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GI Combo 2

Question	Answer
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
tumor suppresor genes	down-regulate normal growth stimulatory pathways
proto-oncogenes	part of signaling pathway that promote normal cell growth and proliferation
DNA repair genes	maintain integrity of genome by repairing errors in nucleotides
risk factors for colorectal cancer	#1 AGE personal/family hx familial syndromes like polyposis race, acromegaly, renal transplant
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
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!
Lynch Syndrome	1. auto dominant 2. 80% risk colon ca 3. dx thru genetic testing 4. colonoscopy q1-2 yr @ age 20
risk factors for colon cancer	sedentary, smoke, fatty, T2DM, androgen deprivation, EtOH
what are protective factors to reduce risk?	ASA, NSAIDS, folate
screening modalities	1. colonoscopy (diagnostic+therapeutic) 2. guiac 3. flex sigmoidoscopy 4. double contrast barium enema 5. CT colonography
tubular polyps	most common and least aggressive
pedunculated polyps	more common and less aggressive than sessile
hypersplastic polyps	usually benign
worst polyps to have?	villous (then tubular villous)
clinical presentation of CRC?	asx most common sx: ab pain, change bowels, hematochezia alarm sx: BRBPR, abd mass
what type of lesions are more common with iron-deficiency anemia?	right sided
obstructions cause lesions on which side?	left
what is the primary sx of rectal lesions?	hematochezia
what is the #1 prognostic factor for CRC?	stage at diagnosis
first line tx for CRC?	excision
TNM staging in CRC: T1	invades submucosa
TNM staging in CRC: T2	invades muscularis propria
TNM staging in CRC: T3	invades pericolorectal tissues
TNM staging in CRC: T4a	reaches surface of visceral peritoneum
TNM staging in CRC: T4b	directly adheres to other organs
TNM staging in CRC: N1	1-3 regional nodes
TNM staging in CRC: N2	4+ regional nodes
which type of CRC is the only type where radiation is a tx?	rectal because it is stationary
what do esophageal cells secrete?	bicarb to alkalinize contents
how does respiration affect the esophagus?	diaphragm pinches the esophagus closed during inspiration
what is a first choice diagnostic if you suspect motility disorder or mechanical obstruction?	barium swallow
what is a first choice diagnostic if you suspect aspiration?	modified swallow @ bedside
when is EGD best?	best when tissue sample is needed or if visual of anatomy is necessary
manometry	evaluates esophageal motility, gives pressures at various points, local anasthetic no sedation
ambulatory intraesophageal pH monitoring	most sensitive to detect GERD to monitor timing, freq, duration of each episode
esophageal impedance	NG catheter based detects changes in resistance to electric current use for any type of reflux
what is the primary problem with GERD?	dysfunctional lower esophageal sphincter where gastric juices or inadequate clearing mechanisms may damage tissue
what factors contribute to GERD?	(increased intraabdominal pressure) hiatal hernia obesity pregnancy (relaxed smooth muscle) ETOH, meds, foods, pregnancy
how do you diagnose GERD?	complete removal of sx from treatment
standard GERD therapy	lifestyle mod, antacids, H2RAs, PPI
what are some drawbacks of PPIs?	dont address LES dysfunction only 80% efficacious less responsive for atypical patients interact with protease inhibitors and plavix
what is an alternative med for functional heartburn?	SSRI
what must a pt exhibit to be a surgical candidate?	normal esophageal function failed medical therapy etc..
4 common causes of esophageal strictures	GERD trauma (physical or chemical) radiation malignancy
tx for esophageal stricture	dilitation with biopsy chronic PPI steroid injections
barretts therapy	PPI anti-reflux surgery endoscopy fro high grade disease
types of esophageal cancer	barretts esophageal adenocarcinoma squamous cell carcinoma of the esophagus
symptoms of esophageal cancer?	dysphagia weight loss dysphonia
achalasia presentation	dysphagia to liquids and solids (better with valsava) chest pain vomit/aspiration absence of GERD or bleching modest weight loss
what is achalasia?	loss of intramural neurons lack of normal peristalsis failure of LES to relax
primary causes? secondary causes of achalasia?	primary is idiopathic secondary due to cancer, chagas, viral, neurodegenerative disorders
achalasia management	sublingual NG CCB botox balloon dilitation esophagetomy goal is to decrease the pressure to open the LES sphincter
what are some motility disorders?	achalasia diffuse esophageal spasm scleroderma
diffuse esophageal spasm	patchy neural degradation non-peristalti contractions dysphagia to solids and liquids
scleroderma of the esophagus	atrophy and sclerosis of the esophageal wall "stovepipe esophagus" combined with GERD
clinical presentation of infectious esophagitis	acute onset, odynophagia, dysphagia, chest pain, systemic sx (plus mroe if host is immunocompromised)
differentials for infectious esophagitis	candida CMV HSV
treatment for infectious esophagitis	antimicrobials steroids hydration
which type of esophagitis is common in kids and teens?	eosinophilic
what are the different types of inflammatory esophagitis?	infectious radiation eosiniophilic corrosive pill-induced
what factors contribute to the formation of gallstones?	hypomotility and high cholesterol decreased bile salts or decreased phospholipids high hormone levels
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)
risk factors for gallstones	age, gender, obesity, severe weight loss, pregnancy(due to high estrogen), TPN, drugs (statins, ceftriaxone), DM, Crohns, spinal cord injuries
what is the best diagnostic tool for stones in the gallbladder?	sonography; 97% sensitive
best diagnostic tool for stones outside gallbladder, specifically in CBD?	endoscopic ultrasound
what are some findings on an ultrasound that may indicate acute cholecysitis?	GB wall edema, pericholecystic fluid, stone seen in the cystic duct
which test is only used to confirm that the cystic duct is plugged in cases of acute cholecystitis?	HIDA scan
what is the gold standard for stones in the common duct as it diagnosis and treats choledocholithiasis?	endoscopic retrograde cholangiopancreatography ERCP
what is a complication of stones?	gallstone ileus where it blocks the iliocecal junction
cholelithiasis	stones in gallbladder
chronic cholecystitis aka "biliary colic"	caused by stones intermittently blocking cystic duct w/NO inflammation of gallbladder mucosa
acute cholecystitis	chronic blocking of cystic duct --not an infection --yes inflammation and dilation of gallbladder --RUQ tenderness and fever
choledocholithiasis	bad stone blocking CBD with sx of pain, jaundice, +Murphys sign and acholic stools
cholangitis	inflammation + obstruction life threatening pain, jaundice, +Murphys sign and acholic stools+fever+chills
biliary pancreatitis	stone blocks ileum or common bile duct
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
meltzer-lyon test	aspiration of bile to assess for cholesterol and calcium bilirubinate crystals
mgmt of chronic cholecystitis?	cholecystectomy
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
what do you suspect if you see leukocytosis w/left shift, elevated LFTs?	acute cholecystitis
RUQ and epigastric pain with pruritis and jaundice	choledocholithiasis
occurrance of stones in CBD w/life threatening symptoms like cholangitis or acute pancreatitis	choledocholithiasis
what LFT values rise with obstruction?	alk phos+GGT+bili
standard treatment for choledocholithiasis	ERCP for diagnosis and removal, often with CBD exploration
impacted stone in CBD, bile stasis, bacterial superinfection of stagnant bile	cholangitis
presents as Charcots Triad: RUQ pain+fever+jaundice or Reynolds Pentad: RUQ=fever+jaundice+AMS+hypOtension	cholangitis
what dx has blood cultures + for enteric bacteria? plus elevated WBC w/left shift?	cholangitis
tx for cholangitis	IV fluids+electrolytes blood cultures antibiotics stone extraction and cholecystectomy
murphy's sign	pain and arrest of inspiration upon deep palpation of right subcostal region
sx of severe hepatitis	most are asymptomatic prodromal syndrome dark urine acholic stools RUQ pain jaundice hepatomegaly splenomegaly w/cervical lymphadenopathy elevated AST/ALT
which hepatitis do you suspect? -acute onset with history of shellfish ingestion, foreign travel, or daycare setting	A
which hepatitis do you suspect? -acute onset with history of sex promiscuity, MSMm IVDA, recent tattoo	acute B
which hepatitis do you suspect? -asymptomatic with mild elevation of transamineases, with multiple risk factors present	chronic B or chronic C
which hepatitis do you suspect? -initial HBV symptoms are worse than expected, or condition suddenly worsens	D co-infection with B
which hepatitis do you suspect? -same presentation as Hep A, but HAV markers are negative	E
common lab features for all heps	transient neutropenia and lymphopenia lymphocytosis electrolyte imbalances prolonged INR normalish alk-phos
management of acute hep	treat each symptom ultrasound to r/o masses, obstruction
when do you admit?	admit with sx of acute liver failure: 1. coagulopathy INR>1.5 2. encephalopathy 3. bilirubin>15
which heps can you be a carrier for?	NOT A
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
where is HAV concentrated?	feces, saliva NOT urine
usually, what is the resolution of HAV like?	most resolve without incidence, no relapsing once you've passed the 6 month mark
cholestatic hepatitis	protracted jaundiced illness with pruritis
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
where is HBV present in the body?	serum and body fluids DNA virus!!
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!
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
how would an acute HBV present?	new onset flu-like sx, RUQ pain, nausea and vomiting -elevated transaminases (in 1000s) -hyperbilirubinemia
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
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
HBV treatment options	interferons, nucleoside analogs (entecavir and tenofovir) for life! lifelong to prevent viremia-->prevent cirrhosis and liver cancer
what are 3 complications of HBV?	1. extrahepatic stuffs: polyarteritis nodosa, glomerulonephritis 2. cirrhosis 3. hepatocellular carcinoma 4. superinfection with HDV
what is the only oncogenic hepatitis?	HBV
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
what does HCV progess to in 10-40 years?	cirrhosis
symptoms of HCV?	almost always asymptomatic, rarely becomes fulminant
who do you NOT treat fro HCV?	continued IVDA, EtOH abusers, psych issues, decompensated liver disease, autoimmune disorder like psoriasis
is Hep C curable?	yes, sometimes pts must maintain sustained virological response SVR
what are SE of HCV anti-viral treatment?	neutropenia, thrombocytopenia, hemolytic anemia
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
what are some clinical signs of chronic HBV/HCV?	jaundice spider angiomas palmar erythema caput medusa hepatosplenomegaly ascites neuro changes gynecomastia
which OTC is preferred in cirrhotic patients for pain mgmt?	acetaminophen over NSAIDS due to bleeding
what vaccines are recommended for HCV infected?	HAV/HBV vaccines influenze pneumococcal
what are some complications of DILI?	cholestasis, fatty liver, granulomatous hepatotoxicity
what type of injury is associated with: steroids, antibiotics	cholestatic injurt
what type of injury is associated with: antivirals, antiarrhythmics, oncotherapy?	fatty liver
what type of injury is associated with: tylenol OD, diuretics, NSAIDS	directly hepatotoxic
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
what are the CAGE questions, ans what is the sensitivity?	cut down annoyed guilty eye opener --93% sensitive, 76% specific
define hepatitis	inflammation of the liver due to any cause
define cirrhosis	architectural distortion of the liver parenchyma due to fibrosis due to any cause
what are 3 types of liver injury obtained by alcohol?	fatty liver=alcohol steohepatitis alcohol hepatitis alcoholic cirrhosis aka Laennecs cirrhosis
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)
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
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
what happens to liver if you suddenly stop drinking?	they may be restored as they regenerate in response to apoptosis
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
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
what is the most predictive test for prognosis with alcohol liver dz?	nutritional status, failure to restore nutrition can lead to death
what are 2 drugs that may help in acute decompensation in ALD?	1. steroids for 4 weeks 2. pentoxifylline reduces hepatorenal syndrome
what nutritional products are needed in ALD to restore?	1. amino acids 2. electrolytes: Mg, K, PO4 3. thiamine (prevents wernickes)
what is the #1 nutritional deficiency seen in alcoholics?	glutathione depletion
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
describe the clinical presentation of late cirrhosis	gynecomastia, hypogonadism, caput medusa, jaundice, ascites, variceal hemorrhage, encephalopathy, atrophy --high bilirubin, low albumin, coagulopathy, low platelets
how do you determine cirrhosis severity?	child-turcotte-pugh score -enceph -ascites -PT/INR -albumin -total bili assign one point for each
what are some poor prognostic predictors for cirrhosis	1. MAP<82 2. GFR<50 3. poor nutritional status 4. hepatomegaly 5. albumin<2.8
define portal hypertension and causes	portal pressure>12mmHg --caused by cirrhosis, but can be seen in ALD, idiopathic, RHF, schistosomiasis
pharm mgmt for PHTN	vasoconstrictors: decreases splanchnic flow and decreases portal venous flow vasodilators: alter intrahepatic resistance
pharm EVH prevention	NSBB reduce risk of bleeding by 40% 1st line
EVH surgical intervention	1. esophageal ligation/banding 2. esophageal sclerotherapy 3. portosystemic shunt 4. transjugular intrahepatic portosystemic shunt TIPS
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
acute EVH surgical intervention	octreotide started in ER --balloon tamponade, TIPS
what are possible causes of ascites?	cirrhosis misc. PHTN related cardiac peritoneal carcinomas
what is the "underfill theory" for ascites?	increased plasma oncotic pressure and decreased portal venous pressure--sodium retention is a 2ndary compensatory mechanism
what is the "peripheral arterial vasodilation theory"?	increase in vascular capacity and decrease in effective plasma volume results in 2ndary sodium retention
fever+ascites+abdominal pain make you think what?	spontaneous bacterial peritonitis SBP
what are the most important lab results after paracentesis?	fluid cell count >250 indicates infection SAAG>1.1 indicates PHTN
diuretic of choice for ascites?	spironolactone +/- furosemide
tx for SBP?	1. 3rd generation cephalosporin 2. albumin for volume expansion and renal perfusion
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
describe hepatorenal syndrome Type 1	severe/rapid progression severe liver failure poorest prognosis survival=2 weeks
describe hepatorenal syndrome type 2	mod/stable renal failure preserved liver function survival=6 months
tx for HRS type 1?	1. transplant 2. terlipressin (may reverse HRS) 3. catecholamines 4. TIPS
3 ways to prevent HRS	1. paracentesis+albumin 2. treating SBP w/ceftriaxone 3. pentoxifylline in ALD
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
what are some possible mechanisms that cause hepatic encephalopathy	1. ammonia toxicity 2. synergistic neurotoxins 3. alteration of serotonin levels 4. excess GABA
what would labs show for enceph?	elevated ammonia high GABA pancytopenia, thrombocytopenia, leukopenia elevated CSF glutamine
key ideas regarding ammonia levels and enceph	level does NOT correlate to severity of enceph -don't r/o enceph if ammonia is normal
pharm tx for high ammonia	1. bowel cleansing 2. avoid protein 3. lactulose 4. rifaximin
possible anatomical problems with pancreas	1. pancreatic duct: stricture, stones, divisum 2. spincter of oddi dysfunction
describe main functions of pancreas	80% exocrine (acinar cells secrete enzymes, fluid and electrolytes) 20% endocrine (islet of langerhans secrete hormones)
what enzymes are secreted exocrine?	amylase, lipase, protease, trypsinogen
what enzymes are secreted endocrine?	alpha: glucagon beta: insulin delta: somatostatin
what happens if the exocrine dysfunctions?	fat malabsorption leads to: 1. fatty stools 2. malabsorption of vit. A, D, E, K
what happens if endocrine malfunctions?	diabetes
what is creatinine a marker for?	dehydration
define acute pancreatitis	enzyme damage to pancreas resulting in discrete episodes of abd pain+elevation serum amylase+elevated lipase
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)
what are the stats regarding alcohol and pancreatitis?	60-90% have h/o alcohol use but only 5% of alcoholics get pancreatitis
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
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
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

Created by: duanea00

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