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
**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
* intragastric pH
26
Antacids should not be given within 2 hours of doses of what 4 medications?
* Tetracycline * Fluoroquinolone * Itraconazole * Iron
27
What are the names of the 4 H2-Receptor Antagonists (H2 Blockers)
* Cimetidine (Tagament) * Ranitidine (Zantac) * Famotidine (Pepcid) * Nizatidine (Axid)
28
**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
H2-Receptor Antagonists (H2 blockers)
29
Which 3 of the 4 H2 blockers have 1st pass hepatic metabolism?
* Cimetidine * Ranitidine * Famotidine
30
**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
H2 Receptor Antagonists (H2 blockers)
31
**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
H2 Receptor Antagonists (H2 blockers)
32
Which H2 blocker is most potent and which is least potent?
* **Most potent:** Famotidine * **Least potent:** Cimetidine
33
**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?
* **Rx:** 10 hours * **OTC:** \<6 hours
34
4 uses of H2 blockers
* Gastroesophageal Reflux Disease (GERD) * Peptic Ulcer Disease (PUD) * Nonulcer Dyspepsia (NUD) * Prevention of Bleeding from Stress-Related Gastritis
35
**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
H2 blockers
36
**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
H2 Receptor Antagonists (H2 blockers)
37
**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
Cimetidine (H2 blocker)
38
**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.
**Cimetidine** H2 blocker
39
**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
Cimetidine
40
**Drug Interaction of which H2 blocker?** •binds 4–10 times less avidly than cimetidine to cytochrome P450.
Ranitidine
41
**Drug interaction of which H2 blocker?** •negligible interaction occurs with
Nizatidine & Famotidine
42