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STEP1 > GI and Endocrine Drugs > Flashcards

GI and Endocrine Drugs Flashcards

1
Q

What area within the brain regulates emesis?

A

the nucleus tractus solitarius in the medulla

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2
Q

The nucleus tractus solitarius regulates emesis and receives input from what three major sites?

A
  • the stomach via vagal afferents
  • the semicircular canals via CN VIII
  • the area postrema located nearby in the 4th ventricle, outside the BBB
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3
Q

Describe how GI irritation modulates the emetic response.

A
  • GI irritation in the form of distention, infection, or chemotherapy leads to mucosal release of serotonin
  • this serotonin binds 5-HT3 receptors on vagal afferents
  • vagal afferents project to the nucleus tractus solitarius and promote emesis
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4
Q

Ondansetron

A
  • a 5-HT3 antagonist used to prevent emesis
  • it blocks binding of serotonin from the gastric mucosa to 5-HT3 receptors on vagal afferents projecting to the nucleus tractus solitarius
  • side effects include constipation, headache, dizziness, serotonin syndrome, and QT prolongation
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5
Q

How do the semicircular canals mediate emesis? What receptors are involved?

A
  • they mediate the emesis associated with vertigo and motion sickness
  • the vestibular system contains H1 receptors, coupled to a Gq cascade, as well as M1 receptors
  • activation of these receptors leads to emesis
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6
Q

How does the area postrema mediate emesis? What receptors are involved?

A
  • the area postrema is located in the fourth ventricle outside the BBB
  • it senses and responds to emetogenic substances in the blood or CSF
  • D2 receptors and NK1 receptors (for substance P) are critical for this mechanism
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7
Q

List five receptor types involve in the emetic response and where they can be found.

A
  • 5-HT3 on vagal afferents in the GI tract
  • H1 in the semicircular canals
  • M1 in the semicircular canals
  • D2 in the area postrema
  • NK1 (for substance P) in the area postrema
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8
Q

What role do antihistamines play as anti-emetics? What is the primary side effect?

A

first generation H1 antagonists, like diphenhydramine and meclizine, are capable of crossing the BBB and can be used to treat motion sickness, but they often cause sedation

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9
Q

Describe scopolamine as an anti-emetic.

A
  • it is an M1 antagonist

- functions in the vestibular system for the treatment of sea sickness and motion sickness

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10
Q

Motion sick (i.e. vestibular nausea) is best treated with what two agents?

A
  • first generation antihistamines like diphenhydramine or meclizine
  • an M1 antagonist like scopolamine
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11
Q

Aprepitant

A
  • an NK1 receptor antagonist (blocks substance P binding)

- functions in the area postrema to inhibit chemotherapy-induced vomiting with very few side effects

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12
Q

Metoclopramide

A
  • a D2 receptor antagonist that acts in the area postrema to inhibit emesis
  • side effect profile includes a pro kinetic effect in the upper GI system, which can be useful in treating ileus, but is contraindicated in those with GI obstruction
  • may cause diarrhea, extra-pyramidal side effects and eventual tardive dyskinesia, sedation, depression, neuroleptic malignant syndrome, and hyperprolactinemia
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13
Q

Describe how gastric acid secretion is regulated.

A
  • parietal cells in the gastric mucosa of the body and fundus secrete acid via an H/K-ATPase
  • these cells express M3 receptors, which can be activated by vagal efferents
  • alternatively gastrin can stimulate enterochromaffin-like cells to release histamine, which activates Gs-coupled H2 receptors expressed by parietal cells
  • gastrin is secreted by G cells in the antrum in response to luminal proteins and when stimulated by GRP from vagal efferents
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14
Q

H2-Blockers

A
  • these drugs, ending in the suffix “-tidine”, block H2 receptors on parietal cells to prevent their activation
  • they are really only effective at reducing nocturnal acid secretion, not post-prandial secretions, thus they are only second line therapy for GERD
  • they have limited side effects except for cimetidine, which inhibits CYP450, can contribute to hyperprolactinemia with galactorrhea, and anti-andronergic effects leading to impotence
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15
Q

PPIs

A
  • a group of drugs ending in the suffix “-prazole”
  • they form disulfide bonds with and irreversibly inhibit the H/K-ATPase on gastric parietal cells
  • considered first-line therapy for acid-related conditions
  • can impair absorption of dication metals such as Ca2+, Mg2+, and Fe2+, leading to osteoporosis and hip fractures, iron deficiency anemia, or hypomagnesia
  • also increase the risk for respiratory infections and C. diff
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16
Q

What role does octreotide play in the treatment of acid-related conditions?

A
  • somatostatin is capable of inhibiting gastrin and ECL cells, reducing gastric acid secretion
  • some gastrinomas even express somatostatin receptors, and in these cases, the somatostatin analog, octreotide, can be used to treat peptic ulcer disease
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17
Q

What is the difference between a laxative and a pro kinetic agent?

A

pro kinetics stimulate GI motility but laxatives work on the contents of the GI tract

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18
Q

Osmotic Laxatives

A
  • a group of non-absorbable substances that draw water into the intestinal lumen, leading to distention, which stimulates peristalsis
  • includes magnesium compounds, milk of magnesia, PEG, and lactulose
  • may cause diarrhea and dehydration
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19
Q

Which laxative is also a suitable treatment for hepatic encephalopathy and how does this work?

A
  • hepatic encephalopathy is a complication of cirrhosis mediated by a buildup of ammonia (NH3)
  • lactulose is a non-absorbable sugar and osmotic laxative, which is metabolized by intestinal flora into acidic metabolites
  • these acidic metabolites cause ammonia to turn to ammonium (NH4+), which is trapped in the intestinal lumen and excreted rather than absorbed
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20
Q

Psyllium

A
  • a bulk-forming laxative

- functions as a hydrophilic colloid that absorbs water and distends the colon, inducing peristalsis

21
Q

Docusate

A
  • a surfactant laxative

- facilities penetration of stool by water and lipids, serving as a stool softener to increase passage of stool

22
Q

Senna

A
  • a stimulant laxative, also known as a cathartic
  • it stimulates the enteric nervous system and cause colonic secretions
  • chronic use causes melanosis coli, a brown pigmentation of the colon
23
Q

Loperamide

A
  • a u-opioid receptor agonist that induces colonic phasic segmenting, an activity that increases colonic transit time
  • used to treat diarrhea because it doesn’t cross the BBB and thus poses no risk for addiction or dependence
24
Q

Diphenoxylate

A
  • a u-opioid receptor agonist that induces colonic phasic segmenting, an activity that increases colonic transit time
  • used to treat diarrhea
  • but does cross the BBB, so it is combined with atropine to prevent abuse
25
Q

Anti-diarrheal agents are contraindicated in patients with what sorts of diarrhea?

A

bloody diarrhea or diarrhea with fever

26
Q

What role does octreotide play in the treatment of diarrhea?

A

it is a somatostatin analog used to treat the diarrhea caused by VIPomas and carcinoid tumors

27
Q

Beta-islet cells are primarily stimulated by what two things?

A

high serum glucose and activation of B2 receptors

28
Q

Describe the mechanism whereby beta-islet cells release insulin in response to high serum glucose.

A
  • glucose enters beta-islet cells through GLUT-2
  • glucose is utilized to produce ATP, and the growing ATP/ADP ratio closes potassium channels, preventing further efflux and depolarizing the cell
  • depolarization activates voltage-gated calcium channels
  • the resulting calcium influx leads to release of insulin
29
Q

Describe the effects of insulin in the periphery and what receptor/mechanism mediates these effects.

A
  • insulin binds a TK receptor
  • binding stimulates anabolic processes like glyconeogenesis, protein synthesis, and fat storage
  • it also stimulates expression of GLUT4 receptors to promote glucose uptake by insulin-dependent tissues
30
Q

Short-Acting Insulin

A
  • includes glulisine, aspart, and lispro
  • rapid acting because they don’t form dimers or hexamers
  • useful for controlling post-prandial glucose levels
31
Q

Regular Insulin

A
  • the only insulin available IV
  • IV administration has a rapid onset and is the preferred treatment for DKA, but be careful and watch K+ levels
  • IV administration can also be useful in the treatment of hyperkalemia, driving potassium into cells, but should be co-administered with glucose to prevent hypoglycemia
32
Q

What is the preferred treatment for DKA?

A

IV regular insulin

33
Q

Which are the two long-acting insulins?

A

detemir and glargine

34
Q

List two treatments for hypoglycemia.

A

with IM glucagon or IV glucose

35
Q

Sulfonylureas

A
  • function by inhibiting potassium channel opening on beta-islet cells, stimulating release of endogenous insulin
  • includes first generation agents like tolbutamide and chlorpropamide, ending in the “-mide” suffix, and second generation agents like glipizide, glyburide, and glimepiride with the “-ride” suffix
  • side effects include weight gain, a risk for hypoglycemia, and possible sulfa-drug reaction
  • first generation also have a disulfiram-like effect and should not be used with alcohol
36
Q

Glinides

A
  • type II DM drugs ending in the suffix “-glinide”
  • function by inhibiting potassium channel opening on beta-islet cells, stimulating release of endogenous insulin
  • carry a risk for weight gain and hypoglycemia but are not sulfa-drugs
37
Q

GLP-1 Agonists

A
  • type II DM drugs ending in the suffix “-tide” (e.g. exenatide or liraglutide)
  • function by activating GLP-1 receptors, which delay gastric emptying (reducing post-prandial glucose peak), promoting satiety, inhibiting glucagon release, and stimulating endogenous insulin release
  • euglycemic so they don’t carry a risk for hypoglycemia or weight gain but may stimulate pancreatitis
38
Q

Gliptins

A
  • function by inhibiting DDP-4 and the breakdown of endogenous GLP-1; thereby, delaying gastric emptying, promoting satiety, inhibiting glucagon release, and promoting insulin release
  • euglycemic so they don’t carry a risk for hypoglycemia or weight gain but increase the risk for URTI
39
Q

Metformin

A
  • functions to increase insulin sensitivity and reduce hepatic gluconeogenesis by activating AMPK
  • may also promote weight stabilization or reduction
  • most common side effects are related to GI distress, including n/v, diarrhea, and anorexia
  • should not be used in those with renal failure as it increases the risk for lactic acidosis
40
Q

Glitazones

A
  • rosiglitazone and pioglitazone, type II DM medications
  • function by activating the intranuclear PPARy receptor, which then serves as a transcription factor for adiponectin
  • PPARy activation increases insulin sensitivity and storage of triglycerides
  • known to cause fluid retention with edema and exacerbation of heart failure, bone reabsorption with atypical fractures, and weight gain
41
Q

Pramlintide

A
  • an amylin analog used to treat type I and type II DM
  • functions like endogenous amylin, secreted in the same granules as insulin, to inhibit appetite, glucagon secretion, and gastric emptying
  • may cause GI upset or hypoglycemia
42
Q

Acarbose

A
  • inhibits alpha-glucosidases in the brush border
  • thus preventing digestion of disaccharides to monosaccharides, inhibiting absorption, and reducing post-prandial glucose spikes in type I DM
  • cause severe GI distress
43
Q

Miglitol

A
  • inhibits alpha-glucosidases in the brush border
  • thus preventing digestion of disaccharides to monosaccharides, inhibiting absorption, and reducing post-prandial glucose spikes in type I DM
  • cause severe GI distress
44
Q

Flozins

A
  • a group of type II DM medications that inhibit SGLT-2, thereby preventing reabsorption of glucose from the PCT
  • may cause UTI or hypotension due to osmotic diuresis and should not be used in those with renal dysfunction
45
Q

Mecasermin

A

an IGF-1 analog, which may cause hypoglycemia

46
Q

Desmopressin

A
  • an ADH agonist
  • activates V2 receptors in the collecting tubules and induces release of VIII and vWF from endothelial cells
  • useful in the treatment of central diabetes insipidous, vWF deficiency, FVIII deficiency, and bed wetting
  • may cause a dilutional hyponatremia
47
Q

Vaptans

A
  • a group of V2-receptor antagonists
  • first line therapy for those with SIADH
  • may cause a hypernatremia or central pontine myelinolysis
48
Q

PTU

A
  • inhibits thyroperoxidase and 5’-deiodinase
  • useful in treating hyperthyroidism as well as thyroid storm
  • may cause an agranulocytosis, hepatotoxicity, drug-induced lupus, ANCA-associated vasculitis
  • not teratogenic, however, so the preferred agent for pregnancy
49
Q

Methiomazole

A
  • inhibits thyroperoxidase
  • not useful in the treatment of thryoid storm but is the preferred drug for hyperthyroidism
  • may cause a lupus-like syndrome or agranulocytosis
  • contraindicated in pregnancy due to teratogenic effects

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