Pharm- Anti-peptic Diseases Flashcards

1
Q

What is the mechanism of histamine binding to parietal cells to cause the H+/K+ ATP to be brought to the membrane?

A

Histamine binds to H2 –> increase in cAMP –> PKA activation –> tubovesicles with pumps brought to apical membrane

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2
Q

Which cells secrete gastrin?

A

G cells

ez to remember lol

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3
Q

Gastrin activates which type of receptors?

A

CCK(B) receptors

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4
Q

Which receptors does Ach activate on the gut?

A

M3

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5
Q

Gastrin and Ach therefore work on what G-protein pathway to increase intracellular Ca++?

A

Gq (activates PLC)

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6
Q

This is the phase of gastric acid secretion when sights, smells, or thoughts stimulate gastrin secretion and vagal stimulation which leads to an increase in gastric acid secretion

A

Cephalic phase

pavlov what UPPP

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7
Q

This is the phase of gastric acid secretion when stretching of the stomach wall and ingestion of amino acidds causes gstrin release.

A

Gastric phase

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8
Q

This is the phase of gastric acid secretion when digested proteins further in the GI tract stimulates gastric acid secretion.

A

Intestinal phase

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9
Q

True or false: prostaglandins stimulate mucous secretion.

A

True

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10
Q

True or false: NSAIDs inhibit mucous secretion.

A

True

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11
Q

What are the 2 most common causes of ulcers?

A

NSAID use and H. pylori

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12
Q

What is the enzyme that H. pylori uses to convert urea to NH3, thus buffering stomach acid?

A

Urease

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13
Q

So yeah, H. pylori is bad, but how does NSAIDs cause ulcers?

A

Remember, NSAIDs inhibit prostaglandins, and prostagandins stimulate mucous secretion. No prostaglandins –> no mucous –> gastric wall damage from lack of protection

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14
Q

This is the condition where there is excess gastrin secretion by a gastrinoma leading to excess gastric acid production.

A

Zollinger Ellison syndrome

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15
Q

These are types of ulcers caused by head trauma leading to heightened vagal tone.

A

Cushings ulcers

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16
Q

How can H2-blockers inhibit acid secretion?

A

remember histamine blocks to H2 receptors on the parietal cell, so if u block the R, the parietal cell never releases HCl

17
Q

What is the suffix for H2-blockers?

A

“-tidine”

like cimetidine and ranitidine

18
Q

Case: a hep C + pt presents with GERD and you are contemplating on prescribing an H2-blocker. Should you prescribe Nizatidine? Why or why not?

A

Yes cuz nizatidine is the only H2 blocker that is eliminated primarily in the kidney.

19
Q

This is the class of drugs that directly inhibit the H/K ATPase, thus decreasing gastric acid secretions.

A

Proton-pump inhibitors (PPI)

20
Q

True or False: PPI’s are secreted in the active form as to allow immediate inhibition when they enter the stomach.

A

False! They’re given as a prodrug and activated when they hit the stomach acid.

21
Q

The gastric acid converts the prodrug PPI into what form?

A

Sulfanemide form

22
Q

Which residue on the H/K ATPase forms a covalent bond with the sulfanemide PPI?

A

Cysteine

23
Q

What are the 3 indications to use a PPI?

A

1) H. pylori-associated ulcers
2) Hemorrhagic ulcers
3) To allow the continued use of NSAIDs in patients with peptic ulcers.

ULCERS

24
Q

Why should you use H2 blockers instead of PPI’s in a pregnant chick?

A

Because PPI’s cross the placenta. cimetidine does too but other H2 blockers dont.

25
Q

What are the 2 most common antacids?

A

aluminum hydroxide and magnesium hydroxide

26
Q

How does subcrafate protect gastric epithelial cells?

A

When sucralfate is placed into an acidic environment, it becomes viscous and binds positively charged proteins such as gastric epithelial cells. This allows it to form a protective layer on the luminal surface of the stomach.

27
Q

Misoprostol is a prostaglandin analogue that can prevent gastric ulcers from what etiology?

A

NSAID-induced ulcers

28
Q

In what type of pt is misoprostol contraindicated? Why?

A

Pregnant chicks cuz it causes uterine contraction

29
Q

This drug is used for irritable bowel syndrome and peptic ulcer disease, and atnagonizes MAchR’s on parietal cells.

A

Dicyclomine