Peptic Ulcer – Top USMLE Diseases

Acute coronary syndrome (ACS) encompasses conditions that include confirmed or suspected myocardial ischemia or myocardial infarction (MI). ACS, which includes non-ST-elevation MI (NSTEMI), ST-elevation MI (STEMI), and unstable angina, usually results from thrombus formation on a ruptured atherosclerotic plaque in the epicardial arteries. Patients most commonly present with chest pain but also may have atypical symptoms. Diagnosis is by clinical history, ECG changes, elevated cardiac enzymes (preferably, high-sensitivity cardiac troponin), and/or evidence of wall motion abnormalities on imaging. Both STEMI and NSTEMI have loss of myocardial tissue, but STEMI is due to transmural ischemia (indicating complete major coronary artery obstruction). NSTEMI occurs because of subendocardial ischemia (indicating partial major coronary artery obstruction). Unstable angina occurs when ischemia does not result in infarction (no troponin elevation and typically with non-ST-elevation changes on ECG). Management of STEMI depends on the timing of the presentation and local resources with regard to thrombolytic therapy versus percutaneous intervention. Both unstable angina and NSTEMI are managed the same way, with both conservative (medical) and invasive strategies available. Additionally, routine medical therapy includes dual antiplatelet therapy, nitrates, oxygen, pain control, and beta-blockers.

Peptic ulcers are mucosal defects > 5 mm in diameter that penetrate the muscularis mucosae in the wall of the stomach or duodenum. Peptic ulcer disease (PUD) results when exposure to acid and digestive enzymes overcomes mucosal defense mechanisms. The most common etiologies are Helicobacter pylori (H. pylori) infection and prolonged use of nonsteroidal antiinflammatory drugs (NSAIDs). Patients may be asymptomatic or present with abdominal pain, nausea, and early satiety. PUD typically responds well to medical treatment with risk factor modification, H. pylori eradication, and acid reduction. If left untreated, PUD can lead to bleeding, perforation, gastric outlet obstruction, and gastric cancer.

Gastritis is inflammation of the gastric mucosa and can be classified by time course (acute or chronic), histologic features, and etiology. It is usually due to an infection (usually by Helicobacter pylori) or an immune-mediated process, but it can also be caused by substances that are direct gastric irritants. Chronic, metaplastic atrophic gastritis may be due to autoimmune or environmental causes and is a risk factor for gastric cancer. Individuals with gastritis may be asymptomatic or may have abdominal pain, dyspepsia, and nausea. Treatment of acute and chronic gastritis due to H. pylori infection involves acid suppression and antibiotics. Other causes are managed by avoiding offending agents and replacing associated deficiencies.

MI is ischemia and death of an area of myocardial tissue due to insufficient blood flow and oxygenation, usually from thrombus formation on a ruptured atherosclerotic plaque in the epicardial arteries. Clinical presentation is most commonly with chest pain, but women and patients with diabetes may have atypical symptoms. Diagnosis is by clinical history, ECG changes, an increase in cardiac enzymes, and evidence of wall motion abnormalities on imaging. Management depends on the timing of the presentation and local resources with regard to thrombolytic therapy versus percutaneous intervention. All patients receive nitrates, pain control, aspirin, anticoagulation, and beta-blockers (unless contraindicated).

Nonsteroidal antiinflammatory drugs (NSAIDs) are a class of medications consisting of aspirin, reversible NSAIDs, and selective NSAIDs. NSAIDs are used as antiplatelet, analgesic, antipyretic, and antiinflammatory agents. Common side effects include GI irritation, prolonged bleeding, and AKI.

Gastric acid medications include proton pump inhibitors (PPIs) and H₂ receptor antagonists (also known as H₂ blockers). The drugs work through different mechanisms to suppress acid secretion by parietal cells in the stomach. The most common indications include peptic ulcer disease, GERD, and dyspepsia. Adverse effects of PPIs include malabsorption, acute interstitial nephritis, and an increased risk of Clostridioides difficile infection. Adverse effects of H₂ blockers include CNS effects, bradycardia/hypotension, gynecomastia, and galactorrhea. Both classes are associated with drug interactions related to the cytochrome P450 system.

Acute kidney injury refers to sudden and often reversible loss of renal function, which develops over days or weeks. Azotemia refers to elevated levels of nitrogen-containing substances in the blood that accompany AKI, which include BUN and creatinine. Uremia refers specifically to the constellation of symptoms that occur with severe renal dysfunction. The etiologies of AKI are classified as prerenal, intrinsic renal, or post-renal, and there is a varied clinical presentation depending on the severity of kidney dysfunction. Acute kidney injury is diagnosed initially by a change in serum creatinine levels, and then the etiology is determined by clinical history, lab testing, imaging, and possibly kidney biopsy. The management of AKI depends on the etiology; however, attention to the individual's volume status and serum electrolytes is always important. If management is unsuccessful and AKI progresses to CKD, then renal replacement therapy with dialysis or kidney transplantation is necessary.

Coronary heart disease (CHD), or ischemic heart disease, describes a situation in which an inadequate supply of blood to the myocardium exists due to a stenosis of the coronary arteries, typically from atherosclerosis. The myocardium becomes ischemic when oxygen supply does not meet oxygen demand. Diagnosis is based on history and ECG findings; cardiac stress tests and catheterizations may also be needed. Treatment is primarily based on reducing the heart's oxygen demand and increasing the delivery of oxygen.

Peptic ulcer disease (PUD) refers to the full-thickness ulcerations of duodenal or gastric mucosa. The ulcerations form when exposure to acid and digestive enzymes overcomes mucosal defense mechanisms. The most common etiologies include Helicobacter pylori (H. pylori) infection and prolonged use of non-steroidal anti-inflammatory drugs (NSAIDs). Patients may be asymptomatic or may present with abdominal pain, nausea, and early satiety. Peptic ulcer disease typically responds well to medical treatment consisting of H. pylori eradication, eliminating risk factors, and proton pump inhibitors (PPIs). If left untreated, it can lead to bleeding, perforation, gastric outlet obstruction, and gastric cancer.

Gastritis refers to inflammation of the gastric mucosa. Gastritis may occur suddenly (acute gastritis) or slowly over time (chronic gastritis). Gastritis may be asymptomatic or with symptoms, including burning abdominal pain (which either worsens or improves with eating), dyspepsia, nausea, and vomiting. The most common etiologies for gastritis are Helicobacter pylori infection and autoimmune disease. Chronic gastritis is a risk factor for gastric cancer. Management involves the use of proton pump inhibitors with antibiotics (in case of H. pylori infection), avoidance of offending agents, and replacement of associated deficiencies.