Quiz 2

(Ref: Harrison 20th edition, p 2216; Harrison 19th edition, page 1906)
 Mechanisms of GERD:
1. Transient LES relaxations
2. LES hypotension
3. Anatomic distortion of the esophagogastic junction inclusive of hiatus hernia
 The acid can reflux can lead to chemical tracheitis leading to nocturnal cough and bronchospasm.
 The acid can reflux can lead to chemical tracheitis leading to nocturnal cough and bronchospasm.
 GERD is often diagnosed in the absence of endoscopic esophagitis, which would otherwise define the disease. In setting of partially treated disease ambulatory 24 hours pH monitoring is done and the outcome is expressed as the percentage of the day that the pH was less than 4 (indicative of recent acid reflux), with values exceeding 5% indicative of GERD

(Ref: Harrison 20th edition, p 2211)
 Cervical esophageal diverticulum (Zenker Diverticulum) is located in Killian-Laimer triangle which is located inferior to the cricopharyngeus in the posterior
midline above the confluence of the longitudinal layer of esophageal muscle. Laimer's triangle is covered only by the circular layer of esophageal muscle.

(Ref: Schwartz 9th edition page 917-921, Harrison 19th p 1925)
Ulcer located along the lesser curve of the stomach and posterior duodenal bulb are at greater risk for severe bleeding and rebreeding due to the proximity of the left gastric artery and gastro – duodenal artery, respectively. The mortality rate for bleeding peptic ulcers is approximately 6%-7%.

(Ref: Harrison 20th edition, p 853)
 Geriatric age group presentation is a risk factor for coronary artery disease. Chest pain can be misleading. The breathlessness and bradycardia and hypotension point towards myocardial infarction.
 Hence the initial evaluation at presentation should be ECG.
 Second – degree heart block (intermittent AV block) may occur as a transient abnormality in inferior wall MI
 Although many patients have a normal pulse rate and blood pressure within the first hour of STEMI, about one – fourth of patients with anterior infarction have manifestations of sympathetic nervous system hyperactivity (tachycardia and / or hypertension), and up to one – half with inferior infarction show evidence of parasympathetic hyperactivity (bradycardia and / or hypotension).

(Ref: Harrison 20th edition, p 2237; Harrison 19th p 1926)
 Dietary modification is the cornerstone of therapy for patients with dumping syndrome.
 Small, multiple meals devoid of simple carbohydrates coupled with elimination of liquids during meals is important.
 Antidiarrheals and anticholinergic agents are complementary to diet. Pectin, which increases the viscosity of intra-luminal contents, may be beneficial in more symptomatic individuals.
 Acarbose, an alpha-glucosidase inhibitor that delays digestion of ingested carbohydrates, has also been shown to be beneficial in the treatment of the late phases of dumping.
 The somatostatin analogue octreotide has been successful in diet-refractory cases