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CLIN PHARM > Clin Pharm Exam I - Drugs > Flashcards

Clin Pharm Exam I - Drugs Flashcards

1
Q

What type of diuretic is acetazolamide?

A

Carbonic anhydrase inhibitor

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2
Q

What is the mechanism for carbonic anhydrase inhibitors?

A
  • Decrease H+
  • Decrease Na absorption via Na/H antiporter
  • K wasting and increased HCO3 secretion ——> milk alkaline diuresis
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3
Q

What are the indications for use of carbonic anhydrase inhibitors?

A
  • Metabolic alkalosis
  • Glaucoma
  • Hyperkalemic Periodic Paralysis (HYPP) in horses

NOT FOR EDEMA

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4
Q

What are the potential toxicities with carbonic anhydrase inhibitors?

A
  • Sulfonamide cross-sensitivity
  • Metabolic acidosis
  • Electrolyte disturbances (K/Na wasting)
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5
Q

What kind of diuretic is mannitol?

A

Osmotic diuretic

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6
Q

What is the mechanism of action for osmotic diuretics?

A
  • Pulls water out of intracellular compartments
  • Holds water in the tubules, inhibiting reabsorption
  • Increases inner medullary blood flow, reducing hypertonicity and favorable gradient for Na/H20 reabsorption
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7
Q

What are the indications for use for osmotic diuretics?

A
  • Relieve intratubular obstruction
  • Increased GFR, renal blood flow, urine production with renal failure
  • Decrease intracranial pressure
  • Decrease intraocular pressure (glaucoma)

CONTRAINDICATED WITH INTRACRANIAL HEMORRHAGE

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8
Q

What types of toxicity are seen with osmotic diuretics?

A

Acute
Rapid volume expansion –> increased blood pressure, hyponatremia

Chronic
- Dehydration, electrolyte disturbances
- Formation of intracellular idiogenic osmoles

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9
Q

What are some other important considerations for osmotic diuretics?

A
  • Only human formulations available
  • Crystals will form in fluid
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10
Q

What type of diuretic is furosemide?

A

Loop diuretic

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11
Q

What is the mechanism for loop diuretics?

A
  • Inhibits the Na/K/Cl symporter –> decreases transcellular Na transport
  • Lower hypertonicity of medulla
  • Increases release of prostaglandins –> increases renal blood flow
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12
Q

What are three important points about the action of loop diuretics?

A
  • Potent, rapidly acting, and short lived
  • Action is limited by the amount of sodium delivered to the loop
  • Needs to be transported into the tubule to have greatest effect
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13
Q

What are the other renal effects of loop diuretics?

A
  • Inhibits Ca and Mg reabsorption
  • Increases K and H+ excretion
  • Enhances PGE2 formation
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14
Q

What are the other non-renal effects of loop diuretics?

A
  • Increased venous compliance
  • Decreased right atrial pressure
  • May prevent exercise induced bronchoconstriction
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15
Q

What are the indications for use for loop diuretics?

A
  • Treatment of edema
  • Increased urine output in renal failure
  • Hypercalcemia
  • Hyperkalemia
  • COPD in horses
  • Exercise induced pulmonary hemorrhage in horses
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16
Q

What are the risks for toxicity with loop diuretics?

A
  • Additive risk for nephrotoxicity when used with other nephrotoxic drugs
  • Additive risk of ototoxicity
  • Hypokalemia
  • Volume depletion/dehydration
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17
Q

What drug interactions are common with loop diuretics?

A

NSAIDs inhibit PGE2 production, and compete with furosemide for transport into the renal tubules

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18
Q

What are some other considerations with loop diuretics?

A
  • 80% bioavailability in healthy dogs (decreased with hypertension)
  • Short half life (only 1 hour when given IV)
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19
Q

What are the contraindications/precautions with loop diuretics?

A
  • Patient with anuria, or who are hypersensitive to the drug
  • Patients with preexisting electrolyte/water balance abnormalities or impaired hepatic function
  • Patients with conditions that may lead to electrolyte/water balance abnormalities
  • Hypotension
  • Hepatic ncephalopathy
  • Patients hypersensitive to sulfonamides
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20
Q

What kind of diuretic are chlorothiazide and hydroclorothiazide?

A

Thiazide diuretics

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21
Q

What is the mechanism of action of thiazide diuretics?

A
  • Inhibits the Na/Cl cotransporter
  • Na remains in the tubular fluid
  • Enhances excretion of Na, Cl, H20, K, Mg, Phos, iodide, and bromide
  • Decreases Ca excretion
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22
Q

What are the indications for use of thiazide diuretics?

A
  • Prevent alcium oxalate uroliths in dogs
  • Enhace the effects of diazoxide treatment of insulinomas in dogs
  • HYPP in horses
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23
Q

What are the risks of toxicity with thiazide diuretics?

A
  • Dehydration
  • Hypokalemia
  • GI effects
  • Alkalosis
  • Cross-reactivity with sulfonamide hypersensitivity
  • Can exacerbate hyperglycemia
  • Ulcerative facial dermatitis in cats
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24
Q

What kind of diuretic is spironolactone?

A

Aldosterone antagonist
K-sparing diuretic

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25
Q

What is the mechanism of action of aldosterone antagonist K-sparing diuretics?

A
  • Completely inhibits aldosterone binding at the level of the distal tubules
  • Increased excretion of Na, Cl, H20
  • Decreased excretion of K, ammonium, and phosphate
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26
Q

What are the indications for use for aldosterone antagonist K-sparing diuretics?

A
  • Adjunctive therapy for congestive heart failure
  • Combined with loop or thiazide diuretic to decrease K wasting
  • Ascites
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27
Q

What are risks of toxicity with aldosterone antagonist K-sparing diuretics?

A
  • Hyperkalemia
  • Dehydration
  • Metabolic acidosis
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28
Q

What are other considerations of aldosterone antagonist K-sparing diuretics?

A
  • Competes with digoxin for renal clearance –> can lead to digoxin toxicity
  • Cross reacts with digoxin assays, interfereing with digoxin monitoring
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29
Q

What type of diuretics are triamterene and amiloride?

A

Sodium channel blocker K-sparing diuretics

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30
Q

What is the mechanism of action of sodium channel blocker K-sparing diuretics?

A
  • Blocks Na channels on luminal side of renal tubular cells
  • Less Na inside cell to exchange for K
  • Less K excreted into the lumen for excretion
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31
Q

What are the indications for use of sodium channel blocker K-sparing diuretics?

A
  • Combine with loop or thiazide diuretic to decrease K wasting
  • Edema in hepatic encephalopathy
  • Not commonly used in vet med
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32
Q

What are the risks of toxicity with sodium channel blocker K-sparing diuretics?

A

Hyperkalemia

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33
Q

What is the general onset of action for acetazolamide?

A

Fast
30 minutes PO

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34
Q

What is the general onset of action for furosemide?

A

Fast
30 minutes IV

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35
Q

What is the general onset of action for thiazides?

A

Medium
2 hours PO

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36
Q

What is the general onset of action for triamterene?

A

Medium
2-4 hours PO

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37
Q

What is the general onset of action for spironolactone?

A

Slow
2-3 days PO

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38
Q

What is the mechanism of action of calcitriol?

A
  • Replaces activated Vitamin D not being made in the kidneys
  • Improved GI Ca absorption
  • Inhibits PTH production
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39
Q

What are the indications for use for calcitriol?

A
  • Renal secondary hyperparathyroidism
  • Hypocalcemia, hypoparathyroidism
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40
Q

What are the risks of toxicity with calcitriol?

A
  • Hypercalcemia
  • Tissue mineralization (DO NOT use if serum phos >6.0 mg/dL)
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41
Q

What is the main pharm consideration with calcitriol?

A

Doesn’t require renal activation like other forms of vitamin D

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42
Q

What type of drugs are epoetin and darbepoetin?

A

Erythrocyte stimulating agents

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43
Q

What is the mechanism of action for erythrocyte stimulating agents?

A

Directly replaces EPO to stimulate RBC production

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44
Q

What is the indication for use for erythrocyte stimulating agents?

A

Clinical anemia <20% due to EPO deficiency (CKD)

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45
Q

What are the risks of toxicity with erythrocyte stimulating agents?

A
  • Hyperviscosity/polycythemia
  • Hypertension
  • Autoantibody formation (70%)
  • Red cell aplasia (30%)
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46
Q

What are some other considerations with erythrocyte stimulating agents?

A
  • Don’t start until PCV <20-22%
  • Target >25% up to low normal PVC
  • Only 60-65% of animals respond
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47
Q

What is the mechanism of action for opiate antitussives?

A

Directly depresses cough center in the medulla via mu/kappa opiate receptors

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48
Q

What are the indications for opiate antitussives?

A

Moderate to severe coughing that interferes with patient QOL

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49
Q

What are the risks of toxicity and drug interaction with opiate antitussives?

A
  • Potential for abuse
  • Sedation
  • Constipation
  • Respiratory depression
  • Excitation/dysphoria in cats and horses
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50
Q

What are some examples of opiate antitussives?

A

Morphine
Codeine
Hydrocodone
Butorphanol

51
Q

What are the characteristics of morphine as an antitussives?

A
  • Low doses inhibit coughing
  • No analgesia or sedation
52
Q

What are the characteristics of codeine as an antitussive?

A
  • Less likely to cause sedation compared to morphine
  • Less potential for addiction/abuse
53
Q

What are the characteristics of hydrocodone as an antitussive?

A
  • Similar to codeine
  • Available in combo with homatropine to curb abuse potential
54
Q

What are the characteristics of butorphanol as an antitussive?

A
  • FDA approved as an antitussive
  • Schedule IV controlled substance
55
Q

What is the mechanism of action for dextromethorphan?

A

Unknown
Opiate derivative but doesn’t stimulate opiate receptors

56
Q

What are the indications for dextromethorphan?

A

Moderate to severe coughing that interferes with patient QOL

57
Q

What are the toxicity/drug interactions with dextromethorphan?

A

Vomiting and CNS toxicity at high doses in dogs and cats

58
Q

What formulation of dextromethorphan should be avoided in dogs and especially cats?

A

Formulations that also contain acetaminophen, antihistamines, and/or decongestants

59
Q

What are the pharmacokinetic considerations with dextromethorphan?

A
  • Poor bioavailability in dogs
  • Very short half life
  • Unknown in cat and horses
60
Q

What is the mechanism of action of tramadol?

A

Opiate with serotonin and alpha-2 activity

61
Q

What are the indications for tramadol?

A

Moderate to severe coughing that interferes with patient QOL

62
Q

What are the toxicity/drug interactions with tramadol?

A
  • Sedation, nausea, vomiting
  • Drugs that inhibit CYP 2D (SSRIs) decreases formation of the active metabolite –> reduces efficacy of tramadol
63
Q

What is the mechanism of action for methylxanthines?

A
  • Not totally understood
  • Inhibition of phosphodiesterase (PDE) –> increased intracellular cAMP levels –> decreased release of inflammatory mediators from mast cells and bronchial smooth muscle relaxation
  • Adenosine receptor antagonists
64
Q

What are the indications for methylxanthines?

A
  • Feline asthma
  • Canine allergic bronchitis
  • Recurrant airway obstruction (heaves/COPD) in horses
  • Poor bronchidilator in cattle
65
Q

What are the toxicity/drug interactions with methylxanthines?

A
  • CNS stimulation
  • Tachycardia
  • Nausea/vomiting
  • Mild diuresis

Clearance relies on CYP 450 enzymes
- Drugs that inhibit this enzymes can lead to toxicity
- Drugs that induce this enzyme can lead to subtherapeutic concentrations

66
Q

What type of drug is theophylline?

A

Methylxanthine bronchodilator

67
Q

What is the mechanism of action for beta-2 adrenergic agonist bronchodilators?

A
  • Beta-2 adrenergic receptors increase intracellular cAMP and cause relaxation of smooth muscle
  • Stimulation of beta-2 receptors on mast cells decreases release of inflammatory mediators
  • Stimulation may increase mucociliary clearance
68
Q

What are the three types of beta-2 adrenergic agonists?

A

Ultra short acting
Longer acting
Ultra long acting

69
Q

What are ultra short acting beta-2 adrenergic agonists used for?

A

To treat acute respiratory crises

70
Q

What are the longer acting beta-2 adrenergic agonists used for?

What are some examples of drugs in this class?

A

Chronic use
Available PO or inhalation

Terbutaline
Metaproterenol
Albuterol

71
Q

What are the toxicity/drug interactions for beta-2 adrenergic agonists?

A
  • Short acting non-specific agents stimulate alpha and beta 1 and 2 receptors –> side effects of hypertension and tachycardia
  • Higher doses of Beta-2 selective agents can stimulate beta-1 receptors = cardiac toxicity
  • Tolerance to beta agonists can occur over time (breaks from the drug may help prevent this)
72
Q

What are the pharmacokinetic considerations for beta-2 adrenergic agonists?

A
  • Epinephrine and isoproteranol last for <1 hour
  • There are masks for horses and inhalation chambers for cats to aid with nebulization
73
Q

What is nebulization?

A

Process of creating small droplets of appropriate size that can be delivered into the airways

74
Q

What is the mechanism of action for anticholinergic bronchodilators?

A

Inhibit acetylcholine receptor activation

75
Q

What are the indications for anticholinergic bronchodilators?

A

Short-term bronchodilators in crisis situations

Adverse effects limit long-term use

76
Q

What are the toxicity/drug interactions with anticholinergic bronchodilators?

A
  • Tachycardia
  • Ileus, constipation, dry mouth
  • CNS excitation followed by depression/coma
  • Decreased mucuciliary clearance
77
Q

What are three examples of anticholinergic bronchodilators?

A

Atropine
Glycopyrrolate
Ipratropium bromide

78
Q

What are the characteristics of atropine as an anticholinergic bronchodilator?

A

Crosses BBB
Potential for colic

79
Q

What are the characteristics of glycopyrrolate as an anticholinergic bronchodilator?

A

Injectable formulation has fewer side effects
DOES NOT CROSS BBB

80
Q

What are the characteristics of ipratropium bromide as an anticholinergic bronchodilator?

A

Not absorbed from airway —-> no systemic adverse effects

81
Q

What type of drug is cromolyn?

A

Anti-inflammatory for reactive airway disease

82
Q

What is the mechanism of action for cromolyn?

A
  • Inhibits mast cell degranulation via interference w/ Ca++ transport across cell membrane
  • No bronchodilatory effects
83
Q

What are the indications for cromolyn?

A

Effective only if administered prior to exposure to allergen in horses

84
Q

What type of drugs are corticosteroids?

A

Anti-inflammatory for reactive airway disease

85
Q

What is the mechanism of action for corticosteroids?

A
  • Decrease inflammation a variety of ways
  • Augments beta-2 adrenergic mediated bronchial smooth muscle relaxation
  • May prevent down-regulation of beta-2 adrenergic receptors
86
Q

What are the indications for corticosteroids as respiratory anti-inflammatory drugs?

A
  • Metered dose inhalers deliver the drug topically to minimize systemic side effects
  • Feline asthma
  • Allergic bronchitis and non-septic pulmonary diseases w/ leukocyte infiltrates in dogs
87
Q

What are the toxicity/drug interactions of glucocorticoids?

A

Dogs: weight gain, GI ulceration, secondary infection

Cats: weight gain, hyperglycemia/risk of DM, secondary infection

88
Q

What are the oral/injectable corticosteroids available?

A
  • Prednisone/prednisolone
  • Methylprednisolone acetate (Depo-Medrol)
  • Dexamethasone
89
Q

What are the inhaled corticosteroids available?

A
  • Flunisolide
  • Budesonide
  • Trimcinolone
  • Beclomethasone diprioprionate
  • Fluticasone proprionate
90
Q

What are expectorants?

A

Drugs that (in theory) increase output of bronchial secretions via decreasing the viscosity of secretions –> enhanced clearance of bronchial exudates –> more productive cough

91
Q

What are the two main expectorants?

A
  • Saline expectorants
  • Guaifenesin
92
Q

What are the characteristics of saline expectorants?

A

Vagal nerve mediated reflex in gastric mucosa stimulates bronchial secretions

93
Q

What are the characteristics of guaifenesin expectorants?

A
  • Muscle relaxant used during anethesia
  • Expectorant side effects
  • Vagal stimulations lead to bronchial secretions
94
Q

What type of drug is acetylcystine?

A

Mucolytic

95
Q

How does acetylcystine work?

A

Sulfhydral groups break the disulfide bonds on mucoproteins

96
Q

What drug type are doxapram and dopram?

A

Respiratory stimulants

97
Q

What is doxapram used for?

A

Stimulating the respiratory center in emergency situations

98
Q

What is the mechanism of action for doxapram?

A
  • CNS stimulant
  • Stimulates carotid and aortic chemoreceptors
  • Transient increases in respiratory rate and volume occur after administration
99
Q

What opiate antitussives are used in horses?

A

Hydrocodone
Butorphanol

100
Q

What non-opiate antitussive is used in horses?

A

Dextromethorphan

101
Q

What is the mechanism of antitussives in horses?

A

Direct suppression of the cough center

102
Q

What is the mechanism of action for methylxanthines in horses?

A

Competitive non-selective phosphodiesterase inhibitor
- Increases cAMP, protein kinase A
- Inhibits TNF-alpha and leukotriene synthesis

Non-selective adenosine receptor antagonist
- Antagonization of A1, A2, and A3 receptors
- Cardiac effects

103
Q

What methylxanthine bronchodilator is used in horses?

A

Theophylline

104
Q

What are the side effects of methylxanthines in horses?

A
  • CNS excitation
  • Arrhythmias
  • Narrow margin of safety
105
Q

What is the mechanism of action of beta-2 adrenergic agonists in horses?

A

Decreased
- Bacterial adherence
- Neutrophil function
- Cholinergic neuro transmission
- Plasma exudation

Increased
- Mucociliary clearance
- Bronchodilation

106
Q

What are the two categories of beta-2 agonists in horses?

What drugs are in each?

A

Selective
- Albuterol
- Clenbuterol
- Salmeterol

Non-selective
- Epinephrine
- Isoproterenol

107
Q

What occurs with down-regulation of beta-2 adrenergic agonists?

A
  • Tolerance/tachyphylaxis
  • Uncoupling of adenylate cyclase
  • Receptor down regulation
108
Q

What are the toxicity/side effects of non-selective beta-2 adrenergic agonists in horses?

A
  • Ultra short-acting

Epinephrine
- Tachycardia
- Muscle fasiculations
- Sweating
- Hypertension

Isoproterenol
- Tachycardia

109
Q

What are the toxicity/side effects of the selective beta-2 adrenergic agonists in horses?

A
  • Tachycardia
  • Sweating
  • Muscle fasciculations
  • Excitation
110
Q

What are three indications for beta-2 adrenergic agonists in horses?

A

1) Emergency therapy in horses with marked airway obstruction or anaphylaxis

2) Before exercise to relieve mild to moderate airway obstruction

3) Before administration of aerosol corticosteroid preparations to improve pulmonary distribution

111
Q

What is the most commonly used beta-2 adrenergic agonist in horses?

What are the characteristics of this drug?

A

Clenbuterol (oral)

  • Partial beta2 agonist
  • Can treat for up to 30 days (tolerance will develop)
  • Excellent bioavailability (87%)
  • Anabolic and lipolytic
  • Anti-inflammatory
  • Tocolytic effect (slow labor in dystocias)
112
Q

Drugs administered as gases/in aerosols can have particles as large as ___________.

A

50 micrometers

113
Q

What size particles does a therapeutic aerosol need to be to get maximum deposition in the lower airways?

A

1-5 micrometers

114
Q

What has the biggest impact on inhaled drug distribution?

A

Pattern of breathing

115
Q

Maximal deposition of inhaled drugs occur when patients take what kind of breaths?

A

Slow, deep breaths with large tidal volumes

116
Q

How is albuterol administered to horses?

A
  • NOT orally (poor bioavailability)
  • Aerosol administration/nebulization
117
Q

What are the characteristics of salmeterol in horses?

A
  • Inhaled
  • Long acting 8-12 hours
  • Anti-inflammatory
  • Inhibits leukotriene/histamine release
  • Reduces eosinophils
  • Used for maintenance in therapy, pre-exercise, and in mild to moderate airway obstruction
118
Q

What is the mechanism of action with anticholinergics in horses?

A
  • Acts on parasympathetic innervations throughout the tracheobronchial tree of the horse
  • Greatest effect in large central airways smooth muscle
  • Parasympathetic blockage of M3 receptors with muscarinic antagonists
119
Q

What are the characteristics of atropine in horses?

A
  • Non-selective M1/M2/M3 antagonist
  • Decreases release of intraellular Ca from the sarcoplasmic reticulum –> Smooth muscle relaxation
  • Rapid bronchodilation in horses
  • Short duration 1/2 - 2 hours
  • Limited use in horses except as a rescue drug
120
Q

What are the side effects of atropine in horses?

A
  • Severe
  • Ileus
  • CNS toxicity
  • Tachycardia
  • Increased mucus viscosity
  • Impaired mucociliary clearance
121
Q

What kind of drug is ipatromium bromide?

A
  • Synthetic anticholinergic
  • Non-selective muscarinic antagonist
122
Q

What are the characteristics of ipatromium bromide?

A
  • Bronchodilation
  • Inhibition of cough
  • Needs nebulized or inhaled
  • Effects within 15-30 minutes, and last 4-6 hours
123
Q

What kind of drugs are pseudoephedrine and phenylpropanolamine (PPA)?

A

respiratory decongestants

124
Q

What is the mechanism of action of respiratory decongestants?

A

Alpha-1 agonist receptor

CLIN PHARM (13 decks)

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