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132 Cards in this Set
- Front
- Back
Labrythine NT cause of N/V
GI NT causes of N/V |
M1 and H1
GI: 5HT3 |
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Area postrema receives following NT
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5HT3, M1, H1, dopamine
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Biliary colic causes N/V by
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stimulating visceral afferent
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Causes of gastroparesis
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s/p vagotomy
pancreatic adenocarcinoma messenteric vascular insufficiency DM scleroderma amyloidosis |
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What is cyclic vomiting syndrome associated with?
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migraine HA, adults with chronic weed use, mostly in children
|
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Tx for chronic idiopathic nausea and functional vomiting
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low dose TCAs
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odansetron and granisetron act as
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5HT3 antagonists
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reglan acts as a
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combined 5HT4 agonist and D2 antagonist
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Treat H pylori with following 2 conditions
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MALT and peptic ulcer
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Conservative management of refractory GERD symptoms
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TCAs, probiotics, exclusion of gas producing foods like legumes
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How much fluid (avg) enters GI, large intestinesper day
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9 L and 1L
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What is the migrating motor complex
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during fasting there is cyclic motilty taht seeks to remove nondigsestible material--lasts about 4min
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Describe defecation
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puborectalis muscle relaxes owing to sacral parasympathetic influence which straightens the rectoanal angle. Rectal distention causes passive relaxtion of the internal anal sphincter.
Sigmorectal contractions increase until the RS angle opens to >15 deg |
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diarrhea classifications
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Acute<2 weeks
Persistant 2-4 weeks Chronic >4 weeks |
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What are the Pathophysiologic mechanisms of Diarrhea
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Secretory
Osmotic Steatorrheal inflammatory Dysmotile Factitial Iatrogenic |
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What causes pancretic cholera AKA hypokalemia achlorhydria
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VIPoma
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What type of thryoid cancer causes diarrhea
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medullary due to calcitonin
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What causes uticaria pigmentosa and diarrhea
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Systemic Mastocytosis mediated with histamine release or direct mast cell inflammation in the colon
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What is translocation in the GI setting
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Long term bowel rest especially in the ICU can lead to movement of enteric pathogens that normally live within the colon to move into the systemic circulation
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WHy is enteral nutrition preferred over parenteral in the ICU setting
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Translocation from bowel rest can lead to sepsis
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enteral feed contraindications
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circ shock, intestinal ischemia, complete mech bowel obstruction, ileus
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What type of feeding is preferred in the setting of pancreatitis?
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jejunostomy feedings
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ICU feedings should include how many nonprotein calories and how many g of protein per kg body mass
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25-30kcal/kg nonprotein and
1.2-1.6g/kg for hypercatabolic state and 0.8-1.0 for normal |
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Which antioxidant is not commonly found in parenteral or enteral feeds in the ICU patient
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selenium
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What is the difference between fermentable fiber and nonfermentable fiber
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Fermentable fiber (cellulose, pectin, gums) degraded in intestines to short chain FA which are energy for large bowel mucosa and it slows gastric emptying and bile salts to alleviate diarrhea
Nonfermentable fiber (lignins): not degraded by intenstinal bacteria but creates osmotic force that absorbs water from lumen and reduces tendency for water diarrhea |
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Who should receive Branch chain FA supplements in enteric feeds
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Trauma victims and hepatic encephalopathy
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Compare gastric vs small bowel motility post op abdominal surgery
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Gastric mobility is often hypomotile for 24-48 hours while the small bowel is often unimpaired
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Name the three endoscopic techniqies used on the small bowel
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capsule,
push-enteroscope is pushed down the small bowel, sometimes with the help of a stiffening overtube that extends from the mouth to the small intestine. The mid-jejunum is usually reached, and the endoscope's instrument channel allows for biopsies or endoscopic therapy , double ballon-a long overtube and endoscope are both equipped with balloons that, when inflated, appose the intestinal wall and allow for pleating of the small intestine over the endoscope and overtube. The double-balloon enteroscope may be passed orally or anally, and the entire small bowel can be visualized in some patients when both approaches are used. Biopsies and endoscopic therapy can be performed throughout the visualized small bowel. |
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% of Post ERCP pancreatitis
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5% and 25% if there is sphincter of oddi dysfunction
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How do you prep for an urgent colonoscopy in presence of hematochezia
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Rapid colonic purge with polyethylene glycol
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Dieulafoy's Lesion
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is a large-caliber arteriole that runs immediately beneath the gastrointestinal mucosa and bleeds through a pinpoint mucosal erosion (Fig. 285-17). Dieulafoy's lesion is seen most commonly on the lesser curvature of the proximal stomach, causes impressive arterial hemorrhage, and may be difficult to diagnose; it is often recognized only after repeated endoscopy for recurrent bleeding. Endoscopic therapy is typically effective for control of bleeding and ablation of the underlying vessel once the lesion has been identified Angiographic embolization or surgical oversewing is considered when endoscopic therapy has failed.
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What endoscopic tx are available for Mallory-Weiss Tear
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1. epinephrine injection,
2. coaptive coagulation, 3. hemoclips 4. band ligation |
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What are Vascular ectasias and how are they treated
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flat mucosal vascular anomalies that are best diagnosed by endoscopy. They usually cause slow intestinal blood loss and have several characteristic distributions in the gastrointestinal tract (Fig. 285-19). Cecal vascular ectasias (senile lesions), gastric antral vascular ectasias ("watermelon stomach"), and radiation-induced rectal ectasias are often responsive to local endoscopic ablative therapy, such as argon plasma coagulation (APC). Patients with diffuse small-bowel vascular ectasias (associated with chronic renal failure and hereditary hemorrhagic telangiectasia) may continue to bleed despite endoscopic treatment of easily accessible lesions by conventional endoscopy. These patients may benefit from double balloon enteroscopy with endoscopic therapy, pharmacologic treatment with octreotide or estrogen/progesterone therapy, or intraoperative enteroscopy.
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What is Charcot's Triad and what does it indicate
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1. jaundice
2. abdominal pain 3. fever Present in about 70% of patients with ascending cholangitis and biliary sepsis |
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Reynald's Pentad
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1. jaundice
2. abdominal pain 3. fever 4. Shock 5. Confusion Promptly restore biliary flow |
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Dysphagia: What is difference in swallowing between stricture vs motility d/o in esophagus
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Esophageal strictures typically cause progressive dysphagia, first for solids, then for liquids
motility disorders often cause intermittent dysphagia for both solids and liquids. |
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Why should Colonoscopy be perfomed in men and postmenopausal women with Fe def anemia?
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even in the absence of detectable occult blood in the stool, approximately 30% of patients will have colon polyps, 10% will have colorectal cancer, and a few additional patients will have colonic vascular lesions.
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Chronic anemia with neg colonscopy and neg EGD, if small bowel is suspected then what is next step
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Capsule endoscopy can provide a dx in 50% of cases which is most commonly mucosal vascular ectasias
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Work up for Hematochezia?
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trivial amounts of hematochezia should be investigated with flexible sigmoidoscopy and anoscopy to exclude large polyps or cancers in the distal bowel.
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Blood on TP only vs blood in the toilet
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Blood on the TP only indicates an anal lesion requiring external inspection, digital examination, anoscopy
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What are the barium studies findings for motor d/o of the esophagus?
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(1) Pharyngeal paralysis with tracheal aspiration
(2) Cricopharyngeal achalasia. the prominent cricopharyngeus, which is recognized by its smoothness and location in the posterior wall. (3) Diffuse esophageal spasm: corkscrew appearance of the lower part of the esophagus. (4) Achalasia: a dilated esophageal body with an air-fluid level and a closed lower esophageal sphincter. (5) Muscular (contractile) lower esophageal ring. The asymmetric contraction visible in has disappeared in, (6) Scleroderma esophagus: dilated esophagus with a stricture and reflux of barium from the stomach into the esophagus |
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Name and Describe the hypertensive esophageal d/o
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In nutcracker esophagus, esophageal contractions are normally peristaltic but hypertensive.
In hypercontracting LES, the normal sphincter relaxation is followed by hypertensive contraction. In hypertensive LES, basal LES pressure is elevated, but sphincter relaxation and contraction are normal |
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Differentiate the pathophysiology DES from the hypertensive d/o
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Nonperistaltic contractions are due to dysfunction of inhibitory nerves. Histopathology shows patchy neural degeneration localized to nerve processes, rather than the prominent degeneration of nerve cell bodies seen in achalasia.
DES may progress to achalasia. Hypertensive peristaltic contractions and hypertensive or hypercontracting LES may represent cholinergic or myogenic hyperactivity. |
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What happens to the LES and peristaltic contractions in achalasia
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the esophageal body loses peristaltic contractions and the LES does not relax normally in response to swallowing.
This mainly due to loss of intramural neurons |
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Primary sx of achalasia
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Dysphagia, chest pain, and regurgitation
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Describe the esophageal lesions in Sceleroderma
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esophageal lesions in systemic sclerosis consist of atrophy of smooth muscle, manifested by weakness in the lower two-thirds of the esophagus and incompetence of the LES.
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Erosive esophagitis may heal by (blank) leading to Barrett's esophagus, a risk factor for adenocarcinoma.
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intestinal metaplasia
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Simple dx of GERD can be made by __________ and ______
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1. History
2. One week trial with 40mg omeprazole with relief of sx |
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Diagnostic studies are indicated in patients with persistent symptoms or symptoms while on therapy, or in those with complications. What are the 3 elements that we need to monitor?
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The diagnostic approach to GERD can be divided into three categories:
(1) documentation of mucosal injury (2) documentation and quantitation of reflux (3) definition of the pathophysiology. |
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Name the PPIs, dosages,their use, and some side effects
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The PPIs are comparably effective:
omeprazole (20 mg/d), lansoprazole (30 mg/d), pantoprazole (40 mg/d), esomeprazole (40 mg/d), or rabeprazole (20 mg/d) for 8 weeks can heal erosive esophagitis in up to 90% of patients. The PPI should be taken 30 min before breakfast. Refractory patients can double the dose. Since GERD is a chronic disease, long-term maintenance therapy is often required, and symptoms may relapse in up to 80% of patients within 1 year if therapy is discontinued. PPIs are most effective in preventing recurrences. The side effects of PPI therapy are generally minimal. However, aggressive acid suppression may cause hypergastrinemia but does not increase the risk for carcinoid tumors or gastrinomas. Vitamin B12 and calcium absorption may be compromised by the treatment. |
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What is acid reflux and what is alkaline reflux
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Acid Reflux is gastric acid
Alkaline reflux is bile salts which are often a reason for PPI, H2 tx failure. |
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Describe the esophagitis that can occur directly from HIV infection
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acute esophageal ulceration associated with oral ulcers and a maculopapular skin rash, which occurs at the time of HIV seroconversion. Some patients with advanced disease have deep, persistent esophageal ulcers requiring treatment with oral glucocorticoids or thalidomide. Some ulcers respond to local steroid injection.
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What meds are responsible for pill esophagitis
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Antibiotics such as doxycycline, tetracycline, oxytetracycline, minocycline, penicillin, and clindamycin account for more than half the cases.
Nonsteroidal anti-inflammatory agents such as aspirin, indomethacin, and ibuprofen may cause injury. Others: potassium chloride, ferrous sulfate or succinate, quinidine, alprenolol, theophylline, ascorbic acid, and pinaverium bromide. Bisphosphonates, particularly alendronate and pamidronate, are more common offenders. Pill-induced esophagitis can be prevented by avoiding the offending agents or taking pills in the upright position with copious amount of fluid. |
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What do imaging studies of eosinophilic esophagitis show?
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Barium esophagogram may show a small-caliber esophagus, isolated esophageal narrowing, or single or multiple esophageal rings.
Esophagoscopy may reveal one or more longitudinal fissures, fixed or transient concentric rings, proximal strictures, and focal white specks (abscesses). Endoscopic ultrasound may show thickening of the esophageal wall. |
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hypopharyngeal webs and iron-deficiency anemia in middle-aged women suggests...
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Plummer-Vinson Syndrome
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Differentiate Lower esophageal mucosal ring vs a muscular ring
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Mucosal ring or Schatzki ring is a thin, weblike constriction located at the squamocolumnar mucosal junction at or near the border of the LES. It may result from GERD or be congenital in origin. It invariably produces dysphagia when the lumen diameter is <1.3 cm. Dysphagia to solids is the only symptom, and it is usually episodic. A lower esophageal ring is one of the common causes of dysphagia. Asymptomatic rings may be present in ~10% of normal individuals. Symptomatic rings and webs are easily treated by dilatation.
lower esophageal muscular ring or contractile ring is located proximal to the site of mucosal rings and may represent an abnormal uppermost segment of the LES. These rings can be recognized by the fact that they are not constant in size and shape. They may also cause dysphagia and should be differentiated from peptic strictures, achalasia, and lower esophageal mucosal rings. Muscular rings do not respond well to dilatation. |
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What leads to a sliding hiatal hernia?
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weakening of the anchors of the gastroesophageal junction to the diaphragm, from longitudinal contraction of the esophagus, or from increased intraabdominal pressure
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Describe the pain experienced in esophageal rupture
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esophageal perforation causes severe retrosternal chest pain, which may be worsened by swallowing and breathing.
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Name 3 locations where foreign bodies most commonly become stuck
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1. cervical esophagus just beyond the UES
2. near the aortic arch 3. above the LES |
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What serologic tests can be ordered for celiac sprue
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IgA endomysial antibody and IgA tissueTransGlutaminase antibody tests, both of which have a 90% sensitivity and 95% specificity for the diagnosis
Antigliadin antibodies are no longer recommended because of their lower sensitivity and specificity. |
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What are three syndromes that occur with EtOH withdrawl
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1. Tremulousness and Hallucinations:
2. Seizures: 3. DT: |
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When do tremulousness and hallucinations occur, the symptoms, and how are they treated?
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within 2 days
tremulousness, agitation, anorexia, nausea, insomnia, tachycardia, and hypertension. Tx with diazepam, 5–20 mg, or chlordiazepoxide, 25–50 mg, orally every 4 hours |
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When do EtOH withdrawl seizures occur after withdrawl?
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occur within 48 hours of abstinence, and within 7–24 hours in approximately two-thirds of cases. Roughly 40% of patients who experience seizures have a single seizure; more than 90% have between one and six seizures. In 85% of the cases, the interval between the first and last seizures is 6 hours or less.
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What are some alarming signs that EtOH withdrawl seizures are due to another cause
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focal seizures
prolonged duration of seizures (>6–12 hours) more than six seizures status epilepticus prolonged postictal state |
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What is the treatment for EtOH withdrawl seizures
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Nothing
Dilantin is usually not required but diazapam and chlorazapam should be given for DT prophylaxis |
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How many days after the last drink do DTs begin and how long does it last?
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3–5 days after cessation of drinking and lasts for up to 72 hours.
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Symptoms of DT
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confusion, agitation, fever, sweating, tachycardia, hypertension, and hallucinations.
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Causes of Death in DT
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Death may result from concomitant infection, pancreatitis, cardiovascular collapse, or trauma.
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Treatment of DT
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diazepam, 10–20 mg intravenously, repeated every 5 minutes as needed until the patient is calm
correction of fluid and electrolyte abnormalities and hypoglycemia The total requirement for diazepam may exceed 100 mg/h. Concomitant beta-adrenergic receptor blockade with atenolol, 50–100 mg/d, also has been recommended. |
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Increased BUN with normal GFR
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■Prerenal azotemia
■Catabolic states ■High-protein diets ■Gastrointestinal bleeding ■Glucocorticoids ■Tetracycline |
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Causes of Increased Albumin
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Dehydration
shock hemoconcentration |
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Causes of Decreased Albumin
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Decreased hepatic synthesis (chronic liver disease, malnutrition, malabsorption, malignancy, congenital analbuminemia [rare]).
Increased losses (nephrotic syndrome, burns, trauma, hemorrhage with fluid replacement, fistulas, enteropathy, acute or chronic glomerulonephritis). Hemodilution (pregnancy, CHF). Drugs: estrogens. |
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What causes NASH
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Results from progression of macrovascular steatosis to steatohepatitis and fibrosis
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Describe NASH histologically
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Characterized histologically by macrovesicular steatosis of NAFLD with
– Focal infiltration by polymorphonuclear neutrophils – Mallory's hyalin – Histologic features are indistinguishable from alcoholic hepatitis |
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What are the causes of Nonalcoholic fatty liver disease (NAFLD)
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DM, obesity, hypertriglyceridemia
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Causes of microvesicular steatosis
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Reye's syndrome
valproic acid toxicity tetracycline acute fatty liver of pregnancy Women in whom fatty liver of pregnancy develops often have a defect in fatty acid oxidation due to reduced long-chain 3-hydroxyacyl-CoA dehydrogenase activity |
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Describe the lab tests for Nonalcoholic fatty liver disease (NAFLD)
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There may be mildly elevated aminotransferase and alkaline phosphatase levels
In contrast to alcoholic liver disease, – Ratio of alanine aminotransferase (ALT) to aspartate aminotransferase (AST) is almost always > 1 in NASH – However, it decreases to < 1 as advanced fibrosis and cirrhosis develop |
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Differentiate the AST/ALT relationship between EtOH liver disease and NAFLD
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In contrast to alcoholic liver disease,
– Ratio of alanine aminotransferase (ALT) to aspartate aminotransferase (AST) is almost always > 1 in NASH – However, it decreases to < 1 as advanced fibrosis and cirrhosis develop |
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Differential Diagnosis of Nonpalpable purpura
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■Trauma
■Senile or solar purpura ■Corticosteroid use ■Idiopathic thrombocytopenic purpura ■Thrombotic thrombocytopenic purpura ■Disseminated intravascular coagulation ■Other thrombocytopenia or platelet dysfunction ■Clotting factor defect ■Vitamin K deficiency ■Warfarin necrosis ■Amyloidosis ■Waldenström's macroglobulinemia ■Scurvy ■Ehlers-Danlos syndrome |
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Differential for palpable purpura
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DDx
Vasculitis ■Polyarteritis nodosa ■Rheumatoid arthritis ■Wegener’s granulomatosis ■Churg-Strauss syndrome ■Henoch-Schönlein purpura ■Systemic lupus erythematosus (SLE) ■Hypersensitivity (leukocytoclastic) vasculitis Infection or emboli ■Meningococcemia ■Gonococcemia ■Endocarditis ■Rocky Mountain spotted fever ■Aspergillus ■Candidiasis ■Ecthyma gangrenosum (neutropenic, pseudomonal) Other ■Sarcoidosis ■Cryoglobulinemia ■Ulcerative colitis ■Crohn’s disease ■Medications |
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Types of Bruises
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Bruises may be referred to by size
ecchymosis (1-3 cm) purpura (3-10 mm) petechia (<3 mm) |
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In the setting of chronic diarrhea, diarrhea that wakes up the patient would indicate which pathology
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Crohns
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In the setting of chronic diarrhea, post prandial diarrhea would inidicate
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IBS
|
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Effective initial treatment for diarrhea only IBS
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Lamotil
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3 types of polyps
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mucosal neoplastic (adenomatous) polyps
mucosal nonneoplastic polyps (hyperplastic, juvenile polyps, hamartomas, inflammatory polyps) submucosal lesions (lipomas, lymphoid aggregates, carcinoids, pneumatosis cystoides intestinalis) |
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Most common polyp removed at colonoscopy. #2
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1. Adenoma 70%
2. Hyperplastic |
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Large hyperplastic polyps located in the proximal colon may evolve into a unique type of premalignant lesion called
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a "serrated adenoma."
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4 Histological Classifications of adenomas
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tubular
villous tubulovillous serrated |
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From normal mucosa, it takes how many years to develop a medium sized polyp and a how many years to cancer
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5 years to polyp
10 years to CA |
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Peutz-Jeghers syndrome
|
hamartomatous polyps throughout the gastrointestinal tract (most notably in the small intestine) as well as mucocutaneous pigmented macules on the lips, buccal mucosa, and skin.
|
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Bethesda Criteria for Colon CA
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(1) colorectal cancer under age 50
(2) synchronous or metachronous colorectal or HNPCC-associated tumor regardless of age (endometrial, stomach, ovary, pancreas, ureter and renal pelvis, biliary tract, brain) (3) colorectal cancer with one or more first-degree relatives with colorectal or HNPCC-related cancer, with one of the cancers occurring before age 50 (4) colorectal cancer with two or more second-degree relatives with colorectal or HNPCC cancer, regardless of age (5) tumors with infiltrating lymphocytes, mucinous/signet ring differentiation, or medullary growth pattern in patients younger than 60 years. |
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Follow up colonoscopy with polyps
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– In 5–10 years for patients with 1–2 small (< 1 cm) tubular adenomas (without villous features or high-grade dysplasia)
– In 3 years for patients with 3–10 adenomas, an adenoma > 1 cm, or an adenoma with villous features or high grade dysplasia – In 1–2 years for patients with > 10 adenomas; consider evaluating these patients for a familial polyposis syndrome |
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Types of GIST
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spindle cell or epitheliod
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MC Location of GIST
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Stomach and proximal Small bowel
|
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What immunohistochemical staining can be performed for GIST
|
80% express CD117 antigen,
|
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Presenting symptoms of Small Bowel lymphoma
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Obstruction
Bleeding Perforation |
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SB Lymphoma occurs most commonly what two areas?
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proximal jejunum-celiac
distal ileum-de novo. |
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Test for Carcinoid tumor
|
measure urinary 5-HIAA
|
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Substances produced by Carcinoid tumors
|
serotonin
substance P neurotensin gastrin somatostatin motilin secretin pancreatic polypeptide |
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Given the GI physiology, how do you treat acute pancreatitis
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NPO to prevent fat and protein from stim CCK release which will stimulate the pancreas
PPI to raise the pH of the starved stomach acid to prevent release of secretin which will stimulate pancreas to release bicarb |
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cholelithiasis caused by which two substances
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80% cholesterol caused
the rest are bilirubin |
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In a study that looked at the autospy results of patients who had had cholecystectomy at some point in their lives, what abnormalities correlated with pain/without pain
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Pain-adhesions of small bowel to gb site (9%); tumours, or tumour-like scars, in the cystic duct-stump and choledochal region found in 15 (15%)
No Pain:peptic ulcers, cystic remnants, or choledochal stones showed no association with the complaints |
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Treatment of constipation
|
Laxative stimulant: bisacodyl, docusate and senna, polyethylene glycol
Stool softener: docusate, senna Laxative: magnesium hydroxide, mineral oil, methylcellulose Osmotic laxative: glycerin, lactulose, polyethylene glycol, sorbitol Bulk laxatives: psyllium, polycarbophil, methylcellulose Enterokinetic agents: 5-HT agonists –tegaserod GI agent, prokinetic: cisapride, domperidone, metoclopramide |
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Clues GERD rather than asthma
|
Adult onset
poor response to meds nocturnal cough nonallergic related to meals |
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Precipatating factors for GERD
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Large meals
Fatty Meals peppermint EtOH caffeine CCBs SSRIs obesity prego(progesterone) |
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Meds to avoid in GERD
|
theophyline
anticolinergics ccb diazapam morphine barbs a blockers |
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GERD resistant to PPI bid x 2 months
|
non-reflux esophagitis: pill, infection, eosinophilic, skin disease
dyspepsia: gastroparesis, PUD, NERD, NUD rapid metabolizer non-compliance dysmotility: achalasia, spasm, nutcracker, g-paresis |
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IBD and thromboembolism
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3 fold increased risk
|
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Why is Nephrolithiasis so common in Crohns
|
caused by hyperoxaluria due to increased intestinal absorption of oxalate
|
|
Heptobiliary complications with Crohns
|
cholelithiasis
benign pericholangitis sclerosing cholangitis autoimmune chronic active hepatitis cirrhosis. |
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Prevalence in Crohns vs UC
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Crohns:7 cases per 100,000
UC:35-100 cases per 100,000 |
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Age of Onset
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UC: any age but peaks are 1-25; 55-65
Crohns: 15-30 mostly ileal and most cases; 60-80 mostly colonic |
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Serum immunochemistry test that can differentiate UC from Crohns
|
+ p-ANCA indicates UC
+ASCA indicates Crohns |
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Do contractions occur in achalsia with aperistalsis
|
Yes. vigorous achalasia has simultaneous contractions that are in sync but not coordinated therefore unable to properly to propel food.
|
|
Surgical technique used for achalasia
|
Heller Myotomy: requires PPI and will have long term GERD
|
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Define long and short segment barret's
|
Long >3cm and short <3cm
|
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Stages of Barrets to Cancer
|
Intestinal Metaplasia that is Negative for Dysplasia ==>indefinite for dysplasia==>Low Grade==>High Grade==> AdenoCA
|
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Types of Esophageal Diverticula
|
Zenker's=Upper E
Traction=MidE Epiphrenic=distal E |
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What Physical signs indicate necrosis in acute pancreatitis
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Fever, Increased WBC
|
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What is the first radiological test to order in setting of suspected acute pancreatitis
|
Ab US to r/o biliary stones, pseudocyst, CBD dilation, ascites
|
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When should a CT be ordered in setting of acute pancreatitis
|
suspicion of necrosis
Organ Failure failure to improve clinically |
|
What does increased ALT indicate in the setting of CBD obstruction, gall stone pancreatitis
|
Hepatocyte compression
|
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What lab value can determine severity of acute pancreatitis
|
CRP: >150 drawn within 48 hours of symptom onset indicates severe acute pancreatitis
|
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What does the PANCREAS acronym stand for in acute pancreatitis treatment
|
P: Pain control usually demerol
A: Antibiotics N: NPO; enteral feedings are better than TPN C: Ca/Mg R:Rest E: electrolytes A: Acid-PPI S: Suction via NG |
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How many L of fluid are given in Acute pancreatitis
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10L/day
|
|
Ransons Criteria at Dx
|
Age>55;
WBC>16; Gluc>200; AST >250; LDH>350 |
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Ransons Criteria at 48 hours
|
HCT decrease by 10%;
BUN increase >5; Base Defecit>4; Ca<8; PaO2<60; Fluid defecit >6L |
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What causes GI Bleed in acute pancreatitis
|
Splenic vein thrombosis
Hemosuccus pacreaticus: Bleed through the Pancreatic duct into duodenum due to erosion of pseudocyst into adjacent vasculature |
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Hormones that promote gastric emptying/inhibit gastric emptying
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Promote: Motilin/Neurotensin
Inhibit (delay): Secretin/SCK |
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What is erythromycin MOA with Gastroparesis therapy
|
Motilin agonist which stimulates antral contractions
|
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Mechansim for Bethanechol(urecholine) in Gastroparesis
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cholinergic that stimulates muscarinics receptors
|
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MOA of Cisparide(porpulsid) in gastroparesis
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facilitates ACH release at myenteric plexus. Not available in US
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