GI & Peptic 1 Flashcards

1
Q

What are the 3 Acid-Peptic Diseases?

A
  • GERD
  • Peptic ulcer (gastric & duodenal)
  • Stress-related mucosal injury
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2
Q

Which condition?

  • mucosal erosions or ulceration arise when the caustic effects of aggressive factors (acid, pepsin, bile)
  • overwhelms the defensive factors of the gastrointestinal mucosa
    • •mucus and bicarbonate secretion, prostaglandins, blood flow processes of restitution and regeneration after cellular injury
A

Acid-Peptic Diseases

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3
Q

Over 90% of peptic ulcers are caused by what 2 things?

A
  • Helicobacter pylori
  • NSAIDs
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4
Q

Give some examples of foods/drinks/meds which can worsen GERD sxs

A
  • fatty meal, peppermint, chocolate
  • Coffee, cola, tea, wine
  • Garlic, onions, chili peppers
  • Spicy foods, OJ, tomato juice
  • Anticholinergics, barbituates, caffeine
  • CCBs, Dopamine, estrogen
  • Nicotine, nitrates, progesterone
  • ASA, bisphosphonates, NSAIDs
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5
Q

What induced this Peptic Ulcer?

  • Chronic
  • Site of damage: Duodenum
  • Depend on Intragastric pH
  • Sxs: epigastric pain
  • Ulcer depth: superficial
  • Less severe GI bleeding, single vessel
A

H. pylori

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6
Q

What induced this Peptic Ulcer?

  • Chronic
  • Site of damage: Stomach
  • Less dependent on Intragastric pH
  • Asymptomatic
  • Deep ulcer depth
  • More severe GI bleeding, single vessel
A

NSAID

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7
Q

What inuced this Peptic Ulcer?

  • Acute
  • Site of damage: Stomach
  • Less dependent on Intragastric pH
  • Asymptomatic
  • Most superficial Ulcer depth
  • GI bleeding is more severe (superficial mucosal capillaries)
A

SRMD

(stress related mucosal disease)

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8
Q

What are the two MOAs of the two drug classes which treat ulcers?

A
  1. agents that reduce intragastric acidity
  2. agents that promote mucosal defense
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9
Q

What medication is used for “Esophageal Clearance” to tx GERD?

A

Bethanechol

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10
Q

What medication is used for “Gastric Emptying” for tx of GERD?

A

Metoclopramide

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11
Q

3 treatments for “Esophageal Mucosal Resistance”

A
  • Alginic Acid
  • Sucralfate
  • Fundoplication
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12
Q

Treatments for “Gastric Acid”

A
  • H2 receptor antagonist (“tidine”)
  • Antacids
  • Proton Pump Inhibitors (PPI) (Omeprazole)
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13
Q

What are the 3 receptors in a Parietal Cell?

A
  • Gastrin (CCK-B)
  • Histamine (H2)
  • Acetylcholine (muscarinic, M3)
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14
Q

Acid Secretion

Which neurotransmitter is released from vagal postganglionic nerves?

A

Acetylcholine

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15
Q

Acid Secretion

Which hormone is released from the antral G cells into the blood?

A

Gastrin

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16
Q
  • When Gastrin, Histamine, & Acetylcholine bind to the parietal cell, this causes an increase in what substance?
  • –> which then stimulates what?
  • –> which stimulates what?
A
  • Cytosolic calcium
  • stimulates protein kinases
  • –> stimulate acid secretion from H+/K+-ATPase (the proton pump)
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17
Q

What are the 3 agents which reduce Intragastric Acidity?

A
  • Antacids
  • H2 receptor antagonists (H2 blockers)
  • Proton Pump Inhibitors (PPI)
18
Q

Which agent?

  • Neutralize or buffer stomach acid
  • Tums, Mylanta, Alka-Seltzer
  • Non-prescription for intermittent heartburn/dyspepsia
  • Weak bases that react w/ gastric hydrochloric acid to form what 2 things?
    • Given how long after a meal effectively neutralizes gastric acid for up to how many hours?
A

Antacids

  • Forms salt & water
  • Single dose of 156mEq of antacid given 1 hour after meal
  • Neutralizes acid for up to 2 hours
19
Q

Which Antacid?

  • Reacts rapidly with HCL to produce carbon dioxide & sodium chloride
  • Adverse effects:
    • CO2 gastric distention & belching
    • Unreacted alkali is readily absorbed, potentially causing metabolic alkalosis when given in high doses or to pts w/ renal insufficiency
  • Sodium chloride absorption may exacerbate fluid retenion in pts w/ HF, HTN, & renal insufficiency
A

Sodium Bicarbonate

20
Q

What are 2 examples of Sodium Bicarbonate Antacids?

A
  • Baking soda
  • Alka seltzer
21
Q

Which Antacid?

  • Less soluble & reacts more slowly w/ HCL to form carbon dioxide & calcium chloride
  • Adverse effects:
    • belching or metabolic alkalosis
    • excessive doses of either sodium bicarb or calicum carbonate w/ calcium-containing products can lead to hypercalcemia, renal insufficiency, and metabolic alkalosis (milk alkali syndrome)
A

Calcium Carbonate

22
Q

What are 2 examples of Calcium Carbonate Antacid

A
  • Tums
  • Os-Cal
23
Q

Which Antacid?

  • react slowly with HCl to form magnesium chloride or aluminum chloride and water
A

Magnesium hydroxide or Aluminum hydroxide

24
Q

Adverse Effects of which antacid?

  • no gas is generated, belching does not occur
  • metabolic alkalosis is also uncommon because of the efficiency of the neutralization reaction
  • unabsorbed magnesium salts may cause an osmotic diarrhea
  • aluminum salts may cause constipation
  • agents are commonly administered together
    • Gelusil, Maalox, Mylanta
    • minimizes the impact on bowel function
  • magnesium and aluminum are absorbed and excreted by the kidneys
    • patients with renal insufficiency should not take these agents long-term
A

Magnesium hydroxide or Aluminum hydroxide

25
Q

Antacids may affect the absorption of other meds by binding the drug by:

  • Reducing its absorption
  • Increasing ______ so that the drug’s dissolution or solubility is altered
A
  • intragastric pH
26
Q

Antacids should not be given within 2 hours of doses of what 4 medications?

A
  • Tetracycline
  • Fluoroquinolone
  • Itraconazole
  • Iron
27
Q

What are the names of the 4 H2-Receptor Antagonists (H2 Blockers)

A
  • Cimetidine (Tagament)
  • Ranitidine (Zantac)
  • Famotidine (Pepcid)
  • Nizatidine (Axid)
28
Q

Pharmacokinetics of which agent?

  • Rapidly absorbed from the intestine
  • 1st pass hepatic metabolism
  • Combination of hepatic metabolism, glomerular filtration, and renal tubular secretion
  • Dose reduction
    • moderate –> severe renal insufficiency
    • Elderly
A

H2-Receptor Antagonists (H2 blockers)

29
Q

Which 3 of the 4 H2 blockers have 1st pass hepatic metabolism?

A
  • Cimetidine
  • Ranitidine
  • Famotidine
30
Q

MOA of what agent?

  • Exhibit competitive inhibition at the parietal cell H2 receptors
  • Suppress basal and meal stimulated acid secretion in a linear, dose dependent manner
  • HIGHLY selective and do not affect H1 or H3 receptors
A

H2 Receptor Antagonists (H2 blockers)

31
Q

MOA of which agent?

  • Volume of gastric secretion & concentration of pepsin are also reduced
  • Reduce acid secretion stimulated by histamine as well as by gastrin & cholinomimetic agents
  • Histamine released from ECL cells by gastrin or vagal stimulation is blocked from binding to parietal cell H2 receptor
  • Direct stimulation of the parietal cell by gastrin or acetylcholine has a diminished effect on acid secretion in the presence of H2 receptor blockade
A

H2 Receptor Antagonists (H2 blockers)

32
Q

Which H2 blocker is most potent and which is least potent?

A
  • Most potent: Famotidine
  • Least potent: Cimetidine
33
Q

H2 Receptor Antagonists (H2 blockers)

  • Prescription doses maintain greater than 50% acid inhibition for how many hours?
  • OTC doses have a duration of acid inhibition of less than how many hours?
A
  • Rx: 10 hours
  • OTC: <6 hours
34
Q

4 uses of H2 blockers

A
  • Gastroesophageal Reflux Disease (GERD)
  • Peptic Ulcer Disease (PUD)
  • Nonulcer Dyspepsia (NUD)
  • Prevention of Bleeding from Stress-Related Gastritis
35
Q

Adverse effects of which agent?

–extremely safe drugs

–occur in less than 3% of patients

–diarrhea, headache, fatigue, myalgias, constipation

–? risk of nosocomial pneumonia in critically ill patients

A

H2 blockers

36
Q

Adverse effects of which agents?

–mental status changes

•confusion, hallucinations, agitation

–intravenous form of this drug

–patients in the intensive care unit

»elderly or who have renal or hepatic dysfunction

A

H2 Receptor Antagonists (H2 blockers)

37
Q

Adverse effects of which agent?

•inhibits binding of dihydrotestosterone to androgen receptors

–inhibits metabolism of estradiol, and increases serum prolactin levels

–gynecomastia or impotence in men

–galactorrhea in women

A

Cimetidine (H2 blocker)

38
Q

Adverse effects of which agent?

–crosses the placenta

•administered to pregnant women only if absolutely necessary

–secreted into breast milk and may therefore affect nursing infants.

A

Cimetidine

H2 blocker

39
Q

Drug Interaction of which H2 blocker?

•Interferes (inhibitor) with several important hepatic cytochrome P450 drug metabolism pathways, including those catalyzed by CYP1A2, CYP2C9, CYP2D6, and CYP3A4

–the half-lives of drugs metabolized by these pathways may be prolonged

A

Cimetidine

40
Q

Drug Interaction of which H2 blocker?

•binds 4–10 times less avidly than cimetidine to cytochrome P450.

A

Ranitidine

41
Q

Drug interaction of which H2 blocker?

•negligible interaction occurs with

A

Nizatidine & Famotidine

42
Q
A