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IPAP 21-2 Soph Semester > GI MEDs > Flashcards

GI MEDs Flashcards

1
Q

Where is pepsinogen found

A

Pepsinogen: inactive form of pepsin found in the Chief cells of the gastric glands

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2
Q

What is pepsin

A

Pepsin: protein splitting enzyme capable of digesting nearly all types of dietary protein and is formed from pepsinogen in the presence of HCl

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3
Q

What is the role of Intirisic Factor

A

Intrinsic Factor: aids in the absorption of vitamin B12 and is found in the Parietal cells of the gastric glands

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4
Q

What stimulates the production of HCL in the Proptoin Pump

A

Acetylcholine (parasympathetic)
Histamine
Gastrin

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5
Q

What is the role of prostaglandins in protection of the GI

A

Inhibit basal and stimulated gastric acid secretion

Diminishes proton pump action

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6
Q

What are the alarm s/s of GERD

A

Alarm Symptoms: dysphagia, odynophagia, bleeding, weight loss, choking, and epigastric mass

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7
Q

What is the nonpharm approach to GERD

A

DIet modification

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8
Q

What medications should be avoided in pts w/ GERD

A

Avoid medications that may reduce LES pressure, delay gastric emptying, or cause direct irritation

Alpha antagonist, anticholinergic, benzodiazepines, CCBs, estrogen, nitrates, opiates, TCAs, theophylline, NSAIDs, and aspirin

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9
Q

What is the pharm approach to moderate GERD

A

Start with H2 inhibitors in addition with antacids for breakthrough GERD symptoms

If symptoms are not controlled after 4 weeks and max dose of H2 inhibitors switch to a Proton Pump Inhibitor (PPI)

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10
Q

What is the pharm approach to frequent GERD

A

Start with PPI

should administer 30-60min prior to meal; may increase to BID dosing if needed

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11
Q

What are the causes of PUD

A

Helicobacter pylori (H.pylori) positive

NSAID induced

Stress Ulcers or Stress-Related Mucosal Damage (SRMD)
SRMD is the preferred term because the mucosal lesions range from superficial gastritis and erosions to deep ulcers

Zollinger-Ellison Syndrome (ZES): gastric acid hypersecretory disease caused by gastrin-secreting tumor and leading to multiple, severe duodenal ulcers

Minor contributor to PUD: inadequate mucosal defense against gastric acid

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12
Q

All pts with PUD should be tested for

A

H. Pylori

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13
Q

What are the noninvasive and invasive Tests for H. Pylori

A

Noninvasive:
Fecal antigen assay
Urea-breath testing (UBT)
Serologic testing

Invasive:
Gastric mucosal biopsies by endoscopy

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14
Q

Wha this the Tx for H. Pylori ulcers

A

Anti-secretory agent: Proton Pump Inhibitor (PPI)

Two antibiotics
1st Line: Triple therapy - clarithromycin + amoxicillin (may replace with metronidazole if allergic to PCN)

2nd Line: Quadruple therapy - for patients that cannot take clarithromycin: tetracycline + metronidazole + bismuth subsalicylate

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15
Q

What is the length of Tx for duodenal ulcers and gastric ulcers

A

If PUD is present, continue PPI for 4-8 weeks for duodenal and 8-12 weeks for gastric ulcers

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16
Q

How are the urea breath test and the stool antigen test performed

A

Urea-breath test (UBT) or stool antigen tests are preferred

Must be off PPI for 1-2 weeks prior to the test

Can wait to confirm until after completion of the PPI course

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17
Q

What is standard triple therapy

A

PPI PO twice daily

Clarithromycin 500 mg PO twice daily
Amoxicillin 1 g orally PO twice daily
(or metronidazole 500 mg PO BID, if PCN allergic)

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18
Q

What is standard Quad therapy

A

PPI PO twice daily

Bismuth subsalicylate 262mg - two tablets PO four times daily

Tetracycline 500mg PO four times daily

Metronidazole 500mg PO three times daily

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19
Q

What does COX-1 do

A

Increase blood flow to gastric mucosa and kidneys

Increase platelet aggregation via thromboxane A2 pathway

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20
Q

What does COX-2 do

A

Increase renal blood flow

Makes PG that activate and sensitize nociceptors (increased pain)

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21
Q

What is the Tx approach to NSAID induced ulcers

A

DC NSAIDS Or reduce
Switch to Acetominphine or Asprin

Celecoxib (Celebrex):
Should be reserved as last line
Associated with cardiovascular risk

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22
Q

What are the prevention methods for stress ulcers

A

Proton Pump Inhibitors (PPI)

Histamine-2 Receptor Antagonists (H2RA)

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23
Q

What is the 1st line therapy for intermittent S/s of acid

A

Antacids

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24
Q

What is the MOA of Sodium Bicarb

A

Mechanism of Action:
Reacts with HCL to produce carbon dioxide and sodium chloride.

CO2 results in gastric distention and belching

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25
Q

What is the MOA of calcium carbonate

A

Calcium Carbonate (Tums, Oscal)

Less acid neutralizing capability compared to sodium bicarbonate and other antacids

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26
Q

What is the MOA and clin use of Mag Hydroxide

A

Mechanism of Action: reacts slowly with HCL to form magnesium chloride and water

Clinical Use: may be used as antacid or laxative (diarrhea)

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27
Q

What is the ADE and caution of Mag Mydroxide

A

Adverse Effects: osmotic diarrhea caused by unabsorbed magnesium salts

Caution: renal insufficient patients should not take magnesium hydroxide long-term

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28
Q

What is the MOA of aluminum hydroxide

A

Mechanism of Action: reacts with HCl to form aluminum chloride and water. Antacid

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29
Q

What is the ADE of aluminum hydroxide

A

Aluminum salts cause constipation

Aluminum is also absorbed and excreted in the kidneys (Renal insufficiency: should not take long-term)

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30
Q

What is the MOA of H2 antagonists

A

Mechanism of Action:
competitively block the binding of histamine to H2 receptors on the parietal cell, inhibiting gastric acid secretion induced by histamine

Suppress basal and meal-stimulated acid secretion

Reduces acid secretion stimulated by gastrin and cholinometic agents

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31
Q

Which is better in erosive esophagitis, PPI or H2 blocker

A

PPI

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32
Q

What are the ADE of H2 blockers

A

CNS effects such as headache, dizziness, fatigue, somnolence, and confusion are most common

Prolonged cimetidine use is associated with rare development of gynecomastia

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33
Q

What is cimetidine

A

H2 blocker

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34
Q

How is cimetidine cleared

A

Competes with the medications and creatinine for tubular secretion in the kidney

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35
Q

What is Ranitidine

A

H2 blocker

Low percentage of side effects and good efficacy

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36
Q

What is Famotidine

A

Pepcid AC

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37
Q

What are the most effective agents for the Tx of GERD

A

PPI

Pantoprazole (Protonix)
Omeprazole (Prilosec)
Omeprazole/Bicarbonate ion (Zegrid)
Esomeprazole (Nexium) 
Rabeprazole (Aciphex) 
Lansoprazole (Prevacid) 
Dexlansoprazole (Dexilant)
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38
Q

What is the MOA of PPI

A

Administered as a prodrug

Irreversibly binds to the H+/K+ ATPase enzyme system (proton pump) of the cells suppressing secretion of hydrogen ions

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39
Q

What is the advantage of PPI over H2RAs

A

Greater degree of acid suppression achieved and typically longer duration of action than H2RAs

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40
Q

What are the newly learned ADE of PPI

A

Increase RSK of FX
Hypomagnesemia
C. DIff
CAP

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41
Q

What is the MOA and clin use of Surcralfate

A

Covers the ulcer site and protects it against acid
Stimulates prostaglandin release
Not absorbed systemically, adverse effects are uncommon
Requires acidic pH for activation

Clinical Use:
Heals peptic ulcers, but not widely used as much because it is not as effective as H2 blockers and PPIs

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42
Q

What is the MOA of misoprostol

A

Prostaglandin Analog
Synthetic, oral prostaglandin E1 analog that has both antisecretory and mucosal protective properties

Clinical Use:
Approved for the prevention of NSAID-induced ulcers in high-risk patients

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43
Q

Can pregnant pts get misoprostol

A

NO

Miscarriages

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44
Q

What is the only combination Rx product that contains metronidazole and tetracycline for the treatment of H. pylori

A

Bismuth, aka petobismol

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45
Q

What is the clin use of Bismuth/ Pepto

A

Nonspecific treatment of dyspepsia and acute diarrhea
Prevention of traveler’s diarrhea
Used in quadruple drug regimens for H. pylori eradication

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46
Q

What are the ADE of Pepto/ bismuth

A

Blackening of Stool
Darkening Of tongue
Renal insufficiency
May bind to other drugs

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47
Q

What is the MOA and Clin Use of Metoclopramide

A

Prokinetic Agent

Dopamine antagonist; stimulates motility of the upper GI track without effecting secretions

Enhances the response to Acetylcholine of tissue in upper GI tract causing enhanced motility and accelerated gastric emptying without stimulating gastric, biliary, or pancreatic secretions

Also block serotonin receptors in the chemoreceptor trigger zone, resulting in the anti-emetic action

Clinical Use: gastroesophageal reflux, prevention of N/V from chemotherapy, impaired gastric emptying (i.e diabetic gastroparesis)

48
Q

What drug helps N/V in chem pts

A

Metoclopramide

5HTs Antagonists

49
Q

What are the MOA and Clin use of Ondansetron/ Granisetron/ Dolasetron/ Palonosetron

A

5hT3 antagonists

Mechanism of Action: block presynaptic serotonin receptors on sensory vagal fibers in gut wall as well as central blockade in the vomiting center and CTZ

Clinical Use:
General medical use
Post-operative nausea and vomiting
Chemotherapy Induced Nausea and Vomiting (CINV) 
Radiation-Induced nausea and vomiting
50
Q

What is the ADE of Ondansetron and other drugs that end in -setron

A

Well tolerated; most common is headache, dizziness, and constipation

QTc prolongation; small but statistically significant prolongation of QT interval (most pronounced with dolasetron)

51
Q

Which 5HT3 has the most pronounces QT elongation effects

A

Dolasetron

52
Q 
What drug class are
 Meclizine (Antivert,Bonine)
Diphenhydramine (Benadryl) 
Dimenhydrinate (Dramamine)
Doxylamine (Unisom)
Doxylamine/pyridoxine (Diclegis)
A

Antihistamines

53
Q

What is the MOA of antihistamines

A

Block histamine H1 at the vestibular apparatus preventing vomiting due to motion sickness
All cause some drowsiness and anticholinergic side effects

54
Q

What drug class are prochloperazine and promethazine

A

Phenothiazines

55
Q

What is the MOA and CLin use of Phenothizies: prochloperazine and promethazine

A

Mechanism of Action:
Block dopamine, muscarinic, and histamine receptors in Chemoreceptor Trigger Zone (CTZ)

Sedation is due to their anti-histamine activity

Clinical Use: effective oral, injectable, and rectal anti-emetics for inpatient and outpatient use

56
Q

What is promethazine

A

A 1st gen antihistamine used for the treatment of nausea, vomiting, and motion sickness

DO NOT USE SubQ

IV formulation should be diluted because of tissue necrosis r

57
Q

What is the MOA and Clin use of scopalamine

A

Mechanism of Action: cholinergic antagonist with greater central (more lipophilic; blocks muscarinic receptors in the vestibular system) than peripheral effects

Clinical Indication: motion sickness; surgical adjunct (blocks short-term memory and decreases saliva)

58
Q

What are the important monitoring and ADE of scopalamine

A

Monitoring: HR, temperature, Urinary Output (UOP)

Adverse Effects: excessive anticholinergic effects (dry mouth: 67%; drowsiness:17%)

59
Q

What is the MOA and Clin use of Droperidol

A

Mechanism of Action: blocks dopamine receptors in chemoreceptor trigger zone (CTZ) of the CNS

Clinical Use:
Butyrophenone antipsychotic, no longer used as antipsychotic

Indicated for Postoperative Nausea/Vomiting (PONV)

Most often used for sedation in endoscopy and surgery, in combination with opioids or benzodiazepines

60
Q

Where is droperidol most often used

A

Most often used for sedation in endoscopy and surgery, in combination with opioids or benzodiazepines

61
Q

What are the ADE of Droperidol, a drug used in sedation for endoscopy

A

EPS, Dystonias, Drowsiness, Agitaton, Confusion

62
Q

What is the MOA and clin of metoclopramide

A

Mechanism of Action:

Dopamine antagonist; stimulates motility of the upper GI track without effecting secretions

Enhances the response to Acetylcholine of tissue in upper GI tract causing enhanced motility and accelerated gastric emptying without stimulating gastric, biliary, or pancreatic secretions

Also block serotonin receptors in the chemoreceptor trigger zone, resulting in the anti-emetic action

Dosed several times a day

Clinical Use: gastroesophageal reflux, prevention of N/V from chemotherapy, impaired gastric emptying (i.e diabetic gastroparesis)

63
Q

What are the ADE of metroclopramide

A

EPS

64
Q

What is the MOA and clin use of Trimethobenzamide

A

Mechanism of Action:

Block emetic impulses in the chemoreceptor trigger zone (CTZ)

Does not cause extrapyramidal symptoms like metoclopramide

Clinical Use:

Used for apomorphine pre-treatment in Parkinson’s patients
Indicated for post-operative N/V and for nausea associated with gastroenteritis

65
Q

What drug is used in the apomorphine pre-treatment in Parkinson’s patients

A

Trimethobenzamide

66
Q

Dexamethasone and Methylprenisone are what drug class

A

Corticosteroids

67
Q

What are the clincal use of corticosteroids

A

Chemotherapy N/V w. 5HT3 Antagonsits (SRAs)

68
Q

How are BZD used to prevent NV

A

Clinical Use: used before the initiation of chemotherapy to reduce anticipatory nausea and vomiting caused by anxiety

Products:
Lorazepam (Ativan)
Diazepam (Valium)

69
Q

What kind of drugs are Dronabinol and Nabilone

A

Cannaboids used to treat NV in chemo pts

And anorexia with AIDS pts

70
Q

What drug is used in conjunction with 5-HT3 antagonist and steroid for both the acute and delayed phases of cisplatin-induced emesis

A

Aprepitant

71
Q

Drugs that end in –prepitant are used to treat what

A

Chemo induce NV

72
Q

What is the Tx approach to mild Diarrhea

A

rehydration fluids + lactose free diet, avoid caffeine

73
Q

What is the Anitbiotic therapy for Travelers Diarrhea

A

Fluoroquinolones

Azithromycin

Rifaximin (Xifaxan) only works in the colon
Rifamixin treats IBS-diarrhea dominant

74
Q

How do you treat antibiotics C. Diff

A

Metronidazole or oral vancomycin

75
Q

How do Opiods agonists stop diarrhea

A

Activates presynaptic opioid receptors (mu receptors) in the enteric nervous system

Inhibit presynaptic cholinergic nerves in the submucosal and mesenteric plexuses

Lead to increase colonic transit time and fecal water absorption

Decreases mass colonic movement and the gastrocolic reflex

76
Q

How is the MOA and clin use of Loperamide

A

Mechanism of Action:
Mu opioid agonist; activates opioid receptors in the enteric system, leading to inhibition of acetylcholine release and decreased peristalsis

Does not cross the BBB

Meperidine derivative

Posses “no” analgesic properties or potential for addiction

Clinical Use:
Control mild to moderate symptoms of non-invasive diarrhea

77
Q

What is the antidiarheal drug for non invasive diarrhea

A

Loperamide ( you know this one, its what you always had to have on hand in the field as a medic) ( doc i shit my pants )

78
Q

What are the common causes of constipation

A 
Altered motility
Neurogenic causes (Parkinson disease)
Endocrine/metabolic disorders (e.g. hypothyroidism, diabetes, hypokalemia, hypercalcemia, uremia)
Pregnancy
Psychogenic causes
Structural abnormalities or obstruction
Nutritional (e.g, reduced fiber and water intake)
Medications
79
Q

What is the MOA and clin use of osmotic Laxatives

A

Mechanism of Action:
Rapid movement of water into the distal small bowel and colon, leads to high volume of liquid stool

Increase volumes leads to bowel distension and reflex urge to defecate

Followed by rapid relief of constipation

Clinical Use:
Acute or intermittent constipation

Preoperative or pre-procedure bowel preparation

80
Q

What type of laxative is magnesium based products

A

Osmotic

81
Q

What kind of laxative is sodium phosphate

A

Osmotic

82
Q

What is the caution with mag sulfate as an osmotic laxative

A

Caution with in patients with renal impairment due to the risk of magnesium intoxication

Electrolyte Abnml

83
Q

What is the black box label for sodium phosphate

A

Nephropathy with oral products

84
Q

What is the MOA and Clin use of lactulose and 70% sorbitol

A

Mechanism of Action: metabolize by colonic bacteria, producing increased osmotic pressure causing fluid accumulation, severe flatus, cramps, and defecation

Clinical Use:
Management of acute, intermittent, or chronic constipation

Lactulose:
Preferred in chronic liver disease in the prevention and treatment of overt hepatic encephalopathy (OHE) episodes and portal systemic encephalopathy (PSE)
Reduces ammonia levels

85
Q

What osmotic laxative is preferred in chronic liver disease

A

Lactulose

86
Q

What kind of laxative is polyethylene solutions

A

Osmotic

Used for preoperative/colon preparation for endoscopic or radiologic procedures

87
Q

How is Polyethylene taken

A

Isotonic solution contain an inert non-absorbable, osmotically active sugar

Induce bowel movement/diarrhea to cleanse the bowel usually within 4 hours

Ingest 2-4 Liters over 2-4 hours

88
Q

What is the 2-4 liters a pt should drink for preoperative/colon preparation for endoscopic or radiologic procedures

A

Polyethylene Gycol

89
Q

What is PEG 3350 power approved for

A

Approved for irritable bowel syndrome constipation dominant (IBS-C)

90
Q

What are Gylcerin suppository and Mineraol Oil

A

Lubircating agents

91
Q

What pts should suppository or mineral oil be used on

A

Management of acute or intermittent constipation

Pediatric patients

92
Q

What are psyllium and wheat dextrin

A

Fiber used to treat constipation

93
Q

What pts should not receive plant fibers

A

Celiac pts

94
Q

What synthetic fiber can be used in celiac pts for constipation

A

Methyl cellulose

95
Q

What kind of laxative is docusate

A

Stool surfactant/ Stool softener

96
Q

How is ducosate used

A

Prevention of opioid induced constipation in combination with Senna or prevention of straining (pregnant/post-operative)

Preferred for prophylaxis not acute treatment of constipation

97
Q

To prevent straining in pregnancy or op pts what stool softener can be used

A

Docusate

98
Q

What is the DOC for IBS in women older than 18 yrs old

A

Lubiprostone

99
Q

What is the DOC in short term emergency Tx of IBS and Chronic Constipation in women older than 55 years old

A

Tegaserod

100
Q

What is Linaclotide used for

A

IBS and Chronic constipation

101
Q

What is the DOC for opiod induced constipation

A

Methyl naltrexone

102
Q

What is the DOC for postoperative ileus

A

Alivmopan

103
Q

What is the DOC for opiod induced constipation in adult pts with chronic non cancer pain

A

Naloxegol

104
Q

Define Ulcerative colitis

A

Superficial, mega colon developing, Risk factor for cancer, that is usually confined to the rectum and terminal colon

Has continuous inflammation

105
Q

Define chrons

A

Cobblestone patchy appearance, that rarely leads to cancer, does not develop mega colon, and can be anywhere from mouth to anus in the GI, and can extend deep to the submucosa

106
Q

What are the 1st line products for IBD

A

Sulfasalazine and Mesalamine

107
Q

What do Sulfasalazine and mesalamine treat

A

IBD: chrons and UC

108
Q

What TCAs can be used to treat IBS

A

Amitriptyline, nortriptyline, and imipramine

Can worsen constipation

109
Q

What SSRIs can be used to treat IBS

A

Fluoxetine, setraline, citalopram, and paroxetine are all viable options

110
Q

What is Rifaximin used for

A

Treats IBS-D

And travelers Diarhhea

111
Q

What is the caution with Rifaxamin

A

Caution in liver impairment

112
Q

What is eluxadoline used for

A

IBS-D

113
Q

What pts should eluxamide, a drug for IBS-D be avoided in

A

should not be used in patients with a history of bile duct obstruction, pancreatitis, severe liver impairment, or severe constipation, and in patients who drink more than three alcoholic beverages per day

114
Q

What is alosetron used for

A

Women with IBS-D

115
Q

What are the black box warnings of alosetron, A 5hT3 antagonist used to treat IBS-D in women

A

Ischemic colitis and Constipation

IPAP 21-2 Soph Semester (20 decks)

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