gastrointestinal disorders chart
TRANSCRIPT
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
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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)
Disease Definition Etiology, Pathogenesis & Complications
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)
Disease Definition Etiology, Pathogenesis & Complications
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,
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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)
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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)
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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:
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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
Disease Definition Etiology, Pathogenesis & Complications
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