#35 – Peptic Ulcer Disease



***LISTEN TO THE PODCAST HERE***



Definitions

  • Dyspepsia
    • Upper abdominal pain or discomfort
  • Gastritis
    • Epithelial or endothelial damage with histologic evidence of inflammation
  • 2 types
    • Gastric
    • Duodenal

Epidemiology

  • Annual incidence in developed countries 0.1-0.19%, or 0.7 cases per 1000 person-years
  • Lifetime prevalence of PUD in 10-20% in pylori (+) patients vs 5-10% in H.pylori (-) patients
  • Increases with age
    • 13x higher risk of bleeding in patients > 70yo
  • More common in males
  • Differences between Gastric and Duodenal Ulcers
    • DU occur up to 20 years before GU
    • DU 5x more common than GU

Etiologies

There are numerous causes of PUD and include infections, stress, medications, alcohol, cirrhosis, neoplasms, etc.  The two main causes in developed countries are:

  • Helicobacter pylori
    • Spiral gram negative rod
    • Decreasing incidence due to better hygiene, OTC medications, and antibiotic use
  • Non-Steroidal Antiflammatory Drugs (NSAIDs)
    • 1-4% per year risk of PUD
    • Risk factors
      • Prior history of PUD or pylori infection
      • Dose
      • Duration
      • Age > 75 years
      • Co-therapy
        • Corticosteroids, anticoagulants, SSRI, bisphosphonates, antiplatelets


Clinical Manifestations

  • Up to 70% of peptic ulcers are asymptomatic
    • Present later with complications
    • Up to 80% present with bleeding without preceding symptoms
  • Dyspepsia is the most common symptoms
    • May also have radiation to the back
  • Relation to food intake
    • GU – Worse
    • DU – Better
  • Night symptoms
    • GU – 1/3 of patients
    • DU – 2/3 of patients
  • Nausea, vomiting, anorexia, early satiety, epigastric fullness


Complications

  • Bleeding
  • Gastric Outlet Obstruction
  • Penetration
    • Change in typical symptoms
  • Perforation
    • 2-10% perforation rate
      • Duodenal – 60%
      • Antrum – 20%
      • Gastric Body – 20%

Red Flags


Work-up

  • Endoscopy
    • Up to 90% sensitivity in identifying ulcer
    • Next step if any red flags
    • Malignant features requiring biopsy:
      • Ulcerated mass protruding from lumen
      • Nodular, clubbed, or fused folds
      • Overhanging, irregular, or thickened ulcer margins
  • H/pylori Testing
    • pylori serology and stool antigen testing
      • May be falsely negative if on concurrent PPI
    • Biopsy testing and histology from endoscopy
    • Urea Breath Test


Initial Management

  • Withdrawal of offending or contributing factors
    • Stop NSAIDs, smoking, EtOH, precipitant foods
  • Antisecretory therapy
    • (+) H. pylori Ulcer
      • Uncomplicated – 14 days
      • Complicated – up to 12 weeks
    • NSAID Induced
      • If stopping – 8 weeks
      • If continuing – indefinitely
    • Non-H.pylori, non-NSAID Ulcer
      • 4-8 weeks
    • PPIs out perform H2A
      • Esomeprazole (Nexium) – 20-40mg daily
      • Lansoprazole (Prevacid) – 15-30mg daily
      • Omeprazole (Prilosec) – 20-40mg daily
      • Pantoprazole (Protonix) – 20-40mg daily
    • High Risk Groups Requiring Indefinite Prophylaxis
      • > 2 cm ulcer on endoscopy and age > 50yo
      • Refractory H. pylori negative, NSAID negative ulcer
      • Failure to eradicate H. pylori
      • Frequently recurrent peptic ulcers (> 2 cases in 1 one)
      • Continued NSAID use
  • H. pylori Eradication
    • Risk factors for Macrolide resistance
      • Prior exposure to macrolide therapy
      • ≥ 15% clarithromycin local resistance rates
      • < 85% eradication rates with clarithromycin triple therapy
    • Initial Therapy
    • Salvage Therapy
      • 20% of patients will fail initial H. pylori eradication

References

  1. Sung JJ, Kuipers EJ, El-Serag HB. Systematic review: the global incidence and prevalence of peptic ulcer disease. Alimentary pharmacology & therapeutics. 2009; 29(9):938-46. [pubmed]
  2. Lin KJ, García Rodríguez LA, Hernández-Díaz S. Systematic review of peptic ulcer disease incidence rates: do studies without validation provide reliable estimates? Pharmacoepidemiology and drug safety. 2011; 20(7):718-28. [pubmed]
  3. Sonnenberg A. Temporal trends and geographical variations of peptic ulcer disease. Alimentary pharmacology & therapeutics. 1995; 9 Suppl 2:3-12. [pubmed]
  4. Thorat MA, Cuzick J. Prophylactic use of aspirin: systematic review of harms and approaches to mitigation in the general population. European journal of epidemiology. 2015; 30(1):5-18. [pubmed]
  5. García Rodríguez LA, Hernández-Díaz S. Risk of uncomplicated peptic ulcer among users of aspirin and nonaspirin nonsteroidal antiinflammatory drugs. American journal of epidemiology. 2004; 159(1):23-31. [pubmed]
  6. Gururatsakul M, Holloway RH, Talley NJ, Holtmann GJ. Association between clinical manifestations of complicated and uncomplicated peptic ulcer and visceral sensory dysfunction. Journal of gastroenterology and hepatology. 2010; 25(6):1162-9. [pubmed]
  7. Wilcox CM, Clark WS. Features associated with painless peptic ulcer bleeding. The American journal of gastroenterology. 1997; 92(8):1289-92. [pubmed]
  8. Paimela H, Paimela L, Myllykangas-Luosujärvi R, Kivilaakso E. Current features of peptic ulcer disease in Finland: incidence of surgery, hospital admissions and mortality for the disease during the past twenty-five years. Scandinavian journal of gastroenterology. 2002; 37(4):399-403. [pubmed]
  9. Malfertheiner P, Megraud F, O’Morain CA. Management of Helicobacter pylori infection-the Maastricht V/Florence Consensus Report. Gut. 2017; 66(1):6-30. [pubmed]
  10. Chiorean MV, Locke GR, Zinsmeister AR, Schleck CD, Melton LJ. Changing rates of Helicobacter pylori testing and treatment in patients with peptic ulcer disease. The American journal of gastroenterology. 2002; 97(12):3015-22. [pubmed]
  11. Yeomans ND, Tulassay Z, Juhász L. A comparison of omeprazole with ranitidine for ulcers associated with nonsteroidal antiinflammatory drugs. Acid Suppression Trial: Ranitidine versus Omeprazole for NSAID-associated Ulcer Treatment (ASTRONAUT) Study Group. The New England journal of medicine. 1998; 338(11):719-26. [pubmed]
  12. Duck WM, Sobel J, Pruckler JM. Antimicrobial resistance incidence and risk factors among Helicobacter pylori-infected persons, United States. Emerging infectious diseases. 2004; 10(6):1088-94. [pubmed]
  13. Chey WD, Leontiadis GI, Howden CW, Moss SF. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. The American journal of gastroenterology. 2017; 112(2):212-239. [pubmed]

Ep-PAINE-nym



Littre’s Hernia

 

Other Known Aliasesnone

DefinitionHernia involving a Meckel’s diverticulum 

Clinical SignificanceNo real clinical significance other than it is an extremely rare type of hernia, but is always included in the typical pimping barrage of surgery students.  It should also be included in the “zebras” of differential diagnoses of RLQ pain.

Image result for littre's herniaImage result for littre's hernia

History – Named after Alexis Littrè (1654-1726), who was a distinguished physician and prolific surgeon at the historic Salpêtriére Teaching Hospital in Paris.  He was inducted into the famed Académie des Sciences in part to his ridiculous dissection of over 200 cadavers in 1684.  He first described an femoral hernia involving an intestinal diverticulum in 1700 in one of his cadaver dissections.

 


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Skandalakis PN, Zoras O, Skandalakis JE, Mirilas P. Littre hernia: surgical anatomy, embryology, and technique of repair. The American surgeon. 2006; 72(3):238-43. [pubmed]
  6. Sturdy DJ.  Science and Social Status: The Members of the Academie Des Sciences 1666-1750. 1995.  Boydell Press
  7. Malling B, Karlsen AA, Hern J.  Littre Hernia: A rare case of incacerated Meckel’s diverticulum.  Ultrasound Int Open.  2017;3(2):E91-92.

PAINE #PANCE Pearl – Gastrointestinal





Question

 

There are many individual lab tests that encompass “liver function tests” or LFTs.  So for this week’s pearl:

  1. List out the tests that make up a liver panel
  2. Explain how they can be grouped together

 



Answer

 

  1. A typical liver panel is made of the following individual lab tests:
    1. Total bilirubin
      1. Indirect bilirubin + direct bilirubin
    2. Aspartate aminotransminase (AST)
    3. Alanine aminotransferase (ALT)
    4. Alkaline phosphatase (ALP)
    5. Gamma-glutamyl transpeptidase (GGT)
    6. Lactate dehydrogenase (LDH)
    7. Albumin
    8. Total protein
  2. The easiest way to quickly interpret LFTs is group these tests into two broad categories:
    1. Hepatocellular (damage to the hepatocytes)
      1. AST
      2. ALT
      3. LDH
    2. Cholestatic (decreased post-hepatic drainage)
      1. Bilirubin
      2. GGT
      3. ALP

 

Now let me make this clear, there is MUCH MORE that goes into interpreting LFTs, but this is good, quick start when you get abnormal LFTs back on your patient.

 

Image result for hepatocellular vs cholestatic


References

  1. Giannini EG, Tesa R, Savarino V.  Liver enzyme alteration: a guide for clinicians.  CMAJ. 2005;172(3):367-379

Ep-PAINE-nym



Meckel’s Diverticulum

 

Other Known Aliasesnone

DefinitionVestigial remnant of the omphalomesenteric duct 

Clinical SignificanceIt is the most common malformation in the GI tract and is mainly asymptomatic.  When symptoms do occur, it commonly presents as painless, rectal bleeding in children.  The “Rule of 2s” will help you remember the facts of this pathology:

  • Effects 2% of the population
  • 2% of these will be symptomatic by age 2
  • 2 types of heterotopic tissue
  • Boy-to-girl ratio is 2:1
  • Usually 2″ in length
  • 2′ from the ileocecal valve

Image result for meckel's diverticulumImage result for meckel's diverticulum

History – Named after Johann Friedrich Meckel, the Younger (1781-1833), who was born into a prestigious medical family, with his father and grandfather already prolific physicians and professors of medicine in Halle, Prussia.  He made tremendous advancements in the area of anatomy and embryonic development with special attention to birth defects and abnormalities, where he pioneered the early study of teratology.  He first described the abnormality which bears his name in 1809.

Johann Friedrich Meckel.jpg


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Stallion A, Shuck JM.  Meckel’s Diverticulum.  Surgical Treatment: Evidence-Based and Problem-Oriented.  2001 [pubmed]
  6. Blackbourne LH.  Surgical Recall.  6th ed. 2012
  7. J. F. Meckel. Über die Divertikel am Darmkanal. Archiv für die Physiologie, Halle, 1809, 9: 421–453
  8. Klunker R, Göbbel L, Musil A, Tönnies H, Schultka R. Johann Friedrich Meckel the Younger (1781-1833) and modern teratology. Annals of Anatomy. 2002; 184(6):535-40. [pubmed]

Ep-PAINE-nym



Grave’s Disease

 

Other Known AliasesAutoimmune hyperthyroidism

Definition – Hyperthyrodism caused by antibodies that stimulate T3/T4 secretion.  The most common antibodies are thyroid-secreting hormone (TSH) and thyrotropin receptor antibody (TRAb). 

Clinical SignificanceClassic clinical manifestations of hyperthyroidism include thyromegaly, ophthalmaopathy, resting tremor, palpitations, weight loss, heat intolerance.  For more in depth analysis of hyperthyroidism, see my 2017 talk at ASPA here.

History – Named after Robert James Graves (1796-1853), who was an prolific Irish physician, surgeon, and educator.  He was named Regius professor of the Institute of Medicine in Trinity College, founded the Dublin Journal of Medical and Chemical Sciences, and was a an early adopter of clinical bedside rounding and teaching with medical students. Dr. Graves wrote a routine clinical lecture series in the London Medical and Surgical Journal and first described a young female patient with ophthalmopathy and goiter in 1835.  Dr. Armand Trousseau then published the collection of these articles in 1864 entitled “Clinical Lectures on the Practice of Medicine” and gave him this eponym.  Another contribution of Dr. Graves was the creation of the second hand on watches to time pulses and the practice of providing food and water with patients with a fever, instead of the common practice of withholding nourishment.

Image result for robert james graves

 


References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Graves RJ.  Newly Observed Affection of the Thyroid Gland. London Medical and Surgical Journal.  1835. Vol.7. Part 2. 512
  6. Graves RJ, Trousseau A.  Clinical Lectures on the Practice of Medicine.  1864.  Dublin.
  7. Smith TJ, Hegedüs L. Graves’ Disease. The New England journal of medicine. 2016; 375(16):1552-1565. [pubmed]