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Clinical Pharmacology I > Exam 3 - GI Part 1 > Flashcards

Exam 3 - GI Part 1 Flashcards

1
Q

Pathophysiology of GERD?

A

Retrograde movement of acid from the stomach into the esophagus; as well as bile acids, pancreatic enzymes, and pepsin.

Leads to increased contact of stomach acid with mucosa.

Caused by low LES tone, increased intra-abdominal pressure, gastric emptying, etc.

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2
Q

Where are gastric acids coming from?

A

Parietal cells secrete gastric acid.

H-K-ATPase secretes hydrogen ions and produces an acidic environment in stomach.

Influenced by histamine affecting H2 receptors, muscarinic receptors, acetylcholine to increase activity of proton pump.

Gastrin secretes more gastric acid.
Paracrine cells release histamine, which are affected by muscacrinic and gastric receptors.

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3
Q

What inhibits secretion of gastric acid?

A

NSAIDs inhibit production of prostaglandins, which means stomach isn’t as protected. Less acid will be secreted.

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4
Q

Epithelial cells function in stomach?

A

Responsible for protecting stomach.

Prostaglandins and muscarinic receptors increase release of bicarbonate for mucus.

Mucus layer on cells has pH of 7.
Gastric lumen can have a pH of 2.

Mucus protects gastric ulcers from being formed.

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5
Q

Risk factors for GERD

A

Obesity, delayed gastric emptying, pregnancy, hiatal hernias, recumbency (laying back), smoking, spicy food

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6
Q

What foods trigger GERD?

A

Alcohol, spicy food, citrus, tomatoes, fatty foods, chocolate, and peppermint

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7
Q

Medications that trigger GERD?

A

Anticholinergics, narcotics, CCBs

Anything that prevents the smooth muscle from contracting and slows peristalsis.

NSAIDs cause GERD by inhibiting prostaglandin synthesis.

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8
Q

What is bisphosphate?

A

Used for osteoporosis, but can stick in the throat and lead to GERD.

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9
Q

Complications of GERD

A

Esophagitis, strictures, anemia from bleeding, Barrett Esophagus, risks for cancer from long-standing reflux.

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10
Q

Clinical Presentations of Esophageal Symptoms

A

Heartburn (pyrosis), followed by regurgitation, belching, and water brash (hyper salivation).

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11
Q

Atypical signs of GERD

A

Pharyngitis, chronic cough horaseness

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12
Q

What are alarming signs of GERD that should be taken care of in ER?

A

Continual pain, dysphagia, odynophagia, unexplained weight loss, GI bleeding, choking, and vommitting.

Esophagus is bright red from coughing, or GI bleed = black tarry stools.

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13
Q

LIfestyle modifications for GERD

A

LIfestyle modifications - don’t eat spicy foods, don’t smoke, weight loss, elevate head of bed, avoid alcohol

Pharmacology intervention and therapy is possible.

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14
Q

How do you treat kids with reflex?

A

Surgery can pull stomach muscle over esophageal sphincter to help close it for kids with bad reflux.

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15
Q

Acid-Peptic Disease

Roles of therapy?

A

Neutralize excess acid, decrease gastric secretion, or enhance gastric mucous defense.

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16
Q

What meds help neutralize excess acid?

A

Antacids - directly neutralize acid in the stomach; best to take in the morning before you eat or afterward when you have symptoms to neutralize (Time when most acid is produced).

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17
Q

Different palatability of GERD meds?

A

Some meds respond better than others

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18
Q

Types of antacids

A

Sodium bicarbonate
Calcium carbonate
Aluminum Hydroxide
Magnesium Hydroxide

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19
Q

How does sodium bicarbonate work?

A

Not super common. Quickly neutralizes acid and produces sodium and alkali load.

Can see fluid retention, because of added sodium. May not be good for salt sensitive. Can also produce gas.

Raises pH of stomach (base), so stomach thinks it needs to produce more acid and have more gastrin release. May need more antacid to counteract. Limited in use.

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20
Q

Calcium Carbonate (Tums)

A

Works rapidly, moderate neutralizing ability, and will absorb calcium.

If they have kidney stones or kidney issues with too much calcium, can exacerbate.

Taking calcium orally can cause constipation.

Chelates other drugs.

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21
Q

Aluminum Hydroxide (Amphagel)

A

Good phosphate binder. Used for patients with chronic kidney disease and hyperphosphatemia.

May see decreased stomach emptying (might increase gastric acid secretion). Forms a cytoprotective effect on mucosa to help with natural barrier.

Will cause constipation.

Have the ability to chelate other drugs - Need to separate antacids from other drugs by taking it an hour before or 4 hours afterwards. Like Bile Acid Sequestrants.

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22
Q

Why do you separate levofloxacin and ciprofloxacin from GERD medicines?

A

They can bind calcium and magnesium! Take an hour before or four afterward.

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23
Q

Magnesium hydroxide (Milk of Magnesia)

“Green Rocket”

A

Good neutralizing ability; see magnesium chloride has low solubility, can have some Mg absorption through tract.

Can cause diarrhea; used for constipation!

Bad for appendicitis, intestinal obstruction, AND renal failure, because you don’t want them to absorb magnesium (Hypermagnesiuma).

MgOH + AlOH (Mylanta, Maalox) - Comes in a liquid suspension. Coats GI tract. Can counteract GI motility.

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24
Q

Problems with antacid treatment at home?

A

They can mask worsening disease, because they don’t know the alarming signs.

Safe in pregnancy, but AVOID sodium bicarbonate - more prone to HTN.

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25
What drugs can bind to antacids?
Tetracycline, fluoroquinolones, and FeSO4.
26
Alginic Acid
Reacts with sodium bicarbonate in saliva to form a viscous solution. Provides a barrier in GI tract of stomach. Patient has to be upright so they don't reflux it. Antacid + alginic acid + Na bicarb = Gaviscon
27
Advantages of antacids
Rapid relief of symptoms, inexpensive, available OTC. Good for breakthrough neutralization, like spicy food.
28
Disadvantages of antacids
Not effective for healing. Multiple doses required throughout the day, worry about constipation or diarrhea, and potential drug interactions.
29
Reduce gastric acid secretion MOA
Block H2 receptor (antagonist); will see decreased acid secretion of parietal cells; including basal, nocturnal, and stimulated acid secretion - covers throughout the day. Lowers H+ in secretions. Reduces pepsin as well, which is a digestive protein in the stomach.
30
H2 Receptor Antagonists - Name them.
Cimetidine - Tagamet (Never use) Ranitidine - Zantac (IV) Famotidine (IV) Nizatidine Well absorbed in GI tract, need renal dose adjustment
31
H2 Receptor Antagonists - When are they used?
PUD, GERD, and Zollinger-Ellison Syndrome ZES - hypersecretory condition of too much stomach acid on a chronic basis; leads to erosions and ulcers.
32
ADR H2 antagonists
WELL TOLERATED DRUGS CNS - confusion and seizures (rare) Thrombocytopenia, rash
33
H2 receptor antagonists - standing in therapy
Effective in 60% of patients, more effective than antacids cause they provide longer coverage throughout the day. Agents equally efficacious and well tolerated; selected based on cost adn pharmacokinetics. Pregnancy category B
34
Why do you think you can only use H2 antagonists for 14 days?
Because if you're on it for a prolonged time, you should see your doctor. Can use to premedicate daily or PRN (Before they eat, so it has time to wrok)
35
Cimetidine - Why don't we use it?
Inhibits CYP3A4 - can be problematic with statins and other drugs
36
Proton pump inhibitors
Inhibit proton pump and block all effects of acetylcholine, histamine, and gastric effects from the end point of that process. Irreversible inhibitors, so parietal cells have to make more acid. 7 days of treatment will inhibit 95% of secretion. Effective. Suicide inhibitors.
37
Name the PPIs.
Esomeprazole, lansoprazole, omeprazole, pantoprazole, rabeprazole Omeprazole and esomeprazole are enantiomers (have same activity). Can be available IV for severe cases of gastric bleeding or hypersecretory conditions.
38
Indications of PPI
Patient who aren't controlled by H2 antagonists, used for Zollinger Ellision, PUD, and GERD
39
ADR of PPI
Hyperplasia of parietal cells in animals. Elevated stomach pH - When acidic, prevents the colonization of bacteria. With increase in pH, bacteria can start to colonize and you worry about aspiration, cause you increase risk of VAP for critically stressed patients who may have gastric ulcers. Higher pH of stomach, decreases absorption of calcium! Bad for osteoporosis patients.
40
PPI and pregnancy
Relatively safe, but antacids are safer, since they're least absorbed
41
How do you administer PPI?
Once a day or thirty minutes before a meal. When they hit normal stomach acid, can be destroyed, so the tablets come with the small beaded coating to survival that low pH. When it gets to the duodenum with higher pH, it dissolves into the blood and allows drug to be absorbed DO NOT CRUSH OR CHEW - you can break the nice acid protective barrier before it can be absorbed. Better than H2 blockers at healing, but are more expensive. Drug increases levels of ketoconazole, itraconazole, and iron salts. Otherwise well-tolerated.
42
ADR OTC Omeprazole
When used OTC, patients can mask more alarming symptoms.
43
When should you not use OTC Omeprazole?
GI bleeding sx: vomiting blood, bloody/black stool, dysphagia
44
You should consult MD before use of Omeprazole if?
``` HB severe > 3 months Nocturnal HB Lightheaded, dizzy, sweating CP, SOB HB with wheezing, coughing, choking Unexplained weight loss ```
45
Omeprazole is approved for who?
>18 years old, Rx is FDA approved in children
46
You should discontinue Omperazole and consult MD if:
HB continues/worsens Need to exceed OTC dosing guidelines HB returns after completing course
47
What is a Gastrin Inhibitor?
Octreotide; somatostatin analog, blocks gastrin release Used for: Gastrinomas (tumors that secrete gastrin), Zollinger-Ellison, Severe diarrhea IV admin. Helps block insulin release, varicocele bleeds in esophagus
48
Mucosal Protecting Agents
Mucosal Protecting Agents
49
What is Colloidal Bismuth (Pepto-Bismol)?
Bismuth subsalicyclate Coats stomach lining Inhibits pepsin activity Imparts black color to feces and oral cavity! Contains salicylates
50
Who should you not give Pepto-Bismol to?
Post-viral kids, can develop Reye's syndrome
51
What is Sucralfate (Carafate)?
Non-absorbable aluminum salt of sucrose octasulfate MOA: sucralfate + acid = paste (Coats stomach) Use: Heme/Onc Stomatitis Comes in liquid form
52
What is Misoprostol?
PGE1 analog *Enhances mucous production Decreases acid production Use: Ulcers from NSAIDS, diarrhea, cramps CI in Pregnancy! (Abortificant) Abortificant = Misoprostol + Methotrexate
53
Which agent is the cheapest and works the fastest at relieving GERD?
Antacids | More fast
54
Which agent works the BEST and lasts the longest, when treating GERD?
PPI's | More potent
55
What are the different phases of GERD tx?
Phase I - Mild, intermittent HB - Antacids and/or OTC H2RA/PPI Phase IIa - Symptomatic relief of GERD - H2RA or PPI Phase IIb - Erosive dz/severe sx - PPI or HD-H2RA (Esomeprazole, Pantoprozole) Phase III - Refractory pt's - Interventional therapy
56
For pts who relapse within 1 yr of discontinuing drug therapy, they require standard doses of maintenance:
Mild disease: H2- blocker | Mod/Sev: PPI
57
Peptic Ulcer Disease
Peptic Ulcer Disease
58
What are the 3 types of PUD's you can develop?
- H. Pylori Ulcers - NSAID ulcers - Stress-related mucosal damage
59
What is the presentation of dyspepsia?
Recurrent pain in upper abdomen | Sx: pain, fullness, bloating, nausea from upper GI tract
60
How do you tx dyspepsia on an NSAID?
Discontinue NSAID! or Decrease dose, or change to COX-2 specific (Celebrex) Try H2RA or PPI if sx continue
61
How do you tx dyspepsia not on an NSAID?
Test for H. Pylori and tx if positive H2RA or PPI if negative result
62
What are alarming symptoms of PUD?
Bleeding, anemia, weight loss
63
Gastric acid secretion in DU vs. GU:
DU: Hypersecretion GU: Normal secretion
64
What are the risk factors for PUD?
``` H. Pylori NSAID use Smoking Genetics Stress ```
65
Clinical presentation for DU:
Localized, relieved by food (food uses up acid) Nocturnal pain/pain 1-3 hrs after meals (when hyper secretion starts again)
66
Clinical presentation of GU:
Diffuse, pain at any time of day Problem with the protective barrier (NOT oversecretion)
67
What are the 3 types of Complicated Ulcers?
GI Bleeding: erosion of ulcer into artery Obstruction: Scarring/edema of duodenal bulb Perforation: Severe abd pain, penetration (burrowing of ulcer into other structures)
68
Tx of Ulcers depends on:
Cause of ulcer (HP or NSAID) Ulcer is initial or recurrent Complications have occurred or not
69
What heals most ulcers in 4-8 weeks?
PPIs, H2RAs and other agents PPIs are faster
70
Which ulcers are larger and more difficult to heal?
GU's, always bathed in acids
71
What are non-pharmacologic therapies for Ulcers?
Eliminate stress, avoid trigger food, avoid NSAIDs, EtOH/smoking cessation
72
What are the tx's for PUD?
H2RA's, PPI, Sucralfate, Antacids, Drugs for H. Pylori
73
H2RA's Efficacy
Healing rate of 70-95% after 4-8 wks More effective than antacid, bc longer lasting effects All agents equally effective
74
H2RA's cost effective?
Yes, much cheaper than PPIs and other therapy IV and liquid form available
75
PPI's efficacy:
Symptom relief and healing in 2-4 wks | Agents equally effective
76
In PUD, what are antacids used for?
PRN for symptoms, breakthrough dyspepsia Calcium carb is best choice (Tums).
77
Tx considerations with Antacids:
Choice of agent depends on patient | DI: bind to Tetracycline, Iron, FQ's
78
How do you dx H. Pylori?
Urea breath test (C13), Stool antigen test, serum antibody test
79
Which agents are used for tx of H. Pylori?
``` Abx: Clarithromycin, Amoxicillin, Metronidazole, Tetracycline RBC: Ranitidine Bismuth Citrate BSS: Bismuth subsalicylate H2RA's PPI's ```
80
H. Pylori tx: Bismuth preps
MOA: Local gastroprotection via stimulation of endogenous PG's, also suppress H. Pylori RBS: Ranitidine + Bismuth + Citrate (Tritec) BSS: Bismuth subsalicylate + Flagyl + TCN (Helidac)
81
What are the H. Pylori tx options?
2 drug - not recommended 3 drug regimen: Clarithromycin Amoxicillin PPI ``` 4 drug regimen: BEST ONE 90-99% efficacy BSS Metronidazole Tetracycline PPI (2 abx, PPI, Protective agent) ```
82
How do you choose H. Pylori tx options?
``` tolerability interactions cost compliance abx resistance ```
83
Initial tx failure of H. Pylori?
Use different abx Use Bismuth 10-14 days of therapy (instead of 7)
84
Who has high risk for GI toxicity from NSAIDs?
``` >60 yo Hx of PUD Use of corticosteroids high dose NSAID use use of anticoag's chronic major organ impairment (CHF) ```
85
What is the patho of NSAID-induced ulcers?
Direct topical irritation of gastric epithelium | Inhibition of COX-1 --> prevents synthesis of GI mucosal prostaglandin (PG)
86
Clinical Presentation H. Pylori Ulcers vs. NSAID-Induced Ulcers:
H-pylori: - DU>GU - pH dependent - Epigastric pain - Superficial ulcer depth - Mild GI bleeding NSAID induced: - GU>DU - Less pH dependent - Often asymptomatic - Deep ulcerations - MORE Severe GI bleeds
87
What is the tx for NSAID induced ulcers?
- Stop NSAID if possible - Eval pt for H. Pylori - H2RA's/PPIs/Sucralfate can be used - PPI preferred
88
NSAID-Ulcers Prophylaxis considered for who?
Pts with h/o ulcer on NSAID who continue it High risk: - Concurrent anticoags/corticosteroids - H/o ulcers - Elderly - High surgical risk - Debiliated pt's
89
What is used for NSAID-ulcer prophylaxis?
MISOPROSTOL (Cytotec) > H2RA Arthrotec = Misoprostol + Diclofenac Pregnany cat X
90
Maintenance therapy of ulcers is considered in who?
- Frequent ulcer recurrences - Hx of ulcer-related bleeding - High-risk pos - Failed HP eradication therapy - Pts with HP(-) ulcers
91
Maintenance of healed ulcers is done with what agents?
NSAIDs discontinued? -Low dose H2RA, PPI, Sucralfate NSAID continued? -Misoprostol or PPI

Clinical Pharmacology I (7 decks)

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