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359 Cards in this Set

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Choledocholithiasis
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
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 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
Cholecystitis
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"
Cholecystectaisa
Dilation of the gallbladder
When do you hospitalize someone for Biliary Colic?
Intractible Pain, vomitting, dehydration

Evidence of more advanced condition.
Most accurate predictor of gallstone disease
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.
Stones in the gallbladder
Cholelithiasis
Inflammation of the Gallbladder
Cholecystitis
Dilation of the gallbladder
Cholecystectasia
Stones in the Common Bile Duct
CHoledocholithiasis
Cholangitis
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]
Inflmmation/infxn of biliary tree
Cholangitis
Primary Sclerosing Cholangitis
Extensive fibrosis of the extra or intra-hepatic bile ducts; frequently seen with ulcerative colitis; presents with recurrent or persistent obstructive jaundice.
HIDA
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)
Gallbladder dyskinesia
Poor ejection fraction of the gallbladder
Poor ejection fraction of the gallbladder
Gallbladder dyskinesia
Gallstone ileus
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.
Interqual Criteria for Admission, Abdominal Pain
1+ of:
-Amylase >500
-Lipase >5x nomral\
-Mental Status Change
-Diverticulitis or Pancreatitis on -X ray
-102+ fever AND >15k WBC
-Protracted vomitting
Asymptomatic Cholelithiasis
Cholesterol insoluble in water and requires Bile Salts and Lecithin to emulsify. Insufficient bile acids and lecithin causes precipitation.
Weight as a risk factor for gallstones
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
Is there a genetic predisposition to gallstones
Pima Indians most at risk
Native Americans, Hispanics, Caucasians

1st degree relative a risk factor
Is gender a risk factor for gallstones?
Yes: female, estrogens enhance secretion of cholesterol into bile. progesterone slows gallbladder emptying.

estrogens and hormone replacement therapy are risk factors
Metabolic Risk Factors for Gallstones
Hypertriglyceridemia↑ cholesterol synth
Diabetes produces hypertriglyceridemia,
also neuropathy reduces motility
GI conditions as a Risk Factor for Gallstones
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.
OMM Considerations with gallstones
Spinal Cord injuries may reduce gallbladder motility

Diabetic neuropathy as well.
The most at risk gallstone pt
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)
Drugs which increase risk of gallstones
clofibrate, octeotide, ceftriaxone

binds calcium and precipitates out of bile

Aspirin and NSAIDs may be protective because of anti-inflammatory actions
Preventing gallstones
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)
The Five F's of Gallstones
Fat, Forty, Fertile, Flatulent, Female
Obese 43 yo female with flatus, LMP 1 week ago
The 5 F's of Gallstone Risk: Fat, Forty, Fertile, Flatulent, Female
The majority of gallstones in adults are which type?
Cholesterol Stones: will produce one single stone.
Will not show up on a plain film
Gallstones on an X ray
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
The majority of gallstones in children are which type?
esp w/ hemolytic anemias like sickle cell Pigment stones: Calcium bilirubinate. Usuallly multiple, will show up on plain film.
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
Cholesterol Stones
most common cause of gallstones in adults; will produce one single stone, will not show up on a plain film
Pigment Stones
Pigment stones (Calcium biolirubinate, majority of stones in children, esp w/ hemolytic anemias like sickle cell) will show up on X ray
"mixed" type gallstones
a mixture of cholesterol, pigment, Ca2+ and phosphate. common in obese pts and those on a calorie rich CHO rich diet
Endoscopic Ultrasound
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
Biliary Colic Abnormal Lab Findings
Excludes Uncomplicated Cholelithiasis: should be normal.
Oral Bile Acids
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
Ursodiol
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
Chronic Cholecystitis
Thickening and fibrosis of gallbladder from long-standing cholelithiasis

histopathologic dx, not clinically relevant
ERCP
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
MRCP
Magnetic Resonance Cholangiopancreatography

Non-invasive imaging preferred way to Dx choledocholithiasis (risk of pancreatitis with ERCP Endoscopic Retrograde Cholangiopancreatography)
Complications of Acute Cholecystitis
Gengrene most common → Perforation → Cholecytoenteric fistula

Gallstone illeus (from mechanical obstrx)
Emphysematous cholecystitis: crepitus from gas producing chlostridial infxn
Charcots Triad
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]
Raynaud's Pentad
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]
Fever, RUQ Pain, Jaundice
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]
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
Porcelain Gallbladder
X ray finding, raises concern for CA

indication for removal first opportunity
epigastric/RUQ "intense dull pressure" radiating to right shoulder for 3 hours. No peritoneal signs.
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
Sudden onset of severe, unrelenting pain in RUQ ± radiation. Jaundice, pale stools, dark urine
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
Severe, steady RUQ/epigastric pain radiating ot right shoulder >6 hours. Positive Murphey's Sign.
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"
RUQ/Epigastric Pain, Nausea, & Vomitting, Elevated Amlyase and Lipase
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
DDx of Gallstone diseases by Labs
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
AST/ALT 1.5x normal
Milld ALT & AST Elevation

Mild <3x normal
Moderate 3-20x normal
Severe >20x normal
AST/ALT 2.5x normal
Milld ALT & AST Elevation

Mild <3x normal
Moderate 3-20x normal
Severe >20x normal
AST/ALT 4x normal
Moderate ALT & AST Elevation

↑↑↑ AST/ALT ±↑AP/GGTP = hepatoceullary injury

Mild <3x normal
Moderate 3-20x normal
Severe >20x normal
AST/ALT 8x normal
Moderate ALT & AST Elevation

↑↑↑ AST/ALT ±↑AP/GGTP = hepatoceullary injury

Mild <3x normal
Moderate 3-20x normal
Severe >20x normal
AST/ALT 12x normal
Moderate ALT & AST Elevation

↑↑↑ AST/ALT ±↑AP/GGTP = hepatoceullary injury

Mild <3x normal
Moderate 3-20x normal
Severe >20x normal
AST/ALT 21x normal
Severe ALT & AST Elevation

↑↑↑ AST/ALT ±↑AP/GGTP = hepatoceullary injury

Mild <3x normal
Moderate 3-20x normal
Severe >20x normal
Alkaline Phosphastase 1.5x normal
Mild Elevation

↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease

Mild <2x normal
Moderate 2-5x normal
Severe >8x normal
Alkaline Phosphastase 2.5x normal
Moderate Elevation

↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease

Mild <2x normal
Moderate 2-5x normal
Severe >8x normal
Alkaline Phosphastase 4x normal
Moderate Elevation

↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease

Mild <2x normal
Moderate 2-5x normal
Severe >8x normal
Alkaline Phosphastase 8x normal
Moderate Elevation

↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease

Mild <2x normal
Moderate 2-5x normal
Severe >8x normal
Gamma glutamyl transpeptidase 1.5x Normal
Mild Elevation

↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease

Mild <3x normal
Moderate 3-10x normal
Severe >10x normal
Gamma glutamyl transpeptidase 2.5x Normal
Mild Elevation

↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease

Mild <3x normal
Moderate 3-10x normal
Severe >10x normal
Gamma glutamyl transpeptidase 4x Normal
Moderate Elevation

↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease

Mild <3x normal
Moderate 3-10x normal
Severe >10x normal
Gamma glutamyl transpeptidase 8x Normal
Moderate Elevation

↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease

Mild <3x normal
Moderate 3-10x normal
Severe >10x normal
Gamma glutamyl transpeptidase 12x Normal
Severe Elevation

↑↑↑ AP/GGTP ±↑AST/ALT = obstructive/infiltrative liver disease

Mild <3x normal
Moderate 3-10x normal
Severe >10x normal
Increased Bilirubin
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
Increased GGTP
transports AA's across lipid membrane
not specific for Liver unless combined w/ ↑AP
then sensitive indicator of obstructive/infiltrative liver disease
Elevated Prothrombin Time
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
Decreased Albumin
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
Cholestasic Liver Disease
↑↑↑ 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
Infiltrative Liver Disease
↑↑↑ 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
Hepatocellular Liver Disease
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)
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)
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)
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)
Marked Elevation of Transaminaes
>2000

drug, toxin, ischemic or acute viral injury

acute obstx choledocholithiasis, autoimmune

[more on this in slides, doubt he will test it]
Moderate Persistent Elevation of Transaminases
250-1000

any type of liver disease, viral and drug induced most common

[more on this in slides, doubt he will test it]
Persistent Mild Elevation of Transaminases
<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]
% of Pts who abuse alcohol who will develop progressive liver injury
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)
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
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
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
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
Causes of Cirrhosis
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
Alcoholic Cirrhosis
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
Findings in Cirrhosis
Temproal wasting
spider angioma
jaundice
firm nodular liver edge
palpable spleen tip
ascites
heme positive stool
asterixis
confusion
Complications of cirrhosis
GI bleed/protal hypertension (esophageal varices)

ascites/spontaneous bacterial peritonitis

bleed into GI→ digest protein into amonia → encephalopathy

infxns
Course of Cirrhosis
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
tired itchy people RUQ punepxlained anorexia
cirrhosis (from primary biliary cirrhosis?)
Asterixis
cirrhosis: you ask them to hold their arms out and hands back and the hands shudder
Cirrhosis
these aren't aren't that great

go back and review slides
Kussmaul
Rapid Deep Sighing Respirations. Compensatory mechanism for metabolic acidosis.

present in DKA not HHS (no acidosis)
Rapid Deep Breaths with Altered Mental Status
Kussmaul breathing: compensatory for metabolic acidosis

present in DKA not HHS (no acidosis)
Alcohol and Blood Sugar
Alcohol predisposes to dvlpt of hypoglycemia because it inhibits glycogen storage and glucoenogenesis
Abnormal Blood Sugar State characterized by tachycardia, diaphoresis, and anxiety
early hypoglycemia, due to SNS activation
Early signs of hypoglycemia
SNS mediated tachycardia, diarphoresis, anxiety
Complications of hypoglycemia
Psychotic behavior and Seizures, coma may dvlp without warning symptoms
Diabetic Ketoacidosis
hyperglycemia, ketonemia, acidemia;

caused by absence of insulin and excess of anti-insulin glucagon, growht hormone, caatchecholamiens, cortisol

→ dehydration, shock and death
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
What are the three major metabolic abnormalities considered in an IDDM patient with altered mental status?
Hypoglycemia: ↓ blood sugar
DKA: hyperglycemia, ketonemia, acidemia
Hyperosmolar Hyperglycemic State: ↓ insulin, ↑ blood sugar, w/o ketosis
What are the initial steps in the approach to a diabetic patient with altered mental status?
-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
hyperglycemia, no insulin w/o ketosis
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
How often is airway management required in the diabetic patient with metabolic complications?
Usually not required should give O2 to anyone with altered mental status
What are the areas of focus in the history of a diabetic patient presenting with altered mental status?
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
How often is the classical triad of polydipsia, polyuria and polyphagia present in DKA?
<half
What are some of the common MISDIAGNOSES made when the real diagnosis is DKA?
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