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PT1 B3 > Lecture 76, 77 -- GI Pharmacology > Flashcards

Lecture 76, 77 -- GI Pharmacology Flashcards

1
Q

name three classes of drugs that effect GI acidity

A

Antacids

H2 antagonists

Proton pump inhibitors

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2
Q

Common indications for acid lower medications

A

GERD
Peptic Ulcer Disease
H pylori
Ibuprofen causing ulcers; typically in the elderly

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3
Q

Describe the Physiology of Acid Secretion…
what is the neural stimulation, endocrine stimulation, and paracrine stimulus?

what cells are involved ?

what is the primary stimulus for acid secretion?

Describe cellular interplay

what is an inhibitor of gastrin? what cell mediates this?

A

1) Neural Stimulation via the Vagus Nerve
2) Endocrine stimulation via Gastrin
3) Paracrine stimulation by histamine release Entero-Chromaffin - Like Cells (ECL)

Parietal Cells - Secretion of H+ in respnse to Histamine
Enterochromaffin Cells – release histamine in response to Gastrin and ACH

G cells – release gastrin to stimulate histmine release from parietal cells

Vagal Nerve — release ACH to stimulate histamine release from parietal cells

THE PRIMARY STIMULUS OF ACID RELEASE IS HISTAMINE SECRETION BY ECL

D cells – secrete somatostatin; an inhibitor of gastrin

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4
Q

Antacids —
Names:

Mechanism

Clinical uses

A

Names: Sodium bicarb, Mg Hydroxde, Alum Hydroxde, Calcium Carbonate

direct acid neutralization in the lumen

occasional GERD, dyspepsia
Useful if determining if CP is related to acid reflux

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5
Q

What different chemical compositions are used and what are the different associated side effects?

A

Sodium Bicarb – systemc alkalosis in renal insuffiency

Mg Hydroxide – osmotic diarrhea

Aluminant hydroxide – constipation, hypophosph

CaCO3 – hypercalcemia, kidney stones

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6
Q

Proton Pump Inhibitors –

Names

Mechanism / Pharmacokinetics

Clinical uses:

A

Names: Omeprazole, Esomeprazole, Pantoprazole

mechanism: directly block parietal cell H/K ATPases of the parietal cells
but first Require conversion to sulfenamide intermediate which forms a an inhibitor complex with the H/K ATPase. This is ultimated degraded

Clinical use:
Primary Rx: PUD, GERD, Reflux Esophagitis, H Pylor (PPI + amoxacillin + azithromycin), Zollinger Ellison Syndrome

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7
Q

PPI -

Side effects – what are (hospitalized) patients more susceptible to?

A

Side effects: Well tolerated;

But can cause: HA, N, Diarrhea, flatulence

Metabolized by p450s

Reduced stomach acid makes it easier for infectious agents to act – Salmonella, C diff, traveler’s diarrhea

Increased risk of bone fracture but no increased risk of bone density

Increased risk of aspiration pneumonia in hospitalized patients (eg lower stomach acid, more germs in the stomach)

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8
Q

H2 Blockers -

Names:

Mechanism:

Clinical uses

A

names: Cimetidine, Ranitidine (zantac), Pamotidine (Pepcid)

Mechanism: Prevent histamine induced activation of acid release from parietal cells by blocking H2 receptor

Indications: GERD, Dyspepsia, PUP
Stress Ulcer Prophylaxis –

Zollinger Ellison syndrome

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9
Q

H2 Blockers -

side effects:
overall –
specific side effects of which 1 drug …

A

Side Effects: Virtually None

Cimetidine – inhibits cytochrome p450 system; interfering with other drugs

Anti-androgenic – some gynocomastia, impotence, decreased libido

Crosses BBB -Confusion in the elderly

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10
Q

what is zollinerger Ellison Syndrome?

what drugs can be used to treat it?

A

H2 Blockers, PPIs

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11
Q

Mucosal Protectants — 3 drugs

A

Bismuth salts (pepto bismol)

Sucralfate (keraphate)

Misoprostol

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12
Q

Bismuth salts

    • mechanism:
    • Clinical Uses:
  • -Side effects
A
    • mechanism: ‘Coats’ ulcers + inflamed areas;
    • Clinical Uses: Gastroenteritis, helps with Nasuea, diarrhea, dyspepsia

–Side effects: black tongue and feces, interaction with anticoagulants

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13
Q

Sucralfate

  • – mechanism
    • when should it be taken?
  • –Clinical Uses –
A

forms a ‘gel-like’ material on ulcers and protects them from actions of acid and digestive enzymes

should be taken ante cebum (before meals)

Clinical USes:
Stress ulcer prophylaxis

Bile reflux gastritis

esophageal ulcers

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14
Q

Misoprostol

  • class of drug ?
    • mechanism?
    • Side effects?
A

Prostaglandin E1 analog stimulates mucopolysaccharide production, decreases acid secretion,

Side effects: caution - induces labor

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15
Q

DRUGS AFFECTING GI MOTILITY

3 classes of drugs

A

Antibiotics: (macrolides)

Cholinomimetics

Dopamine Receptor Antagonists

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16
Q

abx – which abx is used to promote GI motility?

  • mechanism?
  • side effects ?
A

Erythromycin

Activate motilin receptors on smooth muscle

Side effcts: QT prolongation and increased risk for Torsade de Pointes

Not used often clinically

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17
Q

Cholinomimetics
- name a couple drugs

  • mechanism ?
  • side effects

what specific syndrome is treated with IV neostigmine

A

Bethanechol, neostigmine

Mechanism: ACH receptors; potently increase GI motility

Side effects: SLUDGE -- hypersalviation, lacrimation, defacation, N/V

Clinical uses: IV neostigmine is great for Ogilvie’s Syndrome

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18
Q

Dopamine Receptor Antagonists:

name a few drugs

mechanism / effects

side effects

A

Metoclopramide, Domperidone

	○ Increased gastric tone/pressure
	○ Improved antroduodenal coordination
	○ Accelerated gastric emptying

Side effects: Parkinsoninan effects Tardive dyskenesias, dystonia, neuropleptic malignant syndrome

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19
Q

name 5 classes of laxatives:

A

• Fiber/Bulk Formers -

* Osmotic:  
* Stimulant/irritant:
* Stool Softeners:    
* Cl- Channel Secretion:
20
Q

• Fiber/Bulk Formers

  • name some drugs
  • how do they work?
A

psyllium (METAMUCIL

Bulk laxatives” - form gels in the colon causing water retention and distension –> increased peristalsis

21
Q

• Osmotic: laxatives

  • name some drugs
    how do they work?
A

Milk of Magnesia, polyethylene glycol, lactulose

		§ Draw H2O into the intestinal lumen via osmosis resulting in softer/liquid stools and distension induced peristalsis
22
Q

• Stimulant/irritant:

  • name some drugs
  • how do they work
A

• Bisacodyl (e.g., Dulcolax), Senna

§ Stimulates colonic smooth muscle and causes H2O accumulation in lumen; exact mechanisms unclear

23
Q

• Stool Softeners:
- name some

  • mechanism
A

docusate (Colace) – causes fat/H2O to mix and soften the stool

Lubricant – mineral oil softens stools, prevents H2O absorption

24
Q

• Cl- Channel Secretion as laxative

  • name the drug

mechanism

A

○ Lubiprostone (Amitiza) –
§ Mechansims similar to Cholera Toxin – activates ClC-2 chloride channels causing chloride secretion, sodium follows to maintain isoelectric equilibrium, water follows sodium (paracellular)

25
Q

Anti-Diarrhea: name three classes of drugs:

In general when should you not give any anti-diarrheal treatment? what bugs specifically ?

A
  • Antimotility Agents
    • Adsorbents
    • Antisecretory

Do not give in the setting of bacterial infection or inflammation
§ Can possibly result in toxic megacolon –
□ C. difficile, Entamoeba, E. coli 0157:H7,

26
Q

• Antimotility Agents for diarrhea treatment

  • drugs?
  • mechanism?
  • side effect/caution:
A

• Drugs: Loperamide (Immodium), Diphenoxylate-atropine, Tincture of opium

§ Mechanism: act via the opiate receptor to inhibit peristalsis

27
Q

• Adsorbents as anti-diarrheals

  • name a few drugs (several different sub-types); describe their general mechanism

when should you not use the “salicylate” drug?

adverse effect of bile acid and how should be managed?

A

Bismuth subsalicylate —
do not use when patients are taking ASA
Watch out for Reye’s Syndrome in children

Fiber – acts a bulking agent absorbing intraluminal water

Bile Acid Binding Resins: Cholestyramine — nonabsorbable complex with bile acids in the intestines, preventing them from stimulating colonic mucosa to secrete electrolytes and fluid

		• Separate cholestyramine from other medications by at least 2 hours because it can inhibit drug absorption
28
Q

Antisecretory agent as anti-diarrheal

name the drug

how does it work

A

Octreotide (somatostatin analog),

		§ Reduces fluid and electrolyte secretion by stomach and pancreas
		§ Mild antimotility effect
		§ Promotes intestinal electrolyte absorption
29
Q

Describe the pathogenesis of nausea and emesis?

what can induce nausea/emesis ?

what is an important area of the brain

what neurotransmitters are involved

A

Noxious smells/taste, Motion sickness, Gastric Irritants, Emetogenic drugs,

Nuerotransmitters – Serotonin (5HT3) and Dopamine (DA)

Area postrema

30
Q

name 6 classes of drugs that can treat nausea and vomiting

name some drugs in each class

some side effects of each

A

Anticholinergic: scopolamine — SLUDGE

Antihistamine: meclizine, dimenhydrinate (dramamine) — Sedation/drowziness

DA-antagonist: prochlorperazine (compazine), promethazine (phenergan) --- 
Extrapyramidal symptoms (parkinsonian effects, tardive dyskinesia, QT prolongation)

5-HT3 -antagonist: ondansetron (Zofran) — QT prolongation

Cannabinoid: dronabinol – paranoia, CNS depression

Neurokinin antagonist: aprepitant — hiccups, fatigue, infection

31
Q

which anti emetics are best for:

1) Migraine-related nausea
2) Motion sickness

A

Migraines: DA-antagonists (compazine) 5-HT3 -antagonists (zofran)

Anticholinergics (scopalamine), antihistiamine (dramamine)

32
Q

which anti emetics are best for: Chemotherapy-induced N/V

A

5-HT3 –antagonists, corticosteroids, NK antagonists

Others: cannabinoids,

33
Q

which anti emetics are best for

Postoperative N/V

Hyperemesis gravidarum

A

DA antagonists, 5-HT3 –antagonists, NK antagonists

Ginger, antihistamines, DA antagonists, 5-HT3 -antagonists

34
Q

what two diseases fall under the umbrella of Inflammatory bowel disease –

in general what are these diseases ?

A

Crohn’s and Ulcerative Colitis – auto-immune mediate chronic inflammatory conditions of the gut

35
Q

what 4 classes of drugs are used to treat/manage IBD?

A

Aminosalicylates –

Glucocorticoids

Immunomodulators

Biologics — anti TNF alpha, Anti integrin

36
Q

Aminosalicylates as anti-inflammatory for IBD

what is the prodrug?
what is the active agent?
how is it actiavted ?

which IBDs is it used for?
is it used for maintance or induction?

side effects?

A

Sulfasalazine: prodrug

Active Agent: 5-aminosalicylate — used for maintenance and induction

activated by bacteria in tehcolon

used for UC and CD

Side effects: GI, CNS, hematologic side effects

37
Q

Glucocorticoids as anti-inflammatory for IBD

what are some convetional gc?

what is non convetional gc? how is it different?

when are they used?

how are the drugs stopped? why?

side effects?

A

• Conventional Glucocorticoids: Prednisone, methylprednisolone

Budesonide – non systemic GC; controlled release in the ileum and R colon

short-term induction therapy, not a chronic maintenance agent

requires taper when stopping the drug to avoid secondary adrenal insufficiency

Side effects: MANY
fat, moon facies, bursing, muscle wasting, osteoporosis, etc

38
Q

Immunomodulators as anti-inflammatory for IBD

2 drugs —

A

6-mercaptopurine (6MP)/azathioprine (AZA) -

Methotrexate —

39
Q

6-mercaptopurine (6MP)/azathioprine (AZA) - as Immunomodulators as anti-inflammatory for IBD

how is it used for managment of IBD?

which is the prodrug? which is the active agent?

whats important about the metabolism ? what tests should be run regarding prediction of toxicity?

with what drug should this not be combined?

toxicities:

A

AZA – prodrug converted to 6 MP

6MP – eventually metabolized to 6 TGN

Metabolism – 6MP can be converted to some inactive agents via other enzymes (TPMT and Xanthine Oxidase)

test for TPMT – otherwise shuinted towrads to the active 6 TGN and have high levels of myelosuppression

do not combine with allopurinol (xanthine oxidase inhibitor) – or else the drug is shunted towars 6 TGN and increses toxicity

toxic: Leukopenia, thrombocytopenia, bone marrow suppression; incresaed risk of malignancy, infection

used for maintanence of remission of UC and Crohn’s; not for induction

40
Q

• Methotrexate — as Immunomodulators as anti-inflammatory for IBD

mechanism:

clinical uses in regards to UC and CD

A

nhibition of dihydrofolate reductase

□ Clinical use: effective in Maintenance of Remission in CD

• Adverse effects : Hepatotoxicty, myelosuppresion, Interstiital lung idsease (always CXR Before medication)

□ Admin with Folic acid supplementation

Adverse: Teratogenic,

41
Q

Name three Monoclonal antibodies against TNF alpha

which are used for CD, which are used for UC, which are used for both?

side effects

A
  • Infliximab – CD and UC
    * Adalimumab == Cd and UC
    * Certolizumab pegol == CD not UC
side effects: 
Infection
Myelosuppression
inreased risk of malignancy 
Psoriasis, lupus,
42
Q

name two Anti-Integrins monoclonal antibodies:

mechanism/effect?

A
  • Natalizumab and Vedolizumab

* Blocks leukocyte migration from blood vessels to sites of inflammation

43
Q

important side effect of Natalizumab

A
  • Vedolizumab: gut-specific
    * Natalizumab: increased risk of progressive multifocal leukoencephalopathy (PML — resulting from the reactivation of JC virus — high morbidity)
44
Q

Which drugs are used as induction therapy for IBD?

A
  • 5-ASA
    * Glucocorticoids
    * Biologics
45
Q

which drugs are used as maintenacne therapy for IBD?

A
  • 5-ASA
    * 6-MP/AZA
    * Methotrexate

Biologic

PT1 B3 (16 decks)

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