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

Lecture One (GI intro)-Exam 1 Flashcards

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
Q

Cytoprotectants: Misoprostol
* What are the indications? (2)

A
  • Protectant NSAID-induced ulcers or patients at high risk of ulcers
  • Short-term use for gastric or duodenal ulcers
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26
Q

Cytoprotectants: Misprostol
* What are the SE? (3) what is the CI? (1)

A

Adverse effects (dose related):
* Nausea
* Diarrhea
* Abdominal cramping

CI: pregnancy (induce abortions)

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27
Q

Cytoprotectants: Sucralfate
* What is the drug made out of?
* What is the MOA?

A

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

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28
Q

Cytoprotectants: Sucralfate
* What are the overall effects? (3)

A

Physical barrier – promotes healing
* Increases bicarbonate secretion
* Increases mucous viscosity and thickness

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29
Q

Sucralfate:
* What are the SE?(6)

A
  • Consitipation
  • HA
  • dizziness
  • Dry mouth
  • Hyperglycemia
  • Multiple drug interactions
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30
Q

Cytoprotectants: Sucralfate
* What are the indications? (5)

A
  • Duodenal ulcers
  • Dyspepsia
  • Epithelial wounds
  • Mucositis
  • Radiation proctitis
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31
Q

Vomiting reflex
* Located where?
* What does it contain?
* What happens with stimulation?

A

Located in medulla oblingata
* Contains muscarinic receptors
* Stimulation = triggers vomiting reflex

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32
Q

Vomiting reflex
* What are the Four primary stimulators of VC?

A
  • Chemoreceptor trigger zone (CTZ)
  • Vestibular system (VS)
  • GI mechanoreceptors
  • Higher brain centers
33
Q

Vomiting pathophysiology: Chemcoreceptor trigger zone
* Located where?
* Outside what?
* Triggered by what?
* Stimulates what?
* What are the receptors?

A

Receptors: Chem D(2)oN(K1)’t (5)HiT(3)

34
Q

Vestibulat system:
* What is it important for?
* Problems communicated via what?
* Stimulations of what?
* What are the receptors?

A
35
Q

Higher brain centers (cerebrum)
* Response to what?
* Direct stimulation of what?

A
  • Response to emotional, pain, smell, sight
  • Direct stimulation of vomiting center muscarinic receptors
36
Q

Gastrointestinal center
* What is resleased?
* Stimulates what? (2)
* What are the receptors?

A
37
Q

What are the Select Nausea and vomiting etiologies? (10)

A
  • Increased intracranial pressure
  • Vestibular dysfunction
  • Dyspepsia
  • Gastroparesis
  • Infections
  • Medications / chemicals
  • Pregnancy
  • Pain
  • Psychiatric disorder

“I Vow Doctors Get Instant Medical Pregnancy Pain Patches”

38
Q

Antihistamines / anticholinergic agents

A
39
Q

Antihistamines / anticholinergic agents

A
40
Q

5Ht3 / NK-1 receptor antagonists

A
41
Q

5Ht3 / NK-1 receptor antagonists

A
42
Q

Miscellaneous antiemetics

A
43
Q
A
44
Q

Laxatives:
* produce what?
* What are the different mechanisms? (5)

A

Produce bowel movements and relieve constipation

Many different mechanisms
* Osmotic
* Bulk forming
* Stimulant
* Irritant
* Lubricant

45
Q

Osmotic laxatives
* increases what? (2)
* Pull water where?
* Triggers what?

A
  • Increases solute load in intestine
  • Pulls water into GI lumen
  • Increases stool volume and stretches bowel
  • Triggers defecation reflex
46
Q

Laxatives: bulk laxatives
* Insoluble what?
* Takes up what?
* Intestinal wall _
* Stimulation of what?
* Induce what?

A
  • 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
Q

Irritant and stimulant laxatives
* Prevent what?
* Promote what?
* Irriate what?

A
  • 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
Q

Laxatives
* What is generally first line?
* What is second line?
* What is imporant about PEG 3350 AKA Miralax? (2)

A

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
Q

Laxatives
* Magnesium salts (MOM) – caution with what?
* Sodium salts – many what?
* Bisacodyl / senna – severe what?
* What is not effective for treatment?

A
  • 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
50
Q
A

Def know the onset of action

51
Q

Fill in covered part

A

Def know the onset of action

52
Q

Fill in covered spot

A

Def know the onset of action

53
Q

Fill in covered spot

A

Def know the onset of action

54
Q

Fill in covered spot

A

Def know the onset of action

55
Q
A
56
Q

What are secretagogues reserved for?

A

Prescription products reserved for patients with refractory, chronic constipation
* Last line

57
Q

secretagogues

A
58
Q

secretagogues

A
59
Q

Bowel prep regimens
* What is first line?
* What are the two options?
* What can you add?

A
  • First-line includes polyethylene glycol preparations
  • Golytely vs Miralax
  • ± Lubiprostone / bisacodyl
60
Q

Bowel prep regimens
* What is more effective? what is it limited by?
* Specific regimens depend on what?
* Fluids when?

A
  • Split regimens may be more effective->Limited by procedure timing
  • Specific regimens depend on comorbidities
  • Fluids only day -1; nothing red, orange, purple
61
Q
A
62
Q

Melanosis coli
* Secondary to what?
* Active form in colon causes what?
* What is it?
* Resolves how and when?

A
  • 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
Q

Antispasmodics
* What is the MOA of action? (think about what it blocks, decrease and reduce)

A
  • 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
64
Q
A
65
Q

Antispasmodics

A
66
Q
A
67
Q

Antispasmodics

A
68
Q

Prokinetics: metoclopramide
* What is the MOA?

A
  • Inhibits D2, apomorphine, and 5HT3 receptors
  • Increases LES pressure and gastric contractions
  • Mild antiemetic
69
Q

Prokinetics: Macrolide antibiotics
* What are the examples? (2) What does it cause? (2)
* What are the interactions?

A

Erythromycin / azithromycin
* Increase high amplitude gastric contractions
* May cause tachyphylaxis

Interactions
* Avoid concomitant administration with magnesium or aluminum-containing antacids

70
Q

Macrolide antibiotics:
* What are the ADRs? (5)

A
  • GI: nausea, vomiting, diarrhea (erythromycin > clarithromycin > azithromycin)
  • Prolongation of QT – interval
  • Hepatotoxicity
  • Drug interactions CYP3A4 (erythromycin, clarithromycin)
  • Hearing loss (erythromycin)
71
Q

Antidiarrheals:
* Decrease what?
* Increase what?
* Recommended for what?

A
  • Decreased diarrhea frequency
  • Increase consistency of bowel movements
  • Recommended for self-limiting diarrhea
72
Q

Antidiarrheals
* Do not use what?
* Caution with who?
* used in conjuction with what?

A
  • Do not use > 2 days without medical supervision
  • Caution with elderly
  • Used in conjunction with rehydration/refeeding
73
Q

What is the MOA?

A
74
Q

Fill in for the SE and Cautions

A
75
Q

Pancrelipase
* Exogenous digestive hormones and enzymes required for what?
* Ingested with what?

A
  • Exogenous digestive hormones and enzymes required for normal digestion
  • Ingested with meals and snacks to improve digestion and absorption; decrease abdominal pain
76
Q

Pancrelipase:
* What are the indications? (6)

A
  • Exocrine pancreatic insufficiency
  • Pancreatitis
  • Pancreatic surgery
  • Cystic fibrosis
  • Steatorrhea – post gastrectomy syndrome
  • Pancreatic cancer
77
Q

Pancrelipase: Porcine lipase, amylase, and protease
* Lipase –
* Amylase –
* Proteases –

A
  • Lipase – hydrolysis and degradation of fats
  • Amylase – hydrolysis and digestion of starches
  • Proteases – breakdown proteins and amino acids
78
Q

Pancrelipase:
* What is the site of action?
* Minimal what?
* What is the dose?

A
  • 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
Q

Pancrelipase
* What are the SE?
* What is monitoring? (4)

A

Adverse effects – minimal

Monitoring
* Abdominal symptoms
* Weight / growth
* Stool character
* Blood glucose

Pharm III (14 decks)

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