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Pharmacology > GI: Upper GI Tract, PUD, GERD > Flashcards

GI: Upper GI Tract, PUD, GERD Flashcards

1
Q

What are the 3 mediators of secretion of acid into the gastric lumen?

A
  1. Acetylcholine
  2. Gastrin
  3. Histamine
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2
Q

Protein kinase produced by the gastric mediators stimulate what?

A

The potassium-hydrogen-adenosine (K-H-ATPase) pump on the parietal cell surface (proton pump)

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3
Q

What is the main action of the proton pump?

A

Pump protons (mainly H) out of the parietal cells into the gastric lumen as HCl (acid)

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4
Q

What are some of the body’s mechanisms of protection of the gastric lining? (5)

A 
Mucus
PGE
Somatostatin
Bicarb
Blood flow
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5
Q

Peptic ulcers are breaks in the _______ mucosa and are the result of an imbalance of ____ ________ and ______.

A

Intestinal
acid production
protection

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6
Q

Peptic ulcers are located where?

A

Stomach

Duodenum

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7
Q

3 important factors for PUD development:

A

H. pylori
NSAID use
Cigarettes smoking

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8
Q

Goals of PUD therapy:

A

Reduce gastric acidity
Enhance mucosal defenses
Eliminate H.pylori

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9
Q

H. pylori is a gram _____ spiral bacterium and is transmitted ______.

A

Negative

Orally

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10
Q

How does H.pylori cause gastric injury?

A

Production of a cytotoxin
Breakdown of mucosal defenses

(Presence of H.pylori in the GI tract causes a production of urease which converts urea to form an ammonia ‘cloud’ around the bacteria to neutralize local acid and form a protective barrier. Urease also causes damage to the mucosal cell wall. The body responds to the formation of the alkaline cloud by increasing acid secretion.)

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11
Q

H.pylori must be ______ or PUD will _____.

A

eradicated

recur

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12
Q

How do NSAIDs induce GI damage?(systemic and topical)

A

Systemic:
Tips balance of GI protection vs. acid secretion-By inhibition of cyclooxygenase, PGE is decreased, which decreases bicarb and mucus production, decreases blood flow and increases acid secretion. May also damage mucosal by giving off free radicals

Topical: NSAIDs in stomach lumen at a low pH are unionized which allows them to travel to gastric epithelium cells (neutral pH) where they become ionized and trapped= direct cell damage.

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13
Q

GERD is less of an imbalance between gastric acid secretion and protection and more of a disorder in which:

A

the esophageal mucosa is damaged by reflux of acid into the lower esophagus

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14
Q

Drugs that inhibit acid secretion include:(3)

A

H2 antagonists
PPIs
Anticholinergic agents

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15
Q

Drugs that neutralize gastric acid: (1)

A

Antacids

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16
Q

Drugs that protect the gastric mucosa: (3)

A

Sucralfate
Colloidal bismuth
PGE

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17
Q

Drugs used to eradicate H.pylori:

A

Antibiotics

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18
Q

How do H2 antagonists work and what are some examples?

A

Competitive antagonism of H2 receptors to suppress gastric acid secretion
Ex- Ranitidine, Famotidine, Cimetidine, Nizatidine

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19
Q

When do H2 antagonists reach their peak concentration and how are they metabolized and excreted?

A

1-3hrs
Metabolized: Liver
Excreted: Kidneys

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20
Q

AE of H2 antagonists:

A

Diarrhea, HA, muscle pain, constipation, fatigue, confusion/hallucination (IV)

21
Q

What are common DI that can occur with H2 blockers and which one in particular inhibits CYP?

A

Interfere with drugs that require in acidic medium (ex-atazanavir)
Cimetidine inhibits CYP3A4, 2D6, 1A2

22
Q

Which drugs cause a total shutdown of acid release because they work late in the acid production cycle and what are some examples?

A 
PPIs
Lansoprazole
Pantoprazole
Esomeprazole
Omeprazole
Rabeprazole
23
Q

PPIs are _____ that are converted to _____ drugs in the parietal cell canaliculus.

A

prodrug

active

24
Q

MOA of PPIs:

A

Forms a covalent bond with proton pump. The bond is irreversible, new proton pump must be synthesized to replace

25
Q

What is true of PPIs half life and dosing?

A

Short half-life

May need loading dose and frequent dosing

26
Q

How are PPIs metabolized?

A

By the liver via CYP 2C19, 3A4

27
Q

Which PPI can inhibit the metabolism of plavix d/t inhibition of 2C19?

A

Omeprazole

28
Q

How are PPIs related to pregnancy?

A

They cross the placenta and can be found in breast milk

29
Q

AE of PPIs

A

HA, GI disturbance, nausea
Enteric inf d/t compromised defenses (ex-salmonella)
Long-term use may cause increased acid production and carcinoid tumors

30
Q

When is a PPI the preferred treatment?

A

PUD with H.pylori
Hemorrhagic ulcers
PUD in patients who required NSAID use

31
Q

What is the MOA of anticholinergics and an example?

A

Muscarinic ACh receptor antagonist
Decreases acid secretion
Dicyclomine
(least effective)

32
Q

AE of Anticholinergics:

A

Dry mouth, constipation, blurred vision, cardia arrythmia, urinary retention

33
Q

Which drug does not prevent release of gastric acid but is good for acute pain relief and not the treatment of choice for PUD?

A

Antacids. Neutralize acid-fast onset but not long lasting

34
Q

Antacids are a combination between a _____ and a ______.

A

Anion
Cation

(Anions: Carbonate, bicarbonate, citrate, phosphate, hydroxide
Cation: Na+, Ca+2, Mg+2, Al+3)

35
Q

AE of antacids include:

A

Constipation (Al, Ca)
Diarrhea (Mag)
Electrolyte abnormalities

(may combine Al, Ca with Mag to balance AE)

36
Q

Which drug used fornPUD does NOT alter gastric pH?

A

Sucralfate (symptomatic relief)

37
Q

How does sucralfate work?

A
  • Complex salt of sucrose sulfate and aluminum hydroxide
  • Forms a viscous gel that binds to positively charged proteins and sticks to areas of ulceration
  • Protects ulcerated tissue from aggressive factors like pepsin, acid, and bile salts
38
Q

Why is sucralfate difficult to use?

A

Large tablets and frequent administration

39
Q

How does sucralfate produce drug interactions?

A

By binding to the drugs

40
Q

Which drug is a coating agent used in PUD which forms a barrier and stimulates mucosal bicarbonate and PGE2 as well as impeded H.pylori growth?

A

Colloidal Bismuth

41
Q

Which PG analog is used to prevent NSAID induced ulcers?

A

Misoprostol

42
Q

AE and CI of Misoprostol:

A

AE: Abdominal discomfort, diarrhea
CI: Pregnancy

43
Q

What is the classic triple therapy used to treat H.pylori?

A

Amoxicillin
Clarithromycin
PPI

44
Q

What is the quadruple therapy used to treat H.pylori and when is it used?

A

Tetracycline
Metronidazole
PPI
Bismuth

Used when patients fail therapy or a have an allergy to triple therapy

45
Q

Drug of choice for GERD:

A

PPIs

aggressively raise gastric pH for long periods

46
Q

Other second line options for GERD include:

A

H2 antagonists
Antacids
Sucralfate
Metoclopramide

47
Q

How does metoclopramide used to treat GERD?

A

Enhances stomach emptying

Increases LES tone

48
Q

Risk Factors that patient’s should be counseled about regarding GERD (and PUD):

A

Avoid caffeine, alcohol, cigarettes, and NSAIDs

Pharmacology (48 decks)

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