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  1. Classification Of Dysphagia
    • Dysphagia can be classified as oropharyngeal or esophageal.
    • Oropharyngeal dysphagia presents with difficulty swallowing due to inability to properly transfer food from the mouth to the pharynx.
    • Underlying etiologies for oropharyngeal dysphagia can Include stroke,advanced dementia, oropharyngeal malignancy, or neuromuscular disorders (eg. myasthenia gravis).
    • Patients with oropharyngeal dysphagia can also have associated coughing, choking, or nasal regurgitation on swallowing.
    • Other complications can include aspiration pneumonia and weight loss.
    • This patient's history of stroke with coughing and choking on swallowing suggests oropharyngeal dysphagia.
    • Recurrent right lower lobe pneumonia suggests likely aspiration pneumonia.
    • Videofluoroscopic modified barium swallow study : is preferred initially in these patients to evaluate swallowing mechanics, degree of dysfunction, and severity of aspiration.
  2. Carcinoids
    • Carcinoids are well differentiated neuroendocrine tumors found most commonly in the distal small intestine, proximal colon, and lung, with a strong propensity for metastasis to liver.
    • These tumors can secrete several products Including histamine, serotonin, and vasoactive intestinal peptide that are metabolized In the liver.
    • In patients with liver metastasis, these hormones are released directly Into the systemic circulation, leading to carcinoid syndrome.
  3. Hallmark of Carcinoid Syndrome
    • Episodic flushing is the hallmark of carcinoid syndrome and occurs in almost 85% of patients. Severe flushing may be associated with hypotension and tachycardia.
    • Secretory diarrhea may be accompanied by abdominal cramping.
    • Other common features Include cutaneous telangiectasias, bronchospasm, and tricuspid regurgitation.
    • Pathognomonic plaque-like deposits of fibrous tissue occur most commonly on the endocardium on the right side of the heart, leading to tricuspid regurgitation and right-sided heart failure.
    • Elevated 24-hour urinary 5- hydroxyindoleacetlc acid can confirm the diagnosis in most patients.
  4. Features of carcinoid syndrome
    • Clinical manifestations :
    • • Skin: flushing, telangiectasias, cyanosis
    • • Gastrointestinal: diarrhea, cramping
    • • Cardiac: valvular lesions (right > left side)
    • • Pulmonary: bronchospasm
    • • Miscellaneous: Niacin deficiency (dermatitis, diarrhea & dementia)
    • Diagnosis:
    • Elevated 24"hour urinary excretion of 5-HIAA
    • • CT/MRI of abdomen & pelvis to localize tumor
    • • OctreoScan to detect metastases
    • • Echocardiogram (if symptoms of carcinoid heart disease are present)
    • Treatment :
    • • Octreotide for symptomatic patients & prior to surgery/anesthesia
    • • Surgery for liver metastases
  5. D-Xylose
    • D-xylose is a monosaccharide that can be absorbed in the proximal small intestine without degradation by pancreatic or brush border enzymes. It is subsequently excreted in the urine.
    • In the D-xylose test: the patient is given an oral dose of D-xylose, with subsequent assay of urine and venous blood.
    • Patients with proximal small Intestinal mucosal disease (eg, celiac disease) cannot absorb the D xylose in the intestine, and urinary and venous D xylose levels will be low. By contrast, patients with malabsorption due to enzyme deficiencies (eg, chronic pancreatitis) will have normal absorption of D-xylose.
    • A false-positive D-xylose test (ie, decreased urinary excretion of D-xylose despite normal mucosal absorption) can be seen in patients with delayed gastric emptying or impaired glomerular filtration.
  6. Features of malabsorption in celiac disease
    • General : Bulky, foul-smelling, floating stools
    • Fat & protein : Loss of muscle mass, loss of subcutaneous fat, fallgue
    • Iron : Pallor (anemia), fatigue
    • Calcium & vitamin D: Bone pain (osteomalacia), fracture (osteoporosis)
    • Vitamin K : Easy bruising
    • Vitamin A : Hyperkeratosis
  7. Diagnosis Of Celiac Disease
    • The diagnosis of celiac disease Is highly correlated with positive results on serological studies, primarily lgA anti-tissue transglutaminase and lgA anti endomysial antibodies.
    • However, many patients with biopsy-confirmed celiac disease will have negative results on lgA antibody testing due to an associated selective lgA deficiency, which is common in celiac disease.
    • If lgA serology is negative but the suspicion for celiac disease Is high, total lgA should be measured (or lgG-based serologic testing should be done).
  8. Acute Cholangitis
    • Clinical presentation :
    • • Fever, jaundice, right upper quadrant pain (Charcot triad)
    • • Mental status , hypotension (Reynolds pentad)
    • • Liver failure
    • • Acute kidney injury
    • Diagnosis:
    • • Biliary dilation on ultrasound or CT scan
    • • Increase Alkaline phosphatase, gamma-glutamyl transpeptidase, direct bilirubin
    • • Leukocytosis, increase C-reactive protein
    • Treatment :
    • • Biliary drainage: Endoscopic retrograde cholangiopancreatography with sphincterotomy or percutaneous transhepatic cholangiography
    • • Broad-spectrum antibiotics: Beta-lactam/beta lactamase inhibitor, third-generation cephalosporin + metronidazole
  9. Acalculous cholecystitis
    • Risk factors:
    • • Severe trauma, extensive bums, recent surgery (eg, cardiopulmonary, aortic, abdominal)
    • • Prolonged fasting or TPN
    • • Critical illness (sepsis, ICU, mechanical ventilation)
    • Clinical presentation:
    • • Unexplained fever, vague/RUQ abdominal discomfort, leukocytosis
    • • Possible jaundice, RUQ mass, abnormal LFTs
    • Diagnosis:
    • •• Abdominal ultrasound (preferred) Cholescintigraphy (HIDA scan) or abdominal CT scan if ultrasound not diagnostic
  10. Management of gallstones
    • Gallstones without symptoms: No treatment necessary in most patients
    • Gallstones with typical biliary colic symptoms:
    • • Elective laparoscopic cholecystectomy
    • • Possible ursodeoxycholic acid in poor surgical candidates
    • Complicated gallstone disease:
    • (acute cholecystitis, choledocholithiasis, gallstone pancreatitis)
    • • Cholecystectomy within 72 hours
  11. Postcholecystectomy syndrome (PCS)
    • PCS refers to persistent abdominal pain or dyspepsia (eg, nausea) that occurs either postoperatively (early) or months to years (late) after a cholecystectomy.
    • PCS can be due to biliary (eg, retained common bile duct or cystic duct stone, biliary dyskinesia) or extra-biliary (eg, pancreatitis. peptic ulcer disease, coronary artery disease) causes.
    • Patients usually notice the same pain they had prior to surgery, new pain just after surgery, or the same pain that never went away.
    • Laboratory findings can Include elevated alkaline phosphatase, mildly abnormal serum aminotransferases. and dilated common bile duct on abdominal ultrasound.
    • These findings usually suggest common bile duct stones or biliary sphincter of Oddi dysfunction.
    • The next step involves endoscopic ultrasound, endoscopic retrograde cholangio pancreatography (ERCP) or magnetic resonance cholangiopancreatography for final diagnosis and guiding therapy.
    • Treatment for PCS is directed at the causative factor.
  12. Biliary Colic
    • The pain is in the right upper quadrant or epigastric region, often constant (rather than colicky), and accompanied by nausea, vomiting, and right-sided shoulder or subscapular discomfort (referred pain).
    • Patients may have recurrent symptoms that resolve between episodes
  13. Bilairy Colic Vs Cholecystitis
    Features that distinguish biliary colic from cholecystitis are pain resolution within 4-6 hours and absence of abdominal tenderness, fever, and leukocytosis.
  14. Mechanism of billiary colic
    • biliary colic is usually secondary to gallstones. Ingestion of a large (usually fatty) meal stimulates gallbladder contraction.
    • The intra-gallbladder pressure increases on gallbladder contraction against an obstructed cystic duct and causes pain.
    • Subsequent gallbladder relaxation allows the stone to fall back from the duct with subsequent pain resolution.
  15. Mechanism of gallstone formation in pts on TPN
    • The presence of proteins and fatty acids in the duodenum acts as a stimulus for release of cholecystokinin (CCK), which In turn stimulates the contraction of the gallbladder.
    • In patients on total parenteral nutrition or prolonged fasting, the normal stimulus for CCK release and gallbladder contraction is absent.
    • This leads to biliary stasis and promotes the formation of bile sludge and gallstones.
    • Small bowel (ileal) resection also contributes to the formation of gallstones. Decreased entero hepatic circulation of bile acids results in altered hepatic bile composition, which becomes supersaturated with cholesterol and promotes gallstone formation.
  16. Mechanism of stone formation in pregnancy and pts taking OCPs
    • Estrogen-induced Increase in cholesterol secretion is the underlying mechanism for the development of cholesterol gallstones during pregnancy and in women taking oral contraceptives.
    • During pregnancy, estrogen causes an increase in cholesterol secretion and progesterone causes a reduction in bile acid secretion, causing increased cholesterol saturation of bile.
    • Progesterone also slows gallbladder emptying and thus facilitates the formation of cholesterol gallstones during pregnancy.
  17. Chronic mesenteric ischemia
    • Etiology : • Atherosclerosis (smoking, dyslipidemia)
    • Clinical features:
    • • Crampy, postprandial, epigastric pain (intestinal angina),
    • • Food aversion & weight loss, nausea, early satiety and diarrhea
    • Diagnosis:
    • • Signs of malnutrition, abdominal bruit
    • • CT angiography (preferred), Doppler ultrasonography
    • Management:
    • • Risk reduclion (eg, tobacco reduction), nutritional support
    • • Endovascular or open surgical revascularization
  18. Mechanism of bowel angina in Chronic mesenteric ischemia
    • The anginal pain frequently starts within the first hour of eating and slowly resolves over the next 2 hours.
    • The pathophysiology of the pain is most likely related to shunting of blood away from the small intestine to meet the increased demand of the stomach.
    • In patients with atherosclerosis, the celiac or the superior mesenteric arteries may be narrowed and unable to dilate appropriately to maintain adequate blood flow to the intestines
  19. Pancreatic adenocarcinoma
    • Risk factors:
    • • Smoking
    • • Hereditary pancreatitis
    • • Nonhereditary chronic pancreatitis
    • • Obesity & lack of physical activity
    • Clinical presentation:
    • • Systemic symptoms (eg, weight loss, anorexia (>85%)
    • • Abdominal pain/back pain (80%): Insidious onset of gnawing abdominal pain (usually epigastric and radiating to the back), which is worse at night, with eating, or when lying supine.
    • • Jaundice (56%)
    • • Recent-onset atypical diabetes mellitus
    • • Unexplained migratory superficial thrombophlebitis
    • • Hepatomegaly & ascites with metastasis
    • Laboratory studies:
    • • Cholestasis ( Increased alkaline phosphatase & direct bilirubin)
    • • increased Cancer-associated antigen 19-9 (not as a screening test)
    • • Abdominal ultrasound (if jaundiced) or CT scan (if no jaundice)
  20. Cancers in the head of the pancreas (60%-70%)
    • typically present with jaundice (common bile duct obstruction, elevated alkaline phosphatase and bilirubin) and steatorrhea (pancreatic exocrine insufficiency or pancreatic duct blockage).
    • In patients with these findings, abdominal ultrasound is preferred for detecting pancreatic head tumors and excluding other potential causes of biliary obstruction (eg, choledocholithiasis).
    • • Cancers in the body and tall usually do not present with obstructive jaundice. Abdominal CT scan is preferred (more sensitive and specific) and helps exclude other conditions.
    • Ultrasound Is less sensitive for visualizing the pancreatic body and tail (due to overlying bowel gas) and for detecting smaller (<3 cm) tumors.
  21. Overview of chronic pancreatitis
    • Etiology:
    • • Alcohol use
    • • Cystic fibrosis (common in children)
    • • Ductal obstruction (eg, malignancy, stones)
    • • Autoimmune
    • Clinical presentation:
    • • Chronic epigastric pain with intermittent pain-free intervals
    • • Malabsorption-steatorrhea, weight loss
    • • Diabetes mellitus
    • Laboratory results/Imaging:
    • • Amylase/lipase can be normal & nondiagnostic
    • • CT scan or MRCP can show calcifications, dilated ducts & enlarged pancreas
    • Treatment:
    • • Pain management
    • • Alcohol & smoking cessation
    • • Frequent, small meals
    • • Pancreatic enzyme supplements
  22. Common causes of steatorrhea
    • Pancreatic insufficiency:
    • • Chronic pancreatitis due to alcohol abuse, cystic fibrosis, or autoimmune/hereditary pancreatitis
    • • Pancreatic cancer
    • Bile salt-related:
    • • Small-bowel Crohn disease
    • • Bacterial overgrowth
    • • Primary biliary cirrhosis
    • • Primary sclerosing cholangitis
    • • Surgical resection of ileum (at least 60-100 cm)
    • Impaired Intestinal surface epithelium:
    • • Celiac disease
    • • AIDS enteropathy
    • • Giardiasis
    • Other rare causes:
    • • Whipple disease
    • • Zollinger-Ellison syndrome
    • • Medication-induced
  23. Hyperestrinism in Cirrhosis of liver
    • spider angioma and palmar erythema both arise from hyperestrinism due to Impaired hepatic metabolism of circulating estrogens, a process that begins in the cytochrome P450 system.Circulating estrogens affect vascular wall dilation.
    • Spider angioma: consists of a central, dilated arteriole surrounded by smaller radiating vessels.
    • Palmar erythema: Is a result of increased normal speckling of the palm due to increased vasodilation, especially at the thenar and hypothenar eminences.
    • Conditions due to hyperestrinism:
    • Spider angiomata
    • Gynecomastia
    • Loss of sexual hair
    • Testicular atrophy
    • Palmar erythema
  24. Portal Hypertension
    • esophageal varices
    • splenomegaly
    • ascites
    • caput medusae
    • anorectal varices
  25. Caput medusae
    • arise from the dilation of superficial veins on the abdominal wall due to portal hypertension (PH).
    • PH results from increased resistance to portal now at the sinusolds and leads to increased pressure at the portosystemlc collateral veins in the anterior abdomen, rectum, and distal esophagus.
    • This then predisposes to esophageal varices, rectal varices, and caput medusae.
    • Similarly, PH causes enlargement of the spleen (which drains into the portal vein via the splenic vein) due to vascular congestion of the red pulp.
  26. Dupuytren contracture
    • occurs when the palmar fascia thickens and shortens, deforming the hand.
    • It Is usually most notable initially in the fourth and fifth digits and occurs due to fibroblast proliferation and collagen deposition, which are likely worsened by oxidative stress from increased free radical production.
  27. common causes of cirrhosis In the United States :
    include viral hepatitis (C more than B), chronic alcoholism, nonalcoholic fatty liver disease (NAFLD), and hemochromatosis
  28. Hepatic hydrothorax
    • pleural effusion not due to underlying cardiac or pulmonary abnormalities.
    • Hepatic hydrothorax generally results in transudative pleural effusions and is thought to occur due to small defects in the diaphragm.
    • These defects permit peritoneal fluid to pass into the pleural space, which occurs much more commonly on the right side due to the less muscular hemidiaphragm.
    • Patients have dyspnea, cough, pleuritic chest pain, and hypoxemia.
    • Diagnosis involves documentation of the effusion (eg, chest x ray) and testing to exclude other causes (eg, thoracentesis, echocardiogram).
    • Treatment involves salt restriction and diuretic administration. Therapeutic thoracentesis could be attempted in patients with prominent symptoms. Chest tube placement should be avoided as it can result in large-volume protein, fluid, and electrolyte losses as well as other severe complications (eg, renal failure).
    • The definitive option for treatment is liver transplantation, although this may not be appropriate for all patients depending on other factors.
  29. Hepatopulmonary syndrome
    • results from intrapulmonary vascular dilations in the setting of chronic liver disease.
    • Patients frequently have evidence of platypnea (increased dyspnea while upright) or orthodeoxia (oxygen desaturation while upright).
  30. cirrhosis due to Chronic alcohol use
    macrocytic anemia, aspartate aminotransferase [AST] to alanine aminotransferase [Al T] ratio ~2: 1, parotid gland enlargement likely from fatty Infiltration due to chronic alcohol use rather than to cirrhosis itself
  31. Management Of compensated Cirhosis
    • Ultrasound surveillance for HCC with or without AFP every 6 monthly
    • endoscopy surveillance for varices
  32. Management of Variceal hemorrhage
    • Primary prophylaxis can be achieved either with endoscopic variceal ligation (EVL) or administration of a nonselective beta blocker such as propranolol or nadolol.
    • Nonselective beta blockers reduce portal venous pressure by blocking the adrenergic vasodllatory response of the mesenteric arterioles, which results In unopposed alpha-adrenergic tone, vasoconstriction, and reduced portal blood flow.
    • The choice of beta blocker or EVL depends on patient preference and the size of the varices (EVL is preferred for larger varices).
  33. Management Of ascitis
    • Dietary Sodium restriction
    • Diuretics (Frusemide and Spironolactone)
    • Paracentesis
    • Abstinence from alcohol
  34. Management of Hepatic encephalopathy
    • Identify cause : Infections, GI Bleeding
    • Lactulose
    • Rifaximine
  35. Hepatorenal syndrome (HRS)
    • is one of the most dangerous complications of end stage liver disease, occurring in up to 10% of patients with cirrhosis.
    • HRS is characterized by decreased glomerular filtration in the absence of shock, proteinuria, or other clear cause of renal dysfunction, and a failure to respond to a 1.5 L normal saline bolus.
    • It is thought to result from renal vasoconstriction In response to decreased total renal blood flow and vasodilatory substance synthesis.
    • There are 2 subtypes of HRS.
    • Type 1 is rapidly progressive: most patients die within 10 weeks without treatment.
    • Type 2 progresses more slowly, with an average survival of 3-6 months.
    • The most common causes of death are infection and hemorrhage.
    • Unfortunately, no medication has consistently proven beneficial in HRS and the mortality for these patients placed on dialysis is very high.
    • Liver transplantation is the only intervention with established benefit.
  36. Clostridium difficile colitis
    • patient's recent antibiotic use, watery bowel movements, and mild abdominal tenderness suggest possible C. difficile.
    • Risk factors for C difficile include: recent hospitalization, advanced age, or antibiotic use (most commonly fluoroquinolones, penicillins, cephalosporins, and clindamycin).
    • Unexplained leukocytosis in hospitalized patients should raise suspicion for C. difficile, even without diarrhea.
    • C. difficle colitis can range from mild watery diarrhea to fulminant colitis with toxic megacolon.
    • Diagnosis: is usually confirmed with stool studies for C difficile toxin (eg, polymerase chain reaction).
    • Patients with mild to moderate (WBC<15 ,000/mL) C difficile colitis should receive empiric oral metronidazole while awaiting stool studies.
    • Patients with negative studies may require sigmoidoscopy or colonoscopy with biopsy to document pseudomembranous colitis.
    • Severe colitis usually requires oral vancomycin with or without IV metronidazole or a possible switch to intra colonic vancomycin.
    • Fidaxomicin is a bactericidal antibiotic usually reserved for recurrent colitis or as initial therapy for patients with severe colitis who cannot tolerate oral vancomycin.
  37. Clostridium dlfficile colitis
    • Mild-moderate
    • • WBC <15,000/mm,
    • • Creatinine < 1.5x baseline
    • Treatment is: Oral metronidazole
  38. Severe Clostridium Colitis
    • WBC more than 15,000/mml
    • Creatinine more than 1.5x baseline
    • Serum albumin <2.5 g/dl
    • Treatment is : oral Vancomycin. But, if ileus is present add IV Metronidazole and Switch to rectal vancomycin
    • If following features present:
    • • WBC more than 20 ,000/mm3
    • • Lactate more than 2.2 mg/dl
    • • Toxic megacolon
    • • Severe ileus
    • Options:
    • Subtotal colectomy
    • Diverting loop ileostomy with colonic lavage
  39. Pathogenesis of Clostridium difficile
    • Clostridium difficile is a gram-positive, anaerobic bacterium that causes infectious diarrhea in the nosocomial and outpatient setting.
    • Hardy antibiotic-resistant spores are ingested and convert to fully functional bacilli in the colon.
    • Although the organism is noninvasive, pathogenic strains produce exotoxins ("enterotoxin" A and "cytotoxin" B) that penetrate colonic epithelial cells, resulting in apoptosis and the loss of tight junctions.
    • Carriage of toxigenic C. difficile is common, but extensive proliferation is usually required to reach exotoxin levels that are pathogenic.
    • The single greatest risk factor for clinical illness is recent antibiotic use (eg, fluoroquinolones, clindamycin, cephalosporins, penicillins), which disrupts the normal colonic flora (eg, Bacteroides), freeing nutrients and eliminating a crucial epithelial barrier.
    • Other common risk factors include advanced age (>65) and gastric acid suppression (eg, proton pump inhibitor).
  40. Diagnosis and Management of Clostridium difficile
    • C difficile colitis usually manifests with watery diarrhea (~3 stools/day), abdominal cramping, vomiting, low-grade fever, and leukocytosis (- 15,000/mm').
    • Overt melena and bright red blood per rectum are rare.
    • Diagnosis is typically made with stool assay for C difficile exotoxin genes via polymerase chain reaction.
    • Treatment involves the cessation of the inciting antibiotic (If possible), Infection control (contact precautions), and antimicrobial therapy with oral metronidazole or vancomycin.
  41. Colonic Polyp
    • A polyp is a grossly visible protrusion from the flat mucosal surface of the intestine. Most polyps are benign. Polyps can be classified as follows:
    • 1. Hyperplastic polyps: These are the most common non-neoplastic polyps in the colon. These arise from hyperplastic mucosal proliferation. No further workup is needed.
    • 2. Hamartomatous polyps: These include juvenile polyp (a non-malignant lesion, generally removed due to the risk of bleeding) and Peutz Jeghers polyp (generally non-malignant).
    • 3. Adenoma: This is the most common type of polyp found in the colon. It is present in approximately 30-50% of elderly people. These polyps are potentially premalignant; however, <1% of such polyps become malignant. Most polyps are asymptomatic; less than 5% of patients have positive occult stool tests.
  42. Probability of adenomatous polyp turning into malignancy
    • The probability of an adenomatous polyp progressing into cancer can be judged clinically by the lesion's gross appearance, histology, and size.
    • 1. Adenoma can be sessile or stalked (pedunculated). Cancer is seen more commonly in sessile polyps.
    • 2. Histologically, adenoma is divided into tubular, tubulovillous, and the villous variety. Villous adenomas, which are most commonly sessile, are most likely (three times more likely than tubular adenoma for malignant transformation) to become malignant among all three varieties. Second on the list is tubulovillous, followed by tubular adenoma with the least risk of malignant transformation. Therefore, as the villus component increases the risk of malignancy increases.
    • 3. The likelihood of an adenomatous lesion containing invasive cancer also depends on the size of the polyp. The risk is negligible (<2%) with< 1.5 cm polyp. intermediate(2-10%) with 1.5-2.5 cm size polyp, and substantial (10%) with polyps >2.5 cm In size.
  43. Screening of colon cancer
    • Patients at average risk of developing colon cancer should begin screening at age 50 with high-sensitivity fecal occult blood testing (FOBT) annually, flexible sigmoidoscopy every 5 years combined with FOBT every 3 years, or colonoscopy every 10 years.
    • Patients with an affected first-degree relative should begin screening at age 40 or 10 years before the age of the relative's diagnosis.
  44. Lung Cancer Screening
    • Low-dose chest CT is recommended yearly for lung cancer screening in patients who are age 55-80, have a more than 30-pack-year smoking history, and are currently smoking or quit within the past 15 years.
    • Recommended test: • Low-dose chest CT
    • Recommended interval: • Yearly
    • Age for screening : 55-80
    • Eligibility for screening based on smoking history:
    • • Patient has >30-pack-year smoking history
    • • Patient is a current smoker or quit smoking within the last 15 years
    • Termination of screening:
    • • Age >80
    • OR
    • • Patient successfully quit smoking for more than 15 years
    • • Patient has other medical problems that significantly limit life expectancy or ability/willingness to undergo lung cancer surgery
  45. Diarrhoea
    • Diarrhea can be divided into 3 main categories: watery, fatty, and inflammatory.
    • Watery diarrhea can be further broken down into osmotic, secretory, and functional.
    • Hallmarks of secretory diarrhea: include larger daily stool volumes (>1L/day) and diarrhea that occurs even during fasting or sleep.
    • Secretory diarrhea most commonly occurs when luminal ion channels are disrupted in the gastrointestinal tract, resulting in a state of active secretion.
    • A helpful tool in distinguishing osmotic from secretory diarrhea is the stool osmotic gap (SOG): , which calculates the difference between plasma osmolality (considered equivalent to measured stool osmolarity) and double the sum of sodium and potassium ions in stool (corresponding to calculated stool osmolality) SOG = plasma osmolality - 2 x (stool sodium + stool potassium):
    • Secretory diarrhea is due to increased secretions of ions; therefore, the difference between plasma osmolality and measured fecal sodium and potassium is significantly reduced (SOG <50 mOsm/kg).
  46. Common causes of secretory diarrhea :
    • Include bacterial infections (eg, Vibrio cholera), viral infections (eg, rotavirus). congenital disorders of ion transport (eg, cystic fibrosis), early ileocolitis, and postsurgical changes.
    • Secretory diarrhea can occur after bowel resection or cholecystectomy when unabsorbed bile acids reach the colon and result in the direct stimulation of luminal ion channels.
    • In addition, resection of the ileocecal area reduces the ability of the Intestines to actively absorb sodium ions against the electrochemical gradient.
  47. Osmotic diarrhea
    In osmotic diarrhea, nonabsorbed and unmeasured osmotically active agents are present in the gastrointestinal tract. These ions result in an elevated osmotic gap (SOG >125 mOsm/kg).
  48. Diffuse Esophageal Spasm
    • patient's symptoms (ie, spontaneous pain, odynophagia for cold and hot food) are suggestive of diffuse esophageal spasm.
    • Resolution of her chest pain after taking nitroglycerin Is also consistent wlth the diagnosis.
    • Nitrates (and calcium channel blockers) relax not only myocytes in coronary vessels, but also those in the esophagus. thereby alleviating the pain.
    • Esophagography may or may not show other anomalies (eg, corkscrew shape).
    • Esophageal manometry should show repetitive, non-peristaltic, high-amplitude contractions, either spontaneously or after ergonovine stimulation.
  49. Diffuse esophageal spasm
    • Pathophysiology:
    • • Uncoordinated, simultaneous contractions of esophageal body likely related to impaired inhibitory innervation in the esophagus
    • Symptoms:
    • • Intermittent chest pain
    • • Dysphagia for solids & liquids
    • Diagnosis:
    • • Esophagram: "Corkscrew" pattern d/t nonperistaltic contractions
    • • Manometry: Intermittent peristalsis, multiple simultaneous contractions of the middle and lower esophagus. The lower esophageal sphincter usually shows normal relaxation
    • D/D: achalasia (Impaired esophageal motility with incomplete relaxation at the lower esophageal sphincter) and nutcracker esophagus (excessive tone at the lower esophageal sphincter).
    • Treatment:
    • • Calcium channel blockers (Diltiazam)
    • • Alternate: Nitrates, tricyclics
  50. Acute diverticulitis
    • Definition: inflammation due to microperforation of a diverticulum.
    • Etiology: Chronic constipation and a low-fiber, high fat diet are risk factors for diverticular disease.
    • Clinical Features: Patients with diverticulitis present with abdominal pain (usually lower left quadrant), fever, nausea/vomiting, and leukocytosis. Some have urinary urgency, frequency, or dysuria due to bladder irritation from an inflamed sigmoid colon.
    • Investigation: Abdominal CT scan (oral and intravenous contrast) is the best diagnostic test for diverticulitis, differentiating it from other diseases (eg. colon cancer. kidney infection).
    • Findings suggestive of diverticulitis include increased Inflammation in pericolic fat, presence of diverticula, bowel wall thickening, soft tissue masses (eg. phlegmons), and pericolic fluid collections suggesting abscess.
    • Management:
    • • Bowel rest
    • • Antibiotics (eg, ciprofloxacin, metronidazole)
    • Complications:
    • • Abscess, obstruction, fistula, perforation
Card Set:
2017-08-29 12:15:16
liver disease

peptic ulcer Disease
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