Winter Icmd Midterm

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

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

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"

Dilation of the gallbladder

Intractible Pain, vomitting, dehydration

Evidence of more advanced condition.

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.

Cholelithiasis

Cholecystitis

Cholecystectasia

CHoledocholithiasis

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]

Cholangitis

Extensive fibrosis of the extra or intra-hepatic bile ducts; frequently seen with ulcerative colitis; presents with recurrent or persistent obstructive jaundice.

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)

Poor ejection fraction of the gallbladder

Gallbladder dyskinesia

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.

1+ of:
-Amylase >500
-Lipase >5x nomral\
-Mental Status Change
-Diverticulitis or Pancreatitis on -X ray
-102+ fever AND >15k WBC
-Protracted vomitting

Cholesterol insoluble in water and requires Bile Salts and Lecithin to emulsify. Insufficient bile acids and lecithin causes precipitation.

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

Pima Indians most at risk
Native Americans, Hispanics, Caucasians

1st degree relative a risk factor

Yes: female, estrogens enhance secretion of cholesterol into bile. progesterone slows gallbladder emptying.

estrogens and hormone replacement therapy are risk factors

Hypertriglyceridemia↑ cholesterol synth
Diabetes produces hypertriglyceridemia,
also neuropathy reduces motility

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.

Spinal Cord injuries may reduce gallbladder motility

Diabetic neuropathy as well.

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)

clofibrate, octeotide, ceftriaxone

binds calcium and precipitates out of bile

Aspirin and NSAIDs may be protective because of anti-inflammatory actions

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)

Fat, Forty, Fertile, Flatulent, Female

The 5 F's of Gallstone Risk: Fat, Forty, Fertile, Flatulent, Female

Cholesterol Stones: will produce one single stone.
Will not show up on a plain film

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

esp w/ hemolytic anemias like sickle cell Pigment stones: Calcium bilirubinate. Usuallly multiple, will show up on plain film.

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

most common cause of gallstones in adults; will produce one single stone, will not show up on a plain film

Pigment stones (Calcium biolirubinate, majority of stones in children, esp w/ hemolytic anemias like sickle cell) will show up on X ray

a mixture of cholesterol, pigment, Ca2+ and phosphate. common in obese pts and those on a calorie rich CHO rich diet

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

Excludes Uncomplicated Cholelithiasis: should be normal.

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

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

Thickening and fibrosis of gallbladder from long-standing cholelithiasis

histopathologic dx, not clinically relevant

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

Magnetic Resonance Cholangiopancreatography

Non-invasive imaging preferred way to Dx choledocholithiasis (risk of pancreatitis with ERCP Endoscopic Retrograde Cholangiopancreatography)

Gengrene most common → Perforation → Cholecytoenteric fistula

Gallstone illeus (from mechanical obstrx)
Emphysematous cholecystitis: crepitus from gas producing chlostridial infxn

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]

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]

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 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

X ray finding, raises concern for CA

indication for removal first opportunity

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

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

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"

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

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

Milld ALT & AST Elevation

Mild <3x normal
Moderate 3-20x normal
Severe >20x normal

Milld ALT & AST Elevation

Mild <3x normal
Moderate 3-20x normal
Severe >20x normal

Moderate ALT & AST Elevation

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

Mild <3x normal
Moderate 3-20x normal
Severe >20x normal

Moderate ALT & AST Elevation

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

Mild <3x normal
Moderate 3-20x normal
Severe >20x normal

Moderate ALT & AST Elevation

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

Mild <3x normal
Moderate 3-20x normal
Severe >20x normal

Severe ALT & AST Elevation

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

Mild <3x normal
Moderate 3-20x normal
Severe >20x normal

Mild Elevation

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

Mild <2x normal
Moderate 2-5x normal
Severe >8x normal

Moderate Elevation

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

Mild <2x normal
Moderate 2-5x normal
Severe >8x normal

Moderate Elevation

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

Mild <2x normal
Moderate 2-5x normal
Severe >8x normal

Moderate Elevation

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

Mild <2x normal
Moderate 2-5x normal
Severe >8x normal

Mild Elevation

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

Mild <3x normal
Moderate 3-10x normal
Severe >10x normal

Mild Elevation

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

Mild <3x normal
Moderate 3-10x normal
Severe >10x normal

Moderate Elevation

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

Mild <3x normal
Moderate 3-10x normal
Severe >10x normal

Moderate Elevation

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

Mild <3x normal
Moderate 3-10x normal
Severe >10x normal

Severe Elevation

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

Mild <3x normal
Moderate 3-10x normal
Severe >10x normal

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

transports AA's across lipid membrane
not specific for Liver unless combined w/ ↑AP
then sensitive indicator of obstructive/infiltrative liver disease

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

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

↑↑↑ 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

↑↑↑ 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

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)

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)

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)

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)

>2000

drug, toxin, ischemic or acute viral injury

acute obstx choledocholithiasis, autoimmune

[more on this in slides, doubt he will test it]

250-1000

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

[more on this in slides, doubt he will test it]

<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]

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)

alcoholic fatty liver
will occur in 90% of alcohol abusers
not itself a progressive condition, improves with abstinence

Non-alcoholic fatty liver

Causes: Obesity, massive weight loss, total parenteral nutrition, diabetes, hypercholesterol/hyperTAGemia

can result in steatohepatitis and may evolve into cirrhosis

characteristic presentation of alcoholic hepatitis

hepatic bruit in severe cases

often coexistant with signs of cirrhosis/chornic disease

~50% mortality, may resolve with abstinence

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

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

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

Temproal wasting
spider angioma
jaundice
firm nodular liver edge
palpable spleen tip
ascites
heme positive stool
asterixis
confusion

GI bleed/protal hypertension (esophageal varices)

ascites/spontaneous bacterial peritonitis

bleed into GI→ digest protein into amonia → encephalopathy

infxns

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

cirrhosis (from primary biliary cirrhosis?)

cirrhosis: you ask them to hold their arms out and hands back and the hands shudder

these aren't aren't that great

go back and review slides

Rapid Deep Sighing Respirations. Compensatory mechanism for metabolic acidosis.

present in DKA not HHS (no acidosis)

Kussmaul breathing: compensatory for metabolic acidosis

present in DKA not HHS (no acidosis)

Alcohol predisposes to dvlpt of hypoglycemia because it inhibits glycogen storage and glucoenogenesis

early hypoglycemia, due to SNS activation

SNS mediated tachycardia, diarphoresis, anxiety

Psychotic behavior and Seizures, coma may dvlp without warning symptoms

hyperglycemia, ketonemia, acidemia;

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

→ dehydration, shock and death

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

Hypoglycemia: ↓ blood sugar
DKA: hyperglycemia, ketonemia, acidemia
Hyperosmolar Hyperglycemic State: ↓ insulin, ↑ blood sugar, w/o ketosis

-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

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

Usually not required should give O2 to anyone 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

<half

metabolic acidosis → severe abdominal pain

misdx'd as appendicitis/gastroenteritis

? Blood Sugar Emergencies Lecture

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

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

classic triad (occurs <50%) in pre-DKA

"there is no other place for this person to be other than the ICU"

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

hypokalemia may cause extreme pain, misdx'd as acute abdomen

e⁻lyte distrubances → ↓ bowel sounds

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!

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

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

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"

BUN:Cr >10:1 from dehydration

(Cr freely filtered, ~0% secreted/resorbed, ↑ BUN resportion w/ ↓ GFR)

serum creatinine may be elevated due to ketonemia

The serum nitroprusside rxn only measures acetone and acetate; the main ketone of DKA is beta-hydroxybutyrate.

2(Na⁺) + glucose/18 + BUN/2.8

Normal is 290 ± 5

>320 = significant hyperosmolality

glycosuria and ketonuria.

maybe proteinuria and hyaline casts from dehydration

WBC = infx

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

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

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

normal saline alone up to 20% decrease

goal is to decrease 100mg/h

going too fast → cerebral edema & hypoglycemia

goal is to decrease 100mg/h

going too fast → cerebral edema (Δosmolality) & hypoglycemia

Fluids & Insulin

Insluin may be the more important one to convince cells they're not starving

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."

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

Hourly labs of glucose, e⁻lytes, oslmolarity, & ABG's

all recorded on flow sheet

Normal saline administered until stability acheived then switched to 0.45 NaCL

may fall up to 30% in first hour alone just from fluids

as soon as urinary output is obtained and true hyperkalemia is ruled out

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

It will do no harm even in a hyperglycemic pt

seizures occur in 10% of hypoglycemics

oral hypoglycemic agents often long acting, so these pts must be admitted

other complications

does not rule out CA

peptic ulcers
esophagitis/gastritis
esophageal varices
mallory weiss tears

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;

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

longitudinal tears in esophagus 2° to wretching; blood loss usually small and self limiting.

NSAIDs, EtOH, CA ChemoTx etc → hemorrhagic &erosive lesions

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)

only after a full colonscopy has been performed

Hematochezia: Left Side
Melena: Right Side
Change in Bowel Habit: Left Side
Iron Deficiency Anemia: Either

Cancer via Barium Enema

obstruction usually surgical adhesion

Small: think adhesions first, then hernias, CA, intussusception, volvulus

Large: most commonly malignancy, then colonic volvulus, diverticular disease. Almost NEVER adhesions.

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

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

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

Mainstay is antibiotics
admit if worried about complications
drain any abscess

repeated episodes: remove some colon

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

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

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

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

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

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.

Focused Assesment with Sonography for Trauma

Ultrasound the places where fluid is most likely to accumulate in the abdomen

Expensive, but non invasive

detects both presence and source of hemoperitonum

Usually due to medical instrumentation/paraesophageal surgery

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

coins

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

high index of suspicion for ingested/inhaled foreign body

emergency

1. conducts electricity → liquifactive necrosis
2. caustic material leakage

GI consult immediately

obstructiong ureterocele

Endoscopy- best method

alternatively:foley catheer, magill forceps, bougienage (push it into stomach)

surgery for dangerous materials or if signs of peritonitis

yes you should, because they dont usually get them

stuffer--the ones who've just done it without planning to avoid getting caught

yes- suspect Stasis or obstruction

"expulsion or extraction of an embryo or fetus weighing ≤500g from its mother"

typically corresponds to ≤22 weeks

spontaneous or not

retroperitoneal pathology on that side

Embryo <10 weeks
Fetus ≤ 0 weeks

ascities

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

an obstructing mass

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

yes it i- goes away afterwards

by far most are caused by strx or chromosomal abnormalities

1° maternal risk factor = age

look for new branching arteries, and smudging on arteriograms

uterine cancer until proven otherwise

endometrial biopsy

embolize them

may cause dysnfx uterine bleeding

gross hematuria

vauge upper abdominal pain

fatigue, weight loss, anemia (typical caner signs)

most are found by chance..

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

pretty danm good until it breaks out of the capsule (stages 1-2)

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)

to the BONE*

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

take the kidney out

no bile = proximal to duodenum

GU cancer

Barium Swallow finding for pyloric stenosis

medial deviation of mid ureters

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

idiopathic

methysergide

cancers

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

to look for cancers

terminal ileum protruding into the cecum;

ideopathic <2y

>2yo more likely pathological

relieve bladder distension

collect uncontaminated urine

monitor urine output

bladder tests (cytogram/urodynamics)

currant jelly stool

blood from urethra or urethral disruption

acute prostatitis

Hx of urethral strictures

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

dont inflate unless you see urine first

mesentery pulled with bowel into intussception: obstructs venous outflow--> edema, weeping fluid & currant jelly stool

neruogenic bladder

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

Nocturia 2-3 times a nigh

any untoward reaction after food ingestion ranging from toxic reaction such as food poisoning to immune/nonimmune reaction

nonimmune eg lactose intolerance

a J shape

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

trabeculation

immune suppresion against foods we eat

TURP- transurethral resectoscope prostetomy

1. Peanuts
2. Tree Nuts
3. Milk
4. eggs
5 fish
6 shellfish
7 seeds
8 fruits
9 grains

the irrigation fluids used in TURP have low sodium, so this causes water intoxication in the pt.

N/V/CHF

tx diruetics

unconjugated: hemolysis, reduced hepatic removal, altered metabolism

conjugated: decreased excretion, disease of biliary tract

before acute retention occurs

liver disease must be suspected

Urolume stent

green light laser

various ablation techiques

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

renal pelvis

where it crosses the pelvis

going into the bladder

Benign GERD

Non-erosive reflux disease

about 50%

≥60 million Americans experience heartburn daily

20% of those seeking medical attn have serious complications

Proteus

Hoarseness, Coughing, Sleep Apnea, really anything

intractable pain
high grade obstruction

Esophageal Peristasis
Bicarbonate
Mucosal integrity- mucosal damage may be 1° to reflux
LES competance
Gastric Emptying

unenhanced helical computed tomorpgrahy (CT)

autonomic neuropathy of T2DM

may be 1° cause of GERD

shock wave lithotripsy

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."

percutaneous nephrostomy

20% of pts:
Barrets
Ulcer ± bleeding
stricture
LERD → Laryngocarcinoma

shock wave failes
pregnant pt
obese
pt is a bleeder

>55 yo
Anemia/+FOBT
Dysphagia
Respiratory Sx
Early satiety/weight loss
persistent sx w/ Tx

Stress

Urge (sudden need/loss of bladder control)

Overflow (neuro)
Mixed

2° to smoke & EtOH

more common in women in the proximal 2/3 of esophagus

13 million people

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

the proximal 2/3rd of urethra and bladder neck

1. Smoking Cessation
2. Wt loss
3. Elevated head of the bed
4. no foods/liquids after 6 pm

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

multiparous women, pelvic surgery, activity related

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

UTI, new Rx, hematuria, CVA

tomato juice, orange juice, anything with high acidity, spiciness. fat slows emptying. EtOH. peppermint.

diabetic, never feels empty, back problems, surgery

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!

nope

~1/100 in European Populations with appropriate genetics HLA DQ2;
the majority that don't have DQ8

yes it does

HLA DQ2 → MHC2 molecule which presents gliaden

produces 2 things:
anti-tissue transglutaminase antibodies
Cytotoxic cells vs. GI mucosa

this looks for failure of the zone of continence

Flatulence, Bloating

Malabsorption/Malnutrition

Vomiting/Diarrhea

cardiovascular eval, maybe have severe asymptomatic coronary artery disease

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

two flights of stairs test

an external manifestation of celiac disease

inflatable penile implants- 98% couples satisfaction

delete the wheat

1 mg of gluten: a piece of bread smaller than a postage stamp → intestinal inflammation

NO it does not

same as obstructive benign prostate hyperplasia

increased PSA velocity, Low% free PSA is bad

See pathology

hematochezia ≈ UV>>Crohn's

gross hematuria

change in voiding pattern

Probably UC

tranurethral resection of tumor, with lots of check ups

Crohns Disease

radical cystectomy

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)

lung, liver, bone

Crohn's characterized by intermittent exacerbat'ns w/ remissions

Surgery req'd for intractible sx, complciations; but post op recurrences common

pure seminoma

massive hemorrhage
fulminant colitis → toxic megacolon
perf/strx
CA

xray therapy

risk does not ↑ for 8 years
more probable with more severe forms of disease
need to screen frequently
(Crohn's only if colon involved)

retroperitoneal lymph nodes

Uveitis/Episcleritis
Skin- erythema nodosum/pyoderma gangrenosum
arthritis
enthesitis (tendonal insertions)
aphthous ulcers
thrombophlebitis
1° Sclerosing colangitis (w/ UC)

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)

uncircumcised
VD
HPV
Smoking

≥ 1500-2000 you should be able to see something on transvaginal ultrasound

≥6500 should be visible transabdominally

otherwise ectopic

dead/discolored tissue on scrotom

fever/drosiness

genital pain and redness

odor

CUT IT ALL OUT

IBS: Dx of Exlcusion

rubber band ligation

dont pack the anal canal.

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

a cyst or abscess near or in the upper intergluteal cleft- usually has hair and skin debris in it

CBC c diff
TSH
Anti tTGA
Routine Chemistries

w/o warning sx, routine use of colonoscopy & testing in IBD pt <50 not recommended

hairy butted men- with prolonged sitting

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.

BIG time complete excision - and dont close it just let it fill in from the outside

(risk w/o tx minus risk w/ tx)/(risk w/o tx)

richter hernia

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

risk of re-infarction

the neighborhood within which the effect likely lies

imagine the number at the extreme high and extreme low, is this still a good number?

8gms

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

if you dont get out of bed, you dont get any pain meds

absolute risk of control group minus absolute risk of experimental group

that its too early for oral intake of foods

absolute risk with therapy/absolute risk w/o therapy

if RR <1 treatment is beneficial

an N.G feeding tube

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

atelectasis

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

they are misleadingly high

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;

LOTS of metabolic issues

independent: the thing you change
dependent: the thing you measure

roux en Y subtotal gastrectomy

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?

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

60-80%

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

type 2 DM

intra-acinar activation of trypsinogen → cascade of pancreatic enzymes

Social Hx

Classic acute pancreatitis;

typically begins after heavy meal or drinking binge

pts with renal insufficiency

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

no organic cause found

almost never due to pancreatic disease

amylase produced by both salivary glands and pancreas

alcoholics produce 3x normal salivary amylase

vascular, rupture, stones, cysts

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

inflammatory processes

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

pain out of proportion to physical findings

1/3 of all presenting cases

ulcers

ureterocele

biliary colic

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

sitting upright xray

suspicion of statis or obstrx

#1 cause of infx is stasis

native american woman.
fat
crohns disease
drugs

Kidneys Ureter, Bladder X ray

Fat
Female
forty
fertile
fiar skin

KUB = Kidneys Ureter Bladder X ray

Loss of both poas = ascities
Loss of one = retroperitoneal pathology

cholesterol stones

Ureter/Pelvic Junction, common location for pathology:
stenotic is most common

tx: pyeloplasty

pigmented stones

due to high unconjugated bilirubin

surgical treatment for Ureter-Pelvic Jnx pathology (stricture, etc)

intense dull pressure in the RUQ
intolerance of fatty foods, nausea, vomiting, flatuence

Periaortic

this is the onset of cholecystitis (inflammation)

at least 50% is normal

IM diclofenac

cut it out

common bile duct injury

functional gallbladder
small stones
-and have a comorbid condition that prevents surgery