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Spring Pharm Block 4 > FR Review 4 - Respiratory, GI, Narcotics, and NSAIDs > Flashcards

FR Review 4 - Respiratory, GI, Narcotics, and NSAIDs Flashcards

1
Q

Differentiate the management of dry cough vs wet cough.

A

Dry: suppressed only if it is exhausting the patient
Wet: never suppressed

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2
Q

What drug class is the mainstay of asthma treatment and how do they act?

A

Glucocorticoids –> reduce bronchial hyperactivity and inflammation.

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3
Q

By what routes are glucocorticoids administered and which formulation is hydrophilic and why?

A

PO, IV, and Inhalation –> Inhaled steroids are hydrophilic so the drug stays where you put it.

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4
Q

What is a significant AE of inhaled glucocorticoids and why does this occur?

A

Thrush (candida) –> the inhaled steroid stays on the tongue and the patient doesn’t gargle.

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5
Q

What is the mechanism of action of Cromolyn and Nedocromil and by what route are they administered?

A

Mast cell stabilizers - reduce HST on exposure to allergens. Administered by inhalation only.

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6
Q

What is albuterol used for?

A

Short acting B-2 agonist used as a rescue agent

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7
Q

What is the result of administering a parasympatholytic in respiratory disease and which disease is it most used for?

A

Bronchodilation - used primarily in COPD and can be an adjunct in asthma

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8
Q

List two anti-cholinergic agents used in respiratory disease and which is used more frequently?

A

Ipratropium - used more frequently

Tiotropium - long acting agent

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9
Q

What class of drugs is a second-line agent in the management of asthma and what are their AEs?

A

Leukotriene Receptor Antagonists (Montelukast) - relatively few and benign AEs

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10
Q

What is the mechanism of PDE-4 inhibitors?

A

PDE-4 chews up cAMP in the lungs. PDE-4 inhibitors increase cAMP which result in bronchodilation.

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11
Q

What is the primary indication for PDE-4 inhibitors?

A

COPD –> chronic bronchitis, NOT emphysema

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12
Q

What are the instructions to use a MDI?

A

shake –> exhale –> slowly inhale and activate the MDI

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13
Q

What medication class causes ulcers and state three reasons why?

A

NSAIDs - because they are acidic, decrease mucus, and they anti-coagulate.

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14
Q

Describe the mechanism of action of sucralfate.

A

Not absorbed PO - it binds to the ulcer site like a band-aid and protects it from acid.

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15
Q

What drugs will sucralfate interact with?

A

Tetracyclines and Fluoroquinolones because sucralfate has aluminum in it and the other drugs are chelators.

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16
Q

What cells in the stomach produce acid and what are two common pathways by which they are stimulated that we may antagonize pharmacologically?

A

Parietal cells stimulated by H-2 (histamine) receptors and the proton pump.

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17
Q

Name 4 H-2 receptor antagonists.

A

Cimetidine, Famotidine, Nizatidine, Ranitidine.

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18
Q

Are H-2 receptor antagonists available by Px or OTC?

A

Both depending on dose.

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19
Q

If taking only one H-2 receptor antagonist per day, when should it be taken and why?

A

At night - most stomach acid is produced at night.

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20
Q

What are three AEs of H-2 receptor antagonists?

A

Thrombocytopenia
Confusion (especially in elderly or other patients in which the drug may accumulate)
Renally eliminated –> can’t use if CrCl < 50

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21
Q

What 4 drugs will H-2 receptor antagonists interact with and why?

A

Digoxin, itraconazole, iron, atazanavir - these drugs need acid to be absorbed. H2RAs increase pH.

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22
Q

Name five proton pump inhibitors.

A

Omeprazole, Esomeprazole, Lansoperazole, Rabeprazole, Pantoprazole.

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23
Q

T/F: PPIs act faster than H2RAs.

A

False: PPIs are slow on, slow off.

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24
Q

What are prokinetic agents and what are they used for?

A

Increase peristalsis - used as an anti-emitic, GERD, gastroparesis, facilitate feeding tube placement to get it past the pyloric valve.

25
Q

Define gastroparesis and what patients get it?

A

Decrease peristalsis from GI neuropathy - common in DM patients.

26
Q

What is the father of prokinetic agents and what are its effects?

A

Metoclopramide - enhances upper GI smooth muscle response to Ach enhancing GI motility and increased gastric emptying. Also blocks dopamine receptors in the chemo trigger zone (vomit center in CNS).

27
Q

What chronic disease may be exacerbated by metoclopramide use and why?

A

Parkinson’s because it blocks dopamine in the CNS.

28
Q

List two salts included in antacids and what is the major AE associated with each?

A

Al - constipating

Mg - diarrhea

29
Q

What drug commonly mixed with an NSAID can be used in prevention of ulcers?

A

Misoprostol - PG that stimulates production of mucus in the gut.

30
Q

What is the brand name of misoprostol by itself and what is the name of its coformulation?

A

Cytotec - misoprostol by itself

Arthrotec - misoprstol plus diclofenac

31
Q

What are the two main AEs associated with misoprostol?

A

Diarrhea and uterine contractions

32
Q

What are three agents used to manage constipation?

A

Magnesium
Lactulose - draws water to it
Polyethylene glycol - draws water to it

33
Q

Differentiate propylene glycol from polyethylene glycol from ethylene glycol.

A

Propylene Glyc - diluent used to force drugs into solution that would otherwise not dissolve
Polyethylene Glyc - used in colonoscopy prep
Ethylene glycol - antifreeze

34
Q

How is diarrhea caused by antibiotics managed?

A

If typical diarrhea - no management

If C. Diff - treat with PO Vancomycin

35
Q

What agents can be used as anti-diarrheals?

A

Codeine - not commonly used bc it is C-5
Lomotil - combo of diphenoxylate (anti-motility) and atropine (anti-ach that slows peristalsis)
Loperamide

36
Q

What agent is used to treat irritable bowel syndrome?

A

Dicyclomine - Anti-spasmodic anti-Ach agent specific to the colon.

37
Q

What are the classes of drugs used as anti-emetics? What is their MOA? Give an example of each.

A
  1. Antihistamine - meclizine and dimenhydrimate
  2. Phenothiazines - dec vomit center activity - prochlorperazine
  3. Serotonin 3 receptor antagonists - serotonin 3 in brain stimulates N/V - ondansetron
  4. Prokinetics - inc peristalsis - metoclopramide
  5. Benzos - MOA unknonwn - lorazepam
  6. Cannabinoids - pharm grade THC - dronabinol
  7. Steroids - brain tumor and TBI induced N/V - dexamethasone (most lipophilic steroid)
  8. Substance P receptor blocker - P receptor agonism causes pain - aprepitant
38
Q

Which narcotic medication is often given with ampho B to treat the rigors (tremors) caused by ampho B?

A

Meperidine

39
Q

What is the antidote for narcotics and what is the potential adverse effect?

A

Naloxone - may cause acute withdrawal

40
Q

List and describe the three drugs used to ween addicts off of narcotics.

A
  1. Naltrexone: Long acting form of naloxone that reduces euphoria in stable addicts.
  2. Methadone: Very long acting narcotic with large Vd.
  3. Bupenorphine: Opioid agonist/antagonist
41
Q

What drug, related to naltrexone, is used for opioid induced constipation?

A

Methylnaltrexone

42
Q

What chemical is the precursor to inflammatory mediators discussed in the NSAID section and what pathway leads to each inflammatory mediator?

A

Arachadonic Acid (AA)
AA –> COX-1 and CPX-2 –> Prostaglandins
AA –> LO enzyme –> Leukotrienes and Bradykinin

43
Q

What is the mechanism of action of NSAIDs?

A

Blocks COX-1 and COX-2 pathways inhibiting production of prostaglandins.

44
Q

Describe the pathophysiology of an “allergy” to NSAIDs.

A

Some people make excess leukotrienes and bradykinin in response to NSAIDs. Overproduction of bradykinin induces angioedema.

45
Q

What are the “three As” of NSAIDs’ mechanism of action?

A

Anti-inflammatory
Antipyretic
Analgesic

46
Q

Where are COX-1 and COX-2 enzymes primarily found?

A

COX-1 in the gut

COX-2 in the periphery

47
Q

Describe how NSAIDs affect the renal system.

A

PGs maintain patency of the afferent arteriole. NSAIDs constrict the afferent arteriole and reduce GFR –> causes an increase in serum creatinine.

48
Q

What is the primary sign of ASA overdose and why?

A

Tinnitus - NSAIDs increase the level of arachadonic acid which irritates the auditory nerve.

49
Q

What is the indication for IV indomethacin and by what mechanism? What other drug can be used for this indication?

A

Indication for patent ductus arteriosis –> PGs keep things open, indomethacin inhibits PGs. May also use IV ibuprofen (ibuprofen lysine).

50
Q

What is unique about meloxicam and what is the clinical effect of this characteristic?

A

The most Cox-2 selective of all non-selective NSAIDs. It stays in the periphery and has less GI AEs. Good choice for osteoarthritis in the elderly.

51
Q

By what routes is ketorolac administered and what is the maximum time it can be used and why?

A

PO and IM (only IM NSAID) –> max PO use is 5 days because it causes renal toxicity after 5 days.

52
Q

What is the only Cox-2 selective NSAID still on the market and why is it rarely used?

A

Celecoxib –> rarely used bc of cost and worry for increased cardiovascular morbidity and mortality.

53
Q

What are the effects of acetaminophen?

A

Antipyretic and analgesic (poor antiinflammatory)

54
Q

What is true about the distribution of acetaminophen and how is this clinically relevant?

A

Highly lipophilic meaning it will enter the CNS with few effects on the periphery.

55
Q

T/F: Acetaminophen acts as an anti-platelet

A

False –> no effect on platelets

56
Q

What differentiates APAP from the NSAIDs in terms of its metabolism and what is the clinical relevance?

A

It is metabolized by the liver where most NSAIDs are metabolized renally. APAP toxicity causes hepatotoxicity.

57
Q

What is the antidote for APAP overdose?

A

N-acetylcysteine (NAC)

58
Q

What are the effects of ASA that cause patients to be at increased risk for developing peptic ulcer disease?

A

It is an acid.
It decreases mucus production in the stomach.
It is an anti-platelet medication.

Spring Pharm Block 4 (17 decks)

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