GI Pharmacology Flashcards
(107 cards)
1
Q
Proton pump inhibitors (PPIs)
A
Act directly on the H/K/ATPase pump to prevent secretion of acid
2
Q
Indication for PPIs
A
GERD, peptic ulcer disease, treatment of gastritis and for gastrinomas (zollinger-Ellison syndrome)
3
Q
Suffix PPI
A
Prazole
4
Q
Side effects PPI
A
Hip fracture (decreases calcium absorption) Pneumonia (bacteria overgrowth in less acidic environment
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
6
Q
Causes of gastritis
A
Metaplasia, stres, coffee, h pylori
7
Q
PPI and peptic ulcer
A
Caused by h pylori, gastrinomas, and medications
8
Q
Where are peptic ulcers most common
A
Lesser curve of stomach and first part of the duodenum
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
10
Q
Why are PPI more effective than other drugs that aim to reduce acid production
A
Irreversibly blocks h/k/atpase
11
Q
Side effects PPI
A
Hip fracture
Pneumonia
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
13
Q
PPI and bacteria
A
Pneumonia, c diff associated diarrhea
14
Q
H2 blocker
A
Antagonists at the histamine H2 receptor, which are found within parietal cells of the stomach.
15
Q
Suffix H2 blockers
A
Itidine
16
Q
Indications for H2 blockers
A
Indigestion and heartburn (GERD) and promote the healing of ulcers
17
Q
MOA H2 blockers
A
Block histamine H2 receptors in parietal cells of the stomach, leading to reduced acid secretion
18
Q
Examples of H2 blockers
A
Cimetidine, ranitidine, famotidine, and nizatidine
19
Q
Indications for H2 blockers
A
GERD, peptic ulcer
20
Q
How does GERD present
A
Regurgitation, dysphagia, heartburn, night time cough and dyspnea
21
Q
How H2 block help GERD
A
Decrease parietal acid secretion
22
Q
How H2 blocker help peptic ulcer
A
Promote healing of duodenal and gastric ulcers, although recurrence is common when used alone
23
Q
MOA H2 receptor blocker
A
Reversible block H2 receptors as competitive inhibitors
24
Q
What happens when H2 is blocked
A
Reduction of histamine stimulated gastric acid secretion.
25
What happens when histamine binds H2
Stimulates parietal cell acid secretion, in addition to gastric and acetylcholine RAPID effects
26
H2 location
Parietal cells of stomach
27
H2 blocker
Reduce acid secretion rom parietal cells
28
Cimetidine side effects
Decrease creatinine clearance (inhibit tubular secretion)
| Crosses BBB may lead to headache and dizziness and confusion
29
Cimetidine MOA
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
30
Ranitidine side effect
Decreased creatinine clearance via inhibition of tubular secretion
31
What can cimetidine cross
BBB, placenta,
32
Anti androgen effects of cimetidine
Exaggerated effects of estrogen, manifesting as galactorrhea and amenorrhea in women and impotence and gynecomastia in men
33
Cimetidine inhibit p450
Decreases metabolism of particular medications
34
Why increase pneumonia with cimetidine and ranitidine
Increasing pH of stomach so bacteria are able to colonize and migrate
35
CNS changes cimetidine
Espicially elderly who have persisting liver or kidney disease
Hallucinations, confusion, CNS depression or excitation
36
Octreotide
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
37
Indications octreotide
Acute varicella bleeds
Pituitary tumors (GH secreting)
Carcinoid tumors
VIPoma
38
Octreotide and acute varicella bleeds
Somatostatin analog induces splanchnic constriction, leading to decreased portal vessel pressure in bleeding varies
39
Octreotide andpituitary tumors
Inhibits action of TSH and GH from anterior pituitary
Helpful in tumors productive TSH (thyrotropinoma) and GH (gigantism and acromegaly)
40
Octreotide and carcinoid tumors
Decreases secretion of serotonin by the tumor and decreases the breakdown product of serotonin
41
Octreotide and VIPoma
Control diarrhea associated with VIPomas bc blocks the secretion and action of VIP
42
Odansetron
Antiemetic used to control nausea and vomiting in patients undergoing chemo or patients who are postoperative
43
MOA ondansetron
5-HT3 serotonergic antagonist and leads to receptor antagonists activity centrally, causing inhibition of the medullary chemoreceptive zone
44
Side effects ondansetron
Headache and constipation
45
Why not give ondansetron to patients with with congenital arrhythmias , CHF, bradycardia or patients taking QT interval prolonging medications . Why the Qt
Can lead to further QT interval prolongation
46
Indications for ondansetron
Postoperative vomiting
| Chemotherapy (nausea stuff) give 30 min before chemo
47
MOA ondansetron as serotonergic antagonist
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
MOA ondansetron as centrally acting antiemetic
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
Side effects ondansetron
Headache, constipation, QT prolongation
50
Promethazine (phenergan)
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
Side effects promethazine (phenergan)
Respiratory depression, sedation, dry mouth, urinary retention, extrapyramidal symptoms(dystonia, akathisia, Parkinsonism)
52
Who should not take promethazine (phenergan)
Kids under 2, due to increased risk of death, related to severe respiratory depression
53
MOA promethazine
H1 receptor antagonist (antiemetic)
| Weak dopamine antagonist (D2 blocks thus decreasing nausea and vom)
54
Indications for promethazine
Nausea and vomiting, motion sickness
55
Side effects promethazine
Respiratory depression
Sedation, CNS depression
Anticholinergic effects
Extrapyramidal symptoms
56
Metoclopramide
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
Metoclopramide :D2 antagonist
Prevents stimuli at the chemoreceptors trigger zone int he CNS from causing nausea and vomiting along with the serotonin blockade
58
Metoclopramide: enhancing acetylcholine sensitivity
This medication increases resting tone and contraction amplitude of gastric contractions by enhancing acetylcholine sensitivity
59
Side effects metoclopramide
Parkinsonian side effects, such as dystonia and involuntary movements . Furthermore, dopamine antagonism may lead to hyperprolactinemia and galactorrhea in patients.
60
Who should not take metoclopramide
Patients with small bowel obstructions as well a s those with Parkinson’s disease as it may worsen symptoms
61
Indications for metoclopramide
```
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
MOA metoclopramide
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
Combo of D2 antagonism combined with 5HT3 inhibition
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
Side effects metoclopramide
Parkinsonian (D antagonist)
| Galactorrhea (block D no negative inhibition of prolactin release from anterior pituitary—>hyperprolactinemia)
65
Who should not have metoclopramide
Small bowel obstruction(due to increase in gastric motility)
| Parkinson’s disease (bc d antagonist)
66
Sucralfate (Carafate)
Antiulcer agent used in patients with duodenal ulcers
67
MOA sucralfate (carafate)
Creating a barrier that protects existing ulcers from stomach acids and pepsin, allowing healing
68
What is the barrier created by sucralfate (carafate)
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
Does sucralfate decrease acid secretion or neutralize acid
Nope
70
Indications for sucralfate (carafate)
GI ulcer
71
Side effects sucralfate
Constipation
72
In order for sucralfate to work it must be in an __ environment
Acidic
73
What should we not take sucralfate with
Antacids
74
Why give sucralfate on empty stomach
More effective
75
Oral suspension sucralfate
Pill too large to swallow for some
| May give suspension
76
Why may sucralfate decrease absorption of other meds
Give two hours before or after other medications as it may decrease absorption of other medications, espicially phenytoin, digoxin, warfarin, and fluoroquinolone antibiotics
77
Pancreatin, pancrelipase (pancreatic enzymes)
Given as digestive enzyme supplements for those missing pancreatic enzymes or those who have pancreatic insuffiency.
78
What are pancreatin and pancrelipase
Mixtures of several exocrine pancreas produced digestive enzymes, like amylase, lipase and protease
79
Indications for pancreatin and pancrelipase
Cystic fibrosis, pancreatic inadequacy
80
Side effect pancreatin, pancrelipase
GI distress , should also have 34 hour fat excretion measured to measure effectiveness
81
MOA pancreatin and pancrelipase
Produced by exocrine cells
| Enteric coated, delayed release capsules that dissolve in the duodenum and jejunum and should not be crushed or chewed
82
Indications pancreatin, pancrelipase
```
CF (blocked panctic ducts)
pancreatic inadequacy (pancreatitis, obstruction of duct, patients who have had pancreatectomy, leading to impaired function)
```
83
Side effect pancreatic enzymes
GI distress-diarrhea, nausea, vomiting
84
Pancreatic enzymes are inactivated by __ __
Gastric acid
So give H2 blockers and PPIs to decrease stomach acid secretion .
Or enteric coated to prevent inactivation
85
Pancreatic enzymes do a 24 hour fat excretion
There should be a profound decrease in fat excretion as these enzymes help fat absorption
86
Pancreatic enzymes take with every meal and SoCal
Ok
87
Total parent earl nutrition (TPN) or parenteral nutrition (PN)
Feeding can be done intravenously when enteral feeding is contradicted
88
What is in TPN solutions
Fat emulsions (lipids), dextrose, aa, vitamins, and minerals
89
How is TPN, PN administered
Slowly suing an infusion pump, through a large, central vein.
90
Side effects TPN
Nausea, vomiting, hyperglycemia, hyperlipidemia, reseeding syndrome
91
MOA TPN PN
Nutrition given outside GI
92
So not add meds to TPN line
Ok
93
Activated charcoal (actidose)
Agent that binds to poisonous chemicals to prevent toxicity
94
Indication for activated charcoal
Remove ingested large molecule poisons containing carbon.
95
Side effects activated charcoal
Black stools and GI distress characterized by cramping, nausea, vomiting, diarrhea, constipation and vomiting
96
How administer activated charcoal
Oral or NG tube route
97
Administering activated charcoal with an ___ may neutralize the anticipated effects
Antidote
98
What does activated charcoal bind
Large toxic molecules contains carbon atoms
| Acetaminophen, asprin, NSAIDS, tricyclic antidepressants
99
What does activated charcoal have poor affinity for
Heavy metals-caustics, corrosives, alcohols, chlorine’s, lithium, cyanide, iodine, and petroleum distillates
100
What happens to molecules bound to the acvitvated charcoal
Excreted in black colored stools since charcoal cant be absorbed into the blood
101
Indication for activated charcoal
Ingested poison
102
Side effects activated charcoal
Black stool
| GI distress
103
Sometimes cathartic such as __ are administered with the first dose of activated charcoal to stimulate intestinal motility and increase elimination
Sorbitol
104
Who should not be given activated charcoal
Patients with bowel perforation or obstruction bc of GI distress
105
When should you give activated charcoal
ASAP after poison ingestion
106
Gastric lovage
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
Do not give activated charcoal with antidotes
The activated charcoal may absorb the antidote and neutralize the beneficial effects
