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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
Q

What drugs can bind to antacids?

A

Tetracycline, fluoroquinolones, and FeSO4.

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26
Q

Alginic Acid

A

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

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27
Q

Advantages of antacids

A

Rapid relief of symptoms, inexpensive, available OTC. Good for breakthrough neutralization, like spicy food.

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28
Q

Disadvantages of antacids

A

Not effective for healing.

Multiple doses required throughout the day, worry about constipation or diarrhea, and potential drug interactions.

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29
Q

Reduce gastric acid secretion MOA

A

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.

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30
Q

H2 Receptor Antagonists - Name them.

A

Cimetidine - Tagamet (Never use)
Ranitidine - Zantac (IV)
Famotidine (IV)
Nizatidine

Well absorbed in GI tract, need renal dose adjustment

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31
Q

H2 Receptor Antagonists - When are they used?

A

PUD, GERD, and Zollinger-Ellison Syndrome

ZES - hypersecretory condition of too much stomach acid on a chronic basis; leads to erosions and ulcers.

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32
Q

ADR H2 antagonists

A

WELL TOLERATED DRUGS

CNS - confusion and seizures (rare)
Thrombocytopenia, rash

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33
Q

H2 receptor antagonists - standing in therapy

A

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

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34
Q

Why do you think you can only use H2 antagonists for 14 days?

A

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)

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35
Q

Cimetidine - Why don’t we use it?

A

Inhibits CYP3A4 - can be problematic with statins and other drugs

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36
Q

Proton pump inhibitors

A

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.

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37
Q

Name the PPIs.

A

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
Q

Indications of PPI

A

Patient who aren’t controlled by H2 antagonists, used for Zollinger Ellision, PUD, and GERD

39
Q

ADR of PPI

A

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
Q

PPI and pregnancy

A

Relatively safe, but antacids are safer, since they’re least absorbed

41
Q

How do you administer PPI?

A

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
Q

ADR OTC Omeprazole

A

When used OTC, patients can mask more alarming symptoms.

43
Q

When should you not use OTC Omeprazole?

A

GI bleeding sx: vomiting blood, bloody/black stool, dysphagia

44
Q

You should consult MD before use of Omeprazole if?

A 
HB severe > 3 months
Nocturnal HB
Lightheaded, dizzy, sweating
CP, SOB
HB with wheezing, coughing, choking
Unexplained weight loss
45
Q

Omeprazole is approved for who?

A

> 18 years old, Rx is FDA approved in children

46
Q

You should discontinue Omperazole and consult MD if:

A

HB continues/worsens
Need to exceed OTC dosing guidelines
HB returns after completing course

47
Q

What is a Gastrin Inhibitor?

A

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
Q

Mucosal Protecting Agents

A

Mucosal Protecting Agents

49
Q

What is Colloidal Bismuth (Pepto-Bismol)?

A

Bismuth subsalicyclate

Coats stomach lining
Inhibits pepsin activity
Imparts black color to feces and oral cavity!
Contains salicylates

50
Q

Who should you not give Pepto-Bismol to?

A

Post-viral kids, can develop Reye’s syndrome

51
Q

What is Sucralfate (Carafate)?

A

Non-absorbable aluminum salt of sucrose octasulfate

MOA: sucralfate + acid = paste (Coats stomach)

Use: Heme/Onc Stomatitis

Comes in liquid form

52
Q

What is Misoprostol?

A

PGE1 analog

*Enhances mucous production

Decreases acid production

Use: Ulcers from NSAIDS, diarrhea, cramps

CI in Pregnancy! (Abortificant)

Abortificant = Misoprostol + Methotrexate

53
Q

Which agent is the cheapest and works the fastest at relieving GERD?

A

Antacids

More fast

54
Q

Which agent works the BEST and lasts the longest, when treating GERD?

A

PPI’s

More potent

55
Q

What are the different phases of GERD tx?

A

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
Q

For pts who relapse within 1 yr of discontinuing drug therapy, they require standard doses of maintenance:

A

Mild disease: H2- blocker

Mod/Sev: PPI

57
Q

Peptic Ulcer Disease

A

Peptic Ulcer Disease

58
Q

What are the 3 types of PUD’s you can develop?

A
  • H. Pylori Ulcers
  • NSAID ulcers
  • Stress-related mucosal damage
59
Q

What is the presentation of dyspepsia?

A

Recurrent pain in upper abdomen

Sx: pain, fullness, bloating, nausea from upper GI tract

60
Q

How do you tx dyspepsia on an NSAID?

A

Discontinue NSAID! or Decrease dose, or change to COX-2 specific (Celebrex)

Try H2RA or PPI if sx continue

61
Q

How do you tx dyspepsia not on an NSAID?

A

Test for H. Pylori and tx if positive

H2RA or PPI if negative result

62
Q

What are alarming symptoms of PUD?

A

Bleeding, anemia, weight loss

63
Q

Gastric acid secretion in DU vs. GU:

A

DU: Hypersecretion

GU: Normal secretion

64
Q

What are the risk factors for PUD?

A 
H. Pylori
NSAID use
Smoking
Genetics
Stress
65
Q

Clinical presentation for DU:

A

Localized, relieved by food (food uses up acid)

Nocturnal pain/pain 1-3 hrs after meals (when hyper secretion starts again)

66
Q

Clinical presentation of GU:

A

Diffuse, pain at any time of day

Problem with the protective barrier (NOT oversecretion)

67
Q

What are the 3 types of Complicated Ulcers?

A

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
Q

Tx of Ulcers depends on:

A

Cause of ulcer (HP or NSAID)
Ulcer is initial or recurrent
Complications have occurred or not

69
Q

What heals most ulcers in 4-8 weeks?

A

PPIs, H2RAs and other agents

PPIs are faster

70
Q

Which ulcers are larger and more difficult to heal?

A

GU’s, always bathed in acids

71
Q

What are non-pharmacologic therapies for Ulcers?

A

Eliminate stress, avoid trigger food, avoid NSAIDs, EtOH/smoking cessation

72
Q

What are the tx’s for PUD?

A

H2RA’s, PPI, Sucralfate, Antacids, Drugs for H. Pylori

73
Q

H2RA’s Efficacy

A

Healing rate of 70-95% after 4-8 wks
More effective than antacid, bc longer lasting effects
All agents equally effective

74
Q

H2RA’s cost effective?

A

Yes, much cheaper than PPIs and other therapy

IV and liquid form available

75
Q

PPI’s efficacy:

A

Symptom relief and healing in 2-4 wks

Agents equally effective

76
Q

In PUD, what are antacids used for?

A

PRN for symptoms, breakthrough dyspepsia

Calcium carb is best choice (Tums).

77
Q

Tx considerations with Antacids:

A

Choice of agent depends on patient

DI: bind to Tetracycline, Iron, FQ’s

78
Q

How do you dx H. Pylori?

A

Urea breath test (C13), Stool antigen test, serum antibody test

79
Q

Which agents are used for tx of H. Pylori?

A 
Abx: Clarithromycin, Amoxicillin, Metronidazole, Tetracycline
RBC: Ranitidine Bismuth Citrate
BSS: Bismuth subsalicylate
H2RA's
PPI's
80
Q

H. Pylori tx: Bismuth preps

A

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
Q

What are the H. Pylori tx options?

A

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
Q

How do you choose H. Pylori tx options?

A 
tolerability
interactions
cost
compliance
abx resistance
83
Q

Initial tx failure of H. Pylori?

A

Use different abx
Use Bismuth
10-14 days of therapy (instead of 7)

84
Q

Who has high risk for GI toxicity from NSAIDs?

A 
>60 yo
Hx of PUD 
Use of corticosteroids 
high dose NSAID use
use of anticoag's
chronic major organ impairment (CHF)
85
Q

What is the patho of NSAID-induced ulcers?

A

Direct topical irritation of gastric epithelium

Inhibition of COX-1 –> prevents synthesis of GI mucosal prostaglandin (PG)

86
Q

Clinical Presentation

H. Pylori Ulcers vs. NSAID-Induced Ulcers:

A

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
Q

What is the tx for NSAID induced ulcers?

A
  • Stop NSAID if possible
  • Eval pt for H. Pylori
  • H2RA’s/PPIs/Sucralfate can be used - PPI preferred
88
Q

NSAID-Ulcers Prophylaxis considered for who?

A

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
Q

What is used for NSAID-ulcer prophylaxis?

A

MISOPROSTOL (Cytotec) > H2RA

Arthrotec = Misoprostol + Diclofenac
Pregnany cat X

90
Q

Maintenance therapy of ulcers is considered in who?

A
  • Frequent ulcer recurrences
  • Hx of ulcer-related bleeding
  • High-risk pos
  • Failed HP eradication therapy
  • Pts with HP(-) ulcers
91
Q

Maintenance of healed ulcers is done with what agents?

A

NSAIDs discontinued?
-Low dose H2RA, PPI, Sucralfate

NSAID continued?
-Misoprostol or PPI

Clinical Pharmacology I (7 decks)

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