Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phar 301 > Drugs for GI disorders > Flashcards

Drugs for GI disorders Flashcards

1
Q

True/False? The human immune system accounts for the gut microbiome

A

True/False? The human immune system accounts for the gut microbiome

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

True/False? Modern antibiotics do not disrupt the “helpful” bacteria in our microbiome

A

True/False? Modern antibiotics do not disrupt the “helpful” bacteria in our microbiome

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

What drugs treat Peptic Ulcer disease?

A

PPIs, H2 Receptor antagonists, sucralfate, misoprostol, microbial agents to eradicate Helicobacter pylori

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

What drugs treat Gasteresophageal reflux disease?

A

PPIs, H2, receptor antagonists, antacids, metoclopramide

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

What class of drugs treat delayed gastric emptying?

A

Promotility agents

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

What class of drugs treat Constipation?

A

Laxatives

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

What class of drugs treat Diarrhea?

A

Antidiarrheals (duh)

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

What drugs treat irritable bowel disease?

A

Aminosalicylates, TNF-alpha antibodies, immunosuppressants, corticosteroids

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

What is the primary symptom of Peptic Ulcer Disease?

A

Excess acid production or decreased barrier function, which can overwhelm defense mechanisms and allow ulcers to form in varous areas of GIT

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

Where does PUD affect?

A

Upper GIT (stomach, duodenum, lower esophagus)

Wherever the mucosal epithelium can be exposed to acid and pepsin

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

What are the contributing factors of PUD?

A

Helicobacter pylori infection

Nonsteroidal antiinflammatory drugs (NSIDS)

Stress, (esp. in patients with chronic illness)

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

What is the first line treatment for PUD? What happens if the patient has H. pylori infections?

A

Proton pump inhibitors (PPIs)

Patients with H. pylori infections require antimicrobial agents to prevent relapse

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

What is gastroesophageal reflux disease (GERD)?

A

Dysfunctional relaxation of the lower esophageal sphincter that allows the acidic gastric contents to reflux into the esophagus

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

What can GERD lead to?

A

Inflammation, ulcerations, bleeding, possibly Barrett esophagus

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

How is GERD treated commonly?

A

PPIs, H2 histamine receptor antagonists, DA antagonists (increase the tone of the lower esophageal sphincter)

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

True/False? Since COX-1 inhibitors can lead to gastric ulcers, COX-2 inhibitors (such as celecoxib) are prescribed as they are safer

A

True/False? Since COX-1 inhibitors can lead to gastric ulcers, COX-2 inhibitors (such as celecoxib) are prescribed as they are safer

They carry a lower risk of ulcer formation than nonselective NSAIDS but they appear to be associated with an increase in heart attack/stroke

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

What is Omeprazole and what does it do?

A

Proton pump inhibitor, inhibits the parietal cell H+K+-ATPase preventing the pump from functioning

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

What is the advantage of Omeprazole (and any other PPI)?

A

Nonspecificity - will reduce acid secretion independently of how secretion is stimulated

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

Why does Omeprazole accumulate in parietal cells?

A

Because of its pKa

Parietal cells are acidic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

True/False? Omeprazole is a prodrug that is converted to its active form by an enzyme in the parietal cell

A

True/False? Omeprazole is a prodrug that is converted to its active form by an enzyme in the parietal cell

It is converted by acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Does Omeprazole bind to enzymes temporarily?

A

No, covalently and irreversibly modifies the enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Which is superior for NSAID-associated damage prevention, PPIs or H2 receptor agonists?

A

PPIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Esomeprazole?

A

S enantiomer of Omeprazole, much more effective

Higher bioavailability because of lower first-pass metabolism than R isomer

24
Q

What effects do prostaglandins exert to the GI system?

A

Cytoprotection and decreased acid secretion (among others)

25
Q

Can Prostaglanin analogs such as misoprostol be used to prevent NSAID-induced damage?

A

Yes but not used first-line

26
Q

What are antacids what do they do?

A

Inorganic bases that neutrolize hydrochloric acid

27
Q

What are the effects of Magnesium and Aluminum on digestion, respectively?

A

Magnesium: Laxative effect

Aluminum: constipating effect

28
Q

What is Sucralfate?

A

Protective agent
Aluminum salt of sucrose octasulfate

29
Q

What does sucralfate do?

A

Binds electrostatically to positively charged tissue proteins and mucin within the ulcer crater to form a viscous barrier

prevents further damage from acid/pepsin

also binds bile salts/stimulates production of mucosal prostaglandins

30
Q

Does Sucralfate affect gastric acid secretion?

A

no

31
Q

When is Sucralfate used?

A

As an alternative to PPIs or H2 antagonists to promote healing of ulcers

32
Q

What do dopamine receptor antagonists such as metoclopramide do?

A

Promote motility by affecting different GI receptors

Increases tone of Lower esophageal sphincter (GERD)

Increases force of gastric contractions

Antiemetic agent

33
Q

What is the primary symptom of constipation?

A

Abnormally difficult passage of hard/infrequent stools

34
Q

What are some of the causes of constipation?

A

Diet

Pregnancy

drugs (opioids, Al-containing antacids, Iron)

GI, metabolic, or neurological disorders

35
Q

What is the ideal treatment of constipation?

What medication can help if this ideal treatment is insufficient?

A

Dietary and lifestyle change (inc. fluid/fibre intake, physical exercise)

Often a laxative is necessary

36
Q

What are the 6 types of laxatives?

A
  1. Bulk-forming laxatives
  2. Emollients
  3. Lubricants
  4. Saline laxatives
  5. Hyperosmolar agents
  6. Stimulant laxatives
37
Q

What are the characteristics of bulk-forming laxatives?

A

Nonabsorbable cellulose-like materials that remove dietary fibre

They hydrate in the presence of water and swell into a pliable soft mass that activates the defecation reflex (reduces intestinal transit time)

Can have a paradoxical antidiarrheal effect resulting from their ability to bind excess water

38
Q

What are the characteristics of emollients?

A

Ionic detergents that soften feces and permit easier defecation by lowering the surface tension and permitting water to interact more effectively with the solid stool

The most commonly used agent in this category is docusate sodium

39
Q

What are the characteristics of Lubricants?

A

Oral nonabsorbable laxatives that act by lubricating the stool to facilitate passage.

  • They may also act on the colonic epithelium to reduce water passage*
  • eg mineral oil*
40
Q

What are the characteristics of Saline Laxatives?

A

inorganic salts with poorly absorbed cations such as magnesium, or anions such as sulfate or phosphate

Draw water into the intestine by osmotic means, resulting in increased GI propulsion/evacuation

Because of appreciable amounts of Mg may be absorbed, these should be avoided in patients wihth renal insufficiency

41
Q

What are the characteristics of Hyperosmolar agents?

A

Hyperosmolar agents increase intestinal content osmolarity, leading to accumulation of fluid in the colon

Abdominal bloating and flatulence are common side effects as lactulose and sorbitol are poorly absorbed and undergo bacterial fermentation into organic acids and CO2

42
Q

What is the most common hyperosmolar laxative?

A

Polyethylene Glycol (PEG)

poorly absorbed by gut but not metabolised by colonic bacteria

43
Q

What are the characteristics of stimulant laxatives?

A

Anthraquinones are converted by colonic bacteria to their active form

Act on the intestinal epithelium to increase fluid accumulation and contraction

44
Q

What causes Trafellers’ Diarrhea?

A

Enterotoxgenic E. coli (ETEC)

45
Q

How does misoprostol treat severe constipation?

A

By binding to prostanoid receptors 4 on epithelial cells, which triggers a GPCR (increases cAMP)

46
Q

How does Linaclotide function?

A

Mimics the action of endogenous guanylin and uroguanylin, bot guanylate cyclase type C (GC-C) receptor ligand

Increases the flow of electrolytes and water int o the lumen of the GI tract

cGMP into the serosa leads to a reduction in visceral hyperalgesia

Used to treat irritable bowel syndrome with constipation and chronic constipation with no known cause

47
Q

How do opioid antagonists function?

A

Act on enteric neurons to decrease secretion and promote fluid reabsorption from the lumen

Decrease motility resulting in slowed transit through GI tract, allowing greater time for fluid absorption (drier fecal mass)

Can be used as analgesics which would cause constipation

Used to prevent Opioid induced constipation

48
Q

True/False? Opioid Antagonists cross the blood brain barrier

A

True/False? Opioid Antagonists cross the blood brain barrier

49
Q

What is Loperamie and how does it function?

A

Opioid agonist

Specific antidiarrheal agent that does not cross BBB

Antisecretory effect on GIT mediated via mu-opioid receptors

At high doses, decreases motility via mu opioid receptor in myenteric plexa of bowel

50
Q

Should you use Loperamide in the symptomatic treatment of diarrhea caused by enteric organisms such as Shigella and enterohemorragic E. coli or for C. difficile infection?

A

NO

Can be made worse

51
Q

What are the two main manifestations of Inflammatory bowel disease?

A

Ulcerative colitis and Crohn’s disease?

52
Q

What does the current treatment of IBD consist of?

A

Sulfasalazine and Mesalazine

53
Q

What is Mesalamine/Mesalazine? How do they work?

What is Sulfasalazine? How does that work?

A

Unconjugated 5-aminosalicylates (5-ACA)

Rapidly absorbed in jejunum (only 20% reach terminal ileum and colon)

Sulfasalazine is a prodrug that gets converted into mesalazine and sulfapyridine by gut bacteria

Prevents first pass so more drug gets into colon

54
Q

How can glucocorticoids help treat IBD?

A

Illeal-release budesonide in CD and colonic-release budesonide MMX in UC are effective induciton agents

Second generation coritcosteroids have a better safety and tolerability profile

Long term corticosteroid use is not recommended

55
Q
A

Phar 301 (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions