113 terms


type of cell structure in the esophagus
Upper 2/3 - squamaous striated
lower 1/3 - columnar smooth
folds in the stomach are called?
Review the types of cells in the stomach and what they do.
Chief - Pepsinogen
Parietal - H, Intrinsic factor
Gastrin (G-Cells)
Histamine (ECL cells)
Somatostatin (D-Cells)
What are some of the functions of the liver?
1) Gluconeogenesis (non-carbohydrate nutrient into glucose)
2) Glyogenogenesis
3) Filters Stuff
4) Syn. albumin and globulins
Ampulla of Vater
Formed by the union of the common bile duct and the pancreatic duct
Two main control of pancrease by which hormones?
1) Secretin (releases NaHCO3 in response to low pH)
2) CCK - Releases Bile
What are the two types of abd. pain and describe them
1) Visceral
Poorly localized/diffuse (C-Fibers - slow conduction) (organ or visceral peritoneum)

2) Somatic (Parietal)
Localized, intense (parietal periteneum and abd. walll)
Name a few things that will cause Osmotic diarrhea
1) MgSO4
2) PO4
3) Lactose intolerance
4) Sugar subsitutes (ex. sorbitol)
3 main types of diarrhea
1) Osmotic
2) Secretory
3) Motility (increased motility, ex. surgical resection)
Anti-diarrheal plus atropine

Atropine for OD as lomotil is an opiods so if OD then tachycardia to prevent OD
Anatomical difference b/w upper and lower GI bleed
Ligament of Treitz - supsensory ligament from duodenum to diaphragm, sepearates duodenum from ileum
Stimulates parietal cells to secrete more H and intrinsic factors
inhibits gastrin production (when therefore inhibits parietal cells from stimulating H, and intrinsic factors)
Puts out HCO3
When fat/Proteins enter into the duodenum CCK is produced which releases pancreatic crap like typrsinogen and others which is then acted upon by duodenal enterokinase to stimulate trypsinogen to become trypsin and tryspin activates the other pancreatic crap and is all now in its active form to break down fats/proteins.
Where is stuff absorbed in the GI tract
Stomach: Water, Ethanol and ASA
Small Intestine:
Duodenum = Iron, Calcium, Fats, Sugars, Water, Proteins, Vitamins, Magnesium, Sodium
Jejunum = Sugars, Folate and Proteins
Ileum = Bile Salts, Vitamin B12,Vitamin C and Chloride
Colon: Water, Electrolytes and Vitamins
Whats the difference b/w diverticulosis and diverticulitis?
Diverticulosis - outpocketing of diverticula

Diverticulitis - w/ inflammation

-People w/ diverticulitis gen. have pain gen. around the sigmoid colon. Risks can included perforation, and infections
-Colonoscopy is contraindicated during the acute phase
-perforation - get peritoneal signs
-Tx includes clear liquid diet, augmentin or cipro or bactrim w/ flagyl
An EGD stands for?
Endoscopic retrograde cholangiopancreatography - Combined endoscopy and fluroscopy to provide therapeutic and diagnositc interventions for gallbladder, and ductal problems

("like a cath lab for the GI tract")
Endoscopic ultrasound - Diagnostic but can see the tail of the pancrease
S/S - Heartburn, can have a bitter taste in the back of throat

Dx - Endoscopy (rule out lesions)

Tx - Lifestyle (obesity), Antacids like Milk of Magnesia (antacid and also a laxative so will get diarrhea), H2 blockers (ex. famotadine, ranitidine)

Other - Citrus, Peperment, Alcohol - increases acid secretion
H2 blocker for GERD

Also Ranitidine for GERD (both have t*dine at the end)
H2 blocker for GERD

Also Famotadine for GERD (both have t*dine at the end)
What it is - incomplete ability to relax the lower esophageal sphincter

S/S - dysphagia, regurg, C/P

X-Ray - Bird Beak Esophageous (fills up to around 1/3 and then after that it opens, then keeps a little bit of fluid in the esophagous)

Medical - CCB, Nitrates, Botox - Gen don't last long, maybe 6 months
Pneumatic ballon distention - causes small tears, has pain means its workin', single dilation effective in 2/3rds of pts for 2 yrs, 2nd/3rd dilation works in up to 90% for 2 yrs
Surgical - Hellers Myotomy (cut through circular muscle, 80% develop reflux but use a PPI, gen. reserved this procedure for pts who fail medical and 2-3 tries of the pneumatic ballon distention)
Scleroderma (esophageal manifestations)
Develop CREST symptoms - Calcinosis, Raynaud's phenomenon, Esophageal dysfunction, Sclerodactyly, and Telangiectasias.

Esophageal damage causes dysphagia and GERD

Tx - PPI, Gastroprokinetics like erythromycin and azithromycin
Schatzki ring (esophageal ring)
Definition -Narrowing of lower part of esophagus leading to dysphagia

Etiology - caused by a ring of mucosal tissue, ALWAYS ASSOCIATED W/ A HIATAL HERNIA

S/S - intermitent dysphagia especially w/ solid food, feeling that food "sticks" w/ swallowing

Dx - EGD or barium swallow

Tx - TX THE HIATAL HERNIA, gen. no tx but esophageal dilation may be neccesary
Esophageal web
Definition - thin web in esophageous

S/S - dysphagia, possible pain
Plummer-Vison Syndrome
Definition - also characterized by esophageal webs

S/S - Triad of Dysphagia, Fe-Deficiency anemia, esophagitis

Tx - tx. Fe-Def anemia

Other - assoc. webs, Fe-def anemia
Esophageal stricture
Definition - narrowing of the esophageous

Etiology - often associated w/ GERD as the cause

S/S - Dysphagia

Tx - stretch it up
Esophageal neoplasms (2 types)
Adenocarcinoma -
Etiology - GERD, now #1 due to increase in obesity, associated w/ barrets (lower 1/3)

Squamous Cell Carcinoma-
Etiology - ETOH, Smoking (upper 2/3)

Dx - Biopsy

Tx - small/localized - surgery
Large - pallative
Definition - Slow GI motility

Etiology - Diabetes, hypothyroidism, idiopathic

S/S - early saiety, abd pain, N/V

Tx - Dietary modifications (low fat/soft mechanical), prokinetic agents like erythromycin

Other - picket fencing (extreme highs and lows of BGL) may be due to gastroparesis
2 barriers to to stomach acid in...well...the stomach
1) epithelial cells secreting HCO3
2) Mucosal cells secreting Mucous
Hiatal hernia
Definition - protrusion of the stomach into the thorax

Types of hiatal hernias
95% - Sliding - hernia goes above esophageal hiatus and ballons upward w/ the esophagus
5% - paraesophageal - hernia goes above esophageal hiatus and the stomach lies in parrellel w/ the esophagus

S/S - Great mimic - C/P, SOB, Palpitations (stimulation of vagus) all caused from GERD => Majority are symptomless

Tx - Paraesophageal - likely to cause stricture and prob. requires surgery (Do not used meds that lower the LES pressure!!!!)
Peptic Ulcers
Primary Causes - H. Pylori, NSAID, Smoking Zollinger-Ellison syndrome (hypersecretory state)

S/S - Asymptomatic Fe-Deficiency anemia to abd pain (may be epigastric and a dull ache), N/V (most commonly in duodenum)

Dx - endoscopy - see it, biopsy it, therapy

Tx -
Triple combination - PPI, amoxicillin, clarithromycin
H2 receptor blockers (t*dines)
PPI - azoles

Complications -
Zollinger-Ellison Syndrome
Hypersecretory state (increased H in the stomach)
Gastrin secreting tumors, gen. found in the pancrease and duodenum
Elevated serum gastrin
ulcer in an unusual area ex. jejeunum

Gen. found - Gastrinoma triangle (area of the duodenum)

Dx - fasting gastrin test, confirmed by positive secretin test
NAIDS are more likely to cause what kind of ulcer
Gastric ulcer
Whats the deal with eating food and its relation to ulcer differentiation
Peptic ulcers - pain goes away with eating

Gastric ulcers - pain gets worse w/ eating
Definition - Nonspecific inflammation of the stomach

Causes - H. Pylori, NSAID's, B12 deficiency can be associated w/ it

Types -
Acute - Alcohol, NSAID
Chronic - autoimmune, multiple acute attacks

Type A- atrophic gastritis
Type B- nonatrophic gastritis
Purpose - The irreversible end result of a variety of inflammatory, toxic, metabolic and congestive insults to the liver

Causes - Alcohol, Hep B/C

Dx - Liver biopsy is gold standard

S/S -
Musle wasting, palmar erythema, spider angioma, caput medusae

Sequile of events
Hepatocellular dysfunction
Jaundice, coagulopathy, hypoalbuminemia

Portal HTN
ascites, hepatic encdephelopathy

Hepatocellular carcinoma

Other - ultimatley lead to hepatocellular carcinoma
What distinquishes compensated from uncompensated cirrhosis?
constitutional symptoms start to appear
variceal hemmorhage
esophageal varices can be tx w/?
Whats the albumin level in a pt w/ cirrhosis
Some treatment for ascites
salt restriction (2g/day)
weight loss
Hepatocellular carcinoma
Complication of cirrhosis

Blacks more common
name some of the functions of the liver.
1) metabolism of carbohydrates and fats
2) Production of cougulation factors
3) Produce fat soly vitamins (A, D, E, K)
4) Detox
AST - Aspartate aminotransferase
Causes of Elevation - Liver, Muscle, Kidney, Brain, Pancrease, RBC

ALT - Alanine aminotransferase =More Specific for the (L)iver
Causes of Elevation - Liver

Relationships between the two
1) In relation to AST, ALT is generally higher in liver disease except in alcoholic liver disease when the AST is higher.
2) Alcoholic liver disease => AST/ALT ration higher than 3.
3) Acute Hepatocellular Necrosis (viral or toxic causes ie. tylenol OD) => High levels of ALT (15 times higher)
4) Nonalcoholic fatty liver disease (obesity, insulin resistance, diabetes) => Asymptomatic elevations of AST & ALT
Causes - Liver, Bone, Intestines, and Placenta
Conjugated (direct) - Impaired bile flow (since its at the liver that it becomes conjugated)

Unconjugated (indirect) - Blood breakdown overwhelms liver (as it becomes conjugated in the liver)
Increases in liver disease
Responsiveness to Vit K in liver disease
Liver disease - not responsive as decreased production of cougulation factors

Bile duct obstruction - still responsive to Vit K as still making cougulation factors
What is Fulminant Hepatic failure
1) Encephalopathy w/in 8 weeks of symptoms
2) Encephalopathy w/in 2 weeks of jaundice
3) Cougulopathy
Most common type of hepatitis in america
Hep A
What suggests a viral causes of acute hepatitis
Causes of acute hepatitis
Viral Hep A, B, D
Drugs - tylenol, EtOH
Vascular - hypotension
Causes of chronic hepatitis
Viral Hep B, C
Drugs - amiodarone
Hepatitis can be divided into A-E. There are also ones where the source of the virus is from blood therefore its a chronic infection and thoses that are from the feces therefore its an acute infection. Which forms of hepatitis correlate to these findings?
A/E - Feces, Acute
B/C/D - Blood, Chronic
Outcome of the hepatitis A/B?
A- Okay
B - 30% die from cirrhois or hepatocellular carcinoma
Definition - Gallstones

Types -
Cholesterol (75%)
Calcium (Pigmented aka black or brown, 25%)

Etiology -
Cholesterol supersaturation in bile
Gallbladder hypomotility (TPN, no PO foods)

Risk Factors -
Rapid weight loss

S/S - Most asymptomatic
1/3 develop symptoms of biliary colic or chronic choleysitis

Dx - U/S

Tx - surgery
Ursodiol (increase nucleation time, decrease int. absorption)
Biliary colic
Aka Biliary pain

After a meal start hurting in RUQ, may radiate to R. scapula
resolves slowly over 30 min - 3 hrs
Tx for gallstones, decrease int. absorption, increase nucleation time
Definition - Inflammation of the gallbladder

Causes - Cystic duct occlusion by a gallstone

S/S - RUQ or epigastric pain, N/V

Dx - U/S
Murphy's sign
HIDA scan - most sensitive scan

Tx - Fluids, Antibiotics, semiurgent surgical (less than 72 hrs)

Unexplained fever think of Acalculous cholecystitis
Definition - Gallstone is in the common bile duct

S/S - 50% asymptomatic,
Biliary colic, Jaundice

Dx - U/S, ERCP (5% causing pancreatitis)

Tx - ERCP w/ stone extraction
Definitis - Infection proximal to the common bile duct obstruction

S/S -
Charcots Triad
RUQ Pain

Reynolds Pentad-
Charcots Triad plus AMS and Shock

U/S, ERCP (Gold Standard), Blood Cultures for Critters

Tx -
Broad spectrum Antibiotics
Amp/Gent, Extended spectrum PCN, 3rd Gen. Cephalosporins
Biliary Drainage (emergent in certain conditions)

Other - 5-10% mortality
What is Charcots Triad and what does it indicate
Cholangitis - infection proximal to the common bile duct obstruction

RUQ pain
Reynolds Pentad
Cholangitis - infection proximal to the common bile duct obstruction

Charcots Triad of RUQ pain, Jaundice, Fever plus...
Painless Jaundice can be indicitive of? (Not on objectives)
Cholangiocarcinoma (Cancer of the gallbladder)
Amp/Gent, Extended spectrum PCN, 3rd Gen. Cephalosporins can be used for which disease discussed in class? (Related to gallbladder problems)
3 types of diarrhea
1) Secretory
Mechanism - Increased Sec/Dec Abs of Na & Cl
Ex - Cholera, Fatty-acid induced
Characteristics - large volumes and watery

2) Osmotic
Mechanism- nonabsorbable crap in gut lumen
Ex - Lactose intolerance, Mg laxatives, Gen. malabsorption
Characteristics - watery, improves fasting, may have fat globules

3) Motility
Mechanism - Increased motility
Ex - IBS, Scleroderma, Diabetes, Hyperthyroid
Characteristics - variable
Pertinent questions and why are you asking them for a pt w/ diarrhea
Acute - Microbial pathogens, resolve independently of interventions, Starbucks (increased cAMP, Increased fluid secretion)?
Chronic (more than 4 weeks)
unlikely to be infectious

Inflammation, neoplasm, ischemia

Large - small bowel or proximal colonic disease
Small but frequent - L. sided colonic or rectal disease

Ex Mg, Lactose


Family hx?
Celiac disease, IBS
Causes of Chronic diarrhea?
Greater than 4 weeks

Persistant parasitic infections ex. giardiasis
Weight loss
Nutritional deficiencies - Alcohol, pancreatitis
Bloody - IBS, Ulcerative colitis
Lactose intolerance
Laxative abuse
Colon Cancer (always be considered in older pts)
Important critters in Acute Diarrhea
1) E. Coli (Travelers diarrhea by toxins => can be bloody)
2) Vibrio Cholerae (seafood)
3) C. Diff (after antimicrobial therapy)
4) Rotavirus (outbreaks among children)
5) Norovirus (winter outbreaks, closed spaces, ships, nursing homes, schools, etc => 1/3 of all viral diarrheas)
6) Giardia lambia (Day care centers)
7) B. cereus (food)
Which antibiotics should one give for Giardia lambia and C. Diff when they cause diarrhea? Whats the deal w/ these bugs and the risk factors for contracting them?
Giardia lambia - Tinidazole, Nitazoxanide, Metronidazole
(Day care centers)

C. Diff - D/C offending med
1) Metronidazole (500mg)
2) Vancomycin (500mg)
(Antimicrobial therapy)
FYI C.diff and diarrhea (not on objectives)
C. diff can colonized the large bowel in the presense of antibiotics which limit the normal bacteria. Produce cytotoxins that cause mucosal damage and produce a colitis
Food poisoning causing diarrhea can be caused by which two organisms mainly?
1) Staph aureus
2) B. cereus
Mild and moderate cases of diarrhea can be treated w/ what? These meds are not to be used w/ bloody diarrhea, fever, or systemic toxicity. (Not on objectives
1) Pepto-Bismol
2) Loperamide
Acute Pancreatitis
Definition - inflammation pancrease

Causes- (intra-acinar conversion of trypsinogen to trypsin)
Gallstones 45%
Alcohol 35%
Misc (Ex. Increased TG, and drugs) 10%
I don't know 10%

Types -
1) Obstructive - Gallstones
2) Non-Obstructive - ETOH, Trauma (hypovolemia), TG

S/S -
Worse when supine
Abd pain boring into back
Grey Turner (ecchymosis in flank) & Cullens sign (ecchymosis in periumbilical region) means hemorrhagic pancreatitis

Dx -
Lab Amylase, Lipase greater than 3 times normal

Severity - Ransons Criteria => 75% recover w/o therapy, 25% will develop complication, 5-10% overall will die, early deaths w/in 2 weeks associated w/ MOD's from inflammatory mediators and cytokines, later deaths from infections

Tx - (nothing proven to decrease chance of death)
1) Supportive
2) TPN if needed to rest pancrease
3) IV fluids
3) ERCP w/ removal of stones if gallstones obstructing

Other => Necrotizing pancreatis - death of pancrease, do not show up on CT
Ranson Criteria. What is it used for and what is it?
Assessing the severity of acute pancreatitis (mortality less than 1% w/ 2 or less, 10-20% w/ 3-5, 50% w/ 6 or more)

@ dx
1) age greater than 55
2) WBC higher than 16,000
3) BGL above 200
4) LDH 2 times normal
5) ALT 6 times normal

during initial 48 hrs
1) decrease in Hct by 10%
2) serum calcium under 8
3) BUN above 5
4) PO2 (arterial) less than 60
5) Base deficit greater than 4
Fluid sequestration greater than 600 cc's
Chronic Pancreatitis
Definition - Chronic inflammation of pancrease

Causes -
1) Obstructive
2) Non-Obstructive
Alcohol (most common 70%)

Abd Pain
Exocrine - weight loss, Malabsorption
Endocrine - diabetes (80-90% loss)
Biliary stricture - Jaundice

Dx - Secretin stimulation test - Gold standard
Serum trypsinogen (exocrine pancreatic dysfunction)

Tx -
1) Pain control
2) Ocreotide
3) Surgery
4) Mngt complications
5) Pancreatic enzymes

Long term impact
1) Pancreatic cancer
2) Diabetes (once 80-90% of pancrease dies)
Pancreatic cancer
Causes -
Adenocarcinoma (most common!!!)

Risk Factors-
Chronic pancreatitis
Family history

Dx -

Tx -
Maldigestion causes
1) Gastric Dysmotility (Gastric bypass, vagotomy)
2) Exocrine Pancreatic Insufficiency
3) Bile Salt Deficiency
4) Mucosal disease (loss of brush border => sucrase, lactase, maltase)
Malabsorption causes
1) decreased intestinal surface area (most common)
2) decreased circulation and lymphatic drainage
3) Mucosal infiltration with abnormal cells
4) Transport protein mutations
5) Impaired motility
Malabsorption S/S
1) Steatorrhea - Stool that floats
2) Weight loss
3) Diarrhea
4) Anemia (Fe-Def anemia, B12)
5) Vit K deficiency
Test for malabsorption
1) Fecal fat (first test, gold standard)
2) D-Xylose (done after the fecal fat is positive)
3) Breath test (bacterial overgrowth)
4) Small bowel biopsy
5) Schilling tests - Vit B12 malabsorption
How to differentiate malabsorption vs. maldigestion
D-Xylose is decreased in malabsorption and normal in maldigestion
Bacterial overgrowth in the small bowel dx and tx
Dx - Breath test (c-xylose) (H being breated out from fermentation of C6H12O6)

Tx -
Celiac Sprue
Definition - Damange to the mucosal of the gut due to gluten (people must be sensitive to this) (immunological condition)

S/S -
Abd. Pain
Malabsorption symptoms

Dx -
Intestinal biopsy (gold standard)
Tissue IgA Antibody
Tx - Gluten-Free diet
What are the two types of inflammatory bowel diseases? When are the peak incidences of these diseases?
Inflammatory disease of the bowel (believed to be caused by an overactive immune response to GI bugs)

1) Ulcerative Colitis (continous diffuse Mucosal inflammation in colon)
2) Crohns disease (transmural inflammation in a discontinous fashion anywhere in the GI tract)

2 phases of peak incidence => 15-30 and in 60's
Fats increase risk => more common in higher socioeconomic classes and western nations (america and canada)
Ulcerative Colitis
Definition - Inflammatory Bowel disease characterized by continous diffuse Mucosal inflammation in colon

S/S -
Bloody Diarrhea

Major Sites-
1) Pancolitis 47%
2) L. sided disease 25%
3) Proctitis 28%

Dx - Endoscopy

Tx - Mesalamine & Sulfasalazine
Surgery is an option (surgery not an option for Crohns)

Toxic Megacolon => gross dilation of colon w/ fever, abd pain, bloody diarrhea, tachycardia

Other -
Smoking is protective
Crohns Disease
Definition - Inflammatory bowel disease characterized by transmural inflammation in a discontinous fashion anywhere in the GI tract

Normal Diarrhea
Abd Pain Common

Major sites -
1) Ileocolitis - distal small intestine and proximal large bowel 45%
2) ileitis - terminal ileum 22%
3) Colitis 32%

Dx - Endoscopy

Tx -
Acute Flares - Steriods

Other -
Smoking makes it worse
Cobblestoning in the mucosal surface may occur
Differentiating features of ulcerative colitis vs crohns
Ulcerative Colitis -
Rectal involvement
Continous pattern of involvement
No Abd Pain
Blood Diarrhea
Smoking is protective
ulcerations on endocscope
pANCA marker

Crohns Disease -
Rectum spared
Non-continous pattern of involvement
Abd Pain Common
Normal Diarrhea
Smoking makes it worse
Cobblestoneing endoscopic finding
ASCA marker
Intestinal obstruction and abd mass may also be seen
Where is Inflammatory Bowel Disease common?
Western nations, high socioeconomic class
Extraintestinal Manifestation of inflammatory bowel disease? aka ulcerative colitis, crohns disease.
Immune-mediated showing the systematic inflammatory changes from IBD

1) Arthritis - most common
2) Ankylosing sponylitis
3) Hepatobiliary problems
4) Skin disorders ( Pyoderma ganrenosum - ulcer w/ necrotic base generally on the legs, erythema nodosum - raised tender nodules gen over ant. surface of tibia)
5) Ocular problems (Uveitis - Inflam lesion of ant chamber and produces blurred vision, photophobia, episcleritis - burning eyes and scleral injection)
Inflammatory bowel disease patients have what major comorbidity?
Colorectal cancer

Treatment for Inflammatory Bowel Disease
Mild - Antibiotics
Moderate - Steriods (Prednisone, 6 MP/AZA, Methotrexate)
Severe - Cyclosporine/Tacrolimus, Experimental

6-mercaptopurine, azathioprine => prednisone sparing drugs
Flagyl, Prednisone, Sulfa (Pregnancy risk Cat B)
Anti-TNF (TNF promotes inflammation) => Infliximab, Adalimumab, Certolizumab
Anti-inflammatory for Inflammatory bowel disease (TNF promotes inflammation)

Infliximab, Adalimumab, Certolizumab
Microscopic Colitis
Definition - Diarrhea gen. found in middle ages (40-50's), gen. females

Types -
Collagenous colitis - Mainly in females
Lymphocytic colitis

S/S -
Watery diarrhea
Abd Pain

Dx -
Labs gen. normal
Colonoscopy looks normal but histology evidence of inflammation

Symptom management
Which antibody markers can distinquish Ulcerative colitis vs. crohns disease?
pANCA - Ulcerative colitis

ASCA, Omp C - Crohns
H. Pylori can cause what?
Serology for Hepatitis
Name HBsAg AntiHBc IgM AntiHBs
1) Past infection + +
2) Vaccinated +
3) Acute Infection + + +
4) Chronic Infection + +

So IgM only in acute infection
HBsAg you are currently fighting the infection

AntiHBs only if been exposed to it before
AntiHBc you've actually had the disease in the past
What is the association between colon polyps and colon cancer?
Colon cancers are believed to arise from adenomatous polyps (colon epithelia)
What are the 2 types of colon polyps?
1) Hyperplastic (non-neoplastic)
2) Adenomatous (tubular, villous, tubulovillous)
a) High Malignancy potential
b) takes approx. 10 years to progress to cancer
c) Almost all colon cancers arise from adenomas
d) 1% of adenomatous polpys become malignant (but think if you have 100 adenomatous polyps in your colon!!!)
What are the risk factors for colon cancer?
1) age over 50
2) History of Colon rectal cancer (family or self) or adenomatous polyps
3) Inflammatory bowel disease (Crohns & Ulcerative Colitis)
4) Familial adenomatous polyposis (100's of adenomas in colon, nearly 100% risk of cancer if not treated by age of 40)
5) 3 first-degree relatives diagnosed w/ colon rectal cancer w/ one under the age of 50 => start colonoscopy at age 25 or 10 years prior to youngest relative's age of diagnosis [Hereditary non-polyposis colorectal cancer (HNPCC or Lynch syndrome)]
Colon cancer screening recommendations
1) Average Risk => Colonoscopy q 10 years starting at age 50

2) One or two first degree relatives diagnosed w/ colonrectal cancer at any age or adenoma w/ a diagnosis prior to age 60 => Colonoscopy q 5 years starting at age 40

3) Hereditary non-polyposis => start colonoscopy at age 25 or 10 years prior to youngest relative's age of diagnosis, genetic conseuling and testing, Flexible sigmoidoscopy yearly beginning at puberty

4) Personal hx of Colon rectal cancer => Colonoscopy w/in 1 year of resection, repeat @ 3 years, then q 5 years if normal still

5) personal history of colorectal adenomas => q 5 yrs

6) IBS => q 2 yrs after 8 yrs of a dx of pancolitis or after 15 yrs after dx of left sided disease

Hereditary non-polyposis is defined as 3 first-degree relatives diagnosed w/ colon rectal cancer w/ one under the age of 50
Treatment of Colon Cancer, Lets talk about it!
1) Early stages (stage I & II) => Surgery can be curative
2) Intermediate stages (stage III) => Surgery and Chemo
3) Late stage (IV) => Pallation, Hospice

Stage II and III => post-operative radiation and 5-Fluorouracil reduce the recurrance rate, and death rate.

Other Random Facts
1) 45% of pts present w/ advanced (stage III or IV) Colon Cancer
5-Flurouracil is used to treat what GI problem
Colon cancer

Stage II and III => post-operative radiation and 5-Fluorouracil reduce the recurrance rate, and death rate.
Hereditary non-polyposis colorectal cancer (HNPCC or Lynch syndrome)
Occurrence of CRC in at least three 1st degree relatives over at least 2 generations with at least 1 person diagnosed < age 50
CT Colonography
Screen for Colon cancer but can't do a biopsy. This can be done q 5 years for average risk pts to screen for colon cancer.

Disadvantage is if you find something then you need a biopsy so you are going to need to do a colonoscopy anyways
What are the symptoms of IBS?
1) Abd distention
2) Flatulence
3) disordered bowel function
4) Abd pain (generally LLQ)
5) Altered bowel functions
6) Chronically recurring

IBS is probaly due to an abnormality in the gut flora
Serotonin also prob. play a role in GI motility
What is the basic Rome III criteria?
1) Recurrent abdominal pain or discomfort at least 3 days per month in the last 3 months associated with 2 or more of the following:
a) Relieved by defecation; and/or
b) Onset associated with a change in frequency of stool; and/or
c) Onset associated with a change in form (appearance) of stool
d) Diagnostic criteria fulfilled for the last 3 months with symptom onset ≥ 6 months prior to diagnosis.
What are the Red Flags of IBS?
1) Symptoms after 50
2) Family hx of IBD, Celiac Sprue (4 times higher), Colorectal cancer
3) Nocturnal diarrhea
4) GI Bleed
5) Fe-Deficiency anemia
6) Weight loss
What medical treatments are available for IBS and what symptoms do they help control?
1) Diarrhea
a) Loperamide
b) Cholestyramine resin
c) Alosteron

2) Constipation
a) MgOH
b) Lactulose syrup
c) polyethylene glycol
d) 70% sorbitol

3) Abd Pain
a) smooth muscle relaxant
b) TCA's
c) SSRI's
What are the main types of IBS and its prevalence in the US?
1) IBS-D => Diarrhea predominant
2) IBS-C => Constipation predominant