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1. Sebutkan jenis-jenis penyakit upper GI2. A.D. is a
70-year-old woman who retired from teaching about 5 years ago.
Several days
ago, she noticed black tarry stools and was hospitalized for an
upper GI bleed mostlikely secondary to NSAID use. She complains of
feeling tired and occasionally dizzy
for about 1 week. A.D. presents with a 5-year history of
rheumatoid arthritis for which
she takes naproxen 250 mg in the morning and 500 mg in the
evening. She states that prior to admission, she was also taking
prednisone 10 mg daily about a week for herarthritic pain that was
not controlled with naproxen. She denies any history of
previous
ulcer or ulcer-related complication. Other prescription
medications includehydrochlorothiazide 25 mg daily for
hypertension. OTC self-directed medications include
enteric-coated aspirin 81 mg daily, calcium carbonate, and a
multivitamin. A.D. does notuse tobacco or drink caffeinated
beverages but does have an occasional beer with friends.
She denies epigastric pain, nausea, vomiting, anorexia, and
weight loss but notes a recentchange in stool color. A review of
other body systems are noncontributory other than
previously indicated. There are no known food or drug allergies.
Physical examinationreveals a well-developed weak woman in no acute
distress. The abdomen was normal
with no pain on palpation. Bowel sounds were normal with no
guarding, masses,hepatomegaly, or spleenomegaly. The rectum was
normal but with guiaic-positive stool.
Vital signs include a temperature of 98.9F, blood pressure of
100/65, and a heart rate of90 beats/minute. Pertinent laboratory
values include Hgb of 11.0 g/dL, Hct of 35%, blood
urea nitrogen (BUN) 40, and serum creatinine (SrCr) 1.5 mg/dL.
All other laboratoryvalues are within normal limits. What factors
place A.D. at increased risk for developing
an NSAID-induced ulcer and related upper GI bleeding?3. A.D. was
admitted for further evaluation and treatment. An upper endoscopy
(EGD)
revealed two bleeding antral ulcers (0.2 and 0.4 cm). An antral
biopsy was reported to beH. pylori negative. All medications were
discontinued. Oral oxycodone was instituted at
5 mg every 6 hours when needed to control A.D.'s arthritic pain
while she washospitalized. Consideration was given to decreasing
the naproxen dose and switching to
acetaminophen, a nonacetylated salicylate, or a partially
selective NSAID (Table 26-4),but none of these options were
satisfactory for this patient. Treatment was initiated with a
continuous infusion of IV pantoprazole for 3 days and then she
was switched to oralpantoprazole 40 mg BID. A.D. was discharged on
pantoprazole 40 mg QD and naproxen
250 mg in the morning and 500 mg in the evening. All other oral
medications werereinstituted except for the prednisone. Will A.D.'s
gastric ulcer heal if she continues to
take the naproxen?4. Which ulcer-healing regimen would you have
recommended if A.D. was reported to be
H. pylori positive.5. Three months later, A.D. returned to her
gastroenterologist for a follow-up EGD, which
confirmed that the gastric ulcers were healed. On return to her
primary care physician, the pantoprazole was changed to ranitidine
150 mg BID. Other medications at this time
include naproxen 250 mg in the morning and 500 mg in the
evening, enteric-coatedaspirin 81 mg QD, calcium carbonate, and
multivitamins. What pharmacological options
are available to reduce the risk of a NSAID ulcer now that
A.D.'s initial ulcer is healedand she continues to take the
naproxen and aspirin?
6. S.P. is a 71-year-old retired gentleman who was eating dinner
with his wife when heexperienced a sudden onset of chest pain
described as crushing, burning, and squeezing.
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His wife notified emergency personnel, who transported S.P. to
the emergencydepartment. His past medical history reveals some
cardiovascular risk factors, including
age, hypertension, hyperlipidemia, and a sedentary lifestyle.
His medications prior toadmission include aspirin 81 mg daily,
hydrochlorothiazide 25 mg daily, and atorvastatin
40 mg at bedtime. He also takes OTC famotidine 20 mg daily as
needed for dyspepsia.
On examination, he complains of substernal crushing chest pain
that has lasted over 1hour. He is diaphoretic and extremely
anxious. He denies any shortness of breath, painradiating to upper
extremities or jaw, or cough. His vital signs include a temperature
of
99.1F, blood pressure 155/95 mmHg and heart rate of 115
beats/minute. Pertinentlaboratory results at this time are white
blood cell (WBC) count 7,700/mm
3, Hgb 14.2
g/dL, Hct 45%, platelets 270,000/mm3, SrCr 1.1 mg/dL, BUN 11
mg/dL, total cholesterol
161 mg/dL, low-density lipoprotein 96 mg/dL, high-density
lipoprotein 30 mg/dL,
triglycerides 190 mg/dL, sodium (Na) 141 mEq/L, potassium (K)
4.1 mEq/L, andtroponin I 0.3 ng/mL. Electrocardiogram reveals sinus
tachycardia with no evidence of
ST-segment elevation, depression, or T-wave inversion or new
left bundle branch block.Because of S.P.'s cardiovascular risk
factors and indeterminate troponin, he underwent
immediate diagnostic cardiac catheterization, which showed
normal coronaryangiography and an ejection fraction of 65%. S.P.
was diagnosed with noncardiac chest
pain (NCCP). Could S.P.'s chest pain be associated with an
extraesophagealmanifestation of GERD?
7. S.P. responded well to the trial of omeprazole 40 mg orally
twice daily and has not hadchest pain in 2 months. He has heard
that surgical options exist that may eliminate his
need for medications, as they are very expensive for him. Is
S.P. a candidate forantireflux surgery?
