Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

GASTROINTESTINAL DISORDERSSigns & Sx of GI Distress

- abd pain, distension, bloating, chest discomfort, indigestion, dysphagia; anorexia, N/V, wt gain or loss; diarrhea & constipation, tenesmus; jaundice; hemoptysis, hematemesis (vomiting bld), hematochezia (the passage of bld in the feces); melena (dark, tarry stools containing decomposing bld; indicative of bleeding in the upper part of the GIT)

RED FLAGS- progressive wt loss, night sweats & fevers possible malignancy- bright red bld from rectum diverticular disease, UC, tumour- blood in stool hemorrhoids, colorectal CA, diverticular dis, UC, tumour- dizziness, nausea, sweating, hypotension GI bleeding- melena complicated esophageal ulcer, peptic ulcer disease (PUD)

UPPER GI BLEEDING 4X more common than bleeding from the lower GI

major cause of morbidity & mortality alcohol abuse LV cirrhosis portal

HTN esophageal varices (potential source for UGIB)

NSAID use may lead to gastric bleeding

Lab Dx: Hb, BUN:creatinine (↑ w/ UGIB >36 in pt w/out renal insuff), coagulation profile, platelet count (<50 requires platelet transfusion), LV fxn test, plasma fibrinogen, electrolytes

DDx: btwn gastric/duodenal ulcer, gastric/esophageal varices, Mallory-Weiss tear, esophagitis, neoplasm, hemorrhagic gastritis

ABDOMINAL PAIN Categories:Visceral: arises from abdominal organsParietal: arises from outside layer of abdominal organs; pain more localizedSuperficial abd wall pain: asstd w/ injuries to mm or inflm of the skin as in Herpes zosterReferred pain

Extraperitoneal causes:- pneumonia, MI, empyema, rheumatic fever, leukemia, SCA, SC tumour, Herpes zoster, nephritis, prostitis…..many many more (see pp 2 pkg 1)

- Observe position of the pt:- flexed right hip < extension appendicitis- fetal acute pancreatitis- pain < mvmt peritoneal inflm- pain > mvmt ureteral stone, cholecystitis

- Abdominal exam:- palpation, rebound tenderness- Murphy’s sign (+) acute cholecystitis- Grey-turners sign (+) retroperitoneal

bleed- Cullen’s sign (+) “ “

Quality of pain

Sudden Perforation, rupture, torsion

15-45min; > antacids & food

PUD

Several hours Biliary colicSeveral days Pancreatitis

Acute/chronic diarrhea Obstruction, spasm, dilation

Cramping, inter-mittent, stabbing

“ “

Squeezing, steady Biliary colic

Lab Dx: see above; xray in suspected obstruction

DDx: food poisoning, ectopic preg, MI, LU dis, acute pancreatitis, appenditis, peritoneal inflm, cholecystitis, cholelithiasis or KI stone, bowel obstruct’n, testicle/ovary torsion, rupture of aortic aneurysm

Keynotes: DRE may reveal peritoneal

inflm bc anterior rectum has peritoneal surface

include preg test & pelvic exam to rule out ectopic preg

painful soft abd in elderly IBD

point tenderness suggests appendicitis, diverticulitis, cholecystitis

DISEASES OF THE ESOPHAGUS

DYSPHAGIA - subjective awareness of difficulty swallowing dt impaired progression of matter to ST

Pre-esophageal or esophageal origin: solids only obstructionsolids & liquids motor dysfunction

DDx: hiatal hernia, GERD + complications (Barretts metaplasia, esoph stricture),

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

Mechanical/Obstruction1) Intrinsic narrowing: inflamed

esophagus becomes swollen ↓ diameter

2) Extrinsic compression: external compressive forces

Motor/Neurological1)Diff swallowing dt oral lesions,

paralysis of tongue, oropharyngeal anesthesia

2)Dysfxn of peristalsis dt impairment of striated esophageal mm a.r.o. CVA or myopathy of smooth mm as in achalasia & diffuse spasms

intermittent lower esophageal ring (Schatzki)

progressively worsens carcinoma

NB: Rule out globus hystericus: feeling of having a lump in throat unrelated to swallowing; asstd w/ anxiety & grief

esoph web (PVS), ring (Schatzki’s), carcinoma

Mechanical – Obstructive Disorders of the Esophagus

HIATAL HERNIA - A portion of the ST prolapses through the diaphragmatic esophageal hiatus

- 2 types:1)Paraesophageal hernia: widened

esoph hiatus permits fundus of ST to protrude into chest,; GE jxn remains below the diaphragm preventing acid reflux

2)Sliding hiatal hernia: MC, GE jxn migrates into the chest thru the esoph hiatus; as LES moves up into chest it is less effective as a sphincter allowing acid reflux

- caused by factors that ↑ intraabd P such as: constipation, preg, ascites, obesity

- asstd w/ GERD & its complications

Sx: usually asymptomatic

GASTRO-ESOPHAGEAL REFLUX DISEASE (GERD)

reflux of gastric contents into esophagus dt incompetence of LES

Causes: infection, drugs, corrosive chemicals, pregnancy, scleroderma agents that ↓ LES P : caffeine, chocolate, alcohol, nicotine, fats

Complications: esophagitis strictures, ulcerations w/chronic inflammation – scarring pulmonary aspiration Barrett’s esophagus/ Metaplasia

Sx: Heartburn (epigastric/substernal burning) occurs w/I an hour or two after meals & last minutes to hours; radiates up & down thorax (DDx: angina: pain radiates from across chest into back, lasts minutes unless MI develops lasts hours) Chest pain: substernal that may radiate into back, neck, arms, jaw; independent or co-existent w/ heartburn Regurgitation of gastric contents Dysphagia for solids w/ full feeling in throat (may indicate developing stricture) Persistent non-productive cough bloating, belching < lying down after meal, bending over, at night or when fasting angina-like pain d/t stretching and stimulation of visceral afferent fibers of esophagus burning, squeezing

Dx: endoscopy w/ biopsy confirms GERD; esophageal manometry to determine the P & strength of the LES; esophageal pH monitoring, barium swallow

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

hoarseness, repetitive clearing of throat

BARRETT’S ESOPHAGUS/ METAPLASIA

- A metaplastic change of normal squamous epith of the esoph to abnormal columnar epithelium dt chronic irritation

- Specialized metaplastic cells secrete mucous & histologically resemble cells in ST & intestine

Tx: - don’t lay down after eating or elevate head, acid suppressing med (antacids, proton pump inhibitors, histamine rec antagonists)- wt loss to ↓ intraabd P- diet: avoid acid forming foods,

eat smaller meals

ESOPHAGEAL WEBS, RINGS, STRICTURES

Web: smooth, eccentric 2-3mm wide, extension of normal esoph T consisting of mucosa & submucosaRing: smooth, concentric 3-5mm wide extension of T consisting of all 3 layersStricture: about 1-4cm long; develops a.r.o scarring from acid reflux

- most pts asymptomatic and unaware of their condition until found during an endoscopy or barium swallow

Dx & Lab Dx: see pp 2 pkg 2

DDx: congenital, Plummer-Vinson syndrome, chronic inflm, caustic ingestion, autoimmune dis, celiac sprue

Plummer-Vinson Syndrome **Web

- A thin mucosal memb covered by normal squamous epith that grows across the inside of the esophagus from the mucosa (at the level of the cricoid)

- Fe def anemia: depletion of Fe dependent enzymes changes in muscles involved in swallowing mech atrophy of esophageal mucosa web formation- asstd w/ AI conditions such as: RA, pernicious anemia, celiac, thyroiditis

Sx: difficulty swallowing solids Tx: perforation of webs, treat underlying anemia & webs will disappear on their own

Schatzki’s Ring **Ring

- lower esophageal ring located at the junction of esoph & ST

probably present at birth correlated to GERD, pill induced esophagitis, congenital develops when lumen < 12mm (normal 3-4cm)

Sx: - intermittent non-progressive dysphagia for solids

DDx: carcinoma, dysphagia is permanent and progressive

Tx: esophageal dilation w/ intention of fracturing ring, chew food well

Peptic Esophageal Stricture **Stricture

- inflm & ulcer formation scar formation stricture formation

- a result of GERD induced esophagitis (accounts for 70-80% of strictures)- some congenitalHistological changes - edema, cellular infiltration, basal cell hyperplasia, ↑ deposition of collagen on healing

Tx: esophageal dilation, chew food well, long term proton pump inhibitors, avoid substances that ↑ LES P

ESOPHAGEAL DIVERTICULA

congenital or acquired outpouchings at any level of the esophageal wall

often asymptomatic, but may cause dysphagia & regurgitation

Zenker’s Diverticulum(pharyngoesophageal)

most common diverticula just behind cricoid cartilage at approx. the upper esophageal sphincter

contains all layers of wall prolonged stasis of trapped food w/I the diverticulum increases risk of squamous cell carcinoma

CARCINOMA OF THE ESOPHAGUS

obstructive (mechanical esophageal disorders) adenocarcinoma, or squamous cell carcinoma

men tobacco smoking alcoholism vit A & C deficiency lye ingestion achalasia Barrett’s esophagus

Sx: progressive, persistent dysphagia for solids pain indicates extension of tumor beyond wall of esophagus dysphagia for liquids, cough, hoarseness, and weight loss are symptoms of advanced esophageal carcinoma

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

Celiac sprue

Motor – Neurological Disorders of the Esophagus

Achalasia primary esophageal motility disorder char by failure of the LES to relax & absence of esophageal peristalsis cardiospasm, or mega-esophagus, or esophageal aperistalsis

neurogenic disorder: pts have imbalance (excitatory > inhibitory) in neurotransmiss’n from scarring of Auerbach’s plexus LES doesn’t relax when swallowing = obstruction loss of peristaltic activity secondary dilation of esophagus above

Sx: dysphagia for both liquids and solids weight loss (90%)

Associated symptoms: chest pain, regurgitation nocturnal cough d/t dilated lumen → increased sputum → aspiration → pneumonia, bronchiectasis

Dx: “bird’s beak” appearance of lower esoph; esophageal manometry; pH monitoring to rule out GERD; endoscopy to rule out tumour & malignancy

Tx: Ca channel blockers & nitrates to ↓ LES P

Esophageal Spasm strong, uncoordinated, non-propulsive contractions food doesn’t travel down neural defect accompanied by incomplete relaxation of LES similar to achalasia

Sx: intermittent dysphagia for both liquids & solids occasional chest pain, globus hystericus, regurgitation of food odynophasia esp w/extremely cold or hot food chest pain d/t spasm (pain similar to angina location * c/b relieved by nitroglycerin)

Esophageal Tears & Varices

Mallory-Weiss Syndrome - non-transmural tears at the GE jxn - caused by ↑ intraabdominal P dt forceful vomiting and failure of the LES to relax

Sx: hematemesis Tx: surgery to repair tears; females w/ MWS rule out preg

Boerhaave’s Syndrome - transmural perforation of the esophagus

- typically occurs after forceful vomiting; repeated episodes of retching & vomiting-

Sx: sudden onset of severe chest pain in lower thorax & upper abd- SOB- < swallowing, no hematemesis (DDx: MWS has

hematemesis)- tachycardia, sweating, fever, HTN

Tx: *EMERGENCY surgery and drainage required; most lethal perforation of the GIT- best prognosis w/ early dx & surgery w/in 12h

Esophageal Varices - dilated bld vessels w/in the wall of the esophagus

- seen in pts w/ portal HTN (ie cirrhosis of the LV) ↑ bld flow thru vessels leading to esophagus ↑ chance of rupture & bleeding

*Vessels may rupture causing life-threatening hemorrhage

DISEASES OF THE GALLBLADDER, BILE DUCTS, & DISORDERS OF THE PANCREAS

Congenital Abnormalities - includes abnormalities in position, number, size & shape

Ectopia: abn position stasis dt compression gallstone formationDouble GB: abn number & shapeSegmentation: abn size & shape

BILIARY CALCULI presence of calculi in the GB (cholelithiasis) or in the biliary ducts (choledocholthiasis) more freq in women & some ethnic groups risk factors: western diet, family hx Formation depends on:

1) Lithogenic bile production2) GB motility

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

3) Cyrstallization of CHOL (termed “nucleation of gallstones” three types of stones: cholesterol, pigment, and mixed stones (80%); up to 3cm in diameter CHOL rich stones result from: LV not providing enough bile salts & lecithin, ↑ LV synthesis of CHOL, supersaturation of bile w/ CHOL “lithogenic bile”, slow emptying of GB Tx: oral bile acids ↓ biliary secretion of CHOL ↓ in CHOL saturation of bile Complications: infection (cholecystitis), obstruction, acute pancreatitis, perforation gall stone ileus, stricture biliary cirrhosis, malignancy

CHOLELITHIASIS/CHOLEDOCHO-LITHIASIS

gallstones in the gallbladder gallstones in the common bile duct

genetic, sex, obesity, rapid wt loss rapid ↑ in biliary chol saturation, high caloric diet, regional enteritis, CF, Type IV hyperlipidemia, diabetes, long-term parenteral nutrition, Crohn’s, bowel resection

pigment gallstones associated w/chronic hemolytic anemia, chronic LIV dz, cirrhosis, biliary infection, obstruction/

anomalies of the GB or bile ducts

Symptoms occur only when stones migrate to obstruct: cystic duct obstruction: (50%) biliary colic and/or

acute inflammation of GB common bile duct obstruction: (10-20%) biliary

colic, jaundice, inflammation of hepatic bile ducts (cholangitis), or pancreatitis from ascending bacterial inf’n

Dx: ultrasound

BILIARY COLIC pain produced by contraction of biliary tree d/t sudden obstruction & increased intraluminal pressure in bile duct

Complications:- ↑ risk of GB CA w/ cholelithiasis- asymptomatic stones in the common bile

duct are more life-threatening and should be removed

SX:Pain: sudden onset, severe, steady, lasts up to 3hrs,

maximal in RUQ & epigastrum radiates to interscapular area, right scapula,

shoulder, back (rare) episodes are longer than intestinal colic slightly > flexed posture vomiting does not relieve pain consistent relief only w/ narcoticsOther features: N & V often cold sweats fever and chills (asstd w/ acute obstruction &

bacterial infection) jaundice, pruritis uncommon dark urine & light stools abdomen is soft, may dev local tenderness

Dx: ultrasound, abd xray only shows 10% of stones, cholangiogram, ↑ alkaline phosphatase, slightly ↑ transaminases

DDx:1) Gastric ulcer/food poisoning: pain relieved by vomiting2) LV disease3) Hepatitis: v. high transaminases

Tx: surgery, chemical dissolution, oral bile acids

ACUTE CHOLANGITIS bacterial inflammation of the bile ducts close-space infection usually complicated d/t bacteria than ascend from the intestine

biliary colic jaundice shaking chills w/fever

SCLEROSING CHOLANGITIS

inflammation of hepatic bile duct progressive narrowing of bile duct

men 3x >women pruritus right abd pain jaundice fatiguenausea

Lab Dx: elevated serum ALP, ERCP

ACUTE CALCULUSCHOLECYSTITIS

- inflammation of the GB caused by calculi

women>menassociated findings: Hx of biliary sx fatty food intolerance constipation during attack fever jaundice not present in simple cholecystitis

Sx: pain is followed a few hours later by N/V patient lies motionless vomiting does not relieve pain pain is mild or severe biliary colic pain in RUQ, referred to interscapular region, right shoulder associated w/pulmonary edema and inflammation

Dx: ultrasound best initial method, leukocytosis present, xray, cholecystogram during acute attacks

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

local tenderness in RUQ m/b pruritis (d/t bile build up) sx may be mild or masked in elderly & pts taking corticosteroid/immuno-suppressive therapy

Other symptoms cutaneous hyperesthesia (+) Murphy’s sign – pain & inspiratory arrest while palpating RUQ, (+) Courvoisier’s sign – palpable GB, (+) Boas’ sign – tenderness around R scapula

CHRONIC CHOLECYSTITIS

recurrent subacute inflm of GB and sx d/t gallstones

single episode of biliary colic, acute cholecystitis → chronic inflammatory changes

Complications of calculous cholecystitis empyema: suppurative infn in which GB fills w/ purulent material sepsis *BAD* perforation of GB perforation: days to 1 week after acute cholecystitis; 25% mortality; sx of acute peritonitis hydropic gallbladder: obstructed cystic duct GB filled w/ clear, mucous “white bile” fistula: erosion of GB from gallstones fistula to duodenum, colon, ST gallstone ileus: migration of gallstone thru fistula into intestinal tract; may cause colonic obstruction if >2cm acute pancreatitis

ACALCULUS CHOLECYSTIS

2-10% of cases of acute cholecystitis operations, severe trauma, acute medical illness, Strep, diabetes

CANCER OF GALLBLADDER

abnormal thickening of GB wall women 3x >men

mimic those of acute or chronic cholecystitis palpable mass in RUQ signs of obstructive jaundice Sister Mary Joseph lesion : erythematous, retracted excoriated umbilical metastasis

ACUTEPANCREATITIS

acute inflammation of pancreas in which pancreatic enzymes autodigest the gland

main cause: alcohol binge drinking, gallstones less common cause: post-op pancreatitis, abd trauma, hyperlipidemia, drugs, uremia, PUD w/penetration of pancreas, viral infections, biliary colic

Complications- inflm can spread easily & can evolve into hemmorhagic or necrotizing pancreatitis

Sx: pain in epigastrium/abdomen (RUQ), sometimes in periumbilical region pain radiates to back N/V abdominal tenderness < supine (+) Cullen’s sign – retroperitoneal bleeding that causes hematoma at umbilicus, or flank ((+) Turner’s sign ) diminished/absent bowel sounds (d/t pain) → decreased breathing, bloating → decreased BM (not a classic sign)

Lab Dx: ↑ serum amylase, lipase, trypsinogen

CHRONIC PANCREATITIS persistent histological changes after etiologic agent has been removed

alcohol cystic fibrosis common cause in children scarring

SX:Pain in the epigastrium after eating, radiates to back < supine several days to week, usually relieved only by narcotics recurrent attacks often precipitated by alcohol excess

Lab Dx: Xray: pancreatic calcification, m/b left pleural effusion ERCP: diffuse ductal dilatation, irregular beaded appearance Peritoneal aspirate: very high amylase (final stage) US: enlarged pancreas and/or

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

Other features malabsorption in association w/ steatorrhea and clay color, floating, bulky & foul smelling stool jaundice diabetesAssociated findings: vomiting wide-ranging temp shock w/cold clammy skin tenderness in lower epigastrium abdomen is slightly rigid abdominal distention, transient adynamic ileus Cullen’s sign, Grey-Turner’s sign

abscess CT: pancreatic calcification

ADENOCARCINOMA OF THE PANCREAS

Men > women, 55-65 yrs 70% in head of pancreas, 30% in tail risks: hereditary pancreatitis, smokers, diabetics, long term exposure to insecticide DDT, chronic pancreatitis

Sx: constant abd pain (after meals) or periumbilical discomfort pain radiates to back, relieved by sitting up or bending knees jaundice (65%) weight loss (60%) palpable gallbladder (Courvoisier’s sign) palpable epigastric mass

Lab: increase serum amylase

Only 10-20% are respectable at time of dx. 3 months survival w/out resection

DISEASES OF THE STOMACH & DUODENUM

H. Pylori Infection - responsible for 90% of duodenal ulcers & 80% of gastric complaints

- can survive in mucus layer of ST dt secretion of enzyme urease which creates a more alkaline env for itself- only found in gastric mucosa

Asstd w/:- acute gastritis, PUD, MALTomas, GERD, Fe def anemia, skin dis, rheumatic condit’ns

ACUTEGASTRITIS

inflammatory lesions of the gastric mucosa diffuse/localized usually self-limited

2 Types:1) Erosive – hemorrhagic, superficial/deep erosions2) Non-erosive – H.pylori inf’n

drugs (aspirin, NSAIDs, steroids) accidental ingestion of caustic substance (lye, sulfuric acid) stress (eg., trauma w/added shock, sepsis, organ failure) infections (H.pylori, M. tuberculosis, Candida, herpes)

Sx: asymptomatic in 30% 1st sx usually hemorrhage epigastric burning pain N/V occult GI bleeding, when severe associated w/ hematemesis chronic bleeding anemia melena

Dx: endoscopy H.pylori culture serologic testing for anti-Abs urease test (breath or biopsy)

Tx: transfusion, anti-secretory ulcer meds, vasoconstrictors

CHRONIC GASTRITIS characterized by: superficial lymphocyte infiltrate in the lamina propria, progressive inflammatory changes

Type A: less common, involves body & fundus; AI dis that leads to inflm & atrophy of mucosa; achlorhydria is diagnostic, lack of IF pernicious anemia

prolonged use of alcohol, aspirin, etc radiation, thermal injury infections (H. pylori)

association w/gastric polyps, gastric ulcer, and gastric cancer (Type B > Type A)

Symptoms similar for Type A & B: burning epigastric pain dyspepsia/indigestion N/V

Type A sx: plasma Abs to intrinsic factor & parietal cells hypochlorydria, achlorhydria sx of pernicious anemia (pts have few GI complaints)

Dx: endoscopy CBC (anemia)

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

Type B: more common, involves antrum in younger pts, entire ST in elderly; 90% have H.pylori infection, HCl production not affected if only antrum involved bc HCl produced in body of ST

hypergastrinemia hypothyroidism, DM, vitiligo occur more frequently in Type AType B sx: gastric acid level is normal/slightly reduced gastrin cell Abs ↓ gastric secretions serum gastrin elevated

PEPTIC ULCER DISEASE

- A circumscribed ulceration of the mucous membrane that penetrates the muscularis mucosa

- Occurs in areas exposed to acid & pepsin

2 Types of Ulcers:Gastric Ulcers: MC occur along lesser curvature of ST, develop later in life, hyposecretion of HCl, chance of malignancy, < food

Duodenal Ulcers: w/in first few cm of duodenum (bulb), smaller ulcerations, hypersecretion of HCl, benign, > food

Can occur at any age, intermittent dis Family hx of H.pylori, steroids and NSAID, Stress impairs mucosal defense mechanisms excess HCl secretion personality type A, Zollinger-Ellison syndrome < smoking; ↓ healing

complications of PUD: hemorrhage, perforation, penetration of adjacent organ, gastric-outlet obstruction, malignancy (gastric ulcers)RED FLAG: *Emergency inflm of peritoneum: rigid abd, ↓ bowel sounds, occult bld

Sx: burning epigastric pain or RUQ pain, bloating, N/ mb V, anemia may present only w/bleeding (melena, pallor, tachycardia, low BP)

Duodenal ulcers: pain >w/meals, but <2-3hrs after meals weight gain pain may awaken from sleep hypersalivation increased HCl

Gastric ulcers: rarely in pts <40yoa pain < eatingweight loss- tend to have normal/reduced HCl

Dx: endoscopy, xray, family hx

Tx: goal is to neutralize or ↓ gastric acidity, tx for H.pylori inf’n

GASTRIC CARCINOMA

4 Types:1) Protruding: polyp type2) Penetrating: tumour has sharp, well demarcated borders, mb ulcerated3) Spreading: along mucosa or thru wall; edges of ulcers fibrotic “Leather bottle” ST4) Misc

possible etiologic factors: tobacco use, Vit C def., consumption of preserved food, pernicious anemia Risk factors: H.pylori infn, atrophic gastritis, gastric dysplasia, polyps men > women, 60-75yrs

Stages of carcinoma:I: confined to muscularis propriaII: muscularis & serosal invovlIII: gastric & nodal involveIV: residual disV: metastatic

Sx: weight loss, anorexia epigastric pain early satiety vomiting ( weakness & fatigue (2° to bld loss) gross GI bleeding dysphagia palpable left supraclavicular node (Virchows node) suggestive of metastatic disease in chest & abdominal cavity *RED FLAG

Dx: endoscopy w/ biopsy and brush cytology; ↑ serum carcinoembryonic Ag- achlorhydria irt stimulation

indicates malignancy

Tx: surgery, chemo

DISEASES OF THE LIVER

FATTY LIVER DISEASE - excessive accumulation of lipidin hepatocytes

- most common LV response to injury - alcoholic fatty LV mb accom-

panied by inflm, necrosis & permanent damage (cirrhosis)

Diffuse fatty change:- alcoholism, obesity, diabetes- other causes: malnutrition (PEM,

kwashiorkor), metabolic disorders, drugs, systemic illnesses w/ fever (Reye’s syndrome)

Focal Fatty change:- less common; presents as a space occupying

lesion in the LV- asstd w/ alcoholism, obesity, diabetes

Sx: non-tender, asymptomatic hepatomegaly may present w/ RUQ pain & jaundice

Dx: mild ↑ in ALP or transaminase (AST/ALT)- hyperlipidemia- US/CAT show fat deposits- Gold standard = biopsy

Tx: reversible if underlying cause removed;

ALCOHOLIC LIVER DISEASE

- spectrum of clinical sx & pathologic changes caused by EtOH

Major Factors: - Quantity & duration of consumption

Sx:- variable clinical picture; becomes apparent in pts

Lab Dx: ↑ glutamyl transpeptidase (GGT)

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

- progresses to symptomatic alcoholic hepatits

- nutritional status of the pt- genetic & metabolic traits

Prognosis related to the amt of cirrhosis and LV cell necrosis

30’s, severe prob in 40’s- LV may be enlarged, smooth, tender- Cirrhosis may be present & asymptomatic

Tx: stop drinking EtOH..duh!- supportive tx

CIRRHOSIS - widespread fibrosis & nodule formation w/in the LV

- fibrosis is a common response to hepatocell injury or necrosis- caused by: infections, storage disorders, toxic metabolite accum, chemicals & drugs, disturbances in LV bld flow, obstruction of bile flow- fibrosis develops from depostition of collagen irt injury, inflm, necrosis ↓ in hepatic fxn

Sx:- pruritis- portal HTN w/ variceal bleeding, ascites- LV failure renal failure coma- Weakness, anorexia, malaise, wt loss- Obstruction of bile flow jaundice, pruritis,

xanthelasmas- LV may be palpable- normocytic or microcytic anemia

Lab Dx: ↓ serum albuin, ↓ prothrombin time, ↑ serum globulin, ↑ transaminase, ALP normal or ↑, bilirubin normal

PRIMARY BILIARY CIRRHOSIS

- dis of unknown cause char by chronic cholestasis & by progressive destruction of intrahepatic bile ducts

4 Stages: see pp 11 pkg 5- presents insidiously- 90% in women aged 35-70- commonly asstd w/ AI diseases such as RA, scleroderma, sicca cplx, autoimmune thyroiditis- slow progression longer survival

Sx:- 50% asymptomatic w/ abnormalities detected

during bld test- pruritis, non-sp fatigue- enlarged, firm, non-tender LV (50%)- splenomegaly (25%)- skin xanthomas - clubbing, metabolic bone dis, peripheral

neuropathy in some

Dx: biopsy, ultrasound

DDx: - extrahepatic biliary obstruction, chronic hepatits, primary sclerosing cholangitis, drug induced cholestasis

Changes in Liver Function Loss of LV fxn : ↓ urea synthesis, ↑ bld ammonia hepatic encephalopathy ↓ albumin synthesis ascites ↓ clotting factors bleeding

UNCONJUGATEDHYPERBILIRUBINEMIA

increased formation of bilirubin (hemolytic anemia) impaired hepatic uptake (↓d glucoronyl transferase activity) neonatal jaundice (immature glucoronyl transferase)

Causes:- hemolysis, Gilbert’s syndrome, Crigler-Najjar syndrome, neonatal jaundice, drugs (rifampin, chloramphenical)

increased formation of bile does not lead to pruritus impaired hepatic uptake – N ranges of LFTs, absence of urinary bile, characteristic bili fractionation, N LIV histology < stress, excessive exercise, fasting neonatal jaundice – bili (not bound to albumin) deposits in brain tissue → permanent neurological injury may occur & possibly death

CONJUGATED BILIRUBINEMIAS

4 categories: hepatocellular (eg., hepatitis, cirrhosis) obstructive infiltrative (eg., fat LIV)space-occupying lesion (eg., tumor, cyst, abscess)

ACUTE HEPATITIS - a systemic infection affecting predominantly the LV

4 stages of acute hepatitis:1. incubation period2. preicteric phase3. icteric phase4. convalescent period

Typical symptoms of hepatitis include: jaundice – less than 1/3 of pts common cold nausea, fatigue, anorexia, loss of appetite slight fever diffuse muscle pain

Lab Dx: ↑ALP ↑transaminase AST + ALT ↑ serum bilirubin

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

decreased desire to smoke heaviness/fullness/discomfort in RUQ (inflamed, swollen LIV→ glyson’s capsule stretched → pain ascitesIn icteric phase: dark urine cutaneous jaundice lasts several weeksExtrahepatic sx: joint pain (symmetric) – small hand and wrist joints diffuse adenopathy (enlarged LIV) skin rash

Frequently, the infection is asymptomatic and anicteric!

Hepatitis A RNA enterovirus fecal-oral contamination incubation: 15-49d present in stool 2 weeks after infection

N & V jaundice (50% develop) malaise, fever anorexia

Anti-HAV (total)+ IgM anti-HAV+Prior infection: Anti-HAV (total)+ IgM anti-HAV- IgG anti-HAV+

Hepatitis B DNA virus Identified in almost every body fluid (saliva, sweat, blood, breast milk, tears, semen, etc) Risk: sexual contact, sharing razors, breast-feeding, etc Incubation: mean 70-80d Present in blood 2 months after infections

Appear at about 3 months; may be asymptomatic, or symptomatic: Arthralgia N & V jaundice (not every case)May progress to fulminant hepatic failure & death (2%)Chronic carrier →↑risk for early death from cirrhosis or hepatocellular carcinoma

In severe cases of Hep B + C: encephalopathy- toxic involvement of brain present w/I 2wks psychomotor slowing, pt is disoriented and confused flapping tremor – wrist becomes dorsiflexed when asked to spread fingers fulminant → severe LIV failure

HBsAg+, IgM anti-HBc+Prior infection: HBsAg- Anti-HBs+ Anti-HBc+Chronic carrier HBsAg+ IgM anti-HBc-Hep B vaccine HBsAg- Anti-HBs+ Anti-HBc-

Hepatitis C RNA virus parenteral exposure incubation period: mean 50d more than 50% infected ppl become chronic carriers →↑risk of chronic hepatitis, cirrhosis, hepatocellular carcinoma

milder than other hepatitis viruses similar to those of Hep B, except arthralgias less common infreq other manifestations – porphyria cutanea tarda, cryoglobulinemia

Hepatitis D defective RNA virus occurs only in presence of Hep B incubation: 30-18-d

symptoms more severe → fulminant hepatic failure and death in up to 20% pts

anti-HD+

Hepatitis E RNA virus transmitted by RNA virus mild in most pts 20% mortality if acquired during pregnancy

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

CHRONIC HEPATITIS liver cell necrosis and inflammation lasting > 6-12months

alcohol intake over many years accounts for majority of chronic cases HBV, HBC also major causes (injury caused by Immune-med host rxn to viral infection) Wilsons disease in children & young adults

jaundice (variable) Terry’s nails (white nails) spider nevi (angiomas) – sign of damaged estrogen metabolism gynecomastia atrophic testes excessive decrease in weight ascites from portal hypertension

DDx:- alcoholic LV dis, acute viral hepatitis, primary biliary cirrhosis- biopsy needed for definitive dx

HEPATOCELLULAR CARCINOMA

- LV tumour arising from malignant hepatocytes

- HBV & HCV carriers at greater risk- environmental carcinogens- alcoholic cirrhosis

Sx:- abd pain, wt loss, palpable RUQ mass, unexplained deterioration in a pt w/ cirrhosis- fever- first manifestation is an acute abdominal emergency caused by rupture of tuour- painful, growing hepatomegaly, hepatic friction rub, bruit

Dx: ↑ alpha-fetoprotein, biopsy

Fibrolamellar carcinoma, Cholangiocarcinoma, Hepatoblastoma

- other primary LV cancers Dx: based on histology; therapy is of little value and prognosis is poor

DISEASES OF THE SMALL INTESTINE & COLON

Healthy Bowel Flora - Benefits of healthy flora:- Synthesis & excretion of vitamins (K,B12, & other B vit)- Prevent colonization of disease causing pathogens through competition for attachment- Stimulate the dev of immune & lymphatic T in the GIT (Peyer’s patches)- Stimulate the production of cross-reactive Abs

- Ab’s produced against the antigenic cpts of the normal flora cross react w/ certain pathogenic bacteria preventing inf’n

Intestinal Dysbiosis an harmful overgrowth of intestinal bacteria/pathogenic bac (more than 104 ml of tissue)

- caused by: ABC use, poor diet (↑ fat, ↑ sugar, ↓ fiber), compromised GIT (Crohns, IBS) hypochlorydia (↓ HCl)

- gas, bloating, diarrhea, N/V Dx: Stool analysis – measures digestion & maldig thru fecal chymotrypsin, pH, fiber; intestinal abs thru fecal LCFA, SCFA, CHOL

Maldigestion &Malabsorption

- inability to break down lrg molecules in the lumen of the SI

1 . Inadequate digestion dt - pancreatic insufficiency- bile salt def- inadequate mixing of chime, bile,

pancreatic enzymes- 2nd to LV dis, terminal ileal disease impaired enterohep

recycling

2. Mucosal Disorders dt- gluten enteropathy/food sensitiv- intestinal ischemia- leaky get syndrome- intest lymphoma- inadeq absorptive surface dt bowel resection, Crohns

Manifests as:- Fat soluble vitamin def (ADEK)

Sx: night blindness, dry skin, hemolytic anemia in children, neurological prob (CN 2, 7, 9, 10) & bleeding disorders - Iron

Fe abs in duodenum & upper jejunum; malabs leads to ↓ Hb, ↓ serum Fe & ferritin; Sx: anemia, glossitis, koilonychias (spooned nails)

- CalciumCa abs in duod & upper jejunum; binds to Ca binding PRO in cells (CBP ↑ by Vit

D; ↓ abs ↓ serum Ca & Mg; Ca def leads to metabolic bone disease; Sx: tetany, parethesias; Dx: measure serum Ca & Mg, bone scan for ↓ bone mineralizationFolic acid

Abs in jejunum; ↓ abs ↓ RBC folate; Sx: glossitis, megaloblastic anemia; may see ↑ folic acid with bacterial overgrowthVitamin B12

Def caused by terminal ileal dis; Sx: pernicious anemia; prolonged def

- inability to transport molecules across the intestinal mucosa

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

- fibrosis dt systemic sclerosis, radiation enteritis

degeneration of the spinal cord, peripheral neuropathy, dementia; Dx: Schilling Test

CHOSx: generalized malnutrition, wt loss, flatus; Dx: D-xylose test

PROSx: malnutrition, wt loss, amenorrhea, ↓ libido; Dx: measure serum albumin

FATSx: malnutrition, wt loss, steatorrhea; Dx: fecal fat excretion

DIVERTICULAR DISEASE Complications:

- diverticulitis (NB: little to no bleeding)- bleeding (NB: diverticula bleed often)- peptic ulceration- perforation- neoplasm- obstruction: strangulation, invagination = incarceration, twisting, intussusception

Duodenal diverticula w/in 1-2cm of the papilla of Vater saccular outpouchings

common bile duct obstruction may occur dt outpouchings interfering w/ its emptying

asymptomatic in most pts rarely causes upper GI bleeding

- found during endoscopy/autopsy

Jejunal diverticula malabsorption diarrhea, bloating, distention, flatus steatorrhea: bulky & greasy stool anorexia (d/t build up of toxins from undigested food) glossitis (d/t vit def) anemia; pernicious anemia + neuropathy ascites & edema (protein def) osteopenia (Vit D def), osteoporosis & tetany d/t Ca def

Tx: surgical removal of multiple or large diverticuli

Meckel’s diverticulum true diverticulum as it involves all layers of bowel wall average 5-7cm long w/i 60-90cm of ileocecal valve of terminal ileum may contain ST or pancreatic T which may produce HCl

most freq congenital anomaly of the GI tract; represents the remnant of the viteline duct

Complications:- peptic ulceration from HCl prod, perforations, bowel obstruction, neoplasm, GIT strangulation, twisting, incarceration

DDx:1) Acute appendicitis:

Colonic diverticulum outpouchings of mucosa only (not true diverticula) herniation of mucosa/submuc thru the muscular layer; along the teniae at the site of penetrat’n of mesenteric vsls

Pathogenesis: Low-fiber diets: ↑ intraluminal P

especially in the sigmoid colon mucosal herniation → outpouching at focal wall weakness ** vegetarians have a 1/3 incidence of

diverticuli Chronic constipation dt hard, dry fecal

matter; also caused by lack of exercise, ignoring the urge, stress/anxiety, drugs, pregnancy

asymptomatic in uncomplicated diverticulaSx: crampy abd pain in LLQ, pain alternates w/diarrhea and constipation; > BM; bloating

Tx: ↑ stool bulk ↓ intraluminal P; regulate bowel frequency

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

DIVERTICULITIS complication of diverticulosis inflammation of diverticular sacs usually involves the R side of the colon

retention in the diverticula of undigested food residues and bacteria → hard mass called a fecalith compromises bld supply ↑ suscept to invasion by colonic bact, perforation w/ peridiverticular abscesses

Complications: - bowel obstruct’n, abscess formation → peritonitis “L-sided appendicitis” fistula to bladder or vagina may develop (< 25%) bleeding is rare (see next line)

Sx: crampy LLQ pain, fever, constipation/diarrhea, N/V, tenderness, pain < BM

Dx: made on the basis of clinical sx; CT scan performed during acute phases of diverticulitisNB: colonoscopy & barium enema are CI during acute phase dt risk of perforation- after resolution of acute, endoscopy to visualize damage and rule out IBS

DDx:

1) Diverticulosis: multiple non-inflamed diverticuli often bleed from the R side of the colon, while inflamed diverticuli do not

2) IBS:

Tx: ABC, IV fluids, bowel rest (NPO)

Complication of Diverticulitis:BLEEDING

- occurs in 20-25% of cases- 80% spontaneously stop w/ only supportive tx; 20% rebleed

Dt erosion of a penetrating artery at the dome of the diverticulum

Sx: acute and brisk, painless w/impressive episodes of bright red blood per rectum and not associated w/straining

Dx: colonoscopy (after acute bleeding stops), arteriography or rapid sequence nuclear scanning to localize the bleeding portion of the colon

Management of bleeding:- initially, IV fluids & bld replacement; after rebleeding surgical resection

MEGACOLON- Definition: massive distention of colon accompanied by constipation & obstruction

Hirschsprung’s Disease (AganglionicMegacolon)

Congenital malformation of ganglia in the colonic submucosa (Meissner’s) & myenteric (Aurbach’s) plexus inability to defecate Usually involves sigmoid colon

Peristalsis absent in aganglionic segment unable to pass stool functional obstruction at most distal segment → proximal colon dilation 1/5000 live births; MCly in males, familial, asstd w/ other congenital abnorm

Complications: enterocolitis, perforation

- apparent after birth when infant doesn’t pass meconium, abd distension follows; may occur later in life w/mild sx

Sx: severe constipation & vomiting, absence of stool in rectum

Dx: DRE reveals absence of stool in rectum, X-ray shows a dilated proximal segment & a narrow distal segment, biopsy of mucosa/ submuc to confirm

Tx: surgical resection of aganglionic seg; or bypass of contracted seg by attaching normal colon to just above the internal sphincter

Chronic Idiopathic Megacolon

psychogenic megacolon onset at time of toilet training Sx: chronic constipation, abd distention

Dx: barium enema shows entire megacolon is distended & filled w/ stool; no narrow segment found

DDx:1) Hirschsprung’s: DRE in CIM reveals feces in rectum (feces absent in Hirschsprung’s); no narrow segment & normal ganglia found in CIM

Tx: enemas until pt acquires normal BM

Acquired Megacolon

Causes: schizophrenia, depression cerebral atrophy spinal cord injury Parkinson’s scleroderma narcotic drugs (morphine & codeine) esp in bedridden pts

obstipation (constipation d/t obstruction) massive colonic dilatation rectum distended w/feces

DDx:1) Hirschsprung’s: onset is during childhood; acquired megacolon occurs later in life; empty rectum in congenital megacolon

Tx: aimed at identifying underlying cause; use of purgatives that act by irritating the mucosa or by direct stimulation of the plexuses

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

infection by Trypanosoma cruzi (Chaga’s disease) destruction of ganglion cells in colon;

INTESTINAL OBSTRUCTION1) Mechanical obstruction2) Non-mechanical obstruction

Mechanical Obstruction *Dynamic ileus

Extrinsic Lesions:- adhesive bands, internal & external herniasIntrinsic Lesions:- carcinoma, diverticulitis, Crohns, gallstone obstruction, intus-sesception, volvulus (twisting causing obstruction)

- MC causes: carcinoma, sigmoid diverticulitis, volvulus (account for 90% of cases)- extreme prolonged contraction of intestine d/t heavy metal poisoning, uremia, extensive intestinal ulcerations- compensatory contraction of bowel above obstruction → twisting, strangulation, etc

Non-mechanical Obstruction *Adynamic ileus

- Mediated by H from the sympathoadrenal system

- Occurs to some degree after abdominal operation; only lasts 2-3 days

Causes: post-op narcotics, retroperitoneal hematomas asstd w/ vertebral fractures, thoracic dis (fractured ribs, pneumonia, MI), electrolyte imbalance (part K+), intestinal ischemia

Complications: peritonitis d/t ↑d

Small Bowel Obstruction Hallmark: abd distention caused by accumulation of stool, gas, fluid w/in obstructed segment

Sx depend on whether obstruction is complete/ incomplete, transient/ persistent

Sx: cramping, paroxysmal mid-abd pain; pain < the higher the obstruction; btwn intervals of pain, pt is relatively comfortable N/V = very severe; earliest sx; more profuse the higher the obstruction; constipation & abd distention follows vomiting

Complete obstruction = cessation of passage of gas or stool via rectum

Dx: Xray shows air-fluid levels & absence of gasPhysical exam: abd distension dt accumulation of gas & fluid; abd is soft & tender; distension is localized not general; visible peristalsis of ST and small bowel

DDx:1)Large Bowel Obstruct’n: LBO nausea absent

Large Bowel Obstruction - #1 cause : left-sided carcinoma of rectum ; also caused by volvulus of sigmoid or cecum, diverticulitis

Onset of acute pain may occur over a week

Sx: colicky abd pain w/ spasms that may last a few minutes, pain localized in hypogastrium (midline), vomiting m/b absent but nausea is constant and severe, constipation & abd distention; local tenderness w/ rigidity on palpation

IRRITABLE BOWEL SYNDROME(IBS)

motility disorder involving the entire hollow GI tract enhanced visceral activity dysregulation of CNS function (motor, sensory)

recurrent abd pain, usually LLQ altered freq of defecation w/hard stool (constipation), or watery stool (diarrhea) sense of incomplete evacuation feeling of abd distention after food intake excess flatus tender sigmoid full w/feces may be palpated in

exclusion of other conditions relation of sx to environmental and emotional stress

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

LLQ sx always occur in waking state, < stress (depression, anxiety), ingestion of food (indigestion)

ACUTE APPENDICITIS- normal appendix (7cm long x 1cm wide); derived from the cecum- usually lies along anterior surface of cecum, but position is variable leading to difficulties in dx of appendicitis

Acute appendicitis - inflammation of the appendix - primary event is obstruction of the appendiceal lumen by fecalith (67%), inflammation, foreign body or neoplasm → ischemia, 2nd bacterial infection- recent studies: ulceration of mucosa is initial event

Sx: pain: initially, periumbilical &/or epigastric pain → soon localized to RLQ at McBurney’s point, anorexia, in some case N/V- localized abd pain on coughing , light percus- abd tenderness w/in Sherren’s triangle (formed by umbilicus, right ASIS, symphysis pubis), rebound tenderness- low-grade fever (37.7-38.3)

Variability dt position of appendix:Retrocecal appendix: pain and rigidity of abdomen is lessPelvic appendix: if located low, abd wall is not rigid urinary frequency, diarrhea rectal exam will cause pain & inflamed appendix felt as fullness or mass

With rupture: generalized peritonitis diffuse rigidity and tenderness distention and ↓ abd sounds abscess formation win /localized mass &

tenderness can be found

Dx: based on clinical s/sx- (+) Rovsing’s sign, psoas sign, obturator sign- leukocytosis; absence of leukocytosis present in some cases; ↑↑ leukocytes indicates a risk for perforation

DDx:1) Meckels diverticulum: clinically mimics acute appendicitis

INFLAMMATORY BOWEL DISEASE (IBD)

- a motility disorder involving the whole GIT- chronic, non-specific disorder of unknown cause

- MC GI dis in practice; women > men- Upper and lower GI sx from abnormal intestinal motility & spasms, ↑ visceral sensitivity to certain foods

Pathogenesis: genetic predisposition, disturbed immune regulation, certain infectious dis, cigarette smoking

3 major clinical manifestations: abdominal pain (LLQ) diarrhea rectal bleeding

Sx: recurrent abd pain, altered freq of defecation w/ constipation & diarrhea, sense of incomplete evacuation, abd distention after eating, pain > BM, ↑ flatus characteristic passage of mucous

NB: sx almost always occur on waking, < stress or indigestion, sx are variable depending on whether inflam is acute/ chronic, mucosal/transmural, & if it involves the SI/LI

Physical exam: significant abd tenderness & distension unusual; sigmoid C tender & full on palpation

Dx: (made by exclusion) chronic intermittent nature of sx w/ out obvious signs of physical deteriorat’n; relation of sx to env or emotional stress- sigmoidoscopy: reveals prominent vascular pattern, mm spasms, excess normal looking mucous- colonoscopy to exclude inflame or neoplasm- barium enema may reveal spasticity of sigmoid & accentuated haustra

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

DDx:- parasites, candida, diverticular dis, infectious diarrhea, lactose/food intol, celiac, tumour/neoplasm

Tx: exercise, diet mod, dietary fiber w/ spastic colon & constipation

CROHN’S DISEASE - alternating areas of normal & involved mucosa w/ transmural inflammation – “skip lesions”- may occur anywhere in GI tract (from buccal mucosa to colon)- Crohn’s of the small bowel: “regional enteritis”

- ileum involved most often- granulomatous disease- longitudinal, deep ulcers

Complications of transmural inflm: fistula formation: 1. enterocolonic – btwn

diff parts of GI, 2. enterovesical – adjacent hollow viscus, 3. colovaginal, 4. enterocutaneous (btwn GI & skin)

stricture formation 2° to scar format’n bowel obstruction & intraabd abscess

- periods of exacerbation & remission

Sx:Pain: colicky, steady, often in RLQ (ileum), ↑ after meals; not relieved by defecation (in contrast to IBS)- tender mass in RLQ- diarrhea, steatorrhea, occult blood, melenaOther features: systemic symptoms: fever, weight loss, malaise, anorexia intestinal obstruction (25%), massive GI bleeding (2-3%) pseudopolyps uncommon, anal fistula & perirectal abscess common

Extraintestinal manifestations: anemia hepatobiliary disorders increased risk of gallstones peripheral arthritis, ankylosing spondylitis skin problems: erythema nodosum pyoderma gangrenosum (deep ulcerat’n w/ necrotic center) oral lesions – apthous ulcers, stomatitis ocular problem: iritis, episcleritis, uveitis → blurred vision & H/A

Dx:- based on clinical sx w/ findings of ulcerations, long strictured segments (string sign), & skip lesions; - colonscop, biopsy shows granulomas formationXray: cobblestone appearance d/talteratn in ulcers & mucosa

DDx: 1)IBS has abd pain, diarrhea, bloating, but symptoms are more prolonged w/absence of bleeding

2)Xray: deep ulcerations, long strictured segments, skip areas – incontrast to UC & other inflamm conditns3) UC: shallow ulcers, dilation of colon4)Colonoscopy: inflm in contrast to IBS

Tx: anti-inflm, B12 inj, supplemental Vit D, Ca ; anti-diarrheals, probiotics, bowel rest w/ IV fluid; surgery may be necessary for obstruction, fistulas, perforation, growth retardation in children; responds poorly to surgery

ULCERATIVECOLITIS

* see chart in notes pkg 7 page 27 – DDx btwn UC & Crohn’s

Chronic, relapsing inflammatory disorder of rectum and colon

Etiology, pathogenesis similar to Crohn’s

Pathology: microabscesses of the crypts of Lieberkuhn (70%); shallow lesions - inflammation is limited to mucosa & submucosa (Crohn’s = long, deep lesions that are transmural)- confined to rectum and sigmoid colon- continuous lesions, beginning at rectum (Crohn’s has skip lesions)

Sx: bloody diarrhea (more pronounced in Crohn’s)- pain > defecation (aot Crohns – pain not relieved by defecation)- pseudopolyps common- anal fistula & perirectal abscess uncommon- wt loss, fever, LLQ cramping pain- nocturnal passage of a small volume of blood and mucus- abd may or may not be tender- severe anemia dt bleeding

Complications- ↑ risk of colon CA depending on duration & extent of dis; severity not a risk factor- **Toxic megacolon: pt presents w/ fever, tachycardia, anemia, leukocytosis, abd pain;

Dx: clinical s/sx; exclusion of infectious diarrhea, parasites, neoplasm; stool exam shows mucous, bld & WBC- Rectal sigmoidoscopy: friability, edema, hyperemia of mucosa & ulcerations; biopsies must be taken- Barium enema CI in severely ill or toxic pts dt risk of perforation

DDx: 1) IBS: stool of IBS has inflammatory changes & mucus is abnormal

2) Crohns: inflm is transmural as opp to UC (inflm in crypts of lieberkuhn); discontinuous skip lesions (UC has continuous ulceration confined to colon);

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

mid-transverse colon dilated to <6-7cm; perforation & peritonitis may follow- pericholangitis

pseudopolyps uncommon, anal fistula & perirectal abscess common

3) Infectious diarrhea & parasites: stool sample

Tx: (similar to Crohn’s) surgery is indicated for toxic megacolon **, ileoanal anastmosies, massive hemorrhage, carcinoma

ACUTE DIARRHEA

Condition Age Signs & Sx Clinical Dx & Lab Dx

Viral or Bacterial Gastroenteritis

- All ages - abrupt onset, lasts > 1wk; fever, N/V- crampy abd pain- may lead to severe dehydration in children

- stool culture, CBC

Rotavirus - MC < 3 yrs - vomiting, fever- no pain

- peak incidence in winter

Salmonella, Shigella - MC 1-4 yrs - vomiting, abd pain- high fever

- stool culture

Pseudomembranous colitis - hx of ABC usage (eg Clinamycin) - severe colitis w/ pseudomembrane formation- life threatening diarrhea

- Clostridium difficile super infection seen asstd w/ clindamycin use

Laxative use - usually seen in women - mm weakness, lassitude - stool culture for NaOH for phenolphthalein- barium enema- lytes for hypokalemia

Toxins: Clostridium botulism Staphylococcus

- All ages - severe vomiting & diarrhea 2-4hrs after eating contaminated food (meat, dairy)- neurological sx (diplopia, dysarthria, dysphagia, paralysis)

- bioassay of toxins in bld, stool, food- bld & T culture- leukocytosis, thrombocytosis

Dysentary syndrome - hx of prior good health - gastrointestinal sx only- acute, watery diarrhea (may contain bld & mucous)- abd cramps, HA, N/V, fever, malaise

- stool examination for WBC (+) send for stool culture- high fever bld culture

CHRONIC DIARRHEA

IBS - most common cause of chronic diarrhea- MC in young women; high stress individuals

- intermittent D alternating w/ constipation- mucous in stool- incomplete evacuation- < morning asstd w/ urgency

- tender abd to palpation- abd distention, gas

Crohn’s & UC - Adults & children - 1st episode lasts 2wks w/potential recurrence in following weeks & months- wt loss, bloody stools, fever, arthralgia, anemia- inability to gain wt in children

- proctoscopy, colonoscopy, GI radiographs

Lactase Deficiency - infants <1yr- African/Mediterranean decent

- flatulence, vomiting, anorexia- failure to thrive in children

- lactose intolerance test- mucosal biopsy

Diabetes - neurological sx - fasting bld GLU- colony count of gastric contents

Giardiasis - hikers & campers - acute/gradual onset of 1-3wks; may persist - microscopic stool analysis & duodenal

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

for wks to months- ↑ flatulence, foul smelling, explosive, watery diarrhea- mucous in stool- anorexia & wt loss

aspirate for giardia

TUMOURS OF THE SMALL & LARGE INTESTINE

BENIGN TUMORS OF THE SMALL INTESTINE

adenomas, lipomas, leiomyomas - Peutz-Jeghers syndrome: polyposis of SI

Complications:- GI carcinoma before age 40- ↑ risk for extraintestinal carcinomas

Sx: - polyps appear firm and lobulated, 2-3cm in diameter; pedunculated or sessile- m/b associated w/ obstruction or bleeding but are mostly asymptomatic- mucocutaneous pigmentation (perioral skin, lips, buccal mucosa, hands, feet)

MALIGNANT TUMORS OF THE SMALL INTESTINE *rare

Types of tumours adenocarcinomas (duodenal) carcinoid tumors (appendix, ileum) - carcinoid tumours grow v. slowly pt may live for years even if metastatic lymphomas (appendix & ileum) leiomyosarcomas

most common primary small bowel tumor is symptomatic carcinoid, found in appendix may be metastatic from breast, KI, ovaries/testes, melanomas endocrine cell tumors neuroendocrine neoplasms pts almost always have extensive LIV metastasis

Sx: bleeding, bowel obstruction, malabs- Carcinoid syndrome: caused by prod of vasoactive amines (serotonin, histamine, bradykinin) by tumour; sx: cutaneous flushing, cyanosis, diarrhea, abd pain, wheezing

Tx: surgery, poor prognosis

BENIGN TUMORS OF THE LARGE BOWEL

adenomatous polyps precursors of adenocarcinoma ↑ risk when polyps are larger than 2cm, villous vs tubercular, sessile vs pedunculated

Sx: rectal bleeding; large polyps may cause sx of abd obstruction

Dx: barium enema, endoscopy of colonTx: surgery

FAMILIAL POLYPOSIS

multiple adenomas w/in the colon multiple adenomas carpet the colon lesions usu <1cm in diameter w/ tubular histology

Gardner’s syndrome: when osteomas or soft tissue tumors are present by time sx occur, 2/3 pts developed carcinoma

Tx: if colonectomy not performed → adenocarcinoma by age 40

MALIGNANT TUMORS OF LARGE BOWEL:

ADENOCARCINOMA OF THE COLON

- 98% of all colorectal carcinomas Risk factors: Hx of adenomatous polyps UC > Crohn’s familial polyposis hx of other malignancy fam hx of colon CA in 1st ° relative

Strong positive associations: high animal fat consumption (red meat) low fiber consumption obesity ethanol refined sugar cigarette smoking

Metastasis usu involves LIV; however, bone, LUs, and brain also m/b affected

Sx: asymptomatic symptomatic: sx vary depending on location and sizeMC symptoms: GI bleeding (m/b occult, associated w/Fe def anemia) change in bowel habits abdominal pain anorexia/weight loss (advanced) external palpation of abd, or digital exam, may feel mass

CANCER OF THE ANUS & - once symptomatic, prognosis is poor Sx: painless, inconsistent rectal bleeding, Dx: anoscopic exam; if cause of bleeding

Disease Definition Etiology, Pathogenesis & Complications

Signs & Sx Dx & DDx

RECTUM - survival rate: identified in early stage (95% 5yr), metastatic stage (<10% 5yr)

palpable internal/external mass, may have ulcers, polyps, verrucous warts

not identified, further testing req

**High incidence of colorectal CA in pts w/ rectal bleeding

Tx: surgery

COLORECTAL CANCER Sx: asymptomaticLeft-sided tumors: alternating D/C; ↑ risk of obstruction, bld in stool, wt loss, flat lesions that grow in “napkin ring” fashionRight-sided tumors: discomfort after eating, Fe def anemia, bld in stool, wt loss, grow as a polyploidy mass

Dx   : tests for colorectal neoplasm :- Fecal occult bld testing: sensitivity & specificity (sen & sp) 50%- Sigmoidoscopy: lower sens than barium enema & colonoscopy- Barium enema: ↑ sensitivity - Colonoscopy: gold standard

DDx: Crohn’s, UC, IBS, diverticulitis, bowel obstruction, inf’n, PID, ischemic colitis