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Pharmacology -AM > GERD/PUD/IBD > Flashcards

GERD/PUD/IBD Flashcards

1
Q

Combo pack options for H.pylori-associated ulcers

A

Pylori, Helidac, PrevPac
Abx + PPI
$$$

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2
Q

MOA= anti-inflammatory effects to areas of inflammation in the GI tract

A

Aminosalicylates (-salazine)

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3
Q

This can form when there is an imbalance of Gastric acid/pepsin vs Bicarbonate/mucous secretion/prostaglandins

A

PUD

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4
Q

What do you need to test for when using Azathioprine & 6-MPs to avoid the possibility of Azathioprine toxicity?

A

TPMT, it metabolizes Azathioprine to 6-MP. If not present, then need to reduce the dose

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5
Q

Anti-TNF-alpha Biologic drugs used for IBD:

A

Infliximab
Certolizumab
Adalimumab
Golimumab

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6
Q

H2 blockers drugs

A

Cimetidine
Famotidine
Nizatidine
Ranitidine

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7
Q

What is the 4th drug you add if 3 drug treatment for H.pylori fails?

A

Bismuth

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8
Q

AE: Hypersensitivity

A

Azathioprine & 6-MP

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9
Q

Misoprostol (synthetic prostaglandin) MOA

A

inhibits secretion of acid and stimulates secretion of mucous and bicarbonate

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10
Q

Aminosalicylates or sulfasalazine or budesonide (a PO corticosteroid) are often used to treat _______ especially in cases that are less severe (but can be used then, too). These all could be used for acute flares or maintenence.

A

UC or CD

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11
Q

Why would you want to use Cyclosporine for IBD?

A

Used for patients with fulminant or refractory Sx (serious cases)

Also used to prevent organ rejection in transplant patients

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12
Q

What IBD drugs include the possible AE of increased risk of Progressive Multifocal Leukoencephalopathy?

A

Natalizumab
Vedolizumab

(other biologics)

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13
Q

How long could it take for Azathioprine & 6-MP to work with IBD?

A

3-12 months

PO

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14
Q

Bismuth Subsalicylate (Pepto Bismol) use

A

sometimes used in quadruple therapy for treating peptic ulcers

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15
Q

Bismuth Subsalicylate AE

A

black tongue & stools

salicylism (w/ high doses)

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16
Q

Sucralfate MOA

A

non-absorbed, forms paste-like adhesive over ulcer and protects from acids/bile salts/pepsin

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17
Q

Sucralfate administration

A

multiple times daily, large pills- inconvenient

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18
Q

Defect in the gastric or duodenal mucosal wall that extends into the deeper layers of submucosa

A

Peptic Ulcer Disease

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19
Q

gastric acid secretion is inhibited by

A

prostaglandins

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20
Q

One of the Aminosalicylates has worse AE than the others. Which one, and what are the AE?

A

Sulfasalazine

headache, GI fx, fatigue, bone marrow suppression, lowered sperm counts, hepatitis

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21
Q

PPI MOA

A

inhibits gastric H+ pump
(H+=acid=proton, proton pump inhibitor)
reduces secretion of gastric acid

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22
Q

Why would you use Methotrexate for IBD?

A

maintain remission of CD and decrease steroid use

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23
Q

PPI AE

A

headache, diarrhea, constipation, ab pain

increased risk of community acquired pneumonia & c diff

reduced calcium absorption (take calcium citrate for supplementation)

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24
Q

Risk factors for NSAID-induced PUD

A
  • > 60
  • concomitant anticoagulant use
  • preexisting coagulopathy
  • concomitant corticosteroid or SSRI use
  • CV disease
  • Multiple NSAID use
  • High dose NSAID use
  • > 1 month NSAID use
  • NSAID related dyspepsia
  • smoking
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25
Q

MOA of this IBD Tx: host flora may alter inflammatory response

A

Probiotics: L. acidophilus, Bifidobacterium

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26
Q

Antacid drugs

A
  • magnesium hydroxide
  • magnesium hydroxide/aluminum hydroxide
  • calcium carbonate
  • sodium bicarbonate
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27
Q

Antacid use

A

immediate, short acting

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28
Q

gastric acid secretion is stimulated by

A

acetylcholine, gastrin, histamine

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29
Q

The biggest difference between Ulcerative Colitis and Crohn’s disease?

A

Depth and location-

UC: colon & rectum and continuous, does not extend beyond submucosal layer
CD: anywhere mouth to anus and discontinuous, ulcerates deeply- transmural

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30
Q

Benefit of using Anti-TNF-alpha Biologics for IBD (-umab):

A

Decrease in TNF-alpha = reduction of inflammation

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31
Q

Inflammatory response includes atypical type 2 T helper cells that produce pro-inflammatory cytokines: IL-1, IL-6, TNF-alpha

A

Ulcerative Colitis

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32
Q

Tx approach to GERD

A

Lifestyle changes
Patient-directe therapy (OTC meds)
Acid suppressing therapy (Rx meds)
Anti-reflux surgery

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33
Q

Corticosteroids that are not considered systemic corticosteroids:

A

oral budesonide, nasal corticosteroids, inhaled cortiocosteroids.

nasal corticosteroids and inhaled corticosteroids would not help a patient maintain remission of UC or CD because these routes do not affect the GI tract significantly/at all.

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34
Q

Which Aminosalicylates are linked to molecules or formulated for different areas of effect, or # doses/day?

A

Sulfasalzine
Olsalazine
Balsalazine

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35
Q

Inhaled corticosteroids

A 
Beclomethasone
Budesonide
Ciclesonide
Flunisolide
Fluticasone
Mometasone
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36
Q

Benefits of using Natalizumab & Vedolizumab for IBD?

A

reduced inflammation

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37
Q

Sucralfate use

A

specific situations, to reduce the risk of NSAID-induced gastric ulcers

*must stop the NSAID

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38
Q

How do you choose what IBD drugs to use?

A

Based on location and severity of disease

Route of administration that is chosen is also determined based on the location and sometimes severity of the disease.

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39
Q

H2 blockers administration

A

Rx or OTC, PO and some IV

40
Q

Other medications used in the Tx of IBD

A

Antibiotics (CD)
Smoking (transdermal nicotine)- (UC)
Probiotics (mostly UC)

41
Q

If a patient has an active TB or Hep B infection, what meds would you want to avoid using?

A

Anti-TNF-alpha Biologics: infliximab, certolizumab, adalimumab, golimumab

42
Q

Patients with _______ are at a high risk of relapse–50-80% of patients may relapse within a year or two. In contrast, some patients can achieve remission for many years. Expect that most (if not all) patients will be on maintenance therapy indefinitely.

A

UC and CD

43
Q

Antacids *

A

absorption of cations (Mg, Al, Ca) can occur with renal impaired

44
Q

Misoprostol AE

A

GI AE’s are common

  • ab pain
  • flatulence
  • diarrhea & nausea (dose related)
45
Q

Immunosuppressant drugs for IBD

A 
Azathioprine
6-mercaptopurine (6-MP)
Methotrexate
Cyclosporine
Biologics
46
Q

Goals and cautions of IBD Tx

A

Goals: maximize efficacy & minimize toxicity

Cautions:

  • avoid antidiarrheal meds (reduce motility)
  • avoid anticholinergic drugs (reduce motility)
  • avoid NSAIDs (worsen Sx)
  • caution w/ opioids (reduce motility)
47
Q

PPI interactions

A

reduce absorption of drugs that need an acidic environment
CYP450
CYP2C19 - Omeprazole (worst w/ slow metabolism)

48
Q

With this IBD Tx, CD has a minimal response while VSL#3 may reduce pouchitis in patients with ileal pouch anal anastomosis, and it may also prevent relapse in mild-mod UC disease

A

Probiotics: L. acidophilus, Bifidobacterium

49
Q

Antacids MOA

A

React with gastric acid to produce water+ a salt (more neutral). Reduce acidity

50
Q

What do you consider when choosing Tx for IBD?

A 
Patients Sx
Medical Hx
Current medication use
Drug allergies
Extent, location, and severity
51
Q

PPI drugs

A 
Esomeprazole
Lansoprazole
Omeprazole
Pantoprazole
Rabeprazole
Dexlansoprazole
52
Q

Goals of GERD Tx

A

Alleviate Sx
Decrease frequency of recurrent disease
Promote healing of mucosal injury
Prevent complications

53
Q

Misoprostol administration

A

4x day

54
Q

The long term AE effects of this IBD drug include hepatotoxicity, pulmonary fibrosis, and bone marrow suppression

A

Methotrexate

55
Q

Sucralfate interactions

A

prevents absorption of many drugs (digoxin, fluoroquinolone) concern with low TI

56
Q

What are the cons of using Anti-TNF-alpha Biologics for IBD?

A
  • Only available as SubQ or IV
  • expensive
  • serious AE

Infliximab has IV infusion related rxn risks: fever, chest pain, hypoTN, dyspnea

57
Q

Systemic (oral) corticosteroids

A

Prednisone
Prednisolone
Methyprednisolone

58
Q

Non-pharmacologic therapy for PUD

A
  • reduce psychological stress
  • stop smoking
  • avoid alcohol
  • avoid NSAID/ASA use
59
Q

Antacid AE

A
  • Constipation w/ calcium & aluminum
  • Diarrhea w/ magnesium
  • Acid/base imbalance w/ sodium bicarb
60
Q

This IBD drug’s MOA is as a folate antagonist

A

Methotrexate

61
Q

Other biologic immunosuppressant drugs used for IBD (not anti-TNF-alpha):

A

Natalizumab

Vedolizumab

62
Q

GERD lifestyle changes

A
  • eat smaller meals
  • avoid eating in 3 hours prior to bed
  • avoid irritating foods
  • avoid irritating meds (NSAIDs)
  • smoking cessation
  • avoid alcohol
  • wt loss
  • elevate head of the bed
63
Q

This IBD Tx has AE of significant toxicity risks including: nephrotoxicity, risks of infection, seizures, hypertension, LFT abnormalities

A

Cyclosporine

64
Q

Which Aminosalicylate affects different areas based on the route of administration?

A

Mesalamine

PO-> ileum, cecum
Enema -> colon, rectum
Suppository -> rectum

65
Q

Why would you want to use Azathioprine & 6-MP for IBD?

A

maintaining remission and reducing the need for long term corticosteroid use

66
Q

AE include: possible reactivation of serious infx including TB, Hep B, HF, lymphoma

A

Anti-TNF-alpha Biologics: infliximab, certolizumab, adalimumab, golimumab

67
Q

PPI administration

A

PO (can open & mix in)
30-60 minutes before meals
Lasts 18 hours

68
Q

MOA: target immune response or cytokines involved with IBD

A

Immunosuppressants

69
Q

How do you treat NSAID-associated ulcers?

A

discontinue NSAID if possible.

If not, PPI, H2RAs, Sucralfate

70
Q

How do you treat H.pylori-associated ulcers?

A

3 drug combo:
PPI (or H2RA)
Antibiotics- Clarithromycin, Amoxicillin or metronidazole

10-14 days

71
Q

Sucralfate AE

A

constipation, nausea, metallic taste

aluminum toxicity MC with renal failure

72
Q

How do you prevent NSAID-associated ulcers?

A

Use gastroprotection if must use:

  • Misoprostol&raquo_space; H2RAs
  • PPIs&raquo_space; H2RAs
  • Misoprostol = PPIs
  • COX2 selective NSAID = PPI + nonselective NSAID (latter is preferred)
  • PPIs better tolerated than Misoprostol
73
Q

Reasons for H.pylori Tx failure

A

Reinfection
Non-adherance
Antimicrobial resistance (70%)

74
Q

H2 blockers *

A

Dose adjust for renal impaired

Will enter breast milk, cross placenta

75
Q

Misoprostol use

A

in specific situations, to reduce the risk of NSAID-induced gastric ulcers

76
Q

Antacid administration

A

best to take after meals

77
Q

Non-pharmacologic therapy for IBD

A
  • avoid irritating foods
  • B12, folic acid, fat soluble vitamins, iron, etc supplementation if needed
  • Assess for risk of bone loss
  • surgery
78
Q

Antacid interactions

A

Blocks absorption of many drugs, take other drugs 1-2 hrs before and/or 4-6 hrs after

  • ferrous sulfate
  • isoniazid
  • sulfonylureas
  • flouroquinolones
79
Q

Why would you choose to use Aminosalicylates?

A

To induce and maintain remission in mild-moderate IBD

80
Q

Aminosalicylate *

A

Contraindicated in sulfamide allergy

Must supplement with folic acid during pregnancy

81
Q

PPI *

A

Do not stop abruptly, must taper off

82
Q

AE with long term use: cataracts, skin atrophy, HTN, hyperglycemia, adrenal suppression, osteoporosis, increased risk of infection, delayed growth in children

A

corticosteroids

best not to use long term

83
Q

What meds are the last resort choice for IBD Tx?

A

Natalizumab
Vedolizumab

(other biologics)

84
Q

Aminosalicylate drugs

A
  • Mesalamine
  • Sulfasalazine
  • Olsalazine
  • Balsalazine
85
Q

MC causes of PUD

A

H. pylori infection (esp DU)
NSAIDs (esp GU)
Stress-related mucosal damage

86
Q

H2 blockers interactions

A

Reduce efficacy of drugs that require an acidic environment.

Cimetidine reacts w/ CYP450 and interferes with the metabolism of other drugs (warfarin, phenytoin)

87
Q

Bismuth Subsalicylate MOA

A

antimicrobial, inhibits pepsin, increase mucous secretion, works w/ glycoproteins to coat & protect ulcers

88
Q

This IBD drug is Pregnancy Category X

A

Methotrexate

89
Q

H2 blockers MOA

A

inhibits H2 receptors from binding to Histimine (which stimulates gastric secretion) to reduce secretion of gastric acid

90
Q

Inflammatory response includes T-helper type 1 cells that produce pro-inflammatory cytokines: Interferon-gama, TNF-alpha*, IL-1, IL-6, IL-8, IL-12

A

Crohn’s disease

91
Q

H2 blockers AE

A

mostly well tolerated

Confusion w/ elderly & IV

Cimetidine may cause endocrine fx (gynecomastia/galactorrhea)

92
Q

Patient directed GERD therapy options (OTC)

A
  • Antacids- quick, cheap, prn
  • OTC H2 blockers- work in 30 min, prn, less $ than PPIs
  • PPIs- effective, not for prn, use for 2 wks then stop
93
Q

Antibiotics used in IBD Tx

A

Metronidazole -> pouchitis, CD with resection or perianal fistulas

Ciprofloxacin -> refractory active CD

Can also use in combination

94
Q

Misoprostol *

A

Avoid in pregnancy

95
Q

MOA: inhibits purine synthesis, reduction of IBD associated GI inflammation

A

Azathioprine & 6-MP

Pharmacology -AM (4 decks)

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