Step up to Medicine- GI Flashcards
Hemochromatosis (AR d/o) -defect in iron absorption leading to increased iron which will deposit in different organs. Pt is usu asymptomatic with mild elevation of ALT and AST levels. What to do to diagnose?
- obtain iron studies.
- if iron is elevated, order a liver biopsy to confirm
How do you clinically stage colorectal cancer?
clinical staging done with CT scan of chest, abdomen, pelvis and by PE (ascites, hepatomegaly, LAD)
What’s the most common cause of large bowel obstruction in adults?
colorectal cancer
Right sided vs left sided colorectal cancer.
Right-sided colorectal cancer: melena, obstructionis unusual b/c cecum has the largest luminal diameter, occult blood in stool, iron deficiency anemia, changes in bowel habits uncommon
*triad of anemia, weakness and RLQ mass
Left-sided colorectal cancer: more signs of obstruction 2/2 to smaller lumen, changes in bowel habits more common (alternating constipation/diarrhea, narrowing of stools -pencil stools), hematochezia
Rectal cancer makes up 20-30% of all colorectal cancers. Rectal cancer has a higher recurrence rate and lower 5-yr survival rate. List symptoms
hemtochezia, tenesmus, and rectal mass
Surgery is only curative treatment of colorectal cancer. Follow-up is impt! What is part of the follow-up work-up post-surgery for colorectal cancer? Follow-up is impt b/c about 90% of recurrences occur in the first 3 years.
- stool guaiac test
- annual CT of abdomen/pelvis and CXR for up to 5 years
- colonoscopy at 1 year and then every 3 years
- CEA levels every 3-6 months (elevations are sensitive indicators for recurrence, too high can indicate liver involvement)
Colonic polyps: nonneoplastic vs adenamatous. List the 3 non-neoplastic and treatments
Non-neoplastic:
1) hyperplastic (metaplastic polyps): most common (90%), generally remain small and asymptomatic , no specific requirement but usu removed b/c hard to distinguish from adenamatous
2) juvenile polyps
- typically in children younger than 10 & are highly vascular, should remove
3) inflammatory polyps
- “pseudopolyps” are assoc with ulcerative colitis
Colonic polyps: nonneoplastic vs adenamatous. List the 3 adenamatous and treatments
Adenamatous polyps:
1) Tubular (most common) -SMALLEST risk of malignancy
2) Tubulovillous -intermediate risk
3) villous -greatest risk
Treatment for all 3 = removal
Diverticolosis: due to increased intraluminal pressure leading to pouches in the colon wall. What are the risk factors? The most common location?
risk factors: increasin age, lower-fiber diets, positive family history
most common site is sigmoid colon
What is the test of choice for diverticolosis?
Barium enema
*x rays are usu normal therefore not diagnostic
Treatment of diverticulosis (symptoms: vague LLQ discomfort, bloating, constip/diarrhea)
- high fiber foods
- psyllium
A complication of diverticolosis is painless rectal bleeding. Usually it’s clinically insignificant and you don’t do anything for it. But 5% experience severe bleeding. What do you do then?
- even when it’s severe, in most cases, it resolves spontaneously
- colonoscopy may be performed to locate site and mesenteric angiography
- if bleeding is persistent and/or recurrent, surgery may be needed (segmental colectomy)
A complication of diverticolosis is diverticulitis affecting 15-25% of patients. It happens when feces become impacted in the diverticulum leading to erosion and microperforation. What is the diagnostic imaging for diverticulitis?
CT of abdomen and pelvis with oral and IV contrast -reveals a swollen, edematous bowel wall or an abscess
uncomplicated diverticulitis treatment
IV abx, bowel rest (NPO), IV fluids
What are some complications associated with diverticulitis?
- abscess formation (can be drained)
- colovesical fistula
- obstruction
- free colonic perforation
treatment is surgery
Clinical features of diverticulitis:
LLQ pain, fever, leukocytosis
Angiodysplasia of the Colon aka arteriovenous malformations/vascular ectasia -what is it? causes what problems? treatment? dx?
AV malformations are tortuous dilated veins in submucosa of the colon wall that is a common cause of bleeding in pts over age 60. Bleeding is usually low-grade. Colonoscopy is diagnostic choice. It can be treated by colonoscopic coagulation
As many as 25% of pts with bleeding AV malformations have what other valvular abnormality?
aortic stenosis
If someone has severe abdominal pain disproportionate to physical findings, what should you suspect?
acute mesenteric ischemia
List some signs of intestinal infarction? If you suspect acute mesenteric ischemia, what levels should you check?
- hypotension, tachypnea, lactic acidosis, fever, altered mental status
- check lactate level!
What is the definitive diagnostic test for acute mesenteric ischemia?
mesenteric angiography
What is the therapy of choice for the arterial causes of acute mesenteric ischemia (embolic, arterial and non-occlusive)?
vasodilator called papaverine directly into SMA
Chronic mesenteric ischemia is caused by atherosclerotic occlusive disease of main mesenteric vessels. What are some symptoms
abdominal angina dull pain typically post-prandial
significant weight loss
What is the dx modality of choice to detect chronic mesenteric ischemia? What is the definitive treatment?
- mesenteric arteriography
- surgical revascularization is the definitive treatment of choice
What is Ogilvie’s sydrome?
signs, symptoms and radiographic evidence of large bowel obstruction but there is NO MECHANICAL obstruction. This usually affects ill people with recent history of surgery or with serious medical illnesses
When is the colon in impending rupture?
when there is colonic distention and when the colon diameter exceeds 10 cm -decompress immediately
C. diff presents with profuse watery diarrhea, crampy abdominal pain and can lead to toxic megacolon. Treatment is?
d/c offending abx, and give metronidazole or oral vanco
-can give cholestyramine to improve diarrhea
How to diagnose c. diff?
- c. diff toxins in stool is diagnostic but takes up to 25%
- flexible sigmoidoscopy is most rapid and is diagnostic but not used b/c of comfort and expense
What’s the most common site of colonic volvulus? What are some signs of colonic volvulus?
sigmoid colon (75% of all cases), cecum is 25% -acute onset of colicky abdominal pain, obstipation, abdominal distention, anorexia, n/v
Plain abdominal films can be used to assess colonic volvulus. How will they look if it’s a sigmoid volvulus vs cecal volvulous?
What’s the preferred diagnostic and therapeutic test for sigmoid volvulus?
1) sigmoid volvulus: OMEGA LOOP SIGN/bent inner tube shape is a sign of dilated sigmoid colon
2) cecal volvuls: COFFEE BEAN SIGN indicates large air-fluid level in RLQ
Sigmoidoscopy is preferred diagnostic and theraptuic test for sigmoid volvulus
What are the 2 most common causes of cirrhosis?
1) alcohol
2) viral infection, esp hep C
What’s the gold std for diagnosis of cirrhosis?
biopsy
Complications of liver failure (AC, 9H)
Ascites Coagulopathy Hypoalbuminemia portal Hypertension hyperammonemia hepatic encephalopathy hepatorenal syndrome hypoglycemia hyperbilirubinemia/jaudice hyperestrinism hepatocellular carcinoma
Portal hypertension is a complication of cirrhosis: list clinical features, diagnsois and treatment
clinical features: bleeding (hematemesis, melena, hematochezia) 2/2 to esophageal varices is most life-threatening
diagnosis is based on clinical symtpoms, paracentesis can help
treatment is transjugular intrahepatic portal-systemic shunt (TIPS) to lower portal pressure
What are some classic signs of chronic liver disease?
- ascites
- varices
- gynecomastia, testicular atrophy
- palmar erythema, spider angiomas
- hemorrhaids
- caput medusae
Varices are a huge complication of cirrhosis. Clinical features include: massive hematemesis, melena, and exacerbation of hepatic encephalopathy. How to treat?
- stabilize patient
- IV abx given ppx
- IV octreotide is initiated and continued for 3-5 days
- perform emergent upper GI endoscopy for diagnsois and
- treat hemorrhage either with variceal ligation or sclerotherapy
- b blockers as LONG-TERM therapy to prevent rebleeding
The most common complication of cirrhosis is ascites 2/2 to portal hypertension in which there’s accumulation of fluid in the peritoneal cavity due to increased hydrostatic pressure and hypoalbuminemia (reduced oncotic pressure) What are clinical features?
-abdominal distension, shifting dullness, fluid wave
When there’s ascites, you can do paracentesis to determine whether ascites is due to portal HTN or another process like SBP
-measure serum ascites albumin gradient (serum albumin - ascitic albumin)
If it is > 1.1 g/dL, portal HTN is very likely
How to manage ascites?
salt restriction and diuretics in most cases (furosemide and spironolactone)
If you suspect hepatocellular carcinoma in someone with liver cirrhosis, what’s the imaging of choice?
CT-guided biopsy
What are clinical features of of hepatic encephalopathy?
- decreased mental function, confusion, poor concentration, even stupor or coma
- asterixis (“flapping tremor”)
- rigidity, hyperreflexia
- fetor hepaticus -musty odor breath
Treatment for hepatic encephalopathy
- lactolose prevents absorption of ammonia
- neomycin can kill bowel flora to decrease ammonia production by intestinal bacteria
- limit protein to 30g - 40 g/day
Hepatorenal syndrome is end-stage liver disease characterized by progressive renal failure in advanced liver disease 2/2 to renal hypoperfusion due to vasoconstriction of renal vessels. What often precipitates hepatorenal syndrome? Will renal injury respond to volume expansion?
infection or diuretics
kidneys will not respond to volume expansion
Clinical symptoms of hepatorenal syndrome
-azotemia, oliguria, hyponatremia, hypotension, low urine sodium (
Spider angiomas -what’s dilated?
dilated cutaneous arterioles with central red spot and reddish extensions
Liver cirrhosis is assoc with coagulopathy b/c of decreased synthesis of clotting factors. How should you treat it?
give FFP b/c Vit K won’t work on the diseased liver
Wilson’s disease (AR) -decrease ceruloplasmin which usu binds copper to allow it to be excreted by the liver causing copper accumulation in various organs. What are clinical features?
- liver disease
- kayser fleischer rings 2/2 to copper deposition in eyes but do not affect vision
- CNS findings (EPS signs, parkinsonian symptoms, chorea, drooling, incoordination due to copper in basal gangia)
- renal involvement: nephrocalcinosis, aminoaciduria
How to treat someone with Wilson’s disease?
- chelating agents like D-penicillamine which removes and detoxifies excess copper
- zinc (prevents uptake of dietary copper)
- liver transplantation
- monitor pt’s copper levels, urinary copper excretion, ceruloplasmin, liver function, PE for signs of liver or neuro disease, psych helath
Hemochromatosis (AR) -excessive iron absorption in intestine leads to accumulation of ferritin and hemosiderin in various organs leading to fibrosis 2/2 to hydroxyl free radicals generated by the excess iron. What are some complications of hemochromatosis?
- cirrhosis (which can lead to HCC)
- cardiomyopathy
- diabetes mellitis
- arthritis (most commonly in 2nd and third MCP joints, hips and knees)
- hypogonadism (impotence, amenorrhea, loss of libido)
- hypothyroidism
- hyperpigmentation of skin (“bronzelike”)
What’s required for diagnosis of hemochromatosis?
-liver biospy (determines hepatic iron concentration)
HOw to treat hemochromatosis?
-repeated phlebotomies
Hepatocellular adenoma is a benign liver tumor most commonly found in? What do you have to worry about?
in young women (15-40 years of age), OCP use, female sex, and anabolic steroids
-worry about rupture b/c can lead to hemoperitoneum and hemorrhage so resect tumors if > 5 cm that do not regress after stopping OCPs
Cavernous hemangiomas are the most common benign liver tumor. They are usu small and asymptomatic and do not require treatment. How to diagnose?
- diagnose with US or CT scan with IV contrast
- biopsy contraindicated b/c it’s a vascular tumor will cause bleeding
List 8 risk factors of HCC
1) Cirrhosis esp in assoc with alcohol or hep B or C
2) chemical carcinogens (aflatoxin, vinyl chloride, thorotrast)
3) hemochromatosis, wilson’s disease
4) schistosomiasis
5) hepatic adenoma
6) cigarette smoke
7) AAT def
8) glycogen storage disease type 1
Gilbert’s syndrome
AD due to decreased hepatic uridine diphosphate glurcuronyl transferase (UDGT) activity leading to high unconjugated bilirubin. Asymptomatic in most cases, exacerbated by stress, fasting, fever, alcohol, infections. NO TREATMENT.
What is hemobilia?
-blood draining into the duodenum via commonbile duct where the source of bleeding can be anywhere along the biliary tract, the liver, or the ampullary region
Clinical symptoms of hemobilia? what is diagnostic? treatment?
Hemobilia can be caused by trauma (most common), papillary thyroid carcinoma, surgery, tumors, infection
Symptoms: GI bleeding, jaundice, RUQ pain
Arteriogram is diagnostic
Treatment is resuscitation (may require transfusions). If bleeding is severe –> surgery
Liver cysts: polycystic liver cysts and hydatid liver cysts.
1) Polycystic liver cysts: AD, usu assoc with PKD. rarely leads to hepatic fibrosis and liver failure; usu asymptomatic, pts will die from renal complications than liver, treatment is usu asymptomatic
2) Hydatid liver cysts: caused by infection from tapeworm Echinococcus granulosus, cysts in right lobe of liver. small cysts are asymptomatic, larger cysts may cause RUQ pain and rupture into the peritoneal cavity, causing fatal anaphylatic shock. TREATMENT: surgical resection to avoid spilling contents of the cyst into the peritoneal cavity. Mebendazole is given after surgery
Liver abscess: pyogenic liver abscess vs amebic liver abscess -both are commonly found in right lobe
What is the most common cause of pyogenic liver abscess? Clinical presentation? dx? treatment?
pyogenic liver abscess
- most common cause is biliary tract obstruction -obstruction of bile flow allows bacterial proliferation (e coli, klebsiella, proteus, enterococcus, anaerobes)
- other causes: trauma, GI infections
- look quite ill: fever, malaise, anorexia, weight loss, nausea, vomiting, RUQ pain and jaundice
- diagnosed by US or CT
- fatal if untreated
- IV abx and percutaenous drainage of abscess
Liver abscess: pyogenic liver abscess vs amebic liver abscess -both are commonly found in right lobe
Amebic liver abscess found most commonly in what population? Caused by? Clinical picture? Treatment?
Most common in men particularly homosexual men transmitted thru fecal-oral contact caused by intestinal amebiasis (entamoeba histolytica), reaching the liver via portain vein
clinical: fever, RUQ pain, n/v, hepatomegaly, diarrhea
Serologic testing (immunoglobulin G enzyme immunoassay) stablishes diagnosis
E. histolytica stool antigen test is not sensitive
imaging studies can detect abscess but can’t differentiate from pyogenic
IV metronidazole
What is Budd-chiari syndrome? Clinical features?
Liver diease 2/2 occlusion of hepatic venous outflow –> hepatic congestion & microvascular ischemia
Clinical features: resemble those of cirrhosis -hepatomegaly, ascites, RUQ pain, jaundice, variceal bleeding
What is the diagnosis of budd-chiari syndrome?
hepatic venography
serum ascites albumin gradient > 1.1 g/dL
What are some causes of budd-chiari syndrome?
- hypercoaguable states
- myeloproliferative disorders (polycythemia vera)
- pregnancy
- chronic inflammatory diseases
- infections
- malignancies
- trauma
- idiopathic
What are the 3 major causes of jaundice
- hemolysis
- liver disease
- biliary obstruction
Conjugated vs unconjugated bilirubin: color of urine, toxic or not?
- conjugated
- water soluble
- excess is excreted in urine
- therefore, dark urine is only seen with conjugated bilirubin
- nontoxic
- unconjugated
- not water soluble
- cannot be excreted in urine
- TOXIC b/c can cross BBB –> neuro deficits
Dark urine and pale stools signal a _________ hyperbilirubinemia
conjugated
urine + for bilirubin
viral or alcoholic hepatitis, cirrhosis: conjugated, unconjugated or mixed hyperbilirubinemia?
mixed
Rotor’s syndrome and Dubin-Johnson syndrome -problems with?
problem with transporting conjugated bilirubin (decreased intrahepatic excretion) into the canaliculi causing conjugated hyperbilirubinemia
Gilbert’s syndrome and Crigler-Najjar syndrome -problems with?
problems with conjugating bilirubin due to deficient glucuronyl transferase
List clinical findings of cholestasis when there’s blockage of bile flow with an increase in conjugated bilirubin levels
- jaundice, gray stools, dark urine
- pruritus (bile salt deposition in skin)
- elevated alk phosp
- elevated serum cholesterol (impaired excretion)
- skin xanthomas
- malabsorption of fats and fat soluble vitamines (ADEK)
ALT vs AST, which is more sensitive and specific to liver
ALT
If ALT and AST levels are mildly elevated (low hundreds), think?
chronic viral hepatitis or acute alcoholic hepatitis
If ALT and AST levels are moderately elevated (high hundreds to thousands), think?
acute viral hepatitis
If ALT and AST are severely elevated > 10,000, think?
due to extensive hepatic necrosis prob due to:
- ischemia, shock liver (prolonged hypotension or circulatory collapse)
- acetaminophen toxicity
- severe viral hepatitis
What do you expect ALT and AST to be in someone with cirrhosis or metastatic liver disease?
-normal or even low b/c # of healthy liver cells is reduced
ABCDEFGHI -mnemonic for causes of elevations of ALT or AST in asymp patients
Autoimmune hepatitis hepatitis B hepatitis C Drugs or toxins Ethanol Fatty liver Growths (tumors) Hemodynamic disorders Iron (hemochromatosis), Copper (Wilson's), AAT deficiency
If Alk-phosp is high, how to see if it’s liver related or extrahepatic?
order GGT (gamma-glutamyl transferase): if elevated, think liver; if not, think either bone disease or preg
Describe 3 types of gallstones
1) cholesterol stones
- obesity, diabetes, multiple preg, OCP, Chrohn’s, ileal resection, advanced age, native american, cirrhosis, CF
2) pigment stones
- black stones assoc w/ hemolysis or alcoholic cirrhosis
- brown stones assoc with biliary tract infections
3) mixed stones
- majority of stones
What’s the cardinal symptom of gallstones (cholethiasis)?
- biliary colic due to temporary obstruction of cystic duct by a gallstone when pain is caused by gallbladder contracting against obstruction
- therefore pain is commonly reported after eating and at night
What is Boa’s sign?
in cholethiasis, there’s referred right subscapular pain of biliary colic (pain caused by gallbladder contracting against obstruction caused by gallstone of cystic duct)
How to diagnose cholethiasis?
RUQ ultrasound
cholethiasis can cause Acute cholecystitis which is inflammation (NOT INFECTION) of gallbladder wall. What’s the triad? What sign is assoc?
triad: RUQ pain, fever, leukocytosis
+ murphy sign
What’s the imaging of choice for acute cholecysitis?
RUQ ultrasound
use hepatoiminodiacetic acid radionuclide scan (HIDA_ if US is inconclusive
*a positive HIDA scan is when gallbladder is not visualized b/c then there’s an obstruction 4 hrs after injection
Gallstone ileus is a complication of cholecystitis. what is it
when gallstone enters bowel lumen via cholecystoenteric fistua and gets stuck in terminal ileum causes obstruction
Choledocholithiasis is when there’s a stone in the common bile duct. It can be primary or secondary from gallbladder. What is the GOLD STD to diagnose?
GOLD STD -endoscopic retrograde cholangiopancreatography (ERCP) -NOT ONLY DIAGNOSTIC BUT ALSO THERAPEUTIC
-but still do US first
Cholangitis is infection of biliary tract 2/2 to obstruction –> biliary stasis & bacterial growth (60% due to choledocholithiasis). Its clinical features are summarized by a triad called Charcot’s triad. What makes up the triad?
Charcot’s triad signifies cholangitis
-fever, jaundice, RUQ pain
If present with sepsis + AMS –> Reynold’s pentad (CAN BE RAPIDLY FATAL)
What’s the most dreaded and serious complication of acute cholangitis?
hepatic abscess
Porcelain gallbadder -should by ppx removed, why?
porcelain gallbladder is intramural calcification of gallbladder wall. PPX removed b/c can develop into cancer of gallbladder
Primary sclerosing cholangitis -chronic progressive disease of intrahepatic and/or extrahepatic bile ducts characterized by thickening of bile duct walls and narrowing of lumens leading to CIRRHOSIS, PORTAL HTN, LIVER FAILURE. Strong assoc with with IBD?
Ulcerative colitis (p-anca, continuous starting from rectum)
what’s the diagnostic studies of choice for primary sclerosing cholangitis?
ERCP and PTC will reveal multiple areas of bead-like stricturing and bead-like dilatations of intrahepatic and extrahepatic ducts
Primary biliary cirrhosis is a chronic and progressive cholestatic liver disease characterized by destruction of intrahepatic bile ducts with portal inflammation and scarring. What are some clinical features?
- fatigue
- pruitis (early in course of disease) –use cholestyramine
- jaundice (late)
- RUQ discomfort
- Xanthomata and xanthelasmata
- osteoporosis -use calcium, bisphosphonates, vitamin D)
- portal HTN
Primary biliary cirrhosis is a chronic and progressive cholestatic liver disease characterized by destruction of intrahepatic bile ducts with portal inflammation and scarring. How to confirm diagnosis? Also what kind of antibodies are found? Liver transplant is only cure, but what can slow down disease?
Liver biospy to confirm
and antimitochondrial abs found in up to 95% of patients
ursodeoxycholic acid can slow progression of disease
Bile duct stricture has clinical signs of obstructive jaundice. Preferred treatment?
endoscopic stent
What is biliary dyskinesia? How to diagnose?
motor dysfunction of sphincter of oddi –> recurrent episodes of biliary colic w/o evidence of gallstones on US, CT, and ERCP
diagnosed by HIDA scan
1) fill gallbladder with labeled radionuclide
2) give CCK iv which will cause sphincter of oddi to relax and contract gallbladder
3) determine EF of gallblader
* if EF is low, dyskinesia is likely
