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Dysphagia Type 1
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Problem with delivering food or fluid to the esophagus
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decreased ability to initiate the swallowing sequence*
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person may cough to dislodge the solid/liquid or may aspirate when attempting to swallow
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symptoms tend to worsen with liquid rather than solid
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Dysphagia Type 2
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Problem with transporting the bolus (food piece) down the throat
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result of a disorder (structural or neuromuscular)) in which the peristaltic movement of the throat is altered
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persons may feel as though the food is stuck behind the sternum and if underlying pathology is not resolved can worsen to include liquids
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disorders include esophageal diverticula: outpouchings of one or more layers of the esophagus | achalasia: in which the smooth muscle is altered | neoplasms or strictures
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Dysphagia Type 3
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Problem with bolus entering the stomach
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Secondary to lower esophageal dysfunction or lesions that obstruct the pathway
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categorized as a tightness or pain in the substernal area when swallowing
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tumors in the mediastinum or below may reduce LES function and chronic inflammation of the lower esophagus can lead to further inability
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Heartburn/Pyrosis
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caused by a reflux of the gastric fluids
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a substernal burning sensation that radiates up to the neck
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the acid irritates the esophageal mucosa and can also cause spasm of the throat muscles
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Chest pain
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esophageal distention (enlarging) or powerful muscle contractions
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pain radiates to neck, jaw, shoulder and arm (similar to angina pectoris) and odynophagia
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esophageal obstruction ir diffuse esophageal spasm where there is a high magnitude spasm between normal peristalsis
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infection chest pain
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infections in the esophagus in immunocompromised individuals
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dull, aching chest pain
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can worsen heartburn and regular chest pain
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visceral pain
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due to stretching or inflammation
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diffuse, poorly localized pain which can be knawing, burning or cramping
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somatic pain
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injury to abdominal pain, parietal peritoneum, mesentery or diaphragm
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sharp intense pain at the area of injury, well localized
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referred pain
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pain in the same neurosegment felt in other part
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sharp well localized pain that may be felt deep and at a location away from the injury
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acute
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instantaneous onset
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chronic
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gradual onset
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acute diarrhea
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due to acute infection, emotional stress, leakage of liquid stool around impacted stool
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chronic
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symptoms last longer than 4 weeks, due to chronic GI tract infection, alterations in motility or integrity, malabsorption, endocrine disorders
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episodic diarrhea
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probably related to food allergy or ingestion of irritants such as caffeine
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osmotic
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increased amount of poorly soluble nutrient intake such as carbs which pull water into the bowel lumen
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secretory
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caused by toxins that stimulate intestinal fluid secretion and lower absorption, ~ 1L of diarrhea
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exudative (mucus, blood or protein)
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blood, protein and mucus getting into the bowel lumen from the site of inflammation
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motility distrubances
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decreased time and contact of chyme with the absorptive enzymes
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Stomatitis
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ulcerative inflammation of the mouth oral mucosa
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causes:
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viral or bacterial infections, mechanical trauma, irritant exposure (alcohol/tabacco), medication, radiation therapy, autoimmune disorders and nutrient deficiency
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most common type: herpetic gingivostomatitis
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HSV acquired most by children which causes tingling and itching and leave behind painful ulcers that have ruptures and HSV stays dormant in the dorsal ganglia reactivating years later
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treatement:
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antiviral/biotics for infections, topical or systemic steroids for autoimmune causes, general treatment in oral hygiene and topical barriers or steroids
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the stomach pushes up into the chest cavity through the diaphragm
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-
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risk increases with age, women more than men
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-
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2 types: siding hernia (most common), paraesophageal hernia or mixed
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sliding herniais when a portion of the stomach and gastroesophageal junction move up the diaphragm
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-
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paraesophageal hernia is when the greater curvature of the stomach pushes up
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risk factor
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anything that increase intraabdominal pressure such as pregnancy, obesity and chronic straining or coughing
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treatment
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similar to GERD with surgery fro acute manifestations
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life threatning in a large proion of the stomach becomes incarcerated which is rare
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pathoegenesis
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any agent that alters the strength of the LES or increases intraabdominal pressure
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risk factor
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ingesting fatty foods, smoking, alcohol, pregnancy, caffeine, anatomical features such as a hiatal hernia
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clinical manifests: attributed to esophagitis (inflammation)
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heartburn, regurgitation, chest pain, dysphagia (difficulty swallowing))
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treatment
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increase LES strength, esophageal clearance, imprvoe gastric emptying, suppress acidity, avoid dietary risk factors
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treatment (cont.)
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antacids, histamine blockers (sporadic GERDS), proton pump inhibitors have been known to reverse changes from chronic GERD, surgical intervention
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Barrett esophagus
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complication of GERDS where the epithelium of the esophagus changes to another
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leads to a higher risk of cancer
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progression can lead to ulceration, fibrotic scarring, esophageal strictures
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etiology
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disorder of the upper GI tract caused by acids and pepsin which causes injury to the mucosa of the throat, stomach or duodenum
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-
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an increase in the factors that cause ulcers than those that do not
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cause
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NSAIDS, smoking, genetics, h. pyelori which is crucial to the formation of ulcers and thrives in acidic conditions
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H. pyelori
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lowers healing and has a high rate of recurrence
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gastric cause
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breakdown of the mucosal barrier that usually prevents the acid from diffusing to the rest of the body (aspirin, NSAIDS, alcohol and bile)
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duodenal cause
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excess acid secretion and increased activity of the vagus nerve which stimultes the cells to release gastrin which targets cells to release HCl leading to high HCl
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clinical manifests
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epigastric burning pain relived by food or dairy or antacids | life threatening complication such as GI bleeding
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diagnosis
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Upper GI barium contrast radiography, endoscopy to visualize ulcers, testing for h. pyelori
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treatment
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encourage healing of mucosa by reducing acid, prevent recurrence, h. pyelori antibiotics, proton pump inhibitors and sucralfate which forms a protective barrier, no smoking, reduce stress
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etio
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chronic inflammation of rectal and colon mucus, large ulcers forming
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clinical manifest and comlication
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increased risk of cancer after 7 - 10 years, exacebations and remission, bloody diarrhea and lower abdominal pain
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treatment
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corticosteroid, broad spectrum antibiotics, salicylate analog, immunomodulating drugs, IV followed by oral cyclosporine for refractory
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risk factor
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age 40+, high fiber and fat diet, polyps, chronic irritation/inflammation, hereditary
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diagnosis
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recommend colonoscopy every 10 years after reaching risk age
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familial adenomatous polypsis:
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where three or more family members have colorectal cancer, two generations of colorectal cancer or one or more cases of colorectal cancer before age 50
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clinical manifest based on location
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right: tarry, black stool | left side: intermittent cramping with stringy stool with mucus or blood | rectum: change in bowel habits, urgent need to defecate upon waking, rectal fullness, alternating diarrhea/constipation, rectal ache
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prognosis
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the earlier the prognosis the better, based on tumor size, location, invasion, if it metastasized, and uses the TMN classification
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treatment
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colostomy (opening colon via abdomen), surgical removal, chemo or radiation
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partial or complete blockage of samll/large bowel
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mechanical: tumors, hernia, volvolus
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functional: inhibition of peristalsis
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ogilvie: recurrent bout of ileus
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clinical manifest
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increase bowel sound, pain, nausea, vomit
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absence of bowel sounds
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upper jejunal area: vomit, dehydration and electrolyte depletion
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risk factors
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surgery for adhesions
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congenital abnormalities of the bowel
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metastatic cancer esp from female reproductive or intestinal tract
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treatment
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remove mechanical block
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surgical intervention or decompression with tube
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fluid/electrolyte replacement
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other info
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if left untreated can lead to perforation/ischemia, and necrosis
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necrosis leads to bowel gangrene, sepsis and peritonitis
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fluid, gas, water, electrolyte accumulate in bowel
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altered motility or lack of digestive enzyme
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caused by swallowing air, normal bacterial/enzyme activity, or neutralization of bicarb in the upper GI
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belching
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normal expelling of swallowed air
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abdominal distention
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failure to digest nutrients or defect in intestinal motility
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excessive flatus
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bacterial digestion of certain foods that are gas causing (legumes, vegetables)
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alternating diarrhea and constipation accompanied by cramping with no pathology of the GI tract
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etiology also unclear
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clinical manifest
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diarrhea, constipation, cramping, mucus in stool, nausea
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treatment
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antidiarrheal agents, antispasmodic agents, high fiber diet
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etiology
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telescoping of a portion of the bowel into adjacent portion resulting in obstruction (bowel pushes itself into the other.)
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risk factors
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infants and males
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treatment
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surgical
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risk factor
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men are more likely than women, genetic, diet high in nitrosamine, smoking, barrett esophagus, alcohol
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prognosis/diagnosis
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poor prognosis, can quickly metastasize
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treatment
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stent placement, tumor ablation/removal via heat and laser, surgery, radiation and chemotherapy
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benign or malignant, accounts for less than 5 %
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-
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clinical manifest
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depends on the type and extent of obstruction, can lead to biliary stasis (stopping of bile) jaundice, bleeding and ulcers
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treatment
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surgical removal of tumor and parts of the intestine - chemotherapy
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risk factor
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more prevalent in Japan, men older than 30 years, h. pylori infection, epsetein barr, genetic/dietary factors, smoking
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stages
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are determined by penetration into a major muscle of the stomach and looking at the lymphatic system
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treatment
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aspirin has protective benefits, surgical removal
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clinical manifest
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early - asymptomatic | advanced: anorexia, weight loss and bleeding
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clinical manifest
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usually none, but may cause gross bleeding and abdominal pain
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treatment
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varies in size, type and location and removed using a scope
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small, infrequent or difficult bowel movement
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fewer than 3 stools per week
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low fiber, low exercise, slower perstalsis due to aging or pathological disorders
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fecal impaction can occur where the stool starts blocking the GI tract
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a familial intolerance to gluten
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will lead to inflammation and atrophy of intestinal vili
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causes:
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impaired nutrient absorption due to reduced surface area
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diagnosis
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intestinal biopsy, anti tissue transglutaminase anitbody and imunoglobulin A endomysial antibody
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treatment
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gluten free diet, corticosteroids, supplemental folate, b12, and fat soluble vitamin
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etiology
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of unknown cause but usually causes bacterial overgrowth in the large intestine where the mucus membrane is damaged due to fermentation
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samll intestine
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the mucus lining atrophies leading to malabsorption and folate and b12 acid deficiency
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risk factor
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those who live or visit countries along the equator and in adults more than children
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clinical manifestaion
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bloody diarrhea, abdominal distention and fat in stool steatorrhea
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treatment
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antimicrobials, antidiarrheals and vitamin/electrolyte supplement
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dumping of stomach contents into the small intestine after a short amount of time
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most likely due to pyloric sphincter regulation loss - the sphincter is what allows chyme movement from stomach to intestine
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risk factor/cause
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common after gastrectomy, gastric surgery for obesity, cancer or ulcers
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due to the large amount of partially digested food entering the intestine it can cause a shift in osmotic causing diarrhea
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there is also rapid absorption of glucose in the blood leading to very high plasma insulin but results in low energy a few hours later due to no food storage in the stomach
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clinical manifestation
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diarrhea, abdominal pain, rapid fall in blood glucose/hypoglycemia
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treatment
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eating small but more meals about 6 -8 thoughtout the day
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due to removal of majority of the intestines
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causes severe diarrhea and malabsorption
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reduced ability to absorb due to short area to allow for absorption
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(esp if ileocecal valve is removed)
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clinical manifest
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diarrhea
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treatment
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supportive to nutrient intake
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regional enteritis or granulomatous
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affects proximal portion of the colon or terminal ileum
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etio
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chronic inflammation of all layers of the intestinal wall due to obstruction and inflammation of the lymph vessels
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diagnostic findings
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ulcerations, strictures, fibrosis, fistulas
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clinical manifest
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fever, diarrhea, right lower quad pain, RLQ mass, tenderness
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treatment
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alleveiating and reduce inflammation, stop smoking, drugs similar to ulcerative colitis, no definitive care mostly supportive
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etiology
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bleeding caused by tear in the mucosa due to excessive vomiting
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clinical manifest
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vomiting of blood (hematemesis) and passing or large amounts of blood rectally
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diagnosis
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endoscopic examination
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treatment
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blood transfusion thought bleeding may stop on its own, controlling active bleeding with coagulation techniques, epinephrine injection etc.
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etiology
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portal hypertension from alcoholism or viral hepatitis
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causes
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in tropical areas a species of liver fluke
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a high mortality rate and it affects more than half of patients with cirrhosis
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forceful expulsion of the gastric contents through the mouth
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coordinated sequence of abdominal muscles and reverse esophageal perstalsis
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also caused by alterations in the integrity of the GI tract wall and motility (obstruction))
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etiology
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inflammation and necrosis of th large intestine due to clostridium difficile or antibiotics and mediated by bacterial toxins
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clinical manifests
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diarrhea, abdominal pain, leukocytosis, sepsis or perforation
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treatment
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stop antibiotics if possible, treat ischemia or any contributing factors, fecal transplant if severe
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occurs in infants <34 week or low weight infants <5 lbs
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diffuse or patch necrosis
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etiology
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bowel ischemia, perinatal oxygen deficiency, use of hypertonic formula
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clinical manifest
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distended abdomen and stomach and perforation (hole in stomach)
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treatment
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fluids, antibiotics, surgery for ischemia or perforation
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typhlitis
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specialized necrosis in adult cancer patient with poor prognosis
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etiology
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inflammation of the appendix due to fecalith or stone made of feces
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clinical manifest
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periumbilical pain, RLQ pain, nausea, vomit, fever, diarrhea and systemic inflammation
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treatment
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immediate surgical removal, antibiotics, fluids, any localized abscesses may be drained with a tube
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etiology
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presence of diverticula or herniations on the colon - diverticulosis
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cause
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low intake of dietary fiber causing high intraluminal pressure
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clinical manifest
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diverticulosis - asymptomatic | diverticulitis: inflammation of the diverticula has fever, acute lower abdomen pain and leukocytosis
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treatment
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antibiotics and surgery for abscesses
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acute
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precipitated by ingestion of irritating substances such as alcohol, aspirin, non-steroidal anti-inflammatory drugs (NSAIDS), viral bacteria
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clinical manifest
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maybe asymptomatic, anorexia, postprandial discomfort, hematemesis
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treatment
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remove the cause
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chronic
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helicobacter pylori which is transmitted person to person, fecal to oral route or water borne
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complication
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peptic ulcer, atrophic gastritis (thinning of the lining), gastric adenocarcinoma, mucos associated lymphoid tissue and decreased acid + intrinsic factor
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etiology
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inflammation of stomach and small intestine
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chronic
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secondary to another GI disorder
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acute
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direct infection by pathogenic bacteria or toxin
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-
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may be cause by imbalance in the normal flora
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clinical manifests
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diarrhea seceretory, abdominal discomfort, nausea, vomit, fever and malaise
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treatment
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replace fluids and electrolytes
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