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Pharmacology > EXAM #1: GI PHARMACOLOGY > Flashcards

EXAM #1: GI PHARMACOLOGY Flashcards

1
Q

What factors are secreted by parietal cells in the stomach?

A
  • HCl

- Intrinsic factor

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2
Q

Where are parietal cells located in the mucosa?

A

Gastric pit

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3
Q

What is the function of HCl produced by the parietal cells? What about intrinsic factor?

A

HCL

  • Protein digestion
  • Sterilization
  • Nutrient absorption

IF
- Vitamin B12 Absorption

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4
Q

What cell type secretes mucous and bicarbonate in the stomach?

A

Superficial epithelial cells

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5
Q

What are the “gastroprotective” secretions of the stomach?

A

Mucous and bicarbonate

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6
Q

What cell type secretes histamine in the stomach?

A

ECL

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7
Q

What is the function of histamine in the stomach?

A

Promotion of HCl secretion

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8
Q

What is the source of Gastrin in the stomach?

A

G-cells

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9
Q

What is the function of Gastrin in the stomach?

A

Gastrin promotes the secretion of HCl

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10
Q

What is the endocrine mechanism that increases gastric acid secretion?

A

Gastrin

1) Gastrin is secreted into the BLOOD via G-cells of the stomach
2) Gastrin can then mediate acid secretion via direct and indirect mechanisms:
- Direct= stimulate parietal cells to secrete H+
- Indirect= stimulate ECL cells to secrete histamine, which eventually increases acid secretion

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11
Q

What is the paracrine mechanism to increase gastric acid secretion?

A

Histamine

  • Histamine is released from ECL cells onto neighboring parietal cells, stimulating acid secretion
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12
Q

What is the effect of prostaglandins on acid secretion in the stomach?

A

This is the PARACRINE mechanism to negatively regulate the H+-K+ ATPase

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13
Q

What are the two ways that prostaglandins are gastroprotective?

A
  • Negative regulation of the H+-K+ ATPase

- Promotes the secretion of mucous and bicarbonate from gastric epithelial cells

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14
Q

What cells release somatostatin? What is the function of somatostatin?

A

D-cells release somatostatin, which:

1) Inhibits gastrin release from G-cells
2) Inhibits histamine release from ECL cells
3) Inhibits H+-K+-ATPase activity

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15
Q

What are the two most common causes of ulcers in the US?

A

1) NSAIDs

2) H. pylori infection

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16
Q

How do NSAIDs lead to the development of peptic ulcers?

A

Cycloxygenase that leads to decreased prostaglandin synthesis

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17
Q

What are the hallmark symptoms of a gastric ulcer (7)?

A

1) Abdominal pain–exacerbated by meal
2) Nausea
3) Vomiting/ hematemesis/ coffee ground emesis
4) Melena
5) Indigestion
6) Weight loss
7) Fatigue

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18
Q

What is the therapeutic goal of antacids?

A

Neutralize gastric acid by raising the pH greater than 4

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19
Q

How do antacids work?

A

Base + Acid= Salt + Water

Sometimes these can produce CO2–note that there is NOT a target receptor for antacids, simple acid/base chemistry.

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20
Q

List the common antacids in order of the rate of reactivity.

A

1) Sodium bicarboante- fast
2) Calcium carbonate- medium
3) Magnesium hydroxide- slow
4) Aluminum hydroxide- slow

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21
Q

What is the duration of action for antacids? Why is this clinically relevant?

A
  • Duration of action is 1-2 hours
  • B/c of this short duration, they have to be taken often
  • Frequency leads to lower compliance
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22
Q

What are the common adverse effects of antacids?

A
  • Reduced drug bioavaliablity- changes in pH will alter the availability of drugs
  • Greater risk of enteric infection
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23
Q

Why do antacids increase risk of enteric infection?

A

Raise in pH prevents acidic destruction of microograngisms

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24
Q

What are the specific adverse effects of Sodium Bicarboante?

A

1) Metabolic alkalosis
2) Excessive NaCl absorption
3) Gas/bloating

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25
Q

What are the specific adverse effects of Calcium Carbonate?

A

1) Gas/ bloating

2) Acid rebound

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26
Q

What is acid rebound?

A
  • pH increases in stomach

- homeostatic mechanisms promote acid secretion

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27
Q

What antacid produces the most acid rebound?

A

Calcium Carbonate

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28
Q

What are the specific adverse effects of Magnesium Hydroxide?

A

Osmotic diarrhea b/c there is a large amount of salt retained in the lumen of the gut

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29
Q

What are the specific adverse effects of Aluminum Hydroxide?

A

Constipation b/c aluminum will DECREASE peristalsis

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30
Q

What two antacids are commonly seen together? Why?

A

Magnesium hydroxide and Aluminum hydroxide b/c they have opposing side effects i.e. osmotic diarrhea and constipation respectively

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31
Q

List the indications for antacids.

A

1) GERD
2) Peptic ulcers
3) Dyspepsia

32
Q

How does the efficacy of antacids compare to H2 receptor antagonists to heal GERD and Peptic Ulcers?

A

Same but you have to take antacids more often

33
Q

Describe the mechanism of action of H2 receptor antagonists.

A
  • Competitive inhibition of H2 (histamine) receptors
  • Leads to a DECREASE in gastrin-induced HCl secretion
  • Partial block of muscarinic HCl secretion

This blocks the INDIRECT effects of Gastrin on acid secretion, but NOT the DIRECT effects of gastrin

34
Q

What is the suffix that is common to all H2 receptor antagonists?

A

“Idine”

35
Q

List the H2 receptor antagonists.

A

Cimetidine
Ranitidine
Nizatidine
Famotidine

36
Q

What is the duration of H2 receptor antagonists?

A

6-10 hours

Note that this is much longer than antacids

37
Q

What is the common adverse effect of H2 receptor antagonists?

A

Headache

38
Q

What are the specific considerations that need to be taken into account when prescribing Cimetidine?

A

1) CNS effects
2) Endocrine effects
3) Inhibition of CYP metabolism i.e. potential for drug interaction

39
Q

What are the adverse CNS effects Cimetidine?

A
  • Confusion
  • Hallucinations
  • Agitation
40
Q

What are the adverse endocrine effects Cimetidine?

A
  • Inhibition of androgen receptors
  • Inhibition of estradiol metabolism
  • Increased prolactin level
  • Produce gynecomastia in males
41
Q

List the indications for H2 receptor antagonists.

A

1) GERD
2) Peptic Ulcers
3) Dyspepsia
4) Gastritis

42
Q

What is important to remember about H2 receptor antagonists and their onset of action?

A

Must be ABSORBED first

43
Q

What is the mechanism of action of PPIs?

A
  • Inhibit the proton pump
  • Inhibit the effects of
    1) Gastrin
    2) Histamine
    3) ACh
44
Q

Describe the absorption and mechanism of the PPIs.

A

1) Absorbed
2) Circulates
3) Concentrates on the proton pump via transport form the basolateral membrane
4) Antagonizes the proton pump

45
Q

What type of antagonists are the PPIs?

A

Irreversible

I.e. activation of the pump requires new synthesis

46
Q

What is the common suffix among the PPIs?

A

Azole

47
Q

List the PPIs.

A 
Omeprazole 
Lansoprazole 
Rabeprazole 
Esomeprazole 
Pantoprazole
48
Q

How long does it take to get the max dosing effect of the PPIs? Why?

A

3-4 days

  • Proton pumps are made in parietal cells and sequestered in vesicles
  • Upon stimulation, the pumps are inserted into the apical membrane
  • It takes 3-4 days to exhaust all the vesicles
  • B/c proton pumps only work at apical membrane, it takes 3-4 days for maximum effect.
49
Q

What are the common adverse effects of PPIs?

A

1) Decreased drug bioavaliablity
2) Diarrhea
3) Headache
4) Abdominal pain

50
Q

What are the adverse effects that can be seen with chronic PPI therapy?

A
  • Decreased nutrient absorption i.e. B12, iron, Ca++, and zinc
51
Q

What types of infections are hospitalized patients more likely to have on a PPI?

A
  • Enteric infection

- Respiratory infection

52
Q

What are the indications for PPIs.

A

1) GERD
2) Peptic ulcers
3) Dyspepsia
4) Gastritis
5) Hypersecretory disease
6) NSAID-ulcers
7) H.pylori ulcers

53
Q

What class of drugs is the most efficacious inhibitors of acid secretion?

A

PPIs

54
Q

List the gastroprotective drugs.

A

Sucralfate
Misoprostol
Bismuth

55
Q

What is the mechaism of Sucralfate?

A

1) Adheres to the ulcer and creates a physical barrier

2) May stimulate mucus secretion

56
Q

What is the mechanism of bismuth subsalicylate?

A

1) Adheres to the ulcer and creates a physical barrier

2) May stimulate mucus secretion

57
Q

What is the mechaism of action of Misoprostol?

A

Prostaglandin analog

58
Q

What are the functions of ACh in the stomach?

A

BOTH protective and aggressive:

1) Promote mucous and bicarbonate secretion
2) Promote HCl secretion

59
Q

What are the common adverse effects of sucralfate?

A
  • Constipation

- Impaired drug absorption

60
Q

What patient population requires prescribing Sucralfate with caution?

A

Renal insufficient

This is b/c the drug contains some Aluminum, which can be toxic in patients with renal insufficiency

61
Q

What are the common adverse effects of Misoprostol?

A

Cramping
Diarrhea

This is b/c as a PG inducer, it increases smooth muscle contraction, leading to cramping and diarrhea.

62
Q

What is the serious adverse effect of Misoprostol?

A

Abortificient– INDUCES ABORTION

Do NOT give to women of childbearing age, and especially not PREGNANT women–induces uterine contractions

63
Q

What is the common adverse effect of Bismuth subsalicylate?

A

Blackening of the stool and tongue

64
Q

What is the serious adverse effect of Bismuth subsalicylate?

A

High does of salicylate toxicity

65
Q

How do the effects of Bismuth subsalicylate differ in the stomach and intestines?

A
  • Increase PG synthesis in stomach

- Block PG synthesis in intestines

66
Q

Generally, when are mucosal protective indicated?

A

As a 2nd line agent to PPIs

67
Q

What are the specific indications for Sucralfate?

A
  • Stress related ulcers

- Hospitalized patient when you DON’T want to prevent acid secretion (risk of enteric infection/ respiratory infection)

68
Q

What is the specific indication for Misoprostol?

A

NSAID associated ulcers

69
Q

What is the specific indications for Bismuth subsalicylate?

A

1) H. pylori ulcers
2) Traveler’s dirrhea
3) Dyspepsia

70
Q

Explain the etiology of H.pylori associated ulcers.

A
  • Bacteria colonizes the mucusal epithelium of the stomach

- Causes damage at the site of colonization and leads to tissue breakdown i.e. ulcer

71
Q

Aside from ulcers, what more serious diseases is H.pylori associated with?

A

1) Gastric lymphoma

2) Gastric adenocarcinoma

72
Q

What is the first line, “new triple therapy” for treating H. pylori?

A

1) PPI
2) Clarithromycin
3) Amoxicillin or metronidazole (PCN allergy if patient cannot take amoxicillin)

I.e. the strategy is to decrease gastric acid and administer antimicrobial agents

73
Q

Why are two antibiotics given with H. pylori infection?

A

H. pylori has a very high level of drug resistance–giving one antibiotic may lead to the induction of a very resistant strain

74
Q

What is the old triple therapy for H. pylori?

A
  • Bismuth subsalicylate
  • Tetracycline
  • Metronidazole
75
Q

What is quadruple therapy?

A

1) PPI
2) Clarithromycin
3) Amoxicillin or metronidazole (PCN allergy if patient cannot take amoxicillin)

+ Bismuth subsalicylate

Pharmacology (64 decks)

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