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phar 301 > Lecture 17 (after midterm 2) > Flashcards

Lecture 17 (after midterm 2) Flashcards

1
Q

Bacterial functions in the human body

A

1) Maturation of the immune system and gut physiology
2) Synthesis of vitamins and metabolites
3) Digestions of complex glycans derived from food (fibers)
4) Protection from intestinal infection (Clostridioides difficile)

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2
Q

Effect of Gut microbiota on drugs

A

Can metabolize drugs activating, inactivating or toxifying them

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3
Q

What is Peptic Ulcer disease

A

Where the mucosal epithelium is exposed to acid and pepsin
Affects the upper GI tract (stomach, duodenum, and lower esophagus)

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4
Q

What induces the formation of ulcers

A

Excess acid production or impaired barrier function that overwhelms the defense mechanisms in the GIT

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5
Q

What are first line treatments for Peptic Ulcer Disease (PUD)

A

Proton pump inhibitors (given the cause is NOT a bacterial infection)
If caused by Helicobacter pylori, use antimicrobial treatment

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6
Q

Possible causes of Peptic Ulcer Disease (PUD)

A

NSAIDs, stress and chronic illnesses, and Helicobacter pylori infection (bacterial infection)

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7
Q

What is Gastroesophageal Reflux disease (GERD)

A

A dysfunctional relaxation of the lower esophageal sphincter, allowing reflux of acidic gastric contents from the stomach into the esophagus

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8
Q

What can Gastroesophageal Reflux Disease (GERD) lead to

A

Inflammation, bleeding, ulcerations, and Barret esophagus

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9
Q

What is Barrett esophagus

A

Reorganization of the cell lining of the esophagus in response to acid damage
A premalignant condition
Associated with high incidence of transition to cancer

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10
Q

GERD treatment

A

Proton pump inhibitors, histamine (H2) receptor antagonists, and dopamine antagonists (increase the tone of the lower esophageal sphincter)

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11
Q

Function of Antisecretory drugs

A

Prevent secretion of gastric acid in the stomach by parietal cells

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12
Q

How is gastric acid secreted

A

By an ATPase proton pump
Pumps protons into gastric lumen

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13
Q

Which molecules induce gastric acid secretion by parietal cells

A

Acetylcholine, gastrin, and histamine

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14
Q

Mechanism of gastric acid secretion by Acetylcholine

A

Acetylcholine is released from vagus nerve terminals–>Acetylcholine binds the M3 muscarinic receptor on parietal cells–>parietal cells secrete gastric acid

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15
Q

Mechanism of gastric acid secretion by Gastrin

A

Gastrin is released from G cells (in stomach)–> Gastrin then binds to CCK2 receptors or gastrin receptors on parietal cells–>parietal cells secrete gastric acid

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16
Q

Mechanism of gastric acid secretion by Histamine

A

ECL (enterochromaffin-like cells) synthesize histamine–>histamine then binds to H2 receptor on parietal cells

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17
Q

2 pathways of gastric acid secretion

A

Direct and indirect pathways

18
Q

Direct pathway of gastric acid secretion

A

Acetylcholine, gastrin, and histamine bind DIRECTLY to their respective receptors (M3 muscarinic receptors, CCK2 or gastrin receptors, and H2 receptors) on parietal cell’s membrane to SYNERGISTICALLY stimulate acid secretion

19
Q

Indirect pathway of gastric acid secretion

A

Acetylcholine and gastrin bind to their receptors on ECL cells to stimulate secretion of histamine–>histamine then stimulates parietal cells to secrete gastric acid

20
Q

Inhibition of Acetylcholine release to inhibit gastric acid secretion

A

ex. Propantheline
Inhibition by a Muscarinic (cholinergic) antagonist

21
Q

Pathway of acetylcholine gastric acid secretion

A

Acetylcholine released by vagus nerve–> acetylcholine acts on M3 muscarinic receptor (a GPCR)–>activates phospholipase C that converts PIP2 to IP3–>IP3 releases Ca2+ from ER and activates Protein kinase C–>Ca2+ release and Protein kinase C open ATPase proton pump–>release gastric acid

22
Q

Inhibition of Histamine release to induce gastric acid secretion

A

ex. Cimetidine
Inhibition by a Histamine H2 receptor antagonist

23
Q

Pathway of Histamine gastric acid secretion

A

Histamine released by ECL–>histamine acts on H2 receptor (GPCR)–>activates adenylyl cyclase–>increases synthesis of cAMP–> high [cAMP] activates Protein Kinase A–> Protein Kinase A directly opens ATPase proton pump–>releases gastric acid

24
Q

How can histamine inhibition be overcome

A

By food-induced acid secretion via acetylcholine and/or gastrin

25
Q

Inhibition of Parietal cells gastric acid secretion

A

ex. Omeprazole
Proton pump inhibitors
Direct inhibition by blocking ATPase proton pump

26
Q

Function of Proton Pump inhibitors

A

Reduce acid secretion independent of how it is stimulated
Cannot be overcome

27
Q

Pathway of Proton pump inhibition of gastric acid secretion

A

Direct
Prostaglandin E2 binds to EP3 receptor (inhibitor) on parietal cells–>EP3 receptor inhibits adenylyl cyclase–>less cAMP produced–>decreased gastric acid secretion
Indirect
Prostaglandin E2 reduces histamine release from ECL cells and gastrin release from G cells

28
Q

Mechanism of somatostatins in gastric acid secretion

A

Reduce gastric acid secretion by stimulating EP3 receptors (same inhibitory receptors as prostaglandins)

29
Q

Omeprazole in neutral vs ionic form

A

Neutral–>may enter acidic vesicles
Ionic–>stuck in vesicle

30
Q

What is omeprazole

A

Prodrug that is converted to active form by stomach acids

31
Q

Mechanism of omeprazole

A

In active form
Omeprazole covalently and irreversibly binds the ATPase proton pump, inactivating it

32
Q

When to use Proton pump inhibitors

A

ex. Omeprazole
1) NSAID-associated damage prevention
2) Prophylactic treatment to protect the gastric barrier against infections (Clostridium difficile)

33
Q

Side effects of long term use of Proton Pump Inhibitors (PPIs)

A

ex. Omeprazole
Vitamin B12 deficiency and hypomagnesemia
Increased risk of osteoporosis and fractures

34
Q

Effect of NSAIDs on prostaglandins

A

NSAIDs reduce the number of prostaglandins which leads to
1) Increase in acid production
2) Decrease in mucus and bicarbonate production
3) Decreased blood flow
4) Increased risk of ulcers

35
Q

What do NSAIDs inhibit

A

Cyclooxygenase 1 and 2 responsible for the synthesis of prostaglandins
COX1–> constitutively expressed, produces gastric prostaglandins responsible for mucosal integrity
COX2–> induced by inflammatory stimuli

36
Q

Side effects of COX-2 selective NSAIDs

A

ex. coxib, celecoxib
Myocardial infarction and stroke

37
Q

Effect of NSAIDs

A

1) Create local injuries in gastric epithelial cells (due to accumulation)
2) Weak acids so may cross cell membranes and enter gastric epithelial cells
3) Ionized in cytoplasm so may get trapped and accumulate causing cell damage

38
Q

Mechanism of Prostaglandin

A

Activate prostanoid receptors on parietal cells to decrease gastric acid secretion

39
Q

Function of Prostaglandin analog

A

ex. Misoprostol
1) Increases secretion of mucus and bicarbonate
2) Enhances mucosal blood flow
3) Inhibits mucosal cell turnover to enhance mucosal defense

40
Q

When to use Misoprostol (prostaglandin analog)

A

Labour induction of medical abortion

41
Q

Side effect of Misoprostol

A

Frequent diarrhea

phar 301 (23 decks)

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