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Pharmacology > GI Pharmacology > Flashcards

GI Pharmacology Flashcards

1
Q

Proton pump inhibitors (PPIs)

A

Act directly on the H/K/ATPase pump to prevent secretion of acid

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2
Q

Indication for PPIs

A

GERD, peptic ulcer disease, treatment of gastritis and for gastrinomas (zollinger-Ellison syndrome)

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3
Q

Suffix PPI

A

Prazole

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4
Q

Side effects PPI

A 
Hip fracture (decreases calcium absorption)
Pneumonia (bacteria overgrowth in less acidic environment
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5
Q

PPI and zollinger Ellison

A

Caused by gastric secreting tumor of the pancreas that stimulates the acid secreting cells of the stomach to maximal activity.
Cause ulceration

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6
Q

Causes of gastritis

A

Metaplasia, stres, coffee, h pylori

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7
Q

PPI and peptic ulcer

A

Caused by h pylori, gastrinomas, and medications

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8
Q

Where are peptic ulcers most common

A

Lesser curve of stomach and first part of the duodenum

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9
Q

PPI mechanism

A

Inhibit H/K/ATPase located in gastric parietal. Cells

Inhibits gastric secretion be this is the final stage in gastric secretion

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10
Q

Why are PPI more effective than other drugs that aim to reduce acid production

A

Irreversibly blocks h/k/atpase

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11
Q

Side effects PPI

A

Hip fracture

Pneumonia

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12
Q

Hip fracture PPI

A

Malabsorption of Ca
Proton pump inhibitors promote hypochlorhydria and interfere with absorption of ca, leading to increased frequency of hip fracture
Also associated with low mg

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13
Q

PPI and bacteria

A

Pneumonia, c diff associated diarrhea

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14
Q

H2 blocker

A

Antagonists at the histamine H2 receptor, which are found within parietal cells of the stomach.

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15
Q

Suffix H2 blockers

A

Itidine

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16
Q

Indications for H2 blockers

A

Indigestion and heartburn (GERD) and promote the healing of ulcers

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17
Q

MOA H2 blockers

A

Block histamine H2 receptors in parietal cells of the stomach, leading to reduced acid secretion

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18
Q

Examples of H2 blockers

A

Cimetidine, ranitidine, famotidine, and nizatidine

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19
Q

Indications for H2 blockers

A

GERD, peptic ulcer

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20
Q

How does GERD present

A

Regurgitation, dysphagia, heartburn, night time cough and dyspnea

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21
Q

How H2 block help GERD

A

Decrease parietal acid secretion

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22
Q

How H2 blocker help peptic ulcer

A

Promote healing of duodenal and gastric ulcers, although recurrence is common when used alone

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23
Q

MOA H2 receptor blocker

A

Reversible block H2 receptors as competitive inhibitors

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24
Q

What happens when H2 is blocked

A

Reduction of histamine stimulated gastric acid secretion.

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25
Q

What happens when histamine binds H2

A

Stimulates parietal cell acid secretion, in addition to gastric and acetylcholine RAPID effects

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26
Q

H2 location

A

Parietal cells of stomach

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27
Q

H2 blocker

A

Reduce acid secretion rom parietal cells

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28
Q

Cimetidine side effects

A

Decrease creatinine clearance (inhibit tubular secretion)

Crosses BBB may lead to headache and dizziness and confusion

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29
Q

Cimetidine MOA

A

Anti androgen which is a competitive antagonist at DHT receptors
Potent inhibitor of cytochrome p450 enzyme system and may decrease the metabolism of the medications

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30
Q

Ranitidine side effect

A

Decreased creatinine clearance via inhibition of tubular secretion

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31
Q

What can cimetidine cross

A

BBB, placenta,

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32
Q

Anti androgen effects of cimetidine

A

Exaggerated effects of estrogen, manifesting as galactorrhea and amenorrhea in women and impotence and gynecomastia in men

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33
Q

Cimetidine inhibit p450

A

Decreases metabolism of particular medications

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34
Q

Why increase pneumonia with cimetidine and ranitidine

A

Increasing pH of stomach so bacteria are able to colonize and migrate

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35
Q

CNS changes cimetidine

A

Espicially elderly who have persisting liver or kidney disease

Hallucinations, confusion, CNS depression or excitation

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36
Q

Octreotide

A

Long acting somatostatin analog with various indications. It is used acutely to help stop varicella bleeds, for hormone secreting tumors(inhibits secretion. And activity of various endocrine hormones. Helpful in growth hormone secreting tumors, which may cause acromegaly or gigantism . Also treat diarrhea in carcinoid tumors and VIPomas

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37
Q

Indications octreotide

A

Acute varicella bleeds
Pituitary tumors (GH secreting)
Carcinoid tumors
VIPoma

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38
Q

Octreotide and acute varicella bleeds

A

Somatostatin analog induces splanchnic constriction, leading to decreased portal vessel pressure in bleeding varies

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39
Q

Octreotide andpituitary tumors

A

Inhibits action of TSH and GH from anterior pituitary

Helpful in tumors productive TSH (thyrotropinoma) and GH (gigantism and acromegaly)

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40
Q

Octreotide and carcinoid tumors

A

Decreases secretion of serotonin by the tumor and decreases the breakdown product of serotonin

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41
Q

Octreotide and VIPoma

A

Control diarrhea associated with VIPomas bc blocks the secretion and action of VIP

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42
Q

Odansetron

A

Antiemetic used to control nausea and vomiting in patients undergoing chemo or patients who are postoperative

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43
Q

MOA ondansetron

A

5-HT3 serotonergic antagonist and leads to receptor antagonists activity centrally, causing inhibition of the medullary chemoreceptive zone

44
Q

Side effects ondansetron

A

Headache and constipation

45
Q

Why not give ondansetron to patients with with congenital arrhythmias , CHF, bradycardia or patients taking QT interval prolonging medications . Why the Qt

A

Can lead to further QT interval prolongation

46
Q

Indications for ondansetron

A

Postoperative vomiting

Chemotherapy (nausea stuff) give 30 min before chemo

47
Q

MOA ondansetron as serotonergic antagonist

A

Serotonin 5-HT3 receptor antagonist . Antiemetic activity of the drug is brought about through the inhibition of 5-HT3 receptors present both centrally (medullary chemoreceptors zone) and peripherally (GI tract). This inhibition in turn inhibits the visceral afferent stimulation of the vomiting center, as well as through direct inhibition of serotonin activity within the area postrema and the chemoreceptors trigger zone

48
Q

MOA ondansetron as centrally acting antiemetic

A

Antagonist activity , both centrally and at visceral receptors. A large amount of the activity comes from its central inhibition fo the medullary chemoreceptors zone

49
Q

Side effects ondansetron

A

Headache, constipation, QT prolongation

50
Q

Promethazine (phenergan)

A

H1 receptor antagonist and a weak dopamine antagonist that competes with H1 and D2 receptors in the chemoreceptors triggger zone of the brain to decrease nausea, vomiting, and motion sickness

51
Q

Side effects promethazine (phenergan)

A

Respiratory depression, sedation, dry mouth, urinary retention, extrapyramidal symptoms(dystonia, akathisia, Parkinsonism)

52
Q

Who should not take promethazine (phenergan)

A

Kids under 2, due to increased risk of death, related to severe respiratory depression

53
Q

MOA promethazine

A

H1 receptor antagonist (antiemetic)

Weak dopamine antagonist (D2 blocks thus decreasing nausea and vom)

54
Q

Indications for promethazine

A

Nausea and vomiting, motion sickness

55
Q

Side effects promethazine

A

Respiratory depression
Sedation, CNS depression
Anticholinergic effects
Extrapyramidal symptoms

56
Q

Metoclopramide

A

Antiemetic and gastroprokinetic agent, which works as an antagonist at D2 dopaminergic receptors, a 5HT blocker in the CNS as well as enhancing the sensitivity to acetylcholine in gastric tissue and increasing lower esophageal tone

57
Q

Metoclopramide :D2 antagonist

A

Prevents stimuli at the chemoreceptors trigger zone int he CNS from causing nausea and vomiting along with the serotonin blockade

58
Q

Metoclopramide: enhancing acetylcholine sensitivity

A

This medication increases resting tone and contraction amplitude of gastric contractions by enhancing acetylcholine sensitivity

59
Q

Side effects metoclopramide

A

Parkinsonian side effects, such as dystonia and involuntary movements . Furthermore, dopamine antagonism may lead to hyperprolactinemia and galactorrhea in patients.

60
Q

Who should not take metoclopramide

A

Patients with small bowel obstructions as well a s those with Parkinson’s disease as it may worsen symptoms

61
Q

Indications for metoclopramide

A 
Antiemetic  (5HT serotonin receptor antagonist the chemoreceptors trigger zone of the brain to prevent nausea and vomiting)
Promotility agent (helpful in gastroparesis and GERD Asia increases duodenal and jejunal peristalsis improving the tone and amplitude of gastric contractions. This medication. Also increases the lower esophageal sphincter (LES) tone. It is important to also note it does these actions without increasing gastric secretion
62
Q

MOA metoclopramide

A

Increased resting tone of gastric contractions with relaxation of pyloric sphincter and duodenal bulb (motility)

Antagonist at D2-serotonergic blocking activity int he chemoreceptors zone as well as enhancing responsiveness to acetylcholine of gastric tissue.

63
Q

Combo of D2 antagonism combined with 5HT3 inhibition

A

Blocks receptors in the chemoreceptors trigger zone of the CNS from causing nausea and vomiting . Furthermore D2 antagonism contributes to gastroprokinetic activity, but an enhancement of Ach leads to increased gastric emptying though without an increase of gastric secretions

64
Q

Side effects metoclopramide

A

Parkinsonian (D antagonist)

Galactorrhea (block D no negative inhibition of prolactin release from anterior pituitary—>hyperprolactinemia)

65
Q

Who should not have metoclopramide

A

Small bowel obstruction(due to increase in gastric motility)

Parkinson’s disease (bc d antagonist)

66
Q

Sucralfate (Carafate)

A

Antiulcer agent used in patients with duodenal ulcers

67
Q

MOA sucralfate (carafate)

A

Creating a barrier that protects existing ulcers from stomach acids and pepsin, allowing healing

68
Q

What is the barrier created by sucralfate (carafate)

A

Sticky, viscid barrier created by the medication adheres to the ulcer crater for up to 6 hours. The medication does not provide any acid neutralizing response or decrease acid secretion

69
Q

Does sucralfate decrease acid secretion or neutralize acid

A

Nope

70
Q

Indications for sucralfate (carafate)

A

GI ulcer

71
Q

Side effects sucralfate

A

Constipation

72
Q

In order for sucralfate to work it must be in an __ environment

A

Acidic

73
Q

What should we not take sucralfate with

A

Antacids

74
Q

Why give sucralfate on empty stomach

A

More effective

75
Q

Oral suspension sucralfate

A

Pill too large to swallow for some

May give suspension

76
Q

Why may sucralfate decrease absorption of other meds

A

Give two hours before or after other medications as it may decrease absorption of other medications, espicially phenytoin, digoxin, warfarin, and fluoroquinolone antibiotics

77
Q

Pancreatin, pancrelipase (pancreatic enzymes)

A

Given as digestive enzyme supplements for those missing pancreatic enzymes or those who have pancreatic insuffiency.

78
Q

What are pancreatin and pancrelipase

A

Mixtures of several exocrine pancreas produced digestive enzymes, like amylase, lipase and protease

79
Q

Indications for pancreatin and pancrelipase

A

Cystic fibrosis, pancreatic inadequacy

80
Q

Side effect pancreatin, pancrelipase

A

GI distress , should also have 34 hour fat excretion measured to measure effectiveness

81
Q

MOA pancreatin and pancrelipase

A

Produced by exocrine cells

Enteric coated, delayed release capsules that dissolve in the duodenum and jejunum and should not be crushed or chewed

82
Q

Indications pancreatin, pancrelipase

A 
CF (blocked panctic ducts)
pancreatic inadequacy (pancreatitis, obstruction of duct, patients who have had pancreatectomy, leading to impaired function)
83
Q

Side effect pancreatic enzymes

A

GI distress-diarrhea, nausea, vomiting

84
Q

Pancreatic enzymes are inactivated by __ __

A

Gastric acid
So give H2 blockers and PPIs to decrease stomach acid secretion .
Or enteric coated to prevent inactivation

85
Q

Pancreatic enzymes do a 24 hour fat excretion

A

There should be a profound decrease in fat excretion as these enzymes help fat absorption

86
Q

Pancreatic enzymes take with every meal and SoCal

A

Ok

87
Q

Total parent earl nutrition (TPN) or parenteral nutrition (PN)

A

Feeding can be done intravenously when enteral feeding is contradicted

88
Q

What is in TPN solutions

A

Fat emulsions (lipids), dextrose, aa, vitamins, and minerals

89
Q

How is TPN, PN administered

A

Slowly suing an infusion pump, through a large, central vein.

90
Q

Side effects TPN

A

Nausea, vomiting, hyperglycemia, hyperlipidemia, reseeding syndrome

91
Q

MOA TPN PN

A

Nutrition given outside GI

92
Q

So not add meds to TPN line

A

Ok

93
Q

Activated charcoal (actidose)

A

Agent that binds to poisonous chemicals to prevent toxicity

94
Q

Indication for activated charcoal

A

Remove ingested large molecule poisons containing carbon.

95
Q

Side effects activated charcoal

A

Black stools and GI distress characterized by cramping, nausea, vomiting, diarrhea, constipation and vomiting

96
Q

How administer activated charcoal

A

Oral or NG tube route

97
Q

Administering activated charcoal with an ___ may neutralize the anticipated effects

A

Antidote

98
Q

What does activated charcoal bind

A

Large toxic molecules contains carbon atoms

Acetaminophen, asprin, NSAIDS, tricyclic antidepressants

99
Q

What does activated charcoal have poor affinity for

A

Heavy metals-caustics, corrosives, alcohols, chlorine’s, lithium, cyanide, iodine, and petroleum distillates

100
Q

What happens to molecules bound to the acvitvated charcoal

A

Excreted in black colored stools since charcoal cant be absorbed into the blood

101
Q

Indication for activated charcoal

A

Ingested poison

102
Q

Side effects activated charcoal

A

Black stool

GI distress

103
Q

Sometimes cathartic such as __ are administered with the first dose of activated charcoal to stimulate intestinal motility and increase elimination

A

Sorbitol

104
Q

Who should not be given activated charcoal

A

Patients with bowel perforation or obstruction bc of GI distress

105
Q

When should you give activated charcoal

A

ASAP after poison ingestion

106
Q

Gastric lovage

A

The stomach may be pumped within 30 minutes of ingesting toxic substances. Often given after gastric lavage to remove any poisonous substances that have reached beyond the stomach

107
Q

Do not give activated charcoal with antidotes

A

The activated charcoal may absorb the antidote and neutralize the beneficial effects

Pharmacology (52 decks)

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