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Pharmacology > GI diseases > Flashcards

GI diseases Flashcards

1
Q
  1. Parietal cells secrete?
  2. Chief cells secrete?
  3. D cells secrete?
  4. G cells secrete?
A
  1. Hydrochloric acid
  2. Pepsinogen
  3. Somatostatin
  4. Gastrin
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2
Q

Why the main side effect of NSAIDS is GI problems?

A

because it decreases the production of prostaglandins necessary for the protective action against gastric acid on mucosa

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3
Q

Prostaglandins

-function on the GI tract (4)

A
  • increase bicarbonate production from mucous cells
  • dilate blood vessels –> increase blood supply to mucous cells
  • maintain normal function of the mucous
  • form a protective layer
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4
Q

Why does ICU patients have a higher risk of ulcer formation?

A

Because gastric acid production is increased in stress situations

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5
Q

Antacids

  • names
  • mechanism
A

-Aluminium hydroxide, Calcium carbonate, Magnesium hydroxide

  • Reduce intragastric acidity - main mechanism
  • weak bases that react with gastric hydrochloric acid to forma salt and water
  • rapid effect
  • given 1h after meal –> neutralized gastric acid for up to 2h
  • increase intragastric pH + decrease pepsin activity
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6
Q

Why is calcium carbonate not used as an antacids anymore?

A
  • because it produces CO2 which could cause antrum distension
  • CO2 activates G cells –> increase gastrin secretion –> further increase the production of gastric acid
  • if high doses are used –> high amounts of calcium would be absorbed –> systemic effects
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7
Q

Antacids

-may affect the absorption of other medications by:

A
  • binding the drug (reducing it’s absorption)

- increase intragastric pH –> alter the drug’s dissolution or solubility

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8
Q

Antacids - absorption and effect on stool consistency:

  • Magnesium hydroxide
  • Calcium carbonate
  • Aluminium hydroxide
A
  • strong laxative effect, not absorbed from gut
  • absorbed from gut
  • not absorbed from gut, constipating action
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9
Q

H2-receptor antagonists

  • names
  • mechanism of action
A

-Cimetidine, Ranitidine

  • decrease hydrocholoric acid secretion
  • block histamine H2 receptors on parietal cells
  • decrease nocturnal acid but less effect than PPIs against stimulated secretion
  • decrease pepsin secretion
  • not very effective to reduce stimulated gastric acid secretion
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10
Q

H2-receptor antagonists

  • pharmacokinetics
  • unwanted effects
A
  • selective
  • very safe
  • only therapeutic effect –> reduction of gastric acid secretion - 60-70%

-headache, dizziness, diarrhea, constipation

Cimetidine

  • weak anti-androgenic agent (Gynecomastia)
  • potent P450 enzyme inhibitor
  • may increase the concentration of many drugs
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11
Q

Proton pump inhibitors (PPIs)

  • names
  • mechanism of action
A

-Esomeprazole, Omeprazole

  • decrease hydrochloric acid secretion
  • IRREVERSIBLY block H+/K+ ATPase in active gastric parietal cells
  • most potent of all
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12
Q

Proton pump inhibitors (PPIs)

  • pharmacokinetics
  • indications
A
  • given orally (coated to prevent inactivation in the stomach) or parenterally
  • metabolized in the liver
  • 1/2 life of 1-2h
  • may require 3-4d. to achieve their full effectiveness
  • GERD, peptic ulcer, GI bleeding, part of H.pylori eradication therapy, non-ulcer dyspepsia, prevention of stress
  • preventing ulcers caused by NSAIDs
  • Zollinger-Ellison syndrome
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13
Q

Proton pump inhibitors (PPIs)

-steps of how it acts

A

-lipophilic weak bases

  1. Absorbed in the intestines
  2. Reach systemic circulation
  3. Reach parietal cell
  4. Diffuse into the parietal cell canaliculi
  5. With the acidic environment of the lumen they become protonated (active)
  6. Converted to compounds that irreversibly inactivate the parietal cell H+/K+ ATPase
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14
Q

Proton pump inhibitors (PPIs)

  • why are repeated doses necessary?
  • is tolerance possible?
A

Because it doesn’t block ALL the pumps at once. A few days are necessary to see an effect and also if u discontinue the drug.

No, because the cells are not able to adapt due to the fact that almost all of the pumps are inhibited

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15
Q

Mucosal protective agents

-names

A

-Misoprostol, Sucralfate

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16
Q

Mucosal protective agents

-names

A

-Misoprostol, Sucralfate

17
Q

Sucralfate

  • mechanism of action
  • other info
A
  • polymerized in the acid environment - poorly soluble
  • polymer binds to injured tissue and forms a protective coating over ulcer beds
  • an aluminum sucrose sulfate
  • accelerates the healing of peptic ulcers and decrease the recurrence rate
  • toxicitiy is very low - no systemic effects
18
Q

Antibiotics

-H. pylori infection

A
  • chronic infection with H.pylori is present in most patients with recurrent non-NSAID induced peptic ulcers
  • eradication of H.pylori decreases the rate of recurrence of ulcer in these patients
  • Antibiotics + PPIs –> usually at least 2 antibiotics

Omeprazole + Clarithromycin + Amoxicillin
Omeprazole + Clarithromycin + Metronidazole
Omeprazole + Tetracycline + Metronidazole + Bismuth

19
Q

Antibiotics

  • H. pylori infection
  • combination of drugs
A
  • chronic infection with H.pylori is present in most patients with recurrent non-NSAID induced peptic ulcers
  • eradication of H.pylori decreases the rate of recurrence of ulcer in these patients
  • Antibiotics + PPIs –> usually at least 2 antibiotics

Omeprazole + Clarithromycin + Amoxicillin
Omeprazole + Clarithromycin + Metronidazole
Omeprazole + Tetracycline + Metronidazole + Bismuth

20
Q

Sources of input to the vomiting center

A
  1. “Chemoreceptor trigger zone” - activated by different drugs and toxins or by the vesicular nuclei. Dopamine, serotonin, opioid, NK1 receptors
  2. Vestibular system - Muscarinic and histamine receptors
  3. Vagal and spinal afferent nerves from the GI tract
  4. CNS
21
Q

Drugs with antiemetic actions - names

  1. Selective 5-HT3 receptor antagonists
  2. D2 dopamine antagonists
  3. H1 antagonists
  4. Muscarinic receptor antagonists
A
  1. Ondansetron
  2. Metoclopramide, Domperidone
  3. Meclizine
  4. Scopolamine
22
Q

Prokinetic agents

  • names
  • function
  • indication
A
  • Neostigmine, Metoclopramide, Domperidone, Erythromycin
  • increase GI motility
  • GERD, gastroparesis/ post-surgical gastric emptying delay or decreased intestines motility
23
Q

Neostigmine

A
  • acetylcholinesterase inhibitor

- increase acetylcholine in synapsis –> increase peristalsis

24
Q

Metoclopramide, Domperidone

A
  • D2 receptor antagonist
  • decrease sympathetic activity, indirectly increase parasympathetic activity
  • promote GI motility
  • Metoclopramide - can cross blood-brain barrier –> when used chronically can cause symptoms of parkinsonism, hyperprolactinemia, etc.
  • Domperidone - cannot cross blood-brain barrier –> low risk of CNS toxicity
25
Q

Erythromycin

A
  • motilin receptors on GI smooth muscle stimulator

- macrolide antibiotic

26
Q

Laxatives

  • names
  • function
A
  • Docusate, Magnesium hydroxide, Lactulose, Senna, Bisacodyl
  • increase bowel movement
27
Q

Laxatives

  • indications
  • contraindication
A
  • before examination, before/after surgery, before birth (obstipation during pregnancy)
  • drug induced obstipation, intoxication, hemorrhoids

-obstruction of the bowel

28
Q

Laxatives “Vicious Circle)

A

TOLERANCE

  1. Constipation
  2. Drug is given
  3. Defecation + electrolytes loss
  4. Kidneys try to compensate for the electrolyte loss
  5. Reabsorption of sodium and water
  6. increase absorption of sodium = potassium loss
  7. Can lead to hypokalemia (muscle weakness)
  8. Lower motility of bowels
    9/ Could exacerbate constipation
29
Q

Laxatives

-Types

A
  1. Bulk-forming laxatives - 12-72h to work
    - fiber in the food: ass bulk and water
  2. Stool surfactant agents (Softeners) - 12-72h work
    - anionic surfactants: add water and fats
    - Docusate
  3. Osmotic laxatives - 12-72h (oral)/ 30min-1h (rectal) to work
    - create osmotic effect and increase water holding = water secretion
    - Magnesium hydroxide, Lactulose
  4. Stimulant laxatives (Cathartics) - 6-10h to work (fast)
    - act on intestinal mucosa/ enteric nervous system and increase water/electrolyte secretion
    - Senna, Bisacodyl
30
Q

Anti-diarrheal agents

-name

A

-Loperamide, Somatostatin, Ocreotide

31
Q

Loperamide

  • mechanism of action
  • unwanted effects
A
  • opioid agonist –> no unwanted effect but drug effect is only local –> minimal CNS effect
  • activates u opioid receptors in enteric nervous system and slows motility with negligible CNS effect

-mild cramping but little or no CNS toxicity

32
Q

Somatostatin

  • action on the anterior pituitary
  • action on the GI system
A
  • paracrine function in nervous system
  • decrease release of growth hormone, TSH, prolactin
  • decrease release of gastrin, cholecystokinin, secretin, motilin, vasoactive intestinal peptide, gastric inhibitory polypeptide, 5-HT
  • decrease intestinal fluid secretion, motility, gallbladder contraction, portal and splanchnic blood flow
  • decrease pancreatic function: release of glucagon, insulin, exocrine secretory function
33
Q

Ocreotide

  • indications
  • unwanted effects
A
  • acute hemorrhage from esophageal varices in liver cirrhosis (decrease portal venous pressure)
  • diarrheas with: carcinoid syndrome (increase secretion of 5-HT and kallikrein)
  • GI fistulae

-GI –> cramps, nausea, vomiting, diarrhea, constipation, hyperbilirubinemia, gallstones, hyperglycemia or hypoglycemia, hypothyroidism, bradycardia, dizziness, dyspnoae

34
Q

Anti-spasmodics

  • name
  • mechanism of action
  • indications
A
  • Drotaverine
  • causes imbalance of calcium –> decrease activity of the muscle
  • irritable bowel syndrome, abdominal pain and cramps, diarrhea alternating with constipation, flatulence
35
Q

Inflammatory bowel disease

  • treatment for the mild stage of the disease - name
  • mechanism of action
A
  • Sulfasalazine (5-ASA + sulfapyridine)
  • decrease activity of immune cells = decrease synthesis of prostaglandins, leukotrienes, cytokines
  • systemic absorption of the sulfapyridine moiety –> nausea, GI upset, headache, myalgias, bone marrow suppresion
36
Q

Inflammatory bowel disease

-treatment for the moderate stage of the disease - name

A
  • Methotrexate

- immunomodulator

37
Q

Inflammatory bowel disease

-treatment for the severe stage of the disease - name

A
  • Adalimumab, Infliximab

- anti-TNF antibodies

Pharmacology (29 decks)

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