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Unit1_Pharm Flashcards

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1
Q

_______ suppression is still the treatment of choice for acute ulcers and given alone these agents will lead to ulcer healing.

A

Acid

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2
Q

Acid suppression is still the treatment of choice for _____ ulcers and given alone these agents will lead to ulcer healing.

A

acute

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3
Q

_________ therapy is necessary to reduce the rate of recurrence of gastric ulcers (50-80% success) and duodenal ulcers (90-95% success) antibiotic therapy is critical.

A

Antibiotic

These antibiotics are used as components of “triple” or “quadruple” therapy with proton pump inhibitors and H2 antagonists.

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4
Q

What makes up Triple ABX therapy?

A 
Clarithomycine 
\+
Amoxicillin-or-Metronidazole 
\+
PPI
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5
Q

What makes up Quadruple ABX therapy?

A 
Bismuth subsalicylate
\+
Metronidazole
\+
Tetracycline 
\+ 
PPI or H2 Antagonist
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6
Q

What makes up Sequential ABX therapy?

A

Amoxicillin-PPI (5 days) then

Clarithromycin-Tinidazole-PPI (5 days)

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7
Q

What Drug is  Administered as prodrug, absorbed into systemic circulation, then diffuses into parietal cells of stomach where proton catalyzed formation of the active sulfenamide “traps” the drug in the acidic secretory canniculi?

A

Proton Pump Inhibitors

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8
Q

What cells in the GI do PPIs act on?

A

parietal cells in the stomach

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9
Q

What is the active form of a PPI?

A

Active Silfenamide

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10
Q

What type of inhibition does a PPI do?

A

irreversible inhibition of an enzyme [H+/K+ ATPase]

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11
Q

How long does it take for the synthesis of new enzyme that is irreversibly blocked by PPIs? Therefore, this means that PPIs result in what percentage reduction in acid production?

A

18 hours are needed to synthesize new H+/K+ ATPase.

80-95% reduction in acid production. (even tho the half-life of PPIs are 0.5 to 2.0 hours)

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12
Q

How long does it take a PPI to reach steady state levels?

A

2-5 days. b/c not all pumps are active at the time of Rx use.

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13
Q

Which PPIs are the most effective?

A

They all have the same effects

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14
Q

PPI are highly protein-bound with bioavailability of 40-90%. What can you do to improve bioavailability?

A

Admin as an enteric-coated pill or with Sodium Bicarb.

Best to give about 1 hour before meal so that peak plasma level occurs when your pumps are active.

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15
Q

What is the metaboism profile of PPIs?

A

rapid first pass in liver via CYP450. caution with pt. w./ hepatic issues.

no drug accum in chronic renal failure with once-daily dosing.

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16
Q

What diz/Sx can be treated with PPIs?

A
  • GERD
  • Peptic Ulcer Diz
  • NSAID-induced ulcers
  • Prevention of stress gastritis
  • Zollinger-Ellison Syndrome
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17
Q

Which PPI fucks with a blood thinner? What is the name of that blood thinner?

A

Omeprazole inhibits conversion of clopidogrel, and anti-platelet agent (prevents crosslinking of platelets)

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18
Q

Omeprazole [Prilosec] / Esomeprazole [Nexium], Lansoprazole [Prevacid] are what class of drugs?

A

PPIs

Omeprazole is available OTC

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19
Q

What is the MOA of H2 Receptor Antagonist?

A

reversible, competitive block of PARIETAL cells H2 receptors on basolateral membrane.

Better at blocking nocturnal (basal, H2-mediated) acid secretion (90%) than meal-stimulated (ACh- and gastrin-mediated, 60-80%). Since suppression of nocturnal acidity is key to duodenal ulcer healing, evening dosing of H2 antagonists is usually adequate therapy.

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20
Q

Describe the PK profile of H2 receptor antagonist.

A

Rapid absorption from GI tract, decrsed with antacid use.

Less protein binding than PPIs.

Some Hepatic metabolism (no adjustment needed for liver diz)

Elim = renal excretion [need dose adjustment with impaired renal function, think old folks]

half-life = 1 - 4 hours

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21
Q

What are the clinical uses of H2 receptor antagonist?

A
  • GERD
  • Peptic Ulcer Disease
  • Stress-related gastritis
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22
Q

What are the basic common side effects of H2 receptor ANTAGONIST?

A
  • dizziness
  • diarrhea
  • constipation
  • headache
  • some CNS dysfunction

overall they are well tolerated

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23
Q

What are the endocrine ADRs ~w/ H2 receptor antagonists?

A

@ high does ==>

  • Gynecomastia
  • Galactorrhea
  • decreased sperm count
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24
Q

What are the DDi ~w/ H2 receptor antagonists?

A
  • Cimetidine inhibits CYP450 oxidative metabolism.

(Fucks with the effects or toxicity of number of drugs (theophylline, warfarin, phenytoin, carbamazepine, ketoconazole, itraconazole, benzodiazepines)

-All anti-secretory agents can decrease ketoconazole absorption by causing an increase in gastric pH (more basic)

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25
Sucralfate [Carafate] is what class of drug?
Mucosal Protective Agents
26
What is the MOA of Sucralfate?
during acid-induced damage, pepsin will hydrolyze mucosal proteins causing erosion and ulcerations. this process is inhibited by sulfated disaccharide aluminum salt that SELECTIVELY binds to necrotic ulcer tissue to form a protective layer. [up to 6 hours of protection per dose]
27
What are the other possible 2/nd actions of Sucralfate?
decrease back diffusion of H+ and binds to pepsin and bile acids. May stimulate PGE and Epidermal GF production.
28
What are the clinical uses of Sucralfate?
decreased use. limited to adjunct Tx.
29
What are the ADRs ~w/ Sucralfate?
few. Constipation most common
30
Misoprostol [Cytotec] is what class of drug?
PGE1 analog
31
What is the MOA of Misoprostol?
PGE normally act on stomach parietal cells to inhibit cAMP formation --> DECREASE H+ secretion. PGE also stimulate acid neutralizing HCO- formation and cytoprotective mucus formation. Misoprostol is a PGE1 analog = increases this normal physiological func. acid-suppression is does-related [up to 85-95%]
32
Describe the PK of Misoprostol?
- Oral, rapid absorption (w/in 30min) - rapidly de-esterified to active metabolite, 30-min half-life. - dosed 3-4/day
33
What are the clinical uses of Misoprostol?
Tx NSAIDs induced GI ulceration, but rarely used d/t to 4-dose/day and ADRs
34
What are the side effects of Misoprostol use?
- Diarrhea | - No-No-4-Prego
35
What drug class can be used in pain relief (healing) d/t peptic ulceration and acute gastritis?
Gastric Antacids
36
What would be the IDEAL properties of gastric antacids? (4)
1. rapidly increase stomach pH to 4-5. (PD) 2. be non-absorbable (PK) 3. be long-acting (PK) 4. no ADRs
37
Which type of antacids have the HIGHEST levels of systemic actions? (i.e. highest systemic absorption)
NaHCO3 (Sodium bicarb) Al3+, Mg2+, Ca2+ are less absorbed and cleared with normal renal func.
38
Which antacids has diarrhea as an ADR? Which one has constipation as an ADR?
Mg2+ = diarrhea Ca2+ & Al3+ = constipation
39
What are the DDIs of antacids?
may interact with other GI drugs. rule is to space antacid dosing around other drugs. - Decreased absorption due to binding or adsorption interactions in gut (chelation with Al+++ - Ca++ - Mg++): Tetracycline, fluoroquinolones, digoxin, chlorpromazine, indomethacin. - Altered absorption due to effect on gastric emptying. - Altered excretion due to alkaline urine: Aspirin (increase), quinidine (decrease) - Reduced bioavailability of H2 antagonists and ketoconazole via increased gastric pH
40
Which antacids should not be used if pt. has renal issues?
Mg2+ & Sodium Bicarb
41
Which antacids is contraindicated in pregos and prolonged use?
Sodium Bicarb
42
Which antacids may lead to CNS toxicity with chronic use?
Aluminum
43
What class of drugs can be used as empric and Sx-based Tx for various disorders of bowel moliity & Sx relief of esophagus associated w/ GERD?
Prokinetic Agents
44
Overall, what is the MOA of Prokinetc drugs?
direct or indirect AGONIST activity at smooth muscle [M3] receptors.
45
What is the specific MOA of the following Prokinetic Drug? Erythromycin
Erythromycin (+) is an agonist at excitatory (+) at neural and smooth muscle motilin receptors.
46
What is the specific MOA of the following Prokinetic Drug? Cisapride
Cisapride is an agonist (+) at excitatory (+) neural 5-HT4 receptors on enteric nervous system cholinergic motor neurons.
47
What is the specific MOA of the following Prokinetic Drug? Metoclopramide
Metoclopramide is an antagonist (-) at presynaptic dopamine (DA) receptors (D2) that inhibit the release of acetycholine.
48
What is the specific MOA of the following Prokinetic Drug? Neostigmine
Neostigmine inhibits (-) hydrolysis of acetylcholine by acetylcholinesterase (AChE).
49
What is the specific MOA of the following Prokinetic Drug? Bethanechol
Bethanechol acts directly as an agonist (+) at excitatory (+) M3 smooth muscle receptors.
50
Direct activation of M3 muscarinic receptors in the gut (as with older cholinergic agents such as direct receptor agonists [bethanechol] or cholinesterase inhibitors [neostigmine]) will increase GI motility BUT will NOT do so in a coordinated manner; what does this result in?
There will be NO net increase in propulsive activity and will also tend to increase gastric and pancreatic secretions.
51
Prokinetic agents increase gastric motiliyty by increasing the release of what?
ACh from cholinergic neurons in the enteric NS. they at upstream; effects the motor neurons, not the post-synaptic action.
52
What drug is a Dopamine antagonist that blocks presynaptic inhibition of ACh release by dopamine at D2 receptors?
Metoclopramide [Reglan] Produce coordinated contractions that enhances transit of luminal contents. DA-antag = relieves v/n
53
What drug(s) are AGONIST at post-synaptic 5HT4 receptors and DIRECTLY increase ACh release?
- Tegaserod [Zelnorm] - Cisapride [Propusid] * Stimulates motility and increases transit in esophagus, stomach, small intestine and ascending colon * Reduces bloating associated with irritable bowel syndrome
54
What is the PK of Tegaserod?
- Oral - Partially absorption from gut, slowed by food, best given on empty stomach - Two-thirds of dose excreted unchanged in feces; remainder excreted as glucuronide metabolites in urine. Half-life of 11 hours. No dosage adjustments necessary unless severe hepatic or renal impairment, then drug should be avoided.
55
What is the PK of Metoclopramide?
- Oral-IV-IM - Rapid absorption, peak effects within 1 hour. - Metabolized to sulfate and glucuronide conjugates and then excreted in the urine; half-life of 4-6 hours with duration of action 1-2 hours
56
What are the clinical uses of promotility Drugs? (M3 AGONIST)
- diabetic gastroparesis - GERD - constipation-predominant IBS in women (tegaserod)
57
Which promotility drug (M3 AGONIST) may increase QT-interval?
Cisapride promotility drug (M3 AGONIST) *especially if there is CYP450 DDi
58
Which promotility drug (M3 AGONIST) may cause somnolence, dystonic reactions, tardive dyskinesia?
Metoclopramide | b/c it's a DA agonist!
59
Which promotility drug (M3 AGONIST) is mainly used to Tx IBS? and diarrhea and headaches are the most common ADR?
Tegaserod
60
What is the primary use of laxatives?
Tx ACUTE Constipation
61
What can most/all non-acute, simple constipation be treated by?
- proper diet - exercise - adequate fluid intake
62
Laxatives are classified by their MOA, what are they? (4)
- Bulk forming (psyliium, methylcelluose) - Stimulant, i.e. irritant (bisacodyl, senna) - Saline [osmotic] (Mg-Hydroxide, lactulose) - wetting agents (docusate, mineral oil)
63
Which type of laxitive has a MOA that is most similar to normal physiology and is therefore recommended first?
Fiber/bulk forming. Psyliium
64
What is the general MOA of Saline (osmotic) cathartics?
Non-absorptive ions which causes osmotic retention of water in intestine leading to increase peristalsis; *Can be used in "purging doses" for food/drug poisoning.
65
What laxative is reserved for fecal impaction?
Phosphate enema
66
What laxative is used for bowel cleansing before surg, radiological and endoscopic procedures?
Polyethylene glycol - electrolyte solutions (PEGs) Lactulose (indigestible sugars) use with old people.
67
If both Fiber (1st) and saline (2nd) laxatives fail, what do you use next?
Stimulant/irritant (Bisacodyl)
68
What is the MOA of Bisacodyl?
Induced local low-grade inflammation in bowels to stimulate peristalsis. (~w/ activation of PGE-cAMP and NO-cGMP pathways)
69
What are the ADRs of Bisacodyl?
- electrolytes/fluid def. - severe cramping. - most widely abused of the laxative drugs
70
_____1_____ contains a triglyceride that is hydrolyzed in the gut to ricinoleic acid, which then acts primarily in the small intestine to stimulate fluid/electrolyte secretion and speed intestinal transit. It also contains ____2____, an extremely toxic glycoprotein.]
1. Castor oil | 2. Ricin
71
What laxative drugs is primarily used in prevention?
Stool-Wetting agents & Emollients. • Surfactant (docusate [Colace], dioctyl calcium sulfosuccinate [Surfak]) - Acts as stool-softener (facilitates admixture of aqueous and fatty substances) - Used in patients with cardiovascular disease / hernia / postpartum patients. Often used in combination with stimulant laxative when initiating opioid analgesic therapy. • Lubricant (mineral oil, olive oil) that coats fecal contents preventing colonic absorption of fecal water. Use with caution in very young / elderly due to potential for aspiration into lungs.
72
What drug is useful in initiating defecation reflex; commonly used in neonatal / pediatric patients.
Glycerin Suppositories
73
Peripherally acting opioid antagonists are an option for patients taking opioids for non-cancer pain that have failed laxative therapy. What are the two major ones?
Methylnaltrexone [Relistor®] • Given SC, doesn’t cross BBB • Expensive ($700 per day) Naloxegol [Movantik®] • New pegylated derivative of naloxone given orally ($10 per day) • Extensive first-pass metabolism - primarily binds opioid receptors in GI tract only • Increases spontaneous bowel movements without reducing opioid analgesia; well-tolerated
74
What are the classes of Antidiarrheal Agents? (4)
- Opioids - Polycarbophil (Mitrolan) - Adsorbents - Probiotics
75
____________ is an opioid that is effective against traveler’s diarrhea, alone or in combination with antimicrobial agents. Use should be discontinued if no improvement in 48 hours.
Loperamide
76
What are the ADRs of Loperamide in anti-diarrheal use?
OD --> CNS depression and paralytic ileus.  May worsen Shigella infections.
77
What Antidiarrheal Agent is useful in the Tx of BOTH diarrhea & constipation and what is the MOA of each?
Polycarbophil (Mitrolan) * Useful in diarrhea (absorbs 60X weight in H2O). * Constipation (prevents fecal desiccation).
78
Avoid use of ___________ in children under 12 (salicylate risk for Reye’s syndrome)
bismuth subsalicylate
79
What is the rationale for the use of Adsorbents to Tx diarrhea?
Rationale is to adsorb “toxins” that cause irritation (of doubtful value); can also adsorb drugs, nutrients, digestive enzymes.
80
What is the pathophys of IBS?
Irritable Bowel Syndrome: Idiopathic, chronic relapsing disorder characterized by abdominal discomfort (pain, bloating, distention, or cramps) along with alterations in GI motility (diarrhea, constipation, or both).
81
What is the pharma goal of the Tx of IBS?
- Aimed at relieving abdominal pain and discomfort (low dose tricyclic antidepressants) - improving bowel function (antidiarrheal agents [loperamide] if diarrhea or fiber supplements / osmotic laxatives if constipation) - plus two classes of agents specifically for IBS.
82
What is the MOA of 5HT-3 Antagonist in the Tx of IBS? (Alosetron [Lotronex])
Block of 5-HT3 receptors on sensory and motor neurons reduces pain and inhibits colonic motility.
83
Alosetron [Lotronex] is what class of drug?
5HT-3 Antagonist
84
What is the PK of 5HT-3 Antagonist? Alosetron [Lotronex]
- Rapid oral absorption (bioavailability 50-60%). | - extensive P450 metabolism with plasma half-life of 1.5 hours, but much longer duration of effect.
85
What Antidiarrheal is currently restricted to use only for treatment of severe IBS in women with diarrhea as the prominent symptom that have not responded to conventional therapies. Effective in 50-60% of patients.
Alosetron [Lotronex]. 5HT-3 Antagonist
86
What are ADRs of 5HT-3 Antagonist, Alosetron?
- Ischemic Colitis | - Constipation in ~30% of pt.
87
Name a 5HT-4 Agonist:
Tegaserod [Zelnorm]
88
What is the MOA of 5HT-4 Agonist (Tegaserod)?
Agonist at serotonin 5-HT4 receptors that leads to stimulation of release of neurotransmitters involved in peristaltic reflex, promoting gastric emptying and intestinal motility.
89
What is the PK of 5HT-4 Agonist (Tegaserod)?
- Low oral bioavailability (10%), should be taken on empty stomach. - Renal excretion (66%) - Hepatic metabolism (33%); !!! -- should not be given to patients with severe renal or hepatic dysfunction.
90
What are the clinical use of 5HT-4 Agonist (Tegaserod)?
- Restricted to WOMEN under 55yrs. | - IBS pt. with predominant CONSTIPATION or Chronic idiopathic CONSTIPATION that have NOT responded to other Tx.
91
What are ARDs of 5HT-4 Agonist (Tegaserod)?
- diarrhea (10%) in early Tx, self-resolves
92
What drugs is used to Tx the Sx of n/v during chemotheraphy
Metoclopramide used for n/v of chemotherapy
93
What are the side effects of Dopamine Receptor (D2) Antagonists used in Tx GI?
Due to block of D2 receptors at other sites: Extrapyramidal symptoms (movement disorders) Restlessness, fatigue, drowsiness, diarrhea
94
Metoclopramide (also blocks 5HT3) - Prochlorperazine are what class of drugs? (i.e. what are their general MOA?)
Dopamine Receptor (D2) Antagonists
95
What anti-cholinergic agents are described: Primary use: prevention and treatment of motion sickness Some efficacy in post-operative nausea and vomiting Administered transdermally with duration of action of 72 h
Scopolamine
96
What anti-cholinergic agents are described: First generation agents: Good CNS penetration Additional muscarinic receptor blocking actions Available orally - promethazine also IV and rectally Primary use for motion sickness and postoperative emesis
Antihistamines Meclizine – Promethazine Diphenhydramine (Dimenhydrinate)
97
What Drugs cause drug-induced diarrhea?
- Antibiotics (esp. broader spectrum agents): super infection - Colchicine (anti-inflammatory agent for gout) - Digoxin: parasympathomimetic action - Magnesium Antacids: osmotic laxative action - Misoprostol: prostaglandin analog stimulates intestinal musculature - Muscarinic Agonists: increased parasympathetic tone - Reserpine: sympatholytic agent allows parasympathetic dominance in GI tract - SSRIs: elevated synaptic 5HT levels stimulates GI motility

DEMS_BTRAN (8 decks)

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