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Medical Pharmacology Exam 3 > GI Drugs I and II > Flashcards

GI Drugs I and II Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the stomach cell type that secretes acid? What are the 3 stimulants of acid secretion?

A

Parietal cells
Ach
gastrin
histamine

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2
Q

What are the 3 major stimuli for acid secretion and their receptors?

A

Ach - M3 receptors
gastrin - CCK2 receptors
histamine - H2 receptors

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3
Q

What are the two secretions of the stomach epithelia?

A

Mucus

Bicarbonate

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4
Q

An important step in the formation of stomach acid is H2CO3 formation. What is the enzyme responsible?

A

Carbonic anhydrase

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5
Q

What are the 3 ion transporters involved in gastric acid secretion?

A

H+ / K+ antiporter
K+ Cl- symporter
HCO3 / Cl antiporter

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6
Q

Of the 3 major stimulants for the secretion of gastric acid, which are Ca++ dependent and which are cAMP dependent?

A

Gastrin and Ach - Ca++ dependent

Histamine - cAMP

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7
Q

Regarding cephalic stimulated acid response, what nerve is involved and what and where is the target cell?

A

Vagus nerve

Enterochromaffin cell in stomach fundus

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8
Q

What is the neurotransmitter used by enterochrommafin like cells to stmulate acid secretion from parietal cells? What is the target receptor on the parietal cells? This release is [ fast and short / slow and prolonged ]?

A

Histamine
H2 receptors
Slow and prolonged

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9
Q

Slow and prolonged release of acid from parietal cells is produced by stimulation of _ receptor. Rapid release of acid is produced by stimulation of _ receptor. What is the stimulus for the rapid response?

A

H2
M3
Vagus nerve Ach

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10
Q

In addition to the vagus nerve stimulating enterochrommafin like cells to produce acid, what cell type can also stimulate enterochrommafin like cells? What is their target receptor? Where are they located?

A

G cells
CCK2 receptor
Antrum of stomach

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11
Q

Prostaglandins are [protective / non-protective] of the intestinal mucosa. What is the mechanism (2)?

A

Protective

  • Activate Gi GPCRs to inhibit cAMP to decrease acid
  • Increase secretion of mucus and bicarbonate
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12
Q

If prostaglandins downregulate the cAMP dependent acid production, which of the 3 main stimulants of acid secretion is affected by this? (histamine, gastrin, acetylcholine)

A

Histamine - H2 receptor effects is cAMP dependent

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13
Q

What are the 3 examples of proton pump inhibitors provided? What is their mechanism?

A

Omeprazole, esomeprazole and lansoprazole

Covalently bind and irreversibly inhibit H+/K+ ATPase

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14
Q

Proton pump inhibitors are the first line treatment for hyperacidity and ulcers. If they only work for 2 hours, why are they only used 2 times a day?

A

Because of slow turnover of the H+/K+ ATPase at apical surface

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15
Q

What is the acid requirement for proton pump inhibitors?

A

All PPIs are prodrugs, require acid to be activated inot their active forms

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16
Q

How do proton pump inhibitors reach their targets in the parietal cells?

A
  • Absorbed as high pH form into blood

- Enter parietal cell and is activated / trapped

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17
Q

GERD, erosive esophagitis, peptic ulcers and NSAID induced gastric ulcers can all be treated with _

A

proton pump inhibitors

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18
Q

What is Zollinger - Ellison syndrome? How is it treated?

A

Gastrin secreting tumor from pancreas or intestine

proton pump inhibitor

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19
Q

What is the percentage of acid that can be reduced using proton pump inhibitors? Why does the treatment require 2-5 days to work?

A

Up to 90% reduction in stomach acid

Only active proton pumps (small percentage) react with PPIs

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20
Q

How are PPIs cleared from circulation?

A

Through the liver

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21
Q

How does hepatic failure affect PPIs?

A

Reduced clearance of the PPIs

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22
Q

Serum concentration of what drug is increased following PPI use? Activation of what drug is decreased?

A

Warfarin serum concentrations increased

Reduced activation of clopidogrel

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23
Q

What can happen with suddenly stopping the use to PPIs?

A

Rebound hypergastrinemia and gastritis

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24
Q

Which is more powerful in reducing acid secretion, H2 antagonists or PPIs? What cell is the source of the histamine antagonized by H2 receptor blockers?

A

PPIs (90%), H2 blockers (70%) reduction

enterochrommafin like cells

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25
Q

How are H2 receptor blockers excreted?

A

renal organic cation system

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26
Q

What are the 3 examples of H2 receptor antagonists provided? What are their durations of action?

A

Cimetidine 4-5 hrs
Ranitidine 6-8 hrs
Famotidine 10 - 12 hrs

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27
Q

What is the effect of long term use on testosterone? On estradiol? 3 effects in men?

A 
Reduced testosterone binding to receptor
Hydroxylation of estradiol in women (galactorrhea)
-reduced sperm count
-impotence
-gynecomastia
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28
Q

What is the effect of H2 blockers on pepsin and intrinsic factor? How long till tolerance occurs?

A

Reduced pepsin and IF

3 days

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29
Q

What is misoprostol? What is it used for? What 2 agents are preferred to misoprotol for this use?

A

Synthetic analog of PGE1
Used to prevent NSAID induced injury
PPIs and H2 antagonists

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30
Q

What 2 populations should not use misoprostol?

A 
Inflammatory bowel disease patients
Pregnant patients (can increase uterine contractions)
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31
Q

What is sucralfate? How does it work?

A

An octasulfate of sucrose

Forms sticky polymer coating that swells and covers epithelium at neutral pH

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32
Q

What is the use of sucralfate? What types of drugs should be avoided when using sucralfate? Why?

A

Stress ulcers

PPIs, H2 blockers - activated by acid

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33
Q

What is the main side effect of sucralfate? What is its effect on absorption?

A

Constipation

Can reduce absorption of other drugs

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34
Q

How do antacids work? What are the 3 examples provided?

A

Simple neutralize stomach acid
Aluminum hydroxide
Magnesium hydroxide
Calcium carbonate

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35
Q

What is the difference between aluminum and magnesium hydroxide?

A

Al - Slower acting, delays gastric emptying

Mg - faster acting, enhances motility

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36
Q

What drug interaction is likely with aluminum hydroxide?

A

Binds up tetracyclines

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37
Q

What is a side effect observed with use of Mg-trisilicate?

A

Silica is absorbed and can form renal stones

38
Q

What group of patients should not use Mg containing drugs?

A

Patients with renal disease

39
Q

What is the muscarinic antagonist that is used for the treatment of GI symptoms? What is its mechanism? What is the target receptor?

A

Pirenzepine
Blocks transmission of vagal nerve in stomach wall, less ECL and parietal cell stimulation
M1 receptor specific

40
Q

How much reduction in acid production from muscarinic antagonists? What are side effects associated with these drugs? How often are these drugs used?

A

40 - 50 % reduction
Severe anticholinergic effects
Rarely used

41
Q

True or false: Majority of H pylori infections cause disease?

A

False, only 1/3 of infections are pathogenic

42
Q

What is the toxin that confers pathogenicity to H Pylori?

A

Vacuolating endotoxin A

43
Q

What are the 3 components of H pylori treatment?

A

Acid reduction
Antibacterial
Cytoprotection

44
Q

What is the major network of nerves that govern GI motility? Between what 2 structures is it located?

A

Myenteric plexus

Longitudinal and circular GI muscles

45
Q

In addition to histamine, what other neurotransmitter is released by the stimulation of enterochrommafin like cells?

A

Serotonin

46
Q

Following serotonin release and stimulation of primary afferent neurons, local reflex pathways are activated. These reflex pathways cause [relaxation/contraction] orally and [relaxation/contraction] anally?

A

Orally - Contraction

Anally - Relaxation

47
Q

What is the major use of bethanechol? What is its mechanism? What is the general characteristic of associated side effects?

A

Increases urination in post surgical patients
Selective activation of M2 and M3 receptors
Cholinergic - bradycardia, diarrhea, cramps, salivation, etc

48
Q

What is the major treatment for ileus? What is its mechanism?

A

Neostigmine methylsulfate

Acetylcholinesterase inhibitor

49
Q

What is metoclopramide? Why does it work in promoting motility?

A

Dopamine receptor antagonist

Dopamine usually inhibits Ach, these drugs make Ach neurotransmission stronger

50
Q

What is the effect of metoclopramide on GERD? Is it an emetic or antiemetic? Laxative or not?

A

Relieves symptons of GERD, doesn’t promote healing
Antiemetic
Laxative

51
Q

What are the side effects of Long term use of metoclopramide?

A

Parkinson’s like symptoms

Long term - tardive dyskinesias

52
Q

What is the effect of 5HT-4 receptor stimulation? What are the 2 5HT-4 agonists provided? What are their uses?

A
  • Stimulation increases motility
  • Tegaserod - partial agonist - Female IBS
  • Cisapride - full agonist - GERD
53
Q

What is a major consideration with the use of 5HT-4 agonists?

A

Side effects include fatal cardiac arrhythmias

Drugs use restricted by FDA and manufacturers

54
Q

What is motilin? What are the 2 sources?

A

22 amino acid peptide increases motility

Secreted by ECL cells and M cells

55
Q

How are macrolide antibiotics related to motilin? What is the example provided for GI use? What are the uses (4)

A

Imitate motilin
Erthromycin
- Bezoars, ileus, scleroderma and pseudo obstructions

56
Q

A viable alternative to laxatives for most patients is increased _ in the diet?

A

Fiber

57
Q

What are the cathartic non-absorable laxatives provided as examples? (4)

A

Polyethylene glycol
Magnesium hydroxide
Magnesium sulfate
Magnesium citrate

58
Q

What group of patients should not use cathartic non-absorable laxatives (4)

A

Renal insufficiency patients
Cardiac disease patients
Electrolyte abnormality patients
Patients on diuretics

59
Q

What are the 3 sugars that can act as osmotic laxatives?

A

Lactulose
Sorbitol
Mannitol

60
Q

Which of the sugar osmotic laxatives is fermented by colonic bacteria leading to reduced luminal pH and NH4 trapping?

A

Lactulose

61
Q

What are the causes of constipation associated with the use of sugar osmotic laxatives?

A

Constipation from opioids

Constipation from vincristine

62
Q

What is the mechanism by which docusate salts (stool wetting agents) act? What is their effect on defacation frequency?

A

Act as surfactant, mix fatty substances and water in stools

Soften stool, no change in defacation frequency

63
Q

What is the example of irritant laxative provided? What happens during overdose? How can this agent cause gastric irritation (3)?

A

Bisacodyl
With overdose, causes catharsis
- if chewed, mixed with milk or antacids

64
Q

What are the 2 ways castor oil can be used? What is the active component of castor oil?

A

Ricinoleic acid
4 ml - laxative
16 ml - cathartic

65
Q

What is the mechanism by why glycerin works? What is a common route of administration?

A

Increased water retention, stimulates peristalsis and evacuation
Suppositories - BM in 1 hr

66
Q

What are the 3 examples of bulk forming laxatives provided? What is their potential effect on other drugs? What is their potential effect on abdominal obstructions?

A 
Methylcellulose
Psyllium 
Polycarbophil 
Can potentially adsorb other drugs 
Can exacerbate abdominal obstructions
67
Q

While loose watery stools are generally self limiting, what 2 diseases can cause death via loose watery stools?

A

Cholera

Shigellosis

68
Q

What are 2 examples of opioids that can be used as antidiarrheals? How do they differ with regards to CNS effects

A

Diphenoxylate and loperamide

Loperamine doesn’t enter CNS

69
Q

How is diphenoxylate packaged to prevent abuse?

A

Packaged with atropine

70
Q

What is octreotide? What are its uses (4)?

A

Derivative of somatostatin

  • secretory diarrhea of hormone secreting tumors
  • post-surgical gastric dumping syndrome
  • chemotherapy diarrhea
  • Rest pancreas in pancreatitis
71
Q

What is a potential effect of long term use of octreotide?

A

Gallstones

72
Q

What is bismuth subsalicylate? What is the chemically active component?

A

Mix of bismuth and salycylate in magnesium aluminium silicate and oil of wintergreen
- Salicylate is released systemically

73
Q

What are the 2 CNS areas involved in vomiting?

A

CTZ - chemoreceptor trigger zone

Nucleus tractus solitarius of Vagus

74
Q

Among antiemetics, there are 4 examples of 5HT-3 receptor antagonists. What are they? While most are IV and orally administered, which is only available IV? Which has the highest affinity and longest activity?

A

Ondasetron
Granisetron
Dolasetron
Palonosetron (IV only, highest affin., longest activity)

75
Q

What are the 3 dopamine receptor antagonists used as antiemetics? Which is the preferred agent for chemo-induced nausea?

A

Metoclopramide (preferred for chemo- nausea)
Prochlorperazine
Chlorpromazine

76
Q

In addition to use as antiemetics, what is another use of the dopamine receptor antagonists? What receptor is acted on when treating this other condition?

A

Motion sickness

H1 receptor

77
Q

What is a side effect following long term use of the dopamine receptor antagonists? What group of patients are at risk for dissociative dysphoria with these drugs?

A

Parkinson like effects

Psychiatrically normal patients

78
Q

What are the 4 examples of antihistamine antiemetics? What type of emesis are they typically used for? What is another use for these drugs?

A 
Cyclizine
Promethazine
Hydroxyzine
Diphenhydramine
Post-Op emesis
Motion sickness
79
Q

Among the antihistamine antiemetics, which also has anticholinergic effects when used in abdominal cancer patients?

A

Cyclizine

80
Q

Where in the CNS do the antihistamine antiemetics work (2)?

A

Brainstem and vestibular apparatus

81
Q

What was the example of anticholinergic antiemetic provided? What is it used for? Where does it act?

A

Scopolamine
Motion sickness
In the vestibular apparatus

82
Q

What are the 2 examples of emetic provided? Where do they act? What has largely replaced these drugs?

A

Syrup of ipecac and apomorphine
CTZ - chemoreceptor trigger zone
Activated charcoal

83
Q

What is similar between ulcerative colitis and Crohn’s disease? What is different between them (2)?

A

Similar
- Idiopathic inflammatory lesions
Difference
- Colitis - anus to colon only, confluent lesions
- Crohns - All intestines, non confluent lesions

84
Q

What are the examples of 5-ASA based drugs used for the treatment of inflammatory bowel disease? (3) These drugs are prodrugs cleaved by colonic enzymes. What is the common end point? Which are activated in the colon? Which in the small bowel?

A

Slufasalazine (colon)
Mesalamine (jejenum and ileum)
Olsalazine (colon)
Mesalamine (common endpoint of cleavage)

85
Q

What is an example of a glucocorticoid that can be used for Inflammatory bowel disease? What is its function?

A

Budesonide

Inflammatory suppresants

86
Q

What are the 2 thiopurines used for the treatment of inflammatory bowel disease? They are prodrugs, what is their common endpoint? What is their mechanism of action?

A

6-Mercaptopurine and Azathioprine
6 Thioguanine
The 6 thioguanine incorporates into DNA of rapidly proliferating immune cells

87
Q

What is the major use of the thiopurines in treating inflammatory bowel disease?

A

Used to maintain remission in patients

88
Q

Beyond budesonide, 6-Mercaptopurine and Azathioprine, what are 2 other immunosuppresants used to treat inflammatory bowel disease? What cases are they used in? What IBD populations is each used in?

A

Methotrexate - Steroid resistant / dependent patients
Cyclosporine - Glucocorticoid resistant patients

Used for acute disease management

89
Q

What are the examples of anti-TNF antibodies used for the treatment of inflammatory bowel disease? How are they different?

A

Infliximab and adalimumab
Infliximab - humanized mouse anti TNF
Adalimumab - 100% human antibody

90
Q

What is the main use of the antiTNF antibodies? What are the side effects?

A

Maintain remission from IBD

  • respiratory tract infection
  • lack of response to tuberculosis
91
Q

What are 2 drugs used to treat irritable bowel syndrome? (not IBD) What are their receptor targets? What are notable side effects of each?

A

Alosetron - 5HT-3 - Ischemic enterocolitis

Tegaserod - 5HT-4 - Cardiac arrhythmias

Medical Pharmacology Exam 3 (13 decks)

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