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Sketchy Pharmacology Notecards > GI > Flashcards

GI Flashcards

1
Q

What coordinates emesis in the body and where is it located?

A

Nucleus Tractus Solitarus, it is located in the medulla

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2
Q

Where does NTS receive input from?

A

GI tract, vestibular system and the area postrema

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3
Q

How does Gi communicate with NTS

A

Communicates via vagal nerve, when GI gets irritated it releases mucosal serotonin which binds to the 5HT 3 receptors, this leads to signals being sent via afferent vagal nerve to NTS

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4
Q

How does NTS regulate emesis

A

It coordinates with the rest of the medulla to coordinate emesis response

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5
Q

How does vestibular system communicate with NTS?

A

Via CN VIII

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6
Q

What receptors are present in the vestibular system?

A

M1 and H1 receptors

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7
Q

What is Area Postrema and where is it located

A

Area Postrema is a chemoreceptor trigger zone, it responds to presence of emetogenic substances such as chemotherapy agents.It is located adjacent to NTS on the 4th ventricle outside the BBB

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8
Q

What part of the CNS is responsible for sea sickness or motion sickness?

A

Vestibular system

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9
Q

Ondanestron MOA and what is it used for?

A

Antagonist of 5HT-3 receptors on the vagal afferents in the GI tract. Ondanestron is good for treating chemo induced emesis or post op emesis

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10
Q

AE of Ondanestron

A

ConstipationHeadacheDizzinessQT prolongation so it can precipitate torsades and potentially serotonin syndrome

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11
Q

What is serotonin syndrome?

A

It is associated with systemic release of serotonin and leads to symptoms such as rigidity, tremor, hyperthermia, hyperreflexia, and confusion

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12
Q

What drugs can be used to treat motion sickness?

A

1st gen H1 receptor blockers can cross the BBB so they can be used to motion sickness, they also have anti muscarinic properties so they can block both H1 and M1 receptors

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13
Q

Name 1st gen H1 antagonists

A

Diphenhydramine, meclizine, hydroxyzine

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14
Q

Scopolamine

A

Anti muscarinic agent, used clinically to treat vestibular nausea/motion sickness/sea sickness via M1 receptor inhibition.

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15
Q

What kind of receptors does area postrema contain?

A

D2 receptors and neurokonin 1 receptors (NK 1)

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16
Q

MOA of metoclopramide

A

It has 2 principle MOA, it antagonizes D2 receptors in area prostrema to treat chemo induced emesis and it has a pro kinetic effect on GI as it promotes GI motility

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17
Q

What is another use of metoclopramide

A

Activates GI smooth muscles by antagonizing D2 receptors so it is used for treatment of delayed gastric emptying

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18
Q

Contraindications for metocloproamide

A

It can only be used for non obstructive GI obstruction, cannot be used in case of a small bowel obstruction as that can lead to GI perforation

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19
Q

What are the side effects of metoclopramide

A
  1. Prokinetic effects mean it induces diarrheaMost of the side effects of metoclopramide are due to D2 receptor blockade of the CNS and are more common andsevere in elderly patients
    * Drowsiness
    * Depression
    * Extrapyramidal symptoms
    * Tardive dyskinesia
    * Myopathy and rhabdomyolysis Neuroleptic malignant syndrome
    * QT prolongation
    * Prolactinemia
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20
Q

What extrapyramidal symptoms are caused by metoclopramide

A

Dystonia, akathisia, and parkinsonian features.

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21
Q

Explain neuroleptic malignant syndrome

A

Caused directly by inhibiting D2 receptors in CNS fever, rigidity, mental status changes, autonomic instability, and rhabdomyolysis

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22
Q

Why is there elevated prolactin secretion due to metoclopramide? What can elevated prolactin cause?

A

Due to CNS D2 blockade, leads to gynecomastia, impotence, galactorrhea, and menstrual disorders.

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23
Q

What drugs discussed so far are contraindicated in torsades?

A

Onadnestrone and metoclopramide

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24
Q

What other drugs can be used to inhibit emesis?

A

Antipsychotics

25
Q

What is the role of substance P in inducing emesis?

A

Substance P binds to NK1 receptors in Area Postrema, activating it to relay info into the NTS

26
Q

Aprepitant MOA

A

Competitively inhibits the NK1 receptors in Area Postrema, often used in combination with 5HT-3 antagonists to inhibit emesis

27
Q

Why is aprepitant often preferred over other anti emetics?

A

It lacks any effects on serotonin, dopamine and muscarinic receptors so it has a shorter side effects profile

28
Q

What is the function of parietal cells?How do they achieve this?

A

Parietal cells are located on the fundus of the body and release acid into the lumen via the H+/K+ ATPase. K+ goes into the cell, H+ goes out of the cell using the energy from 1 ATP.

29
Q

What regulates acid secretion by parietal cells?

A
  • Histamine is released by the ECL (Enterochromaffin-like) cell, activating H2 receptors on the parietal cell on the basolateral membrane
  • ECL cells in turn respond to gastrin released by G cells
  • G cells are located in the antrum of the stomach and release G protein in the presence of intraluminal peptides into the circulation
  • Gastrin binds to CCKB receptors on ECL and parietal cells
  • Additionally vagus nerve releases gastrin releasing peptide (GRP instead of ACh) to directly stimulate parietal cells
30
Q

Name H2 receptor blockers

A

Ranitidine, cimetidine, famotidine, nizatidine

31
Q

MOA of H2 receptor antagonists, their effectiveness and clinical indications

A

Inhibit histamine regulated acid secretion however they are not 100% effective since parietal cells can be stimulated by gastrin and vagus nerveClinical uses:1. Nocturnal secretion of acid since this is largely histamine related2. Second line treatment for GERD, gastric and duodenal ulcers

32
Q

What mostly controls post prandial acid secretion and what is a clinical concequence to this?

A

Vagus nerve, H2 blockers are not effective for inhibiting post prandial acid production

33
Q

AE of H2 blockers?

A

Generally safe drugs with little adverse effects:1. Cimetidine inhibits CYP4502. Cimetidine inhibits binding of DHT to androgen receptor, together with inhibitng estrogen metabolism it can lead to gynacomastia, impotence and prolactinomia

34
Q

MOA of PPIs

A

Proton Pump Inhibitors (PPIs) irreversibly inhibit the H+/K+ ATPase by covalently binding to them

35
Q

Indications of PPIs

A

Effectively inhibit and shut down acid production, much more effectively than H2 blockers

  • GERD, gastric and duodenal ulcers
  • NSAIDs induced gastric ulcers
  • Gastrinoma/Zollinger Ellison syndrome
  • H. pylori infection
36
Q

What are the side effects of PPIs

A
  • Increased risk of infections especially C. Diff
  • Increased risk of respiratory infections such as pneumonia
  • Decreased absorption of Ca, Fe and Mg
  • Osteoporosis and hypomagnesia
37
Q

What other drug can be used to inhibit gastric acid production?

A

Octeotride

38
Q

What are osmotic laxatives?

A

Nonabsorbale substances taht draw water into the intestinal lumen, lead to distention and eventual peristalsis

39
Q

Name osmotic laxatives

A

Mg compounds such as MgOH and mg citrateLactulosePolyethylene glycol (PEG)

40
Q

AE of Mg compounds?

A

Prolong use can cause hypermagenesia

41
Q

What is PEG and how is it administered?

A

Non absorbable sugar, acts as an osmotic diuretic, administered with electrolytes

42
Q

Lactulose MOAand what is its useother than a laxative?

A

Lactulose is metabolised by colonic bacteria, producing severe flatulence and cramps in the process, it can also be used to treat hepatic encephalopathy

43
Q

Explain hepatic encephalopathy

A

Hepatic encephalopathy is a neurologic complication of cirrhosis due to the buildup of ammonia (inability to convert it into urea) and other toxins. A primary source of ammonia comes from intestinal bacteria degrading Nitrogen products. In patients with cirrhosis, GI bleeding can percipitate hepatic encephalopathy as intestinal bacteria break down hemoglobin, creating nitrogen products and ammonia; excess dietary protein intake is another potential trigger

44
Q

How does lactulose help with hepatic encephalopathy?

A

Intestinal bacteria metabolize lactulose into acidic metabolites, lowering the pH of the intestinal lumen. The acidic environment created turns toxic ammonia (NH3) into ammonium (NH4+), which gets trapped in the lumen and secreted.

45
Q

Rifaximin indications and MOA

A

Rifaximin (a poorly absorbed antibiotic)can also help treat hepatic encephalopathy by killing the intestinal bacteria responsible for toxic ammonia (NH3) production.

46
Q

AE of laxatives.

A

Laxatives can cause diarrhea and dehydration.

47
Q

What are bulk forming fibers?

A

Indigestible hydrophilic colloid -> absorbs water -> distention -> peristalsis

48
Q

Name bulk forming laxatives

A

Psyllium, methylcellulose, and synthetic fibers

49
Q

Name stool softners

A

Oral enema, docusate, and glycerine sopository.

50
Q

MOA of stool surfactants (softners)?

A

Facilitate penetration of stool by water and lipids, can be administered orally or rectally

51
Q

What are stimulant laxatives?

A

Stimulant laxatives/ Cathartics stimulate bowel movement through the enteric nervous system

52
Q

Senna MOA and AE

A

Senna is a stimulant laxative (aka cathartic), which means it stimulates the enteric nervous system and colonic secretions.Chronic use of senna causes melanosis coli (brown pigmentation of the colon).

53
Q

How does opioids treat diarrhea?

A

Activating mu receptors in the GI tract, these exist in high density in the GI tract and their action leads to significant GI side effects

54
Q

Loperamide

A

Loperamide is an opioid agonist that does not cross the BBB and therefore has no analgesic properties or potential for addiction. Opioid agonists (e.g. loperamide and diphenoxylate) increase the colonic phasic segmenting activity of the colon, increasing the colonic transit time

55
Q

Diphenoxylate

A

Diphenoxylate is an opioid agonist used to treat diarrhea that has some ability to cross the BBB -> combine with small doses of atropine to prevent abuse (gives the user adverse symptoms in order to combat euphoria)

56
Q

What are the AE of diphenoxylate and loperamide?

A

Causes constipation

57
Q

What is a VIPoma?

A

VIPoma’s are pancreatic endocrine tumors that secrete vasoactive-intestinal-peptide which can cause systemic symptoms such as flushing, wheezing, and a secretory diarrhea

58
Q

What is a carcinoid syndrome?

A

Carcinoid syndrome is usually due to an ileal tumor with hepatic metastasis that is secreting a number of substances, including serotonin which can cause secretory diarrhea.

59
Q

How do you treat VIPoma and carcinoid tumor pharmacologically?

A

Octreotide

Sketchy Pharmacology Notecards (14 decks)

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