gastrointestinal disorders chart

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 PancreatitisAcute/chronic

diarrheaObstruction, spasm,

dilationCramping, 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


Signs & Sx Dx & DDx

DISEASES OF THE ESOPHAGUSDYSPHAGIA - subjective awareness of difficulty

swallowing dt impaired progression of matter to ST

Mechanical/Obstruction

1)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

Pre-esophageal or esophageal origin:

•solids only obstruction

•solids & liquids motor dysfunction

•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

DDx: hiatal hernia, GERD + complications (Barretts metaplasia, esoph stricture), esoph web (PVS), ring (Schatzki’s), carcinoma

Mechanical – Obstructive Disorders of the EsophagusHIATAL 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

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

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


Signs & Sx Dx & DDx

Complications:esophagitisstrictures, ulcerationsw/chronic inflammation – scarringpulmonary aspiration

Barrett’s esophagus/ Metaplasia

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 coughbloating, belching

< lying down after meal, bending over, at night or when fastingangina-like pain d/t stretching and stimulation of visceral afferent fibers of esophagusburning, squeezinghoarseness, 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 birthcorrelated 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 - inflm & ulcer formation scar - a result of GERD induced esophagitis Tx: esophageal dilation, chew


Signs & Sx Dx & DDx

Stricture **Stricture

formation stricture formation (accounts for 70-80% of strictures)- some congenitalHistological changes - edema, cellular infiltration, basal cell hyperplasia, ↑ deposition of collagen on healing

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 diverticulajust behind cricoid cartilage at approx. the upper esophageal sphincter

contains all layers of wallprolonged 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

mentobacco smokingalcoholismvit A & C deficiencylye ingestionachalasiaBarrett’s esophagus Celiac sprue

Sx: progressive, persistent dysphagia for solids

pain indicates extension of tumor beyond wall of esophagusdysphagia for liquids, cough, hoarseness, and weight loss are symptoms of advanced esophageal carcinoma

Motor – Neurological Disorders of the EsophagusAchalasia primary esophageal motility

disorder char by failure of the LES to relax & absence of esophageal peristalsiscardiospasm, 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 solidsweight 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 downneural defect accompanied by incomplete relaxation of LES similar to achalasia

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

Esophageal Tears & VaricesMallory-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


Signs & Sx Dx & DDx

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 PANCREASCongenital 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 groupsrisk factors: western diet, family hxFormation depends on:

1) Lithogenic bile production2) GB motility3) 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,

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


Signs & Sx Dx & DDx

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

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 ductsclose-space infectionusually complicated d/t bacteria than ascend from the intestine

biliary colicjaundiceshaking chills w/fever

SCLEROSING CHOLANGITIS

inflammation of hepatic bile ductprogressive narrowing of bile duct

men 3x >women pruritus

right abd painjaundicefatiguenausea

Lab Dx: elevated serum ALP, ERCP

ACUTE CALCULUSCHOLECYSTITIS

- inflammation of the GB caused by calculi

women>menassociated findings:

Hx of biliary sxfatty food intoleranceconstipation during attack

fever

jaundice not present in simple cholecystitislocal 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

Sx: pain is followed a few hours later by N/Vpatient lies motionlessvomiting does not relieve painpain is mild or severebiliary colicpain in RUQ, referred to interscapular region, right shoulderassociated w/pulmonary edema and inflammationOther symptoms

cutaneous hyperesthesia

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

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

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


Signs & Sx Dx & DDx

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 >2cmacute pancreatitis

ACALCULUS CHOLECYSTIS

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

CANCER OF GALLBLADDER

abnormal thickening of GB wallwomen 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 regionpain 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 childrenscarring

SX:Pain

in the epigastrium after eating, radiates to back < supineseveral days to week, usually relieved only by narcoticsrecurrent attacks often precipitated by alcohol excessOther features

malabsorption in association w/ steatorrhea

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


Signs & Sx Dx & DDx

and clay color, floating, bulky & foul smelling stooljaundicediabetesAssociated findings:vomiting wide-ranging tempshock w/cold clammy skintenderness in lower epigastrium abdomen is slightly rigidabdominal distention, transient adynamic ileusCullen’s sign, Grey-Turner’s sign

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 discomfortpain radiates to back, relieved by sitting up or bending kneesjaundice (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 & DUODENUMH. 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/localizedusually 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 hemorrhageepigastric burning painN/V

occult GI bleeding, when severe associated w/ hematemesis chronic bleeding anemia melena

Dx:endoscopy

H.pylori cultureserologic testing for anti-Absurease 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

prolonged use of alcohol, aspirin, etcradiation, thermal injury

infections (H. pylori)

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

Symptoms similar for Type A & B:burning epigastric paindyspepsia/indigestion

N/V

Type A sx:

Dx:endoscopyCBC (anemia)


Signs & Sx Dx & DDx

body & fundus; AI dis that leads to inflm & atrophy of mucosa; achlorhydria is diagnostic, lack of IF pernicious anemia

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

A) plasma Abs to intrinsic factor & parietal cellshypochlorydria, achlorhydria

sx of pernicious anemia (pts have few GI complaints)hypergastrinemiahypothyroidism, DM, vitiligo occur more frequently in Type AType B sx:

gastric acid level is normal/slightly reducedgastrin cell Abs

↓ gastric secretionsserum 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 secretionpersonality 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, anemiamay present only w/bleeding (melena, pallor, tachycardia, low BP)

Duodenal ulcers:pain >w/meals, but <2-3hrs after mealsweight gainpain may awaken from sleephypersalivationincreased HCl

Gastric ulcers:rarely in pts <40yoapain < 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 anemiaRisk factors: H.pylori infn, atrophic gastritis, gastric dysplasia, polypsmen > women, 60-75yrs

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

Sx:

weight loss, anorexiaepigastric painearly satiety

vomiting (

weakness & fatigue (2° to bld loss)gross GI bleedingdysphagia

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 LIVERFATTY LIVER DISEASE - excessive accumulation of lipidin

hepatocytesDiffuse fatty change:- alcoholism, obesity, diabetes

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

Dx: mild ↑ in ALP or transaminase (AST/ALT)


Signs & Sx Dx & DDx

- most common LV response to injury

- alcoholic fatty LV mb accom-panied by inflm, necrosis & permanent damage (cirrhosis)

- 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

- 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

- progresses to symptomatic alcoholic hepatits

Major Factors: - Quantity & duration of consumption- nutritional status of the pt- genetic & metabolic traits

Prognosis related to the amt of cirrhosis and LV cell necrosis

Sx:- variable clinical picture; becomes apparent in

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

Lab Dx: ↑ glutamyl transpeptidase (GGT)

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 pruritusimpaired 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,


Signs & Sx Dx & DDx

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 ptscommon coldnausea, fatigue, anorexia, loss of appetiteslight feverdiffuse muscle paindecreased desire to smoke

heaviness/fullness/discomfort in RUQ (inflamed, swollen LIV→ glyson’s capsule stretched → painascitesIn icteric phase:dark urinecutaneous 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!

Lab Dx:↑ALP

↑transaminase AST + ALT

↑ serum bilirubin

Hepatitis A RNA enterovirus fecal-oral contaminationincubation: 15-49dpresent in stool 2 weeks after infection

N & Vjaundice (50% develop)malaise, feveranorexia

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, etcIncubation: mean 70-80dPresent in blood 2 months after infections

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

HBsAg+,

IgM anti-HBc+Prior infection:

HBsAg-

Anti-HBs+

Anti-HBc+Chronic carrier


Signs & Sx Dx & DDx

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 fingersfulminant → severe LIV failure

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 commoninfreq other manifestations – porphyria cutanea tarda, cryoglobulinemia

Hepatitis D defective RNA virus occurs only in presence of Hep Bincubation: 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

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 metabolismgynecomastiaatrophic testesexcessive decrease in weightascites 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 & COLONHealthy 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)


Signs & Sx Dx & DDx

- 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

- inability to transport molecules across the intestinal mucosa

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- fibrosis dt systemic sclerosis, radiation enteritis

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 mineralization

Folic acidAbs in jejunum; ↓ abs ↓ RBC folate; Sx: glossitis, megaloblastic anemia; may see ↑ folic acid with bacterial overgrowth

Vitamin B12Def caused by terminal ileal dis; Sx: pernicious anemia; prolonged def degeneration of the spinal cord, peripheral neuropathy, dementia; Dx:

Schilling TestCHO

Sx: generalized malnutrition, wt loss, flatus; Dx: D-xylose testPRO

Sx: malnutrition, wt loss, amenorrhea, ↓ libido; Dx: measure serum albuminFAT

Sx: 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 Vatersaccular outpouchings

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

asymptomatic in most ptsrarely causes upper GI bleeding

- found during endoscopy/autopsy

Jejunal diverticula malabsorption diarrhea, bloating, distention, flatus

steatorrhea: bulky & greasy stool

Tx: surgical removal of multiple or large diverticuli


Signs & Sx Dx & DDx

anorexia (d/t build up of toxins from undigested food)glossitis (d/t vit def)

anemia; pernicious anemia + neuropathyascites & edema (protein def)osteopenia (Vit D def), osteoporosis & tetany d/t Ca def

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 ileummay 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

DIVERTICULITIS complication of diverticulosis

inflammation of diverticular sacsusually 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)


Signs & Sx Dx & DDx

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 defecateUsually 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 trainingSx: 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, depressioncerebral atrophyspinal cord injuryParkinson’ssclerodermanarcotic drugs (morphine & codeine) esp in bedridden pts

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

obstipation (constipation d/t obstruction)massive colonic dilatationrectum 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

INTESTINAL OBSTRUCTION1) Mechanical obstruction2) Non-mechanical obstruction

Mechanical Obstruction *Dynamic ileus

Extrinsic Lesions:- adhesive bands, internal & external herniasIntrinsic Lesions:

- MC causes: carcinoma, sigmoid diverticulitis, volvulus (account for 90% of cases)- extreme prolonged contraction of


Signs & Sx Dx & DDx

- carcinoma, diverticulitis, Crohns, gallstone obstruction, intus-sesception, volvulus (twisting causing obstruction)

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 tractenhanced visceral activitydysregulation of CNS function (motor, sensory)

recurrent abd pain, usually LLQaltered freq of defecation w/hard stool (constipation), or watery stool (diarrhea)sense of incomplete evacuation

feeling of abd distention after food intakeexcess flatus

tender sigmoid full w/feces may be palpated in LLQ

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

exclusion of other conditions

relation of sx to environmental and emotional stress


Signs & Sx Dx & DDx

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 rigidurinary frequency, diarrhearectal 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

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


Signs & Sx Dx & DDx

involves the SI/LIDDx:- 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:anemiahepatobiliary disordersincreased risk of gallstonesperipheral arthritis, ankylosing spondylitisskin problems: erythema nodosum

pyoderma gangrenosum (deep ulcerat’n w/ necrotic center)

oral lesions – apthous ulcers, stomatitisocular 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 conditns

3) UC: shallow ulcers, dilation of colon

4)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

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:


Signs & Sx Dx & DDx

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

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); 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 DIARRHEAIBS - 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


Signs & Sx Dx & DDx

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

- microscopic stool analysis & duodenal aspirate for giardia

TUMOURS OF THE SMALL & LARGE INTESTINEBENIGN 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, melanomasendocrine cell tumorsneuroendocrine neoplasmspts 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 - 98% of all colorectal carcinomas Risk factors:• Hx of adenomatous polyps

Sx: asymptomatic symptomatic: sx vary depending on location and size


Signs & Sx Dx & DDx

OF LARGE BOWEL:

ADENOCARCINOMA OF THE COLON

• 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

MC symptoms:GI bleeding (m/b occult, associated w/Fe def anemia)

change in bowel habits abdominal painanorexia/weight loss (advanced)

external palpation of abd, or digital exam, may feel mass

CANCER OF THE ANUS & RECTUM

- once symptomatic, prognosis is poor- survival rate: identified in early stage (95% 5yr), metastatic stage (<10% 5yr)

Sx: painless, inconsistent rectal bleeding, palpable internal/external mass, may have ulcers, polyps, verrucous warts

Dx: anoscopic exam; if cause of bleeding not identified, further testing req

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

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

gastrointestinal disorders chart

Documents

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