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359 Cards in this Set
- Front
- Back
Choledocholithiasis
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Common bile duct stones
Sx: Hx colicky pain, sudden onset of severe, unrelenting pain in RUQ ± radiation. Obstructive jaundice w/ pale stools and dark urine. Labs: Leukocytosis, ↑ conjugated/direct bilirubin, ↑ alkaline phosphatase, ↑ GGT. Normal GGT unlikely choledocholithiasis. Imaging: US shows shows ducts >8mm ± stones. ERCP allows dx and tx, (MRCP less invasive no tx) Tx: Fluids, bedrest, anti-emetics analgesics. ERCP c shpincterotomy to remove iimpacted stones acutely, followed by cholecytectomy |
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Biliary Colic
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Pain due to gallbladder contraction, usually 1-2 hours postrpandial in response to a fatty meal. Increased pressure form forcing stone against th ebile duct opening. Stomes fall back away as ballbladder relaxes. most accurate predictor of gallstone diesease.
Sx: epigastric/RUQ "intense dull pressure" radiating to right shoulder. No peritoneal signs. >6 hours = cholecystitis (a different monster) Lab Results: Normal Dx: Ultrasound Tx: Elective Outpatient Laproscopic Cholecystectomy. 2 week recovery if laproscopic. Most common complication = Bile Duct Injury |
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Cholecystitis
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Inflammation of the gallbladder
Sx: Severe, steady RUQ/epigastric pain radiating ot right shoulder >6 hours. Positive Murphey's Sign. [Sick, Febrile, Guarding] Dx: combination of Hx, PE, lab and imaging (US, HIDA) Lab: leukocytosis, Liver fnx minimally elevated Tx: NPO, IV Fluids, analgesics (diclofenac non-narcotic), broad spectrum antibiotics, NG tube if vomitting and surgery w/in 72 h of attack Complciations: Gengrene most common → Perforation → Cholecytoenteric fistula; mechanical ileus, crepitus from clostridia "Emphysematous cholecystitis" |
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Cholecystectaisa
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Dilation of the gallbladder
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When do you hospitalize someone for Biliary Colic?
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Intractible Pain, vomitting, dehydration
Evidence of more advanced condition. |
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Most accurate predictor of gallstone disease
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Biliary Colic: Pain due to gallbladder contraction, usually in response to a fatty meal. Increased pressure form forcing stone against th ebile duct opening. Stomes fall back away as ballbladder relaxes.
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Stones in the gallbladder
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Cholelithiasis
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Inflammation of the Gallbladder
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Cholecystitis
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Dilation of the gallbladder
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Cholecystectasia
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Stones in the Common Bile Duct
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CHoledocholithiasis
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Cholangitis
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Obstrx (Stones, CA, Strixr) → Stasis → E coli, Klebsiella, Enterobacter Infx
Charcots Triad: Fever (Infxn), RUQ Pain Jaundice Raynauds Pentad: Triad + Mental Status Changes and Hypotension Tests: Leukocytosis w/ left shift, elevated alkaloine phosphates, GGT and direct bilirubin. Imaging: US = common bile duct dilation and stones. CT w/ IV contrast or MRCP to determine level of obstrx Tx: Immediate ERCP w/ sphincterotomy, [Blood Cultures, indwelling pain for decompression, antibiotics] |
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Inflmmation/infxn of biliary tree
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Cholangitis
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Primary Sclerosing Cholangitis
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Extensive fibrosis of the extra or intra-hepatic bile ducts; frequently seen with ulcerative colitis; presents with recurrent or persistent obstructive jaundice.
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HIDA
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isotope labelled hepatobiliary imaging technique
injected dye will be sequestered in gallbladder (if not = Liver dysfnx) give cholecystokinin (CCK) to induce contraction Gallbladder dyskinesia is anejection fraction <40% (reduced) |
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Gallbladder dyskinesia
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Poor ejection fraction of the gallbladder
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Poor ejection fraction of the gallbladder
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Gallbladder dyskinesia
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Gallstone ileus
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small intestinal obstruction due to a large stone that erodes through the gallbladder wall into the duodenum, producing a cholecytoenteric fistula and then obstructing the small bowel.
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Interqual Criteria for Admission, Abdominal Pain
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1+ of:
-Amylase >500 -Lipase >5x nomral\ -Mental Status Change -Diverticulitis or Pancreatitis on -X ray -102+ fever AND >15k WBC -Protracted vomitting |
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Asymptomatic Cholelithiasis
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Cholesterol insoluble in water and requires Bile Salts and Lecithin to emulsify. Insufficient bile acids and lecithin causes precipitation.
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Weight as a risk factor for gallstones
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BMI >30 ↑ cholesterol secretion
rapid weight loss >3.3lbs/wk also a risk factor (reduced bile acid/lecithin prodxn?) prolonged fasting 5+d leads to biliary "sludge" resolved w/ refeeding |
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Is there a genetic predisposition to gallstones
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Pima Indians most at risk
Native Americans, Hispanics, Caucasians 1st degree relative a risk factor |
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Is gender a risk factor for gallstones?
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Yes: female, estrogens enhance secretion of cholesterol into bile. progesterone slows gallbladder emptying.
estrogens and hormone replacement therapy are risk factors |
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Metabolic Risk Factors for Gallstones
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Hypertriglyceridemia↑ cholesterol synth
Diabetes produces hypertriglyceridemia, also neuropathy reduces motility |
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GI conditions as a Risk Factor for Gallstones
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Ileal Resction or Chrones disease:
1/3 of all pts with terminal ileum disruption have decreased bile salt resorption Cirrhosis pts have reduced synthesis of bile salts. |
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OMM Considerations with gallstones
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Spinal Cord injuries may reduce gallbladder motility
Diabetic neuropathy as well. |
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The most at risk gallstone pt
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Aging obese cirrhotic diabetic pregnant Pima Indian woman who has stopped eating to loose weight w/ spinal cord injury and malabsoprtion in the terminal ileum who is currently taking drugs like clofibrate, octerotide, or ceftriaxone.
(5 F's: Fat, Forty , Fertile Flatulent, Female) |
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Drugs which increase risk of gallstones
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clofibrate, octeotide, ceftriaxone
binds calcium and precipitates out of bile Aspirin and NSAIDs may be protective because of anti-inflammatory actions |
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Preventing gallstones
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Low CHO, low fat, high fiber diet, physical activity and coffee all appear to be protective.
Ascorbic Acid has been shown protective in women. Aspirin/NSAIDS may also be protective (anti-inflammatory) |
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The Five F's of Gallstones
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Fat, Forty, Fertile, Flatulent, Female
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Obese 43 yo female with flatus, LMP 1 week ago
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The 5 F's of Gallstone Risk: Fat, Forty, Fertile, Flatulent, Female
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The majority of gallstones in adults are which type?
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Cholesterol Stones: will produce one single stone.
Will not show up on a plain film |
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Gallstones on an X ray
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Cholesterol stones (majoirty of stones in adults) will not show up
Pigment stones (Calcium biolirubinate, majority of stones in children, esp w/ hemolytic anemias like sickle cell) will |
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The majority of gallstones in children are which type?
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esp w/ hemolytic anemias like sickle cell Pigment stones: Calcium bilirubinate. Usuallly multiple, will show up on plain film.
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Which gallstone type is usually found as multiple stones
Which gallstone type is usually found as a single stone |
Usually find multiple pigment stones: calcium bilirubinate, majority of stones in children esp w/ hemolytic anemias like sickle cell, will show up on plain film
Usually find solitary Cholesterol stones, majority of stones in adults, will not show up on plain film |
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Cholesterol Stones
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most common cause of gallstones in adults; will produce one single stone, will not show up on a plain film
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Pigment Stones
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Pigment stones (Calcium biolirubinate, majority of stones in children, esp w/ hemolytic anemias like sickle cell) will show up on X ray
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"mixed" type gallstones
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a mixture of cholesterol, pigment, Ca2+ and phosphate. common in obese pts and those on a calorie rich CHO rich diet
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Endoscopic Ultrasound
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A diagnostic procedure used as a follow up to negative ultrasound for suspected cholelithiasis.
Pass scope into stomach Advantages: more sensitive than skin US, able to exclude PUD |
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Biliary Colic Abnormal Lab Findings
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Excludes Uncomplicated Cholelithiasis: should be normal.
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Oral Bile Acids
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Ursodiol, for dissolving gallstones, best for small cholesterol stones
legnthy procedure, 30% success rate and 50% recurrence limited to pts with comorbid condition which prevents operation and those which do not want surgery. Used prophylactically in pts who have bariatric surgery to prevent dvlp 2nd to rapid weight loss |
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Ursodiol
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Oral Bile Acids, for dissolving gallstones, best for small cholesterol stones
legnthy procedure, 30% success rate and 50% recurrence limited to pts with comorbid condition which prevents operation and those which do not want surgery. Used prophylactically in pts who have bariatric surgery to prevent dvlp 2nd to rapid weight loss |
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Chronic Cholecystitis
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Thickening and fibrosis of gallbladder from long-standing cholelithiasis
histopathologic dx, not clinically relevant |
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ERCP
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Endoscopic Retrograde Cholangiopancreatography
best way to Dx/Tx choledocholithiasis/Cholangitis: permits simultanous stone extraction and stent implacement usually a simultanous sphincterotomy (cut sphincter of Oddi muscles) w/ electrocautery risk of pancreatitis, so best to make non-invasive Dx w/ MRCP Magnetic Resonance Cholangiopancreatography |
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MRCP
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Magnetic Resonance Cholangiopancreatography
Non-invasive imaging preferred way to Dx choledocholithiasis (risk of pancreatitis with ERCP Endoscopic Retrograde Cholangiopancreatography) |
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Complications of Acute Cholecystitis
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Gengrene most common → Perforation → Cholecytoenteric fistula
Gallstone illeus (from mechanical obstrx) Emphysematous cholecystitis: crepitus from gas producing chlostridial infxn |
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Charcots Triad
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Cholangitis: Bile Tree Infxn
Charcots Triad: Fever (Infxn), RUQ Pain Jaundice Raynauds Pentad: Triad + Mental Status Changes and Hypotension Obstrx (Stones, CA, Strixr) → Stasis → E coli, Klebsiella, Enterobacter Infx Tests: Leukocytosis w/ left shift, elevated alkaloine phosphates, GGT and direct bilirubin. Imaging: US = common bile duct dilation and stones. CT w/ IV contrast or MRCP to determine level of obstrx Tx: Immediate ERCP w/ sphincterotomy, [Blood Cultures, indwelling pain for decompression, antibiotics] |
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Raynaud's Pentad
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Cholangitis
Charcots Triad: Fever (Infxn), RUQ Pain Jaundice Raynauds Pentad: Triad + Mental Status Changes and Hypotension Obstrx (Stones, CA, Strixr) → Stasis → E coli, Klebsiella, Enterobacter Infx Tests: Leukocytosis w/ left shift, elevated alkaloine phosphates, GGT and direct bilirubin. Imaging: US = common bile duct dilation and stones. CT w/ IV contrast or MRCP to determine level of obstrx Tx: Immediate ERCP w/ sphincterotomy, [Blood Cultures, indwelling pain for decompression, antibiotics] |
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Fever, RUQ Pain, Jaundice
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Charcot's Triad: Cholangitis
[Raynauds Pentad: Triad + Mental Status Changes and Hypotension] Obstrx (Stones, CA, Strixr) → Stasis → E coli, Klebsiella, Enterobacter Infx Tests: Leukocytosis w/ left shift, elevated alkaloine phosphates, GGT and direct bilirubin. Imaging: US = common bile duct dilation and stones. CT w/ IV contrast or MRCP to determine level of obstrx Tx: Immediate ERCP w/ sphincterotomy, [Blood Cultures, indwelling pain for decompression, antibiotics] |
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Gallstone Pancreatitis
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Gallstone in common bile duct impacts in duodenal papilla
Tx; immeidate ERCP with sphincterotomy gallbladder should be removed, but important to let pancreatitis resolve before surgery |
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Porcelain Gallbladder
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X ray finding, raises concern for CA
indication for removal first opportunity |
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epigastric/RUQ "intense dull pressure" radiating to right shoulder for 3 hours. No peritoneal signs.
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Biliary Colic: Pain due to gallbladder contraction, usually 1-2 hours postrpandial in response to a fatty meal. Increased pressure form forcing stone against th ebile duct opening. Stomes fall back away as ballbladder relaxes. most accurate predictor of gallstone disease.
>6 hours = cholecystitis (a different monster) Lab Results: Normal Dx: Ultrasound Tx: Elective Outpatient Laproscopic Cholecystectomy. 2 week recovery if laproscopic. Most common complication = Bile Duct Injury |
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Sudden onset of severe, unrelenting pain in RUQ ± radiation. Jaundice, pale stools, dark urine
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Choledocholithiasis: Common bile duct stones
Labs: Leukocytosis, ↑ conjugated/direct bilirubin, ↑ alkaline phosphatase, ↑ GGT. Normal GGT unlikely choledocholithiasis. Imaging: US shows shows ducts >8mm ± stones. ERCP allows dx and tx, (MRCP less invasive no tx) Tx: Fluids, bedrest, anti-emetics analgesics. ERCP c shpincterotomy to remove iimpacted stones acutely, followed by cholecytectomy |
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Severe, steady RUQ/epigastric pain radiating ot right shoulder >6 hours. Positive Murphey's Sign.
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Cholecystitis: Inflammation of the gallbladder
Sx: [Front, Sick, Febrile, Guarding] Dx: combination of Hx, PE, lab and imaging (US, HIDA) Lab: leukocytosis, Liver fnx minimally elevated Tx: NPO, IV Fluids, analgesics (diclofenac non-narcotic), broad spectrum antibiotics, NG tube if vomitting and surgery w/in 72 h of attack Complciations: Gengrene most common → Perforation → Cholecytoenteric fistula; mechanical ileus, crepitus from clostridia "Emphysematous cholecystitis" |
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RUQ/Epigastric Pain, Nausea, & Vomitting, Elevated Amlyase and Lipase
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Gallstone Pancreatitis: Gallstone in common bile duct impacts in duodenal papilla
Tx; immeidate ERCP with sphincterotomy gallbladder should be removed, but important to let pancreatitis resolve before surgery |
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DDx of Gallstone diseases by Labs
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Normal: Gallstones, Chornic Cholecystitis
Acute Cholecystitis: Leukocytosis Choledocholithiaisis: Leukocytosis, ↑ conjugated/direct bilirubin, ↑ alkaline phosphatase, ↑ GGT. Cholangitis: Leukocytosis, ↑ conjugated/direct bilirubin, ↑ alkaline phosphatase, ↑ GGT., and Leukocytosis w/ left shift Gallstone pancreatitis: elevated lipase/amylase |
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AST/ALT 1.5x normal
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Milld ALT & AST Elevation
Mild <3x normal Moderate 3-20x normal Severe >20x normal |
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AST/ALT 2.5x normal
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Milld ALT & AST Elevation
Mild <3x normal Moderate 3-20x normal Severe >20x normal |
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AST/ALT 4x normal
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Moderate ALT & AST Elevation
↑↑↑ AST/ALT ±↑AP/GGTP = hepatoceullary injury Mild <3x normal Moderate 3-20x normal Severe >20x normal |
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AST/ALT 8x normal
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Moderate ALT & AST Elevation
↑↑↑ AST/ALT ±↑AP/GGTP = hepatoceullary injury Mild <3x normal Moderate 3-20x normal Severe >20x normal |
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AST/ALT 12x normal
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Moderate ALT & AST Elevation
↑↑↑ AST/ALT ±↑AP/GGTP = hepatoceullary injury Mild <3x normal Moderate 3-20x normal Severe >20x normal |
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AST/ALT 21x normal
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Severe ALT & AST Elevation
↑↑↑ AST/ALT ±↑AP/GGTP = hepatoceullary injury Mild <3x normal Moderate 3-20x normal Severe >20x normal |
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Alkaline Phosphastase 1.5x normal
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Mild Elevation
↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease Mild <2x normal Moderate 2-5x normal Severe >8x normal |
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Alkaline Phosphastase 2.5x normal
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Moderate Elevation
↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease Mild <2x normal Moderate 2-5x normal Severe >8x normal |
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Alkaline Phosphastase 4x normal
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Moderate Elevation
↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease Mild <2x normal Moderate 2-5x normal Severe >8x normal |
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Alkaline Phosphastase 8x normal
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Moderate Elevation
↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease Mild <2x normal Moderate 2-5x normal Severe >8x normal |
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Gamma glutamyl transpeptidase 1.5x Normal
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Mild Elevation
↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease Mild <3x normal Moderate 3-10x normal Severe >10x normal |
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Gamma glutamyl transpeptidase 2.5x Normal
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Mild Elevation
↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease Mild <3x normal Moderate 3-10x normal Severe >10x normal |
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Gamma glutamyl transpeptidase 4x Normal
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Moderate Elevation
↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease Mild <3x normal Moderate 3-10x normal Severe >10x normal |
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Gamma glutamyl transpeptidase 8x Normal
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Moderate Elevation
↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease Mild <3x normal Moderate 3-10x normal Severe >10x normal |
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Gamma glutamyl transpeptidase 12x Normal
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Severe Elevation
↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease Mild <3x normal Moderate 3-10x normal Severe >10x normal |
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Increased Bilirubin
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Conjugated alone = infiltrative/obstrx liver disease
↑↑↑ AP/GGTP ±↑AST/ALT Unconjugated alone = increased production, hemolysis, ineffective erythropoesis, resportion of hematoma or muscle injury Conjugated + Unconguated = Hepatocellular Injury ↑↑↑ AST/ALT ±↑AP/GGTP |
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Increased GGTP
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transports AA's across lipid membrane
not specific for Liver unless combined w/ ↑AP then sensitive indicator of obstructive/infiltrative liver disease |
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Elevated Prothrombin Time
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All but Factor VIII produced by Liver
DDx: Vitamin K deficiency, Warfarin, DIC, Rare Congenital defects, LIVER DISEASE Either hepatocellular injury: vitamin K unresponsive or Obstructive/Infiltrative → Cholestasis → vitamin K malabsorption, vitamin K responsive |
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Decreased Albumin
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Approx 10g/day synthed, Half-life 20 days,
reflects variety of hepatic factors: nutrition, volume, vascular integrity, catabolism, hormonal factors, blood loss insensitive marker for hepatic fnx ↓ albumin expected more in hepatocelluar than obstrx/infiltrative liver dysfnx |
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Cholestasic Liver Disease
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↑↑↑ AP/GGTP ±↑AST/ALT
Causes: Drugs, Viral, Toxins, Tumors, stones, strictures, etc Sx: Jaundice, Abdominal Pain, Fever, Malabsorption ↑conjugated bilirubin (seeping back into blood) ↑ PT, vitamin K reponsive (malabsportion) ±↑cholesterol (indicates chronic) same as Infiltrative |
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Infiltrative Liver Disease
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↑↑↑ AP/GGTP ±↑AST/ALT
Causes: accumulation of abnormal tissue: fat, tumor, granulomas, cysts, abscesses, amyloid, etc. Sx: RUQ pain, hepatomegaly, weight loss, fever ↑conjugated bilirubin (seeping back into blood) ↑ PT, vitamin K reponsive (malabsportion) ±↑cholesterol (indicates chronic) Same as Cholestatic |
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Hepatocellular Liver Disease
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Viral hepatitis, drugs, toxins, autoimmune, ischemic etc
Sx: Anorexia, Nausea/Vomiting, RUQ pain, Jaundice, Bleeding, Coma ↑↑↑ AST/ALT ±↑GGT ↑unconjugated & conjugated bilirubin (, not being converted, what is converted seeping back into blood) ↑ PT, vitamin K unreponsive (problem with synthesis) ↓ albumin (synth) ±↓cholesterol (synth indicates chronic) |
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Abnormal Liver Fnx +
Sx: Jaundice, Abdominal Pain, Fever, Malabsorption |
Cholestatic Liver disease (obstructive),
Causes: Drugs, Viral, Toxins, Tumors, stones, strictures, etc similar labs as Infiltrative liver disease ↑↑↑ AP/GGTP ±↑AST/ALT ↑conjugated bilirubin (seeping back into blood) ↑ PT, vitamin K reponsive (malabsportion) ±↑cholesterol (indicates chronic) |
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Abnormal Liver Fnx +
Sx: Anorexia, Nausea/Vomiting, RUQ pain, Jaundice |
Hepatocellular Liver Disease: Viral hepatitis, drugs, toxins, autoimmune, ischemic etc
↑↑↑ AST/ALT ±↑GGT ↑unconjugated & conjugated bilirubin (, not being converted, what is converted seeping back into blood) ↑ PT, vitamin K unreponsive (problem with synthesis) ↓ albumin (synth) ±↓cholesterol (synth indicates chronic) |
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Abnormal Liver Fnx +
Sx: RUQ pain, hepatomegaly, weight loss, fever |
Infiltrative Liver Disease: accumulation of abnormal tissue: fat, tumor, granulomas, cysts, abscesses, amyloid, etc.
similar labs as obstructive liver disease↑↑↑ AP/GGTP ±↑AST/ALT ↑conjugated bilirubin (seeping back into blood) ↑ PT, vitamin K reponsive (malabsportion) ±↑cholesterol (indicates chronic) |
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Marked Elevation of Transaminaes
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>2000
drug, toxin, ischemic or acute viral injury acute obstx choledocholithiasis, autoimmune [more on this in slides, doubt he will test it] |
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Moderate Persistent Elevation of Transaminases
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250-1000
any type of liver disease, viral and drug induced most common [more on this in slides, doubt he will test it] |
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Persistent Mild Elevation of Transaminases
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<250
Any liver disease characterized by modest hepatic inflam and necrosis Most commonly: obese diabetic hyperlipidemic female: non-EtOHlic fatty liver infiltration [more on this in slides, doubt he will test it] |
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% of Pts who abuse alcohol who will develop progressive liver injury
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the majority of pts who absue EtOH will NOT dvlp progressive liver injury
90% will dvlop Alcoholic fatty liver, with elevated AST & ALT at a ratio of AST: ALT >2:1 of those ~30% will dvlp a progressive condition, alcoholic hepatitis/alcoholic cirrhosis (w/ some overlap) |
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aSx Enlarged Liver
↑↑AST ↑ALT AST:ALT >2:1 |
alcoholic fatty liver
will occur in 90% of alcohol abusers not itself a progressive condition, improves with abstinence |
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aSx Enlarged Liver
↑AST ↑ALT AST<ALT |
Non-alcoholic fatty liver
Causes: Obesity, massive weight loss, total parenteral nutrition, diabetes, hypercholesterol/hyperTAGemia can result in steatohepatitis and may evolve into cirrhosis |
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Anoexia, modest fever, hepatomegaly and tenderness, jaundice, dark urine, light stools
↑AST, ↑ALT, both <200 ↑GGT ↑↑bilirubin |
characteristic presentation of alcoholic hepatitis
hepatic bruit in severe cases often coexistant with signs of cirrhosis/chornic disease ~50% mortality, may resolve with abstinence |
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Alcoholic Hepatitis
Sx, Labs, Px |
Sx: Anoexia, modest fever, hepatomegaly and tenderness, jaundice, dark urine, light stools, hepatic bruit in severe cases
often coexistant with signs of cirrhosis/chornic disease ↑AST, ↑ALT both <200 ↑GGT ↑↑bilirubin ~50% mortality, may resolve with abstinence |
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Causes of Cirrhosis
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Most commonly Primary biliary cirrhosis, autoimmune disease of middle aged women after having children
Else: alcohol, hepatitis C>B>>others, [non-EtOH steatohepatitis, metabolic liver diseasses, primary sclerosing cholangitis |
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Alcoholic Cirrhosis
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EtOH prevents oxidation of hepatic FA's fnx as irritant cause chronic inflammation → pericentral fibrosis (reversible) →macronodular fibrosis → micronodular fibrosis: hepatocytes suffocated
continued EtOH 30% 5 year survival discontinued EtOH 60% 5 year survival |
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Findings in Cirrhosis
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Temproal wasting
spider angioma jaundice firm nodular liver edge palpable spleen tip ascites heme positive stool asterixis confusion |
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Complications of cirrhosis
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GI bleed/protal hypertension (esophageal varices)
ascites/spontaneous bacterial peritonitis bleed into GI→ digest protein into amonia → encephalopathy infxns |
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Course of Cirrhosis
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NO elective surgery
50% mortality, correlates to severity index Child-Pugh Classl Liver transplants allocated based on MELD score, NELDNa also includes calcliation factoring possible hyponatreamia |
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tired itchy people RUQ punepxlained anorexia
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cirrhosis (from primary biliary cirrhosis?)
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Asterixis
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cirrhosis: you ask them to hold their arms out and hands back and the hands shudder
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Cirrhosis
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these aren't aren't that great
go back and review slides |
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Kussmaul
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Rapid Deep Sighing Respirations. Compensatory mechanism for metabolic acidosis.
present in DKA not HHS (no acidosis) |
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Rapid Deep Breaths with Altered Mental Status
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Kussmaul breathing: compensatory for metabolic acidosis
present in DKA not HHS (no acidosis) |
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Alcohol and Blood Sugar
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Alcohol predisposes to dvlpt of hypoglycemia because it inhibits glycogen storage and glucoenogenesis
|
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Abnormal Blood Sugar State characterized by tachycardia, diaphoresis, and anxiety
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early hypoglycemia, due to SNS activation
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Early signs of hypoglycemia
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SNS mediated tachycardia, diarphoresis, anxiety
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Complications of hypoglycemia
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Psychotic behavior and Seizures, coma may dvlp without warning symptoms
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Diabetic Ketoacidosis
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hyperglycemia, ketonemia, acidemia;
caused by absence of insulin and excess of anti-insulin glucagon, growht hormone, caatchecholamiens, cortisol → dehydration, shock and death |
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hyperosmolar hyperglycemic state
|
aka hyperosmolar coma (though coma only 1/4)
"an old, old person, probably DMT2 w/ IR" lack of insulin + hyperglycemia w/o ketosis brain swelling → abnormal respiration mortality is high from MI/CVA |
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What are the three major metabolic abnormalities considered in an IDDM patient with altered mental status?
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Hypoglycemia: ↓ blood sugar
DKA: hyperglycemia, ketonemia, acidemia Hyperosmolar Hyperglycemic State: ↓ insulin, ↑ blood sugar, w/o ketosis |
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What are the initial steps in the approach to a diabetic patient with altered mental status?
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-Airway- support rarely req'd, should be assessed first
-O2: given to any pt with AMS -Circulation: Hypotension → 2 IV's of isotonic crystaloid (crappy diabetic veins = 2 lines) -Blood: specimines for glucose -Dextrose: if not hyperglycemic -Monitor: looking at T wave for [K+] problems, check for ischemia as source of metabolic stress -Naoloxone to avoid missing an occult opioid intoxiciation -ABG's, VBG's to assess ° of acidosis -Urine: glucose, ketone, UA looking for dehydration and infx -Coma scale: to look for improvement or deterioration -Flow Sheet: serial recordings of lab/I/O/Mental Status findings |
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hyperglycemia, no insulin w/o ketosis
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hyperglycemic hyperosmotic state, aka hyperosmolar coma (though coma only 1/4)
"an old, old person, probably DMT2 w/ IR" brain swelling → abnormal respiration mortality is high from MI/CVA |
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How often is airway management required in the diabetic patient with metabolic complications?
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Usually not required should give O2 to anyone with altered mental status
|
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What are the areas of focus in the history of a diabetic patient presenting with altered mental status?
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Prior glycemic problems, & freq; known complications: neuropathy, nephropathy, vascular disease?
Rx: esp insulin/hypoglycemic agents, beta-blockers: mask the SNS warning signs of hypoglycemia, Mental Status altering drugs ↑/↓ in food intake, exercise, stress classical history: polyruria, polyphagia, polydipsia, actually present in <50% of DKA usual mental status? (HHS "90 yo comes in cookoo as a loon--is he normally like that?") GI complaints: DKA metabolic acidosis → severe abodminal pain |
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How often is the classical triad of polydipsia, polyuria and polyphagia present in DKA?
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<half
|
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What are some of the common MISDIAGNOSES made when the real diagnosis is DKA?
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metabolic acidosis → severe abdominal pain
misdx'd as appendicitis/gastroenteritis |
|
Know the flow chart of approach to treatment/diagnosis in the patient with altered mental status.
|
? Blood Sugar Emergencies Lecture
|
|
[K+] in DKA
|
falsely normal or high
will fall precipitously w/ treatment EKG: if T is normal or w/ U wave → supplement [K+] Tall peaked T wave consistent with hyperkalemia → withhold K treatment |
|
EKG of DKA
|
first, looking for a silent MI
[K] usually falsely normal or high will fall precipitously w/ treatment EKG: if T is normal or w/ U wave → supplement [K+] Tall peaked T wave consistent with hyperkalemia → withhold K treatment |
|
polyruria, polyphagia, polydipsia in someone on an insulin regulating regiment
|
classic triad (occurs <50%) in pre-DKA
|
|
To what floor would you admit a DKA
|
"there is no other place for this person to be other than the ICU"
|
|
HEENT in DKA
|
trauma - may be 1° or 2° to DKA (as a stressor or a fall from AMS)
malignant otitis externa rapidly progressive meningitis a consideration in any AMS |
|
Abdomen in DKA
|
hypokalemia may cause extreme pain, misdx'd as acute abdomen
e⁻lyte distrubances → ↓ bowel sounds |
|
What is a commonly used definition of DKA (laboratory values)?
|
Glucose in excess of 300, usually 500-800.
Ketonemia with serum ketones present >1:2 Acidemia with pH < 7.30 or bicarbonate < 15 mEq/liter, ACIDOSIS MAY BE PROFOUND! |
|
Discuss the importance of the CBC in the diabetic patient with altered mental status; what do changes indicate?
|
White count may be up to 20k w/o sepsis, this is from demargination 2° to stress
Left shift suggestive of infx hematocrit will be elevated 2° to dehydration |
|
Discuss the importance of electrolytes in the diabetic patient with altered mental status, what do changes indicate?
|
Na⁺ deficit will appear on e⁻lyte panel: this is falsely lowered due to hyperglycemia "you look like a fool when you admit someone with DKA and freak out about low sodium"
K⁺ defcits average 5mEg/kg, this will be fasely normal due to compensatory mechanism for acidosis and will fall precipitously with treatment Serum Mg & P often abnormal &will rapidly ↨ w/ Tx |
|
What is a common sodium deficit in a patient with DKA?
|
6mEq/kg
this is falsely lowered due to hyperglycemia "you look like a fool when you admit someone with DKA and freak out about low sodium" |
|
How is renal function testing results changed in diabetics with altered mental status?
|
BUN:Cr >10:1 from dehydration
(Cr freely filtered, ~0% secreted/resorbed, ↑ BUN resportion w/ ↓ GFR) serum creatinine may be elevated due to ketonemia |
|
Why might measured ketones be low or normal in a patient with true DKA?
|
The serum nitroprusside rxn only measures acetone and acetate; the main ketone of DKA is beta-hydroxybutyrate.
|
|
How do you calculate serum osmolality and what is normal, and what is abnormal?
|
2(Na⁺) + glucose/18 + BUN/2.8
Normal is 290 ± 5 >320 = significant hyperosmolality |
|
How might the urinalysis be affected in a diabetic patient with altered mental status?
|
glycosuria and ketonuria.
maybe proteinuria and hyaline casts from dehydration WBC = infx |
|
What are the seven principles of management of a patient with altered mental status?
|
1 Restore fluid volume
2 normalize blood glucose 3 clear ketosis 4 correct acidosis 5 correct & maintaine e⁻lytes 6 gradually restore equilibrium to serum osmolality 7 closely monitor clinical & labs |
|
Discuss the management of hypoglycemia.
|
hypoglycemia from oral hypoglycemic agents req's admission because λ so long
if awake & wont aspirate: oral glucose followed by protein meal Unable: IV glucose or IM glucagon → Gng if glycogen stores available |
|
What is the MOST IMPORTANT part of therapy in DKA, and how is it managed initially?
|
Fluid administration, average of 6L deficit
if hemodynamically unstable 2 L of 0.9 NaCl more stable 1 bolus over 30 min + 1 drip over ~2 hours, reassess |
|
How much might the serum glucose level fall in DKA with appropriate fluid management alone in the first hour?
|
normal saline alone up to 20% decrease
goal is to decrease 100mg/h going too fast → cerebral edema & hypoglycemia |
|
What is the goal of decreasing the glucose level in DKA (i.e. rate of decrease/hour) what are the consequences of going too fast?
|
goal is to decrease 100mg/h
going too fast → cerebral edema (Δosmolality) & hypoglycemia |
|
In DKA, what therapy is REQUIRED to clear ketones and free fatty acids?
|
Fluids & Insulin
Insluin may be the more important one to convince cells they're not starving |
|
When is bicarbonate therapy used in the treatment of DKA? What untoward events are associated with bicarbonate therapy, thus making the treatment of DKA patients with bicarbonate controversial?
|
Controversial Tx at Best, may cause severe cerebral edema; only given to severly acidemic pts pH<7.0 or Bicarb <10
"I haven't given it since residency, I would rather them be acidotic longer and treat the ultimate cause." |
|
When and how is potassium therapy regulated in DKA?
|
K⁺ administered to pt w/ urinary output and no peaked T waves on EKG
often added in 2nd Liter as KP since P will be low as well changed ourly based on e⁻lyte values |
|
What are the components of close clinical and laboratory monitoring in DKA?
|
Hourly labs of glucose, e⁻lytes, oslmolarity, & ABG's
all recorded on flow sheet |
|
What is the fluid management of a patient in hyperosmolar hyperglycemic state?
|
Normal saline administered until stability acheived then switched to 0.45 NaCL
|
|
How much might the serum glucose level fall in hyperosmolar hyperglycemic state (HHS) with appropriate fluid management alone in the first hour?
|
may fall up to 30% in first hour alone just from fluids
|
|
When is potassium therapy begun in HHS?
|
as soon as urinary output is obtained and true hyperkalemia is ruled out
|
|
How is close clinical and laboratory monitoring different in HHS from DKA?
|
Flow sheets of hourly lab results of glucose, e⁻lytes osmolality (ABG's)
disease state often correlated with serious co-existing problems which need to be adressed |
|
Why is glucose sometimes given empirically to diabetic patients presenting with altered mental status?
|
It will do no harm even in a hyperglycemic pt
seizures occur in 10% of hypoglycemics |
|
How is disposition potentially different in hypoglycemia patients based on the cause of the hypoglycemia?
|
oral hypoglycemic agents often long acting, so these pts must be admitted
|
|
A discrepancy between laboratory and clinical findings should make the physician consider….
|
other complications
|
|
Hemorrhoids as a source of GI bleeds
|
does not rule out CA
|
|
4 most common causes of upper GI bleeds
|
peptic ulcers
esophagitis/gastritis esophageal varices mallory weiss tears |
|
Esophageal Varices: progression, tx
|
Acute phase: onset of active hemorrhage
latter phase: high risk of recurrence for ~2 mo, usually w/in days only 50% will stop bleeding on their own hemodynamic resuscitation: aggressive w/ IV fluids & blood, 2 large bore IV's (&don't let the nurse trick you into putting in a central line) Complications: aspiration, sepsis, hepatic encephalopathy, renal failure DOC: ocreotide (somatostatin), decreases portal pressure proton pump inhibitor infusion sclerotherapy (injx kills vessels) or variceal band ligation; 20% failure rate → sengstaken blakemore baloon tamponade; |
|
PUD Tx
|
Acid suppression on H2 blockers & proton pump inhibitors
endoscopic tx to find a bleed: injection therapy, thermal coagulation, hemostatic clips, etc surgery for perforation or refractory bleed |
|
Mallory Weiss Tears
|
longitudinal tears in esophagus 2° to wretching; blood loss usually small and self limiting.
|
|
Pathogenesis of Esophagitis/Gastritis
|
NSAIDs, EtOH, CA ChemoTx etc → hemorrhagic &erosive lesions
|
|
Angiodysplasia
|
an AVM wherein blood vessels lack smooth muscle → dilated tortuous submucosal vessels most often cecum/right colon (largest segment = largest wall tensin)
intermittent occlusion → dilation episodic and self limited bleeding of venous origin (as opposed to divertiulitis) |
|
GI bleed or pain. When do you rule out a colon cancer?
|
only after a full colonscopy has been performed
|
|
Where is the colon cancer:
Hematochezia Melena Change in Bowel Habit Iron Deficiency Anemia |
Hematochezia: Left Side
Melena: Right Side Change in Bowel Habit: Left Side Iron Deficiency Anemia: Either |
|
Apple Core Lesion in Colon
|
Cancer via Barium Enema
|
|
Air Fluid Levels in the GI tract
|
obstruction usually surgical adhesion
|
|
Contrast the causes of small bowel versus large bowel obstruction.
|
Small: think adhesions first, then hernias, CA, intussusception, volvulus
Large: most commonly malignancy, then colonic volvulus, diverticular disease. Almost NEVER adhesions. |
|
Colonic volvulus.
who is more likely to get which? |
The colon twists on its mesentery & strangulates; abrupt onset of sx.
cecal from congenital abscence of mesentery: ~50yo at presentation; best treated surgically; sigmoid:old, old person in nursing home, Hx chronic constipation; tx:advancing sigmoidoscope trhough twisted segment to untwist it Contra:gangrene → surgery |
|
SBO Tx
|
NPO
IV hydration Anti-emetics Pain Meds NG Tube- suck ou the air most of the time pts will get better at this point. If not or recurrent: SURGERY |
|
Diverticular disease: pathogenesis, common complications
|
high intralumenal pressure + relative weakness of wall
pressure greatest where lumen narrowest- sigmoid colon complications: -most common = inflammation- Diverticulitis generally left sided 2° to fecal inspission & bacterial proliferation; perforation generally within mesentery or limited by omentum or adjacent strx; free perforation may occur -arterial bleeding in 10%, painless generally right-sided & massive but self-limited |
|
Tx Divertiulitis
|
Mainstay is antibiotics
admit if worried about complications drain any abscess repeated episodes: remove some colon |
|
Anal Abscess
|
infected anal glands 2° to obstrx
~10 glands circumferentially w/in anal canal at dentate line may look like a giant zit w/o whitehead; may only be pain; Diagnostic Method: CT with contrast, if you have 1 abscess you may have several Tx: Surgical Drainage immediately. Antibiotics not indicated without cellulitis. ("Drainage, Drainage, Drainage") Complications: 50% dvlp anus→skin fistula w/w/o drainage |
|
Anal fistula
|
occurs 505 of the time w/ perianal absces whether you drain it or not.
may be associated with crohn's, UC, or TB anus → skin lined with epithlium and granulation tissue persistent blood stained malodorous discharged for the duration; commonly blocked → bouts of inflammation and recurrent abscesses the only tx is surgical excision |
|
Rectal Prolapse
|
Type I: false procidentia, partial or mucosal prolapse. Usually <2 cm long produces radial folds at jnx w/ anal skin
Type II: true procidentia, complete prolappse:full thickness extrusion of rectal wall, chracterized by concentric folds in prolapsed mucosa Tx: manual reduction complications: irritation, ulceration generally painless and in children; 2° to an underlying cause: CF, constipation, parasite |
|
Common causes of blunt abdominal truama:
|
75% MVA (incl pedestrians), 15% blows, 10% falls
worst for solid organs: most often injures kidneys, then spleen & liver Tx: ABCDisability (Mental.Neurologic Status) Expose: remove all clothes despite absence of abdominal pain & hemodynamic stability: abdominal injury in 7% of pts w/ trauma & DISTRACTING injuries and 10% who ONLY PRESENT FOR HEAD INJURY |
|
Diagnostic Workup with BAT
|
Dx: F.A.S.T. US exam, Diagnostic Peritoneal Lavage, CT
Laproscopy if pt persistently hypotensive/losing blood, clear evidence of persistent GI bleeding/pneumoperitoneum/or diaphragmatic rupture, or clear evidence of organ damage |
|
Diagnostic Peritoneal Levage
|
Invasive procedure for peritoneal intraperitoneal hemoorhage
cut a hole in the pt and try to drain for blood. if nothing comes out, hang a bag and let it go in, then drop the bag and let everything flow back into it. |
|
FAST exam for BAT
|
Focused Assesment with Sonography for Trauma
Ultrasound the places where fluid is most likely to accumulate in the abdomen |
|
CT scanning for BAT
|
Expensive, but non invasive
detects both presence and source of hemoperitonum |
|
Esophageal Perforation
|
Usually due to medical instrumentation/paraesophageal surgery
|
|
Boerhaave's syndrome
|
spontaneous perforation of the erpution 2° to ↑ intraesophageal pressure + ↓ intrathoracic pressure causes by straining or vomiting
may be completely spontaneous (no preexisting conditions), though w/ preexisting conditions ↑ mortality generally excruviantingly painful, commonly Hx of EtOH & PUD Dx: suggested on CXR, confirmed with CT or esophageal contrast study (no barium, might get into lungs) Tx: surgery w/in 24h; if healthy just close it, if not healthy, it comes out & they're going to need a PEG tube |
|
Most commonly ingested foreign body
|
coins
|
|
Foreign Body Dx
|
Dx: CXR
flat objects in the esophagus usually orient in coronal plane, best seen on AP projection objects in trachea orient into the sagittal plane, best seen in lateral projection 1/3 of ingested FB's radiolucent, CT is next step Tx: urgent removal if -object is sharp, long and is in esophagus or stomach -airway compromise -disk battery -near complete esophageal obstrx -SSx of inflammation/obstrx low risk & beyond the stomach, watch for FB in stool, follow up XR & removal if not exiting |
|
Child comes in CC cough w/ abrupt onset, no signs of URI
|
high index of suspicion for ingested/inhaled foreign body
|
|
Swallowed Disc Battery
|
emergency
1. conducts electricity → liquifactive necrosis 2. caustic material leakage GI consult immediately |
|
What does green onion sign associated with?
|
obstructiong ureterocele
|
|
Esophageal FB removal
|
Endoscopy- best method
alternatively:foley catheer, magill forceps, bougienage (push it into stomach) surgery for dangerous materials or if signs of peritonitis |
|
should you be worried about UTI's in children?
|
yes you should, because they dont usually get them
|
|
More dangerous to be a drug packer or a stuffer
|
stuffer--the ones who've just done it without planning to avoid getting caught
|
|
Should you be worried about recurrent UTI's in adults?
|
yes- suspect Stasis or obstruction
|
|
Define abortion
|
"expulsion or extraction of an embryo or fetus weighing ≤500g from its mother"
typically corresponds to ≤22 weeks spontaneous or not |
|
What does loss of a psoas shadow mean?
|
retroperitoneal pathology on that side
|
|
Embryo vs Fetus
|
Embryo <10 weeks
Fetus ≤ 0 weeks |
|
What does loss of BOTH psoas shadows mean?
|
ascities
|
|
Different types of abortions
|
Threatened- bleeding through closed cervical os, fetal loss may not occur, VAST majority w/ fetal cardiac activity at 7+ weeks will not abort
Inevitable: dilated cervix, ↑ bleeding, painful uterine contractions. abortion is imminent Missed- in utero death of fetus ≤20th week; ± vaginal bleeding, cervix closed, women notice that early sx of pregnancy (weight gain, nausea) have ended, may retain pregnancy for a long time. Complete- ≤12 weeks, 100% of uterine contents expelled, uterus & cervix return to small, well contracted state. mild-no pain Incomplete- >12 weeks, fetus passed but significant placental tissue retained aka abortion with retained POC products of conception; os open, uterus not well contracted, potential hypovolemic shock; painful contractions Septic |
|
What should you be worried of if the ureter runs more midline, rather than lateral?
|
an obstructing mass
|
|
Define dysfunctional uterine bleeding.
|
Diagnosis of exclusion: no organic dysfnx; probably hormonal in origin (unopposed estrogen, endometrium outgrows its own blood supply and necrotizes)
Tx: iron supplements hormonal therapy: progesterone pelvic rest accurate pad count TIMELY OBGYN (may need histerectomy) Good follow up instrx |
|
Is hydronephorsis ok in pregnancy?
|
yes it i- goes away afterwards
|
|
Causes of spontaneous abortion
|
by far most are caused by strx or chromosomal abnormalities
1° maternal risk factor = age |
|
How do you recognize neovasuclar tumors of the kidneys?
|
look for new branching arteries, and smudging on arteriograms
|
|
Post-menopausal uterine bleeding
|
uterine cancer until proven otherwise
endometrial biopsy |
|
How do you kill neovascular tumors in the kidney?
|
embolize them
|
|
Fibroids
|
may cause dysnfx uterine bleeding
|
|
What is the presentation of renal carcinoma?
|
gross hematuria
vauge upper abdominal pain fatigue, weight loss, anemia (typical caner signs) most are found by chance.. |
|
the most common form of tracheoesophageal fistula
what are the associated defects? |
esophageal atresia with distal tracheoesophageal fistula
the esophagus from the mouth comes to a blind end as the the lower esophagus fistulizes with the trachea associated defects = VACTERL Vertebral anomalies Anal Atresia (Imperforate Anus) Cardiac Anomalies TEF Renal Anomalies Limb Anomalies- polydactyly, absent thumbs, etc |
|
How good is the survival of renal cell carcinoma?
|
pretty danm good until it breaks out of the capsule (stages 1-2)
|
|
single artery umbilical cord
newborn baby drooling with bubbling mucus |
Esophageal Atreisa- this card is not an objective
vulnerable to aspiration pneumonia, first feeding should be delayed until simplest test: place an NG tube via mouth, dx study:CXR w/ tube coiled in the esophageal pouch. no barium, extreme aspiration risk Tx is surgical Complications: dysmotility, GER, etc arising from abnormal esophagus, tracheomalacia (soft trachea that collapses easily) |
|
Where are the common metastasis sites of Renal carcinoma?*
|
to the BONE*
|
|
Pyloric Stenosis
|
HYPOCHLOREMIC METABOLIC ALKALOSIS
& VISIBLE PERISTALTIC WAVES US of pylorus preferred: elongation &^ Thickening barrium shows STRING SIGN [rest not bolded in slides:] First born males begin projectile vomitting ≤1mo massively enlarged stomach from retained food, palpable "olive" hypertorphied pylorus, No bile because proximal to duodenum, jaundice w/ unconjugated hyperbilirubinemia 2° to dehdyration Tx: correct dehydration & alkalosis then surgical pyloromyotomy |
|
What is the best treatment for renal cell carcinoma?
|
take the kidney out
|
|
1 mo old begins projectile vomiting
|
no bile = proximal to duodenum
|
|
What will you automatically have after a 50 pack year hx of smoking?
|
GU cancer
|
|
String Sign
|
Barium Swallow finding for pyloric stenosis
|
|
What is the sign of retroperiotenal fibrosis?
|
medial deviation of mid ureters
|
|
Functional Abdominal Bowel Pain
|
Recurrent abdominal Bowel Pain, peaks ~9 ± 2 year
diagnosis of exclusion after full Hx, PE and Lab Workup no association with meals, no relief with deification most associated with stress and perfectionism: pain in morning prevents school attendance IBS is a subset of FAP w/ Δ stool habitus; constipation ↔ diarrhea; is releived by defication Warning Signs for more serious illnes: vomiting, abnormal labs, fever, bilious emesis, growth failure/delayed puberty, blood in stools/hemetemesis, weight loss/night waking (from pain); Do not over test w/o warning signs tx: break the anxiety cycle by helping child return to normal activities |
|
What are the main causes of retroperiotenal fibrosis?
|
idiopathic
methysergide cancers |
|
IBS
|
IBS is a subset of FAP w/ Δ stool habitus;
diagnosis of exclusion after full Hx, PE and Lab Workup constipation ↔ diarrhea; is releived by defication no association with meals, no relief with deification most associated with stress and perfectionism: pain in morning prevents school attendance Warning Signs for more serious illnes: vomiting, abnormal labs, fever, bilious emesis, growth failure/delayed puberty, blood in stools/hemetemesis, weight loss/night waking (from pain); Do not over test w/o warning signs tx: break the anxiety cycle by helping child return to normal activities; fiber supplenets useful for IBS |
|
why is it important to always retract the foreskin?
|
to look for cancers
|
|
Most common type of intussception
|
terminal ileum protruding into the cecum;
ideopathic <2y >2yo more likely pathological |
|
What are the four indications to insert a foley cath?
|
relieve bladder distension
collect uncontaminated urine monitor urine output bladder tests (cytogram/urodynamics) |
|
classic late finding of intussception
|
currant jelly stool
|
|
what are the three contraindications for foley catheters?
|
blood from urethra or urethral disruption
acute prostatitis Hx of urethral strictures |
|
infant with sudden onset of crampy abdominal pain; knees are drawn up, pallor; cries out every ~15 minutes, refuses feedings
glassy-eyed, lethargic between bouts. bilious vomiting, reduced pain as time goes on |
intussception
less pressure & pain as segmente becomes fatigued Dx & Tx: barium enema; child MUST have adequate fluid resuscitation before radiographic intervention; surgeons like to be present because if reduction is not complete, emergency surgery is required |
|
What is the golden rule of inflating foley cath?
|
dont inflate unless you see urine first
|
|
[Progression of Intussception]
|
mesentery pulled with bowel into intussception: obstructs venous outflow--> edema, weeping fluid & currant jelly stool
|
|
what is the chirstmas tree bladder a sign of?
|
neruogenic bladder
|
|
Tx of Intussception
|
Dx & Tx: barium enema; child MUST have adequate fluid resuscitation before radiographic intervention; surgeons like to be present because if reduction is not complete, emergency surgery is required
|
|
What is the most significant symptom of obstructive prostatic hyperplasia?
|
Nocturia 2-3 times a nigh
|
|
Adverse Reaction to Food
|
any untoward reaction after food ingestion ranging from toxic reaction such as food poisoning to immune/nonimmune reaction
nonimmune eg lactose intolerance |
|
what shape do the ureters make in obstructive benign prostate hyperplasia ?
|
a J shape
|
|
Which types of foods cause IgE mediated reactions
|
90% of IgE mediated reactions caused by [yes this is an objective]:
(top 6 are also the top 6 causes of anaphylaxis) 1. Peanuts 2. Tree Nuts 3. Cow's Milk 4. Eggs 5. Fish 6. Shellfish Sowbean Wheat |
|
What shape does the bladder take on in obstructive benign prostate hyperplasia?
|
trabeculation
|
|
Oral Tolerance
|
immune suppresion against foods we eat
|
|
What is the gold standard treatment for obstructive benign prostate hyperplasia?
|
TURP- transurethral resectoscope prostetomy
|
|
Rank the Frequency of Common Foods which Cause Anaphylaxis in Children
|
1. Peanuts
2. Tree Nuts 3. Milk 4. eggs 5 fish 6 shellfish 7 seeds 8 fruits 9 grains |
|
what is Post TURP syndrome?
|
the irrigation fluids used in TURP have low sodium, so this causes water intoxication in the pt.
N/V/CHF tx diruetics |
|
Distinguish between uncongjuated and conjugated hyperbilirubinema
|
unconjugated: hemolysis, reduced hepatic removal, altered metabolism
conjugated: decreased excretion, disease of biliary tract |
|
When is it best to treat post TURP syndrome?
|
before acute retention occurs
|
|
infant with dark urine or light stools
|
liver disease must be suspected
|
|
What are the less invasive treatments of obstructive benign prostate hyperplasia?
|
Urolume stent
green light laser various ablation techiques |
|
Diagnostic Criteria for GERD
|
there is no official dx criteria
no specific test endoscopy is the procedure of choice therapeutic trial is the test barium swallow- low S/S Esophageal manometry only if surgical candidate 24h ambulatory pH monitor |
|
where are the three common locations for kidney stones?
|
renal pelvis
where it crosses the pelvis going into the bladder |
|
NERD
|
Benign GERD
Non-erosive reflux disease |
|
How common is recurrence of kidney stones?
|
about 50%
|
|
Epidemiology of GERD
|
≥60 million Americans experience heartburn daily
20% of those seeking medical attn have serious complications |
|
What bug causes staghorn stones, or recurrent kidney stones?
|
Proteus
|
|
Atypical Presentation of GERD
|
Hoarseness, Coughing, Sleep Apnea, really anything
|
|
What are the inducations of uroogical intervention with urinary stones?
|
intractable pain
high grade obstruction |
|
Major physiological protective mechanisms against reflux
|
Esophageal Peristasis
Bicarbonate Mucosal integrity- mucosal damage may be 1° to reflux LES competance Gastric Emptying |
|
What is the BEST radiographic technique for diagnosing urolithiasis?
|
unenhanced helical computed tomorpgrahy (CT)
|
|
Diabetic gastroparesis
|
autonomic neuropathy of T2DM
may be 1° cause of GERD |
|
What is the best way to remove simple renal caculi?
|
shock wave lithotripsy
|
|
hiatal hernia & GERD
|
May contribute but "lots of people with hiatal hernias and no GERD, lots of people with GERD and no hernia. They are not one in the same."
|
|
What is the best treatment for complex renal stones?
|
percutaneous nephrostomy
|
|
Complications of GERD
|
20% of pts:
Barrets Ulcer ± bleeding stricture LERD → Laryngocarcinoma |
|
When is ureterocopy the best treatment for small stones?
|
shock wave failes
pregnant pt obese pt is a bleeder |
|
Alarm sx w/ GERD
|
>55 yo
Anemia/+FOBT Dysphagia Respiratory Sx Early satiety/weight loss persistent sx w/ Tx |
|
What are the four types of incontinenece?
|
Stress
Urge (sudden need/loss of bladder control) Overflow (neuro) Mixed |
|
Squamous cell carcinoma of the esophagus
|
2° to smoke & EtOH
more common in women in the proximal 2/3 of esophagus |
|
How many people have stress urinary incontinence?
|
13 million people
|
|
Adenocarcinoma of the esophagus
|
2° to Barrett's
most common in white males in distal 1/3 of the esophagus ↑450% among white men over the last 3 decades |
|
What part of the urinary system is the "zone of continence"?
|
the proximal 2/3rd of urethra and bladder neck
|
|
Initial Approach to GERD
|
1. Smoking Cessation
2. Wt loss 3. Elevated head of the bed 4. no foods/liquids after 6 pm |
|
Tx of GERD, persistent after lifestyle modifications
|
Phase 2: H2 receptor antagonst "I don't think they're worth a damn"-Finch
Phase 3: Proton Pump Inhibitors-- you need H⁺ to absorb Ca²⁺ and Mg²⁺ Phase 4: Surgery Nissen-fundo plication- create a sphincter by wrapping fundus around cardia |
|
What history suggests Stress incontinence
|
multiparous women, pelvic surgery, activity related
|
|
What happens when a GERD pt stops taking proton pump inhibitors
|
gastrin production → H+ prodxn
if you don't have H+ gastrin goes way up if you stop taking H+ pump inhibitors, Sx return with a vengence |
|
What history suggest urge incontinence?
|
UTI, new Rx, hematuria, CVA
|
|
Foods for GERD pts to avoid
|
tomato juice, orange juice, anything with high acidity, spiciness. fat slows emptying. EtOH. peppermint.
|
|
What history suggest overflow incontinence?
|
diabetic, never feels empty, back problems, surgery
|
|
Criteria for Celiac Disease Dx
|
Positive IgA tissue transglutiminase abs
biopsy consistent with celiac disase: villous atrophy Need BOTH for Dx Response to gluten free diet--not an appropriate diagnostic method! |
|
does a cystocele cause incontinence ?
|
nope
|
|
Epidemiology of Celiac Disease
|
~1/100 in European Populations with appropriate genetics HLA DQ2;
the majority that don't have DQ8 |
|
does a cystourethrocele mean incontinence?
|
yes it does
|
|
pathogenesis of celiac disease
|
HLA DQ2 → MHC2 molecule which presents gliaden
produces 2 things: anti-tissue transglutaminase antibodies Cytotoxic cells vs. GI mucosa |
|
What does the marshall test for incontinence do?
|
this looks for failure of the zone of continence
|
|
GI Sx of Celiac
|
Flatulence, Bloating
Malabsorption/Malnutrition Vomiting/Diarrhea |
|
What do young men with ED need a work up for?
|
cardiovascular eval, maybe have severe asymptomatic coronary artery disease
|
|
Non-GI Sx of Celiac
|
D: rickets, osteomalacia, osteoporosis
A: night blindness, rash E: peripheral neuropathy, ataxia K: bleeding Iron, Folate/B12: Anemia weight loss 2x mortality risk: SI adenocarcinoma, Enteropathy Associated T cell Lymphoma EATL; risk returns to nomormal after 5 years on gluten-free diet |
|
what test is given before giving viagra?
|
two flights of stairs test
|
|
pruritic herpetiform dermatitis on extensor surfaces
|
an external manifestation of celiac disease
|
|
what is THE BEST treatment for ED?
|
inflatable penile implants- 98% couples satisfaction
|
|
Tx for celiac disease
|
delete the wheat
1 mg of gluten: a piece of bread smaller than a postage stamp → intestinal inflammation |
|
does prostate cancer cause bone mets?
|
NO it does not
|
|
What are the symptoms of prostate cancer?
|
same as obstructive benign prostate hyperplasia
increased PSA velocity, Low% free PSA is bad |
|
Crohn's vs UC
|
See pathology
hematochezia ≈ UV>>Crohn's |
|
What are the signs of bladder cancer?
|
gross hematuria
change in voiding pattern |
|
Bright Red Bloody Dairrhea
non-infectious process |
Probably UC
|
|
how do you treat superficial bladder cancer?
|
tranurethral resection of tumor, with lots of check ups
|
|
Cobblestoning
|
Crohns Disease
|
|
what is the treatment for invasive bladder cancer?
|
radical cystectomy
|
|
Complications of Chron's Disase
|
Sinus tracts → perforation
strictures/obstrx fistua entero-enteric, -vesicle, -cutaneous abscess perianal disease ↑ risk of colon cancer (many of these complications 2° to transmural nature of crohn's, not manifested in UC) |
|
Where does testicular cancer metastasis to?
|
lung, liver, bone
|
|
Natural Hx of Crohn's Disease
|
Crohn's characterized by intermittent exacerbat'ns w/ remissions
Surgery req'd for intractible sx, complciations; but post op recurrences common |
|
What is the most common type of testicular cancer?
|
pure seminoma
|
|
Complications of UC
|
massive hemorrhage
fulminant colitis → toxic megacolon perf/strx CA |
|
What is the treatment for a pure seminoma?
|
xray therapy
|
|
Screening IBD for Colon CA
|
risk does not ↑ for 8 years
more probable with more severe forms of disease need to screen frequently (Crohn's only if colon involved) |
|
what nodes does testes cancer go to first?
|
retroperitoneal lymph nodes
|
|
Extra-GI complications of IBD
|
Uveitis/Episcleritis
Skin- erythema nodosum/pyoderma gangrenosum arthritis enthesitis (tendonal insertions) aphthous ulcers thrombophlebitis 1° Sclerosing colangitis (w/ UC) |
|
Workup for a pt with vaginal bleeding, pelvic pain and a positive pregnancy test
|
Physical Exam: Dilated Os? Blood?
hemoglobin/hematocrit QUANTITATIVE Serum Beta hCG Pelvic US Rh factor Blood Type and Screeen managemetn depends on stability; unstable require OB consult & possible dilation & curettage (D&C) |
|
What are the risk factors for penile cancer?
|
uncircumcised
VD HPV Smoking |
|
hCG
|
≥ 1500-2000 you should be able to see something on transvaginal ultrasound
≥6500 should be visible transabdominally otherwise ectopic |
|
What are the signs of fourniers gangrene?
|
dead/discolored tissue on scrotom
fever/drosiness genital pain and redness odor |
|
What is the Tx for fourniers gangrene?
|
CUT IT ALL OUT
|
|
Most common GI dx
|
IBS: Dx of Exlcusion
|
|
What is the BEST treatment for internal hemorrhoids?
|
rubber band ligation
dont pack the anal canal. |
|
IBS
|
abdominal pain and altered bowel habitus in absence of organic, biochemical, serological, structural causes
Dx of Exclusion 15% of US population, and only 15% seek medial attn improvement with defication onset with Δfreq/form of stool |
|
What is a pilonidal cyst?
|
a cyst or abscess near or in the upper intergluteal cleft- usually has hair and skin debris in it
|
|
IBS colonoscopies
|
CBC c diff
TSH Anti tTGA Routine Chemistries w/o warning sx, routine use of colonoscopy & testing in IBD pt <50 not recommended |
|
who gets pilonidal cysts?
|
hairy butted men- with prolonged sitting
|
|
lost to follow up
|
want <20%
pts lost often have diffierent prognoses, or are suffering adverse otucomes/death, or are doing so well they did not return to clinic. |
|
how do you treat pilonidal cyst
|
BIG time complete excision - and dont close it just let it fill in from the outside
|
|
Relative Risk Reduction
|
(risk w/o tx minus risk w/ tx)/(risk w/o tx)
|
|
what kind of hernia produces bowel perforation without obstruction?
|
richter hernia
|
|
p value
|
the smaller the p value, the more likely there is a systemic difference;
if you want your two test groups to be equal you want a p > 0.05 if you want your treatment to be value you want a p < 0.05 |
|
What is the risk of having anesthesia withing 3 months of an MI?
|
risk of re-infarction
|
|
confidence interval
|
the neighborhood within which the effect likely lies
imagine the number at the extreme high and extreme low, is this still a good number? |
|
what is an acceptable pre-op Hgb in healthy people
|
8gms
|
|
Absolute risk
|
the % of pts in group who had a bad outcome. there is an absolute risk for the control group, there is an absolute risk for the experimental group
|
|
What is Newhoffs law?
|
if you dont get out of bed, you dont get any pain meds
|
|
Absolute risk reduction
|
absolute risk of control group minus absolute risk of experimental group
|
|
what do hiccups indicate post surgery?
|
that its too early for oral intake of foods
|
|
Relative risk
|
absolute risk with therapy/absolute risk w/o therapy
if RR <1 treatment is beneficial |
|
how do you fix post of ileus due to gastric atony?
|
an N.G feeding tube
|
|
NNT
|
1/(absolute risk without therapy/absolute risk with therapy)
functionally: the number of subjects that would have to undergo the treatment in question to avoid one negative otucome; most NNT's ≈10 |
|
What is the most likely cause of fever post op in the first 24-48?
|
atelectasis
|
|
importance of randomization in clinical trials
|
clinical outomes result from many causes:
undelrying severity presence of comorbidity known & unknown prognostic factors non-randomized studies tend to show larger tx effects than randomized randomziation is the best way to equally distribute unkown and unknown determinants of treatment outcoems |
|
how are HgB and Hct affected by acute bleeding?
|
they are misleadingly high
|
|
intention-to-treat protocol
|
analyzing pts in the group to which they were assigned, regardless of whether they continued the treatment or moved from placebo to tx group.
preserves the value of randomization; |
|
What is the problem with the jejunoileal bypass?
|
LOTS of metabolic issues
|
|
independent & dependent variables
|
independent: the thing you change
dependent: the thing you measure |
|
What is the most effective weight loss surgery?
|
roux en Y subtotal gastrectomy
|
|
Establishing internal validity
|
1. Was the assignment of pts to tx randomized (distributes unknown variables evenly)
2. Were the groups similar at the start of the trial (distributes known variables evenly via stratified randomization, want p<0.05) 3. Was the follow up sufficiently long & complete? (want <20% of pts lost to follow up) 4. Were pts analyzed in groups to which they were assigned 5. Were pts, health workers & study personnel "blind" to tx? If something like surgery where the pt and doc must know- follow up analysts should be blind. 6 How large was the treatment effect? |
|
Chronic Pancreatitis
|
Usually due to alcoholism, progresses to diabetes
chronic intermittent pain, steatorrhea Imaging makes the Dx Tx: teetotalling, reduced dietary fat, pancreatic enzyme supplements before meals, possible ductal decompression, rarely surgical resection |
|
how much per cent excess weight is lost with roux en Y subtotal gastectormy?
|
60-80%
|
|
Acute pancreatitis
etiologies |
mild will be self limited
severe may lead to mulitorgan failure, ≤30% mortality if infected Etiology: Gallstones & alcohol abuse acct for ≤80% of all cases T.H.I.S. is B.A.D. : Trauma, HyperTAGemia, hyperCa²⁺emia, Idiopathic, Scorpion bite, Biliary, Alcohol, Drugs most probable candidate: Old Black Man with AIDS & a congenital abnormality |
|
What disease (other than being fat) is often cured with gastric bypass surgery?
|
type 2 DM
|
|
Mechanism of Injury
|
intra-acinar activation of trypsinogen → cascade of pancreatic enzymes
|
|
what part of the history does a living will and religious restriction go into?
|
Social Hx
|
|
Sudden onset of constant, dull boring epigastric pain which radiates to back and flanks, improved by leaning forward
|
Classic acute pancreatitis;
typically begins after heavy meal or drinking binge |
|
Who should not be given lactated ringers solution?
|
pts with renal insufficiency
|
|
Lab Tests for Pancreatitis
|
Amylase and Lipase = Pancreatic Enzymes
CMP, CBC, GGTP Liver Enzymes to look for gallstone blockage Ca², cholesterol, TAGs may be etiology/complication CBC: HCT>47 predictive of severe necrotizing pancreatitis CRP a useful marker at 36+ hrs |
|
What is nonspecific abdominal pain?
|
no organic cause found
|
|
aSx hyperamylasemia
|
almost never due to pancreatic disease
amylase produced by both salivary glands and pancreas alcoholics produce 3x normal salivary amylase |
|
what is the most likely origin of rapid onset severe abdominal pain?
|
vascular, rupture, stones, cysts
|
|
prognosticating acute pancreatitis
|
Ranson's Critera: ≥3 points ≈ severe acute pancreatitis
APACHE II: >8 ≈ S.A.P. <<Most sensitive & specific Balthazar Critera: based on CECT A-E, A is best, E is worst Glasgow Criteria Imrie Critera CECT: Contrast Enhanced CT Scan to assess severity &prognosis |
|
What is the most likely origin of slow insidious onset abdominal pain?
|
inflammatory processes
|
|
treatment of acute pancreatitis
|
1. Intravascular Volume Replacement, most important
2. Analgesia/Pancreatic Rest 3. Antibiotics for fever, significantly reduces mortality if infx 4. Relieve obstrx/ surgical debridement Enteral nutrition w/ NG tube PAST DUODENUM |
|
What is the classic finding for mesenteric ischemia or pancratitis?
|
pain out of proportion to physical findings
|
|
Frequency of UG problems in 1° Care setting
|
1/3 of all presenting cases
|
|
what kind of abdominal pain is relived with eating?
|
ulcers
|
|
Green Onion deformity
|
ureterocele
|
|
what kind of abdominal pain is worse after eating
|
biliary colic
|
|
Child with a UTI
|
Children don't get UTI's → urological obstrx? chronic retention? anomaly?
#1 cause of infx is stasis worst thing you can do is give them antibiotics and send them home |
|
what xray position is best for looking for free air under the diaphragm (as in a perforation)
|
sitting upright xray
|
|
Adult w/ recurrent UTI following Rx
|
suspicion of statis or obstrx
#1 cause of infx is stasis |
|
What are the major risks of causes gall stones?
|
native american woman.
fat crohns disease drugs |
|
KUB
|
Kidneys Ureter, Bladder X ray
|
|
What are the 5 "F"s of gallstones?
|
Fat
Female forty fertile fiar skin |
|
Loss of Psoas Shadow on KUB
|
KUB = Kidneys Ureter Bladder X ray
Loss of both poas = ascities Loss of one = retroperitoneal pathology |
|
What type of gallstone is usually found in adults, as a solitary stone?
|
cholesterol stones
|
|
UPJ
|
Ureter/Pelvic Junction, common location for pathology:
stenotic is most common tx: pyeloplasty |
|
what type of gallstone is usually found in kids, as multiple stones?
|
pigmented stones
due to high unconjugated bilirubin |
|
Pyeloplasty
|
surgical treatment for Ureter-Pelvic Jnx pathology (stricture, etc)
|
|
What is the pain of gallstones like?
|
intense dull pressure in the RUQ
intolerance of fatty foods, nausea, vomiting, flatuence |
|
Sentinel LN's for Testes CA
|
Periaortic
|
|
What does the diagnosis change to if gallstone pain lasts longer than 6 hours?
|
this is the onset of cholecystitis (inflammation)
|
|
What is the normal ejection fraction for the gallbladder when adminstering CCK?
|
at least 50% is normal
|
|
what NSAID has been shown to stop the progression of gallstones to cholecystitis?
|
IM diclofenac
|
|
What is the best therapy for symptomatic gallstones?
|
cut it out
|
|
what is the most common complication of laparoscopic cholecystectomy?
|
common bile duct injury
|
|
What kind of pt gets oral bile acids to dissolve stones, rather than surgery?
|
functional gallbladder
small stones -and have a comorbid condition that prevents surgery |