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Free STEP3 Exam Braindumps (page: 4)

Page 4 of 202
PDF with 804 Questions

A 50-year-old female presents to your office for evaluation of solid food dysphagia without weight loss. Symptoms have been present for 6 months and are progressive. The patient has had two episodes of near impaction, but copious water ingestion and repeated swallows allowed the food bolus to pass. She has never had to present to the ER for disimpaction. She drinks five to six beers per day, loves spicy foods, and smokes a pack of cigarettes daily with a total lifetime history of 30 pack-years. She has had intermittent heartburn symptoms for years and has not sought treatment. She takes hydrochlorothiazide for hypertension. Review of symptoms reveals chronic cough. Physical examination is unremarkable. Upper endoscopy reveals a distal esophageal stricture with inflammatory changes. Esophageal biopsies reveal benign mucosa with chronic inflammation. Gastric biopsies are unremarkable. Helicobacter pylori testing is negative.

What is the most likely etiology of the patient's stricture?

  1. alcohol ingestion
  2. tobacco use
  3. gastroesophageal reflux
  4. hydrochlorothiazide
  5. spicy food ingestion

Answer(s): C

Explanation:

The patient has a peptic stricture, seen in the setting of long-standing untreated gastroesophageal reflux with esophagitis. The history of progressive solid food dysphagia without weight loss is typical. Tobacco, alcohol, thiazide diuretics, and spicy foods do not predispose to benign esophageal strictures. The patient has developed a peptic stricture, a serious complication of GERD. The patient needs esophageal dilation (either with mechanical or pneumatic dilators) and maximal acid suppression. PPI therapy is superior to histamine receptor antagonist therapy in terms of healing erosive esophagitis. Patients with long-standing GERD are at increased risk of developing Barrett esophagus, a risk factor for esophageal adenocarcinoma. GERD is not a risk factor for esophageal squamous cell cancer, gastric cancer, or duodenal cancer. Patients with chronic H. pylori infection (which this patient did not have) are at increased risk for a form of gastric lymphoma known as a MALT-oma.



A 50-year-old female presents to your office for evaluation of solid food dysphagia without weight loss. Symptoms have been present for 6 months and are progressive. The patient has had two episodes of near impaction, but copious water ingestion and repeated swallows allowed the food bolus to pass. She has never had to present to the ER for disimpaction. She drinks five to six beers per day, loves spicy foods, and smokes a pack of cigarettes daily with a total lifetime history of 30 pack-years. She has had intermittent heartburn symptoms for years and has not sought treatment. She takes hydrochlorothiazide for hypertension. Review of symptoms reveals chronic cough. Physical examination is unremarkable. Upper endoscopy reveals a distal esophageal stricture with inflammatory changes. Esophageal biopsies reveal benign mucosa with chronic inflammation. Gastric biopsies are unremarkable. Helicobacter pylori testing is negative.

What is the next best step in therapy for this patient?

  1. esophageal dilation
  2. histamine receptor antagonist therapy
  3. PPI therapy
  4. esophageal dilation with histamine receptor antagonist therapy
  5. esophageal dilation with PPI inhibitor therapy

Answer(s): E

Explanation:

The patient has a peptic stricture, seen in the setting of long-standing untreated gastroesophageal reflux with esophagitis. The history of progressive solid food dysphagia without weight loss is typical. Tobacco, alcohol, thiazide diuretics, and spicy foods do not predispose to benign esophageal strictures. The patient has developed a peptic stricture, a serious complication of GERD. The patient needs esophageal dilation (either with mechanical or pneumatic dilators) and maximal acid suppression. PPI therapy is superior to histamine receptor antagonist therapy in terms of healing erosive esophagitis. Patients with long-standing GERD are at increased risk of developing Barrett esophagus, a risk factor for esophageal adenocarcinoma. GERD is not a risk factor for esophageal squamous cell cancer, gastric cancer, or duodenal cancer. Patients with
chronic H. pylori infection (which this patient did not have) are at increased risk for a form of gastric lymphoma known as a MALT-oma.



A 50-year-old female presents to your office for evaluation of solid food dysphagia without weight loss. Symptoms have been present for 6 months and are progressive. The patient has had two episodes of near impaction, but copious water ingestion and repeated swallows allowed the food bolus to pass. She has never had to present to the ER for disimpaction. She drinks five to six beers per day, loves spicy foods, and smokes a pack of cigarettes daily with a total lifetime history of 30 pack-years. She has had intermittent heartburn symptoms for years and has not sought treatment. She takes hydrochlorothiazide for hypertension. Review of symptoms reveals chronic cough. Physical examination is unremarkable. Upper endoscopy reveals a distal esophageal stricture with inflammatory changes. Esophageal biopsies reveal benign mucosa with chronic inflammation. Gastric biopsies are unremarkable. Helicobacter pylori testing is negative.

The patient is at increased risk for which of the following illnesses?

  1. esophageal squamous cell cancer
  2. esophageal adenocarcinoma
  3. gastric cancer
  4. gastric lymphoma
  5. duodenal adenocarcinoma

Answer(s): B

Explanation:

The patient has a peptic stricture, seen in the setting of long-standing untreated gastroesophageal reflux with esophagitis. The history of progressive solid food dysphagia without weight loss is typical. Tobacco, alcohol, thiazide diuretics, and spicy foods do not predispose to benign esophageal strictures. The patient has developed a peptic stricture, a serious complication of GERD. The patient needs esophageal dilation (either with mechanical or pneumatic dilators) and maximal acid suppression. PPI therapy is superior to histamine receptor antagonist therapy in terms of healing erosive esophagitis. Patients with long-standing GERD are at increased risk of developing Barrett esophagus, a risk factor for esophageal adenocarcinoma. GERD is not a risk factor for esophageal squamous cell cancer, gastric cancer, or duodenal cancer. Patients with
chronic H. pylori infection (which this patient did not have) are at increased risk for a form of gastric lymphoma known as a MALT-oma.



A 65-year-old man presents to your office for evaluation of abdominal pain. The patient states that he has epigastric pain that radiates to his back. The pain is worse with eating and improves with fasting. The pain has been present for 6 months and is gradually worsening. The patient has lost 15 lbs but feels his oral intake has been adequate. He complains of greasy stools and frequent thirst and urination. Examination reveals a thin male with temporal wasting and oderate abdominal pain with palpation. The patient consumes approximately 1015 beers per day and smokes a pack of cigarettes per day for the past 20 years.
What would be the best initial test to do in this patient?

  1. spot fecal fat collection
  2. 72-hour fecal fat collection
  3. CT scan of the abdomen
  4. ERCP
  5. upper endoscopy

Answer(s): C

Explanation:

The patient's history and examination are worrisome for pancreatic disease, and he has strong signs of pancreatic insufficiency. His long history of alcohol use suggests the possibility of chronic pancreatitis or pancreatic cancer. Fecal fat studies would only confirm or quantify his steatorrhea. ACT scan would image the pancreas for changes consistent with chronic pancreatitis (duct dilation, calcifications, pseudocysts) and could look for a neoplasm of the pancreas as well. ERCP is not indicated as a first- line test in patients with abdominal pain given its risk of causing acute pancreatitis. Upper endoscopy would be helpful to rule out peptic ulcer disease and other gastric complaints, but would not provide more global information about the abdomen.
The patient has greasy stools and weight loss, findings seen in patients with steatorrhea due to chronic pancreatitis.

Patients with steatorrhea malabsorb fat-soluble vitamins (vitamins A, D, E, and K). "Night blindness" (poor night vision) due to vitamin Adeficiency is common among patients with advanced chronic pancreatitis and likely led to this patient's motor vehicle accident. The patient has DM as a consequence of pancreatic endocrine insufficiency, another feature of chronic pancreatitis. Diabetes develops when greater than 80- 90% of the gland has been destroyed. Patients with chronic pancreatitis have a coexisting loss of glucagon from islet cells and, thus, often become brittle diabetics, with hypoglycemia seen after insulin administration. Vitamin K and B12 deficiency, which the patient may have, do not cause hypoglycemia. The patient was previously noted to eat well, so inadequate oral intake is unlikely. Diabetic education should decrease the rate of chronic insulin overdosage.

The patient has pancreatic exocrine insufficiency and thus cannot produce enough pancreatic enzymes to digest his food. Pancreatic enzyme replacement therapy in tablet form is a mainstay of therapy for chronic pancreatitis. It can rapidly reverse this problem by providing exogenously produced pancreatic enzymes to break down fats, carbohydrates, and proteins for absorption in the small bowel. The patient would not benefit from additional oral feedings without enzyme supplementation and would only worsen his steatorrhea by doing so. He can take food orally, so feeding via gastrostomy, TPN, or PPN are not indicated. The patient's worsening pain and weight loss despite therapy is worrisome for the development of pancreatic cancer. CA-19-9 is
frequently (but not universally) elevated in pancreatic cancers, although it can be elevated in cholangiocarcinoma as well. PSA is associated with prostate cancer. CEA is associated with colon cancer. CA-125 is associated with ovarian cancer. AFP is associated with hepatocellular carcinoma.






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