GI Flashcards Preview

Clinical Medicine > GI > Flashcards

Flashcards in GI Deck (166):

what are the 4 distinct layers of histo in GI tract?

serosa, muscularis, submucosa, mucosa


which salivary gland produces mucous? which produces water, electrolytes and enzymes?

mucous=sublingual and submandibular; water, electrolytes and enzyems=parotid


what is in saliva?

mucus, IgA (to prevent bacterial infection), lipase, alpha amylase, and bicarbonate


what is absorbed in the stomach?

asprin, alcohol, NSAIDSs


what influences gastric motility?

vagus nerve stimulation, stomach distention from contents, and enteric nerve stimulation via acetylcholine


what decreases the rate of gastric emptying?

fatty foods, food in SI, smaller volume of food in stomach


which phase of digestion is characterized by each of the following?
vagus nerve and acetylcholine leading to increased HcL
food and stomach distention leading to G cells to produce gastrin and gastrin to stimulate parietal cells
chyme in duodenum decreases gastric secretion

cephalic; gastric; intestinal


Increased WBC with ?

infections, pain, alcoholic hepatitis or stress.


Decreases WBCs with ?

viral infection.


Decreased Hgb and hematocrit in ?

GI bleeding (celiac, IBC, cancer),


elevated INR in ?

liver dz (less clotting factors being produced),


macrocytic anemia in ?

B12 and folate deficiency (think malabsorption and ETOH),


microcytic anemia in ?

Fe def


Decreases platelets in?



which LFT is specific for the liver?



what are the possible causes of GI issues?

impaired digestion/absorption, altered secretion, altered transit, immune dysreg, infection, impaired gut blood flow, malignancy, functional


what are common upper GI complainsts?

abd pain, dysphagia, halitosis, nausea, vomiting, heartburn, regurg, hematoemesis


what are common lower GI complaints?

hematochezia, constipation, diarrhea, abd pain, bloating


what's in the ddx for difficulty swallowing?

eosinophilic esophagitis, stricture/schatzki's ring, GERD related esophagitis, malgnancy, infectious/med induced, oropharyngeal issues, motility disorders


what's in the ddx for heartburn?

eosinophilic esophagitis, esophageal sensitivity, functional dyspepsia, GERD


what's in the ddx for odynophagia?

pill induced esophagiits, GERD related esophagitis, candida, esophageal spasm


what's in the ddx for indigestion?

GERD, biliary colic, functional dyspepsia, gastroparesis, celiac sprue, H. pylori


what factors increase the total daily expenditure needs?

a. This increases with injury, surgery, infection, trauma, fever, long bone fracture, pregnancy/lactation, chronic lung disease, congen. heart disease, cancer/AIDS, hyperthyroidism, inflammatory disease, and activity. There are specific formulas to use based on each of these. Total daily expenditure (TDE)=BEE x IF (injury factor) x AF (activity factor)


what is the best way to image the luminal GItract? (esophagus, stomach, small bowel, large bowel, etc)?

luminal contrast studies like esophagram, SBFT, barium/gastrografin


what is the best way to image the upper abdominal solid organs like the gallbladder, liver, pancreas?

cross sectional techniques like CT, US, MRI


what is the normal amount of radiation that each person gets per year? how much does a CT scan give? X-ray?

3 mSv; CT gives 14 mSv; ABD xray 0.7 msV, CXR 0.1 msv


what are some indications for an ABD XRAY?

assess stomach, small owel, or colon, evaluate air fluid levels, or ileus, evaluate free air, tube or catheter drain position, and abdominal calcifications


when is a double contrast esophagram indicated?

for detecting subtle, early mucosal neoplastic or inflammatory lesion, gives see through image with greater mucosal detail


when is a single contrast esophagram indicated?

Single contrast good for demonstrating contour abnormalities, strictures, and polypoid filling defects, esp good if poor phys condition or uncooperative


when is barium the contrast of choice? gastrografin?

use water soluble gastrografin if perforation suspected (barium causes mediastinitis); use barium if aspiration suspected (gastrografin causes pneumonitis


should someone be NPO for upper GI X-ray with contrast? what can an upper GI identify?

yes for 8 hrs; evaluate motility, contour, obstruction and abnormaltiies of lumen of gstomach. Eval PUD, f/u on abnormal studies, post surg eval.


what are the indications for a small bowel follow through?

suspected low transit time,observe mucosal contour, bowel loop distribution, crohn's, obscure GI bleeding, anemia, obstruction. but it can miss subtle changes or masses. Gastrografin can be CI if obstruction b/c it will pull fluid into lumen and aggravate the obstruction.


what's the procedure for a small bowel follow through?

NPO after evening meal. pt drinks 2 cups of thin barium; overhead films obtained q 15-20 minutes until barium reaches the colon


what are the indications for a barium enema? how is it done?

single contrast is faster, less expensive; double contrast is slower but better at finding small lesions, IBD, and rectal eval. Bowel obstruction/pseudoobstruction, suspected diverticulitis, IBD, f/u abnormal imaging, anemia; clear liquids 24 hrs before exam, laxatives evening before and day of exam, supp AM of exam. This can be skipped/modified in acute situations or IBD.


what are the indications for abdominal CT? how is it done?

more detailed than xray; used in almost every type of abdominal disease and symptom: abdm pain, suspected inflammatory condition (appendicitis, diverticulitis, abscess), eval of tumors, enlarged organs, suspected obstruction, guide bx or aspiration; If no contrast, no prep. If oral contrast (to highlight lumen+/- IV contrast (to highlight vasculature and organs, this not safe in renal insufficiency +/- rectal contrast of barium or water-sol, prep is NPO for 6 hrs except for the contrast given at 2, 1 and 1/2 hr before exam. If looking at colon it requires full colonscopy prep.


what is a CT colongraphy? when is it indicated?

a virtual colonoscopy: if colonscopy incomplete you could do this. But remember its way more radiation and you can't fix stuff while looking like you can in colonscopy. no sedation req'd, no bowel prep, air used per rectum to distend colon, exam only takes 2-3 min, images processed.


non invasive technique for evaluating the biliary and pancreatic ductal systems using magnetic resonance



MRCP indications, procedure

liver (1st line for liver stuff) , biliary, pancreas, vasculature visualization.useful if cannot have contrast, Or for clarifying liver lesions, not good for bowel.don't use gadolinium in renal insufficiency.; procedure: no prep, no contrast (in MRCP the bile acts as contras)


what is an MR enterographyy?

an MRI of the small bowel. detailed imaging of small bowel and tumors, abscesses, and active or complications of crohns


what are some indications for an abdominal ultrasound?

indications: imaging biliary, liver, portal system, spleen, gallbladder, kidneys, bladder. Eval blood flow. Can't visualize LUQ b/c of gas in stomach or if excessive fat like obesity. Can guide paracentesis/bx.
procedure: nPO 8 hrs


gastric emptying study indications, procedure

for nausea, vomiting, early satiety or to dx gastroparesis (nerve damage to stomach I dm; NPO 8 hrs; procedure: inaccurate results if taking narcotics (slows it), metoclopramide (anti vomiting but causes tongue thrusting) or erythromycin


if you want to assess/dx: GERD for >5 yrs, dysphagia/odynophagia, anemia, epigastric abdominal pain, recurrent or chronic N/V, F/u on abnormal imaging, screening for esophageal varices and celiac spruel to tx: GI bleeding, esophageal variceal banding, esophageal pyloric channel dilation, bx, stent, small bowel capsule placement: what test is indicated?



what is the procedure for a EGD?

NPO for 8 hrs, hold anticoags except ASA and plavix. IV conscious sedation, lay on left side, oral-esophageal intubation (gagging normal), lasts about 15 min


what can a flexible sigmoidoscopy ID? when is it indicate? is sedation req'd?

can ID about 50% of cancerous tumors and adenomas +/- FOBT. For screening asx pts + fOBT, evaluate diarrhea, proctitis, rectal pain or abn imaging. CI: diverticulitis, toxic megacolon, recent bowel surgery. no sedation typically. Usu 1st give 2 fleet enemas,2 and 1 hr before procedure. Hold anticoags 3-5 days before except ASA and plavix. Sometimes give mg citrate.


what are the indications for a colonoscopy? procedure?

dx: iron deficiency anemia, GI bleeding, abdm pain, abn CT, BE, GGE, IBD, diarrhea. Screen for colon cx. Tx: GI bleeding, dilation of stricture, place stent, decompress colon, take out polyps. Recommended q 10 yrs for adults >50 yrs with avg risk or AA >45 yrs
procedure: clear liquids 24 hours beforehand. Laxatives: either 4L of golytely, or 2L of moviprep + 1 L clear liquids. + NPO for 8 hrs prior. IV conscious sedation, lay on left side, scope advanced to cecum or terminal ileum. Takes about 20-30 min.


what are the indications for a small bowel video capsuel? procedure? limitations?

obscure GI bleeding, crohn's, abnormal imaging; procedure: clear liquids 24 before exam, colon prep, nPO after MN. No iron 7 days before exam. Perfored after EGD and colonscopy. capusle is passed through stool and not collected, if retention it may require surgery.; limitations: can't get bx, can't ID exact location of findings, false positives, legnthy viewing time


indications and procedure for endoscopic ultrasounds

dx, bx and stage esophageal, pancreatic cx, or lymph nodes. Evaluate chronic pancreatitis and pancreatic cysts. Evalute gallbladder, bile, and pancreatic ducts for stones, liver lesions, and rectal and peri rectal lesion eval. Tx: drain pancreatic pseudopsysts, celiac plexus nerve block.; procedure: npo 8 hrs, same procedure as EGD.


what are the indications, procedure, risk of endoscopic retrograde cholangiopancreatography?

dx: obstructive jaundice, fistula, tumors, elevated LFTS, abnormal MRCP, pancreatits, tx: remove CBD stones, stent malignant biliary obstruction, SOD=sphincterotomy, resect papillary tumors, unroof choledochocele, pancreatic divisum-minor papillotomy; procedure: nPO 8 hrs, hold anticoags. Pt lies prone, intubation, takes about 30 min. side viewing scope to look at duodenm, major duodenal papilla, and ampulla of vater, can look at bile ducts, gallbaldder, and pancreatic ducts; risks: complications of pancreattiis, infection, bleeding, perforation, injury


what's in the ddx for abdominal pain?

aortic aneurysm, acute appendicitis, cholangitis, cholecystitis, cholelithiasis, colitis, diveritculitis, gastroenteritis, gynecologic, incarcerated hernia, IBD, ileus, intestinal obstruction, malignancy, pancreatitis, PUD, PID, sickle cell crisis, epidydmitis, testicular torsion, abdominal trauma, bladder distention, cystits, nephrolithiasis, pyelonephritis, mesenteric vascular occlusion


what do each of the following alarm signs signify?
nausea/vomiting , fever, acholic stools or tea colored urine ; black stool , bloody stools, hematemesis,

nausea/vomiting (MI, appendicitis, bowerl obstruction, choelcystitis, incarcerated or strangulated hernia, pancreatitis vs. gastroenteritis), fever (appendicitis, cholangitis, cholecystiits, diverticulitis vs viral syndrome), acholic stools or tea colored urine (biliary obstruction vs. dehydration); black stool (GI bleeding vs. iron supplements), bloody stools, hematemesis,


what do each of the following alarm signs mean? constipation , pain before vomiting , migration of periumbilical pain to RLQ , RLQ pain ), RUQ pain , jaundice

constipation (bowel obstruction, hypercalcemia vs. dehydration), pain before vomiting (appendicitis), migration of periumbilical pain to RLQ (appendiciits), RLQ pain (appendicitis vs. mesenteric adenitis), RUQ pain (cholecystitis), jaundice (biliary obstruction, cholangitis),


what do each of the following alarm signs mean? focal neuro deficit , abrupt onset pain, abrupt and tearing pain, migratory pain , tearing quality pain

focal neuro deficit (aortic dissection), abrupt onset pain (aortic dissection), abrupt and tearing pain (aortic disseciton), migratory pain (aortic dissection), tearing quality pain (aortic dissection)


what do these qualities mean in terms of what the dx could be? AA: worse with eating , better with eating , assoc with N/V , tearing pain , crampy pain , assoc with emesis of undigested food, emesis of undigested foods with acidic juices but no bile , bloody emesis

AA: worse with eating (pancreatitis, gastric ulcer, mesenteric ischemia), better with eating (duodenal ulcer, GERD), assoc with N/V (pancreatitis, bowel obstruction, biliary colic), tearing pain (aortic dissection), crampy pain (distention of hollow tube like bowel, bile duct, ureter), assoc with emesis of undigested food (esophageal obstruction), emesis of undigested foods with acidic juices but no bile (gastroparesis or gastric outlet obstruction), bloody emesis (GERD, esopahgeal or gastric varices, PUD, gastric cancer, aortoenteric fistula)


what do these qualities mean in terms of what the dx could be?RADIATION: to back to right shoulder , to left shoulder , to left arm or neck

to back (pancreatitis, duodenal ulcer, gastric ulcer, aortic dissection) to right shoulder (biliary colic, cholecystitis), to left shoulder (splenomegaly or splenic infarction), to left arm or neck (MI),


what do these qualities mean in terms of what the dx could be?SEVERITY: pain suddenly improve from 8/9 to 2/3 pain hurt most at onset

pain suddenly improve from 8/9 to 2/3 (perforated appendix), pain hurt most at onset (aortic dissection),


what do these qualities mean in terms of what the dx could be?TIMING: continuous with intermittent waves of worsening , multiple waves of pain that increase in intesnity then stop abruptly for short periods of time, recent abx, pain occur once monthly around 2 wks after or beginning of menses, ocass assoc with vaginal spotting

continuous with intermittent waves of worsening (biliary colic, renal colic, small bowerl obstruction), multiple waves of pain that increase in intesnity then stop abruptly for short periods of time (small bowerl obstruction), recent abx (colitis from c. diff), pain occur once monthly around 2 wks after or beginning of menses, ocass assoc with vaginal spotting (mittelschmerz)


what are the different categories of ddx for constipation?

anorectal obstructions, strictures, metabolic and endocrine conditions, neurogenic disorders , musuclar and CT disorders , meds side effect, colorectal motility dysfunction , psychosocial


what's in the ddx for constipation?

anorectal obstructions(anal fissure, colon or rectal cancer, colonic polyps, fecal impaction, ileus, megarectum, strictures (diverticular, IBD, postradiation, or postischemic), thrombosed hemorroids, defecatory disorders, pregnancy) metabolic and endocrine conditions (DM, hypercalcemia, hyperPTism, hypokalmeia, hypomg, lead poisoning, preg, uremia) neurogenic disorders (autonomic neuropathy, chagas disease, hirschsprung diseae, neurofibromatosis, CNS disorders, MS, parkinsons, spinal cord trauma, CVA) musuclar and CT disorders (amyloidosis, systemic sclerosis, myotonic dystrophy) meds side effect, colorectal motility dysfunction (slow transit constipation, constipation predominant IBS, defecatory disorders, idiopathic chronic constipation) psychosocial (depression, low fiber, sedentary lifestyle, somatization)


what do these alarm sx for constipation signify? (and what are the benign causes of them after the vs.?)
unintentional weight loss ,recent onset , hematochezia, melena , sig abd pain , change in stool caliber i.e. gotten narrower , nausea, vomiting , fever , back pain, saddle anesthesia, leg weakness/numbness, difficulty urinating

unintentional weight loss (colon cancer, depression) recent onset (colon cancer, metabolic or endocrine disorder vs. med, psyschosocoial or immobility), hematochezia, melena (serious conditions like colon cancer, diverticulosis, stricture, anal fissure or ulcer vs hemorrhoids) sig abd pain (cancer, diverticulitis vs. IBS, side effect of meds, hemorrhoids) change in stool caliber i.e. gotten narrower (colon cancer, stricture, anal fissure vs. IBS) nausea, vomiting (bowel obstruction vs. IBS) fever (diverticulitis, cancer ) back pain, saddle anesthesia, leg weakness/numbness, difficulty urinating (spinal cord process)


what are the causes of elevated unconjugated bilirubin? conjugated?

20% or less conjugated means there is hemolysis (too much breakdown of heme and its all unconjugated), resportipn hematoma, or something wrong with the conjugating enzyme or fasting, illness, or stress. 20-80% conjugated can mean hepatic dysfunction or impaired bile flow.


what does decreased albumin measure? how long is its half-life?

marker for liver protein synthesis. decreased in liver dysfunction but this does not occur acutely. Acute decreases wit severe systemic illness, malabsorption, or protein loss from GI or renal. half life of 21 days


what can a decreased PT or an elevated INR indicate?

if decreased PT it can mean the liver is not functioning correctly to make its coag factors; if increased INR it means the same thing


what questions should you ask if someone has elevated LFTs?

etoh, new meds, abx in past 3 months, any OTC/herbals, hx of IV or nasal drugs (hep C), sig wt gain (fatty liver), blood transfusions, fmhx of liver dz, dark urine, yellowing of eyes or skin, abd pain, fever, bowel changes, hx of AI (crohns, i.e.), tatoos, travel


what's in the ddx for elevated LFTs?

Hep A-E, fatty infiltration of liver (NAFLD, NASH), AI hepatitis, hemochromatosis, celiac sprue, idiopathic, ischemia, wilson's disease, other viral (CMV, EBV), primary sclerosing cholangitis, primary biliary cirrhosis, thyroid dysfcn, cancer (liver, mets, pancreatic, cholangiocarcinoma), biliary etiology (gallstones), alcohol, toxins, meds


when is a liver bx indicated?

bx if serologic and imaging unrevealing and LFTs persistently 2x normal limit, to assess fibrosis levels, to confirm: AI, wilsons, PBC, hemochromatosis or if tx is ineffective


definition and sx of chronic and acute hepatitis

acute: 6 mo, often no sx, may be fatigued


fulminant liver failure definition, causes, labs, tx

def: prescence of acute liver failure within 8 wks of the onset of jaundice in a pt without previous liver dz
causes: acetaminophen, idiopathic, idiosyncrtic drug rxn, hep B, ischemia, Hep A
labs: high AST/ALT with excption of wilsons, elevated total bilirubin, elevated INR
tx: eliminate offending agent, contract transplant ASAP!


Hepatitis A:
eti and transmission
lab tests
pt ed

epi: any age; incidence decreasing in US esp since vaccine, live/travel in underdeveloped areas, exposure to those with jaundice, exposue to young kids in day care, eating shellfish (rare), ivdu
eti and transmission: ingestion of contaminated food/water, fecal-oral transmission or contact with infected person. Incubation 2-6 wks.
RFs: live/travel in underdeveloped areas, exposure to those with jaundice, exposue to young kids in day care, eating shellfish (rare), ivdu
presentation: 6 usu


what do each of the following antibodies or antigens indicate: HBsAg, HBsAb, HBcAb, HBcAb IgM, HBeAb, HBeAg and how do they aid in dx or tx?

HBsAg (surface antigen) is the protein on the surface of HBV and indicates ongoing infection and infectious. HBsAb is an ab for the surface antigen and indicates recovery, immunity, or vaccination. HBcAb is an antibody to the core of the virus and indicates ongoing or previous infection (core antibody shows up before surface Ab). HBcAb IgM indicates a recent infection, within


what are the different "phases" of Hep B? which are infectious?

Phases: Active diseae: high viral level and increased LFTs. Carrier: low viral level and normal LFTs (can't infect). Immune tolerant: high viral level and normal LFTs (as long as they have normal enzymes their body is fine with the virus but they can still infect others!)


what is the tx for acute and chronic hep B?

for acute tx is supportive, for chronic it depends on LFTs, HBV DNA level, HBeAg status, and fibrosis level of liver. Antiviral meds: Tenofovir is gold std. (usu no resistance, if the virus recurrs its usu d/t pt non adherence)


when and how should pts with chronic hep B be monitored?

monitor for chronic hep B: AFP and liver US q 6 mo for: AA 50, asian men >40, cirrhosis with Hep B, Fm Hx of HCC (start screening ASAP)


Hepatitis B:
eti and transmission
lab tests

epi: common in asia and africa where usu acquired perinatally o r in early childhood, decreased indicidence in US with immunization. Progression to chronic disease is more common in young children.
eti and transmission: inc 60-150 days. HBV can survive on a surface for 7 days.
RFs: for disease: healthcare/occup. Exposure, IVDU/nasal, sexual exposure, mother to child transmission, sharing razors/toothbrush/blood contact, hemodialysis, from disease: cirrhosis of liver or liver cancer
presentation: more severe if >60 yo. Ranges from asx to chronic hepatitis to cirrhosis to HCC.
lab tests: for antigens and antibodies
tx: for acute tx is supportive, for chronic it depends on LFTs, HBV DNA level, HBeAg status, and fibrosis level of liver. Antiviral meds: Tenofovir is gold std. (usu no resistance, if the virus recurrs its usu d/t pt non adherence)


what are the specific recommendations for hep B infected pregnant women?

If pregnant and HBsAG+ need to check LFTs and HBV DNA PCR q 3 mo and 6 months post partum. Higher DNA levels=higher risk of transmission. Tx if viral load greater than 200,000--rec'd to start tx 6-8 wks prior to delivery, and give vaccine and immunoglobulin to infant at birth


what are the subclasses of hep C and what is most common?

acute (clear virus without tx) vs. chronic. Different gentoypes:1a, 1b (MC), 2 and 3 (easily eradicated), 4,5,6 less common.


Hepatitis C:
eti and transmission
lab tests
pt ed

epi: 3.2 mill worldwide with chronic HCV
eti and transmission: Hepatitis C virus, sx occur 4-12 wks after exposure, transmitted primarily through blood
RFs: for dz: blood transfusion piror to 1992 (when anti-HCV was introduced), recipients of clotting factors before 1987, tattoos/body piercings in unhygeniec places, IVDU/nasal, HIV, vertical transmission can happen but uncommon; from dz: 60-70% get chronic liver disease, 5-20% get cirrhosis, 1-5% will die from HCC or cirrhosis
presentation: sx occur 4-12 wks after exposure. Often silent. Can include fever, tiredness, loss of appetite, N/V, dark urine, abd pain, joint pain, gray colord stools and yellowing of skin or eyes
lab tests: test for HCV Ab, HCV RNA by PCR, HCV genotype, infection can be detected about 10 wks after exposure and 97% of those >6 mo after exposure
tx: 15-25% will clear virus without tx, the others will progress to chronic disease. For genotype 1 use combo pill with sofosbuvir and ledipasvir (Harvoni) for 8-24 wks depending on certain factors.
pt ed: avoid etoh, ask provider before starting rx, oTC, or supps


drug induced liver disease: definition, subclasses and causes, tx

definition: dx of exclusion with a compatible hx, neg tests for hep A,B,C, no alcoholism, sepsis, or AI, and normal liver and biliary imaging
subclasses:direct from hepatotoxic agent, dose related vs. indirect: not inherently hepatotoxic and not dose related but it induces or alters a pre existing liver condition.
causes: direct: usu d/t ingestion of a drug, can take weeks after to see sx. Usu a cholestatic pattern of injury but can be hepatocellular. Top 10 meds: amoxicillin/clavulanic acid, isoniazid, nitrofurantoin, bactrim, minocycline, cefazolin, azithromycin, ciprofloxacin, diclofenac, levofloxacin. other hepatotoxins: niacin, asparaginase, oxaliplaitn. indirect: usu reactivation of HepB (rituximab, infliximab, imatinib), acute flare of Hep C (HIV therapies), trigger of AI hep (interferon beta), exacerbation of NASH (mirtazapine, prednisone).
dx: dx of exclusion. Sometimes need liver bx. Use


AI hepatitis
eti and transmission
lab tests

epi: most common in middle aged women, assoc with other AI, but can occur at any age
RFs: other AI disease
presentation: from fatigue to fulminant hepatitis, jaundice, joint aches
lab tests: increased IgG (best indicator). high ANA or positive smooth muscle aB but these are nonspecific. elevated total protein (b/c such high immunoglobulins)
dx: usu very high enzymes, need a liver bx to confirm before tx started.
tx: steroids: prednisone 40 mg daily. Maintenance with mercaptopurine or azathioprine. Usually life long.


primary sclerosing cholangitis

definition: inflammatino and fibrosis of bile duct
epi: mostly men >40 with diffuse inflammatin and fibrosis of the biliary tree.
assoc: assoc with ulcerative colitis; increased r/o cholangiocarcinoma
sx: jaundice, itching, typical sx with hepaitits
labs: alk phos elevated, +p-ANCA, elevatd tbili 50% of the time at dx; ERCP can reveal beaded and strictured pattern in bile ducts
tx: low dose ursodiol
monitoring: for end stage liver disease


primary biliary cirrhosis:

epi: mostly women in 40-60s
eti: causes destruction of interlobular and septal bile ducts. AI?
sx: excoriations from itching, xanthelasmas and xanthomas
labs: alk phos elevated, ALT/AST mild to mod elevatsions, +AMA, elevated IgM, elevatd cholesterol and HDl
tx: ursodeoxycolic acid. Or cholestyramine, rifamipin, gabapentin for the itching.
monitoring:for osteoporosis, esophageal varices, and liver failure


metabolic liver disease:

types: wilsons: A1A: deficiency of proteins causes proteins that aren't degraded to be deposited in liver, also goes with pulm dysfcn. wilsons: autosomal recessive disorder leadng to excessive copper dep in liver, eyes, kidneys, joints, and RBCs.
RFS: A1A: fm hx of emphysema or copd.
SX: wilsons may present with neur deficits like tremors, stuff in eyes,
labs: AIA: decreased A1a; wilsons: decreased ceruloplasmin, increased 24 hr urine copper, increasaed dry wt of copper on liver bx
tx: A1A: no tx once liver complications, can give alpha 1 proteinase inhibitor injections for pulm issues, needs transplant.wilsons: copper chelation vs. transplant if fulminant failure.


hereidtary hemochromatosis:

def: autosomal recessive disease where abnormal iron storage disease where Fe builds up in liver, heart, pancrease, and pituitary gland
epi: MC in northern european ancestry
sx; asx or sx: fatigue, malaise, arthralgias, excessively tan.
labs: elevated iron sats, increased ferritin >1000, genetic testing for HFE mutations (but doesn't r/o if neg),
dx: liver bx with hepatic iron measurement.
tx: phlebotomy every 1-2 wks until ferritin at 50-100. lifetime maintaince q 3-4 mons. and screen family members.


what are the normal functions of the liver?

glucose homeostasis, plasma protein synthesis, lipid and lipoprotein synthesis, bile acid synthesis and secretion (absorbs fat and minerals), vitamin storage (B12, A,D,E,K), biotransformation/detoxification/excretion of endogenous and exogenous compounds like drugs, toxins, etc.;


T or F: LFTs directly measure liver function and/or severity of disease

F: but help us determine patterns of liver/biliary cell injury


what are the alarm signs for diarrhea and what do they mean?

weight loss (>5 lbs) (with normal appetite: hyperthyroidism, malabsorption; with wt loss before the diarrhea: neoplasm, DM, tuberculosis, malabsorption); fever (invasive pathogens (salmonella, shigella, campylobacter), cytotoxic organisms with mucosal inflammation (c. diff), IBD vs. enteric viruses; bloody stools (dysentery) (IBD/ulcerative colitis, malignancy, ischemic colitiis, infection with invasive pathognen vs. hemorrhoids, beet ingestion) awakening from sleep: organic causes (IBD, DM vs. self limited viral syndrome); fm hx of colon cancer, IBD, multiple endocrine neoplasia or celiac sprue, age >50 with change in sx (organic eti), immunocompromised host (infection)


what's in the ddx for diarrhea?

functional diarrhea, infectious diarrhea, IBD, malabsorption, laxative use, medicaed related (including caffeine and alcohol), post op, malignancies, collagenous colitis, idiopathic, hyperthyroidism, ischemic colitis


pt ed

epi 10-20% of americans
eti: cholesterol stones: imbalance of cholesterol (hypersecretion) and lecithin/bile salts+stasis (b/c there is less water soluble parts the stones preciptate out); pigment stones (excess bile pigment (unconjugated bilirubin precipitates) or chronic hemolysis or decreased bilirubin conjugation) black(in gallbladder) more common than brown(from e coli in ducts).
RFs: 5Fs for cholesterol stones: fair, female, forty, fertile, fat (excess cholesterol) for pigment stones: cirrhosis(increased RBC turnover from splenomegaly), increased hemolysis (sickle cell, thalassemia), asian population; or crohns (decreased absorption of bile salts in terminal ileum), or decreased enteral stimulation of gall bladder (ICU, TPN, major trauma, paralysis); RFs from dz: cholecystitis, choledocholithiasis
presentation: abrupt onset, RUQ or epigastric pain with radiation to R scapula, minutes to hours duration that resolves slowly, sharp, stready and severe pain; fatty foods aggravate it, nothing relieves it, may have assoc N/V, may have RUQ tenderness or epigastric pain. NO FEVER OR palpable mass.
dx: normal LFTs, RUQ US
tx: nothing if no pain or complications. Can do cholecystectomy esp if recurrent, ursodeoxycholic acid (ursodiol), lithotripsy
pt ed: avoid rapid wt loss, extreme dieting. Estrogen/OCP can increase r/o stones. Avoid meals high in fat after dx.


abrupt onset, RUQ or epigastric pain with radiation to R scapula, minutes to hours duration that resolves slowly, sharp, stready and severe pain; fatty foods aggravate it, nothing relieves it, may have assoc N/V, may have RUQ tenderness or epigastric pain + fever,leukocytosis, and positive murphy's sign




et: calculs cholecystitis: stone wedged in cystic duct resulting in inflammation from mechanical, chemical, and bacterial causes. Acalculous: inflammation from gall bladder stasis and ischemia, or secondary infection
RFs: for acalculus: critically ill pts (dehydration, fever, absence of PO feeds), trauma pts, HIV, use of TPN; can get gangrenous gallbaldder, emphysematous gallbaldder
dx: RUQ US will show GB wall thickening, pericholecystic fluid, and sonographic murphys sign (from probe hurting them). HIDA scan will show whether or not radiotracer can enter gall bladder or not, could also inject radioactive CCK to get gall bladder to contract., elevated WBCs, possibly increased LFTs if irritating liver
tx: NPO, IVF, pain management, abx (include GNR, anaerobe coverage) cholecystectomy or cholecystotomy tube if not healthy enough to have gall bladder out


abrupt onset, RUQ or epigastric pain with radiation to R scapula, minutes to hours duration that resolves slowly, sharp, stready and severe pain; fatty foods aggravate it, nothing relieves it, may have assoc N/V, may have RUQ tenderness or epigastric pain + jaundice or asymptomatic




eti stone in the common bile duct
RFs: cholangitis, cholecystitis, pancreatitis, stricture
dx: elevated conjugated bilirubin, alk phos, normal AST/ALT, possibly elevated lipase/amylase (if irritating the pancreas) RUQ US shows CBD stone (inferred from dilated cbd>6 mm) If unclear: ERCP, MRCP, cholangiogram
tx: ERCP with stone extraction and papillotomy or cholecystectomy (usu within 6 wks if you think more are in there)



eti: obstruction in bile duct from stone, malignancy, stricture, or infection with fluke
sx: charcot's triad: RUQ pain, fever, jaundice
dx: RUQ US may show obstruction and help rule out alternate dx (like cholecystitis) may have elevated WBCs, bilirubin and alk phos(cholestasis), possible mild elevation of AST/ALT (from things being backed up and flowing into liver)
tx: abx (broad + gram neg rods), biliary decompression in about 20% of the cases is required: ERCP + stone extraction and stents



eti: adenocarcinoma of bile ducts, gallbladder, ampulla of vater
RFs: porcelain gall bladder (chronic inflammation and changes), chronic biliary and liver inflammation, primary sclerosing cholangitis, asian descent (r/o infection with liver fluke),
sx: abd pain, jaundice, wt loss, clay colored stools.
dx: elevated bilirubin or alk phos, CT, abd US, cytoglogy via ERCP
tx: surg resection +/- chemo and radiation if caught early, or it can be done palliatively
px; often mets at dx, 20% 5 yr survival


acute and chronic pancreatitis:

eti acute: gallstones (40%), alcohol (30%), drugs, hypertriglyceridemia, hypercalcemia, obstructive or structural reasons, infections, AI, ischemic, post ERCP, trauma, scorpion sting chronic: etoh, AI, cystic fibrosis
RFs: acute: shock, multisystem organ failure, pseudocyst (walled off), pancreatic necrosis, infection, abscess chronic: malabsorptino/pancreatic insuffieicny, DM, pseuodocysts, necrosis
dx: acute: elevated amylase(not as specific b/c also secreted by salivary glands), elevated lipase ( more specific) +/- elevated bilirubin, transaminases, prognostic; WBC, hct, BUN, Ca, glucose, CRP. Imaging: abdominal CT to see inflammation, adominal US to maybe see stones, MRI/MRCp chronic: amylase/lipase may be normal but you may see calcifications with abdominal CT and MRCP
tx: acute: IVF, bowel rest and advance when sx abate, pain control with meds. Only abx for severe cases. ERCP +sphincterotomy for CBD stone.chronic: etoh cesation, IVF, NPO, and analgesics for acute attacks, relive obstructions


sudden onset, pain in epigastric region that radiates to back, sometimes lUQ/RUQ, duration of hours to days, study, boring pain, aggravated by alcohol binges, relieved by leaning forward, constant and progressive in timing, assoc with N/V; epigastric tenderness + guarding, decreased bowel sounds, +/- jaundice, cullen's sign (periumbilical bruising), grey turner's (flank bruising), fever, tachycardia and hypotension. they'll look and feel sick

acute pancreatitis


how does chronic pancreatitis differ from acute in presentation?

chronic: acute attacks, wt loss, fatty stools


pancreatic cx:

eti: MC is adenocarcinoma, others are acinar, endocrine, cystic
RFs: obesity, smoking, chronic pancreatitis, hereditary
sx: painless jaundice, wt loss, early satiety/loss of appeitte, new diabetes, unexplained pancreatitis, may be itchy
dx: pancreatic protocol CT, Eus with bx, MRI/MRCP, CA 19-9 increased (tumor marker)
tx: whipple's procedure + chemo: remove pancreatic head, duodenum, CBD, gallbladder +/- partial gastrectomy; if locally advanced: chemo; if mets: chemo +palliative
px: poor. If mets only 11 mos.



eti: diverticulosi-> micro or macro perf of diverticulum. Micro=infection contained by pericolonic fat, mesentery or adjacent organs. Macro=infection gets farther out and peritonitis and pericolonic abscess can occur. Pressure +small sigmoid colon causes diverticulae.
RFs: men 70, western diet, obesity smoking
sx: constant LLQ pain, N,V,D, fever, hematochezia uncommon
dx: may have mild leukocytosis, CMP if dehydrated, may have bacteria in urine culture. CT abd and pelvis with contrast is dx. Abd xray may reveal free air showing peritonitis or perforation.
tx: conservative tx for uncomplicated diverticulitis (outpt, cipro+metro, control pain and nausea, clear liquid diet, consider complications if not improved in 2-3 days and colonscopy in 6-8 wks to confirm dx and eval for colorectal cx, IBD, and ischemic colitis) if complicated: in pt, CT scan for surg and abscess? NPO, IVF, IV abx. if abscess: can drain with help of CT guided percutaneous drainage and consider sigmoid colectomy once recovered.



subclasses: 1st degree: no prolapse just prominent blood vessels 2nd deree: prolpase when bearing down but spontaeously reduced 3rd: prolapse on bearing down and requires manual reduction 4th: prolapsed and cannot be manually reduced
eti: anal cushions usu prevent tearing in defecation, aid in continence and provide anal sensation and complete seal in closure. In hemorrhoids they enlarge and get distally displaced.
ask ;does something come out and go back in? or is it there all the time?
RFs: 50-80% of pop; mC cause of lower GI bledding
sx: external: don't bleed excessively, may thrombose, often don't need tx; intenral :not painful ,bleed and prolapse, cause mucus secretion
tx: external: fiber (20-30g) in lots of water bid; stool softener, sitz bath for 6 wks, topical steroids or anesthetics; internal: rubber band ligation, infrared coag, sclerotherapy, excision, just beware of incontinence issues!


anal abscesses:

subclasses: MC in perianal, then ischoanal, intersphincteric then supralevator
eti: obstruction of the cryptoglandular opening results in accumulatino of glandular secretions and a growing area for E. coli, enterococcus or bacteroides
RFs: can cause: fistula, necrotizing fasciits, perineal sepsis (pain, fever, inability to void)
sx: pruritis, pain, usu lesion at anal openingg, red and fluctuant lesion, may have systemic sx like fever and leukocytosis
dx: dx of ischiorectal with digital exam showing a fluctuant mass above the anal opening.
tx: perianal: incisoin and drainage or cruciate or elliptical incision. Can do packing if needed for hemostasis. Abx if cellulitis, valvular heart disease, immunocompromised, DM, or corticosteroids, + sitz baths. Same tx for ischiorectal.


rectal prolpase



epi: MC in kids and elderly
eti: kids: CF, parasitic infections of intestine or long term diarrhea; adults: constipation, muscle or nerve problems, mutliple vaginal deliveries

sx: presents gradually; initial sx only with bowel movements, later feels like something is falling out +/- fecal incontinence

tx:surgery usu not needed. Tx cause. Surgery for adults to repair weakend anal sphincter and pelvic muscles.


anal fissure



epi:younger to middle aged men
eti: C/D or increased anal pressure and decreased blood flow which results in poor healing

sx: pain during and after defecation, BRBPR with bowel movements only, fissure on examination

tx: increase qfiber with lots of water, sitz baths, surgery if doesn't heal. Can treat with topical nitroglycerin, calcium channel blocker or botox or sphincterotomy


which type of hernia is most commonly incarcerated b/c its a smaller opening?



what is the only thing that will treat inguinal hernias and can prevent incarceration and strangulation?



what's the pathophys behind pancreatitis?

damage to ductal epithelium causes leakage of digestive juices and activation of proteolytic and lipolytic enzymes. These cause vascular injury, capillary and lymphatic obstruction, and acinar cell injury release more enzymes. Eventually it activtes the kallikrein system and there is gross vsodilation and vascular permability leaking to shock and acute renal failure which can lead to acute respiratory distress syndrome and death


what's in the ddx for cholelithiasis?

PUD, GERD, nonulcer dyspepsia, IBS, sphincter of oddi dysfcn, hepatitis and perihepattis, hepatic abscess, neprholithiaiss, pyelonephritis, peirneprhic abscess, pneumonia, angina pectoris, pancreatitis, ruptured ectopic pregnancy, appendicitis


can hand sanitizer kill c. diff spores?

no--etoh does not kill it


acute diarrhea:

def: stool with increased water content, volume or frequency (acute 4 wks
epi:avg adult 4x/yr, children experience 7-15 cases by age 5; causes deaths around the world
eti: acute: MC viral (non bloody: norovirus, rotavirus, adenovirus, astrovirus), bacterial (nonbloody: enterotoxigenic e. coli, vibrio, shigella, salmonella, yersinia vs. bloody aeromonas, campylobacter, e. coli (with shiga like toxin), shigella, salmonella, yersinia), parasite (giardia, cryptosporidium, isospora or cyclospora, entamoeba histolytica) or toxins (c. diff, staph aureus, bacilius cereus, c. perfringens), or recent abx use (think c. diff!)
labs: if suspected c. diff: PCR for cdiff toxins A and B. if non infectious, reserve stool cultures for those with grossly bloody stool, severe dehydration, signs of inflammatory idisease (pus in stool, foul smelling) lasting more thn 3-7 days, suspected nosocomial infections or immunosuppression.check for ova/parasites only if in high risk group. and endoscopy or colonic bx for difficult cases.
rfs: dehydration, esp in children w/ higher body water content, increased metabolic rate and increased body surface area to mass index (can happen within 24 hrs)
tx: tx dehydration first (oral preferable), then evaluate etiology. Acute Viral eti is supportive tx with oral rehydration salts (avoid juice, soft drinks, and sports drinks) as much as they want, eat a normal diet once vomiting stops, and can take imodium or simethicone to ease the cramping. food poisoning is supportive and self limited. use antimicrobials guided by bacterial findings.


diarrhea ddx

determine if watery, fatty,or inflammatory (pus, blood, small volume, adb pain). functional diarrhea, infectious diarrhea, IBD, malabsorption, laxative use, medicaed related (including caffeine and alcohol), post op, malignancies, collagenous colitis, idiopathic, hyperthyroidism, ischemic colitis


diarrhea sx

more bowel movements than usual (frequent watery voluminous ones indicate small bowel eti, whereas small volumes with lower abdominal pain signify large bowel eti); abd pain in periumbilical region (small bowel), lower abdominal pain (large bowel patho), generalized abd pain (IBS, ischemic bowel, celiac sprue), incomplete emptying or only passing mucus (anorectal inflammation like ulcerative colitis), pain relieved after bowel movement (IBS), mucus (IBS), greasy, pale, foul smelling, bloating, difficult to flush stool +/- wt loss (steatorrhea from malabsorption), abrupt onset (viral, bacterial), gradual onset (IBD, IBS), abdominal bloating (IBS, lactose intol, viral, abx, nonulcer dyspepsia, celiac sprue), increased flatulence (IBS, carbohydrate malabsorption, viral), straining+urgency+incomplete evac (ulcerative colitis, IBS, proctitis), N/V (viral gastroenteritis, bowel obstruction) arthritic pain (reactive arthritis after infection, IBD), arthritis, urethritis or conjuctivitis (reiter syndrome after infection with GI pahogen), worsening with dairy or milk products (lactose intol), sx after eating rye/wheat/barley (celiac sprue), chew sugarless gum (sorbitol ingestion), sx persist if stop eating (secretory diarrea), travel (giardia, cryptosporidium, etc), recent abx use (c. diff), new meds, hosp recently (c. diff), surgery like vagotomy, intestinal resection (lack of absorptive surface, decreased transit time, malabsorption of bile acids), ill contacts (food borne outbreaks), onset 14 hrs with vomiting (viral), with dysentery (enterohemorrhagic e. coli), with fever or dysentery (salmonella, shigella, campylobacter), work in day care (rotavirus, shigella, giardia, cryptosporidium), pets (salmonella), anal intercourse (herpes simplex, gonorrhea, chlamydia, shigella, salmonella, campylobacter, giardia, cryptosporidium), HIV (cryptosporidium, microsporidium, isospora, cytomegalovirus, diseases that run in family (IBD, multiple endocrine neoplasia), laxatives (laxative abuse), unhappy with body image (laxative abuse), assoc body flushing (carcinoid syndrome)


what do each of these PE signs, + diarrhea, signify?
lymphadenopathy , exopthalmia . , dermatitis herpetiforms, scars, hypermotility, tenderness, masses, rectal exam

lymphadenopathy (if chronic infection or malignancy), exopthalmia if d/t hyperthyroid. , dermatitis herpetiforms (blisters on body from celiacs), abdomen (scars, hypermotility, tenderness, masses), rectal exam


what labs/tests should you do in diarrhea?

if suspected c. diff: PCR for cdiff toxins A and B. if non infectious, reserve stool cultures for those with grossly bloody stool, severe dehydration, signs of inflammatory idisease (pus in stool, foul smelling) lasting more thn 3-7 days, suspected nosocomial infections or immunosuppression.check for ova/parasites only if in high risk group. and endoscopy or colonic bx for difficult cases. can check CBC, CMP and albumin (to see if not abosrbing protein), ESR, LFTs, TSH. 2nd line: check for ova and parasites, fecal leukocyte level/FOBT, fecal calcoprotein(neutrophil activity helps identify IBD)


what does an anorectal manometry test measure? what is normal?

measures anorectal pressures/squeezing; sphincter should relax when rectum squeezes


what's an indication for a colon transit test?

when evaluating constipatin that has normal manometry


what do the different results of a colonic transit test show? what is normal?

normal: 5 or fewer rings should reamin after 3-5 days. if most rings are scattered after 3-5 days that shows slow /hypomotility of colon. If rings gathered in sigmoid colon=funcitonal outlet obstruction.


what causes constipation in kids? is it normal? when do you do testing?

common in kids. Most is idiopathic. Often from transition from breast milk to cows milk. Or transition to school (psych). No need for testing if no red flags: no failue to thrive, no absent reflexes, no urinary incontinence.



defcongenital blocka ge of large intestine
eti: poor muscle movement in bowel or missing nerves causes blockages in infants.
rfs/assoc with down syndrome
sx constipatino, stool in LLQ, explosive stool on withdrawal of finger
labsFOBT for infants with constipation
tx abnormal section must be removed



def: infrequqent bowel movements (


what is the normal process of swallowing?

2. Swallowing: 1st 1/3 is voluntary. Then soft palate elevates to close off nasopharynx, epiglottis closes over larynx to seal off trachea, and larynx is pulled upward to facilitate esophageal opening. Pharyngeal constrictors contract and peristalsis brings bolus downward. Mediated by acetylcholine, nitric oxide and vaso active intestinal peptide.



def: occurs when mucosa is exposed to acid containing gastric secretions
eti: 1) dysfunctioning LES (lower pressure (although most pts have normal pressure), or not getting held together tightly by intraabdominal location or diaphagm or transient relaxation of LES b/c of gastric distention that triggers the vasovagal reflex) , 2) bicarb secretion or hypersecretion of acid (or reflux of bile or alkaline pancreatic secretions), can also be 3) d/t hiatal hernia in which case part of the stomach is above the sphincter and it can't close all the way. 4) or abnormal esophageal clearance aka motility (usually it can clear the reflux via bicarb or peristalsis, the dysfcn of this can be exacerbated by impaired salivation from anticholingeric meds, scleroderma, sjogren syndrome, or oral radiation therapy) 5) delayed gastric emptying (gastroparesis=slow or partial outlet obstruction)
rfs: tobacco, etoh, fatty foods, overeating, tight clothing, obesity, hiatal hernia, pregnancy; refs from dz: barrett's esophagus
sx: "heart burn" 30-60 min after eating or when supine, regurgitation, dysphagia ("stuck"), +/-atypical/extraesophageal signs: asthma, chronic cough, chronic laryngitis, sore throat, hoarseness, globus sensation, noncardiac chest pain)
dx: if tx empirically with antisecretory works then that is dx. If there are alarm sx (troublesmoe dysphagia, odyngophagia, wt loss, iron def anemia, resistant sx) then consider upper endoscopy w/ bx or barium upper GI series or esophageal pH testing.
labs: endoscopy with bx may show edema and hyperemia of larynx, vocal cord erythema, polyps, granulomas, ulcers or hyperemia and lymphoid hyperplasia of posterior pharynx or dental erosion. Consider barium upper GI series or esophageal pH testing and esopahgeal manometry
tx: pharm: empirically w/ antisecretory tx or antacids or oral H2 receptor blockers and lifestyle mods. Heal esophagitis if present. Prevent complications. Non pharm: Elevated head of bead 6 inches, no food/drink for 2-3 hrs before bedtime, stop smoking, decrease etoh, modify diet to smaller portions, less fat and avoid peppermint, spearmint, citrus juices, tomato, chocolate, etoh, coffee, tea, cola, spicy foods, lose wt. avoid NSAIDs. if they don't respond to tx: can do nissen fundoplicaiton surgery


barrett's esophagus:
Rsf for/from

def: intestinal metaplasia of distal esophagus
eti/pathophys: strat squamous turns to columnar with goblet cells and paneth cells from chronic acid exposure
Rsf for/from: GERD, 40-100x inc r/o cx
PE: red, velvety mucosa, may have ulcerations, bleeding and stricture
tx :fundoplication surgery and acid suppression won't help. Just surveillance via endoscope q2 years with biopsies


espohagitis: (of the 5 types)

epi: "infectious: most common in immunosuppressed
pill-induced: often in those who are bed bound/hospitalized/laying down
caustic: kids ingesting stuff
radiation induced: cx pts receiving radiation
eosinophilicpeds pts"
eti: "infectious: most common in immunosuppressed (candida, HSV, CMV)
pill-induced:injury thru prolonged direct contact with med i.e. nSAIDS, KCL, quinidine, vit c, iron, abx (doxy, tetra, clinda, TMP-SMX)
caustic: ingestin of alkali (worst--disintegraes mucosa and goes deep, ph>11 worst and most household products are 9-11pH) or acidic solutions (coag necrosis + eschar)
radiation induced: stricture or narrowing of esophagus, perf or rupture, fistula or hole
eosinophilic: dense eosinophilic infiltration of the esophageal mucosa"
rfS: for pill induced: bed bound or hospitalized (pill not moved down with gravity)
sx: "infectious: odynophagia, dysphagia, substernal chest pain, oral thrush (candida or viral), infection at other site (CMV: colon, retina), oral ulcers (herpes)
pill-induced: may occur suddnely or slowly, severe retrosternal CP, odynophagia, dysphagia
caustic: severe burning, chest pain, gagging, dysphagia, drooling, +/- stridor/wheezing
radiation induced: dysphagia, heartburn, CP, nausea, food impaction



labs/tests: "infectious: endoscope showing small deep ulcerations (herpes) or diffuse, linear, white-yellow plaques and fungal hyphae (candida), 1 large shallow superficial ulcer (CMV)
pill-induced: endoscopy may show shallow or deep ulcers, stricture, hemorrhage, or perforation
caustic: laryngoscopy, endoscoy, xrays
radiation induced
eosinophilic: endoscopy shows narrowed lumen, longitudinal furrows, circular ridges, friability, easily torn, 15-25 eosinophils/hpf on bx"
tx: "infectious: empiric systemic tx with fluconozaole for candida, ganciclovir for immune restoration if HIV+ (cytomegalovirus), sxatic or anti viral (if immunocompromised) for herpes
pill-induced: eliminate offending pill, sx
caustic: ABCs, assess mucosa/observation, if less severe offer clearliquids and feed as tolerated; if moderate (2nd degree burn) steroids +/-abx; if severe: NG tube ,gastrostomy +/- steroids
radiation induced: G tube or J tube permanently to bypass esophagus, tx pain
eosinophilic: topical steroids (fluticasone) oral steroids"
monitoring: monitor via UGI series in known ingesiton cases in 3-6 weeks for milder cases nd in 2-3 weeks in more severe cases. Keep an eye on them b/c they will have inflammation and vascular thrombosis and granulations tissue, weeakening of esophageal wall which increases risk of perf. this risk is gone after 3 wks.


what is mallory weiss syndrome? what are refs? sx? dx/test?

non penetrating, linear mucosal tear at GE jcn from sudden rise in transabdominal pressure
hx of retching, vomiting b/c of weakening muscles +/- hemataemesis +/- melena
rfs: etoh, bulimia, increasing age, hiatal hernia
dx via endoscopy to see tear at GE jcn
tx: stabilize, transfuse in most, electrocoagulation to stop bleeding, epinephrine, and arterial embolizaion. Most will stop sponataneously


zenker's diverticulum

def: protrusion of pharngeal mucosa at pharyngoesophageal jcn loss of elasticity of UES
sx: dypshagia, regurg, cough, halitosis, gurgling, wt loss, swelling in neck
dx: barium swallow
tx: observe, myotomy, diverticuloectomy
complications: aspiration, pneumonia, lung abscess


what are the diff ways to tx esophageal varices?

endoscopy ASAP when hemodynamically stable + banding or sclerotherapy, can do balloon tube tamponade, transvenous intrahepatic portosystemic shunts (TIPS), surgical shunts, or liver transplant



defdegernation of ganglion cells in myenteric plexus and LES can't relax when swallowing
rf: squamous cell carcinoma
sx: gradual, progressive dysphagia with solids and liquids, wt loss, pain/substernal discomfort after meals, regurg of undigested food esp at night, aspiration, may have adopted other maneuvers for eating (taking small bites,etc)
dx: barium study (will show "birds beak" of distended esophagus proximal to LES), CXR, manometry, endoscopy, chest CT
tx: relieve obstruction via nitrates/CCBs to relax the smooth muscle, +/- dilation, myotomy, botox to relax the muscle
px: can return to normal if caught early


upper esophageal sphincter dysfcn

eti weak pharyngeal muscles
sx: cervical dysphagia, solids are worse, chronic cough +/- zenker's diverticulum+F46
tests: barium study, endoscopy, manometry
tx: myotomy


neoplasms in esophagus:
rfs for dz
refs from dz

rfs: scc: etoh, tobacco, achalasia, chronich iron deficiency, tylosis (thickening of palms and soles, white patches in mouth) adenocarcinoma: barrett's esophagus
refs from dz:bleeding, mets (to lung, liver, adrenals MC), obstruction, fistula
sx; most present late with dysphagia, wt loss,pain, hoarseness, regurg, aspiration, hematemesis
labs: CXR may show lymphadenopathy, pulm/bony mets, tracheoesophageal fistula. Barium may show polypoid , infiltrative or ulcerative lesion or apple core lesion, esophagoscopy/bronchopscopy, CT/PET to look for mets
dx: CXR may show lymphadenopathy, pulm/bony mets, tracheoesophageal fistula. Barium may show polypoid , infiltrative or ulcerative lesion, esophagoscopy/bronchopscopy, CT/PET to look for mets
tx: surg, radiation, chemo combos. If stage I and Ia=surgery.If Iib or IIIA: combo of surg and chemo; stage IIIb and Iv: incurable, palliative


what do the following sx mean ? PMH or fmhx of gastric or duodenal ulcer , smoke , hx of heavy etoh use , NSAIDS, >45, duration , burning pain , stabbing , severe/unbearable crampy/colicky), epigastric , substernal ), RUQ , periumbilical , LUQ , pain remains in same place , radiate to back, radiate from epigastrium to chest or neck

PMH or fmhx of gastric or duodenal ulcer (PUD), smoke (pUD, reflux esophagitis, gastric cx), hx of heavy etoh use (gastritis, reflux esophagitis, PUD, pancreatitis, esophageal cancer), NSAIDS, >45 (malig more likely), duration (more serious dx tend to have shorter interval until presentatoin), burning pain (gastritis, duodenal ulcer, gasrtric ulcer), stabbing (pancreatitis, duodenal ulcer, gastric ulcer), severe/unbearable (acute pancreatitis, perforated viscus), crampy/colicky (biliary colic, IBS, intestinal obstrution), epigastric (gastritis, esophagitis, duodenal ulcer, peptic ulcer, pancreatitis, gastric or esopageal malignancy, pancreatic cx, colon cancer (in trans), functional dyspepsia), substernal (ischemic heart disease, esophagitis), RUQ (biliary colic, IBS, hepatoma), periumbilical (small bowel disease or obstruction), LUQ (IBS, lesion in tail of pancreas), pain remains in same place (gastric ulcer), radiate to back (pancreaitis), radiate from epigastrium to chest or neck (GERD, ischemic heart disease, esophageal spasm),


what do these mean?
constant pain , intermittnet , abrupt onset , gradual increae in intestinty, steady for 30 min to 2 hrs before subsiding, reaches peak in 15045 minutes and subsides , wakes from sleep, N/V , melena, chronic cough or hoarseness , dark urine or yellow skin , belching , feelfull , heartburn or regurg , passing gas , lost wt ,diffculty swallowing , bloated , change in stool frq , constipated , mucus with stool ), BRBPR , sx worse or better with meals

constant pain (malignancy), intermittnet (gastritis, pUD, biliary colic, IBS, meds) abrupt onset (acute panc., perf viscus, vascular thrombosis), gradual increae in intestinty (PUD, biliary colic), steady for 30 min to 2 hrs before subsiding (Pud), reaches peak in 15045 minutes and subsides (biliary colic), wakes from sleep (PUD), N/V (PUD, gastric cx, biliary colic), melena (PUD, gastric or colon cx), chronic cough or hoarseness (GERD), dark urine or yellow skin (biliary dz), belching (biliary, IBS, GERD), feelfull (IBS), heartburn or regurg (GERD), passing gas (IBS, malabsoprtion, biliary) lost wt (gastric or esph cx, PUD, colon cx, intraabdominal malig, malasbp) diffculty swallowing (GERD, esophagitis, esophageal stricture, esophageal cx), bloated (IBS), change in stool frq (IBS), constipated (colon cx, IBS), mucus with stool (IBS, IBD), BRBPR (colon cx, diverticulosis, brisly bleeding peptic ulcer, hemorrhoids, IBD), sx worse or better with meals


esophagitis (of all subtypes)

eti: "erosive/hemorrhagic: poss portal HTN, caustic ingestoi, radiation
NSAID: nsaids
stress: critical illness i.e. mech vent, coagulopathy, trauma, burns, shock, sepsis, organ failure
alcoholic: etoh may cause dyspepsia, nausea, emesis, and minor hematemeis but prob not erosive gastritis
non erosive/nonspecific: usu d/t h. pylori or pernicious anemia based on histo assessment
h.pylori: sits in gastric mucosa and cuases inflammation via pMNs and lymphocytes
pernicious anemia: AIdisorder with glands that don't produce enough hcl and don't absorb vit b12"
rf: H. pylori gastritis can cause gastric adenocarcinoma and low grade B cell gastric lymphoma
sx:"erosive/hemorrhagic: often asx, +/- anorexia, epigastric pain, N/V, +/-hemataemesis (coffee ground), bloody aspirate, melena
non erosive/nonspecific
h.pylori: nausea, abd pain with acute infection that progresses to chronic, may cause peptic ulcer
pernicious anemia"


gastritis: (all subtypes)

labs/test: "erosive/hemorrhagic: upper endoscopy will show hemorrhages, petechiae, erosions, focal or diffuse lesions, may have low Fe
NSAID: endscopy if show alarm sx
stress: mucosal erosions and sub epithelial hemorrhages, poss overt bleeding, look for treatable causes with endoscopy to look for txable causes
non erosive/nonspecific
h.pylori: test anyone with past or fm hx of PUD or gastric adenocarcinoma via fecal antigen immunoassay, IgG ab testing or urea breath test (must d/c PPI for 7-14 days and abx 28 days prior to this) will have a cobblestone appearance on endoscopy
pernicious anemia: histo shows gland atrophy and intestinal metaplasia and pareital cell antibodies against proton pumps"
tx: """erosive/hemorrhagic
NSAID: d/c NSAID or reduce dose or give with meals. Can add PPI.
Stress: tx pts with RFs (coagulopathy with low platelets or high iNR and resp failure or on mech vent 48+ hours)prophylactically withPPI, H2 blockers or omeprazole
alcoholic: tx empirically with h2 blockers, PPI or sucralfate for 2-4 wks and stop etoh
non erosive/nonspecific
pernicious anemia"""
monitoring: monitor pernicious anemia gastritis with endoscopy periodically to check poss development of multicentric carcinoid tumors


peptic ulcer dz

def: GI tract problem caused by mucosal damage secondary to pepsin and gastric acid secretion
epi:incidence decreasing d/t better tx of h pylori, safer nSAIDS, and acid suppressive meds
eti: most have H pylori or NSAID hx, some idiopathic, zollinger ellison syndrome, stress/illness, bisphosphonates (osteoporosis meds), amphetamines
pathophys: increased vagal activity +/- h. pylori +/- parietal cell hyperplasia and reduced alkaline secretions. Mostly occur along lesser curvature of stomach and anterior or posterir wall of duodenal bulb
RFs: smoker, male, etoh abuse


peptic ulcer dz

sx: recurrent episodes of epigasric discomfort/pain that usu radiates to back, may be burning or piercing, relived by eating or antacids, wakes pt at night, occurs between meals,loss of appeite, N/V, heartburn, wt loss, intermitten pain lasting 2-8 wks at a time. if perf: sudden change in inensity and rhytmicity of ulcer sx with severe and constant pain that radiates to the back and is unresponsive to antacids or food
pe: may show palor, signs of hemodynamic instability, abdominal rigidity or tenderness, rectal exam/stool guiac, may have hx of melena, hematemesis
labs/tests: endoscopy if alarm sx or older; test for h. pylori via bx if endoscopy, serology or stool antigen or urea breath test. Perform endoscopy if: want ot look for cx, esophagitis, or duodenitis, to look for bleeding, visible vessels, to obtain bx from ulcers to exclude malignancy, to obtain bx to sample h. pylori, for tx measures like stopping bleeding, etc. check CBC or FOBT for blood loss in stools or anemia.


peptic ulcer dz: complications, tx and management of complications

complications: complications: hemorrhage, gastric outflow obstruction (via edema and inflammation), intractability (persistent ulcer after intense and prolonged therapy--consider poor compliance, ctonued use of ulcerogenic drugs, and other dx like crohns, other bacterial infection and viral infections), penetration (pain suddenly more severe, may radiate to back, may perf panc, liver, or biliary tree)
tx: if + for h. pylori tx with triple tx of abx and 1 PPI. d/c the event of perforation: tx with fluids, correct electrolyte imbalances, NG suction, and prophylactic abx. If hemorrhage start fluids, transfusions, and endoscopy with laser or thermal txs to sto bleeding or mechanically compress with clips, start IV PPIs. If gastric outflow: NG asp, gastric lavage, IV PPIS, ABX to tx h. pylori and stop NSAIDS. penetration: IV PPI and close monitoring, consider surgeyr if no improvement


gastrin secreting tumor resulting in hypergastrinemia and hypersecetion of acid; consider for those with fmhx of ulcers, with ulcers refractory to std tx, with multiple ulcers or large ones, with ulcers distal to duodenal bulb,

zollinger ellison syndrome


gastric adenocarcinoma

epic: high indicence in japan, colombia, costa rica,hungary
refs from dz: mayget peritoneal or pleural effusions, bleeding in stomach, obstruction of gastric outlet, GE jcn or small owerl, intrahepatic jaundice, extrahepatic jaundice, starvation and cachexia
sx: dyspeptic sx (N/V, indigestion, loss of appeitte, post prandial fullness), hematemesis, palpable enlarged stomach with succussion splash, enlarged lymph nodes, with wt loss, >45 yrs, +/-iron def anemia and occult blood in stools;
tests: CBC, CMP, tumor markers (CEA, CA 19-9), EGD, double contrast upper GI or barium swallow, CXR, CT, MRI, EUS
tx: depends on staging. Usu diff surgerys +/- adjuvant chemo


gastic lymphoma

sx: dyspepsia, wt loss, anemia, +- abnorm on upper GI like thickened folds, ulcer, mass or infiltrating lesions,
tests: endoscopic bx req'd; abd CT and endoscopic US are req'd for staging. Determine if primary or secondary tumor.
tx: depends on staging. Tx h. pylori infection. Surgery not recommended. Tx with chemo or radiation.


what are some of the complications of gastric surgery?

diarrhea, dumping syndrome (N/V/D, flushing, diaphoresis post prandially), early satiety, bile reflux, afferent loop syndrome , maldigestion and malabsorption (esp of b12), recurrent ulceration


what does alcoholic liver dz refer to?

fatty liver, etoh hepatitis, etoh cirrhosis


fatty liver

EPI: women>men
eti: short periods of alcohol abuse (14-21 drinks per wk men) (11-14 drinks/wk women) or genetic mutations in alcohol dehydrogenase, obesity, +/- nafld/nash, possibly hormone related effects
pathophys: alcohol is broken down into acetaldehyde by alcohol dehydrogenase and then to acetate by aldehyde dehydrogenase which changes the oxidation reduction state in cell and oxidation is reduced and fatty acids increase in cell.


alcoholic hepatits

RFS: drinking 6-8 drinks daily for years +/-cirrhosis
sx: weakness, N/V,anorexia +/- portal HTN, GI bleeding, hepatic encephalopathy
PE: may have hepatomegaly, fever, tachycarida, jaundice, abdominal distention, ascites
labs/tests: may have low hgb, high MCV (>100), AST>ALT (both less than 5x normal but usu AST 2xgreater), increased total bilirubin and triglycerides and WBC count, may have elevatd INR. ALSO there may be some + findigns here that mimic other diseases: high iron or ferritin, elevated anti-nuclear antibody or smooth muscle antibody (ANA,AMA) and cholecystitis on US
tx: based on algorithm--see maddrey discriminant function, model for end stage liver disease, lille model and
Non pharml: abstinence > 6 months before transplant, psych eval, tx withdrawal, avoid narcotics, good nutritonal program, evaluate for infection (like SBP, pneumonia, cellulitis) Evaluate: based on scores of algorithms which help calculate their mortality risk (discriminant fcn and MELD) and response to steroids (lille). If their maddrey disciminant fcn score is >32 then they have a r/o death >50%, if MELD score (predicts 90 day survival) is low, prob need transplant. If lille model at day 7 (evaluates how they have been responding to tx so far via age, albumin, creatinine, PT, total bilirubin at day 0 and 7) shows >0.56 they are a null responder and prob need transplant. if 32 or encephalopathy and check efficacy with lille model


non alcoholic fatty liver dz

def; accumulation of fat (usu TGs) in hepatocytes that results from insulin resistance. It progreses from nonalcoholic fatty liver to non alcoholic steatohepatitis
subclasses: hepatic steatosis (benign) and non alcoholic steatohepatitis (NASH)
epi: MC chronic liver dz in world
eti: primary vs. secondary. Primary is elevated fats via insulin resistance (ie. DMII), dyslipidemia or obesity(metabolic syndrome) vs. secondary which is d/t nutritoin (starvation or parenteral nutrition), drugs (amiodarone, methotrexate, tamoxifen, glucocorticoids, valproate, anti retroviral drugs), toxins, or infection, wilsons, acute fatty liver of pregnancy, alcohol abuse
rfs: BMI >30, age >40, DMII, HTN, elevated ALT
sx: usu asymptomatic
labs/tests: may have some ALT/AST elevation, levels usu fluctate and may be normal sometimes. Need US (less useful if obese), CT, or MRI to visualize the fatty infiltration
dx: liver bx is gold std which will reveal lobular and portal inflammation, mallory bodies nand ballooning. can use imaging. Need to exclude caues by Hep B, C, AI, etoh.
tx: gradual wt loss (not quick) of 10-20% of body wt and prevent DMII, HTN, and hyperlipidemia


what is the most common complication of cirrhosis?



ascites: pathphys, labs, and tx

increased hepatic sinusoidal pressure causes vasodilation of splanchnic and system vessels, which then causes baroreceptors to think BP is low and the renin-angiotensin aldosterone system kicks in and kidneys absorb more sodium and water
labs: check SAAG if suspecting cause other than cirrhosis. (serum ascites albumin gradient). Serum albumin-ascites albumin. If 1 its from cirrhosis or liver disease, if >2.5 its cardiac ascites; if


what is hepatic encephalopathy, sx, and how is it treated?

def: confusional state assoc with liver dz. unknown toxins pass by diseased liver and cause changes elsewhere. usu induced by some event like GIB, infection, dehyration, MI, med non compliance
sx: inverted sleep wake cycle, asterixis, poor attention, irritability and drowsiness, poor memory in early stages, in later stages obtundation and coma
tx: lactulose titrated to 2-3 loose stools daily, or can give via enemas or down NG tube +/- rifaxamin or metronidazole. Avoid sedatives and pain meds. Treat exacerbating cause if found. +/- zinc


rfs for or from

def: progressive hepatic fibrosis and distortion of hepatic architecture
subclasses: compensated (still feel ok and not getting ascites, varices or encephalopahty) vs. decompensated (in hospital with infections, etc)
eti: etoh, NASH, Hep B or C, PBC/PSC, AI, hemochromatosis, right sided heart failure (congestion that affects liver)
rfs for or from: ascites, encephalopathy
PE: hypotensive, hepatosplenomegaly, spider angiomata, palmar erythema, scleral icertus with advanced dz may see abdominal distention, muscle wasting in extremities, edema of legs, asterixis
labs; may have decreassed hgb and platelets, decreased albumin, increased INR, increased total bilirubin
usually irreversible


who is at risk for hepatocellular carcinoma, how is it dx'd and how is it tax's?

10-20% from chronic HBV, 80-90% from cirrhosis; CT/MRI that shows arterial enhancement with venous washout. AFP >2000. liver transplant if only 1 tumor


in what ways is a iFOB/FIT test better than a guaiac for detecting occult blood?

it doesn't detect animal blood or upper GI bleeds, its more sensitive and specific and you only need 1 sample


colon cx:

epi:3rd most common cancer after breast/prostate, lung. Lifetime risk 1:19 large decline in incidence from detection and removal of polyps
eti: genetic+environment. Pathologic changes in normal cells change them into invasive carcinoma. 75% are sporadic with no RFs (except age >50) that can be ID, 15% are familial but no identified gene and 8% are hereditary with a specific gene, and 1-2% comes from IBD. mets to liver, lungs, brain, LNs
RFs for dz: lifestyle/dietary (low fiber, overweight, red meat or processed meats, etoh >2/day, smoking BUT protective factors are calcium/dairy, vit D., fruit, vegetable intake, physical activity, and NSAIDS, ASA, estrogen). Age>50, male gender, race/ethnicity (AA and ashkenazi jews), familial hx of colorectal cx (1st deg relative


colorectal cx
sx (depending on where at in colon)
monitoring after surgery/chemo

sx: 1)asymtpomaic 2)MC: suspicous sx or signs, also indicates more advanced dz 3)emergency admissoin from intestinal obstruction, peritonitis, acute GI bleed. Left sided cx will present with constipation or diarrhea, poss. obstruction, poss. change in bowel or hematochezia since that lumen is smaller with solid stool. Right sided has a larger lumen and liquid stool and will usu be more advanced when you fid it and may present with occult blood loss and/or iron deficiency anemia. it may also present once mets with abdominal distention, RUQ, early satiety if mets to live, or supraclavicular adenopathy.
tx: stage I and II: surgery and chemo if high risk, stage III surgery +adjuvant chemo (usu 6 months), stage IV with limitd mets do surg+chemo, nonresectable mets=palliatvive care
monitoring: for those with cx: stage I surveillance colonscopies; stage II and III: office visits and CEA q3-6 mos for 3 yrs, then 1 6 mos for yrs 4-5, + colonscopies @yr1 +q3-5 yrs., or if no radiation for rectal cx need increased surveillance of sigmoidoscopy q6 mos for 3-5 yrs.


what are the screening recommendation for those with avg risk, those with familial adenopolyposis and those with lynch and those with IBD?

the best test is the test that gets done: colonoscopy q 10yrpreferred, sigmoidoscopy +FOBT 15 yrs, other options: barium enema with air contrast, virtual colonoscopy (expensive and not always covered by insurance) and stool DNA. : ALL >50 q 10 years until 75if adequately screened and negative or 75-80 (if never screened and healthy) not rec'd above 85. (if . screen all with familial adenomatous polyposis at age 12 (they have a 100% change of cancer if +for gene and should get a colectomy). Screen those with hereditary non polyposis colorectal cx ("lynch syndrome") at age 20-25 or 10 years before youngest case. screening ~q yr with bx for those with ulcerative colitis and crohns. other labs to help dx and guide tx: CT of abdomen, pelvis, chest, LFTS (for liver mets), CBC, alk phos, CEA (cx marker)


someone comes into your office and wants to know how they can prevent colon cx: what do you tell theM?

they can't necessarily prevent it but can reduce their risk: to decreaes their risk they can exercise >150 min/week, lose wt, eat less red meat, drink 10g fiber/day (decreases risk by 10%) fruits and veggies, quit smoking
and get screened with a colonoscopy!


pathphys of inflammatory bowel disease

genetic predisposition + immunologic dysfunction + environmental influences; immune mediated chronic intestinal inflammation with periods of flaring and quiescence. Genes involved but they aren't mendelian. 1st degree relatives have 5-20 fold increased chance of developing IBD and 2 parents with IBD give their kid a 36% chance of developing it. these genes are involved in immunoregulation, mucosal barrier integrity, microbial clearance. whereas normal hosts are able to clear infections, down regulation innate immuen responses and heal without stimulating effector T cells, genetically susceptible hosts can't clear the pathogen, they activate the pathogenic T cell responses and they progress to chronic intestinal inflammation.


what sx is the hallmark of ulcerative colitis?

bloody diarrhea


what are the differences in factors that are protective and risky for UC and CD?

protective for uc: Smoking, appendectomy, high fiber, NSAIDS, infection in early life, high fiber, breastfeeding, protective for crowns: High fiber, infection in early life, breast feeding, NSAIDS. Rsf: UC: Abx, infections when older CD: Smoking, appendectomy, OCP, abx infections when older


what are the differences in histo findings for UC and CD?

uc: Lesions are mucosal, friable, may start at rectum and extends proximally in a continuous fashion. Inflammatory process causes vascular congestion, focal hemorrhage and granularity. ONLY IN COLON. MC in recto-sigmoid region, 2nd mC beyond sigmoid. Less commonly pancolitis or backwash ileitis. cd: Lesions are transmural or full thickness and bowel wall can become thickened, fibrotic, or stricured (high r/o SBO). Deep ulcers and granulomas. Cobblestoning from submucosal edema. Can be found anywhere in GI tract. mC in terminal ileum. Mostly in SB or SB+colon. Can be just colitis or oral or gastroduodenal. Rectum often spared.


what tests are the best for UC and cd?

sigmoidoscopy and colonoscopy, respectively +/- CT, MRI


what extra intestinal manifestations are specific to CD? uc?

mouth ulcerations, cholelithiasis, nephrolithiasis (imp. Absorp. Of oxalate); UC: Higher rate of colorectal cx, Primary sclerosing cholangitis


what questions should you ask if someone has elevated LFTs?

assess etoh intake, recent med changes, abx in past 3 months, OTC or herbal meds, hx of IV or nasal drug use (hepB orC), sig wt gain (fatty liver), blood transfusions, fm hx of liver dz, dark urine, noticed yellowing of eyes or skin, abdominal pain, fever, malaise, bowel changes, change in appetite, hx of other AI disease (crohn's, UC), tattoos, travel


what's in the ddx for elevated LFTs?

HepA-E, fatty infiltration of liver (NAFLD, NASH), AI hepatitis, hemochromatosis, celiac sprue, idiopathic, ischemia, wilsons dz, other viral dz (CMV,EBV?), PSC, PBC, thyroid dysfcn, cancer (primary or mets), biliary eti (gallstones), alcohol, toxins, meds


how do you recognize someone in fulminant liver failure? what do you do?

prescence of acute liver failure within 8 wks of the onset of jaundice in a pt without previous liver dz, or a pt with any degree of encephalopathy, INR >1.5 and not on warfarin, no cirrhosis, any degree of encephalopathy, increased INR (>1.5), very high AST/ALT (except wilsons--only mildly elevated) and elevated total bilirubin, elevated INR. ab (not very sensitive or specific) , urea breath, stool antigen, endoscopic bx is gold std, culture is most specific, can check for urease activity (CLOtest)


if someone has elevated LFTs, what labs should you get?

Labs: Hep A total antibody (IgG or total b/c IgM will be gone in 3-6 months), Hep B core (shows if previous or ongoing infection), Hep B surface antigen (shows if in active dz), surface antibody (shows if in recovery or immunity), Hep C antibody, antinuclear antibody and smooth muscle antibody (AI), antimitochondrial antibody, iron, TIBC, ferritin, INR, CBC with platelets, IgA (AI), IgG, IgM, tissue transglutaminase IgA, lipid panel, consider fasting insulin, TSh; Images: US, doppler if concerend for portal vein thrombus, CT if concern for pancreatic process, mRI if concern for liver masses, fibroscan if concern for fibrosis. if imaging/labs not helpful do a bx to confirm if AI, wilsons, PBC, hemochromatosis or to assess if tx is effective


what are the alarm signs with jaundice?

fever (cholangitis, gallstone, acute hepatitis, sepsis vs. hematoma), RUQ pain (cholangitis, gallstone, acute hepatitis, budd-chari syndrome, right sided heart failure vs. varicella zoster, RLL pneumonia, right sided pleural effusion, peptic ulcer, atypical renal colic, musculoskeletal pain) conufsion (cholangitis, hepatic encephalopaty, sepsis, intracranial bleed from coagulopathy, hypoglycemia, seizure vs. delirium) mucosal or cutaneous bleeding (thrombocytopenia from fulminanet hepatic failure or hyperspelnism, disseminated intravascular coagulation, falciparum malaria vs. minor trauma to site), back pain (acute severe hemolysis vs. M/S pain), pregnancy (hyperemesis gravidarum, acute fatty liver of pregnancy, eclampsia, HELLP syndrome, intrahepatic cholestasis of pregnancy) dark urine (hemoglobinuria from acute hemolysis, bilirubinura, gross hematuria from coagulopathy vs dehydration, meds; rifampin causes orange urine, beets cause red urine, myoglobinuria from rhabdomyolysis) involuntary weight loss (pancreatic or hepatobiliary cancer)


what do each of the following things mean if jaundice is also present?previous biliary surgery, new meds/supps, etoh, IV drugs, 40, exposures to people with hepatitis or sex with them, blood transfusions, fm hx , jaundiced with prior illnesses , diabetic , sickle cell, hx of UC , hx of heart failure ), blood clots, abrupt onset ), onset of weeks to months ,recurrent and self limited episodes , epigastric pain , N/V , prodrome of malaise, fatigue and anorexia , clay colored stools , silver stool , hematuria or flank pain , increased abdominal girth ), pruritis bruisability , missed menses, arthralgias

previous biliary surgery, new meds/supps, etoh, IV drugs, 40 (PBC, hemochromatosis, cx of pancreas or bile ducts), exposures to people with hepatitis or sex with them, blood transfusions (hemolysis, hep B/C in past ones), fm hx (hemochromatosis, wilsons, other fm hx stuff), jaundiced with prior illnesses (gilbert syndrome), diabetic (NAFLD or diabetes could be a manifestation of hemochromatosis), sickle cell, hx of UC (PSC), hx of heart failure (decompensated HF or constrictive pericarditis), blood clots, abrupt onset (stones, cholangitis, acute hepatitis, hemolysis, sepsis), onset of weeks to months (pancreatic and hepatobiliary cxs, chronic cirrhosis, infiltrative liver dz, HF)recurrent and self limited episodes (biliary colic), epigastric pain (pancreatitis, panc cx), N/V (choledocholithiasis, cholangitis, acute hepatitis, sepsis), prodrome of malaise, fatigue and anorexia (viral hepatitis, pancreatic or hepatobiliary cx), clay colored stools (biliary duct obstruction), silver stool (cx at head of pancreas causing melena without bile), hematuria or flank pain (renal cell carcinoma with hepatic dysfcn), increased abdominal girth (ascites from chronic liver dz or abdominal mass from cx), pruritis (cholestatic process like PBC, meds, cholestasis) bruisability (coagulopathy), missed menses(pregnancy), arthralgias (prodrome of viral hepatitis or hemochromatosis)