PHARM Lecture 1 Flashcards

1
Q

Pathophysiology of GERD

A
  • decreased LES pressure
  • Anatomic factors
  • esophageal clearance
  • mucosal resistance
  • gastric emptying
  • composition of refluxae
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2
Q

The treatment goal for GERD

A
  • alleviate/eliminate symptoms
  • decrease frequency, duration and recurrence
    -promote healing and injured mucosa
  • prevent complications
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3
Q

Non-pharmacologic therapy

A
  • elevated head of bed 6”-8” while sleeping
    -weight reduction
    -avoid high-risk foods
    -protein-rich diet to increase LES pressures
    -small meals
    -avoid eating junk food before bed
    -avoid smoking/alcohol
    -avoid tight-fitting clothing
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4
Q

Pharmacologic therapy

A

Antacid, H2 antagonist, and PPI

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5
Q

Antacid MOA

A

neutralize acid and raise intragastric PH, increase LES pressure

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6
Q

Efficacy of antacid

A

short duration, can take used PRN in adjunctive to H2RA and PPI

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7
Q

Onset and duration of antacids

A

Onse: 5 minutes
Duration: 30 minutes

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8
Q

Dosing for antacid

A

generally 2 tablets after meals

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9
Q

When to use antacid

A

minor GERD symptoms , <2 times/week

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10
Q

Adverse effects of magnesium

A

diarrhea

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11
Q

Contraindication for magnesium

A

impaired renal excretion or on dialysis

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12
Q

Adverse effects of aluminum

A

constipation
rare - bone demineralization, intestinal obstruction

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13
Q

relationship of aluminum with phosphate

A

decrease phosphorus concentration which leads to bone demineralization

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14
Q

contraindication for sodium

A

CKD,CHF, HTN

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15
Q

adverse effects of calcium

A

constipation

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16
Q

Drug interactions of antacids

A

tetracycline, fluoroquinolones, z pac, ferrous sulfate, ketoconazole, itraconazole, levothyroxine

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17
Q

Which medication relays on acidic environment for absorption

A

ketoconazole, itraconazole, levothyroxine

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18
Q

H2 receptor antagonists meds

A

-ends in dine
*cimetadine
* famotidine
*rantidine - associated with carcinogen

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19
Q

MOA of H2RA

A

competitive inhibition of histamine at H2 receptors of gastric parietal cells –> inhibits gastric acid secretion and increase pH

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20
Q

Onset and duration of H2RA

A

Onset: 30 minutes
Duration: 4-10 hours

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21
Q

Dosing of H2RA

A

generally BID
- reduce dosing if CrCl < 50mL/min

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22
Q

Adverse effects of H2RA

A

headache, fatigue, dizziness, constipation/diarrhea
* thrombocytopenia

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23
Q

Drug interaction with H2RA

A

Cimetidine is a moderate inhibitor of CYP1A2, CYP2C19 and CYP3A4

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24
Q

PPI

A

ends in -prazole

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25
Q

MOA of PPI

A

block gastric acid secretion by inhibiting gastric H+/K+ in gastric parietal cells

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26
Q

Onset and duration of PPI

A

Onset: 2-3 hours, up to 4 days
Duration: 24 hours

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27
Q

Dosing for PPI

A

Standard: once daily with food
BID dosing: severe or complicated GERD
- no renal accumulation or dose adjustment

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28
Q

Can you use PPI PRN

A

No, need to combine with H2RA and antacid due to slow onset

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29
Q

adverse effects of PPI

A

headache, dizziness, n/v/d

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30
Q

Drug interactions of PPI

A

-methotrexate: increase MTX toxicity
- clopidogrel (omeprazole, esomeprazole, rabeprazole)
-HIV meds need acidic environment

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31
Q

PPI-Clopidogrel drug interactions

A

Clopidogrel is metabolized to its active metabolite by CYP2C19 but some of the PPI can inhibit CYP2C19

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32
Q

Treatment for mild GERD (<2 times/week and NOT troublesome)

A
  • antacid and/or H2RA BID or PPI once daily
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33
Q

Symptomatic relief of GERD (>2 times week or troublesome)

A

PPI daily (4-8 weeks) or H2RA BID (6-12 weeks)

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34
Q

Alarm symptoms

A

weightloss more than 10%, family history of cancer, anemia, persistent vomiting

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35
Q

Treatment for Alarm symptoms

A

EGD or further diagnostic testing needed

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36
Q

Treatment for chest pain reflux

A
  • cardiac workup
  • PPI BID for 4 weeks
    if symptoms persists consider diagnostic testing
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37
Q

Moderate-sever symptoms treatment/ esophageal injury

A

PPI daily or BID for 8-16 weeks or H2RA QID (except famotidine BID) or interventional therapy

38
Q

Patients with atypical GERD treatment

A

PPI BID for 3-4 months

39
Q

Elderly patient with GERD treatment

A

older than 60 years old
- PPI once daily

40
Q

Atypical symptoms of GERD

A
  • chest pain
    -asthma
    -poor dentition
    -jaw pain
41
Q

Refractory Gerd treatment

A
  • ensure compliance, further testing, test H.pylori status
    treatment
  • increase dose
    -switch to another PPI
    -add H2RA at bedtime
    -antireflux surgery
42
Q

Concerns with discontinuing therapy

A

can cause rebound

43
Q

Common cause of PUD

A

NSAIDs and H.pylori

44
Q

Nonpharmacologic therapy for PUD

A

reduce stress, smoking cessation

45
Q

Pathophysiology of H.pylori infection

A

gram negative rod
- produce cytotoxins that damage mucosal cells

46
Q

diagnostic h.pylori

A

Biopsy urease and urea breath test

47
Q

what causes a false negative for H.pylori testing

A

If the patient is on PPI, bismuth, antibiotics

48
Q

How long to withhold meds for H.pylori testing

A

1-2 weeks before test
4 weeks for bismuth or antibiotics

49
Q

What medication cause QTc prolongation

A

Clarithromycin

50
Q

Which medication cause discolored urine and bodily fluids

A

metronidazole

51
Q

Which medication is a strong CYP3A4 inhibitor

A

Clarithromycin

52
Q

SE of Bismuth

A

discoloring of tongue and stools, GI upset, tinnitus

53
Q

Which medication is a contraindication for <8 y/o and pregnancy

A

tetracycline

54
Q
  1. PCN allergy: none
  2. MCL exposure: none
A

Bismuth quadruple, nonbismuth quadruple, triple therapy with amoxicillin

55
Q
  1. PCN allergy: no
  2. MCL exposure: no
A

Bismuth quadruple, PPI triple with metronidazole

56
Q

PCN allergy: N
MCL exposure: Y

A

Bismuth quadruple
levofloxacine or triple sequential

57
Q

PCN: Y
MCL exposure: Y

A

Bismuth quadruple

58
Q

1st line treatment for H.pylori

A

Bismuth- based quadruple therapy and concomitant PPI triple therapy (non bismuth quadruple)

59
Q

Alternative 1st line for H.pylori

A

PPI triple therapy

60
Q

Which treatment are you concerned about compliance issue for H.pylori

A

Bismuth-based quadruple therapy
- pt needs to take it QID

61
Q

Meds included in the Bismuth-based quadruple therapy

A

PPI BID
Bismuth QID
Metronidazole QID
Tetracyclein QID

62
Q

Meds in non-bismuth quadruple therapy

A

PPI BID
Clarithromycin BID
Amoxicillin BID
Metronidazole BID

63
Q

Meds in PPI triple therapy

A

PPi BID
Clarithromycin BID
Amoxicillin BID or Metronidazole BID

64
Q

When to test for eradication of H.pylori

A

4 weeks after therapy completion

65
Q

Treatment failure for H.pylori

A

Patient adherence, resistant organisms, low intragastric pH, high bacterial load

66
Q

How long to use PPI for H.pylori infection

A

additional 4 weeks after the completing therapy

67
Q

Which NSAIDs is COX 1 selective

A

ketorolac

68
Q

Which NSAIDs is COX 2 selective

A

Celecoxib

69
Q

Why do NSAIDs increase the risk of ulcers

A

COX 1 inhibits prostaglandins which is important GI protective barriers

70
Q

NSAIDs Boxed Warning

A

GI risk for general NSAIDs, the cardiovascular risk associated with celecoxib

71
Q

Explain the GI risk and CV risk associated with Aspirin

A

GI risk moderate, CV risk is low/protective

72
Q

Explain the GI risk and CV risk associated with Celecoxib

A

GI risk: low, CV risk: moderate - high

73
Q

Patient factors for increased NSAID toxicity

A

> 65 y/o, concomitant anticoagulant use, previous PUD or PUD complications, multiple NSAID use, cigarette smokers

74
Q

NSAID induced treatment

A

Discontinue or lower dose of NSAID, use alternative pain meds and
- PPI once daily for 4 weeks
- H2RA for 6-8 weeks
-Sucralfate for 6-8 weeks

75
Q

Adverse effects of Sucralfate

A

constipation

76
Q

Purpose of Sucralfate

A

mucosal coating agent

77
Q

D-D interactions for sucralfate

A

inhibits drug absorption
- space out from other meds by 2 hours
- take antacids at least 30 minutes before or after sucralfate (has aluminum in it)

78
Q

NSAID induced prevention

A

PPI, misoprostol

79
Q

Adverse effects of misoprostol

A

diarrhea, abdominal cramping

80
Q

Contraindication for misprostol

A

pregnancy

81
Q

What is misoprostol

A

synthetic prostaglandin E (protective) which reduces GI side effects

82
Q

Are H2RA and antacids recommended for NSAID ulcer prophylaxis?

A

No

83
Q

low CV risk (not on aspirin)
low GI risk (0 risk factors)

A

NSAID alone

84
Q

Low GI risk (0 risk factors)
High GI risk (on ASA)

A

Naproxen + PPI or misoprostol

85
Q

Moderate (1-2 RF)
Low CV risk

A

NSAID + PPI or Misoprostol

86
Q

High CV risk (on ASA)
Moderate GI risk

A

Naproxen + PPI or misoprostol

87
Q

High GI risk ( > 2 RF or history of complicated ulcer)
Low CV risk (not on ASA)

A

Alternative therapy is possible or COX 2 inhibitor + PPI or misoprostol

88
Q

High CV risk
High GI risk

A

Avoid NSAID and COX 2 inhibitors

89
Q

Pathophysiology of stress-related mucosal damages

A

Decreased blood flow leads to ischemia and bleeding
- 75% of critically ill patient develop SMRD

90
Q

Prophylaxis for stress related mucosal damage

A

H2RA is preferred, and PPI are potential alternative
**Prophylaxis are not needed if the patient is discharged from ICU and/or risk factors no longer present*

91
Q

Concerns with chronic PPI use

A

Risk of fractures, infections, and interfere with vitamin/mineral absorption

92
Q

How long can you use PPI without concerns

A

up to 3 years