7 Matching Annotations
  1. Jul 2023
  2. May 2023
    1. History and Physical Examination ++ Managing indigestion requires a thorough interview. GERD classically produces heartburn, a substernal warmth that moves toward the neck. Heartburn often is exacerbated by meals and may awaken the patient. Associated symptoms include regurgitation of acid or nonacidic fluid and water brash, the reflex release of salty saliva into the mouth. Atypical symptoms include pharyngitis, asthma, cough, bronchitis, hoarseness, and chest pain that mimics angina. Some patients with acid reflux on esophageal pH testing note abdominal pain instead of heartburn. ++ Dyspeptic patients report symptoms referable to the upper abdomen that may be meal-related (postprandial distress syndrome) or independent of food ingestion (epigastric pain syndrome). The history in functional dyspepsia may also report symptoms of GERD, IBS, or idiopathic gastroparesis. ++ The physical exam with GERD and functional dyspepsia usually is normal. In atypical GERD, pharyngeal erythema and wheezing may be noted. Recurrent regurgitation may cause poor dentition. Dyspeptics may exhibit epigastric tenderness or distention. ++ Discriminating functional from organic causes of indigestion mandates excluding certain historic and exam features. Odynophagia suggests esophageal infection. Dysphagia is concerning for a benign or malignant esophageal blockage. Other alarm features include unexplained weight loss, recurrent vomiting, dysphagia, occult or gross bleeding, nocturnal symptoms, jaundice, palpable mass or adenopathy, and a family history of gastrointestinal neoplasm. Patients with an abdominal wall source of upper abdominal pain may exhibit a positive Carnett’s sign of increased tenderness with tensing of abdominal muscles upon lifting the head from the exam table. +++ Diagnostic Testing ++ Because indigestion is prevalent and most cases result from GERD or functional dyspepsia, it is generally recommended to perform no more than limited and directed diagnostic testing in most individuals. ++ After excluding alarm factors (Table 45-3), patients with typical GERD do not need further evaluation and are treated empirically. Upper endoscopy is indicated only in cases with atypical symptoms or these alarm factors. For heartburn >5 years in duration, especially in patients >50 years old, endoscopy is advocated to screen for Barrett’s metaplasia. Endoscopy is not needed in low-risk patients who respond to acid suppressants. Ambulatory esophageal pH testing using a catheter method or a wireless capsule endoscopically attached to the esophageal wall is considered for drug-refractory symptoms and atypical symptoms like unexplained chest pain. High-resolution esophageal manometry is ordered when surgical treatment of GERD is considered. A low LES pressure predicts failure of drug therapy and provides a rationale to proceed to surgery. Poor esophageal body peristalsis raises concern about postoperative dysphagia and directs the choice of surgical technique. Nonacidic reflux may be detected by combined esophageal impedance-pH testing in medication-unresponsive patients.

      [Start: History and Physical Examination]

      • Does the patient complain of heartburn?
        • Yes:
          • Does heartburn worsen after meals or awaken the patient?
            • Yes: GERD is likely. Proceed to treatment empirically.
            • No: Consider atypical GERD. Check for pharyngeal erythema, wheezing, and poor dentition.
        • No:
          • Does the patient have upper abdominal pain?
            • Yes:
              • Is the pain meal-related (postprandial distress syndrome) or independent of food ingestion (epigastric pain syndrome)?
                • Postprandial distress syndrome: Likely functional dyspepsia. Check for GERD, IBS, or idiopathic gastroparesis.
                • Epigastric pain syndrome: Further evaluation needed.
            • No: Proceed to next question.
      • Does the patient exhibit any alarm features? (unexplained weight loss, recurrent vomiting, dysphagia, occult or gross bleeding, nocturnal symptoms, jaundice, palpable mass or adenopathy, family history of gastrointestinal neoplasm)
        • Yes: Further evaluation needed.
        • No: Proceed to next question.
      • Does the patient exhibit any historic or exam features concerning for organic causes of indigestion?
        • Yes: Further evaluation needed.
        • No: No further evaluation needed. Treat empirically for GERD or functional dyspepsia.

      [End: History and Physical Examination]

      [Start: Diagnostic Testing]

      • Typical GERD:
        • No further evaluation needed. Treat empirically.
      • Atypical symptoms or alarm factors present:
        • Upper endoscopy is indicated.
      • Heartburn >5 years in duration, especially in patients >50 years old:
        • Endoscopy is advocated to screen for Barrett's metaplasia.
      • Low-risk patients who respond to acid suppressants:
        • Endoscopy is not needed.
      • Drug-refractory symptoms and atypical symptoms like unexplained chest pain:
        • Ambulatory esophageal pH testing using a catheter method or a wireless capsule endoscopically attached to the esophageal wall is considered.
      • Surgical treatment of GERD is considered:
        • High-resolution esophageal manometry is ordered.
          • Low LES pressure predicts failure of drug therapy.
          • Poor esophageal body peristalsis raises concern about postoperative dysphagia and directs the choice of surgical technique.
      • Nonacidic reflux may be detected by combined esophageal impedance-pH testing in medication-unresponsive patients.

      [End: Diagnostic Testing]

    1. History

      Symptoms of dysphagia ↓

      Localization of dysphagia: - Suprasternal notch: oropharyngeal or esophageal etiology - Chest: esophageal etiology ↓

      Nasal regurgitation and tracheobronchial aspiration: oropharyngeal dysphagia ↓

      Hoarseness: - Precedes dysphagia: laryngeal primary lesion - Develops after dysphagia: compromise of the recurrent laryngeal nerve ↓

      Type of food causing dysphagia: - Intermittent dysphagia with solid food only: structural dysphagia - Constant dysphagia with both liquids and solids: esophageal motor abnormality - Scleroderma: mild dysphagia for solids only - Oropharyngeal dysphagia: greater difficulty with liquids than solids ↓

      Progression of dysphagia: - Over weeks to months: neoplasia - Unchanged or slowly progressive over years: benign disease process ↓

      Food impaction: structural dysphagia ↓

      Chest pain: motor disorders, structural disorders, or reflux disease ↓

      History: - Prolonged heartburn: peptic stricture or esophageal adenocarcinoma - Prolonged nasogastric intubation, surgery, ingestion of caustic agents or pills, radiation or chemotherapy, mucocutaneous diseases: isolate the cause of dysphagia - Odynophagia: ulceration, infectious or pill-induced esophagitis - AIDS or other immunocompromised states: opportunistic infections or tumors - Atopy: eosinophilic esophagitis - Medication use: pill esophagitis and opioid-induced esophageal dysmotility ↓

      Physical examination: - Signs of bulbar or pseudobulbar palsy, generalized neuromuscular disease: oral and pharyngeal dysphagia - Thyromegaly or lymphadenopathy: esophageal dysphagia - Inflammatory or infectious lesions in the mouth and pharynx: oral and pharyngeal dysphagia - Changes in the skin and oral mucosa: scleroderma or mucocutaneous diseases involving the esophagus ↓

      Diagnostic procedures: - Oral or pharyngeal dysphagia: fluoroscopic swallow study, otolaryngoscopic and neurologic evaluation - Esophageal dysphagia: upper endoscopy, mucosal biopsies

    2. Physiologically, the UES consists of the cricopharyngeus muscle, the adjacent inferior pharyngeal constrictor, and the proximal portion of the cervical esophagus. UES innervation is derived from the vagus nerve, whereas the innervation to the musculature acting on the UES to facilitate its opening during swallowing comes from the fifth, seventh, and twelfth cranial nerves. The UES remains closed at rest owing to both its inherent elastic properties and neurogenically mediated contraction of the cricopharyngeus muscle. UES opening during swallowing involves both cessation of vagal excitation to the cricopharyngeus and simultaneous contraction of the suprahyoid and geniohyoid muscles that pull open the UES in conjunction with the upward and forward displacement of the larynx. ++ The neuromuscular apparatus for peristalsis is distinct in proximal and distal parts of the esophagus. The cervical esophagus, like the pharyngeal musculature, consists of striated muscle and is directly innervated by lower motor neurons of the vagus nerve. Peristalsis in the proximal esophagus is governed by the sequential activation of the vagal motor neurons in the nucleus ambiguus. In contrast, the distal esophagus and LES are composed of smooth muscle and are controlled by excitatory and inhibitory neurons within the esophageal myenteric plexus. Medullary preganglionic neurons from the dorsal motor nucleus of the vagus trigger peristalsis via these ganglionic neurons during primary peristalsis. Neurotransmitters of the excitatory ganglionic neurons are acetylcholine and substance P; those of the inhibitory neurons are vasoactive intestinal peptide and nitric oxide. Peristalsis results from the patterned activation of inhibitory followed by excitatory ganglionic neurons, with progressive dominance of the inhibitory neurons distally. Similarly, LES relaxation occurs with the onset of deglutitive inhibition and persists until the peristaltic sequence is complete. At rest, the LES is contracted because of excitatory ganglionic stimulation and its intrinsic myogenic tone, a property that distinguishes it from the adjacent esophagus. The function of the LES is supplemented by the surrounding muscle of the right diaphragmatic crus, which acts as an external sphincter during inspiration, cough, or abdominal straining.

      Start Preparation phase - Food is masticated - Food is mixed with saliva Transfer phase - Bolus is pushed into the pharynx by the tongue Pharyngeal swallow response - Bolus entry into the hypopharynx initiates the response - Larynx is elevated and pulled forward - Upper esophageal sphincter (UES) opening facilitated - Tongue pulsion propels bolus through UES - Peristaltic contraction clears residue from pharynx and esophagus Primary peristalsis - Peristaltic contractions elicited in response to a swallow - Sequenced inhibition followed by contraction of the musculature along the entire length of the esophagus Deglutitive inhibition - Inhibition that precedes the peristaltic contraction Secondary peristalsis - Activated by local distention of the esophagus - Begins at the point of distention and proceeds distally Tertiary esophageal contractions - Nonperistaltic, disordered esophageal contractions

      Musculature and innervation - Striated musculature of the oral cavity, pharynx, UES, and cervical esophagus - Lower motor neurons carried in cranial nerves innervate muscles - Oral cavity muscles innervated by the fifth (trigeminal) and seventh (facial) cranial nerves - Tongue innervated by the twelfth (hypoglossal) cranial nerve - Pharyngeal muscles innervated by the ninth (glossopharyngeal) and tenth (vagus) cranial nerves - UES innervation derived from the vagus nerve - Innervation to musculature acting on the UES to facilitate its opening during swallowing comes from the fifth, seventh, and twelfth cranial nerves - UES closed at rest owing to both its inherent elastic properties and neurogenically mediated contraction of the cricopharyngeus muscle - Cervical esophagus consists of striated muscle and is directly innervated by lower motor neurons of the vagus nerve - Distal esophagus and LES composed of smooth muscle and are controlled by excitatory and inhibitory neurons within the esophageal myenteric plexus - Medullary preganglionic neurons from the dorsal motor nucleus of the vagus trigger peristalsis via these ganglionic neurons during primary peristalsis - Neurotransmitters of the excitatory ganglionic neurons are acetylcholine and substance P; those of the inhibitory neurons are vasoactive intestinal peptide and nitric oxide - Peristalsis results from the patterned activation of inhibitory followed by excitatory ganglionic neurons, with progressive dominance of the inhibitory neurons distally - LES relaxation occurs with the onset of deglutitive inhibition and persists until the peristaltic sequence is complete - LES is contracted at rest because of excitatory ganglionic stimulation and its intrinsic myogenic tone, a property that distinguishes it from the adjacent esophagus - Function of the LES is supplemented by the surrounding muscle of the right diaphragmatic crus, which acts as an external sphincter during inspiration, cough, or abdominal straining.

      End

  3. Jan 2022
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  4. Mar 2021
  5. Nov 2020