Pharmacology Exam 4 Flashcards

1
Q

What is tiotropium used to treat?

A

Long term COPD

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2
Q

What drug class is tiotropium?

A

muscarinic receptor antagonist (anticholinergic)

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3
Q

How does tiotropium work?

A

Acts on M3 muscarinic receptors located on smooth muscles leading to a rduction in smooth muscle contraction and mucus secretion –> bronchodilatory effect

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4
Q

What are the adverse effects with montelukast?

A

Skin rash, mood changes, tremors, HA, abd pain, heartburn, upset stomach, N/D, tooth pain, fever, stuffiness, cough, hoarsness

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5
Q

What patient teaching should accompany the prescription of montelukast?

A

This will not work fast enough to treat an asthma attack that has already begun. May take several weeks to work

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6
Q

What patient teaching should be provided when prescribing inhaled corticosteroids?

A

Use bronchodilator first. Rinse mouth after use. Use even when not having symptoms

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7
Q

What ethnic background should not be prescribed long acting beta agonists?

A

African Americans. Can worsen asthma symptoms.

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8
Q

What medication would you prescribe for a patient taking propranolol with bronchospasm?

A

Ipratroprium (Atrovent)

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9
Q

What is the MOA of albuterol?

A

Activates beta adrenergic receptors and produces relaxation of pulmonary smooth muscles and dilation of the airways

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10
Q

What is the MOA of inhaled corticosteroids?

A

Inhibits IgE and mast cell mediated migration of inflammatory cells into bronchial tissues

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11
Q

When is it appropriate to use a short acting beta agonist?

A

In acute asthma attacks

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12
Q

What is the MOA of inhaled muscarinic receptor (anticholinergic) antagonists?

A

Reduce smooth muscle contraction and mucous secretion

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13
Q

What are the adverse effects associated with inhaled corticosteroids?

A

Oral thrush, cough, unpleasant taste, hoarseness, sore throat, oral irritation

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14
Q

What special populations should not be prescribed pseudoephedrine?

A

children less than 4
anyone taking an MAO-I
patients with severe HTN or CAD

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15
Q

What drug should be prescribed for a patient with nasal congestion with HTN?

A

nasal oxymetazoline or nasal azelastine

decongestants worsen HTN

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16
Q

What are the adverse effects of antihistamines?

A

sedation
GI upset, dry mouth/throat, urinary retention, dysuria
blurred vision, tinnitus, fatigue, HA, irritability

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17
Q

What conditions should cause a patient to avoid the use of antihistamines?

A
patients less than 6 or greater than 60
narrow-angle glaucoma 
Patients with BPH
Patients taking MAOIs
Do not use while breastfeeding
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18
Q

What is the MOA of codeine in the suppression of cough?

A

direct action on receptos in the cough center of the medulla

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19
Q

What medications are considered antitussives?

A

cough suppressants: codeine, dextromethrophan, benzonatate

20
Q

How are URI treated?

A

antibiotics, steroids, decongestant and expectorants, supportive care (rest, fluids)

21
Q

What patient education should be provided for a patient taking antacids?

A

Aluminum and Calcium-based antacids can cause constipation.
Magnesium can cause diarrhea.
Alkalosis may occur in patients with renal impairment
These may interfere with other medications

22
Q

What is the MOA of loperamide?

A

binds to the opiate receptors on the intestinal wall, which slows gastric motility and reduces the loss of fluid and electrolytes.
Decreases fecal volume, increases viscosity/bulk, and decreases loss of fluids and electrolytes

23
Q

What are the adverse effects of bisdmuth subsalicylate?

A

rebound constipation
gray/black stools
black tongue

24
Q

What special population should not be administered bismuth subsalicylate?

A

children and adolescents during recovery of flu/varicella

aspirin hypersensitivity

25
Q

When should bismuth subsalicylate be administered?

A

traveler’s diarrhea
take before each meal and at bedtime for up to 4x/day up to 3 weeks
Administer after each loose stool up to the max daily dose

26
Q

What lab values should be monitored with long-term administration of PPI?

A

iron studies, CBC, vit B12

calcium, bone-density monitoring

27
Q

Why is osteoporosis a risk when taking omeprazole?

A

inhibition of stomach acid decreases calcium absorption. PPIs speed up bone mineral loss

28
Q

What is the most rapid acting laxative and why?

A

Rectal administration of stimulants, like bisacodyl
(Onset 15-60 minutes)
stimulates peristalsis

29
Q

How does metoclopramide improve GERD?

A

increases lower esophageal tone, relaxes the pyloric sphincter and duodenal bulb, increases peristalsis resulting in accelerated gastric emptying and increases speed of gastric transit

30
Q

What is the Step Down approache with GERD?

A

PPI for 8 weeks
If no resolution, continue for 4-8 weeks then reduce PPI dose for 8 more weeks
If no relieve refer to GI
Idea is to step down to lowest dose of PPI that achieves symptom relief

31
Q

What is the Step UP approach with GERD?

A

Lifestyle modifcation and OTC antacids
Add H2R2 blocker and PPI if symptoms continue
Typically reserved for patients with mild GERD or occasioanl symptoms
If symptoms continue after 4-8 weeks or if endoscopy shows erosion –> start PPI

32
Q

What is the first line of therapy for PUD with a positive H. pylori infection?

A

Triple therapy:
PPI BID x8-12 weeks and two antibiotics for 10-14 days (Amox and Clarithormycin)

Quadruple therapy: PPI BID 8-12 weeks and 2 abx for 10-14 days plush bismuth subsalicylate for 14 days

33
Q

How will you treat N/V?

A

first line therapy is vitamin B6 and doxylamine, especially in pregnant women
Zofran can be used in children but can cause constipation
Ginger

34
Q

How will you treat constipation in children?

A

Mira-lax is first-line therapy
Bulk form laxatives are the safest
Lacutolose can be given if bulk is ineffective

35
Q

what are the disadvantages of using stimulant laxatives for prolonged periods?

A

long term use can lead to loss of colon function. constipation can become increasingly worse and unresponsive to laxatives

36
Q

What is the MOA of the phenothiazine antiemetics?

A

block dopamine receptors in the chemoreceptor trigger zone. also bind/block cholinergic, alpha1-adrenergic and histamine 1 receptors

37
Q

What is the MOA of docusate sodium?

A

Surfactant. reduces surface tension of the oil-water interface on the stool and facilitates water absorption into the stool, producing softening action

38
Q

What is the MOA of PPIs?

A

Binds irreversibly to proton pump on gastric parietal cells and block the secretion of hydrogen ions, which combine with chloride ions in the stomach lumen to form gastric acid

39
Q

What is the MOA of ondansetron?

A

highly selective 5-HT3 receptor antagonist

Blocks serotonin both peripherally on vagal nerve terminals and centrally in the chemoreceptor trigger zone

40
Q

What is the contraindications to the use of misoprostol?

A

Pregnancy or prior uterine surgery

41
Q

How will you choose a diuretic in the treatment of HTN?

A

Assess renal fx, including GFR, BUN, and creatinine

Thiazide diuretics should be prescribed to patients with A GFR greater than 40-45 ml/min

42
Q

What is the MOA of the Loop diuretics?

A

inhibit reabsorption of sodium in the ascending loop of the nephron which results in increased excretion of water in the urine
cause substantial diuresis of up to 20% of the filtered load of sodium, chloride, and water

43
Q

MOA of thiazide diuretics? (hydrochlorothiazide, chlorothiazide, chlorthalidone)

A

acts on the distal convulated tubule and leads to the retention of water in the urine as it follows the sodium particles. decreases preload on the heart which decreases BP, vasodilates and decreases resistance

44
Q

MOA of carbonic anhydrase inhibiotors (diuretics) (acetazolamide, methazolamide)

A

inhibit the enzyme carbonic anhydrase in the proximal confulated tubule which results in bicarbonate accumulation in the urine and decreased sodium absorption

45
Q

MOA of potassium sparing diuretics (spironlactone, amiloride, epleronone, triamterene)

A

do not stimulate potassium secretion in the urine so potassium is spared