, Pancreatitis

150
Q

What do you start a DM2 patient with very high glucose on first?

151
Q

What is the backbone of all HA1C treatments?

152
Q

Zosinamide (Zonegran)

A

Calcium Channel Blocker

153
Q

Zosinamide (Zonegran) Pharmikokinetics

A

Low Protein Binding, PO only, Hepatic metabolism, kidney excretion

154
Q

Zosinamide (Zonegran) ADE

A

CNS: Somnolence, Agitation, cognitive impairment, Renal Stones, Sulfa Moity

155
Q

Lamotrigine (Lamictal)

A

Calcium Channel Blocker

156
Q

Lamotrigine (Lamictal) Pharmikokinetics

A

Low protein binding, PO

157
Q

Lamotrigine (Lamictal) ADE

A

BBW for skin rxn if patient is positive for allelle (TENS or SJS). DDI with Valproic acid (Adjust dosing)

158
Q

Rufinaminde (Banzel)

A

Calcium Channel Blocker

159
Q

Rufinaminde (Banzel) Pharmikokinetics

A

Hepatic metabolism, CYP Inducer

160
Q

Rufinaminde (Banzel) ADE

A

Short QT interval, multi-organ hypersensitivity

161
Q

Lascosamide (Vimpat)

A

Calcium Channel Blocker

162
Q

Lascosamide (Vimpat) Pharmikokinetics

A

100% bioavailible PO, hepatic metabolism, renal elimination

163
Q

Lascosamide (Vimpat) ADE

A

Prolong QT interval, heart block, no DDI

164
Q

Valproate

A

GABAergic Agent

165
Q

GABAergic Agent MOA

A

Increase the activity of the inhibitory neurotransmitter GABA in order to prevent and treat seizures

166
Q

Valproate Pharmicokinetics

A

Many forms, stick to one. Highly protein bound. Inhibit CYP450**, Concentration 50-100 or higher if needed

167
Q

Valproate ADE

A

BBW for hepatotoxicity, tetrogenaity and pancreatitis. Weight gain, thrombocytopenia, Hyperammonemia, Displacement reaction (Phenytoin), Increase Lamotrigine levels (Skin Rxn), CYP Inhibitor

168
Q

Gabapentin

A

GABAergic Agent

169
Q

Gabapentin Pharmikokinetics

A

Oral, renal elimination

170
Q

Gabapentin ADE

A

CNS: Somnolence, dizziness, ataxia, emotional lability, agitation. No DDI. Withdrawl

171
Q

Tigabine (Gabatril)

A

GABAergic Agent

172
Q

Tigabine (Gabaril) Pharmikokinetics

A

Highly protein bound

173
Q

Tigabine (Gabaril) ADE

A

Hallucinations/paranoia, Displacement DI

174
Q

Vigabatrin (Sabril)

A

GABAergic Agent

175
Q

Vigabatrin (Sabril)

A

MUST be an approved provider

176
Q

Vigabatrin (Sabril)

A

BBW - Irriversible vision loss

177
Q

Clobaxam (Onfi)

A

GABAergic Agent

178
Q

Clobaxam (Onfi) Pharmikokinetics

A

PO, Highly protein bound

179
Q

Clobaxam (Onfi) ADE

A

Benzo affects

180
Q

PHENObarbitol

A

GABAergic Agent

181
Q

PHENObarbitol Pharmikokinetics

A

PO only, Highly protein bound

182
Q

PENTObarbitol

A

GABAergic Agent

183
Q

PHENObarbitol ADE

A

Benzo affects

184
Q

PENTObarbitol Pharmikokinetics

185
Q

PENOTbaribol ADE

A

Benzo affects

186
Q

What is the first drug you reach for with status epilipticus?

A

IV Benzos, IM Midazolam, PR diazepam

Advanced Pharm (2 decks)

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