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Y2B1 - GIT πŸ“• > Pharmacology πŸ’Š > Flashcards

Pharmacology πŸ’Š Flashcards

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1
Q

what are the drugs that affect GIT motility?

A

β–ͺ Drugs increase GIT motility: (Treat constipation)
A- Prokinetic drugs
B- Laxatives

β–ͺ Drugs decrease GIT motility: (Treat diarrhea)
A- Antidiarrheal drugs
B- Antispasmodic drugs

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2
Q

what is the definition of prokinetic drugs?

A

Drugs that increase upper GIT motility and increase gastric empting.

β€œUpper GIT = Stomach & esophagus”

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3
Q

give examples for prokinetic drugs

A

Including:

  1. Dopamineregic blockers: e.g. Metoclopramide and Domperidone.
  2. Serotonin (5-HT4) agonists: e.g. Mosapride
  3. Cholinomimetic agents: e.g. Bethanechol.
  4. Macrolide antibiotics: e.g. Erythromycin
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4
Q

what is the mechanism of action of metoclopramide?

A
  • Blocking of dopamine (D) receptors (central & peripheral) leading to decrease the inhibitory action of dopamine on the GIT motility.
  • Enhances cholinergic transmission in GIT.
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5
Q

what are the therapeutic uses of metoclopramide?

A
  • Gastroesophageal reflux (GERD): to enhance gastric emptying and ↑ LES pressure.
  • Disorders of gastric emptying: e.g. diabetic gastroparesis (feeling a full stomach) and postoperative gastric retention.
  • Before small bowel endoscopy: to enhance gastric evacuation and peristaltic movement.
  • Before emergency surgery and labor (to evacuate the stomach and prevent aspiration of gastric contents).
  • Treatment of nausea and vomiting of various causes (Antiemetic action due to blockade of D2 R in VC and CTZ).
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6
Q

what are the adverse effects of metoclopramide?

A
  • Sedation (the most common).
  • Extrapyramidal effects (dystonia and dyskinesia): due to blockade
    of D2 in the basal ganglia.
  • Hyperprolactinemia due to blockade of D2 in the pituitary gland.
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7
Q

what is the mechanism of action of domperidone?

A
  • It blocks peripheral D2 receptors in GIT
  • Block D2 R in CRTZ (it does NOT cross BBB ie. No central effect).
  • Antiemetic effect: less than metoclopramide.
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8
Q

what are the therapeutic uses of domperidone?

A
  • The same uses as metoclopramide.
  • To counteract nausea and vomiting caused by levodopa during treatment of Parkinson’s disease: Because it can block D receptors in CRTZ but not those in the basal ganglia responsible for parkinsonism.
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9
Q

what are the adverse effects of domperidone?

A

Domperidone may ↑ QT interval and predispose to serious arrhythmia and sudden death.

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10
Q

compare between metoclopramide and domperidone

A
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11
Q

what is the mechanism of action of bethanechol?

A
  • Bethanechol stimulates muscarinic M3 in the smooth muscle of the GIT and myenteric plexus.
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12
Q

what are the uses of bethanechol? and why is its usage limited nowdays?

A

It was used in the past for the treatment of GERD and gastroparesis, but now, it is rarely used for this indication due to multiple cholinergic side effects.

Remember: Bethanechol is never given in IV route

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13
Q

what is the mechanism of action of macrolide antbiotics like erythromycin (in cases of constipation)?

A
  • Macrolide antibiotics such as erythromycin directly stimulate motilin receptors on GIT smooth muscle and promote the onset of a migrating motor complex.
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14
Q

what are the adverse effects of erythromycin (related to GIT)?

A
  • Intravenous erythromycin (3 mg/kg) is beneficial in some patients with gastroparesis; however, tolerance rapidly develops.
  • It may be used in patients with acute upper GIT hemorrhage to promote gastric emptying of blood before endoscopy.
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15
Q

what are laxatives?

A

They are agents used to enhance lower GIT motility

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16
Q

what are examples of laxatives?

A
  1. Bulk-forming agents:
    [Dietary fibers – Methylcellulose – Bran]
  2. Osmotic laxatives:
    [Mg sulfate & Na salts – Lactulose – Polyethylene glycol]
  3. Irritant (or stimulant) laxatives: β€œhave very strong effect”
    [Castor oil – Senna – Bisacodyl]
  4. Stool softeners:
    Docusate sodium
  5. Lubricant laxatives:
    [Liquid paraffin – Glycerin suppositories – Evacuant enema]
  6. Chloride channel activators: β€œrelatively safe”
    Lubiprostone
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17
Q

what is the mechanism of action of Bulk-forming agents?

A

They are non-digestible fibers; they retain water in the gut and distend the large intestine β†’ activation of stretch receptors β†’ stimulation of peristalsis.

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18
Q

what is the adverse effects of Bulk-forming agents?

A

they are safe laxatives but may cause:

  • Bloating and abdominal distension.
  • ↓ Absorption of some drugs e.g. digoxin.
  • They may form masses in the gut leading to intestinal obstruction.
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19
Q

what is the mechanism of action of osmotic laxatives?

A

They are retained in the gut lumen and retain water by their osmotic effect β†’ activation of stretch receptors β†’ stimulation of peristalsis.

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20
Q

what are the adverse effects of osmotic laxatives?

A
  • Mg & Na salts (saline laxatives) may be absorbed systemically and produce hypermagnesemia and hypernatremia especially in patients with renal failure.
  • Lactulose may produce abdominal discomfort. β€œhowever, it is the most safe one”
  • Polyethylene glycol may produce electrolyte disturbance (hypokalemia).
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21
Q

which osmotic laxative can be used in pregnancy?

A

Lactulose

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22
Q

what is the mechanism of action of irritant (stimulant) laxatives?

A
  • Produce inflammation (irritation) of the intestinal mucosa: increase cAMP and inhibit Na+/K+ ATPase enzyme leading to: Accumulation of water and electrolytes in the gut lumen.
  • Direct stimulation of peristalsis by stimulation of myenteric plexus.
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23
Q

what are the adverse effects of irritant (stimulant) laxatives?

A
  • Prolonged use β†’ degeneration of gut nervous plexus β†’ atonic (cathartic) colon (should not be used more than 10 days).
  • Stimulation of uterine contraction and abortion
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24
Q

Laxative dependence

A
  • Irritant laxatives cause complete evacuation of the colon.
  • The colon requires 2-5 days before the normal fecal mass can
    be reestablished.
  • The patient becomes worry regarding the lack of bowel
    movement during this period and may use the laxative again and a vicious cycle is established leading to partial or complete loss of normal bowel function.
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25
Q

what are the adverse effects of senna?

A
  1. It passes in urine and cause urine discoloration
  2. It passes in breast milk and cause cathartic effect in the baby.
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26
Q

Bisacodyl

A
  • It is prepared as enteric coated tablets to avoid gastric irritation.
  • If it is given with milk or with other drugs that change gastric pH,
  • the enteric coating may dissolve in the stomach and cause gastric irritation and pain.
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27
Q

what is the mechanism of action of stool softeners?

A

they are anionic surfactants that enable additional water and fats to be incorporated in the stool, making it easier to move through the GIT.

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28
Q

what is the mechanism of action of lubricant laxatives?

A
  • Glycerin has hygroscopic effect. It draws water from rectal mucosa and lubricates the anal canal.
  • It also stimulates reflex rectal contractions and promotes stool evacuation in 15-20 min.
  • Evacuant enema (tape water with mineral oil, hypertonic sorbitol, MgSO4) are safe for administration to facilitate passage of stool in painful anal conditions.
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29
Q

what is the mechanism of action of chloride channel activators?

A
  • It acts by activating chloride channels to increase fluid secretion in the intestinal lumen.
  • This eases the passage of stool and causes little change in electrolyte balance.
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30
Q

wha is lubiprostone used in?

A

treatment of chronic constipation, irritable bowel syndrome (IBS)

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31
Q

Are there any adverse effects for Chloride channel activators?

A
  • tolerance or dependency has not been associated with this drug.
  • Also, drug– drug interactions appear minimal
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32
Q

General indications of laxatives

A
  • Constipation: laxatives should not be used for prolonged duration to avoid laxative dependence.
  • To fasten excretion of toxic substances from the GIT.
  • To prepare the bowel before X-ray or colonoscopy.
  • Hepatic encephalopathy (lactulose): to kill ammonia producing bacteria.
  • Painful anal conditions e.g. anal fissure or piles.
  • Postoperative: e.g. after hemorrhoids (piles) to avoid strain.
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33
Q

Contraindications of laxatives

A
  • Laxatives are dangerous in cases of undiagnosed abdominal pain or
    inflammatory bowel disease. They may lead to intestinal perforation.
  • Organic obstruction of the GIT.
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34
Q

what are antiddiarrheal drugs?

A

Drugs used to decrease passage of frequent unformed stool.

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35
Q

what are the Drugs used in treatment of diarrhea through decreasing GIT motility in GIT?

A
  1. Anti-cholinergic drugs:(Atropine, hyoscine and propantheline)
  2. Synthetic opioids: diphenoxylate and loperamide
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36
Q

what is the mechanism of action of anticholinergic drugs in treatment of diarhhea?

A

Blocking M3 receptor in intestinal smooth muscle:
βœ“ ↓ colonic peristalsis: Antidiarrheal action
βœ“ Relieve cramps associated with diarrhea: Antispasmodic action

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37
Q

what is the mechanism of action of synthetic opiods in treatment of diarrhea?

A
  • They act on opioid ΞΌ (mu) receptors enteric nervous system (ENS) leading to ↑ segmenting (non-propulsive) contractions of the intestine and increase resistance to flow through the lumen.
  • They act on opioid Ξ΄ (delta) receptors in the ENS leading to ↑ water absorption and ↓ water secretion.
  • They act on presynaptic opioid receptors in the ENS leading to ↓ Ach release.
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38
Q

what is the difference between Diphenoxylate and loperamide?

A

Loperamide cannot cross BBB but diphenoxylate can cross BBB poorly (no CNS effects in usual therapeutic doses) but it can cause addiction if used in large doses and for prolonged duration.

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39
Q

what is lomotil?

A

Lomotil is a combination of diphenoxylate 2.5 mg + atropine 0.25 mg: produce more ↓↓ in intestinal motility and decrease liability for abuse.

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40
Q

what are the side effects of Drugs used in treatment of diarrhea through decreasing GIT motility?

β€œlike anticholinergics and Synthetic opioids”

A
  • Anti-cholinergic side effects.
  • Addiction: if used for prolonged duration.
41
Q

what are the treatment options of diarrhea?

A
  1. Maintenance of fluid and electrolyte balance
  2. Non-specific antidiarrheal agents (should be applied after exclusion of other relevant causes of diarrhea)
  3. Specific antidiarrheal agents: treatment of the cause
42
Q

Maintenance of fluid and electrolyte balance in treatment of diarrhea

A
  • Is the first priority especially in extreme of age.
  • Using oral Rehydration Therapy (ORT): Balanced salt solution containing electrolytes and glucose
  • Or Intravenous solutions: in severe dehydration.
43
Q

Non-specific antidiarrheal agents (should be applied after exclusion of other relevant causes of diarrhea)

A
  • Drugs decrease lower GIT motility
  • Drugs bind to toxins as Adsorbents(Kaolin, pectin, activated charcoal)
    or bind bile acid as cholestyramine
44
Q

Specific antidiarrheal agents: treatment of the cause

A
  • antimicrobials for infectious diarrhea.
  • Anti-inflammatory drugs for inflammatory bowel diseases.
45
Q

what is the classification of smooth muscle relaxants?

A
  • Anticholinergic drugs: atropine, propantheline, hyoscine
  • Direct smooth muscle relaxants: papaverine, mebeverine, alverine, drotaverine.
  • Mixtures: Librax (clidinium + chlordiazepoxide).
46
Q

give examples for smooth muscle relaxants

A
  • Papaverine: natural opium alkaloid
  • Mebeverine, alverine, drotaverine: synthetic drugs
47
Q

what is the Mechanism of action of direct smooth muscle relaxants?

A

Inhibition of PDE enzyme lead to increase cAMP and smooth muscle relaxation

48
Q

what are the uses of Direct smooth muscle relaxants?

A

Spasms of the GIT, bile duct and genitourinary tract.

49
Q

what are the side effects of Direct smooth muscle relaxants?

A
  • Cardiac arrhythmia.
  • Abnormal liver functions in the form of ↑ serum transaminases
    and alkaline phosphatase.
  • Headache and dizziness
50
Q

what are the contraindications of Direct smooth muscle relaxants?

A
  • Paralytic ileus.
  • Constipation for more than one week
51
Q

what is librax?

A
  • Chlordiazepoxide: benzodiazepine that has antianxiety effect.
  • Clidinium:anticholinergic drug which ↓ GIT motility
52
Q

what are the uses of librax?

A
  • Spasms of the GIT, bile duct and genitourinary tract.
  • Treatment of irritable bowel syndrome (IBS).
53
Q

what are the side effects of librax?

A
  • Atropine-like actions e.g, dry mouth, urine retention, etc.
  • CNS depression (benzodiazepine): Sedation, drowsiness, confusion,
    etc.
54
Q

what are the contraindications of librax?

A

as direct smooth muscle relaxant:

  • Paralytic ileus.
  • Constipation for more than one week.
55
Q

what is the definition of peptic ulcer?

A
  • Ulceration of the duodenum or stomach due to imbalance between local invasive force (e.g. HCl and pepsin) and protective mechanisms.
56
Q

HSDDI

what are the invasive factors causing peptic ulcer?

A

- Stress:↑ HCl and pepsin secretion by parietal cells.
- Diet: coffee, alcohol and spices.
- Drugs: NSAIDs, corticosteroids, morphine,methylxanthines, etc.
- Infection with Helicobacter pylori.

57
Q

what are the defensive mechanisms preventing peptic ulcer?

A
  • Mucus production by gastric mucosa.
  • Pancreatic bicarbonate secretion.
  • Good mucosal blood flow.
  • Local PGE2 and PGI2 production.
58
Q

what is the shape and site of H.Pylori?

A
  • H. pylori is spiral gram -ve flagellates found in the antrum of human stomach
59
Q

how is H.Pylori diagnosed?

A
  • Infection with H. pylori can be diagnosed by endoscopic biopsy or serological markers.
60
Q

how does Acetylcholine, Gastrin & Histamine affect HCL secretion?

A
  • Ach: ↑ HCl secretion through M1 receptors β†’ ↑ intracellular Ca2+.
  • Gastrin: ↑ HCl secretion through G receptors β†’ ↑ intracellular Ca2+.
  • Histamine: ↑ HCl secretion through H2 receptors β†’ ↑ intracellular cAMP.
  • Both Ca2+ and cAMP activate H+/K+ ATPase at the membrane of the parietal cell to secrete H+ into the gastric lumen (proton pump).
61
Q

how do PGE2 & PGI2 affect HCL secretion?

A

act on PG receptors β†’ ↓ cAMP β†’ ↓ HCl secretion.

62
Q

non-drug therapy of peptic ulcer

A
  • Rest and Sedation: they improve healing and relief pain of DU.
  • Stop Smoking, Spices, alcohol, coffee, and tea: because they ↑ HCl.
  • Avoid Stress: because stress ↑ HCl.
  • Avoid ulcerogenic drugs: e.g. NSAIDs.
  • Diet:
    1. Frequent small meals in DU in order to buffer high acidity.
    2. Encourage milk and fats.
    3. Avoid Spices and fried food
63
Q

give examples for H2 blockers

A

(Cimetidine – Ranitidine – Famotidine - Nizatidine)

64
Q

pharmacological therapy of peptic ulcer

A

Drugs that ↓ HCl secretion (Antisecretory drugs):
- H2 blockers: cimetidine, ranitidine, famotidine.
- Proton pump inhibitors: omeprazole, lanzoprazole, etc.

Drugs that ↑ mucosal defense mechanisms (cytoprotective drugs):
- Sucralfate
- Colloid bismuth compounds: e.g. bismuth subcitrate.
- Carbenoxolone
- PGE1 analogues: misoprostol.

Drugs that neutralize HCl:
- antacids

Antimicrobial drugs for H. pylori

65
Q

what is the Mechanism and pharmacological effects of H2 blockers?

A
  • They act as competitive inhibitors of histamine H2-receptors on the parietal cell, This results in a marked ↓ in histamine-stimulated HCl secretion
66
Q

ulcer & its complications

what are the therapeutic uses of H2 blockers?

A
  • Duodenal and gastric ulcers.
  • Prophylaxis & treatment of stress ulcers (e.g. after burn or major trauma).
  • Reflux esophagitis.
  • With ulcerogenic drugs (e.g. NSAIDs) to protect the gastric mucosa from injury.
67
Q

what are the adverse effects of H2 blockers?

A
  • GIT disturbance
  • CNS symptoms: headache, slurred speech, delirium, coma, etc.
  • Tolerance
  • Cimetidine has anti-androgenic effects (due to block of androgen receptors) leading to ↓ sperm count, impotence and gynecomastia.
  • Cimetidine inhibits hepatic microsomal enzymes (P450) leading to ↓ metabolism of other drugs e.g. theophylline, warfarin, sulphonylureas, etc.
68
Q

precautions when using H2 blockers

A
  • Avoid sudden withdrawal to prevent rebound ulceration.
  • Avoid combination of cimetidine with drugs having narrow therapeutic index (because cimetidine inhibits microsomal P450 and ↑ their toxicity).
69
Q

give examples for Proton pump inhibitors

A

(Omeprazole – Lansoprazole – Pantoprazole)

70
Q

what is the mechanism of action of Proton pump inhibitors?

A
  • They are prodrugs, They are converted into the active form in the gastric mucosa
  • Produce irreversible inhibition of gastric H+/K+ ATPase enzyme leading to ↓ both basal and stimulated HCl secretion to around the zero level for 1-2 days.
  • Their bioavailability is decreased significantly by food and, ideally, should be administered 1 hour before a meal.
71
Q

what are the therapeutic uses of Proton pump inhibitors?

A

The same as H2 blockers (dose of omeprazole: 20-40 mg/day orally for 4-6 weeks then 10-20 mg/day for 4-6 months to prevent recurrence).

72
Q

what are the adverse effects of Proton pump inhibitors?

A
  • GIT disturbance: abdominal colic, nausea, vomiting and transient increase of liver enzymes.
  • Headache, dizziness, skin rash,
  • Decrease vit B12 absorption after > 12 weeks of therapy due to interference with intrinsic factor secretion by the stomach (megaloblastic anemia).
  • Osteoporosis
  • Inhibition of gastric acidity leads to alteration of bioavailability of some drugs e.g. ketoconazole, digoxin, and iron.
  • Infection eg, RT pneumonia, C. diffecil infection
  • Omeprazole in high dose induced gastric carcinoid tumor in rats.

Drug interaction:
- PPI (Omeprazole) inhibits microsomal P450 enzymes leading to:
1. Decreases metabolism of some drugs and increase their toxicity eg, phenytoin, warfarin.
2. Decrease activation of clopidogrel.

73
Q

what is the mechanism of action of Sucralfate?

A
  • It needs acidic medium to be activated. In the presence of acidic medium, it forms a complex with protein debris at the ulcer base and forms a physical barrier (so not taken with antacids, H2 blockers, or PPIs).
  • It ↓ pepsin secretion and ↑ secretion of endogenous PGs.
74
Q

what are the adverse effects of Sucralfate?

A
  • Constipation (due to presence of aluminum).
  • ↓↓ absorption of tetracycline, digoxin and phenytoin.
  • Contain aluminum metal which may accumulate in cases of renal failure causing toxicity, so it should be avoided in renal failure.
75
Q

give examples for Bismuth compounds

A

Bismuth subsalicylate and subcitrate

76
Q

what is the mechanism of action of bismuth compounds?

A
  • As sucrlfate
  • It has additional antimicrobial activity against H. pylori.
77
Q

what are the adverse effects of Bismuth compounds?

A
  • Black stool and teeth discoloration.
  • Encephalopathy in presence of renal failure
78
Q

what are the contraindications of Bismuth compounds?

A

Chronic renal failure and CNS diseases.

79
Q

give an example for Synthetic PGE1 analogue

A

Misoprostol

80
Q

what is the mechanism of action of Synthetic PGE1 analogues?

A
  • It acts on specific receptors on gastric parietal cells to ↓ histamine-stimulated HCl secretion.
  • ↑ mucus and bicarbonate secretion (cytoprotective action).
  • ↑ mucosal blood flow and stimulates mucosal cellular regeneration.
81
Q

what are the therapeutic uses of Synthetic PGE1 analogues?

A

Prevention of peptic ulcer in high risk patients e.g. those on long term use of NSAIDs for chronic inflammatory diseases. [misoprostol 200 microgram is combined with naproxen or diclofenac in single tablet].

82
Q

what are the adverse effects of Synthetic PGE1 analogues?

A
  • Diarrhea and cramping pain: due to ↑ GIT motility and water secretion.
  • Uterine contractions during pregnancy β†’ abortion.
83
Q

when are Synthetic PGE1 analogues contraindicated?

A

pregnancy

84
Q

what is the definition of antacids?

A

Antacids are weak bases that are taken orally and partially neutralize gastric acid and reduce pepsin activity.

85
Q

what is the use of antiacids?

A

They are used as symptomatic relief of hyperacidity and should not be used as long-term treatment.

86
Q

examples of antiacids

A
  • Sodium bicarbonate
  • Calcium carbonate
  • Magnesium and aluminum salts (Mg hydroxide and Aluminium hydroxide)
87
Q

CCDR

what are the adverse effects of antiacids

A

Change in bowel habits:
- Al3+ hydroxide causes constipation, while Mg2+ hydroxide cause diarrhea. For this reason, both salts are combined together to manage this problem.

Rebound hyperacidity:
- with Ca2+ and NaHCO3 containing antacids.

Cation overload:
- Na+ salts β†’ hypertension and systemic alkalosis.
- Ca2+ salts β†’ hypercalcemia, renal stones .

Decrease absorption of other drugs:
- the metal ion in some preparations can chelate other drugs especially tetracycline, digitalis and iron (2 hours interval is essential)

88
Q

what is the main cause for recurrence of peptic ulcer?

A

Infection with H. pylori is a main cause of recurrence of PU.

89
Q

drugs used for treatment of H.Pylori and sequential protocol

A
90
Q

Triple therapy of Helicobacter-Pylori

A
91
Q

HAVE

what are the steps of therapy of bleeding peptic ulcer?

A
  • Hospitalization and Fresh blood transfusion.
  • Acid suppression with high dose PPIs by continuous i.v. infusion is the standard of care e.g. omeprazole 80 mg i.v. bolus followed by 8 mg/h for 72h.
  • Vitamin K1: 10 mg i.m or s.c.
  • Endoscopic therapy: several types of endoscopic treatments are available
92
Q

what is the definition of GERD?

A
  • It is the syndrome consisting of esophageal mucosal damage produced by retrograde flow of gastric contents into the esophagus.
  • It is primary due to ineffective or incompetent lower esophageal sphincter (LES).
93
Q

treatment of GERD

A

Non- Drug Measures:
- Sleeping on a high pillow: most damage to the esophagus occurs at night when swallowing is much reduced and acid can remain in contact with the mucosa of the esophagus for long period.

  • Avoid:
    1. Large meals and eating before sleeping.
    2. Alcohol, smoking, spicy foods and coffee.
    3. Aspirin and NSAIDs.
    4. Tight clothes around the abdomen.
    5. Weight reduction (Enhance, Don’t avoid)

————————————————————————–

Drug treatment:
- Decreasing HCl secretion: (H2 blockers and proton pump inhibitors).
- Antacids and antacid combinations:(Gaviscon).
- Prokinetic drugs.
- Surgical treatment: if medical therapy failed.

94
Q

what is the chemical composition of gaviscon?

A

(alginic acid + Mg-trisilicate + Al-hydroxide + NaHCO3)

95
Q

what is the mechanism of action of gaviscon?

A

Alginic acid in presence of saliva and NaHCO3 forms a highly viscous foamy solution of Na-alginate that floats on the gastric contents as a raft and prevents gastric reflux.

96
Q

what is the definition of prokinetic drugs?

A

Drugs that increase upper GIT motility and increase gastric empting.

97
Q

give examples for prokinetic drugs

A

1. Dopaminergic blockers: e.g. Metoclopramide and Domperidone.
2. Serotonin (5-HT4) agonists: e.g. Mosapride
3. Cholinomimetic agents: e.g. Bethanechol.
4. Macrolide antibiotics: e.g.Erythromycin

98
Q

sequence of most effective drugs against NSAID induced ulcers

A
  1. Misoprostol
  2. PPI
  3. H2 Blockers

Y2B1 - GIT πŸ“• (9 decks)

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