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Micro & Immunology · patient case with 2 questions

Medical history review before treatment

Patient: 60-year-old patient completing a medical history update.

Chief complaint: Routine care.

History: Reports a diagnosis of peptic ulcer disease treated some years ago, and current treatment with atorvastatin for hyperlipidemia.

Findings: No acute dental findings. History review only.

Question 1

Which microorganism is responsible for the majority of peptic ulcers?

  1. Helicobacter pylori
  2. Streptococcus pyogenes
  3. Clostridioides difficile
  4. Escherichia coli
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Correct answer: A. Helicobacter pylori

  • A. CORRECT. HELICOBACTER PYLORI, a gram-negative spiral bacterium, colonizes gastric mucosa and produces urease, neutralizing acid around itself and damaging the mucosal barrier. It accounts for the large majority of duodenal and gastric ulcers not caused by NSAIDs. Relevant dentally: NSAID analgesia should be used cautiously in ulcer patients.
  • B. S. pyogenes causes pharyngitis, erysipelas and skin infection.
  • C. C. difficile causes antibiotic-associated pseudomembranous colitis, a colonic disease.
  • D. E. coli causes urinary and enteric infection, not peptic ulceration.

Note: NSAID use is the other major cause. Together, H. pylori and NSAIDs account for the large majority of peptic ulcers, which is a relevant consideration when prescribing analgesics for this patient.

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Question 2

What is the mechanism of action of his lipid-lowering medication?

  1. Inhibition of HMG-CoA reductase
  2. Bile acid sequestration in the gut lumen
  3. Activation of lipoprotein lipase
  4. Inhibition of intestinal cholesterol absorption
Show answer and explanation

Correct answer: A. Inhibition of HMG-CoA reductase

  • A. CORRECT. Statins competitively inhibit HMG-CoA REDUCTASE, the rate-limiting enzyme of the mevalonate pathway. Reduced hepatic cholesterol synthesis upregulates LDL receptors and clears LDL from the circulation. Dental relevance: statins are CYP3A4 substrates, so azole antifungals and macrolides raise statin levels and myopathy risk.
  • B. Bile acid sequestration describes cholestyramine and colesevelam.
  • C. Fibrates increase lipoprotein lipase activity via PPAR-alpha, targeting triglycerides rather than LDL.
  • D. Blocking intestinal absorption at the NPC1L1 transporter is the mechanism of ezetimibe.

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