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DT4- Exam 2 > Santanam GI Drugs X2-Melissa > Flashcards

Santanam GI Drugs X2-Melissa Flashcards

1
Q

Describe the neuronal, hormonal, and paracrine regulation of gastric acid secretion.

Which cells are responsible for secreting gastric acid?
Where in the stomach are these cells located?

A

Neuronal:
Ach–> M3-R (Gq coupled)–> ^Ca2+/IP3–> ^K+/H+ATPase

Hormonal:
Gastrin–> CCK2-R (Gq coupled)–> ^Ca2+/IP3–> ^K+/H+ATPase

Paracrine:
Histamine–> H2R (Gs coupled)–> ^cAMP–> ^K+/H+ATPase

**Gastric acid secreted by PARIETAL CELLS (body and funds)

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2
Q

What is the role of enterochromaffin cells in regulating gastric acid secretion?

A

Gastrin + Ach stimulate enterochromaffin cells to produce HISTAMINE–> ^ Parietal cell H+ secretion

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3
Q

List three “defense mechanisms” against acid erosion of the stomach and esophagus:

A

1) LES
2) Secretion of gastric mucus layer
3) Secretion of gastric bicarb anions

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4
Q

Describe the role of prostaglandins in mediating acid secretion:

Which two prostaglandins are important here?
To which receptor do they bind?
On which cells do they act?
Upon what are these actions contingent?

A

PGE2 + PGI2–> EP3-R on parietal + gastric epi cells…

1) INHIBIT cAMP (H2) in parietal cells–> DECREASE H+
2) Stimulate gastric epi cells to ^ mucus + ^ HCO3 prodxn

**Note: Effects require adequate mucosal blood flow

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5
Q

What must be done to treat peptic ulcer disease prior to management of acid secretion (2)?

A
  • Irradiate H. pylori (if infected)

- Stop NSAID use (if NSAID induced)

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6
Q

How do antacid work?

A

Act as weak bases to neutralize gastric acid:
Antiacid + HCL–> H2O + CO2 + Chloride salt

**DO NOT AFFECT ACID PRODUCTION ITSELF

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7
Q

Which antacid is systemic?

What is important about it?

A
  • NaHCO3 (aka Baking soda/Alka seltzer)

Absorbed systemically –> transient metabolic alkalosis

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8
Q

Which antacids are non-systemic (4)?

A
  • CaCO3 (Tums)
  • Al (OH)3
  • Mg(OH)2
  • Mylanta + Gelusil (Al, Mg combos)

These are NOT absorbed systemically and do NOT cause alkalosis

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9
Q

What is simethicone?

A

surfactant added to antacids; decreases foaming + esophageal reflux

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10
Q

What is one important consideration when prescribing antacids to patient with CHF?

A

sodium levels

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11
Q

What is one important possible ADR associated with CaCO3 and other Ca2+ containing antacids?

A

Rebound acid secretion

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12
Q

What are GI ADRs associated with Al and Mg antacids?
What is one metabolic ADR?
What health conditions must you consider when prescribing these antacids?

A

Al = MINIMUM poops (constipation)
Mg = MEGA poops (diarrhea)
Combo drugs = varying effects

Both Al and Mg bind PO4–> Phosphate salts–> HYPOphosphatemia

Must consider RENAL INSUFFICIENCY (inadequate excretion–> toxicity)

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13
Q

How do antacids affect performance of other drugs (2)?

A
  • ^ gastric pH–> alter bioavailability
    (Fe, Ketoconazole, theophylline, ABX)

-Al, Mg alter GI motility–> alter absorption

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14
Q

What is the MOA of H2R antagonists?
When are they especially effective?
List 4 of these drugs.

A

Cimetidine, Ranitidine, Nizatidine, Famotidine
“IDINE’s”

MOA:
Competitive inhibit H2R–>
1) DECREASE volume/ H+ content gastric juice (60%)
2) DECREASE pepsin

**Especially effective AT NIGHT (NOCTURNAL ACID INHIB–BASAL acid secretion)

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15
Q

List the 4 therapeutic uses for H2R antagonists:

A

1) Gastric + duodenal ulcers
2) GERD (w/o erosive esophagitis)
3) Zollinger Ellinson Syndrome
4) Acute Stress Ulcers (i.e. following surgery)

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16
Q

Which H2R antagonist interacts with CYP450s?

HOW does it interact with CYP450s?

A

Cimetidine–CYP450 INHIBITOR

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17
Q

What is the #1 drug class used to treat PUD?

A

Proton pump inhibitors

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18
Q

What is the MOA for proton pump inhibitors (PPIs)?

List three go these drugs?

A

Omeprazole, Esomeprazole, Lansoprazole
“PRAZOLE” Drugs

MOA: Prodrugs–activated by stomach acid
IRREVERSIBLE inhib H+/K+ATPase–>
DECREASE BASAL + MEAL STIMULATED ACID prodxn

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19
Q

What are three therapeutic uses for ALL PPI’s

A

1) PUD (faster sx relief and healing than H2R antagonist)
2) GERD +/- erosive esophagitis
3) Zollinger Ellinson syndrome

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20
Q

Which PPI is approved for use WITH NSAIDS in patients with NSAID asstd gastric ulcers?

A

Lansoprazole

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21
Q

What is one random weird possible ADR associated with PPI use? What is one POSSIBLE yet unestablished ADR?

A

Can cause CNS effects (rarely); asstd with gastric cancer in animal models

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22
Q

Which PPIs interact with CYP450s? How?

A

Omeprazole, Esomeprazole INHIBIT CYP2C19

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23
Q

Which PPIs interact with clopidogril?

How?

A

Omeprazole, Esomeprazole inhibit conversion of clopidogril to active form–> NO ANTIPLATELET EFFECTS

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24
Q

What is Mesoprostol?

How does it work?

A

PGE1 analog–>

1) Decrease H+ secretion
2) ^ mucus + ^ HCO3- production

25
Q

What is the primary therapeutic use for mesoprostol?

A

Coadmin w NSAIDS to prevent PUD

26
Q

What are the most common ADRs asstd with Mesoprostol?

When is it contraindicated?

A
  • GI (n/v/d) upset; can ^ IBD asstd. diarrhea

- DO NOT GIVE TO PREGGOS (^ uterine contraction)

27
Q

What is sucralfate?

How does it work (2)?

A

Sulfated sucrose polyaluminum

1) Forms polymers (sticky coating gel) @ pH UNDER 4–>
Coats ulcer craters–> protects from further erosion (basically a band-aid for your belly)
2) ^ PGE2 production

**Note that it requires acidic pH to work!!!

28
Q

What is one ADR associated with sucralfate?

A

Released Al can cause constipation (minimum poops)

29
Q

What is the MOA for bismuth compounds (4)?

A

1) Coats crater ulcers (better healing rate than H2R antag.)
2) ^ mucus + HCO3- production
3) Inhibits pepsin
4) Antibacterial towards H. Pylori

30
Q

What is the ADR associated with Bismuth compounds that you have to remember because it is weird?

A

Darkens oral cavity and stool ( due to sulfide reaction w bacterial H2S)

31
Q

Quick, what the the most important ADR associated with Metaclopramide!?

A

Tardive dyskinesia or parkinson’s like syndrome from D2 inhibition!!!!!

NEVER FORGET THIS!!!

32
Q

Ok, now what is the MOA (3) for metaclopromide and what is it used to treat (2)?

A

Cholinergic agonist; D2 antagonist; Prokinetic in gut–>

1) ^ esophageal clearance
2) ^LES tone
3) ^ gastric emptying
* *Ultimately DECREASE REFLUX…

Therapeutic use:
Mostly for diabetic gastroporeisis; also GERD w/o erosive esophagitis

33
Q

What is triple therapy for H. pylori infection?

A

14 days, 2x per day :

PPI + clarithro + (metronidazole OR amoxicillin)

34
Q

What is quadruple therapy for H. pylori infection?

A

14 days:
2x / day: PPI
3x / day: metronidazole
4 x / day: Bismuth subsalicylate + tetracycline

OR
2x / day: H2R antagonist
4 x / day: Bismuth subsalicylate + tetracycline + metronidazole

35
Q

Describe how GERD is treated in stages I-III

A

1) Treat sporadic GERD with antacids/ lifestyle mod.
2) PPI better than H2RA for frequent sx
3) Chronic and unrelenting gets PPI 2x per day

36
Q

Which laxatives are luminally active (3)

A
  • Hydrophilic colloids (bulk forming fiber etc)
  • Osmotic agents (unabaorbably salts/ sugars)
  • Stool wetting agents (surfactants) and emollients (mineral oil)
37
Q

Which laxatives are nonspecific stimulants/ irritants (3)

A
  • Diphenylmethanes (Bisacodyl)
  • Anthraquinones (senna, casara)
  • Castor Oil

Work in 6-8 hours (castor oil works faster)

“CADi is an irritating character in Mean Girls”

38
Q

Which laxatives are pro kinetic agents (2)

A
  • 5HT4 agonists

- Opioid receptor antagonists

39
Q

What is the difference between laxation and catharsis?

A

Laxation is a little “laxed”–just poop out the rectal stuff

Catharsis is CATHARTIC (poop out ENTIRE colon contents)

40
Q

List some natural (3) and synthetic bulk (2) forming laxatives and describe how they work? When should you AVOID them?

A

Natural: bran, whole grain, psyllium
Synthetic: methylcellulose, calcium polycarbophil

Absorb water to soften stool + ^ bulk; do not take if impacted; work in 1-3 days

41
Q

List some osmotic laxatives and describe how they work:

A
  • Saline laxatives (Mg and PO4 salts) retain H2O in colon to increase motility
  • Lactulose and mannitol = non-absorbable sugars–> hydrolyzed to SHORT CHAIN FAs–> pull H2O into stool–> ^ motility + soften stool

Work in 1-3 hours

42
Q

What type of laxative is Bisacodyl? How does it work?

A

Stimulant laxative–> Stimulates H2O and electrolyte secretion into lumen

43
Q

What are two surfactant laxatives and how do they work?

A

Docusates + Castor oil–>

1) Decreases stool surface tension–> ^ mixing of FA + Aqueous substance (emulsification)–> ^ easy poops
2) ^ H2O + electrolyte secretion

44
Q

How does Castor Oil work as a laxative?

A

Cleaved to RICINOLEIC ACID–> ANIONIC SURFACTANT–> purge in 1-6 hours

45
Q

How does mineral oil work as a laxative?

What are two potential concerns with use?

A

Non-absorbed oil lubricant softens stool; works in 2-3 days

  • Decrease Vit.ADEK absorption
  • Possible lipid pneumonitis if aspirated
46
Q

What two drugs are used to treat Idiopathic constipation and IBS?

A
  • Lubiprostone

- Linaclotide

47
Q

Lubiprostone:

MOA? For what is it the DOC?

A

Metabolite of PGE1–> opens Cl- channels on GI epi–>
^ intestinal electrolyte + fluid secretion–> Accelerates stool transit time

DOC for opioid induced constipaiton

48
Q

Linaclotide:

MOA? Black box warning?

A

Activates Guanylate cyclase-C R’s–> ^cGMP–> ^CFTR activity–> ^ intestinal Cl + HCO3 into lumen–> ^ fluid + Accelerate transit time

THIS KILLED BABY MICE: DO NOT GIVE THIS TO PATIENTS UNDER 18 YOA (BLACK BOX)

49
Q

In whom are laxatives CI?

A

Appendicitis and other obvious situations; remember that laxatives are often abused and they are also used +/- enema or suppositories before surgery to clean patients out…

50
Q

What are the most important things to do when treating diarrhea (2)?

A
  • Maintain hydration and electrolyte balance

- Discontinue offending drugs if drug induced

51
Q

What is the MOA for Opioid antidiarrheals: Loperamide and Diphynoxylate?
What is commonly mixed into preparations of these drugs?
What are they used to treat?

A

Loperamide and Diphenoxylate are commonly mixed with Atropine (muscarinic antagonism to inhibit abuse)

  • u agonists w poor CNS penetration–> decrease motility
  • Treats severe travelers’ diarrhea (Loperamide + antimicrobial = DOC)
52
Q

What is a potential ADR associated with Diphenoxylate + atropine?

A

CNS effects with HIGH doses (central u receptors)

53
Q

What are two ways to treat traveler’s diarrhea?

A
  • Loperamide + antimicrobial

- Bismuth (antiinflammatory, anti-secretory, antibacterial)

54
Q

How does H pylori affect somatostatin secretion?

A

Decreases D cells–> decreases somatostatin production–> decreases inhibition of gastric acid secretion

55
Q

What is octreatide?

How is it used to treat GI pathology?

A

Somatostatin analog–> 100% down regulates GI activity

  • Decrease GI endocrine secretion (including intestinal fluid + bicarb)
  • Decrease GI motility

Treats diarrhea caused by hormone secreting GI tumors; chemo, AIDS, DM asstd. diarrhea

***Think carcinoid tumor!! Rx gave me this at least 2x

56
Q

Describe treatment for MILD IBD:

*The pyramid is actually important. I had an Rx question about treating IBD in different stages of severity

A
  • Topical corticosteroids
  • ABX
  • Glucocorticoid (budensonide)
57
Q

Describe treatment for MODERATE IBD:

A

These patients fail initial therapy

  • Oral corticosteroids
  • Immunomodulators (azothiaprine, 6-mercaptopurine, MTX)
  • Anti-TNF Abs
58
Q

Describe treatment for SEVERE IBD; When do you give Natalizumab or Cyclosporine?

A

These patients fail moderate therapy

  • IV corticosteroids
  • Anti-TNF Abs
  • Surgery
  • *Natalizumab after failing anti-TNF Abs + immunomod.
  • *Cyclosporine after failing IV corticosteroids (This was the Rx question)

DT4- Exam 2 (12 decks)

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