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Pharm III > Lecture One (GI intro)-Exam 1 > Flashcards

Lecture One (GI intro)-Exam 1 Flashcards

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1
Q

What are medications that increase Gastric pH? (3)

A
  • Antacids
  • Histamine 2 blockers
  • Proton pump inhibitors
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2
Q

Stomach acid pathophysiology
* What does mucous and mucous neck cells do?
* What does parietal cells do?

A

Mucous and mucous neck cells:
* Produce thick mucous that helps protects the surface of the stomach

Parietal cells:
* Produce hydrochloric acid (HCl) that produces low pH environment

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3
Q

Stomach acid pathophysiology
* What do chief cells do?
* What does enterochromaffin like cells do?
* What does G-cells do?

A

Chief cells:
* Produce pepsinogen – protein digestion
* Lipase – fat digestion

Enterochromaffin-like cells:
* Produces histamine

G-cells:
* Produce gastrin – regulates gastric activity

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4
Q

Stomach acid pathophysiology
* What does the food stimulate? What does that result in?

A

Food stimulates the vagus nerve to release acetylcholine (Ach) resulting in:
* Direct stimulation of parietal cells via muscarinic (M3) receptor
* Indirect stimulation of parietal cells via stimulation of ECL and G-cells

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5
Q

Stomach acid pathophysiology: parietal cells via stimulation of
* WHat does ECL cells and G cells release and bind to?

A

ECL cell
* Releases histamine – binds to histamine H2 receptor

G-cell
* Releases gastrin – binds to CCK-B receptors

  • ECL – enterochromaffin-like cell
  • CCK-B –cholecystokinin B
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6
Q

Stomach acid pathophysiology
* H2 receptor activation cause?
* What does M3 and CCK-B activation cause?

A
  • H2 receptor activation -> increases cAMP
  • M3 and CCK-B activation -> increases intracellular calcium
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7
Q

Stomach acid pathophysiology
* Pathways converge to ultimately activate what?
* What happens to Cl- and H+? what does those form?

A
  • Pathways converge to ultimately activate H+/K+ proton pump
  • Actively pumps H+ out of cell
  • Cl- passively transported out
  • Form hydrochloric acid in the stomach lumen – ideal for digestion
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8
Q

Antacids
* What does it not do?
* what does it do?
* Recommended for what?
* What products?

A
  • DO NOT decrease acid secretion
  • DO directly neutralize HCl
  • Recommended for intermittent use
  • Multiple combination products
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9
Q

Antacids
* Reacts with what? What does that form?
* What increaes and decreases?

A

React with HCl to form salt and water
* Increases gastric pH
* Decreases conversion of pepsinogen to pepsin
* May increase LES pressure

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10
Q
A
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11
Q

Focus on sodium bicarb

A
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12
Q

Antacids
* What are the multiple drug interaction causes? (3)

A
  • Alteration in gastric pH
  • Adsorbing medications
  • Physically blocking absorption
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13
Q

Antacids
* What do you need to do for medications that can interact?
* What are there significant itneractions with? (6)

A
  • Separate administration of antacids and interacting medications: Take 1 hour before or two hours after antacids
  • Significant interactions with: Tetracyclines, ferrous sulfate, sulfonylureas, quinolones, ketoconazole, voriconazole
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14
Q

Alginic acid (Gaviscon)
* Does not do what?
* Does do what?
* Viscous solution that does what?
* Generally used in conjunction with what?

A
  • DOES NOT decrease gastric pH greatly or increase LES pressure
  • DOES float on the surface of stomach contents
  • Viscous solution that coats and protects the esophagus when refluxed
  • Generally used in conjunction with other antacids (e.g., calcium carbonate)
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15
Q

H2 receptor antagonists
* What does it do? What are the results of that? (3)

A

Competitively, reversibly block H2 receptors
* Decrease activation of proton pump
* Decrease production of nighttime and food-induced acid secretion
* Acid secretion reduction > 90%

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16
Q

H2 receptor antagonists
* What are the indications? (4)

A
  • Peptic ulcer disease (PUD)
  • Ulcer prophylaxis
  • GERD
  • Zollinger-Ellison disease
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17
Q

H2 receptor antagonist
* What are the unique characteritics of Clinetidine?
* What are the SE of H2RAs?
* Dose reduction?
* Monitor for what?
* May cause what?

A
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18
Q

Proton pump inhibitors
* What is the MOA?
* What are examples?

A

Irreversibly binds and inhibit parietal cell proton pumps

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19
Q

Proton pump inhibitors
* more effective than what? How?
* What is the onset?
* What is the duration of activity?
* Decreases drug absorption how?

A
  • More effective than H2 antagonists via Decrease acid secretion > 99%
  • Onset: 3-4 days for full effect
  • Duration of activity: 2-5 days
  • Decreases drug absorption by increasing gastric pH
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20
Q

Proton pump inhibitors
* What does omeprazole inhibit?

A

Inhibits CY3A4 and 2C19

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21
Q

PPIs

A
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22
Q

Check what levels?

A
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23
Q

PPI doses
* What are the doages forms?

A
  • IV
  • Tablets
  • Capsules
  • Powder packs
  • Dissolvable tablets
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24
Q

cytoprotectants: misoprostol
* Wwhat is the MOA? (think about what is stimulates, increases, decreases and improves)

A
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25
Cytoprotectants: Misoprostol * What are the indications? (2)
* Protectant NSAID-induced ulcers or patients at high risk of ulcers * Short-term use for gastric or duodenal ulcers
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Cytoprotectants: Misprostol * What are the SE? (3) what is the CI? (1)
Adverse effects (dose related): * Nausea * Diarrhea * Abdominal cramping CI: pregnancy (induce abortions)
27
Cytoprotectants: Sucralfate * What is the drug made out of? * What is the MOA?
Aluminum hydroxide + sulfated sucrose molecules Acidic environment * Disassociate into aluminum salt and sucrose sulfate * Negatively charged sucrose sulfate binds to positively charged proteins in base of gastric erosion and in the mucosal membrane
28
Cytoprotectants: Sucralfate * What are the overall effects? (3)
Physical barrier – promotes healing * Increases bicarbonate secretion * Increases mucous viscosity and thickness
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Sucralfate: * What are the SE?(6)
* Consitipation * HA * dizziness * Dry mouth * Hyperglycemia * Multiple drug interactions
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Cytoprotectants: Sucralfate * What are the indications? (5)
* Duodenal ulcers * Dyspepsia * Epithelial wounds * Mucositis * Radiation proctitis
31
Vomiting reflex * Located where? * What does it contain? * What happens with stimulation?
Located in medulla oblingata * Contains muscarinic receptors * Stimulation = triggers vomiting reflex
32
Vomiting reflex * What are the Four primary stimulators of VC?
* Chemoreceptor trigger zone (CTZ) * Vestibular system (VS) * GI mechanoreceptors * Higher brain centers
33
Vomiting pathophysiology: Chemcoreceptor trigger zone * Located where? * Outside what? * Triggered by what? * Stimulates what? * What are the receptors?
## Footnote Receptors: Chem D(2)oN(K1)'t (5)HiT(3)
34
Vestibulat system: * What is it important for? * Problems communicated via what? * Stimulations of what? * What are the receptors?
35
Higher brain centers (cerebrum) * Response to what? * Direct stimulation of what?
* Response to emotional, pain, smell, sight * Direct stimulation of vomiting center muscarinic receptors
36
Gastrointestinal center * What is resleased? * Stimulates what? (2) * What are the receptors?
37
What are the Select Nausea and vomiting etiologies? (10)
* Increased intracranial pressure * Vestibular dysfunction * Dyspepsia * Gastroparesis * Infections * Medications / chemicals * Pregnancy * Pain * Psychiatric disorder ## Footnote "I Vow Doctors Get Instant Medical Pregnancy Pain Patches"
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Antihistamines / anticholinergic agents
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Antihistamines / anticholinergic agents
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5Ht3 / NK-1 receptor antagonists
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5Ht3 / NK-1 receptor antagonists
42
Miscellaneous antiemetics
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Laxatives: * produce what? * What are the different mechanisms? (5)
Produce bowel movements and relieve constipation Many different mechanisms * Osmotic * Bulk forming * Stimulant * Irritant * Lubricant
45
Osmotic laxatives * increases what? (2) * Pull water where? * Triggers what?
* Increases solute load in intestine * Pulls water into GI lumen * Increases stool volume and stretches bowel * Triggers defecation reflex
46
Laxatives: bulk laxatives * Insoluble what? * Takes up what? * Intestinal wall _ * Stimulation of what? * Induce what?
* Insoluble methylcellulose fibers * Take up water in the large intestine forming a large mass * Intestinal wall distension * Stimulation of mechanoreceptors * Induce contraction and relaxation of intestinal smooth muscle
47
Irritant and stimulant laxatives * Prevent what? * Promote what? * Irriate what?
* Prevent water reabsorption in the colon and / or * Promote water secretion from the intestinal mucosa * Irritate nerve fibers of the intestinal mucosa * Stimulate defecation
48
Laxatives * What is generally first line? * What is second line? * What is imporant about PEG 3350 AKA Miralax? (2)
Bulk laxatives generally first line Osmotic laxatives second line if no response to bulk laxatives PEG 3350 AKA Miralax * More effective than lactulose * Safe for infants
49
Laxatives * Magnesium salts (MOM) – caution with what? * Sodium salts – many what? * Bisacodyl / senna – severe what? * What is not effective for treatment?
* Magnesium salts (MOM) – caution with renal failure * Sodium salts – many electrolyte abnormalities * Bisacodyl / senna – severe cramping and melanosis coli * Stool softeners not effective for treatment
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What are secretagogues reserved for?
Prescription products reserved for patients with refractory, chronic constipation * Last line
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secretagogues
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secretagogues
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Bowel prep regimens * What is first line? * What are the two options? * What can you add?
* First-line includes polyethylene glycol preparations * Golytely vs Miralax * ± Lubiprostone / bisacodyl
60
Bowel prep regimens * What is more effective? what is it limited by? * Specific regimens depend on what? * Fluids when?
* Split regimens may be more effective->Limited by procedure timing * Specific regimens depend on comorbidities * Fluids only day -1; nothing red, orange, purple
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62
Melanosis coli * Secondary to what? * Active form in colon causes what? * What is it? * Resolves how and when?
* Secondary to chronic senna use * Active form in colon causes cell apoptosis and death of cells lining the colon * Dark pigmentation of cells * Resolves spontaneously if laxatives stopped-> Could take up to 1 year for full resolution
63
Antispasmodics * What is the MOA of action? (think about what it blocks, decrease and reduce)
* Blocks acetylcholine from binding to muscarinic receptors * M3 receptor in smooth muscle * Blocks histamine and bradykinin receptors * Decreases GIT peristalsis and secretions from stomach to colon * Reduces spasms
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Antispasmodics
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Antispasmodics
68
Prokinetics: metoclopramide * What is the MOA?
* Inhibits D2, apomorphine, and 5HT3 receptors * Increases LES pressure and gastric contractions * Mild antiemetic
69
Prokinetics: Macrolide antibiotics * What are the examples? (2) What does it cause? (2) * What are the interactions?
Erythromycin / azithromycin * Increase high amplitude gastric contractions * May cause tachyphylaxis Interactions * Avoid concomitant administration with magnesium or aluminum-containing antacids
70
Macrolide antibiotics: * What are the ADRs? (5)
* GI: nausea, vomiting, diarrhea (erythromycin > clarithromycin > azithromycin) * Prolongation of QT – interval * Hepatotoxicity * Drug interactions CYP3A4 (erythromycin, clarithromycin) * Hearing loss (erythromycin)
71
Antidiarrheals: * Decrease what? * Increase what? * Recommended for what?
* Decreased diarrhea frequency * Increase consistency of bowel movements * Recommended for self-limiting diarrhea
72
Antidiarrheals * Do not use what? * Caution with who? * used in conjuction with what?
* Do not use > 2 days without medical supervision * Caution with elderly * Used in conjunction with rehydration/refeeding
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What is the MOA?
74
Fill in for the SE and Cautions
75
Pancrelipase * Exogenous digestive hormones and enzymes required for what? * Ingested with what?
* Exogenous digestive hormones and enzymes required for normal digestion * Ingested with meals and snacks to improve digestion and absorption; decrease abdominal pain
76
Pancrelipase: * What are the indications? (6)
* Exocrine pancreatic insufficiency * Pancreatitis * Pancreatic surgery * Cystic fibrosis * Steatorrhea – post gastrectomy syndrome * Pancreatic cancer
77
Pancrelipase: Porcine lipase, amylase, and protease * Lipase – * Amylase – * Proteases –
* Lipase – hydrolysis and degradation of fats * Amylase – hydrolysis and digestion of starches * Proteases – breakdown proteins and amino acids
78
Pancrelipase: * What is the site of action? * Minimal what? * What is the dose?
* Site of action: duodenum * Minimal systemic absorption * Based on lipase component * 500 to 2500 units/kg/dose with each meal * 50% dose per snack
79
Pancrelipase * What are the SE? * What is monitoring? (4)
Adverse effects – minimal Monitoring * Abdominal symptoms * Weight / growth * Stool character * Blood glucose

Pharm III (14 decks)

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