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Pharmacology Flashcards

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1
Q

6 Types of Drugs for Acid Neutralization; which is the most potent drug that we use today?

A
  • anatacids, muscurinic receptor antagonists (anti-cholinergics), gastrin receptor antagonists, H2-receptor antagonists, prostaglandin analogs, proton pump inhibitors
  • PPIs are the most potent
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2
Q

2 Types of Mucosa Protective Agents

A
  • bismuth chelate and sucralfate
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3
Q

Antacids

A
  • a mixture of Mg and Al salts to neutralize stomach acid
  • provides symptomatic relief only (but can promote the healing of DUODENAL ulcers if used long enough)
  • side effects: bloating, hypokalemia, constipation (aluminum), diarrhea (magnesium)
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4
Q

Muscurinic Receptor Antagonists (anti-cholinergics)

A
  • block muscurinic receptors from binding to ACh = less stimulation for HCl secretion
  • M3 antagonists decrease direct ACh stimulation of parietal cells
  • M1 antagonists decrease ACh stimulation of ECL cells to inhibit histamine secretion, thus decreasing HCl production
  • (G cells do not use ACh; they respond to the more specific muscarinic transmitter, GRP)
  • “-pine” (Atropine, Pirenzepine, Telenzipine)
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5
Q

Atropine

A
  • a muscurinic receptor antagonist

- non-specific, so has a bunch of side effects associated with its anti-cholinergic action

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6
Q

Pirenzepine, Telenzepine

A
  • muscurinic receptor antagonists

- M1-specific (ECL cell activation via ACh), so they have less side-effects compared to Atropine

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7
Q

Gastrin Receptor Antagonists

A
  • blocks the gastrin receptors (CCK-B) of parietal and ECL cells, preventing HCl secretion
  • Proglumide; a general antagonist that blocks both CCK-B and CCK-A (blocking the latter results in CNS side effects)
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8
Q

H2-Receptor Antagonists

A
  • blocks the histamine H2-receptors of parietal cells, preventing HCl secretion
  • “-tidine” (Cimetidine, Ranitidine, Famotidine, Nizatidine)
  • REVERSIBLE
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9
Q

Cimetidine was the 1st H2-receptor antagonist used; what side effect lead to it being no longer used?

A
  • it resulted in increased estrogen levels
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10
Q

Prostaglandin Analogs

A
  • PGE1 analogs that act as agonists to the prostaglanin receptors, resulting in decreased HCl secretion and increased mucus and bicarb secretion
  • prevents NSAID-induced peptic ulcers (NSAIDs block PGE1)
  • Misoprostol
  • side effects: diarrhea, cramping, uterine contraction (so avoid using during pregnancy!)
  • (also used to maintain a PDA!)
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11
Q

Proton Pump Inhibitors (PPIs)

A
  • bind to and IRREVERSIBLEY inhibit the H+-K+-ATPase of the parietal cells, preventing HCl secretion
  • they are initially inactive pro-drugs that are activated in the acidic environment of the stomach
  • they are the most potent inhibitors of acid secretion
  • “-prazole” (Omeprazole, Esomeprazole, Pantoprazole)
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12
Q

What’s the mechanism of action for mucosa protective agents?

A
  • they create a barrier over the stomach to provide physical protection against the acid
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13
Q

Bismuth Chelate (4 actions)

A
  • a chemical that coats any ulcers, absorbs pepsin, increases prostaglandin synthesis, and increases bicarb secretion
  • side effects: nausea, blackening of tongue and feces
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14
Q

Sucralfate

A
  • forms gel complexes with mucus to coat any ulcers

- side effects are more limited than bismuth chelate’s (about 15% of patients have mild constipation)

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15
Q

Prokinetics

A
  • these agents increase the emptying of the stomach and increase the lower esophageal sphincter pressure to inhibit reflux
  • these help treat GERD, but do NOT treat P.U.D.
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16
Q

Triple Therapy for H. pylori Infection

A
  • Amoxicillin + Clarithromycin + PPI (Omeprazole)

- (if patient has Penicillin allergy, replace Amoxicillin with Metronidazole)

17
Q

Quadruple Therapy for H. pylori Infection

A
  • triple therapy + a mucosa protective agent (bismuth chelate)
18
Q

There are approximately only ___ antivirals available for use. Most are for which two viruses?

A
  • only about 30; most are against HIV and herpes
19
Q

What are the 7 basic steps involved in viral replication (and hence the 7 targets for antivirals)?

A
  • attachment (Maraviroc; HIV) –> penetration –> uncoating (Amantadine) –> replication/transcription (interferon, nuceloside analogs, RT inhibitors) –> translation (interferon) –> assembly (protease inhibitors) –> release (Relenza, Tamiflu)
  • (HIV has an additional step: gag cleavage via HIV aspartic protease; inhibited by Saquinavir and Indinavir)
20
Q

Maraviroc

A
  • HIV antiviral
  • target: the CCR5 chemokine receptor that HIV binds to
  • mechanism: binds to CCR5, altering its conformation without inhibiting it = prevents HIV binding, but allows normal function
21
Q

Amantadine

A
  • target: the viral-encoded M2 ion channel, which is necessary to trigger the uncoating phase
  • mechanism: blocks the M2 ion channel, preventing the H+ uptake needed to trigger uncoating
22
Q

When using nucleotide analogs as antiviral therapy, why are the doses given very frequently?

A
  • because viral replication is very rapid!
23
Q

Acyclovir

A
  • a reverse transcriptase inhibitor
  • a very efficient drug that only gets activated in the presence of the herpes virus, so it only works on infected cells = very few side effects
24
Q

How are nucleotide analogs and reverse transcriptase inhibitors activated?

A
  • they require 3 consecutive phosphorylations
  • (in the case of Acyclovir, the 1st phosphorylation is from the herpes virus itself, which is why the drug only works in the presence of the virus)
25
Q

T or F: HIV actually leaves the host cell in an immature form.

A
  • true!
  • HIV requires a unique cleavage event once it buds off from the host cell in order to be activated; this “gag cleavage” is mediated by HIV aspartic protease
26
Q

Indinavir, Saquinavir

A
  • HIV antivirals that target the virus’s unique cleavage event
  • they inhibit the HIV aspartic protease needed to mediate the gag cleavage
27
Q

What 4 drug treatments are available for Inflammatory Bowel Disease? Which is the most effective?

A
  • 5-aminosalicylates: designed to reach the colon (so most used for UC); topical action - requires massive amounts to work; Sulfasalazine
  • coritcosteroids: interfere with NF-KB signaling, turning off inflammation; don’t use chronically
  • thiopurines: originally developed to treat leukemia; analogs of guanine that interfere with 2nd messenger signaling involved in inflammation; very slow onset (about 16 weeks); 6-Mercaptopurine, Azathiopurine
  • anti-TNFalpha monoclonal antibodies/ biologicals: quite effective for both UC and CD, but more effective for CD; Infliximab, Adalimumab
  • most effective: combo of a thiopurine (AZA) + anti-TNF antibodies
  • can also use methotrexate (mainly works for CD)
  • (corticosteroids for initial, 5-ASA for UC, 6-MP for CD, methotrexate if 6-MP no good, anti-TNFs for both types)
28
Q

The vomiting center has ________ receptors; a major component of the vomiting center is the ______________, which has _______ receptors.

A
  • vomiting center: mACh (muscarinic receptors)
  • major component: chemoreceptor trigger zone (CTZ), uses dopamine D2-receptors + serotonin 5HT3-receptors
  • (the CTZ lies outside the BBB)
29
Q

Note the vomiting pathway due to pain, repulsive sights/sounds, emotions; due to motion sickness; due to toxins/drugs; and due to stimuli from the pharynx/gut

A
  • pain/sights/sounds/emotion: sensory –> CNS –> higher brain centers –> vomiting center
  • motion sickness: labyrinth –> vestibular nuclei (H1 + mACh receptors) –> CTZ –> vomiting center
  • toxins/drugs: multiple pathways –> CTZ –> vomiting center
  • stimuli from gut option 1: visceral afferents (5-HT3 receptors) –> CTZ –> vomiting center
  • stimuli from gut option 2: visceral afferents –> nucleus of solitary tract (H1 and mACh receptors) –> vomiting center
30
Q

Five types of anti-emetic drugs and what each is used for.

A
  • H1-receptor antagonists: motion sickness and stimuli from pharynx/stomach (most effective as prophylaxis)
  • muscarinic-receptor antagonists: same as above + the vomiting center, making it a good general purpose anti-emetic
  • dopamine-receptor antagonists: inhibits the CTZ, good general anti-emetic (but no effect on the emotional/sensory trigger)
  • 5HT3-receptor antagonists: inhibit the CTZ + the visceral afferents from pharynx/stomach stimuli, making them good for treating emesis due to chemotherapy
  • sympathomimetics (NA counteracts effects of ACh)
31
Q

Apomorphine

A
  • a pro-emetic drug; it’s a dopamine agonist, acting on the CTZ to induce emesis
32
Q

3 main types of medications for bowel movements

A
  • purgatives (laxatives; increase GIT motility), prokinetics (increase GIT motility w/o purgation) and antidiarrheals (decrease GIT motility)
33
Q

How do we treat Giardiasis?

A
  • with the antibiotic/antiprotozoal metronidazole
34
Q

” -prazole “

A
  • proton pump inhibitors
35
Q

” -tidine “

A
  • H2 blockers

- “it takes 2 to DINE” (2 for H2, DINE for “ -dine”

36
Q

” -pine”

A
  • anti-cholinergics (muscarinic antagonists)
37
Q

6-MP

A
  • 6-mercaptopurine (prodrug = azathioprine)
  • a thiopurine used to treat IBD; mainstay treatment for CD and for patients with UC that don’t respond to 5-ASA
  • MOA: inhibits de novo purine synthesis to induce immunosuppression
38
Q

5-ASA

A
  • 5-aminosalicylcic acid; Sulfasalazine
  • a mainstay treatment for ulcerative colitis (less effective for CD)
  • works very well, but poor compliance is quite common and often results in a flare-up

GIT (14 decks)

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