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Pharmacology 3A > GI medications & Antiemetic medications > Flashcards

GI medications & Antiemetic medications Flashcards

1
Q

Which hormones directly stimulate acid secretion by parietal cells?

A

Gastrin and Histamine

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2
Q

Gastric acid secretion is regulated by what?

A

Neural (parasympathetic) and hormonal (gastrin, histamine) mechanisms

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3
Q

Drugs that neutralise or inhibit gastric acid secretion include?

A

Antacids, H2 - receptor antagonists, proton pump inhibitors, anticholinergics, and cytoprotective agents.

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4
Q

What is different about Antacid–drug interactions?

A

In general, antacids have been reported most frequently to reduce or delay the absorption of many drugs.

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5
Q

True or False? Antacids are chemical compounds that buffer or neutralise hydrochloric acid in the stomach and thereby raise the gastric pH.

A

True

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6
Q

How do proton pump inhibitors reduce gastric acid secretion?

A

by irreversibly inhibiting the hydrogen–potassium adenosine triphosphatase (ATPase) enzyme system at the secretory surface of the gastric parietal cells.

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7
Q

What infection causes chronic active gastritis and is associated with the development of gastric and duodenal ulcers, and is implicated in the development of gastric carcinoma?

A

Helicobacter pylori

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8
Q

Antacids:
What is their MOA?

A

The mechanism of action of antacids involves neutralizing stomach acid by increasing the pH level in the stomach, thereby reducing the acidity and providing relief from symptoms of acid indigestion or heartburn.

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9
Q

What are the common ADRs of antacids?

A

Flatulence, bloating, chalky taste, electrolyte imbalance

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10
Q

Proton pump inhibitors :
What is their MOA?

A

Blocks the enzyme H+/K+ ATPase, also known as the proton pump, in the gastric parietal cells. By inhibiting the proton pump, PPIs reduce the production of stomach acid, leading to a decrease in gastric acidity.

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11
Q

List some commonly used PPIs by generic name

A

Omeprazole, Pantoprazole, Lansoprazole

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12
Q

What are some precautions/contraindications for PPIs?

A

Caution with concurrent administration of with diazepam, phenytoin, warfarin
Can decrease absorption of medications that require an acid environment

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13
Q

What is some patient education for a patient taking an antiacid?

A
  1. Antacids impede the absorption of other medications so should only be taken 2 hours before or 2 hours after other medications
  2. Electrolyte disturbance can impact on cardiac function (arrythmias)
  3. There can be Rebound acidity with prolonged use
  4. Can mask a more serious underlying condition (H.pylori, peptic ulcer)
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14
Q

Are antacids absorbed?

A

Antacids are not significantly absorbed into the bloodstream. They primarily work locally in the stomach to neutralize stomach acid.

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15
Q

Why should antacid administration be separated from the administration of many other medications?

A

Antacid administration should be separated from the administration of many other medications because antacids can interfere with the absorption and effectiveness of certain medications. They can alter the pH of the stomach, affecting the absorption of drugs that require an acidic environment for optimal absorption.

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16
Q

In what circumstances are antacids contraindicated?

A

Antacids are generally contraindicated in individuals with known allergies or hypersensitivity to the ingredients of the antacid.

They should also be used with caution in individuals with kidney disease, heart disease, or high blood pressure, as some antacids can contain ingredients that may worsen these conditions.

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17
Q

Why are PPIs indicated?

A

Peptic ulcer disease
Gastritis
GORD
H.Pylori

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18
Q

List common ADRs of PPIs

A

GI upset, headache, dizziness, skin rash

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19
Q

What is some patient education for PPIs?

A
  1. Do not open, crush or chew the capsules
  2. Not for long term use
  3. Should follow guidelines for step down therapy and not stop abruptly as can cause rebound acidity
20
Q

What is the treatment of H.Pylori – helicobacter pylori?

A

Triple therapy - With PPIs and Antibiotics

21
Q

What is the physiology of vomiting?

A

Vomiting, or emesis, is a complex physiological process. It begins with a feeling of nausea and is triggered by various stimuli such as toxins, motion, or medications. Triggers the chemoreceptor trigger ZONE (CTZ)
The vomiting center in the brainstem (medulla) is then activated, initiating a coordinated response. Abdominal muscles contract forcefully, the lower esophageal sphincter relaxes, and reverse peristalsis occurs, pushing stomach contents upward. The upper esophageal sphincter opens, allowing expulsion of the contents through the mouth.

22
Q

What are the names of the cells that secrete HCL into the stomach?

A

parietal cells, or oxyntic cells.

23
Q

What endogenous chemicals are responsible for promoting HCL acid secretion in the stomach?

A

primarily histamine, gastrin, and acetylcholine.

Histamine is released from enterochromaffin-like (ECL) cells, gastrin is released from G cells in the stomach, and acetylcholine is released from nerve fibers that innervate the stomach.

24
Q

What are the protective mechanisms that protect the lining of the stomach from HCL?

A

Mucus Production, Bicarbonate Secretion,Tight Junctions, and Prostaglandins

25
Q

What is GORD, what are the common causes and what are the clinical manifestations for the patient?

A

GORD (Gastroesophageal Reflux Disease) is a chronic condition characterized by the reflux of stomach acid and contents into the esophagus.

Common causes of GORD include a weak or malfunctioning lower esophageal sphincter (LES) that allows acid to flow backward, hiatal hernia, obesity, and certain lifestyle factors.

Clinical manifestations of GORD can include heartburn, regurgitation of acid or food, chest pain, difficulty swallowing, coughing, and hoarseness.

26
Q

What is peptic ulcer disease, what are the common causes, treatments and what are the clinical manifestations for the patient?

A

Peptic ulcer disease refers to open sores that develop on the lining of the stomach, upper small intestine, or esophagus.

The most common causes of peptic ulcers are infection with Helicobacter pylori bacteria and long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs).

Treatment options for peptic ulcers include antibiotics to eradicate H. pylori infection, acid-suppressing medications like proton pump inhibitors (PPIs), histamine H2 receptor blockers, and lifestyle modifications.

Clinical manifestations of peptic ulcers may include abdominal pain, indigestion, bloating, nausea, vomiting, and gastrointestinal bleeding (which can lead to symptoms like black, tarry stools or vomiting blood

27
Q

True or False? When drugs from different categories are used effectiveness is increased because more than one pathway is blocked.

A

True

28
Q

What is the MOA of ondansetron?

A

Ondansetron is a serotonin 5-HT3 receptor antagonist. It works by selectively blocking serotonin receptors in the gut and in the central nervous system (CNS). By doing so, it reduces the sensitivity of these receptors to serotonin, a neurotransmitter involved in triggering nausea and vomiting.

29
Q

What are the ADRs of ondansetron?

A

Constipation
Headache
Dizziness
Anxiety

30
Q

What is the patient education for ondansetron?

A

Discuss drug interactions (Tramadol, opiods, cns depressants)

Discuss side effects (constipation, headache, dizziness, and anxiety)

31
Q

What are some indications for ondansetron?

A

Ondansetron is commonly used to prevent and treat nausea and vomiting associated with chemotherapy, radiation therapy, and surgery (post op nausea and vomiting)

32
Q

What are the drug interactions with ondansetron?

A

Tramadol – opposing effects of both ondansetron & tramadol, the analgesic effect is lessened.

Caution with opioids due to the increased risk of constipation with both opioids & ondansetron

Caution with other CNS depressants e.g. benzodiazepines, opioids & some antipsychotics = increased risk of serotonin syndrome

33
Q

What is the MOA of metoclopramide?

A

Metoclopramide works by selectively blocking dopamine receptors in the CTZ and vomiting center. This reduces sensitivity of these receptors to dopamine which helps to reduce the vomiting reflex. Metoclopramide also increases motility of the GI tract = accelerated gastric emptying.

34
Q

What are the ADRs of metoclopramide?

A

Diarrhea
Drowsiness
Restlessness
Headaches
Extrapyramidal effects (tardive dyskinesia / parkinsonian)
Hypotension

35
Q

What is the patient education for metoclopramide?

A

Discuss side effects
Discuss precautions/contraindications (Contraindicated with bowel obstruction and parkinsons disease)

36
Q

What are the indications for metoclopramide?

A

It is used to treat various conditions, including post-operative nausea and vomiting, and gastroparesis.

37
Q

What are the precautions/contraindications for metoclopramide?

A

Precautions / contraindications
Contraindicated with bowel obstruction
Contraindicated for persons with Parkinson’s Disease

38
Q

What is the MOA of the antihistamine - Cyclizine?

A

Cyclizine is an antihistamine with antiemetic properties. It works by blocking histamine H1 receptors in the brain and vestibular system. By inhibiting these receptors, cyclizine helps reduce signals associated with motion sickness and nausea.

39
Q

What are the ADRs of the antihistamine - Cyclizine?

A

Drowsiness
GI upset
Anticholinergic effects (blurred vision, dry mouth, constipation, dizzyness)

40
Q

What drug class is cyclizine?

A

An antihistamine

41
Q

What is the patient education for Cyclizine?

A

Discuss side effects such as how there will be drowsiness and this can impair the pts ability to drive/use machinery

Advise to take 30mins/60mins before travel if indicated for motion sickness.

42
Q

What are the indications for Cyclizine?

A

Used for motion sickness, vertigo, palliative care

43
Q

What are some factors to consider when making the decison which several antiemetic to administer?

A

What is the cause of the nausea & vomiting
Co-existing conditions - e.g. Parkinson’s disease, bowel obstruction
Concurrent use of other CNS medications e.g. opioids, sedatives, antipsychotics

44
Q

What are Anticholinergics (Discuss Indication, MOA, and ADRs)

A

They are a class of medications used for motion sickness.

They work by blocking acetylcholine at muscarinic receptors in the inner ear

They have anticholinergic effects (blurred vision, dry mouth, constipation, dizzyness)

45
Q

Where is the vomiting centre and the CTZ?

A

The vomiting center is located in the medulla oblongata of the brainstem.

The CTZ, also known as the chemoreceptor trigger zone, is located near the fourth ventricle in the brain.

46
Q

What mechanisms stimulate both the vomiting centre and the CTZ?

A

Chemical Stimuli: Various substances in the blood, such as drugs, toxins, and metabolic waste products, can directly stimulate the CTZ or activate receptors in the vomiting center.

Vestibular System: Disturbances in the balance and equilibrium sensed by the inner ear can activate receptors in the CTZ and the vomiting center. Motion sickness is an example of this mechanism.

Higher Brain Centers: Emotional stress, anxiety, and psychological factors can stimulate the vomiting center through connections with higher brain centers.

47
Q

Which receptors are triggered throughout the emetic process?

A

Serotonin 5-HT3 receptors: Activation of these receptors is involved in the initiation of vomiting.

Dopamine D2 receptors: These receptors are involved in the coordination and regulation of vomiting.

Muscarinic receptors: Stimulation of these receptors can trigger the vomiting reflex.

NK1 receptors: Substance P, a neurotransmitter involved in the vomiting reflex, acts on NK1 receptors. .

Pharmacology 3A (18 decks)

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