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389 Cards in this Set
- Front
- Back
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In which group does infectious esophagitis typically occur?
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Immunocompromised patients
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What are the most organism causing infectious esophagitis?
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Candida albicans
Herpes simplex Cytomegalovirus |
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What are the clinical manifestations of infectious esophagitis
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SEVERE odynophagia
dsyphagia, wt loss, upper GI bleeding |
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How do you diagnose infectious esophagitis? What will be seen with each of the 3 organisms (candidiasis, herpes, CMV)?
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Barium swallow
Candidiasis: shaggy mucosa Herpes: many small volcanic ulcers CMV: large, deep linear ulcer |
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What is the definitive test for infectious esophagitis? What will be seen with each of the 3 organisms (candidiasis, herpes, CMV)?
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Biopsy
Candidiasis: many, small, white-yellow plaques. Herpes: many vesicles that ulcerate to from small, shallow, volcanic ulcers CMV: large, deep linear ulcers |
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How is candida esophagitis treated
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Oral nystatin or clotrimazole
(w/AIDS IV fluconazole) |
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How do you treat herpes esophagitis
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oral or IV acyclovir
(if resistent, use valacyclovir or famciclovir or IV foscarnet) |
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How do you treat CMV esophagitis
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IV ganciclovir
(if resistent, IV foscarnet) |
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What pt's most commonly experience pill-induced esophagitis
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elderly patients or those not taking meds correctly
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What are the common drugs that cause pill induced esophagitis
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doxycycline/tetracycline
Potassium chloride Vitamin C NSAIDs Quinidine Alendronate Iron |
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What are the symptoms of pill-induced esophagitis
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odynophagia accompanied by dysphagia
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How do you treat pill-induced esophagitis
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sucralfate suspension
*stop offending agent |
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What is the main cause of radiation induced esophagitis
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radiation to the chest at levels exceeding 3000cGy
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What are the clinical manifestations of radiation induced esophagitis
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severe esophagitis and ulcerations
substernal chest pain, odynophagia and dysphagia |
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What can potentiate the injury of radiation induced esophagitis
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Concomitant chemotherapy with cytotoxic agents
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How do you treat pill-induced esophagitis?
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sucralfate suspension
nutritional supplement delay radiation |
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What are the most common symptoms of esophageal motility disorders
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chest pain, dysphagia or both
*dysphagia with solids & liquids |
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What is the cause of oropharyngeal motor disorder
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neuromuscular disorders of the oropharynx or skeletal muscles of the esophagus
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What are the clinical manifestations of oropharyngeal motor disorder
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difficulty in bolus tranfer to esophagus, nasal regurgitation, or coughing with swallowing
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What diseases often accompany oropharyngeal motor disorder
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Parkinson's disease, ALS, MS, and myasthenia gravis
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How is oropharyngeal motor disorder diagnosed
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modified barium swallow with videofluoroscopy
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What is the cause of esophageal motor disorder? Give examples
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disease of the smooth muscle of the esophagus
stricture, cancer, schatzki's rink, achalasia, diffuse esopohageal spasm and scleroderma |
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In patients with esophageal motor disorder, what is the main difficulty
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dysphagia with solids ONLY
(unlike oropharyngeal motor disorder, there is no difficulty with transfer of bolus, regurgitation, or coughing) |
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How do you diagnose esophageal motor disorder
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manometry to evaluate peristaltic and sphincter functions
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What is the most common esophageal motor disorder? What is the etiology
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achalasia
unknown |
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Describe the pathophysiology of achalasia
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1. Degeneration of nerves in Auerbach's plexus, vagus nerve, and swallowing center
2. This leads to increase in lower esophageal sphincter pressure (LES). 3. This pressure causes incomplete relaxation of the LES with swallowing 4. Aperistalsis in the esophagus |
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What are the clinical manifestations of achalasia
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dysphagia of liquids AND solids as well as regurgitation
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How do you diagnose achalasia? What does it show?
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Barium swallow
dilated esophagus, air-fluid level, delayed esophageal emptying, and a smooth tapered ******Bird's Beak" deformity at the LES |
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What diagnostic test is used to confirm achalasia
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esophageal manometry
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What is the treatment for achalasia
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muscle relaxant before meals: nifedipine
endoscopic injection of botulinum toxin or pneumatic dilation |
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What is the key factor that differentiates diffuse esophageal spasm from other motility disorders?
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signs and symptoms are intermittent
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What is the pathophysiology of diffuse esophageal spasm
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associated with degeneration of Auerbach's plexus
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What are the symptoms for diffuse esophageal spasm
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chest pain, dysphagia, or both
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How do you diagnose diffuse esophageal spasm? What does it show?
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barium swallow
***CORKSCREW*** prominent, spontaneous, nonpropulsive, tertiary contractions |
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How do you treat diffuse esophageal spasm
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SUPPORTIVE
Smooth muscle relaxant: nifedipine Antidepressant: Amitriptyline, imipramine Relaxation exercises, biofeedback, or counseling |
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What is one of the top causes of upper GI bleeding
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Mallory Weiss tear
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Where does a Mallory Weiss tear most often occur
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distal esophagus at the GE junction
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When do Mallory Weiss tears most often occur
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after a bout of vomiting or retching
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When does the bleeding of a Mallory Weiss tear occur
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when the tear occurs involving the underlying venous or arterial plelxus
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Patients with what disease are at increased risk for Mallory Weiss tear
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patients with portal hypertension
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What is the typical presentation of Mallory Weiss tear
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middle-aged male
hematemesis following episode of vomiting after drinking ALCOHOL |
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What is the procedure of choice in a suspected Mallory Weiss tear? What will this look like?
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endoscopy
elongated or elliptical ulcer at the GE junction |
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What is the treatment for Mallory Weiss tear?
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(usually stops spontaneously)
If not... Injection and thermal coagulation |
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In what cases should you avoid thermal coagulation for a Mallory Weiss tear?
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patients with portal hypertension or esophageal varices
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What is the main complication associated with a Mallory weiss tear
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re-bleeding
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What age group is predominantly affected by esophageal neoplasm
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60-70 year olds
males |
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What are the two types of esophageal neoplasm and what do they typically involve?
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Adenocarcinoma: distal esophagus
Squamous cell: middle or distal esophagus |
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What is the most common presenting symptoms of esophageal neoplasm
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progressive dsyphagia (first solids then liquids)
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What are the symptoms of esophageal neoplasm
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odynophagia, chest pain, wt loss and anorexia
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What is the initial diagnostic test for esophageal neoplasm and what will it show?
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barium esophogram: narrowingof the lumen at the tumor site and dilation proximal to the tumor
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How is esophageal neoplasm confirmed once the barium esophogram has been performed
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upper endoscopy with biopsy
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What is the treatment for each type of esophageal neoplasm
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Squamous cell: chemo and surgery
Adenocarcinoma: surgery or chemo (not sensitve to radiation) |
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What is the overall 5-year survival rate for esophageal neoplasm
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10-30%
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What are the main risk factors for adenocarcinoma of the esophagus
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Barrett's esophagus and GERD, smoking, alcohol consumption, history of colon cancer, obesity
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What are the main risk factors for squamous cell carcinoma of the esophagus
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smoking, alcohol consumption, history of radiation therapy, achalasia
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Which of the following leads to Barrett's esphagus?
A. Pyloric stenosis B. Mallory Weiss tear C. esophageal stricture D. GERD |
D. GERD
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What type of things cause esophageal strictures
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esophageal webs and rings, and diverticula
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What are esophageal webs and rings
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thin diaphragm-like structures that interrupt the esophageal lumen
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What are the 3 main types of strictures
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Cervical esophageal webs
Lower esophageal ring (Schatzki's ring) Zenker's diverticulum |
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Who is most commonly affected by cervical esophageal webs
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females
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What is it called when cervical esophageal webs are associated with iron deficiency anemia
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Plummer-Vinson syndrome
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What is the major complaint of cervical esophageal webs
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intermittent solid food dysphagia
(often + iron deficiency) |
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What is the study of choice to diagnose cervical esophageal webs? How is this also a treatment?
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cine-esophagrography
(this endoscopic exam may be curative because it will rupture the web) |
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What is a common cause of intermittent solid food dysphagia that tends to occur when patients are eating quickly?
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Lower esophageal ring (Schatzki's ring)
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What is another name for lower esophageal ring?
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Schatzki's ring
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What is the diagnostic test of choice for Lower esophageal ring (Schatzki's ring)
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barium esophagram
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What is the treatment for Lower esophageal ring (Schatzki's ring)
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dilation of the ring
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What is Zenker's diverticulum
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an outpouching of the esophagus between the inferior pharyngeal constrictor and cricopharyngeal muscles
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How does Zenker's diverticulum often present
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asymptomatic (possibly dysphagia and regurgitation)
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How might one describe a large Zenker's diverticulum
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spontaneous regurgitation of food ingested several hours previously
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How do you diagnose Zenker's Diverticulum
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barium esophagram
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What is the treatment for Zenker's diverticulum
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surgery
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Define esophageal varices
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venous collaterals that develop as a result of portal hypertension
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What are some of the main causes of esophageal varices
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prehepatic thrombosis
hepatic disease postsinusoidal disease alcoholic liver disease viral hepatitis |
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What are the frequently seen predisposing factors for esophageal varices
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History of chronic liver disease and cirrhosis
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What are the clinical manifestations of esophageal varices
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hematemesis, melena, hematochezia and dizziness
(+signs of cirrhosis and portal hypertension) elevated LFT's and bilirubin and PT decreased albumin and cholesterol |
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What is the test of choice for esophageal varices
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endoscopy
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What are medical treatments for esophageal varices
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IV vasopressin
IV nitroglycerin IV octreotide balloon tamponade |
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What are endoscopic therapies for esophageal varices
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*************Tx of choice:
endoscopic hemostasis Includes: endoscopic injection sclerotherapy variceal band ligation |
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What are the main complications of esophageal varices
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hemorrhage and death if uncontrolled
(stops spontaneously 50% of time) |
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What is GERD
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a process that refers to the effortless movement of gastric contents from the stomach to the esophagus
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Who does GERD most commonly affect
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men more than women
white people |
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What iss the pathophysiology behind GERD
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acid contents of the stomach reflux into the esophagus and remains long enough to overcome the resistence of the esoophageal epithelium
*Due to increased frequency of transient LES relaxationsrecurrent heartburn |
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What is the hallmark symptom of GERD
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recurrent heartburn
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What are alarm symptoms in GERD? What should be considered if these are present?
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dysphagia, GI bleeding or weight loss
stricture or adenocarcinoma |
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What are some extraesophageal symptoms associated with GERD
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pharyngitis, earache, gingivitis, laryngitis, chronic cough, asthma and aspiration pneumonia
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How do you diagnose GERD
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history of recurrent heartburn and a positive response to acid-suppression drugs
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In patients with alarm symptoms of GERD, what tests should be performed and what do these tests monitor
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Upper GI series: detects grossly abnormal reflux
Esophageal pH monitoring: ***GOLD STANDARD Bernstein's test: establishes GERD as a cause of symptoms |
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What is the first step in treatment for GERD? Give examples
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Lifestyle modifications
-elevate head of bed 6 inches -stop smoking -stop alcohol -decrease dietary fat -decrease meal size -avoid bedtime snacks -avoid chocolate, peppermint, coffee, tea, colas and citrus fruit drinks |
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What are the drug treatments for GERD
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Anacids: Mylanta
H2 receptor antagonists: decrease HCl secretion: cimetidine, famotidine PPI's: decrease HCl secretion and gastric volume: Omeprazole |
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What is gastritis?
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inflammation of the gastric mucosa
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What is the #1 cause of gastritis?
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H. pylori
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What are the causes of gastritis?
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H. Pylori
Autoimmune (pernicious anemia) Environmental Chemical (bile, NSAIDs) |
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What are the clinical manifestations of gastritis
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epigastric pain, n/v
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How do you diagnose gastritis
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1. H. Pylori: detesct by serolgoy testing, urea-breath test or stool antigen testing
2. Endoscopy: note erosions and petechial hemorrhages |
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How do you treat gastritis
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1. H. Pylori: antibiotics and PPI's
2. NSAIDs: discontinue drugs 3. Medical therapy with PPIs or H2 antagonists |
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What is the most common type of cell causing gastric carcinoma
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adenocarcinoma
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Who is typically affected by gastric neoplasm
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50-70 year olds
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What are the environmental, genetic and predisposing conditions that are often factors in the development of gastric neoplasm
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Environmental: H. Pylori, dietary (excess salt, nitrates/nitrites, deficiency in fiber)
Genetic: Blood group A Conditions: chronic gastritis, pernicious anemia, large gastric adenomatous polyps, chronic peptic ulcer |
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What are the symptoms of gastric neoplasm
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bloating, dysphagia, epigastric pain, early satiety
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How can gastric neoplasm be differentiated from GERD/gastritits
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antacids do NOT relieve the pain
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What can be seen on physical exam in a patient with gastric neoplasm
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cachectic with epigastric mass
signs of metastases (hepatomegaly and jaundice, lymph node involvement in left supraclavicular region (Vircho's node) or periumbilical nodes (St. Mary Joseph's node) |
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How do you diagnose gastric neoplasm
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upper endoscopy w/biopsy
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What is the 5year survival rate for gastric neoplasm
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20%
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What is the highest chance for cure in a pt with gastric neoplasm
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surgical resection
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Is gastric neoplasm responsive to chemo
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somewhat
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Does radiation alone work for gastric neoplasm
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NO, but effective in improving survival if given with chemo
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What are the 2 most common causes of peptic ulcer disease (PUD)
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H. Pylori and NSAIDs
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What is an unusual cause of PUD (excluding pylori and NSAIDs)
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a gastrinoma = Zollinger-Ellison syndrome
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What is Zollinger-Ellison syndrome
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a tumor that secretes excess amounts of gastrin and gastric acid hypersection
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What is a common symptom of Zollinger-Ellison syndrome
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diarrhea
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Where are most Zollinger-Ellison syndrome tumor found
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pancreas and duodenum
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What do lab studies reveal in Zollinger-Ellison syndrome
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markedly elevated serum gastrin levels
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How do you treat Zollinger-Ellison syndrome
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a PPI and surgery
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What are the clinical manifestations of PUD
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burning, epigastric pain WORSE on empty stomach or at night
GI bleeding |
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How do you diagnose PUD
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Upper GI endoscopy (important to biopsy gastric ulcers due to risk for cancer)
*Duodenal ulcers are almost never malignant, biopsy NOT needed Barium contrast studies Gastrin levels Test for H. Pylori |
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What tests can be done to diagnose PUD and what are they useful for
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Urea breath test: diagnosis and follow-up
Stool antigen test: diagnosis and follow-up Rapid urease test: requires endoscopy Histology and Culture: requires endoscopy |
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What is the treatment for PUD
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H2 receptor antagonists
PPI's Antimicrobial: multiple drugs Stop NSAIDs Surgery |
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When is surgery done for PUD
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in intractable of persistent disease
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What surgical procedures are used for PUD
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Truncal vagotomy w/pyloroplasty
Highly selective vagotomy w/o pyloroplasty |
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List 2 complications of PUD
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Upper GI bleeding
Perforation |
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What is the treatment for H. Pylori infection
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PPI + Amoxicillin (1gBID) + Metronidazole/Clarithromycin (500mgBID)
possibly add bismuth subsalicylate (2tabs QID) |
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What is pyloric stenosis
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hypertrophy of the pyloric circular muscle causing projective nonbilious vomiting (vomit may be blood-tinged)
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Who is most commonly affected by pyloric stenosis
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males, and those with +family history
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When is the usual onset of pyloric stenosis
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usually 3 weeks of age, but can be as old as 5months
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What can be seen on PE in a pt with pyloric stenosis
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a palpable olive-shaped mass in mid epigastrium
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What 2 imaging tests can be used to diagnose pyloric stenosis: what do they show?
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Ultrasound: elongated pyloric channel and thickened pyloric wall
Radiographic contrast studies: **String sign- from elongated pyloric channel **Shoulder sign - bulge of pyloric muscle into antrum |
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What might be seen on lab tests in a pt with pyloric stenosis
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hypochloremic alkalosis with hypokalemia
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What is the treatment for pyloric stenosis
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surgery - pyloromyotomy
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What is acute cholecystitis
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sustained obstruction of the cystic duct
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What are symptoms of acute cholecystitis
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RUQ pain +6hrs
+Murphy's sign fever (maybe) |
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What do labs reveal in acute cholecystitis
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leukocytosis and mild elevation in LFT's
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What imaging tests are used to diagnose acute cholecystitis and what will be seen with each
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Ultrasonography: detects stones, gallbladder wall thickening or pericholecystic fluid
Hepatobiliary Scintigraphy: uses radioacive isotope - if it doesn't appear in 4 hours in gallbladder, think acute cholecystitis |
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What is pericholecystic fluid highly specific for
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acute cholecystitis and not chronic disease
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How do you treat acute cholecystitis
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Laparoscopic or open cholecystectomy
broad-spectrum antibiotics |
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What are the 2 types of cholelithiasis stones
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cholesterol & pigmented
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What are the risk factors for cholelithiasis
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fat, female, forty
increasing age female pregnancy estrogens obesity native americans cirrhosis hemolytic anemiaa |
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What are the symptoms of cholelithiasis
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episodic, intermittent RUQ pain radiating to right side of back or shoulder
wave-like cramping that occurs 15mins-2hrs after eating Pain lasts up to 4hrs with n/v |
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What are complications of cholelithiasis
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acute cholecystitis, common bile duct stones, pancreatitis, cholangitis
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How do you diagnose cholelithiaisis
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U/S: see stones
Oral cholecystography: gallbladder fxn CT/MRI ERCP |
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What is the treatment for cholelithiasis
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if asymptomatic - leave alone
surgical cholecystectomy |
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What are the nonsurgical treatments for cholelithiasis
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Ursodeoxycholic acid (stones greater than 1.5cm
extracorporeal shock wave lithotripsy |
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What are the 3 phases and their associated clinical manifestations for hepatitis
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1. Incubation period: asymptomatic,detected in blood, labs normal
2. Preicteric phase: malaise, nausea, decreased appetite, abdominal pain. Viral specific antibodies start to appear, serum transaminases elevate 3. Icteric phase: symptoms worse, jaundice appears. Urine darkes in color, and stool becomes lighter in color. Serum transaminases reach peak (10x upper limit of normal) |
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Hepatitis A
List the 1. Genome 2. Method of spread 3. Incubation period 4. Antibody 5. Screening Assay 6. Prophylaxis 7. Treatment |
1. RNA
2. fecal-oral 3. 25 days 4. Anti-HAV 5. Anti-HAV immmunoglobA 6. HAV vaccine 7. HAV immunoglobulin for household/sexual contacts |
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Hepatitis B
List the 1. Genome 2. Method of spread 3. Incubation period 4. Antibody 5. Screening Assay 6. Prophylaxis 7. Treatment |
1. DNA
2. Parenteral/sexual 3. 75 days 4. Anti-HBs/HBc/HBe 5.HBsAg, Anti-HBc immunoM 6.vaccine at birth 7. postexposure prophylaxiw with hep B immune globulin |
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Hepatitis C
List the 1. Genome 2. Method of spread 3. Incubation period 4. Antibody 5. Screening Assay 6. Prophylaxis 7. Treatment |
1. RNA
2. Parenteral 3. 50 days 4. Anti-HCV 5. Anti-HCV 6. no 7. none for acute |
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Hepatitis D
List the 1. Genome 2. Method of spread 3. Incubation period 4. Antibody 5. Screening Assay 6. Prophylaxis 7. Treatment |
1. RNA
2. Parenteral, sexual 3.30-150 days 4. Anti-HDV 5. HBsAg 6. hep B vaccine 7. supportive |
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Hepatitis E
List the 1. Genome 2. Method of spread 3. Incubation period 4. Antibody 5. Screening Assay 6. Prophylaxis 7. Treatment |
1. RNA
2. fecal-oral 3. 35 days 4. Anti-HEV 5. history 6. no 7. none |
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What are the results of chronic hepatitis
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all have chronic inflammatory injury of the liver that can lead to cirrhosis and end-stage liver disease
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What are the causes of chronic hepatitis
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Hepatitis B,D, and C
autoimmune hepatitis drug-induced chronic hepatitis Wilson's disease |
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What are the clinical manifestations of chronic hepatitis
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Non-specific, mild, intermittent
MC: fatigue PE: liver tenderness |
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What do lab tests reveal in chronic hepatitis
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elevated tranaminases (x5) w/o elevation in aldaline phophatase
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What is the treatment for chronic hepB
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a. pegylated interferon-alpha
b. oral nucleoside analogs such as lamuvidine and adefovir dipivoxil c. avoid immunosuppressive drugs |
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What is the treatment for chronic hepD
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prolonged treatment with interferon-alpha
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What is the treatment for chronic HepC
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interferon-alpha and ribavirin
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What is the treatment for autoimmune chronic hepatitis
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corticosteroids: prednisone or azathioprine
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What is the treatment for drug induced chronic hepatitis
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discontinue drug
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What is the treatment for Wilson's disease causing chronic hepatitis
|
copper chelation improves survival but does not reverse cirrhosis
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What is the most common malignant tumor of the liver
|
metastatic tumors
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What are the most frequent primary tumors to spread to the liver
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GI (colon, stomach, and pancreas), lng and breast
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What is mean survival of liver cancer
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6 months
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What is the most common primary malignancy of the liver
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hepatocellular carcinoma
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What are the primary causes of hepatocellular carcinoma
|
complicaiton of chronic liver dz and cirrhosis (hepC, alcohol, hemochromatosis)
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What is the clinical presentation of liver cancer
|
abdominal pain, palpable abdominal pass, constitutional symptoms
obstructive jaundice |
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Where can primary hepatocellular caracinoma metastasize to
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lymph nodes and lung
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What lab and imaging tests are used to diagnose liver cancer
|
alpha-fetoprotein elevated
CT: lesion of primar and metastatic liver carcinoma |
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What is the diagnosis of liver carcinoma confirmed by
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biopsy
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What is the treatment for liver carcinoma
|
resection or transplantation:
systemic chemo and radiation are limited value |
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What does liver cirrhosis represent
|
end stage of chronic liver disease
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What is cirrhosis due to
|
chronic wound healing in the liver after chronic damage
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List causes of cirrhosis
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Alcohol abuse
Hepatitis (B,D,C) Metabolic disorders (hemochromotosis, Wilson's disease, alpha-1-antitrypsin deficiency, CF) Autoimmune hepatitis Biliary disorders (sclersing cholangitis, primary biliary cirrhosis) Drugs and toxins (carbon tetrachloride, dimethylnitrosamine, methotrexate, amiodarone) |
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What are the symptoms of cirrhosis
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weakness, fatigue, wt loss, anorexia, and abdominal pain
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What are the PE findings of cirrhosis
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jaundice, edema, dermatologic changes
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What are the dermatologic changes seen in cirrhosis
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spider angiomas, telangiectasias, palmar erythema, purpura, and signs of feminization
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What screening test are helpful in diagnosis of cirrhosis
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LFT's, iron studies, renal function, ceruloplasmin, CBC, viral hepatitis serology markers, antinuclear antibodies, alpha-fetoprotein, ammonia level
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What are the imaging studies used to diagnose cirrhosis
|
abdominal U/S:liver shape, size, and composition
CT with liver biopsy |
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What is the treatment for cirrhosis
|
treat underlying cause
abstain from alcohol |
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What is the treatment for autoimmune hepatitis
|
immunosuppressive therapy (corticosteroids and azathioprine)
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What is the treatment for hemochromatosis causing cirrhosis
|
frequent phlebotomies
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What is the treatement for Wilson's disease
|
a chelating agent (penicillamine)
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What is the treatment for primary biliary cirrhosis
|
a bile acid, ursodeoxycholic acid
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What is the treatment of choice for end-stage liver disease
|
transplantation
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What are the complications of liver transplant
|
jaundice
variceal bleeding ascites spontaneous bacterial peritonitis encephalpathy hypersplenism |
|
|
What is the tumor marker for hepatocellular carcinoma
|
alpha-fetoprotein
|
|
|
What is acute pancreatitis
|
inflammatory disease of the pancreas due to activaiton of digestive enzymes and autodigestion
|
|
|
What are the causes of acute pancreatitis
|
Alcohol
Gallstone Pancreatic obstruction Drugs: azathiprine, ddI, furosemid, ACEi, and estrogens hypertriglyceridemia |
|
|
What is the typical presentation of a pt with acute pancreatitis
|
abdominal pain, n/v,
pain is constant, located in epigastric radiating to the back, PE: rebound guarding, decreased bowel sounds, |
|
|
What are the 2 signs seen in acute pancreatitis
|
Grey-Turner's: ecchymoses on the flanks
Cullen's sign: periumbilical ecchymosis |
|
|
What lab results are seen in acute pancreatitis
|
increased amylase and lipase
leukocytosis mild hyperglycemia hypocalcemia elevated bilirubin, ald phos and transaminases |
|
|
When does amylase increase and how long does it stay elevated...what about lipase
|
Amylase: elevated in first 2-12hrs (stays for 3-5days)
Lipase: elevated in first 12 hours (decreasing over 7-10days) |
|
|
What imaging results can be used to diagnose acute pancreatitis and what will be seen on each
|
U/S: gallstones and pancreatic edema
CT: extend of local complications MRCP: shows stones - ERCP has the ability to removethem |
|
|
What is ranson's criteria
|
predictor of course for acute pancreatitis
<2: 1%mortality rate 3+: complicated course |
|
|
What are Ranson's criteria on admission
|
ON ADMISSION:
age>55 WBC>16,000 Aspartate aminotransferase >250 LDH>350 Glucose>200 |
|
|
What are Ranson's criteria 48hrs after admission
|
Hct decrease by >10%
BUN increase by 5% Calcium <8 Arterial PO2 <60 Base deficit>4, fluid sequestration >6L |
|
|
What is the treatment for acute pancreatitis
|
SUPPORTIVE
fluid balance (no po til abdominal pain resolved) pain control abstain from alcohol w/gallstones- remove them |
|
|
What are the complications of acute pancreatitis
|
PANCREATIC NECROSIS
sigsn of sepsis: do CT guided aspiration + abx PSEUDOCYSTS u/s or CT remove large cysts SYSTEMIC as result of hypovolemia, ARDS |
|
|
What is chronic pancreatitis and what is it cause by
|
permanent and progressivedamage tothe pancreas, mainly caused by ETOH, manifest as intermittent attacks of acute pancreatitis
|
|
|
What are the clinical manifestations of chronic pancreatitis
|
abdominapain
wt loss, diarrhea, steatorrhea, DM |
|
|
How is chronic pancreatitis diagnosed
|
Hx -
PANCREATIC EXOCRINE FXN 72hr fecal fat secretin or cholecystokinin stimulation PANCREATIC STRUCTURE X-ray for calcification u/s ERCP *most sensitive and specific |
|
|
What is the treatment for chronic pancreatitis
|
avoid ETOH
pain control (opiates) manage pancreatic insufficiency (enzyme replacement for steatorrhea and decrease dietary fat) |
|
|
What is the most common pancreatic neoplasm
|
ductal adenocarcinoma
|
|
|
what is the most common location of pancreatic neoplasm
|
head of pancreas
|
|
|
what is the 4th most common cause of cancer death
|
pancreatic
|
|
|
What is the 5-year survival rate of pancreatic cancer
|
5%
|
|
|
What are the risk factors for pancreatic cancer
|
smoking, obesity, chronic pnacreatitis, high intake of animal fat, prolonged exposure to petroleum products
|
|
|
What are the most common presenting symptoms of pancreatic cancer
|
epigastric pian
obstructive jaundice wt loss (typically found in late disease) |
|
|
What are early signs of pancreatic cancer
|
nonspecific abdominal pain, n/v/ anorxia, malaise
|
|
|
What is noted on PE in a pt with pancreatic cancer...what is this sign called
|
Courvoisier's sign: palpably distended, nontender gallbladder
|
|
|
What 2 things are used for the diagnosis of pancreatic cancer
|
CT of abdomen is test of choice***
Tumor marker CA19-9 |
|
|
How do you treat pancreatic cancer
|
surgical resection if no metastases
followed by cehmo (5-fluorouracil) Possible biliary and gastric bypass |
|
|
What is appendicits?
|
acute inflaammation of the appendix, typically due to obstruction by a fecalith
|
|
|
What is the most common age to get appendicitis
|
10-30 years
|
|
|
What is the clinical presentation of appendicitis and PE findings
|
colicky, periumbilical or epigastric abdominal pain
n/v anorexia fever becomes more constant and severe and localizes to RLQ McBurney's point and rebound tenderness |
|
|
What are the PE signs of appendicitis
|
McBurneys
Robsings, psoas, obturator |
|
|
What 2 labs and 1 imaging studies are used to diagnose appendicitis
|
Labs: leukocytosis w/left shift
U/A normal (few WBCs and RBCs) U/S or CT scan of the appendix (dilated appendix and thickened wall) |
|
|
What is the treatment for appendicitis
|
surgical removal of the appendix
broad-spectrum abx with perforation |
|
|
What is constipation
|
a perception of abnormal bowel movements (less than 2 bowel movements per week)
|
|
|
What are the symptoms of constipation
|
bloating,
abdominal pain or discomfort difficult defecation anal pain nausea |
|
|
How do you diagnose constipation
|
screen for systemic disease with CBC, chem profile and thyroid function
If conservative tx fails: colonic transit study, pelvic floor fxn |
|
|
What is the treatment for constipation
|
Limit meds
exercise and hydraiton increase fiber laxatives |
|
|
What are the 3 types of laxatives
|
osmotic, emollient, stimulant
|
|
|
How do osmotic laxatives work
|
soften stool
within 3 hrs -Nonabsorbable sugars (lactulose or sorbitol - cramping -Saline: mag hydroxide: watch for hypermagnesemia in pt w/renal failure |
|
|
How do emollient laxatives work...give examples
|
Docusate sodium/Mineral oil
promote stool softening Risk of aspiration pneumonitis |
|
|
How do stimulant laxatives work...give examples
|
Senna or Bisacodyl
Good for acute constipation Work within 12 hrs with oral admin and 60mins with rectal |
|
|
What is diverticulosis
|
when the vasa recta penetrates the circular muscle layers between the taenia coli
|
|
|
How is diverticulosis manifest
-symptoms -PE -labs |
ASYMPTOMATIC
intermittent crampin abdominal pain in LLQ mild LLQ tenderness normal labs FOB- |
|
|
How do you diagnose diverticulosis
|
barium enema: multiple deverticula (typically involving the descending and sigmoid colon)
|
|
|
What should be avoided if diverticulitis is suspected
|
endoscopy
|
|
|
What is the primary treatment for diverticulosis
|
Pain control
Normal bowel acitvity: increase fiber, decrease fat, avoid nuts and seeds |
|
|
What is acute diverticulitis
|
perforation of a diverticulum causing acute infection
|
|
|
How often does diverticulosis turn to diverticulitis
|
20%
|
|
|
What are the symptoms of diverticulities
|
gradual onset of LLQ pain (persisting and accompanied by colonic cpasms and loose bowel movements)
anorexia, n/v fever |
|
|
How is diverticulitis diagnosed
-labs -imaging |
-leukocytosis
-RBCs and WBCs in urine -barium enema (**SAWTOOTH) pattern -CT: look for inflammation, thickening of bowel wall, abscess formation and diverticula |
|
|
How is diverticulitis treated medically and surgically
|
pain control, hydration, broad-spectrum abx
colectomy in recurrent disease |
|
|
What are complications of diverticulitis
|
fistula formation
colonic obstruction abscess formation peritonitis hemorrhage |
|
|
What causes 50% of lower GI bleeds
|
diverticular hemorrhage
|
|
|
What is the clinical manifestation of diverticular hemorrhage
-symptoms -PE -labs |
1 dark to bright red blood per rectum in moderate to large amounts
2 painless bleeding 3. Hgb and Hct normal at first, then decrease |
|
|
How do you diagnose diverticular hemorrhage
|
RBC scans
Endoscopic evaluation |
|
|
How do you treat diverticular hemorrhage
|
USUALLY SPONTANEOUS
IV fluids, blood transfusions Colectomy if needed |
|
|
What is duodenal atresia caused by
|
failure to recanalize lumen after solid phase of intestinal development
|
|
|
What is a common medical problem to have prior to duodenal atresia
|
polyhydramnios
-1/4 of cases seen with Down's syndrome Others: malrotation, esophageal atresia and congenital heart disease |
|
|
What are clinical manifestations of duodenatl atresia
|
1st day: bilious vomiting w/o abdominal distention
|
|
|
How do you diagnose duodenal atresia
|
AXR revealing double-bubble sign
|
|
|
What is the treatment of duodenal atresia
|
Decompression of GI tract and IV fluids
surgery, duodenoduodenostomy |
|
|
What is ulcerative colitis
|
inflammation confined to the mucosa and submucosa
|
|
|
What part of the GI tract does UC affect
|
colon ONLY
|
|
|
What is the peak age of onset for UC
|
15-25 and 55-65
|
|
|
What are the clinical manifestations of UC
symptoms labs |
***Blood diarrhea
rectal/lower quadrant pain urgency and fecal incontinence leukocytosis, anemia, elevated ESR |
|
|
What are extra-intestinal manifestations of UC
|
-arthritis
-ankylosing spondylitis -hepatitis/cirrhosis -sclersoing cholangits -pyoderma gangrenosum -erythema nodosum -uveitis |
|
|
How is UC diagnosed
|
PATHOLOGY
inflammation begins in rectum and extends proximallya certain distance and stops clear separation between inflamed and noninflamed tissue is noted |
|
|
What is seen on barium enema for UC
|
loss of haustra markings, narrowing of the lumen, straightening of the colon
|
|
|
What is seen on endoscopy in UC
|
diffuses erythema iwth edema and loss of vascular pattern in the rectum
inflammation begins in the rectum and extends proximally |
|
|
What is the treatment for UC
|
1. Supportive: antidiarrheals, nutrition
2. Aminosalicylates 3. Corticosteroids 4. Immunomodulator (block lymphocyte prolif) 5. Surgery: colectomy |
|
|
What are complications with UC
|
toxic megacolon
increased risk for colon cancer |
|
|
What is Crohn's disease
|
inflammation extending through the intestinal wall from mucosa to serosa
throughout GI tract (commonly small bowel and colon) same peak ages as UC |
|
|
What are the clinical manifestations of Crohns
|
abdomina pain, diarrhea, wt loss
aphthou ulcer on oral mucosa, tender abdomen, perianal disease labs: leukocytosis, anemia, elevated ESR |
|
|
How do you diagnose Crohn's
|
PATHOLOGY
**cobblestone mucosa **rectal sparing **skip lesions |
|
|
What is seen on barium enema and endoscopy with Crohns
|
aphthous ulcers...cobblestone appearance
fistulas and strictures |
|
|
What is the tx for Crohn's disease
|
1. Supportive: antidiarrheals, nutrition
2. Aminosalicylates 3. Corticosteroids 4. Immunomodulator (block lymphocyte prolif) 5. Surgery: segmental resection 6 Abx: abscesses 7. Infliximab |
|
|
Whatis intussusception
|
invagination of one part of the bowel into itself
|
|
|
What is the most frequen cause of intestinal obstruction during the first 2 years of life
|
intussusception
|
|
|
Are male or females more affected by intussusception
|
males 3:1
|
|
|
Where is the most common location of intussusception
|
ileocolic
|
|
|
What is the key finding with intussusception
|
**Currant jelly stool
|
|
|
What are the symptoms, PE, and labs seen in intussusception
|
paroxysmal clicky abdominal pain, followed by vomit and diarrhea
bloody diarrhea (currant jelly) PE: abdomen distended and tender **sausage shaped mass in upper-mid abdomen AMS, lethargy, seizures |
|
|
What is seen on imaging studies for intussusception
|
AXR: paucity of bowel gas
U/S: single or hypoechoic ring w/hyperechoic center (**target/donut sign) |
|
|
What test is diagnostic and therapeutic for intussusception
|
barium enema
|
|
|
What is the tx for intussusception
|
decompression of the intestine
rehydrate (surgery if reduction doesn't work with barium enema) |
|
|
What is IBS
|
abnormality in motor fxn (smooth muscle) and disturbed sensation (visceral hypersensitivity)
|
|
|
When and to whom does IBS usually present
|
females
age 30-50 |
|
|
What is the major symptom of IBS
|
chronic or recurrent abdominal pain...relieved by defecation
|
|
|
What are symptoms of IBS
|
chronic or recurrent abdominal pain...relieved by defecation
alternating between diarrhea and constipation bloating, heartburn, nausea - no vomit |
|
|
How do you diagnose IBS
|
hx
3months of... abdomina pain relieved by defecation or associated with a change in frequency and/or consistency of stool 2+ of... altered stool frequency alterred stool form altered stool passage passage of mucuus |
|
|
What is the treatment for IBS
|
counseling
avoid unnecessary meds increase fiber, decrease fat antispasmodics anti-depressants |
|
|
Explain the blood flow to the GI tract
|
1. celiac trunk supplies the liver, biliary tract, spleen, stomach, duodenum and pancreas
2. superior mesenteric artery supplies the duodenum, pancreas, small intestine, ascending colon and part of the transverse colon 3. Inferior mesenteric artery supplies the part of the transverse colon, descending colon and rectum |
|
|
What is acute arterial mesenteric ischemia - what significant medical history does a patient with this have
|
ischemia to GI tract
-heart disease and arrhythmias, CHF, recent MI or hypotension |
|
|
What are the clinical manifestations of acute arterial mesenteric ischemia
|
sudden abdominal pain with abdominal tenderness on exam
|
|
|
How is acute arterial mesenteric ischemia diagnosed
|
Labs: leukocytosis, metabolic acidosis, elevated amylase
AXR: *************"THUMBPRINTING" formless loops of small intestine, ileus CT , U/S or angiogram may also be helful |
|
|
What is the tx for acute arterial mesenteric ischemia
|
treat underlying cause
laparotomy required to restore blood flow to organ |
|
|
What is the most common ischemic injury to the GI tract
|
ischemic colitis
|
|
|
At what age is ischemic colitis commonly seen
|
60+
|
|
|
What is the cause of ischemic colitis
|
unknown
|
|
|
What are the symptoms of ischemic colitis
|
sudden, mild, crampy, LLQ pain, urge to defecate
bright red blood per rectum PE: mild tenderness |
|
|
How do you diagnose ischemic colitis
|
No peritonitis-->do colonoscopy
Barium studies "THUMBPRINTING" |
|
|
What is the tx for ischemic colitis
|
Usually resolves in 24-48 hrs
Bowel rest, abx, supportive peritonitis or gangrene present - colon resection |
|
|
What is malabsorption
|
refers to impaired transport across mucosa
|
|
|
Describe the pathophysiology behind malabsorption
|
1. impaired luminal hydrolysis
2. Impaired mucosal function 3. impaired removal of nutrients from the mucosa |
|
|
What are the symptoms of malabsorption
|
Steatorrhea
pale, bulky,greasy stools watery diarrhea stools float Abdominal distention, increased flatus Wt loss |
|
|
How do you diagnose malabsorption
|
1. Tests for fat absorption: qualitative or quantitative fecal fat (increased)
2. Tests for carb absorption: D-Xylose test (low levels suggest mucosal dysfxn) 3. Tests for small bowel bacteria (glucose breath hydrogen test & quantitative culture of jejunum aspirate) 4. Bloods: CBC, Chem7,PT, B12, folate, iron, carotene 5. Radiology: small-bowel follow-through, CT 6. Pathology: bx |
|
|
What specific diseases can cause malabsorption
|
celiac spruue
small bowel bacterial overgrowth Disaccharidase deficiency |
|
|
What is the cause of celiac sprue
|
abnormal immune response to glutten (glutten in wheat, barley, rye and oats)
|
|
|
How is celiac sprue diagnosed
|
Bx: atrophy of villi in SI
Labs: antigliadin and antiendomysial antibodies Remove from diet and challenge |
|
|
What is the tx of celiac sprue
|
no more glutten!
|
|
|
How does small bowel bacterial overgrowth cause malabsorption
|
interfering with bile acids, and protein and carb absorption are affected secondary to mucosal damage
|
|
|
How is diagnosis of small bowel bacterial overgrowth diagnosed and how is it treated
|
showing evidence of malabsorption and bacterial overgrowthth
abx |
|
|
What is disaccharid deficiency
|
lactase deficiency that progresses with age
|
|
|
What are the symptoms of disaccharide deficiency
|
diarrhea is profuse and osmotic gap may exist
|
|
|
What is the tx for disaccharide deficiency
|
avoid agent
|
|
|
What is small bowel obstruction
|
Mechanical obstruction implies a physical barrier to the movement of intestinal contents
|
|
|
What is paralytic ileus (adynamic ileus)
|
a disorder that has a neurogenic disruption of peristalsis as the cause of failure to move intestinal contents forward - not mechanical
|
|
|
What is the most common cause of SBO
|
adhesions
then neoplasm hernia intussusception volvulus |
|
|
What is volvulus
|
rotation of bowel loops around a fixed point
|
|
|
what is voluvulus due to
|
congenital abnormalities or adahesion
onset is abrupt, and strangulation occurs rapidly |
|
|
What are the clinical manifestations of SBO
|
based on location
High: vomit, intermittent pain no distention Middle: vomit, moderate distnetion, intermittent crescendo, colicky abdominal pain Low: feculen vomit, marked distention and variable pain |
|
|
If a patient has signs of shock in considering SBO what should be considered
|
strangulation obstruction
|
|
|
How do you diagnose SBO
|
******AXR: stepwise pattern of dilated small intestine w/air fluid levels
|
|
|
What is the treatment for SBO
|
partial - decompress via nasogastric tube
complete: surgery |
|
|
What is the most common site for large bowel obstruction
|
sigmoid colon
|
|
|
What are common etiologies of LBO
|
carcinoma, diverticulitis, fecal impaction and inflammatory diseases
|
|
|
How does LBO present
|
-deep visceral cramping pain referred to hypogastrium
-constipation -vomit -abdominal distention and typany ***High pitched tinkles with gurgles on auscultation |
|
|
How do you diagnose and confirm LBO
|
AXR shows dilated large intestine
Barium enema confirms diagnose and determines locaiton |
|
|
What is the treatment for LBO
|
decompression and surgery
|
|
|
What is toxic megacolon
|
a rare-life threatening form of ulcerative colitis
|
|
|
What are the clinical manifestations of toxic megacolon
|
fever, tachycardia, abdominal distention and signs of peritonitis
|
|
|
How do you diagnose toxic megacolon
|
-Leukcytosis
-AXR: dilated colon >6cm |
|
|
How do you treat toxic megacolon
|
fluid management
IV steroids and abx no improvement in 24-48hrs or signs of perforation - do surgery |
|
|
What is an anal fissure due to
|
a split in the anoderm
|
|
|
What is the difference between an anal fissure and skin tag
|
an ulcer is a chronic fissure
a skin take (sentinel pile) is associated with a mature ulcer |
|
|
When are anal fissures most commonly caused
|
during defecation of a large firm stool
|
|
|
What is the clinical presentation of an anal fissure
|
severe anal pain and bleeding with defecation
blood in stool or on toilet paper |
|
|
What are the PE findings for an anal fissure
|
linear tear with a white ulcerated base
|
|
|
How is an anal fissure diagnosed
|
on PE
|
|
|
What is the tx for anal fissures
|
stool softeners, bulding agents, and sitz baths
If this does not work, internal anal sphincterotomy |
|
|
What do anorectal abscesses/fistulas arise from
|
arise from infected anal glands
|
|
|
What are the clinical manifestations for an anorectal abscess/fistula
|
severe continuous throbbing anal pain - worse with ambulation and straining
PE: tender mass palpable externally in the perianal area |
|
|
What is the treatment for anorectal abscess/fistula - What happens if not treated
|
surgical drainage
may spread resulting in tissue loss may devlop fistual-in-ano |
|
|
What is a major complication of fecal impaction
|
large bowel obstruction
|
|
|
What are predisposing condition to fecal impaction
|
severe psychiatric disease
prolonged bed rest neurogenic disease of the colon spinal cord disease constipating meds |
|
|
What are clinical manifestations of fecal impaction
|
pelvic pain
diarrhea n/v abdominal distention PE: rectal exam w/hard, dry stool |
|
|
What is the tx for fecal impaction
|
enemas or digital disimpaction
*maintain soft stools |
|
|
What is the difference in location between internal and external hemorrhoids
|
Internal - ABOVE dentate line
External - BELOW dentate line |
|
|
What is a major risk factor for hemorrhoids
|
prolonged straining with defecation
|
|
|
What is the staging for internal hemorrhoids
|
1st degree: bleeding only
2nd degree: bleeding and prolapse that reduces spontaneously 3rd degree: bleeding and prolapse that requires manual reduction 4th degree: bleeding with incarceration that cannon be reduced |
|
|
What is the difference in symptoms of internal vs external hemorrhoids
|
Internal: NO PAIN, bright red stool per rectum, mucus discharge and rectal fullness
External: SEVERE PAIN and perianal mass |
|
|
How do you diagnose hemorrhoids
|
anoscopy..if anemia present, rule-out malignancy
|
|
|
What is the treatment for hemorrhoids
|
Dietary changes, stool softeners, bulking agents, increased fluids
excisional hemorrhoidectomy for large ones |
|
|
Where are most anal neoplasms found
|
NOT the anus but found in anal canal or anal margin
|
|
|
What are some risk factors for anal neoplasms
|
anogenital warts, hx of pelvic cancer and smoking
|
|
|
What histology will most likely be found in the anal margin with neoplasm
|
squamous cell, basal cell, Bowen's disease and Paget's disease
|
|
|
What type of anal carcinoma histology will be found in the anal canal
|
epidermoid carcinoma
|
|
|
What are the clinical manifestations of anal neoplasm
|
rectal mass, bleeding, pain, discharge, itching and tenesmus
|
|
|
How is anal neoplasm diagnosed
|
biopsy
|
|
|
How are anal neoplasms treated
|
Wide local excision of the mass
Radiation and chemo for large or metastatic tumors |
|
|
When is pilonidal disease most often seen
|
white males ages 15-40
increased risk in hirsute obese individuals |
|
|
What are the symptoms and PE findings of pilonidal disease
|
-small, mid-line pits or abscesses near the midline of the coccyx or sacrum
PE; suppurative or draining abscess with hair protruding form openings |
|
|
How are pilonidal cysts treated
|
drainage and deroofing of the abscess
maintain hygiene til abscess heals |
|
|
Where are adenomatous polyps often found
|
distal colon and rectum
|
|
|
What are the risk factors for malignancy in a pt with a polyp
|
related to polyp size and level of dysplasia (more common in elderly)
|
|
|
What are the clinical manifestations of polyps
|
typically asymptomatic
May have + FOB or hematochezia |
|
|
How do you diagnose a polyp
|
endoscopic exam or barium study
*****Gold Standard: colonoscopy with biopsy |
|
|
What is the treatment for polyps
|
removal or destruction of polyp
f/u colonoscopy recommended in 3 years, or earlier if multiple or large polyps have been removed |
|
|
What are the two types of hiatal hernias
|
paraesophageal and sliding
|
|
|
Define paraesophageal hernia
|
all or part of the stomach herniates into the thorax...occuring tothe left of the nondisplaced gastroesophageal junction
|
|
|
What are the cause of sliding hiatal hernias
|
decreased resting pressure in the LES
|
|
|
How do paraesophageal hernias present
|
typically asymptomatic (if symptoms, due to obstruction)
|
|
|
What are the symptoms of sliding hiatal hernias
|
reflux (esp when laying down)
n/v in children dysphagia |
|
|
How do you diagnose a hiatal hernia
|
upper GI series
|
|
|
How do you treat a paraesophageal hernia
|
surgical repair
|
|
|
How do you treat a sliding hiatal hernia
|
surgery if persistent or recurrent
Meds: prokinetic drugs, H2 receptor blockers or PPIs |
|
|
What is the most effective surgery for a sliding hiatal hernia
|
Nissen fundoplication
|
|
|
When is an incisional (ventral) hernia seen
|
hx of prior abdominal surgery
|
|
|
What are the risk factors for incisional (ventral) hernia
|
poor surgical technique, wound infection, age, obesity and placement of drains
|
|
|
What is the main symptom of an incisional hernia
|
mass at site of prio surgery
|
|
|
How do you diagnose an incisional hernia
|
clinical finding
|
|
|
Tx for incisional hernia
|
surgical repair
|
|
|
What are indirect inguinal hernias and when do they usually present?
|
-congenital hernias typically presenting during the first year of life
(may not appear until patient is older when the increased intra-abdominal pressure and dilated internal inguinal ring allow abdominal contents to enter the cavity |
|
|
What are direct inguinal hernias
|
acquire as a result of weakness of the transversalis fascia in ***Hesselbach's triangle
|
|
|
What are the clinical manifestations of inguinal hernias
|
ASYMPTOMATIC W/GROIN MASS
ask pt to cough, note tissue in inguinal ring with indirect: some feel dragging sensation or radiation to scrotum |
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|
Oh PE what will you see in a direct inguinal hernia
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when standing, hernia appears as a symmetric circular swelling at the external ring
it disappears when the patient is supine |
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On PE what will you see in an indirect inguinal hernia
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descending into the scrotum
Present as an elliptical swelling that does not reduce easily |
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How do you treat inguinal hernias
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indirect: likely to become incarcerated or strangulated - surgery!
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What sex is more likely to have an umbilical hernia
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females
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What is an umbilical hernia caused by
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gradual loosening of the tissue around the umbilical ring
(in children, umbilical ring didn't close) |
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What are predisoposing factors for umbilical hernias
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multiple pregnancies
ascites obesity large intra-abdominal tumors |
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What is the clinical presentation of an umbilical hernia
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increasing mass at the umbilical ring
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What is the treatment for umbilical hernias
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children: obliterate spontaneously by 12 months
Surgery to avoid incarceration or strangulation |
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What is phenylketonuria
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an inborn error of metabolism - an autosomal recessive disorder with decreased activity of phenylalanine hydroxylase
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What is the incidence of phenylketonuria
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1 in 10,000 live births
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What are the clinical manifestations of phenylketonuria
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if untreated, develop severe mental retardation, hyperactivity, seizure, light complexion and eczema
-urine has mouse-like odor |
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How do you diagnose phenylketonuria
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infancy screening between 24hrs and 3 weeks of age
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What is the treatment for phenylketonuria
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limit dietary intake of phenylalanine to permit normal growth and development
dietary changes throughout life |
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What vitamins are fat-soluble
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A, D, K
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Vitamin: Thiamine (B1)
1. function 2 deficiency 3 toxicity 4 Source 5 Note |
1. neural conduction
2. Beriberi 3. Lethargy, ataxia 4. pork, liver, organ meat, legumes, grains, wheat |
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Vitamin: Niacin (B3)
1. function 2 deficiency 3 toxicity 4 Source 5 Note |
1. NAD/NADP
2. Pellagra coenzyme 3. flushing, hyperglycemia, liver damage 4. fish, liver, meat, poultry, grains, eggs, milk 5. lowers LDL and increases HDL |
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Vitamin: A
1. function 2 deficiency 3 toxicity 4 Source 5 Note |
1. visual pigments, cell differentiation, gene regulation
2. night blindness 3. hepatocellular mecrosis, intracranial hypertension 4. Liver, dairy, yellow and dark green leafy vegetables 5. teratogenic early in pregnancy, toxic in large amounts |
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Vitamin: Riboflavin
1. function 2 deficiency 3 toxicity 4 Source 5 Note |
1. Coenzyme
2. Cheilosis, glossitis, angular stomatitis 3. none 4. milk, dairy, organ meats, green leafy vegetables |
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Vitamin C
1. function 2 deficiency 3 toxicity 4 Source 5 Note |
1. Antioxidant
2. Scurvy 3. nausea, diarrhea 4. citrus fruits, tomato 5. decreased levels impair wound healing |
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Vitamin: D
1. function 2 deficiency 3 toxicity 4 Source 5 Note |
1. calcium homeostasis, bone metabolism
2. rickets, osteomalacia 3. renal damage, hypercalcemia 4. milk, liver, eggs, salmon, tuna 5. toxic in large amounts |
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Vitamin K
1. function 2 deficiency 3 toxicity 4 Source 5 Note |
1. Blood clotting
2. hemorrhage 3. with IV admin, dyspnea and CV collapse can occur 4. liver, oils, green leafy veggies. Synthesized by the intestinal tract, bacteria 5. interferes with warfarin. Toxic in large amounts |
