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Pharm of Acid-Peptic Disorders Flashcards

1
Q

What is the most common cause of peptic ulcers?

A

H. pylori infection.

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2
Q

What is the 2nd most common cause of peptic ulcers?

A

Medication-induced (NSAIDs).

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3
Q

What is the role of gastric acid? What cells produce it?

A

Digestion of proteins
Activates pepsinogen to pepsin, which activates the other digestive enzymes
Absorption of calcium, iron, B12
Suppresses bacterial growth

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4
Q

Cephalic Phase of Gastric Acid Secretion

A

Vagus nerve mediated. ACh is the NT. It binds to muscarinic receptors on parietal cells due to the taste, thought, smell, sight, and swallowing of food.

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5
Q

Gastric Phase of Gastric Acid Secretion

A

Occurs due to the release of gastrin from G cells and binding to parietal cells to produce gastric acid in response to food or distention of the stomach.

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6
Q

What cells produce gastric acid?

A

Parietal cells.
Cl- exits the cell.
H+ exits via the K+/H+ pump.
HCO3- enters the blood via HCO3-/Cl- pump and is released by the pancreas to neutralize chyme in the duodenum.

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7
Q

What stimulates production of HCl from parietal cells?

A

Gastrin, Histamine, ACh.

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8
Q

What are the products of parietal cells?

A

HCl & intrinsic factor (for absorption of B12).

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9
Q

Acetylcholine

A

Major neural stimulator of parietal cells.
Increases gastrin release, stimulates parietal cells, stimulates enterochromaffin cells (Histamine-producing), and inhibits somatostatin.

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10
Q

Gastrin

A

The major endocrine regulator of HCl release from parietal cells.
Released from G cells in the gastric antrum in response to protein in meal, gastric distention.
Triggers HCl production. Also binds to EC cells and triggers release of histamine.

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11
Q

Histamine

A

Major autocrine/paracrine stimulator of parietal cells. H2 utilizes Gs coupled adendyly cyclase and cAMP to stimulate HCl secretion.

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12
Q

Somatostatin

A

Produced by S cells of the duodenum in response to gastric acid in the duodenum. Inhibits parietal cells by Gs coupled receptors and decreasing cAMP.

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13
Q

Prostaglandins

A

Autocrine factors secreted by macrophages and enothelial cells to inhibit acid secretion by decreasing cAMP.
Stimulates secretion of mucin and bicarb.
Inhibited by NSAIDs.

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14
Q

Pepsin

A

Zymogen activated by HCl. Activates the other digestive enzymes.
Becomes inactivated at pH >4.

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15
Q

What are the defensive mechanisms the gastric mucosa has against ulceration?

A 
Mucin layer
Lumenal Bicarbonate
Somatostatin (< HCl production)
Prostaglandins (< HCl production)
Blood flow provides substrates/removes toxins
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16
Q

What must you consider when treating gastric ulcers?

A

What is the underlying cause?
If H. pylori, get rid of bacteria!
If medications, stop taking them! (NSAIDs).
Stop alcohol/smoking.

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17
Q

What is the main goal of treatment of gastric ulcers?

A

Decrease acid production.

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18
Q

What class of drugs is the most effective suppressor of gastric acid secretion and thus the DOC for treating gastric ulcers?

A

Proton pump inhibitors.
MOA: Act directly on the H+/K+ pump to prevent the production of acid from parietal cells of the stomach. Irreversible.
Multiple doses are necessary to inactivate all proton pumps.
Pro-drugs activated by food.
Most effective when parietal cell is stimulated post-prandially; because the amount of H+/K+ pumps is greatest after a prolonged fast, best to take it 20-30 minutes BEFORE eating breakfast.

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19
Q

PPIs: Examples

A

Esomeprazole, Lansoprazole, Omeprazole

-zole

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20
Q

Pharmacokinetics of PPIs

A

Rapidly absorbed.
Highly protein bound.
Extensively metabolized in the liver by P450.
Mostly excreted by the kidneys.

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21
Q

When should PPIs be taken?

A

20-30 minutes before breakfast since food will stimulate acid production after an overnight fast.
If 2x/day, take again 20-30 minutes before last meal.

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22
Q

Indications for PPIs

A 
Peptic Ulcer Disease
GERD
Esophagitis
Barrett's esophagus
H. pylori ulcers (w/ antibiotic)
NSAID-induced ulcers
Stress ulcer prophylaxis
Zollinger-Ellison Syndrome (cancer of gastrin-producing G cells)
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23
Q

Adverse Effects of PPIs

A

Nausea, abdominal pain, constipation/diarrhrea, flatulence, INCREASED GASTRIN LEVEL led to hyperplasia of enterochromaffin cells (Histamine-producing) leads to rebound hypersecretion of HCl once PPI is discontinued

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24
Q

A patient presents with NSAID-related gastric ulcers, but he is on Clopidogrel. What is of concern when giving PPIs? Which is safe for this patient?

A

PPIs may inhibit CYP2C19, which decreases metabolism and clopidogrel’s anti-platelet effect.
Dexlansoprazole is the only one approved for use with clopidogrel.

25
A 52-year-old male presents with GERD. The resident wants to prescribe a PPI after endoscopy. He asks you when the patient should take his meds. What do you say?
20-30 minutes before breakfast.
26
H2R Antagonists
MOA: Prevent the release of histamine from enterochromaffin cells, which decreased HCl production from parietal cells, by reversibly binding to H2 receptors. Most prominent effects on basal acid secretion. Common ones: Ranitidine, Famotidine.
27
Pharmacokinetics of H2R blockers
Absorbed quickly w/ peak concentration in 1-2 hours. Only a small percentage is protein-bound. Small amount metabolized in the liver. Both metabolized and unmetabolized products are excreted by the kidneys.
28
Indications for H2R Blockers
Peptic Ulcer Disease GERD Prophylaxis of stress ulcers Treatment/prevention of NSAID-induced ulcers Only used for Zollinger-Ellison if PPIs are contraindicated
29
Adverse Effects of H2R Blockers
Diarrhea, constipation, drowsiness, fatigue, muscular pain.
30
Cimetidine Side Effects
``` CNS- confusion, delirium, hallucinations, slurred speech, headaches. Cardiac toxicity Genecomastia/galactorrhea Reduction in sperm count/impotence Myelosuppression Liver failure/transplant rejection Increase in creatine Vitamin deficiency ```
31
Why does Cimedtidine have so many side effects?
It inhibits cytochrome P450 more than other drugs in its class. Interactions include warfarin, pheytoin, caffeine, TCA's, metronidazole.
32
Misoprostol
Prostaglandin analogue; would decrease HCl production by decreasing cAMP. Stimulates bicarb/mucin secretion. Improves mucosal blood flow. More common for RA tx. Diarrhea is most common SE. Can cause spontaneous abortions, so not used often especially in females of childbearing age.
33
Sucrafate
Produces a viscous, sticky gel in acidic environments (pH t alter gastric acid or pepsin secretion or buffer acid; for symptom relief.
34
Dosing of Sucrafate
Acts for up to 6 hrs. after a dose | Should be taken on an empty stomach one hour before meals; do not eat for at least 2 hours after taking it.
35
Indications for Sucrafate
Duodenal ulcer.
36
Side Effects of Sucralfate
Constipation. | May produce aluminum toxicity, especially in chronic kidney disease leading to neurotoxicity and anemia.
37
Antacids
Attempt to directly neutralize acid environment of the gastric mucosa. Food in the stomach prolongs neutralizing effects. Less effective than other methods for mild heartburn.
38
Formulations of Antacids
Aluminum carbonate- Mylanta, Maalox liquids Calcium carbonate - Tums, Maalox tablets, Rolaids Magnesium carbonate - Maalox liquid, Milk of Magnesia, Rolaids Sodium bicarb- Alka-Selzer
39
Adverse effects of Magnesium-containing antacids
Diarrhea, weakness, hypocalcemia, arrhythmias.
40
Adverse effects of calcium-containing antacids
Hypercalcemia, alkalosis, renal impairment (milk-alkali syndrome)
41
Adverse effects of Aluminum-containing antacids
Neurotoxicty, anemia
42
Bismuth Subsalicylate
AKA Pepto Bismal, Kaopectate For nausea, heartburn, indigestion, upset stomach, diarrhea. Used in combination with PPIs/antibiotics for H. pylori induced ulcers. Doesn't inhibit/neutralize acid. Can cause black stool due to reaction with H2S in colon; not necessarily upper GI bleed!
43
A 36-year-old teacher complains of increasing frequency of hearburn that doesn't respond to OTC H2R antagonists. She reports high levels of work-related stress, which is aggrevated by heartburn several times a week. Otherwise, she is in good health with no risk of cardiac risk factors or alar signs. What agent do you prescribe?
PPI 20-30 minutes before 1st meal of the day.
44
A patient presents with GERD. You are concerned about complications such as esophagitis, stricture formation, or Barrett's esophagus. What is your goal of treatment? What do you prescribe?
Complete symptom recovery and healing of inflammation. | PPIs.
45
Stages of Heartburn
1: sporadic, uncomplicated heartburn; 2-3 episodes/week and can be modified by lifestyle modification and antacids. 2: > 2-3 episods/week; treat w/ PPI 3: chronic, unrelenting symptoms; endoscopic exam shows complications; tx: PPI twice daily (30 minutes b4 dinner; 30 b4 last meal) or PPI before breakfast and H2R antagonist at bedtime. Requires patient compliance.
46
A 38-year-old male presents with frequent heartburn that interferes with his daily routine. He has no alarm symptoms or cardiac risk factors. What treatment do you prescribe?
Trial of PPI therapy.
47
What are the 2 most common causes of Peptic Ulcer Disease?
H. pylori infection & NSAID use.
48
A patient presents with peptic ulcer disease caused by H. pylori. What is the mainstay of treatment? What if patient is allergic to penicillin?
PPI 2x/day, Amoxicillin, and Clarithromycin for 7-14 days. | Use Metronidazole instead of Amoxi.
49
Why is sequential antibiotic therapy needed for H. pylori infections?
To prevent resistance.
50
Risk Factors for GI bleeds secondary to Peptic Ulcer Disease
``` NSAIDs H. pylori infection Corticosteroids Mechanical ventilation > 48 hours Coagulopathy ```
51
What are symptoms of an actively bleeding ulcer?
Low BP, high heart rate, low hemoglobin/hematocrit, increased BUN/Creatine.
52
How long do you keep a post-ulcer bleed patient on a PPI drip?
72 hours to prevent risk of rebleeding.
53
Treatment for Acute GI bleeds
Endoscopic treatment
54
Why does PPI work for prevention of secondary GI bleeds?
Clot formation, clot lysis, and mucosal healing are pH-dependent processes that work better at high pH. Pepsin is inhibited and leads to stabilization of clots.
55
Stress Ulcers
Mucosal ereosions which primarily occur in the stomach, but can be found in distal esophagus or duodenum due to an inbalance between gastric acid production by parietal cells and protective mechanisms.
56
Risk Factors for Stress Ulcer Development
Critically ill, mechanical ventilation > 48 hours, shock sepsis, hepatic/renal failure, prior hx of upper GI bleeding.
57
Who received prophylactic treatment for stress ulceration? What are they given?
Anyone in the ICU. | IV PPI or H2R blockers.
58
Who are at high risk of developing stress ulcers during hospitalization?
Older patients Blood thinners Mechanical ventilation > 48 hours
59
Zollinger-Ellison Syndrome
Gastrinomas - pancreatic tumors associated with MEN syndrome Severe ulcers occur in unusual locations (jenunum/ileum) Tx: PPI 2x/day Surgical removal

GI (6 decks)

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