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GI Week 1 > Lecture 6: Pharmacology of Peptic Acid > Flashcards

Lecture 6: Pharmacology of Peptic Acid Flashcards

1
Q

What are the causes of PUD?

A 
PUD includes inflammatory mucosal disorders of the upper GI tract and can involve any of the upper GI organs
For example 
	i. esophagus = reflux esophagitis
	ii. stomach
	iii. duodenum ulcer
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2
Q

What are the environmental factors (CAT) that lead to PUD?

A
  1. Caffeine
  2. Alcohol
  3. Tobacco
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3
Q

What are the three types of receptors in the parietal cell?

A
  1. histamine receptor (H2)
  2. acetylcholine (M3 subtype) receptor
  3. Gastrin/CCK-B receptor
    Each receptor has own ligand
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4
Q

What 3 things that contribute to H+ in

Parietal cells?

A
  1. gastrin
  2. acetylcholine
  3. histamine
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5
Q

What are the key characteristics of the

H/K ATPase?

A
  1. ATP dependent
  2. rate of secretion of HCL depends
    Completely on proton pump
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6
Q

What are the key characteristics of pepsin?

A

Aggressive factor #2
Derived from pepsinogen
A protease secreted by chief cells
Ability to damage the GI tract is pH dependent
Inactivated at pH > 4.0
IRREVERSIBLY inactivated at pH > 6
Too much pepsin can digest proteins on surface epithelium

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7
Q

What is the mechanism by which H. pylori promotes PUD?

A

MULTIFACTORIAL
Aggressive factor 3
Modifies NH3 with urease
Can increase acid output (antrum) or decrease acid output with increased gastrin output
Induces inflammation due to increase of COX-2
Decreased mucosal defenses

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8
Q

What prostaglandins are produced by COX?

A

PGE1 and PGE2

Fucked up by NSAIDS

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9
Q

What are the key factors for Bile?

A

Aggressive factor 5
Can be damaging to GI tract even in the absence of acid
-this effect is counterintuitive since bile neutralizes acid
-the reflux of bile into the stomach/esophagus is usually prevented
Injury from bile (bile gastritis) mainly occurs in patients who have had surgery in which pylorus has been disrupted (pyloroplasty)

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10
Q

What produces bicarbonate?

A
  1. Brunner’s glands
  2. stomach/duodenal surface epithelial cells
  3. mucus neck cells
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11
Q

What do prostaglandins E1 and E2 do?

A

Protective factors

  1. enhance other cytoprotective mechanisms
  2. increase bicarb
  3. increase mucous thickness
  4. increase mucosal blood flow (because of increase in vasodilation)
  5. Reduces production of H+ (receptor on parietal cells)
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12
Q

How do we inhibit acid production?

A
  1. Histamine (H2) receptor antagonists

2. Proton pump inhibitors

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13
Q

What are types of H2 receptor antagonists?

A
  1. Cimetidine (TAGAMET)
  2. Ranitidine (ZANTAC)
  3. Nizatidine (AXID)
  4. Famotidine (PEPCID)
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14
Q

What is Tagamet?

A

A H2 antagonist

Decreases H+ production by parietal cells

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15
Q

What is zantac?

A

A H2 antagonist

Decreases H+ production by parietal cells

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16
Q

What are characteristics of H1 antagonists?

A

Allergy medications

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17
Q

What are the characteristics of H2 antagonists?

A 
Doesn’t do shit for allergies
Only decrease acid production
1. rapidly absorbed and quick onset
2. p450 hepatic metabolism
3. renal excretion
4. elevates pH to inactivate pepsin
18
Q

What are the adverse effects of Tagamet (cimetidine)?

A

Binds to P450 so it is CONTRAINDICATED in drugs that use P450 to be broken down, such as

i. warfarin
2. diazepam

19
Q

Why do H2 antagonists may fail?

A

Because they leave two receptors (acetylcholine and gastrin) unopposed so not as effective

20
Q

What are the types of Proton pump inhibitors?

A
  1. Omeprazole (Prilosec)
  2. Lansoprazole (Prevacid)
  3. Rabeprazole (Aciphex)
  4. Pantroprazole (Protonix)
  5. Esomeprazole (Nexium)
21
Q

What is Prilosec?

A

A proton pump inhibitor

Omeprazole

22
Q

What is the MoA of PPIs?

A

IRREVERSIBLY blocks H/K atpase which leads to them being permanently inactivated
This means that new atpase has to be synthesized
Much more effective

23
Q

What are the key characteristics of PPIs?

A
  1. Intentionally delivered as prodrugs formulated within an acid resistant coating
  2. outer layer is dissolved in alkaline medium
  3. lipophilic prodrug is inactive at neutral/alkaline pH
  4. PPIs diffuse readily across lipid membranes and acidified compartments
24
Q

What happens once PPI reaches parietal cell?

A
  1. Trapped by binding to H+
  2. Activated by coupling to sulfonated group (Sulfon)
  3. Activated form with Sulfon and H+ will bind to the H/K pump
25
Q

What is the PK of PPI?

A

Degraded by gastric acid
Plasma halflife is 1-2 hours but duration is 24-36 hours
Highly effective with a single 20 mg dose inhibiting 65% of acid secretion

26
Q

What are the adverse effects of PPI?

A

Loss of negative inhibition
Because less acid means NO somatostatin produced and you might fuck up its production permanently

  1. cause significant increase in gastrin production
    • interference with negative feedback loop
    • gastric carcinoid tumors in rats
  2. long term use leads to hip fracture
    • reduced calcium absorption
    • reduced acid production of osteoclasts
  3. gastric acid is an important barrier to colonization and infection of stomach and intestine from ingested bacteria
    • suggestion of increased respiratory infections
27
Q

How do we neutralize secreted acids?

A

Antacids

28
Q

What is the MoA of antacids?

A

Weak bases that neutralize HCl to form salt and water

Most often to relive dyspepsia

29
Q

What are the types of antacid?

A
  1. Aluminum and magnesium hydroxides
    - Mylanta and Maloox
  2. Sodium Bicarbonate-
    - Alka seltzer
  3. Calcium carbonate
    - Tums and OsCal
30
Q

What is alkaseltzer?

A

Sodium bicarbonate

Neutralizes HCL

31
Q

What are tums?

A

Calcium bicarbonate

Neutralizes HCL

32
Q

What are the adverse effects of antacids?

A
  1. chalky taste that affects absorption of other drugs like tetracyclines
  2. Mg2+ leads to diarrhea, muscle weakness, renal failure
  3. Al2+ leads to
    • constipation
    • binds phosphate
    • osteomalacia
  4. Ca
    • may cause rebound acid secretion -
    • nephrocalcinosis
    • milk alkali syndrome
33
Q

What is osteomalacia?

A

Softening of the bones

34
Q

What drugs enhance cytoprotection?

A
  1. Sucralfate

2. Misoprostol

35
Q

What is the treatment plan for patients who absolutely need NSAID?

A
  1. long term use of PPI
  2. concomitant use of PGE Analogue
  3. Use of coxibs in carefully selected patients
36
Q

What is a coxib?

A

A selective Cox2 inhibitor

37
Q

What are the characteristics of misoprostol?

A

PGE2 analogue
Effective primary prevention of GU in patient while taking NSAIDS
Side effects = abortion and diarrhea

38
Q

What is Sucralfate?

A

A complex salt of sucrose sulfat and AlOH3
Binds to GI mucosa and acts within lumen
Stimulates mucus and HCO3- + PGE2 production
Increases resistance to proteolysis by pepsin
Binds to area of ulceration but has no direct effect on acid production!

39
Q

What is H. pylori?

A

Gram negative microaerophilic bacterium

40
Q

How do you treat H pylori?

A

Triple or quadruple regimens

  1. Clarithromycin, amoxicillin and PPI
  2. Metronidazole, levofloxacin, PPI and bismuth subsalicyclate

GI Week 1 (6 decks)

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