PHARM Lecture 1 Flashcards

(92 cards)

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
MOA of PPI
block gastric acid secretion by inhibiting gastric H+/K+ in gastric parietal cells
26
Onset and duration of PPI
Onset: 2-3 hours, up to 4 days Duration: 24 hours
27
Dosing for PPI
Standard: once daily with food BID dosing: severe or complicated GERD - no renal accumulation or dose adjustment
28
Can you use PPI PRN
No, need to combine with H2RA and antacid due to slow onset
29
adverse effects of PPI
headache, dizziness, n/v/d
30
Drug interactions of PPI
-methotrexate: increase MTX toxicity - clopidogrel (omeprazole, esomeprazole, rabeprazole) -HIV meds need acidic environment
31
PPI-Clopidogrel drug interactions
Clopidogrel is metabolized to its active metabolite by CYP2C19 but some of the PPI can inhibit CYP2C19
32
Treatment for mild GERD (<2 times/week and NOT troublesome)
- antacid and/or H2RA BID or PPI once daily
33
Symptomatic relief of GERD (>2 times week or troublesome)
PPI daily (4-8 weeks) or H2RA BID (6-12 weeks)
34
Alarm symptoms
weightloss more than 10%, family history of cancer, anemia, persistent vomiting
35
Treatment for Alarm symptoms
EGD or further diagnostic testing needed
36
Treatment for chest pain reflux
- cardiac workup - PPI BID for 4 weeks if symptoms persists consider diagnostic testing
37
Moderate-sever symptoms treatment/ esophageal injury
PPI daily or BID for 8-16 weeks or H2RA QID (except famotidine BID) or interventional therapy
38
Patients with atypical GERD treatment
PPI BID for 3-4 months
39
Elderly patient with GERD treatment
older than 60 years old - PPI once daily
40
Atypical symptoms of GERD
- chest pain -asthma -poor dentition -jaw pain
41
Refractory Gerd treatment
- ensure compliance, further testing, test H.pylori status treatment - increase dose -switch to another PPI -add H2RA at bedtime -antireflux surgery
42
Concerns with discontinuing therapy
can cause rebound
43
Common cause of PUD
NSAIDs and H.pylori
44
Nonpharmacologic therapy for PUD
reduce stress, smoking cessation
45
Pathophysiology of H.pylori infection
gram negative rod - produce cytotoxins that damage mucosal cells
46
diagnostic h.pylori
Biopsy urease and urea breath test
47
what causes a false negative for H.pylori testing
If the patient is on PPI, bismuth, antibiotics
48
How long to withhold meds for H.pylori testing
1-2 weeks before test 4 weeks for bismuth or antibiotics
49
What medication cause QTc prolongation
Clarithromycin
50
Which medication cause discolored urine and bodily fluids
metronidazole
51
Which medication is a strong CYP3A4 inhibitor
Clarithromycin
52
SE of Bismuth
discoloring of tongue and stools, GI upset, tinnitus
53
Which medication is a contraindication for <8 y/o and pregnancy
tetracycline
54
1. PCN allergy: none 2. MCL exposure: none
Bismuth quadruple, nonbismuth quadruple, triple therapy with amoxicillin
55
1. PCN allergy: no 2. MCL exposure: no
Bismuth quadruple, PPI triple with metronidazole
56
PCN allergy: N MCL exposure: Y
Bismuth quadruple levofloxacine or triple sequential
57
PCN: Y MCL exposure: Y
Bismuth quadruple
58
1st line treatment for H.pylori
Bismuth- based quadruple therapy and concomitant PPI triple therapy (non bismuth quadruple)
59
Alternative 1st line for H.pylori
PPI triple therapy
60
Which treatment are you concerned about compliance issue for H.pylori
Bismuth-based quadruple therapy - pt needs to take it QID
61
Meds included in the Bismuth-based quadruple therapy
PPI BID Bismuth QID Metronidazole QID Tetracyclein QID
62
Meds in non-bismuth quadruple therapy
PPI BID Clarithromycin BID Amoxicillin BID Metronidazole BID
63
Meds in PPI triple therapy
PPi BID Clarithromycin BID Amoxicillin BID or Metronidazole BID
64
When to test for eradication of H.pylori
4 weeks after therapy completion
65
Treatment failure for H.pylori
Patient adherence, resistant organisms, low intragastric pH, high bacterial load
66
How long to use PPI for H.pylori infection
additional 4 weeks after the completing therapy
67
Which NSAIDs is COX 1 selective
ketorolac
68
Which NSAIDs is COX 2 selective
Celecoxib
69
Why do NSAIDs increase the risk of ulcers
COX 1 inhibits prostaglandins which is important GI protective barriers
70
NSAIDs Boxed Warning
GI risk for general NSAIDs, the cardiovascular risk associated with celecoxib
71
Explain the GI risk and CV risk associated with Aspirin
GI risk moderate, CV risk is low/protective
72
Explain the GI risk and CV risk associated with Celecoxib
GI risk: low, CV risk: moderate - high
73
Patient factors for increased NSAID toxicity
>65 y/o, concomitant anticoagulant use, previous PUD or PUD complications, multiple NSAID use, cigarette smokers
74
NSAID induced treatment
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
Adverse effects of Sucralfate
constipation
76
Purpose of Sucralfate
mucosal coating agent
77
D-D interactions for sucralfate
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
NSAID induced prevention
PPI, misoprostol
79
Adverse effects of misoprostol
diarrhea, abdominal cramping
80
Contraindication for misprostol
pregnancy
81
What is misoprostol
synthetic prostaglandin E (protective) which reduces GI side effects
82
Are H2RA and antacids recommended for NSAID ulcer prophylaxis?
No
83
low CV risk (not on aspirin) low GI risk (0 risk factors)
NSAID alone
84
Low GI risk (0 risk factors) High GI risk (on ASA)
Naproxen + PPI or misoprostol
85
Moderate (1-2 RF) Low CV risk
NSAID + PPI or Misoprostol
86
High CV risk (on ASA) Moderate GI risk
Naproxen + PPI or misoprostol
87
High GI risk ( > 2 RF or history of complicated ulcer) Low CV risk (not on ASA)
Alternative therapy is possible or COX 2 inhibitor + PPI or misoprostol
88
High CV risk High GI risk
Avoid NSAID and COX 2 inhibitors
89
Pathophysiology of stress-related mucosal damages
Decreased blood flow leads to ischemia and bleeding - 75% of critically ill patient develop SMRD
90
Prophylaxis for stress related mucosal damage
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
Concerns with chronic PPI use
Risk of fractures, infections, and interfere with vitamin/mineral absorption
92
How long can you use PPI without concerns
up to 3 years