Test 3 Flashcards
Used to treat Ogilvie syndrome
NPO, NG tube, Neostigmine
What is neostigmine’s MOA?
reversible ACh inhibitor, indirectly stimulates nic. and musc. receptors to cause colonic contraction.
Side effect of neostigmine?
bradycardia
Continuous dilation of small intestine and colon
Ileus
Most common cause of acute intestinal obstruction?
Adhesions
What is the difference in pain presentation from closed loop obstruction and strangulation?
Closed loop obstruction with functioning ileocecal valve causes cramping and midabdominal pain with colicky behavior. Strangulation is more steady, severe, and localized.
High pitched hyperactive bowel sounds like “tinkling”
Acute intestinal obstruction
What two things do you have to establish with obstructions?
Strangulation vs nonstrangulation
Partial vs complete obstruction
What imaging do you order for an obstruction?
Abdominal x-ray is step on. Look for transition point. If x ray doesn’t work, go with CT abdomen and pelvis with IV and PO contrast.
How do you treat a strangulated obstruction?
Must do surgery. Only time you can avoid surgery is if there’s no strangulation, no increasing abd. pain, and no increasing WBC
What is the most common abdominal emergency in early childhood?
Intussusception
Where do intussusceptions usually occur?
ileocecal junction
What is the classic triad associated with intussusception?
Pain, currant jelly stool, sausage shaped abdominal mass on the right side.
What do you have to do before treating an intussusception?
Have an NG tube placed. Observe afterward in hospital for 12-24 hours.
What do you do for a SMALL BOWEL intussusception?
Usually nothing, many will resolve spontaneously.
Elliptical incision removal, rubber band ligation, laser phototherapy, cryosurgery, and infrared coagulation are treatment examples of what condition?
hemorrhoids
A tear in the anoderm distal to the dentate line, becomes chronic in 40% of patients
Anal fissure
If an anal fissure has raised edges, is it acute or chronic?
Chronic. If it was acute it would look like a paper cut
Constant pain, fever, malaise, patch of redness, indurated skin, mass on exam
Anal abscess
When do you give antibiotics to a pt with an anal abscess?
Only if they are immunosuppressed or have Crohn’s
What is the most common cause of anal fistulas?
Anal abscess. Originate from infected anal crypt gland.
Intermittent rectal pain after having an I/D
Anal fistula
Where are the highest rates of colorectal cancer?
Australia, New Zealand, Europe, North America. More common in males
What kind of polyps are the worst case scenario for getting CRC?
Sessile Villous Adenomatous Polyps
If an adenomatous polyp is found, when do you repeat colonoscopy?
Every 3-5 years
CRC screening in someone with family hx of 1st degree relative?
age 40 or 10 years before youngest family diagnosis <60
CRC screening in someone who has adenomatous polyps >1cm, villous, or tubulovillous polyps?
age 40 or 10 years before youngest polyp diagnosis <60
CRC screening in someone who had abdominal radiation?
Begin screening 10 years after radiation or age 35, whichever is later
CRC screening for African American patient?
Start at 45 because they have the highest CRC rates and a 20% higher mortality, and it occurs at a younger age
When should you perform a DRE on routine physical exam?
Anyone over 40
Lynch Syndrome (HNPCC) has a predominance of _______ sided lesions
Right sided.
Extracolonic cancers are very common
CRC screening for someone with lynch syndrome?
Every 2 years starting at age 25
How do we know if someone has Lynch?
3+ relatives with documented CRC, one of which is a 1st degree reltaive; one+ cases of CRC < age 50; CRC involves at least 2 generations
CRC risk factors that DO NOT change screening recommendations?
Diabetes and alcohol use
CRC protective factors
Physical activity, Vitamin D, Fish consumption, ASA and NSAIDS, Postmenopausal hormone therapy
CRC that presents with fatigue, palpitation, iron deficiency anemia, and no change in bowel habits
Right sided, cecum
CRC that presents with obstruction, abdominal cramping, “apple core” lesion
Left sided
CRC that presents with hematochezia, tenesmus, narrow or “ribbon” stool. Anemia is uncommon
Rectosigmoid colon
TNM: T
depth of tumor penetration
TNM: N
Presence of lymph node involvement
TNM: M
Presence or absence of metastasis
What route does metastasis usually take? What’s an exception?
spread through lymph nodes and portal venous system. Liver is the most common site. distal rectal cancer can bypass portal system and reach lungs through paravertebral venous plexus.
Screening recommendation for IBD after pancolitis
8-10 years
Screening recommendation for left sided colitis
15 years
What do Kuppfer cells do?
Macrophages that break down dead RBCs found in liver.
The development of severe acute liver injury with encephalopathy and imparied syntehtic function (INR >1.5) in a patient without cirrhosis or preexisting liver disease.
Acute liver failure (<26 weeks)
Euphoria/depression, mild confusion, slurred speech, disordered sleep, may/may not have asterixis. Normal EEG
Grade 1 hepatic encephalopathy
Lethargy and marked confusion. Has asterixis. Abnormal EEG.
Grade II hepatic encephalopathy
Marked confusion, incoherent, sleeping but arousable, asterixis and abnormal EEG
Grade III hepatic encephalopathy
What labs should you order in someone you suspect with acute liver failure?
AST, ALT, Alk Phos, GGT, Total bilirubin, Albumin, INR, Acetaminophen level, Hepatitis panel, Ammonia level +/- BMP
How much do men and women have to drink to develop alcohol fatty liver?
> 60g of alcohol/day for men, >20g/day for women.
Men: 5 beers, 5 glasses of wine, 7 shots per day
Women: 4 beers, 2 glasses of wine, 2 shots per day
What imaging is best used to diagnose alcohol fatty liver?
Ultrasound.
LFTs are usually 2x ULN
Moderate elevations of AST and ALT less than 300. AST: ALT is at least 2:1.
Findings of Alcoholic hepatitis
What would you expect to find on biopsy in someone with alcoholic hepatitis?
Neutrophils
NAFLD without inflammation or fibrosis
Simple hepatic steatosis
NAFLD with necroinflammatory component
NASH
NAFLD with cryptogenic cirrhosis
non-alcoholic cirrhosis
Most common liver disorder in western industrialized countries?
NAFLD. Excessive importation of free fatty acids is related.
Screening recommendation for someone who has cirrhosis?
Transabdominal ultrasound every 6 months regardless of cause
Most common cause of death among patients with NAFLD
Cardiovascular disease
Incubates for 30 days, self limited. Rarely leads to fulminant hepatic failure. Does NOT become chronic. What will normalize first, LFTs or bilirubin?
Hepatitis A.
LFTs normalize first,
then bilirubin will normalize
Labs for hep A?
ALT>AST, often > 1000. Bilirubin will peak AFTER ALT and AST peak.
Gold standard: IgM anti-HAV. will be positive at the onset of symptoms.
Urticarial rash, petechiae, arthralgias/arthritis of small joints followed by constitutional symptoms that take over
Hepatitis B
Lab testing during acute phase of hep b?
Viral hepatitis B panel, Hep C, HIV testing.
ALT>AST
First thing that will be positive after HBV infection and will only be positive in someone who CURRENTLY has the virus
HBsAg
Checks if someone is immune to HBV virus
Anti-HBs (antibody to hep b surface antigen)
Nonspecific marker of acute, chronic, or resolved HBV infection. Tells you the real virus was there.
Anti-HBc
Positive tells you there was a recent infection of HBV within the last 6 months
IgM anti-HBc
Marker of high degree of infectivity in someone who has the real virus
HBeAg (hep b envelope antigen)
May be present in an infected or immune person. Suggests a low viral titer and low degree of infectivity
Anti-HBe
HBsAg positive for >6 months. Serum HBV DNA >100,000 copies. Persistent/intermittent elevation of AST/ALT levels.
Chronic hepatitis B
What genotype of HBV is most likely to become chronic?
genotype C
Labs in chronic hep B
May be normal. During exacerbations, ALT may be as high as 50x ULN
Who should get screening ultrasounds Q6-12 months with hep B?
Cirrhosis, family hx, africans, disease >40 years with persistent/intermittent serum elevations
What are the most common genotypes of HCV in the US?
Genotype 1a and 1b, also the most difficult to treat (75% of cases)
Where would you find genotype 4 HCV?
Africa
75% of patients with Hep C were born when?
1945-1965
How likely will Hep C become chronic?
60-80% of patients become chronically infected. Of those, over a quarter will develop cirrhosis.
Screening recommendation if IVDU or HIV + MSM for hep c
Annual testing
Screening recommendation for hep c if born between 1945-65
once in lifetime
What test do you order for routine Hep C screening?
HCV antibody test. If positve, check HCV RNA to confirm.
Acute Hepatitis C occurs how long after exposure to the virus?
2-26 weeks. Average is 7-8 weeks.
When will AST, ALT labs rise in comparison to RNA with hep c?
They will rise a few weeks before positive RNA can be detected.
HCV-RNA can be positive ___________ after exposure
days to 8 weeks
HCV antibody is positive as early as _______ after exposure.
8 weeks. Does not determine acute from chronic.
If you suspect acute hep C based on elevated LFTs and jaundice, check _______ immediately.
HCV RNA.
Check anti-HCV immediately and at week 12
When should you initiate treatment of acute hep C infection?
12 weeks after exposure to allow for possible spontaneous clearance. If you treat during the acute infection, they have a >80% chance of acquiring sustained virologic response.
In what case scenario would you NOT wait 12 weeks to treat hep C?
High inoculum volume, asymptomatic acute HCV. Genotype 1–treat for 24 weeks. Any other genotype treat for 12
Hep C RNA is different in acute and chronic infection how?
Acute–positive within 2 weeks and fluctuates
Chronic– remains steady. Increase in ALT precedes development of Ab
+RNA and high ALT, negative Ab
acute HCV more likely
+RNA, +Ab, normal or low ALT
Chronic HCV is more likely
What is the most common symptom of chronic hep C?
Fatigue
True or false: There is a strong correlation between LFTs and liver histology.
False
What are most symptoms from hep C from?
Development of cirrhosis.
What is the most common cause of death from hep C?
Complications of cirrhosis (portal HTN)
What is the most common cause of death from hep B?
HCC
What genotype of hep C has a higher ate of HCC?
1b
What is the best predictor of progression to cirrhosis in hepatitis C?
Amount of inflammation and fibrosis on liver biopsy.
AA have slower progression
What is genotype 1 treatment of hepatitis C?
Peginterferon, Ribavirin plus Protease inhibitor
What are the hardest genotypes of hep C to treat?
1 and 4
What are side effects of hep C antivirals?
Flu-like symptoms, anemia, neutropenia, thrombocytopenia, rash, hair loss, thyroid dysfunction, mood changes
Protease inhibitors that disrupt replication of HCV that has shown to increase viral response especially in patients who have genotype 1 or who have failed therapy before
Boceprivir and Telaprevir
When would you give telaprevir without boceprivir?
Only indicated for null responders.
Give both for genotype 1
How do you treat Hep C in someone who can’t be on a protease inhibitor?
Treat with ribavirin and peginterferon for 48 weeks
Hep C with evidence of cirrhosis sreening
Q6 month ultrasound
Hep C without evidence of cirrhosis screening
Q12 month ultrasound
How is hep D transmitted?
Sex, blood, bodily fluids. Needs hep B
How is hep E transmitted?
Fecal-oral, rare in US. Test IgM anti-HEV
Characterized by progressive hepatic fibrosis, distortion of hepatic architecture, forming regenerative nodules (incongruent surface of the liver)
Cirrhosis
Most common causes of cirrhosis?
viral hepatitis, alcoholic liver disease, hemochromatosis, NAFLD
Methotrexate, INH, and alpha-1 antitrypsin deficiency may cause what?
cirrhosis
Causes of decompensated cirrhosis
Processing problems
Hormone Imbalances
Portal Hypertension
How would someone have trouble processing bilirubin with cirrhosis?
If you aren’t making albumin, unconjugated bilrubin can’t bind to it to become water soluble and go to the liver.
Also, some people just can’t conjugate the bilirubin with glucuronic acid, or it can’t get out of the liver.
Where will you notice jaundice first?
Under the tongue
Why would someone have trouble processing ammonia with cirrhosis?
Amino acids produce ammonia when they’re metabolized, which has to be converted to urea by the liver. Sick liver can’t do this.
Clinical result of liver’s inability to process ammonia?
hepatic encephalopathy
How does ammonia cause encephalopathy?
Ammonia crosses BBB and is used by brain cells to convert glutamate to glutamine. Too much glutamine = increased osmotic pressure in brain cell = swelling = confusion
What is the treatment of hepatic encephalopathy?
First line is Lactulose laxative. Goal is 2-3 loose stools/day.
FSH stimulates what?
Sertoli cells to make sperm
LH stimulates what?
Leydig cells to make testosterone
What converts testosterone to estradiol?
Aromatase (made by the liver)
spider angiomata, palmar erythema, and gynecomastia are a result of what?
High levels of estrogen, occurs in 2/3 of patients with cirrhosis.
Caused ultimately by too much aromatase and SHBG production by the liver.
Hormone problems occur most often in what kind of cirrhosis?
Alcoholic cirrhosis
serum LH, FSH levels high, serum testosterone low
Primary hypogonadism (testicle problem)
Serum LH, FSH levels low or normal, serum testosterone low
Secondary hypogonadism. (pituitary/hypothalamus problem)
How does liver disease cause portal hypertension?
decreases vascular radius from fibrosis, decreased production of NO, Body makes collaterals and connects to the systemic system through this
Physical manifestations of portal HTN
Caput medusa, hemorrhoids.
Complications: ascites, esophageal varices, spontaneous bacterial peritonitis, hepatorenal syndrome
Treatment of ascites
Salt restriction WITH diuretic. Should be on BOTH spironolactone and furosemide.
Where do most esophageal varix hemorrhages occur?
Superficial to the GE junction
Recommendation for screening for varices
All patients with cirrhosis should have EGD to document existence of varices. Negative–repeat Q2-3 years. Positive, repeat yearly.
Those who have 1 eisode of bleeding have ______% chance of rebleed within ____.
60-80%, 1 year.
1/3 of further rebleeding episodes are fatal.
Treatment of esophageal varices bleeding
LIgation during endoscopy. Nonselective beta blockers–propranolol (Indur) is the drug of choice. Reduces portal and collateral blood flow
SBP is almost always seen in what disease?
ESLD
Labs for diagnosing cirrhosis
Alk Phos elevated but less than 3X ULN Worse INR, worse hepatic dysfunction. Hyponatremia is common. CBC: Thrombocytopenia is most common Anemia Splenomegaly
Anemia from iron deficiency from acute or chronic GI blood loss
Microcytic
Anemia from folate deficiency
Macrocytic
What is the best imaging study to order to diagnose cirrhosis?
Abdominal ultrasound.
LIver biopsy is the gold standard, but not usually needed.
What does a fibrotest or fibrosure test assess?
Takes a bunch of factors into account to classify if patients have mild fibrosis, significant fibrosis, or indeterminate
Rapid, noninvaisve ultrasound done using a special probe to measure hepatic tissue stiffness.
Elastography
Classification system used to determine severity of liver disease according to ascites, bilirubin and albumin, prothrombin time, and degree of encephalopathy. Used to determine who should have hepatic dose adjustments.
Child Pugh
Prognostic model to help estimate disease severity, survival, and transplant. Measures bilirubin, creatinine, INR.
MELD score.
Avg score for transplant is 20, avg time to transplant is 321 days.
Primary cancer of the liver that occurs mostly in patients with underlying chronic liver disease and cirrhosis.
Hepatocellular Carcinoma
What is the trend of HCC?
Doubled in last 20 years, increasing in AA population. Mostly men and Caucasians.
Most common physical sign of HCC?
Hepatomegaly
Diagnosis of HCC?
Abdominal ultrasound. Can use CT or MRI to clarify, then diagnosis is made on biopsy. Uses TNM classification to stage.
Common bile duct ends where?
Sphincter of Oddi
How does common bile duct drain into duodenum?
Ampulla of Vater or major duodenal papilla
Exocrine function of pancreas?
Digestive enzymes from Acinar cells and ductal cells
What do acinar cells do?
Stimulated by CCK, releases trysinogen, lipase, and amylase
What does lipase need to be totally active?
colipase and bile salts
What do ductal cells do?
Release bicarbonate by stimulating secretin. Helps buffer acidic fluid from entering the duodenum from the stomach
Endocrine function of the pancreas?
Langerhan’s cells.
Beta cells—Insulin
Alpha cells – Glucagon
Delta cells – Somatostatin
What is the most common cause of pancreatitis?
Gallstones! Cause 40% of all cases.
Cause reflux of bile into pancreatic duct and edema
Causes of acute pancreatitis
Alcohol (30%), idiopathic (30%), triglycerides >1000 mg/dL, Post-ERCP
Acute onset. Persistent, severe epigastric pain. May have radiation to the back that is partially relieved by sitting up or bending forward. Most have N/V.
Acute pancreatitis
Pain is localized with abrupt onset, colicky
Gallstone pancreatitis
Painless disease with unexplained hypotension in post-op or critical care pt
Pancreatitis
Mild ttp in epigastrum
Mild pancreatitis
Diffuse, intense pain, may have ileus secondary to inflammation. Look for Cullen’s sign and Grey-Turner’s sign
Severe pancreatitis
Lab findings for pancreatitis: Serum amylase
rises within 6-12 hours of onset, half life of 10 hours, normal in 3-5 days. Amylase 3x ULN is magic number. Alcoholic pancreatitis and hyperTG will possibly have normal amylase.
If a patient presents to the ER >24 hours after onset of pancreatitis, what test may be more helpful?
Serum lipase. Rises 4-8 hours after onset, peaks at 24 hours, normal in 8-14 days. Better test in someone with alcoholic pancreatitis.
Imaging for acute pancreatitis
Abdominal and chest x rays
If you need to go further, CT abdomen with IV contrast
What is the colon cutoff sign?
lack of air distal to splenic flexure due to spasm of descending colon in response to pancreatic inflammation. Indicates severe disease.
What is the diagnostic criteria of pancreatitis?
Need to meet 2 of the following 3:
- Acute onset of persistent, severe epigastric pain often radiating to the back
- Elevation of serum lipase or amylase 3X ULN
- Characteristic findings on CT, MRI, or U/S
What % of patients with acute pancreatitis will develop severe pancreatitis?
15-25%
What tool is used to predict severity of pancreatitis?
Ranson’s criteria about mortality.
Looks at age (>55), WBC (350), AST (>250). (GA LAW)
After 48 hrs:
HCT fall, BUN inc, low Calcium, pO2, base deficit, fluid sequestration (C. HOBBS)
If a patient with acute pancreatitis feels better, do they have to come in for follow up?
Yes, in a month to make sure complications don’t occur.
Acute peripancreatic fluid collection, acute necrotic collection, pseudocyst, walled-off necrosis
Treatment of pancreatitis
Recognize severity first.
Mild–NPO
Mod-Severe: PO intake not tolerated because of inflammation and extrinsic fluid collections.
No recommendation for prophylactic antibiotics
No problems with exocrine/endocrine function or digestion. Diffuse morphology
Acute pancreatitis
Digestion, endo/exocrine problems. Morphology is patchy with focal infiltrate and fibrosis.
Chronic pancreatitis.
Causes of chronic pancreatitis
Most common: alcohol abuse
Smoking, hereditary pancreatitis (marked increase of pancreatic adenocarcinoma)
Obstructed duct, systemic disase, idiopathic
Common denominators of chronic pancreatitis
- Hypersecretion of protein that is NOT compensated by bicarb (ductal bicarb secretion impaired)
- Inflammatory and patchy histology changes in exocrine pancreas
What is the predominant feature of chronic pancreatitis?
Abdominal pain
How much of the pancreas needs to be lost to have pancreatic insufficiency? What other problems can develop?
90% Diabetes Mellitus (insulin requring, affects alpha and beta cells), fat and protein deficiency
“classic triad” of chronic pancreatitis
- Pancreatic calcifications
- Steatorrhea
- DM
What is the best imaging for chronic pancreatitis? What is the worst?
Best: MRCP–uses no radiation, no contrast
Worst: Ultrasound (least sensitive and specific)
What should you suspect when total bilirubin and alk phos are elevated in pancreatitis?
Obstruction from fibrosis, stricture, stone/calcification or edema
When should you take pancreatic enzyme supplementation?
First bite of a meal.
Examples are Pancreaze, Creon, Ultresa
How does CCK cause pain?
Releasing factors stimulate duodenum to release CCK. CCK stimulates pancreas to secrete digestive enzymes, which also degrade the releasing factors. When no enzymes are produced, releasing factors are never degraded so the pancreas keeps trying to make more enzymes. Result is pain from way too many digestive enzymes.
Pain management for pancreatitis
TCA + short course of opiates and NSAIDs for 3 weeks.
Where do most pseudocysts occur and what can it cause?
2/3 are in the tail of the pancreas.
Abd. pain, obstruction, vascular occlusion, spontaneous infection, pseudoaneurysm (digestion of nearby vessel)
Treatment of pseudocysts
Drainage if >6 cm or persisted for >6 weeks
Postprandial pain and early satiety
Duodenal obstruction
Pain and elevated LFTs
Bile duct obstruction
95% of malignant neoplasms in pancreatic cancer arise from where?
Exocrine elements.
85% of tumors are adenocarcinomas arising from ductal epithelium.
Generalized pain or epigastric/back pain. May be intermittent and worse with eating, worse at night. Weight loss, anorexia, diarrhea, steatorrhea, vomiting, may see Virchow’s nodes, etc
Pancreatic cancer
Where do most pancreatic tumors occur?
Head of the pancreas (60-70%)
These are more likely to present with jaundice, steatorrhea, and weight loss
How do you diagnose pancreatic cancer?
Can’t just rely on symptoms. Need to do imagine and liver function testing. Transabdominal U/S, CT scan
Confirm with biopsy
What is the role of tumor markers in pancreatic cancer?
CA19-9 is related to tumor size.
Degree of elevation at presentation and post-op setting associated with prognostic predictions.
What stimulates the gallbladder?
CCK
Vagus and splanchnic nerves
Where is ALT found? What is it correlated with?
Found in high concentrations of the liver, low concentrations in heart and kidney.
ALT and trunk fat are related–more central adiposity may have falsely elevated ALT
Where is AST found? What is it correlated with?
Found in tissues of high metabolic activity. Heart, liver, skeletal muscle, kidney, brain, pancreas, spleen, lungs.
Level of elevation correlates with number of damaged cells and time since injury. Evaluates liver and heart disease
What can cause increased AST?
Acute MI, liver disease, tissue trauma (infection, hyperthermia, brain trauma, injury), Hypothyroidism
Where is Alkaline Phosphatase found? What does it correlate with?
Originates in bone, liver, placenta.
Tumor marker, index of liver and bone disease.
Rises with biliary tract obstruction AND rise is out of proportion to AST, ALT elevations.
Liver disease, hyperparathyroidism, CHF, CKD, ulcerative colitis
True or false: There is no increase in AP with osteoporosis.
True
GGT will be elevated when? When do you check it?
Elevated Alk Phos can be from bone or liver. Cehck GGT–will be elevated with liver disease but normal with bone disease
GGT is associated with what?
Sensitive to amount of alcohol consumed in chronic drinkers, elevated in all forms of liver disease/liver cancer
Disproportionate elevation in serum ALT and AST compared to ALP
hepatic cause
Disproportionate elevation in serum ALP compared to ALT and AST
biliary cause
AST>ALT (2:1)
Alcohol
ALT>AST
Hepatic cause
How long do LFTs need to be elevated to be chronic? How high to be mild?
Chronic: 6 months +
Mild: Less than 5X ULN
Work up of chronic LFT elevation?
- Identify meds that can cause this
- Assess alcohol abuse
- Hepatitis?
4. - Consider NASH
Risk factors for developing gallstones
Female, 40, fat, fertile (pregnancy) Rapid weight loss Genetics (native americans) Cirrhosis HyperTG Gallbladder stasis from DM, TPN, spinal cord injury, use of octreotide
What is the biggest contributing substance to biliary sludge?
Cholesterol
Gallstone disease will have what kind of PE findings, labs?
normal
Biliary colic that is actually usually constant, dull/achy in RUQ or epigastrum, radiate to back or right shoulder, diaphoresis, n/v, NOT made worse with movement, lasts 30 minutes, plateus in an hour. Entire attack lasts less than 6 hours.
Gallstone disease, biliary colic
Visceral in origin, GB wall is not inflamed
Chest pain, general abd. pain, belching, fluid regurgitation, abd. distention/bloating, retrosternal burning, n/v
atypical presentation of gallstone disease
What if you were expecting to see gallstones on ultrasound and didn’t?
Repeat in a few weeks
4-6 hours of prolonged biliary colic, assocaited fever, pain and peritoneal inflammation, abnormal labs
acute cholecystitis
fever, leukocytosis, hypotension, mental status changes
Acute cholangitis (complication of choledocolithiasis)
What will you find on CCK Cholescintigraphy in pt with functional gb d/o?
Low ejection fraction
Treatment of gallstones with biliary symptoms
Elective cholecystectomy because this will prevent repeated attacks and complications. Pain management with NSAIDS or IV Keterolac (Toradol). May use opioids if cannot take NSAIDS but ALL opioids increase tone at sphincter of Oddi
RUQ pain, fever, leukocytosis associated with gallbladder inflammation/gallstones.
+ Murphy’s sign (pain on palpation of GB)
Will lay still since movement makes it worse
Acute cholecystitis
Looks the same as acute cholecystitis but NOT associated with gallstones
Acalculous cholecystitis
Result of mechanical irritation or recurrent GB attacks, end result is fibrosis and thickening of GB
Chronic cholecystitis
What is a porcelain gallbladder?
Uncommon manifestation of chronic cholecystitis. GB becomes calcified, can identify on plain xray. increases risk of developing GB carcinoma (poor prognosis).
Always get cholecystectomy
Labs for acute cholecystitis
Leukocytosis (may have abdnemia)
LFTs should be normal in uncomplicated case
U/S is test of choice. CT misses 1/5 of gallstones because they are the same radiodensity as bile
What would you expect to see on ultrasound of acute cholecystitis?
- Gallstone in cystic duct
- GB wall thickening >2-4 mm
- Gall bladder distention
- Perichoecystic fluid
5 . Air in gallbladder wall (gangrenous) - Ultrasonographic murphy’s sign
- Dilation of common bile duct or intrahepatic ducts
Role of Cholescintigraphy (HIDA Scan)
HIDA is injected and selectively taken up by hepatocytes and secreted into bile. Can visualize GB, cystic duct, CBD and small bowel within 30-60 minutes. test is considered positive if GB does not visualize within 60 minutes.
Since acute cholecystitis will go away on its own in 7-10 days, why treat it?
Complications are common! Gallbladder gangrene with subsequent perforation is the most common. Patients need cholecystectomy.
Fistula and ileus can also happen.
Antibiotic guidelines for acute cholecystitis
If WBC >12.5, clinical findings of temp >101.3, air in GB, elderly, immunocompromised
What antibiotics are used to treat acute cholecystitis?
First line is monotherapy with Piperacillin/Tazobactam (Zosyn)
OR
Ceftriaxone (Rocephin) PLUS Metronidazole (Flagyl)
OR
Levaquin Plus Flagyl
NSAIDs (Toradol) for pain.
What can chronic cholecystitis cause?
Increased risk of gallbladder cancer
Risk factors for acalculous cholecystitis?
Prolonged fasting (endotoxin is released from bile)
Increased serum bilirubin, alk phos, and GGT out of proportion to AST and ALT elevations
Choledocolithiasis
Treatment of choledocolithiasis
Locate stone, remove it
Use ERCP. If can’t do ERCP, perform cholecystectomy
Stone gets stuck in ampulla of Vater and blocks bile output. Stagnant bile becomes infected and bacteria spreads back up ductal system into liver. (bacterial translocation into biliary tract)
Asending cholangitis
Most common offender of ascending cholangitis?
E. Coli! (Up to 50%)
Klebsiella, Enterobacter. Also some gram positives, anaerobes are rarely the sole infecting organism.
Classic presentation of ascending cholangitis
Charcot’s triad (Fever, Jaundice, RUQ Pain)
Reynold’s Pentad (Charcot’s triad plus hypotension and altered mental status)
What if you suspect acute cholangitis but they lack Charcot’s triad?
Transabdominal ultrasound. If positive on stones or CBD dilation, perform ERCP in 24 hours.
Progressive inflammation, fibrosis, and structuring or med. and large intrahepatic and extrahepatic bile ducts. This condition has a strong association with what?
Primary Sclerosing Cholangitis
Strong association with ulcerative colitis (can occur years after colectomy for UC)
Who is primary sclerosing cholangitis more common in? What is time of survival without liver transplant?
70% are men.
Average time is 10-12 years after diagnosis without liver transplant
Fatigue, itching, intermittent fever, chills, RUQ pain. How do you diagnose this?
Primary Sclerosing Cholangitis
Cholangiography (ERCP, MRCP)
Biopsy can support but isn’t diagnostic
Labs for primary sclerosing cholangitis
Cholestatic pattern on LFTs
Positive p-ANCA 80% of the time.
Negative antimitochondrial antibodies
T-lymphocyte mediated attack on small intralobular bile ducts
Primary biliary cirrhosis
\+ Antimitochondrial antibodies White women Fatigue, pruritus, hyperpigmentation of skin 30-65 years old Rheumatic symptoms
Primary biliary cirrhosis
Diagnose with liver biopsy and perform serum testing
