3 - GI Flashcards

1
Q

Where in the GI tract is PUD most common?

A

Lesser curvature of the stomach

Duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The defensive factors of the GI mucosa include:

A

Mucus

Bicarbonate

Blood Flow

Prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why are prostaglandins so helpful to the mucosa?

A

Stimulate secretion of mucus and bicarbonate

promote vasodilation

suppress gastric acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why isn’t H. Pylori destroyed in the stomach?

A

It resides in between the epithelial cells and the mucus barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why are NSAIDs so harmful to the gut?

A

Because they inhibit prostaglandin growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Acid itself is almost never enough to cause PUD. The only disease in which gastric acid consistently causes PUD is:

A

Zollinger-Ellison Syndrome

(a tumor that secretes gastrin, causing MASSIVE amounts of acid release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the factors that aggressively attack the Mucosa?

A

H. Pylori

NSAIDs

Gastric Acid

Pepsin

Smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

If a patient is at risk for a peptic ulcer but has to take NSAIDs, what can be done prophylactically?

A

You can start them on a PPI (omeprazole). Can also do misoprostol, but it causes diarrhea so it’s not preferred

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

If NSAIDs can’t be discontinued and the patient has an ulcer, how should treatment proceed?

A

A PPI is the best choice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How big a role does diet play in PUD?

A

Actually, very minor role

the ulcer diet really doesn’t accelerate healing and their no evidence that caffeine promotes ulcer formation

BUT frequency can have an effect. Eater smaller more frequent meals can promote healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which ABX are most often employed to combat H Pylori?

A

Clarithromycin

Amoxicillin

Bismuth

Tetracycline

Metronidazole

Tinidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which ABX is used alone to treat H Pylori?

A

None of them!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

H2 RECEPTOR BLOCKERS

MOA AND DRUG LIST

A

Cimetidine (Tagamet)

H2 receptors cause acid secretion

Suppresses both basal secretion AND secretion stimulated by gastrin and acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When should cimetidine and antacids be taken?

A

At least an hour apart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PROTON PUMP INHIBITORS

MOA AND DRUG LIST

A

Omeprazole

Prodrug that’s converted to active form in the parietal cells

Causes irreversible inhibition of H,K-ATPase pump, blocking acid formation

Inhibits basal and stimulated gastric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which is more effective: PPIs or H2 blockers?

A

PPIs!

They also act faster

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why do H2 blockers and PPIs increase the risk of pneumonia?

A

Anytime you decrease the acidity of the stomach, you allow bacteria to proliferate

This results in a secondary increase in the colonization of the respiratory tract AND impaired WBC function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When are patients at highest risk of developing pneumonia if they take a PPI?

A

Only within the first few days. After that the risk drops off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does acid secretion impact osteoporosis?

A

decreased acid secretion means decreased absorption of calcium

20
Q

Which electrolyte is most impacted by long term PPI use?

A

Magnesium (causes hypomagnesemia)

21
Q

SUCRALFATE

MOA

A

Promotes healing by creating a protective gel that adheres to the ulcer crater, creating a barrier to the back diffusion of H ions

DOES NOT have any effect on acid secretion

22
Q

How can the adverse GI effects of antacids be minimized?

A

Combine an antacid that causes diarrhea (magnesium hydroxide) with one that causes constipation (aluminum hydroxide)

OR give it with sodium

23
Q

There are four groups of antacids:

A

Aluminum Compounds

Magnesium Compounds

Calcium Compounds

Sodium Compounds

24
Q

Why do bulk-forming laxatives work?

A

They basically cause the poop to swell, softening the stool and stretching the intestinal wall (which stimulates peristalsis)

25
Q

How is it that bulk-forming agents can relieve both constipation and diarrhea?

A

In diarrhea, they increase bulk and reduce runniness

I constipation they loosen the stool and promote peristalsis

26
Q

SURFACTANT LAXATIVES

MOA AND DRUG LIST

A

Docusate

Lowers surface tension, which facilitates penetration of water into the feces

27
Q

STIMULANT LAXATIVES

MOA AND DRUG LIST

A

Senna, Bisacodyl, Castor Oil

Stimulate intestinal motility AND increase the amount of water in the gut lumen

28
Q

There are only two appropriate uses for stimulant laxatives:

A

Opioid induced constipation

slow intestinal transit constipation

29
Q

Where is the vomiting center located?

A

The medulla

30
Q

Stimuli that directly activate the vomiting center include:

A

Signals from the cerebral cortex (fear, anxiety)

Signals from sensory organs (noxious smells, upsetting sights, pain)

Signals from the vestibulocochlear apparatus (motion sickness)

31
Q

Indirect-acting stimuli activate the vomiting center by:

A

activating the Chemoreceptor Triggering Zone (CTZ), which in turn activates the vomiting center

32
Q

Which receptors are involved in the vomiting response?

A

Serotonin

Glucocorticoids

Substance P

Neruokinin-1

Dopamine

Acetylcholine

Histamine

33
Q

SEROTONIN RECEPTOR ANTAGONISTS

MOA AND DRUG LIST

A

Ondansetron

Blocks 5-HT3 Receptors in the CTZ and on afferent vagal neurons in the upper GI tract

34
Q

Zofran is even more effective when it is combined with:

A

dexamethasone

35
Q

Which glucocorticoids are used to treat N/V?

A

Decadron and Solu-Medrol

36
Q

SUBSTANCE P ANTAGONISTS

MOA AND DRUG LIST

A

Aprepitant (Emend)

Must be combined with other antiemetic drugs (ideally a glucocorticoid) for maximal effectiveness

Has a very long duration of action

37
Q

PHENOTHIAZINES

MOA AND DRUG LIST

A

Compazine, Phenergan

Dopamine Antagonists

block Dopamine-2 receptors in the CTZ

38
Q

BUTYROPHENONES

MOA AND DRUG LIST

A

Haldol, Droperidol

block Dopamine-2 receptors in the CTZ

39
Q

METOCLOPRAMIDE

CLASSIFICATION AND MOA

A

Dopamine blocker

40
Q

What is the first line treatment for N/V of pregnancy?

A

Doxylamine plus Vitamin B6 (pyridoxine)

A fixed dose formulation is available (Diclectin/Diclegis)

41
Q

What is the most effective drug for prevention and treatment of motion sickness?

A

Scopolamine (Muscarinic antagonist)

42
Q

Which antihistamines are used for N/V? Why?

A

Dramamine, Meclizine, Cyclizine

They block receptors for acetylcholine in addition to receptors for histamine

43
Q

What is the most effective anti-diarrheal agent?

A

Opioids:

Loperamide, Difenoxin, Diphenoxylate

44
Q

Is loperamide potentially dangerous for abuse?

A

No. Does not readily cross the blood brain barrier

45
Q

Which infectious diarrheas DO need to be treated with ABX?

A

Salmonella, Shigella, Campylobacter, Clostridium