Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology II > GI Drugs > Flashcards

GI Drugs Flashcards

1
Q

Name an H2 receptor antagonists

A

ranitidine; famotidine

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

Name a PPI

A

omeprazole

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

List 3 antacids

A

Mg(OH)2; Al(OH)3; CaCO3

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

List some mucosal protective agents

A

sucralfate; bismuth subsalicylate

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

Anti-emetics

A

metoclopramide; ondansetron

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

Stimulant laxative

A

lubiprostone

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

What is a saline laxative

A

Mg(OH)2

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

Antidiarrheal

A

loperamide, alosetron*

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

What is a mesalamine?

A

sulfasalazine

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

List a thiopurine anti-metabolite

A

azathioprine

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

Name a TNF alpha inhibitor

A

infliximab

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

What is the MOA of H2 blockers?

A

Directly block histamine-stimulated gastric acid
secretion – H2 receptor blockers
Blunt parietal cell responses to ACh and gastrin

Very low toxicity – but reduce dose in _renal dysfunction _

*CROSSES PLACENTA

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

What are H2 blockers proven to prevent?

A

gastric and duodenal ulcers
GERD

*can use as prophylaxis for NSAID induced ulcers (better for duodenal)

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

What is the MOA of PPIs?

A

Irreversible inhibition of parietal cell proton pump
(H+/K+-ATPase) results in prolonged (90-98%) inhibition
of gastric acid secretion

The weak base accumulates in parietal cell
canaliculus, then protonated form of drug binds
covalently to enzyme. PPIs are acid labile, so need
enteric coating to get past stomach

Only work with acid secretion

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

True/false: PPIs are administered as prodrugs.

A

True

In order to get through stomach to be absorbed in the intestine. ITs a base, absorbed in the parietal cell; once it crosses over to canaliculi of parietal cell (acidic) becomes protonated and doesn’t come out

*Has a short 1/2 life but effects long term. *

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

What is the effect of PPIs vs. H2 blockers on acid secretion during the day?

A

Note excellent control of nocturnal acid (less Ach/gastrin) for both H2 block and PPI, but PPI much better during the day

H2 is good nocturnally

17
Q

What are PPIs proven to have efficacy for, and what are they a DOC for?

A

Efficacy proven in ulcers and GERD

First choice in Zollinger-Ellison syndrome

18
Q

What is the MOA of antacids?

A

Weak bases that are poorly absorbed (so stay in GI lumen) and directly neutralize stomach acid

Good for occasional heartburn –
but for long term use compliance is not
as good as for H2 blockers or
omeprazole

19
Q

What are some DIs to be concerned about for antacids?

A

Antacids can increase or decrease the
absorption of many classes of drugs

Al(OH)3 or CaCO3: Decreased absorption
of tetracycline, isoniazid, ketoconazole, etc

Increase in urinary pH alters
elimination of *acidic (e.g., salicylates)
and basic (e.g., quinidine) drugs *

20
Q

How do you treat H. Pylori infection?

A

Treatment: usually a PPI plus several antibiotics

21
Q

True/false: you can administer sucralfate with other antacids.

A

FALSE

22
Q

How does sucralfate work?

A

Forms paste-like gel at low pH that adheres
to positively charged proteins of epithelial cells as well as ulcer craters.

PROBLEM: Can adsorb other drugs – e.g.,
tetracycline, phenytoin, digoxin – _wait 2 hrs
before admin of sucralfate_

23
Q

How does Pepto bismol work?

A

Binds selectively to ulcers to protect against acid and pepsin

CAUTION: Blackens stool/tongue

24
Q

How does metoclopramide work as an antiemetic?

A

Central CNS: 5-HT4 receptor agonist; 5-HT3 receptor antagonist (vagal/CNS), also D2

Blocking stimulus to the brain, tries to keep things going in one direction . . .
Enhances ACh release in myenteric plexus and
improved tone in esophageal sphincter

Used for chemotherapy-induced nausea and
vomiting

25
Q

What is an adverse effect of metoclopramide?

A

Adverse: Dopamine D2 receptor antagonist activity
that can cause extrapyramidal (Parkinsonism-like)
symptoms and tardive dyskinesia

** 2009 FDA black box warning: long term use can
result in irreversible muscle spasms (dyskinesia)**

26
Q

How does odansetron work?

A

Selective 5-HT3 receptor antagonist- effective when
administered prior to chemotherapy or surgery.

****has little or no effects on
muscarinic or dopaminergic receptors. **

27
Q

True/false: lubiprostone is approved for chronic constipation use.

A

TRUE

28
Q

What is the MOA of luboprostone?

A

**Cl channel activator: **increases intestinal fluid secretion, results in increased number of bowel movements

Recall that Cl moves out into GI lumen and takes water with it.

TYPE C for PREGNANCY

29
Q

What is an example of a saline laxative?

A

** Mg(OH)2**

hypertonic solution, osmotic pressure leads to
accumulation of fluids in GI tract and
stimulation of peristalsis

Cathartic dose leads to complete
evacuation in less than 3 hours (e.g., for
colonoscopy prep)

30
Q

What is the prototype anti-diarrheal agent?

A

Loperamide
Opioids with low abuse potential because they are very poorly absorbed from the GI

Slows intestinal transit time due to
stimulation of mu opioid receptors in
intestinal smooth muscle

Adverse: toxic megacolon, CNS tox (less with lop)

Avoid in patients with ulcerative colitis or acute
bacillary or amoebic dysentery

31
Q

What do you treat IBS-D with?

A

• Loperamide

• Restricted Use Drug: If standard therapies fail, the
5-HT3 receptor antagonist alosetron is FDA approved
for women with diarrhea-predominant IBS
Mech: _decreased colonic motility via enteric and CNS
blockade of 5-HT3 receptors._

_**AR: ischemic colitis_

32
Q

What do you use to treat IBS-C?

A

Mg(OH)2

33
Q

How do you treat active IBD?

A

Both ulcerative colitis and Crohn’s disease:
• Glucocorticoids (prednisone) t_o rapidly reduce
ulceration and cause initial remission _

• Long term therapy: immunosuppressives
including purine anti-metabolites azathioprine
or 6-mercaptopurine, takes several months for full effect

Adverse: bone marrow
suppression, rashes, fever, nausea

34
Q

What is a first line tx for ulcerative colitis?

A

sulfasalazine
• Mech: interferes with intermediates in
inflammatory pathways – topical 5-ASA
(onto intestinal wall) is effective, _not
systemic_5-ASA

Adverse: up to 40% of pts cannot tolerate.

35
Q

What is infliximab used for?

A

Crohn’s disease

_Immunosuppresant: antibody to TNF-alpha. Binds to TNF-alpha to block
its inflammatory effects at TNF receptors._

Also approved for ulcerative colitis
– Adverse: increased infections

36
Q

What are the stimuli for acid secretion?

A

Stimulus: food (esp peptides), vagus (stretch receptor, release ACh to stimulate gastrin release), direct stimulation of G cells stimulate gastrin release . . . gastrin stimulates histamine and parietal cells >> HCl

37
Q

Pathways for acid secretion

A

Gastrin and ACH work through a calcium dependent pathway (could use a muscarinic antagonist, but not preferable)

Histamine works through H2 receptors (cyclic AMP pathway)

H/K ATP ase >> HCL

38
Q

Antacids causing diarrhea/constipation

A

MgOH diarrhea producing

Al- constipation

Pharmacology II (7 decks)

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