Question Set: PUD Case



A 32-year-old white female was referred to a hepatologist for a liver biopsy following presentation to an emergency department (ED) where she had complained of fever and flank pain secondary to pyelonephritis from obstructive renal calculi. Past history was remarkable for a needle stick injury (the patient was a registered critical care nurse), sustained 10 years earlier in 1982 from a patient believed to be infected with non-A, non-B hepatitis. Six weeks subsequent to the needle stick, she became ill with a mild flu-like syndrome. She was not icteric and no laboratory tests were obtained. Routine physical exams following this exposure revealed sporadic elevations in liver function tests (LFTs). No further workup was obtained until her visit to the ED.On physical exam in the ED, the patient was found to be well developed, well nourished, and in no acute distress. She was anicteric. Lymph nodes were negative, chest was clear to auscultation, and there was no hepatosplenomegaly.No spider angioma or palmar erythema was present, and there was no edema of the extremities. The patient was very active and did not complain of fatigue or malaise. There was no evidence or history of decompensated liver disease or cirrhosis.At the ED visit, laboratory values revealed a markedly elevated white blood cell count. Urinalysis was positive for blood, white blood cells, and bacteria.Liver function tests were abnormal, with an aspartate aminotransferase (AST) of 48 U/L and an alanine aminotransferase (ALT) of 60 U/L. In light of these elevated LFTs, a complete hepatitis profile was obtained. The patient was found to be hepatitis C (HCV) antibody positive. She subsequently tested positive for HCV by polymerase chain reaction (PCR).The patient was referred to a hepatologist who procured a percutaneous liver biopsy to establish baseline liver condition. Interferon alpha (IFN) therapy was initiated after careful consideration of side effects versus possible benefits. The patient began a drug regimen of 3 million international units (MIU) administered subcutaneously three times a week.A decrease in LFTs was noted after 4 weeks of therapy. Liver function tests continued to decline and were normalized by week 8. The IFN was well tolerated except for complaints of fatigue and headache. After 26 weeks of drug therapy, the patient tested negative for the presence of serum HCV via PCR. At that time, the IFN dosage was reduced to 1.5 MIU three times per week. Liver function tests remained normal for eight more weeks, when they increased markedly. A new serum HCV test was positive, and the IFN dosage was increased to 3 MIU three times per week. Though LFTs returned to normal, side effects worsened, with hair thinning and mood swings compounding the chronic headache and fatigue. Drug therapy was discontinued at the patient's request because of the worsening side effects. Following discontinuation of IFN therapy, LFTs showed a rebound effect, reaching new highs (see Figure 1).The patient remained off IFN therapy for 16 months. After reading about several new treatment modalities, the patient expressed interest in undergoing the IFN protocol in the Reichard study,[1] which documented a positive response from prolonged IFN therapy. With the guidance of a hepatologist, the patient began the new protocol of 3 MIU three times weekly for 52 weeks.After 4 weeks of therapy LFTs normalized, and HCV was not detectable in the serum after 16 weeks of drug therapy (see Figure 2). Adverse reactions continued to be present but were better tolerated secondary to increased sleep, decreased stress, daily exercise, and a low-fat diet. Flu-like syndrome and hair thinning were the primary complaints.Starting at week 60, the IFN dosage was weaned in increments of one-half million units every 4 weeks (ie, 2.5 MIU at week 60, 2.0 MIU at week 64, 1.5 MIU at week 68). At 1.5 MIU, the patient reverted to a seropositive state and all therapies were ceased as reevaluation was deemed necessary. Since the patient was asymptomatic with minimal liver damage, a decision was reached between the patient and her physician to discontinue any further IFN treatment. Liver function tests and HCV RNA by PCR continue to be monitored every 4 to 6 months to follow any progression or worsening of the disease. Currently the patient remains asymptomatic with no apparent worsening of her liver function. She leads an active life.Case #57 yo AAM with PMH of hepatitis C, EtOH abuse, HTN is referred to the GI clinic because of elevated LFTs.He has no complaints.PMH:IVDA with heroin and cocaine 3o years ago, hepatitis C, heavy EtOH abuse, HTNRectal bleeding for 2 months - colonoscopy showed 9 benign polyps (one tubular adenoma and 8 hyperplastic polyps).Medications:Tenormin, LisinoprilSH:Drug abuse as described above.He told his PCP that he is "in remission" from alcohol.On closer questioning, the patient admitted to long term EtOH abuse in binging sprees, drinking 3-5 bottles of wine whenever he can afford it. The last binge was just 2 weeks ago. Ironically, he finances his EtOH abuse with the money he is receiving for disability because of his liver disease.Physical examination:WD/WN in NADNo signs of chronic liver diseaseHEENT: no teeth (lost in brawls as per patient)The rest of the exam was normalWhat is your diagnosis?Hepatitis and EtOH abuseWhat labs would you order?CBC, CMP, AFPLiver U/SWhat about hepatitis C genotype?Sure, the treatment response depends on the genotype. Type 1 is bad with only 40% response rate to INF + Ribavirin after 12 months. Type 2 and 3 is good with 80% response rate after just 60 months.This patient's genotype is 1a.Laboratory resultsCMP, hepatitis profile; Hepatitis C viral load and genotypeHe already had some labs several months ago showing that LFTs are persistently elevated.Look at the HDL, it is high because of the EtOH abuse.AFP is 6.2.Should we start antiviral treatment with INF and Ribavirin?No. EtOH abuse is a contraindication to the antiviral treatment of hepatitis C. In fact, in the AFP article posted below a similar case is described in the clinical scenarios at the end.What happened?Patient was referred to Rosary Hall (a drug abuse counseling center) and a F/U appointment was made in 1 month to monitor the progress.Liver U/S and repeat LFT were ordered.All patients with chronic hepatitis C need AFP and liver U/S every 6 months to screen for hepatocellular CA.What did we learn from this case?Take a careful history of drug abuse.You cannot treat hepatitis C patients if they are still drinking heavily.EtOH abuse has a detrimental effect on hepatitis C liver disease (interestingly, this is not the case with hepatitis B).Even if you treat this patient, his chance of response is virtually zero because of the genotype and EtOH abuse. African American patients also have a lower response rate.We should first help this patient stop drinking before treating his hepatitis CCC:PU is a 42 yo WM presenting to your pharmacy requesting refills for his prescriptions. He places twobottles of Maalox on the counter and says, “I hope this stuff works. My doctor said I have dyspepsia”.HPI:Patient reports to have had no stomach problems in the distant past. Several weeks ago, he began having a “cramping” pain “all around” in his stomach while he eats. He frequently feels nauseous and sometimes vomits. The liquid antacids seem to help relieve the pain. He does not visit his physician regularly. Today he called the doctor’s office to ask for something to help his stomach and the nurse instructed him to use the Maalox until his appointment next month.MEDS:Voltaren XR (diclofenac, extended-release) 100 mg po qdMaalox 30 cc po pc & qhsPeptoBismol, occasional use (1-2 times a week)Allergies:PCN, Erythromycin (hives with both)PMH:Arthritis in both knees x 3 years. SH:Smokes 1 pack per day x 18 years. Drinks average of 6 beers on weekends. Divorced x 6 months. Has worked as a 911 Operator for the past 3 years.FH:Mother died in car accident 4 years ago. Father died of stroke, age 66. No siblings or children.ROS:Denies vision, dry mouth, cough, CP, SOB, frequent/ urination. Admits to feeling tired for thepast couple months. + headaches several times a week. + black stools, 2 episodes in the last week. + dizziness “only a couple of times” when he stood up from the couch. + knee pain mostly in the morning; relieved by Voltaren. + weight loss of 10 pounds over past couple months.PE:Gen:Thin, slightly pale gentleman, appears stated age.Vitals:Sitting:BP 134/86 P 96 regStanding: BP 120/80 P 105 regRR 18 unlabored Temp (po) 37C Ht 5 ft 10 in Wt 150# HEENT:NC/AT (normocephalic, atraumatic)Neck:– bruit, – JVDCOR:S1, S2, No S3 or S4, No M/R/GABD:Mild tenderness, – guarding, – massesRect:Guiaic-positiveEXT:– edema, – lesionsLABS (6 weeks ago):Chem-7:Na140(135-145 mg/dL)CBC: WBC 9.1 (4.5-10.5 Th/mm3)K 4.0(3.5-5 mEq/dL) RBC 4.23 (4.3-5.9 Mil/mm3)Cl105(101-111 mEq/dL) Hgb 11.0 (13.9-16.3 mg/dL)HCO326.8(23-29 mEq/dL) Hct 33 (42-52%)BUN32(6-20 mg/dL) MCV 79 (80-97)Cr1.3(0.5-1.2 mg/dL) MCH 26 (27-33 pg)Glu106(70-120 mg/dL)Question Set: PUD Case Develop a problem list for this patient. Prioritize the problems by indicating which ones need to be treated now, and those that can be addressed at another time. ProblemPriorityUlcer related dyspepsia causing chronic blood lossShould be treated ASAPPossible complication due to PUD, obstruction or malignancyProblem can be addressed nowEdema and JVD may be due to mild CHF or possible liver dysfunctionProblem can be addressed laterIron deficiency anemia due to chronic blood lossProblem can be addressed laterSmokingProblem can be addressed later2.State whether you think the patient has a gastric or duodenal ulcer. List the subjective findings to Support your choice. This patient has gastric ulcerSubjective findings that support the presence of a GU:Pain precipitated by foodCramping pain extended over a wide area of abdomenPain relived by antacidsPain associated with N/V and weight lossNo nocturnal painPossible NSAID related etiology3.List the risk factors for peptic ulcer disease specific for this patient.Chronic use of NSAID’sSmokingAlcohol consumptionStressful lifestyle4.In order to better assess the patient’s chief complaint, what additional data would you like to get?A-Ask the patient the following questions:When did the pain start and how quickly did it progress?Did you have any similar episodes previously?How long dose the pain last?What brings on the pain?How sever is the pain? Can you rate it on a scale from 1-10?Do you have any other sensation or feeling around the same time the pain starts?Is your bowel movements regular?What are you using Pepto-Bismol for?How much caffeine do you consume daily?Ask about his diet.Any H/O other medical problemsB-objective data:Endoscopy for visualization of the ulcer, CLO test for H.pylori, check for obstruction or malignancyLiver function testsECGSerology for hepatitis5.Looking at the available objective data (PE and Labs), assess the etiology and severity of the Patient’s abdominal problem.NSAID-induced gastric ulcer disease with chronic bleeding and possible obstruction and/or tumor.? Hepatitis or liver dysfunction6.How should the patient’s abdominal complaint be managed at this time? Describe an appropriate therapeutic plan (changes or additions to his current medication regimen; include drug name(s), doses, duration) For management of PUD1-non-drug modalities:Stop smokingAvoid alcoholAvoid caffeine and aggravating foods2-drug therapyThere are 2 therapeutic options for Tx of the PUDDiscontinue voltaren and use an analgesic like acetaminophen or less damaging NSAID like selective COX-2 inhibitors e.g Celebrex 100-200 mg po bid↓If volatren must be continued↓Administer voltaren with food and/or antacid↓Ranitidine po 150 mg BID or 300mg hs for 8-12 weeks↓High dose PPI are the DOC for ulcer healing in this situationOmeprazole po 20 mg bid for 4-8 weeksEvaluate patient for resolution of symptoms and/or healing of ulcer↓↓After ulcer heals and patient is asymptomatic.Prophylactic therapy is indicatedThe agent of choice is misoprostol PO 200mcg QID↓If the ulcer did not heal or patient still has symptomsOmeprazole po 40 mg/day for 4-8 weeks↓H2RA or PPI are effective in relieving Sx, but may be dangerous by masking symptoms related to complications↓IF HP is present start eradication regimen:BSS po 525mg qid + Metronidazole po 500mg qid +tetracycline 500 mg po qid + Omeprazole po 20 mg bidFor 10 daysFollowed by omperazole po 20mg bid until eradication is documented.Followed by prophylactic therapy with misoprostol as above if volatren is continued.↓Maalox 30 cc po before meals and before bedtime as needed to control pain can be added to either regimen7.What monitoring parameters would you follow to ensure the therapy you described above? Has achieved the desired therapeutic effect? Pain reliefFrequency of antacid useDecrease in abdominal discomfort, postprandial fullness, flatulence, Acid regurgitation, heartburn, and nausea and vomiting.Weight gainGuaiac test on stoolCBCTesting for HPEndoscopic evidence of ulcer healing8.What parameters would you monitor to determine that the patient’s disease is worsening (in spite of treatment) or that the patient is suffering side effects?Acute changes in quality of painSymptoms and signs of bleeding: hematemesis , melena, black stool, guaiac stool, CBCFailure to respond to antacidsMonitor Scr, CBC, ALT, AST, CNS statusMonitor for drug interactions (e.g metronidazole and etoh) ................
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