GI Combo 2
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| 85% of colorectal cancers are predicted to arise from _______, and the genes involving cancer are _____, ____, _____ | adenomatous polyps
1. tumor suppressor genes
2. proto-onco genes
3. DNA repair genes
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| tumor suppresor genes | down-regulate normal growth stimulatory pathways
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| proto-oncogenes | part of signaling pathway that promote normal cell growth and proliferation
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| DNA repair genes | maintain integrity of genome by repairing errors in nucleotides
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| risk factors for colorectal cancer | #1 AGE
personal/family hx
familial syndromes like polyposis
race, acromegaly, renal transplant
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| familial adenomatous polyposis (FAP) | 1. autosomal dominant
2. 100% chance colon cancer wo prophylactic tx
3. flexible sigmoidoscopy from age 12 til 1st polyp found, then COLECTOMY!
4. 30-100% also get upper GI polyps
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| attenuated FAP | 1. onset +10 years than FAP
2. 10-99 polyps
3. screen with colonoscopy starting 10 years younger than relative with disease
*auto dom too!*
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| Lynch Syndrome | 1. auto dominant
2. 80% risk colon ca
3. dx thru genetic testing
4. colonoscopy q1-2 yr @ age 20
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| risk factors for colon cancer | sedentary, smoke, fatty, T2DM, androgen deprivation, EtOH
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| what are protective factors to reduce risk? | ASA, NSAIDS, folate
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| screening modalities | 1. *colonoscopy* (diagnostic+therapeutic)
2. guiac
3. flex sigmoidoscopy
4. double contrast barium enema
5. CT colonography
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| tubular polyps | most common and least aggressive
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| pedunculated polyps | more common and less aggressive than sessile
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| hypersplastic polyps | usually benign
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| worst polyps to have? | villous (then tubular villous)
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| clinical presentation of CRC? | asx
most common sx: ab pain, change bowels, hematochezia
alarm sx: BRBPR, abd mass
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| what type of lesions are more common with iron-deficiency anemia? | right sided
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| obstructions cause lesions on which side? | left
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| what is the primary sx of rectal lesions? | hematochezia
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| what is the #1 prognostic factor for CRC? | stage at diagnosis
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| first line tx for CRC? | excision
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| TNM staging in CRC: T1 | invades submucosa
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| TNM staging in CRC: T2 | invades muscularis propria
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| TNM staging in CRC: T3 | invades pericolorectal tissues
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| TNM staging in CRC: T4a | reaches surface of visceral peritoneum
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| TNM staging in CRC: T4b | directly adheres to other organs
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| TNM staging in CRC: N1 | 1-3 regional nodes
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| TNM staging in CRC: N2 | 4+ regional nodes
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| which type of CRC is the only type where radiation is a tx? | rectal because it is stationary
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| what do esophageal cells secrete? | bicarb to alkalinize contents
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| how does respiration affect the esophagus? | diaphragm pinches the esophagus closed during inspiration
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| what is a first choice diagnostic if you suspect motility disorder or mechanical obstruction? | barium swallow
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| what is a first choice diagnostic if you suspect aspiration? | modified swallow @ bedside
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| when is EGD best? | best when tissue sample is needed or if visual of anatomy is necessary
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| manometry | evaluates esophageal motility, gives pressures at various points, local anasthetic no sedation
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| ambulatory intraesophageal pH monitoring | most sensitive to detect GERD to monitor timing, freq, duration of each episode
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| esophageal impedance | NG catheter based
detects changes in resistance to electric current
use for any type of reflux
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| what is the primary problem with GERD? | dysfunctional lower esophageal sphincter where gastric juices or inadequate clearing mechanisms may damage tissue
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| what factors contribute to GERD? | (increased intraabdominal pressure)
hiatal hernia
obesity
pregnancy
(relaxed smooth muscle)
ETOH, meds, foods, pregnancy
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| how do you diagnose GERD? | complete removal of sx from treatment
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| standard GERD therapy | lifestyle mod, antacids, H2RAs, PPI
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| what are some drawbacks of PPIs? | dont address LES dysfunction
only 80% efficacious
less responsive for atypical patients
*interact with protease inhibitors and plavix*
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| what is an alternative med for functional heartburn? | SSRI
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| what must a pt exhibit to be a surgical candidate? | normal esophageal function
failed medical therapy
etc..
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| 4 common causes of esophageal strictures | GERD
trauma (physical or chemical)
radiation
malignancy
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| tx for esophageal stricture | dilitation with biopsy
chronic PPI
steroid injections
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| barretts therapy | PPI
anti-reflux surgery
endoscopy fro high grade disease
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| types of esophageal cancer | barretts
esophageal adenocarcinoma
squamous cell carcinoma of the esophagus
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| symptoms of esophageal cancer? | dysphagia
weight loss
dysphonia
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| achalasia presentation | dysphagia to liquids and solids (better with valsava)
chest pain
vomit/aspiration
absence of GERD or bleching
modest weight loss
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| what is achalasia? | loss of intramural neurons
lack of normal peristalsis
failure of LES to relax
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| primary causes? secondary causes of achalasia? | primary is idiopathic
secondary due to cancer, chagas, viral, neurodegenerative disorders
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| achalasia management | sublingual NG
CCB
botox
balloon dilitation
esophagetomy
*goal is to decrease the pressure to open the LES sphincter*
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| what are some motility disorders? | achalasia
diffuse esophageal spasm
scleroderma
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| diffuse esophageal spasm | patchy neural degradation
non-peristalti contractions
dysphagia to solids and liquids
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| scleroderma of the esophagus | atrophy and sclerosis of the esophageal wall
"stovepipe esophagus"
combined with GERD
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| clinical presentation of infectious esophagitis | acute onset, odynophagia, dysphagia, chest pain, systemic sx (plus mroe if host is immunocompromised)
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| differentials for infectious esophagitis | candida
CMV
HSV
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| treatment for infectious esophagitis | antimicrobials
steroids
hydration
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| which type of esophagitis is common in kids and teens? | eosinophilic
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| what are the different types of inflammatory esophagitis? | infectious
radiation
eosiniophilic
corrosive
pill-induced
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| what factors contribute to the formation of gallstones? | hypomotility and high cholesterol
decreased bile salts or decreased phospholipids
high hormone levels
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| what conditions may contribute to the formation of black gallstones? | hemolytic diseases like sickle cell, prosthetic heart valves
(black due to bilirubin coming out of solution)
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| risk factors for gallstones | age, gender, obesity, severe weight loss, pregnancy(due to high estrogen), TPN, drugs (statins, ceftriaxone), DM, Crohns, spinal cord injuries
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| what is the best diagnostic tool for stones in the gallbladder? | sonography; 97% sensitive
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| best diagnostic tool for stones outside gallbladder, specifically in CBD? | endoscopic ultrasound
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| what are some findings on an ultrasound that may indicate acute cholecysitis? | GB wall edema, pericholecystic fluid, stone seen in the cystic duct
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| which test is only used to confirm that the cystic duct is plugged in cases of acute cholecystitis? | HIDA scan
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| what is the gold standard for stones in the common duct as it diagnosis and treats choledocholithiasis? | endoscopic retrograde cholangiopancreatography
ERCP
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| what is a complication of stones? | gallstone ileus where it blocks the iliocecal junction
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| cholelithiasis | stones in gallbladder
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| chronic cholecystitis aka "biliary colic" | caused by stones intermittently blocking cystic duct w/NO inflammation of gallbladder mucosa
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| acute cholecystitis | chronic blocking of cystic duct
--not an infection
--yes inflammation and dilation of gallbladder
--RUQ tenderness and fever
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| choledocholithiasis | bad
stone blocking CBD with sx of pain, jaundice, +Murphys sign and acholic stools
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| cholangitis | inflammation + obstruction
life threatening
pain, jaundice, +Murphys sign and acholic stools+fever+chills
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| biliary pancreatitis | stone blocks ileum or common bile duct
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| upper abdominal pain, usually epigastric or RUQ, that gradually increases over 15 minutes-plateaus-resolves. pain becomes more obvious during periods of weight loss or prolonged bed rest | chronic cholecystitis
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| meltzer-lyon test | aspiration of bile to assess for cholesterol and calcium bilirubinate crystals
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| mgmt of chronic cholecystitis? | cholecystectomy
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| abd pain, RUQ tenderness, fever and leukocytosis due to obstruction of cystic duct...causing stasis of bile, damage of gallbladder mucosa, and therefore release if inflammatory mediators | acute cholecystitis
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| what do you suspect if you see leukocytosis w/left shift, elevated LFTs? | acute cholecystitis
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| RUQ and epigastric pain with pruritis and jaundice | choledocholithiasis
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| occurrance of stones in CBD w/life threatening symptoms like cholangitis or acute pancreatitis | choledocholithiasis
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| what LFT values rise with obstruction? | alk phos+GGT+bili
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| standard treatment for choledocholithiasis | ERCP for diagnosis and removal, often with CBD exploration
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| impacted stone in CBD, bile stasis, bacterial superinfection of stagnant bile | cholangitis
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| presents as Charcots Triad: RUQ pain+fever+jaundice or Reynolds Pentad: RUQ=fever+jaundice+AMS+hypOtension | cholangitis
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| what dx has blood cultures + for enteric bacteria? plus elevated WBC w/left shift? | cholangitis
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| tx for cholangitis | IV fluids+electrolytes
blood cultures
antibiotics
stone extraction and cholecystectomy
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| murphy's sign | pain and arrest of inspiration upon deep palpation of right subcostal region
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| sx of severe hepatitis | *most are asymptomatic*
prodromal syndrome
dark urine
acholic stools
RUQ pain
jaundice
hepatomegaly
splenomegaly w/cervical lymphadenopathy
*elevated AST/ALT*
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| which hepatitis do you suspect? -acute onset with history of shellfish ingestion, foreign travel, or daycare setting | A
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| which hepatitis do you suspect? -acute onset with history of sex promiscuity, MSMm IVDA, recent tattoo | acute B
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| which hepatitis do you suspect? -asymptomatic with mild elevation of transamineases, with multiple risk factors present | chronic B or chronic C
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| which hepatitis do you suspect? -initial HBV symptoms are worse than expected, or condition suddenly worsens | D co-infection with B
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| which hepatitis do you suspect? -same presentation as Hep A, but HAV markers are negative | E
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| common lab features for all heps | transient neutropenia and lymphopenia
lymphocytosis
electrolyte imbalances
prolonged INR
normalish alk-phos
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| management of acute hep | treat each symptom
ultrasound to r/o masses, obstruction
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| when do you admit? | admit with sx of acute liver failure:
1. coagulopathy INR>1.5
2. encephalopathy
3. bilirubin>15
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| which heps can you be a carrier for? | NOT A
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| what is the early ab response for HAV? late response? | 1. HAV IgM during acute phase + elevated ALT/AST
--lasts for several months
2. Chronic phase, IgM falls and IgG appears
--remains + for life, and provides immunity
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| where is HAV concentrated? | feces, saliva
NOT urine
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| usually, what is the resolution of HAV like? | most resolve without incidence, no relapsing once you've passed the 6 month mark
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| cholestatic hepatitis | protracted jaundiced illness with pruritis
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| what key indicators may lead you to suspect HEV? | recent foreign travel
Hep presentation, but HAV Ab negative
detect HEV RNA in serum or stool
increasing titer of IgG anti-HEV
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| where is HBV present in the body? | serum and body fluids
DNA virus!!
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| what is the actual cause of liver damage in regard to the HBV? | the immune response to the virus damages the hepatocytes, the virus itself does not destroy the liver
*therefore the HBV viral load does NOT indicate how sick the patient is! liver enzymes do!*
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| how does the age of exposure to HBV affect survivability? | childhood: 90-95% have chronic infection
adult: 90-95% clear the virus
immunocompromised at risk for chronic infection
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| how would an acute HBV present? | new onset flu-like sx, RUQ pain, nausea and vomiting
-elevated transaminases (in 1000s)
-hyperbilirubinemia
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| which serologies can tell you if pt is vaccinated against HBV or recovered from HBV? | HBsAb + in both
HBc Total Ab +: immune/recovered
HBc Total Ab -: vaccinated
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| when do you treat HBV? | 1. anyone with +viral load and elevated liver enzymes
2. viral load>2000,
3. normal AST>ALT
4. evidence of fibrosis on biopsy
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| HBV treatment options | interferons, nucleoside analogs (entecavir and tenofovir) for life! *lifelong to prevent viremia-->prevent cirrhosis and liver cancer*
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| what are 3 complications of HBV? | 1. extrahepatic stuffs: polyarteritis nodosa, glomerulonephritis
2. cirrhosis
3. hepatocellular carcinoma
4. superinfection with HDV
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| what is the only oncogenic hepatitis? | HBV
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| what patient education points are necessary for HBV infected pts? | 1. viral supression for life
2. bi-annual HCC screening
3. vaccinate partners and household contacts
4. EtOh abstinence
5. MUST go to hepatologist if undergo immunosuppressive therapy due to virus reactivation
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| what does HCV progess to in 10-40 years? | cirrhosis
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| symptoms of HCV? | almost always asymptomatic, rarely becomes fulminant
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| who do you NOT treat fro HCV? | continued IVDA, EtOH abusers, psych issues, decompensated liver disease, autoimmune disorder like psoriasis
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| is Hep C curable? | yes, sometimes
*pts must maintain sustained virological response SVR*
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| what are SE of HCV anti-viral treatment? | neutropenia, thrombocytopenia, hemolytic anemia
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| HCV education points | 1. don't wait til u feel sick--by then you need a transplant
2. "cured" individuals can be reinfected
3. low neonatal transmission
4. variable disease progression
5. HCC testing required if cirrhotic
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| what are some clinical signs of chronic HBV/HCV? | jaundice
spider angiomas
palmar erythema
caput medusa
hepatosplenomegaly
ascites
neuro changes
gynecomastia
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| which OTC is preferred in cirrhotic patients for pain mgmt? | acetaminophen over NSAIDS due to bleeding
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| what vaccines are recommended for HCV infected? | HAV/HBV vaccines
influenze
pneumococcal
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| what are some complications of DILI? | cholestasis, fatty liver, granulomatous hepatotoxicity
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| what type of injury is associated with: steroids, antibiotics | cholestatic injurt
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| what type of injury is associated with: antivirals, antiarrhythmics, oncotherapy? | fatty liver
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| what type of injury is associated with: tylenol OD, diuretics, NSAIDS | directly hepatotoxic
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| HCC signs and symptoms? | often asymptomatic until large cancer
pain with palpable mass
friction rub/bruit over liver
blood tinged ascites
--weight loss, bloody ascites, night fevers
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| what are the CAGE questions, ans what is the sensitivity? | cut down
annoyed
guilty
eye opener
--93% sensitive, 76% specific
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| define hepatitis | inflammation of the liver due to any cause
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| define cirrhosis | architectural distortion of the liver parenchyma due to fibrosis due to any cause
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| what are 3 types of liver injury obtained by alcohol? | fatty liver=alcohol steohepatitis
alcohol hepatitis
alcoholic cirrhosis aka Laennecs cirrhosis
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| how are liver zones classified, and what are they? | based upon proximity to oxygen supply
--zone 1 is around portal tracts
--zone 3 close to central vein (oxygen poor)
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| basic pathogenesis of alcohol on the liver | 1. etoh injures hepatocytes and then they swell
"degeneration and intracellular accumulation"
2. TGs accumulate in hepatocytes and compounds already existing problems "steatosis"
3. apoptosis and zonal distribution of necrosis
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| what is the true cause of liver inflammation with alcohol? | immune system sends WBC in an inlammatory response, which destroy antigen presenting hepatocytes
--apoptosis itself does NOT cause inflammation
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| what happens to liver if you suddenly stop drinking? | they may be restored as they regenerate in response to apoptosis
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| describe how inflammation leads to cirrhosis | inflammation causes collagen deposits to form, which affect hepatic blood flow and perfusion of hepatocytes...this subdivides the liver into nodules which are surrounded by scar tissue-->cirrhosis
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| what labs do you order for alcohol liver disease? what are you looking for? | 1. LFTs (AST2-3x>ALT and elevated GGT)
2. PT/INR
3.CBC w/MCV>100
4. BAL
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| what is the most predictive test for prognosis with alcohol liver dz? | nutritional status, failure to restore nutrition can lead to death
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| what are 2 drugs that may help in acute decompensation in ALD? | 1. steroids for 4 weeks
2. pentoxifylline reduces hepatorenal syndrome
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| what nutritional products are needed in ALD to restore? | 1. amino acids
2. electrolytes: Mg, K, PO4
3. thiamine (prevents wernickes)
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| what is the #1 nutritional deficiency seen in alcoholics? | glutathione depletion
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| describe the clinical presentation of early cirrhosis | asymptomatic where dysfunction is noted in labs
--#1 low platelets
--weakness and fatigue, possible spider angiomas, palmar erythma
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| describe the clinical presentation of late cirrhosis | gynecomastia, hypogonadism, caput medusa, jaundice, ascites, variceal hemorrhage, encephalopathy, atrophy
--high bilirubin, low albumin, coagulopathy, low platelets
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| how do you determine cirrhosis severity? | child-turcotte-pugh score
-enceph
-ascites
-PT/INR
-albumin
-total bili
*assign one point for each*
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| what are some poor prognostic predictors for cirrhosis | 1. MAP<82
2. GFR<50
3. poor nutritional status
4. hepatomegaly
5. albumin<2.8
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| define portal hypertension and causes | portal pressure>12mmHg
--caused by cirrhosis, but can be seen in ALD, idiopathic, RHF, schistosomiasis
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| pharm mgmt for PHTN | vasoconstrictors: decreases splanchnic flow and decreases portal venous flow
vasodilators: alter intrahepatic resistance
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| pharm EVH prevention | NSBB reduce risk of bleeding by 40% *1st line*
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| EVH surgical intervention | 1. esophageal ligation/banding
2. esophageal sclerotherapy
3. portosystemic shunt
4. transjugular intrahepatic portosystemic shunt TIPS
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| acute EVH mgmt | 1. fluids + colloids
2. NG tube
3. correct coagulopathy
4. airway protection
5. abx therapy
6. EGD to determine site of bleeding
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| acute EVH surgical intervention | octreotide started in ER
--balloon tamponade, TIPS
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| what are possible causes of ascites? | cirrhosis
misc. PHTN related
cardiac
peritoneal carcinomas
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| what is the "underfill theory" for ascites? | increased plasma oncotic pressure and decreased portal venous pressure--sodium retention is a 2ndary compensatory mechanism
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| what is the "peripheral arterial vasodilation theory"? | increase in vascular capacity and decrease in effective plasma volume results in 2ndary sodium retention
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| fever+ascites+abdominal pain make you think what? | spontaneous bacterial peritonitis SBP
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| what are the most important lab results after paracentesis? | *fluid cell count*
>250 indicates infection
SAAG>1.1 indicates PHTN
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| diuretic of choice for ascites? | spironolactone +/- furosemide
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| tx for SBP? | 1. 3rd generation cephalosporin
2. albumin for volume expansion and renal perfusion
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| what is hepatorenal syndrome? | 1. renal failure defined by creatinine>1.5 in pts with advanced liver dz or PHTN
2. decreased GFR
3. activation of endogenous vasoactive systems
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| describe hepatorenal syndrome Type 1 | severe/rapid progression
severe liver failure
poorest prognosis
survival=2 weeks
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| describe hepatorenal syndrome type 2 | mod/stable renal failure
preserved liver function
survival=6 months
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| tx for HRS type 1? | 1. transplant
2. terlipressin (may reverse HRS)
3. catecholamines
4. TIPS
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| 3 ways to prevent HRS | 1. paracentesis+albumin
2. treating SBP w/ceftriaxone
3. pentoxifylline in ALD
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| what causes hepatic encephalopathy? | 1. reduction in production of compounds made by liver that maintain CNS function
2. failure of liver to detox neuroactive compounds that arise from the gut
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| what are some possible mechanisms that cause hepatic encephalopathy | 1. ammonia toxicity
2. synergistic neurotoxins
3. alteration of serotonin levels
4. excess GABA
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| what would labs show for enceph? | elevated ammonia
high GABA
pancytopenia, thrombocytopenia, leukopenia
elevated CSF glutamine
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| key ideas regarding ammonia levels and enceph | level does NOT correlate to severity of enceph
-don't r/o enceph if ammonia is normal
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| pharm tx for high ammonia | 1. bowel cleansing
2. avoid protein
3. lactulose
4. rifaximin
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| possible anatomical problems with pancreas | 1. pancreatic duct: stricture, stones, divisum
2. spincter of oddi dysfunction
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| describe main functions of pancreas | 80% exocrine (acinar cells secrete enzymes, fluid and electrolytes)
20% endocrine (islet of langerhans secrete hormones)
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| what enzymes are secreted exocrine? | amylase, lipase, protease, trypsinogen
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| what enzymes are secreted endocrine? | alpha: glucagon
beta: insulin
delta: somatostatin
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| what happens if the exocrine dysfunctions? | fat malabsorption leads to:
1. fatty stools
2. malabsorption of vit. A, D, E, K
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| what happens if endocrine malfunctions? | diabetes
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| what is creatinine a marker for? | dehydration
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| define acute pancreatitis | enzyme damage to pancreas resulting in discrete episodes of abd pain+elevation serum amylase+elevated lipase
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| 6 possible mechanisms for acute pancreatitis | 1. premature activation of pancreatic enzymes
2. stones
3. strictures
4. direct injury (acetaldehyde)
5. hereditary
6. elevated TG (too many chylomicrons cause clogging)
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| what are the stats regarding alcohol and pancreatitis? | 60-90% have h/o alcohol use
but only 5% of alcoholics get pancreatitis
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| clinical presentation of alcohol pancreatitis | 1. abdominal pain that radiates to the back (RUQ or epigastric +nausea/vomiting)
2. amylase/lipase>3xupper limit
3. pancreatitis findings on CT w/contrast
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| why would you use an abdominal ultrasound if you suspect pancreatitis? | to rule out gallbladder or bile duct dilation
*cannot see pancreas cause its retroperitoneal*
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| alcohol pancreatitis mgmt | 1. hydration w/bolus
2. pain mgmt
3. nutrition (NPO<3-5 days)
🗑
|
||||
| what is the next step in biliary pancreatitis if the stone has passed? if stone is present? | passed: cholecystectomy
present: ERCP
🗑
|
||||
| define chronic pancreatits | chronic inflammatory process leading to irreversible fibrosis of pancreas
*loss of function and structure*
🗑
|
||||
| how do you diagnose chronic pancreatitis | steatorrhea-->weight loss, low vitamins A,D,E,K
diabetes
abdominal pain
🗑
|
||||
| what labs might you run if you suspect chronic pancreatitis? | fecal fat
fecal elastase
secretin stimulation test
🗑
|
||||
| what is the best imaging technique for chronic pancreatitis? | endoscopic ultrasound that shows:
-hyperechoic foci, lobularity, stranding, irregular pancreatic duct
🗑
|
||||
| what does painless jaundice indicate? | tumor at the head of the pancreas
🗑
|
||||
| what are the stats for pancreatic adenocarcinoma? | 4th leading cause of cancer deaths
incidence=death rate
🗑
|
||||
| risk factors for adenocarcinoma | smoking, chronic pancreatitis, DM in non-obese, genetics
🗑
|
||||
| what are colon tics? what causes them? where located? | protrusions of the mucosa thru muscularis
-caused by low fiber diet, motility abnormalities, aging
-westerners: left colon/sigmoid
-asians: right colon
🗑
|
||||
| what are the stats for diverticulosis and its manifestation? | 70% are asymptomatic
15-25% develop diverticulitis
5-15% develop diverticular bleeding
🗑
|
||||
| presentation of diverticulosis | 1. functional sx: intermittent lower abdominal pain, abnormal bowel, bloating
2. diverticulitis
3. lower GI bleeding
🗑
|
||||
| uncomplicated diverticulitis | small perforations w/contained infection limited to wall of colon and adjacent adventitia
🗑
|
||||
| complicated diverticulitis | abscess, fistula, stricture, bleeding, rarely with free perforation
🗑
|
||||
| what risk factors make you consider diverticulitis? | 1. middle aged or older
2. lower abd pain > several days
3. nausea, distension
4. low grade fever, lower abdominal tenderness
🗑
|
||||
| what are indications for admitting to hospital with diverticulitis? | mod-severe sx
suspicion of complication
unclear diagnosis (appendicitis?)
failure to improve in 24-72 hours
🗑
|
||||
| what is the primary imaging technique if suspected complicated diverticulitis? | CT confirms dx, and rules out other differentials and may detect complications like fistula
🗑
|
||||
| what follow up test is run 4-6 weeks after recovery from diverticulitis? | barium enema and colonoscopy to confirm dx and r/o IBD
🗑
|
||||
| initial mgmt for diverticulitis? | NPO
antibiotic coverage for aerobic and anaerobics
CT w/oral contrast
surgical consult
monitoring for complications
🗑
|
||||
| what signs indicate fistula complications? | polymicrobial UTIs
air/stool in urethra or vagina
air in bladder on CT
🗑
|
||||
| what is the most common cause of LGIB? | diverticulitis assoc. with medium sized arteries
🗑
|
||||
| clinical presentation of diverticular bleeding? | painless
mod-large amounts of blood
BRBPR
spontaneously stops in 75%
🗑
|
||||
| gold standard for acute LGIB evaluation? | colonoscopy
🗑
|
||||
| define ulcerative colitis | chronic inflammatory disorder that affects colon, commonly affects 20s-30 y/o in industrialized countries and high socioeconomic status
🗑
|
||||
| ulcerative colitis always begins where? | rectum
🗑
|
||||
| symptoms of UC? | diarrhea, rectal bleeding, mucus, tenesmus, urgency, abd pain, fever, wt loss
🗑
|
||||
| clinical presentation of mild UC | appear in no distress
affected colon may be mildly tender
may find blood on rectal exam
🗑
|
||||
| clinical presentation of severe UC | ill appearing
tachy, fever, orthostasis, wt loss
diffuse abdominal tenderness
🗑
|
||||
| lab findings for UC | anemia, leukocytosis/thrombocytosis
iron deficiency
hypoalbuminemia
elevated ESR, CRP
🗑
|
||||
| what drug is a common culprit for pancreatitis? | azathioprine
🗑
|
||||
| describe the macroscopic appearance of ulcerative colitis | -most severe distally, progressively less proximally
-atrophic, featureless colon with shortening/narrowing
🗑
|
||||
| microscopic appearance of UC | -inflammatory infiltrate
-crypt abscess
-localized to mucosa and submucosa
-NO granulomas
🗑
|
||||
| what are the treatment goals for UC? | 1. induce remission
2. maintain remission
🗑
|
||||
| patients with UC are at greater risk fro what? | developing colon cancer
🗑
|
||||
| what are indications for colectomy with UC? | 1. colon cancer
2. medically refractory dz
3. uncontrolled bleeding
4. colonic perf
5. toxic megacolon
🗑
|
||||
| how do you reduce risk for colon cancer in pts with UC? | 1. regular surveillance
2. 5-ASA tx
3. decrease inflammation of UC
🗑
|
||||
| what is a potentially fatal complication of UC? describe it.... | toxic megacolon
--presents as severe colitis w/pain and decreased bowel sounds
--dx confirmed by X-ray
🗑
|
||||
| toxic megacolon treatment | bowel rest via TPN
electrolyte repletion
daily Xrays
steroids
abx therapy
r/o infections like cdiff or cmv
🗑
|
||||
| describe basics of crohns disease | -affects GI tract mouth to anus
-may skip areas
-transmural inflammation
-*granulomas present*
🗑
|
||||
| where is the most common site for crohns? | 50% iliocolic
30% ileal
20% colonic
🗑
|
||||
| 3 types of CD | inflammatory
penetrating (fistulas/abscess)
stricturing
🗑
|
||||
| typical presentation of crohns disease | -iliocolonic disease (obstruction, anorexia, acute RLQ pain)
-colonic disease (bloody diarrhea, wt loss)
-perianal disease (stenosis, fissures, fistulas)
🗑
|
||||
| 5 ways to confirm dx of CD | 1. colonoscopy with ileoscopy
2. radiology
3. capsule endoscopy
4. EGD
5. pathology shows granulomas w/patchy inflammation
🗑
|
||||
| treatments for CD | -steroids (budesonide)
-5-ASA
-abx (flagyl/cipro)
-immunomodulators (azathioprine)
-biologic agents
-surgery
-smoking cessation
🗑
|
||||
| what extra-intestinal diseases are associated with IBD? | SKIN
-pyoderma gangrenosum
-erythema nodosum
EYE
-episcleritis
-scleritis
-uretis
JOINTS
-peripheral arthritis
PRIMARY SCLEROSING CHOLANGITIS
🗑
|
||||
| describe microscopic colitis | -presents 50-70 y/o w/females mostly
-chronic watery diarrhea
-normal appearing colon
-abnormal histology showing inflammation
🗑
|
||||
| best treatment for microscopic colitis? | budesonide
🗑
|
||||
| etiology of microscopic colitis | unknown
-possibly inflammatory disorder arising from abnormal immune response
🗑
|
||||
| define IBS | abdominal pain at least 2-3 days per month, present for 3 out of 12 months:
-better with defecation
-onset w/change stool appearance
-onset w/change frequency
"irregularly irregular*
🗑
|
||||
| what is SIBO? | 1. "small bacterial overgrowth"
2. leads to dysmotility
3. frequency of IBS increases after acute gastroenteritis
🗑
|
||||
| what is MMC? | -migrating motor complex
"housekeeper" that sweeps debris/bacteria out of small intestine after meals
🗑
|
||||
| what happens when you lose MMC? | SIBO which may lead to constipation or diarrhea
🗑
|
||||
| how is SIBO detected? how is it controlled | detected by breath tests
controlled with abx (metronizadole, doxy, rifaximin)
🗑
|
||||
| how is the brain-gut axis affected in IBS? | -decreased threhold for visceral pain, normal threshold for somatic pain
-cortical and limbic isssues-->psych factors
🗑
|
||||
| can IBS coexist with IBD? | yes
🗑
|
||||
| what labs should you initially run for IBS? | CBC
TSH
glucose
stool WBC
FFS for diarrhea
*colonoscopy if >50 yo*
🗑
|
||||
| alarm signs for IBS | fever, GI bleed, weight loss
+45 yo onset
family hx of CRC/IBD
🗑
|
||||
| drug therapy fro IBS | bulking agents
smooth muscle relaxants
loperamide
SSRIs
peppermint oil
probiotics
🗑
|
||||
| what is a pitfall of severe IBS? | patient requests surgery when not necessary
🗑
|
||||
| ligament of treitz | tissue that connects the duodenum to the diaphragm, and divides the GI tract into upper and lower
🗑
|
||||
| bright red blood or coffee ground emesis indicates... | LGIB
🗑
|
||||
| BRBPR or marroon stools indicates... | mostly LGIB, or a brisk UGIB
🗑
|
||||
| what are 3 non-GI causes of blood in stool? | epistaxis, bleeding gums, ingestion of blood
🗑
|
||||
| 1st step in assessing GI bleed? second? | 1. determine the severity of the bleeding via vitals, blood pressure, and pulse rate
2. resuscitation
🗑
|
||||
| how do vitals correspond with bleeding severity? | normal BP and HR--> less than 10% total body volume
orthostatic>20 mg drop--> 10-20% moderate
shock-->more than 25% severe
🗑
|
||||
| what steps constitute "resuscitation"? | 1. vascular access (2x18 gauge IVs placed)
2. IV fluids
3. oxygen (or entubation if severe UGIB)
4. frequent vital monitoring
5. start blood transfusions
6. all unstable are admitted to ICU
🗑
|
||||
| what are the criteria for receiving PRBC? | 1. continuously unstable vitals
2. low blood counts
--HCT<30 in elderly/sick or HCT<20-25 in healthy
3. >3liters give warmed blood!!
🗑
|
||||
| when should you perform NG lavage? | pt with hematochezia w/suspicion that bleeding is from UGI source, esp. if pt is hemodynamically unstable
🗑
|
||||
| what are some risks of endoscopy? | bleeding, pain, infection
perforation
aspiration of gastric contents
adverse effects to sedation
🗑
|
||||
| how does a tagged RBC scan work? | (nuclear medicine) RBCs are tagged with radioactive tracer, injected into patient, and identifies bleeding sites--usually LGIB
--good cause non-invasive and safe, bad cause inaccuracy
🗑
|
||||
| angiography | (interventional radiology) injection of IV contrast into vessels to localize bleeding, only detects if >.5ml/min
🗑
|
||||
| what is the order of diagnostics to run for suspected LGIB? | endoscopy
tagged RBC scan
angiography
barium contrast
capsule endoscopy
🗑
|
||||
| when is barium contrast not recommended? capsule endoscopy? | -acute bleeders and contrast may interfere with future diagnostic tests
-acute bleeders cause it takes hours to complete
🗑
|
||||
| causes of UGIB | peptic ulcers
gastritis
varicies
mallory-weiss tears
esophagitis
gastric varicies
🗑
|
||||
| what is the most common cause of UGIB? | peptic ulcers (55%)
🗑
|
||||
| incidence of bleeding from ____ ulcers is 2x that of ____ ulcers | duodenal ulcers are twice as likely to bleed as gastric ulcers
🗑
|
||||
| clinical presentation of PUD? | melena, hematemesis, nausea, vomiting
epigastric pain
hx of GERD, heartburn, indigestion
🗑
|
||||
| which ulcer gets worse with food? | gastric
🗑
|
||||
| how do duodenal ulcers manifest distinct from gastric? | relieved with food but worsen 2-5 hours after eating or on an empty stomach
🗑
|
||||
| risk factors for PUD?/ | #1 NSAID use
H. pylori infection
anti-coagulant therapy
stress
alcohol
🗑
|
||||
| PUD treatment | resuscitate and stabilize
stop aspirin/NSAIDS
start PPI (inhibits acid production so stomach can heal)
NPO
🗑
|
||||
| what are some treatments that can be performed on endoscopy? | thermal therapy (cauterize)
injection w/epi or saline
endoclips or lasers
🗑
|
||||
| define gastritis | injury to gastric mucosa with inflammation
-endoscopically defined as mucosal hemorrhage, erythema, erosions<5mm
🗑
|
||||
| first episode of esophageal variceal hemorrhage has a ____ mortality rate | 20%
🗑
|
||||
| presentation of esophageal varicies | evidence of cirrhosis and/or liver disease
hematemesis and melena and/or BRBPR
hemodynamically unstable
🗑
|
||||
| mgmt of acute EV bleed | 1. resuscitation (blood replacement, FFP+platelets)
2. IV octreotide infusion (decreases portal pressure)
3. prophy abx to prevent SBP
4. possible entubation
5. EV ligation/banding or sclerotherapy
🗑
|
||||
| what are some surgical interventions for aute EV bleed? | ligation/banding
sclerotherapy (botox into varicies)
balloon tamponade
TIPS
🗑
|
||||
| TIPS | transjugular intrahepatic portosystemic shunt
creates a shunt between portal and hepatic veins which decreases portal pressure and decompresses varicies
🗑
|
||||
| mallory-weiss tears | -longitudinal mucosal laceration in distal esophagus and/or proximal stomach
-usually caused by forceful vomiting
🗑
|
||||
| clinical presentation of mallory-weiss tears | hematemesis, melena
hx of non-bloody vomiting/forceful wretching
epgastric pain or back pain
🗑
|
||||
| what is seen in 40-80% of mallory-weiss tears? | heavy alcohol use leading to vomiting
🗑
|
||||
| gold standard for mallory-weiss? | EGD
🗑
|
||||
| what part of the world do most gastric cancers occur? | developing countries, not too common in US
🗑
|
||||
| clinical presentation of gastric cancer | early stages are asymptomatic
occult GI w/wo iron deficiency
only 20-30% with obvious bleeding
🗑
|
||||
| physical exam findings for advanced gastric cancer | palpable abdominal mass
lymphadenopathy due to mets
ascites
🗑
|
||||
| gold standard for gastric cancer diagnosis | EGD so you can get biopsies and treat bleeding if present
🗑
|
||||
| an elderly patient with LGIB, suspect.... | diverticulosis or angiodysplasia
🗑
|
||||
| younger patient with a LGIB, suspect... | infection or inflammatory causes
🗑
|
||||
| diverticulosis | outpouching of the colon
occurs in areas where vessels penetrate the colonic wall
most common in the sigmoid colon
🗑
|
||||
| diverticulitis | infection and inflammation of the diverticula
🗑
|
||||
| diverticulosis presentation | acute, painless hematochezia--BRBPR or melena
bleeding spontaneously stops
blood loss is not hemodynamically significant except with comorbidities
🗑
|
||||
| diagnostics for diverticulosis | colonoscopy
barium studies
CT
🗑
|
||||
| clinical presentation of colon cancer | acute lower GI bleeding is UNcommon..usually occult
weight loss
change in stool caliber or frequency
🗑
|
||||
| tenesmus | sense of urgency or straining to empty an already empty bowel
🗑
|
||||
| dysentery | bloody diarrhea from colorectal source (occult blood)
🗑
|
||||
| melanotic stool | black/tarry stool suggesting GI tract source
🗑
|
||||
| hematochezia | BRBPR suggests colorectal source
🗑
|
||||
| what causes diarrhea? | an increase in intestinal fluids and/or transit time secondary to 1+ of the 8 alterations
🗑
|
||||
| what are the 8 alterations that cause diarrhea? | 1. infection (bacteria, virus, parasite)
2. increased intestinal secretion
3. structural change (surgery)
4. change GI enviro (abx)
5. iatrogenic (meds, hospital)
6. endocrine (thyroid)
7. systemic (IBD)
8. malabsorptive (celiac)
🗑
|
||||
| what are other possibilites to consider before making a diagnosis of diarrhea? | incontinence, hyperdefication, hyperthyroidism
🗑
|
||||
| what % of acute diarrhea is mild and self-limiting? | 90%
🗑
|
||||
| 3 history questions when estab. diarrhea dx | duration
frequency
baseline poop schedule
🗑
|
||||
| 3 most common pathogens for diarrhea | c. jejuni
roto/norovirus
salmonella, shigella, e.coli
🗑
|
||||
| under what conditions do you order a stool culture for diarrhea? | protracted or if pt is immunocompromised....NOT for travelers diarrhea
🗑
|
||||
| what do you suspect if TD becomes persistent or has relapses? | parasite/protozoa
🗑
|
||||
| 2 post-infective conditions for pts that were treated for TD? | IBS and lactose intolerance
🗑
|
||||
| what chronic inflammatory dz must be consideredin all cases of acute diarrhea? | ulcerative colitis
🗑
|
||||
| essential checklist of a physical exam in patients with diarrhea | 1. weight change
2. vitals
3. turgor/hydrations status
4. lymph nodes
5. pain
6. mental status changes
7. belly appearance/tenderness
8. enlarged organs
9. require extra help/support than usual?
🗑
|
||||
| how do you assess dehydration? | cap refill, turgor, BP, radial pulse, urine output
🗑
|
||||
| diagnostic studies: why would you order 24hr stool for weight? | elevated in secretory states
🗑
|
||||
| diagnostic studies: why would you order 24hr stool for fat? | elevated in malabsorptive states
🗑
|
||||
| diagnostic studies: why would you order fecal leukocytes or lactoferrin? | measurement of inflammation, dx IBD
🗑
|
||||
| diagnostic studies: why would you order bacterial culture? | salmonella, shigella, campy
🗑
|
||||
| diagnostic studies: why would you order fecal antigen? | giardia and e. histolytica
🗑
|
||||
| diagnostic studies: why would you order acid fast? | crypto and cyclosporin
🗑
|
||||
| treatment for acute non-inflammatory | loperamide, pepto
🗑
|
||||
| empiric treatment for TD | FQ, bactrim, z-pac
🗑
|
||||
| empiric treatment for acute inflammatory | FQ or bactrim
🗑
|
||||
| classifications of chronic diarrhea: osmotic | solutes lead to retention of luminal fluid-->elevated osmotic gap that resolve with FASTING
ex: sorbitol, milk of mag, lactulose, lactose intolerances, malabsorptive states
🗑
|
||||
| classifications of chronic diarrhea: secretory | excess NaCl is actively secreted into lumen and water follows-->large volume diarrhea, normal osmotic gap
ex: vibrio, post-cholecystectomy, ZE syndrome, meds
🗑
|
||||
| classifications of chronic diarrhea: inflammatory | ulcerative colitis, crohns, microscopic colitis (elderly), radiation enteritis
🗑
|
||||
| classifications of chronic diarrhea: meds | SSRI, NSAIDS, PPI, metformin, abx, cholinesterase inhibitors, Mg antacids, ALLi
🗑
|
||||
| classifications of chronic diarrhea: malabsorption syndromes | celiac/sprue
small bowel resection
chronic pancreatitis
motility disorders (DM, scleroderma)
🗑
|
||||
| classifications of chronic diarrhea: motility disorders | vagotomy
partial gastrectomy
hyperthyroidism
IBS
🗑
|
||||
| classifications of chronic diarrhea: chronic infections | parasites/protozoa
roundworm
CMV
abx associated colitis
🗑
|
||||
| CRAP? | chronic
recurrent
abdominal
pain
🗑
|
||||
| meds that cause constipation | opiods, CCB, diuretics, anti-ACh, psychotropics, NSAIDS, clonidine, supplements Ca and Fe
🗑
|
||||
| what red flag makes you consider malignancy instead of constipation? | 50+ with new onset constipation
🗑
|
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