surgpath_2.1 the gastrointestinal tract (robbins) - table

7/27/2019 SURGPATH_2.1 the Gastrointestinal Tract (Robbins) - Table

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From 2015 2B edited by Anj. Anne. How. Jerro. Mark. Joseph. Tin Page 1 of8

II.1 Gastrointestinal TractRobbins

I. THE ESOPHAGUSA. ANATOMIC ANOMALIESDISEASE ETIOLOGY CLINICAL MANIFESTATIONS MORPHOLOGY

Atresia

CHD Other GIT malformations Incompatible with life

Portion of esophagus is replaced bythin, noncanalized cord, with blind

pouches above and below the atreticsegment

Fistula Connection between the esophagus

and the trachea or a mainstembronchus

Stenosis GERD, Caustric burns,

Radiotherapy

Congenital, Scleroderma Episodic dysphagia Esophageal wall fibrous thickening

Mucosal webs

Congenital Long-standing reflux

esophagitis

Chronic graft-vs.-hostdisease

Plummer-Vinson Syndrome:Cheilosis, glossitis, irondeficiency anemia

Episodic dysphagia UPPEResophageal muscosal

overgrowths

Esophagealrings

congenital heart disease,neurologic problems, GU orother GI malformations

Aspiration, suffocationfrom food, pneumonia,fluid & electrolyte

imbalance

Episodic dysphagia

LOWEResophageal muscosalovergrowths

A ring: if above thegastroesophageal junction

B or Schatzki ring: if at thegastroesophageal juction

Muscularis propria hypertrophy

B. LESIONS ASSOCIATED WITH MOTOR DYSFUNCTIONDISEASE ETIOLOGY CLINICAL MANIFESTATIONS MORPHOLOGY

Achalasia

inhibitory neurondysfunction

degeneration of CNS orperipheral nerves (DM,amyloidosis, cancer)

protozoal (Toxoplasma)infection of esophagealmyenteric plexus ofnerves.

Progressive dysphagia Aperistalsis Nocturnal regurgitation and

aspiration of undigestedfood.

COMPLICATIONS

Inc risk of SCC (~5%). Candida esophagitis. Aspiration pneumonia. Airway obstruction.

Proximal esophageal dilation Thickened or thinned muscular walls Regurgitation with mucosal dage

SecondaryAchalasia

Chagas disease Disorders of the vagal dorsal motor nuclei (polio, surgical ablation) Diabetic autonomic neuropathy Infiltrative disorders (malignancy, amyloidosis, sarcoidosis)

Hiatal Hernia

unknown. Rolling hernias can be

secondary to surgery.

Crura (muscles) ofdiaphragm and theesophagus are not close

enough.

COMPLICATIONS

ulceration with bleeding &perforation.

Rolling hernias can havestrangulation & obstruction.

Sliding (axial):

Shortened esophagus Traction of upper stomach into

thorax

Bell-like dilation of stomach w/in thethoracic cavity

Paraesophageal (rolling): Cardia of stomach dissects into the

thorax adjacent to the esophagus

Diverticula Outpouchings of the alimentary tract

containing one or more wall layers

ZenkerDiverticulum

disordered cricopharyngealmotor function

Dysphagia, foodregurgitation, mass in theneck

Aspiration with pneumonia UPPER esophagus


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I.5 The Thyroid Gland (Robbins) Page 2 of8

TractionDiverticulum

congenital or result ofmotor dysfunction

asymptomatic Mid-esophagealEpiphrenic

Diverticulum

discoordination ofperistalsis & lower

sphincter relaxation

Nocturnal regurgitation ofmassive amounts of fluid

Just above lower esophagealsphincter

Lacerations(Mallory-WeissSyndrome)

Episodes of excessivevomiting

Failure of LES relaxation Alcohol

Massive hematemesis Inflammation Residual ulcer Mediastinitis Peritonitis

longitudinal tears across theesophagogastric junction or in theupper stomach are mucosal orsometimes entirely through the wallwith perforation.

BoerhaaveSyndrome

Large amounts of alcohol Pressure rupture of the esophagusjust above the diaphragm

EsophagealVarices

Portal hypertension 90% of patients with

alcoholic cirrhosis haveesophageal varices.

Schistosomiasis

no symptoms until rupturewith hematemesis

90% chance of recurrence

Tortuous, dilated veins in distalesophageal submucosa/mucosa.

Irregular luminal protrusion ofoverlying mucosa

Superficial ulceration, inflammation,adherent blood clots

C. ESOPHAGITISDISEASE ETIOLOGY CLINICAL MANIFESTATIONS MORPHOLOGY

Reflux

Esophagitis

antireflux mechanisms

Sliding hiatal hernias Delayed gastric emptying

and gastric volume

the esophageal mucosa

In adults Dysphagia Heartburn Regurgitation of gastric

contents in the mouth

Hematemesis Melena Stricture or Barrett

esophagus

Hyperemia and edema

Thickened basal zone & thinning ofsuperficial epithelial layers

Neutrophil or eosinophil infiltration Superficial necrosis and ulceration

with adherent inflammatory exudate

BarrettEsophagus

long-standinggastroesophageal refluxdisease (GERD).

In adults may lead to adenocarcinoma

Gross: irregular circumferentialband of red, velvety mucosa at thegastroesophageal junction, withlinear streaks or patches of similar

mucosa in the distal esophagus

Microscopic: Normal squamousmucosa of distal esophagus replaced

by metaplastic intestinal-likecolumnar epithelium

Infectious andChemicalEsophagitis

Causes:

Prolonged gastric intubation Ingestion of irritants: alcohol corrosive acids or alkalis, excessive hot fluids, smoking Bacteria, viral (Herpesvirus, CMV) or fungal (candidiasis, mucormycosis, aspergillosis) infection Uremia, Chemo- or radiotherapy, Graft-vs-host disease, Autoimmune diseases, Chron disease Systemic desquamative disorders (pemphigoid, epidermolysis bullosa)

II. THE STOMACHA. CONGENITAL ANOMALIES

DISEASE ETIOLOGY CLINICAL MANIFESTATIONS MORPHOLOGY

Pancreaticheterotopia In the gastric muscle wall

DiaphragmaticHernia

Weakness of thediaphragm

Fatal if with respiratoryimpairment with pulmonaryhypoplasia

In utero displacement of thestomach cephalad

Pyloric Stenosis Male to female ratio 4:1 Hypertrophy or hyperplasia of pyloric

muscularis propria

Visible peristalsis Palpable firm ovoid mass

B. GASTRITIS

Acute Gastritis

NSAIDs, EtOH, tobacco,stress, uremia,chemotherapy, ischemia,radiation, systemic

infections.

Gross: edema and hyperaemia,acute hemorrhagic erosive gastritis

Microscopic: neutrophil invasion,erosion

ChronicGastritis

H. pylori colonization ofmucosa EtOH, tobacco,post-surgical, obstruction,Crohn disease

Gross: reddened, boggy, coarse-textured mucosa Histologically: Lymphocyte and plasma cell infiltrate in lamina propria Intraepithelial neutrophilic infil8s Mucosal gland atrophy Metaplasia of surface columnar epithelium to intestinal-type Dysplasia in long standing C. Gastritis


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C. PEPTIC ULCER DISEASE

Peptic Ulcer exposure to acid and pepticjuices

Epigastric gnawing, burning,or aching pain, worse atnight and 1-3 hrs after

meals.

Nausea, vomiting, bloating,belching, weight loss

COMPLICATIONS:Hemorrhage, perforation,peritonitis, scarring

Gross: sharply punched-out defectwith overhanging mucosal borders;smooth, clean ulcer bases

Microscopic: necrotic debris;granulation tissue; deep scarring

Acute GastricUlceration

Severe stress shock,extensive burns, severtrauma (Curling ulcers)

ICP (Cushing ulcers) NSAIDs

Acute gastric erosions orulcers

Ulcers less than 1cm in diameter Ulcer base is brown (blood)

D. MISCELLANEOUS CONDITIONS

Gastric Dilation

Gastric outlet obstruction(pyloric stenosis, tumors)

Gastric and intestinal atony(ileus)

Rarely, gastric rupture

Bezoars Phytobezoar trichobezoar (hairball) Luminal concretions

Eosinophilicgastritis

Heavy eosinophilicinfiltration of the mucosaor submucosa

Idiopathic; AllergyHypertrophicGastropathy

Hypoalbuminemia risk for PUD Protein-losing enteropathy

Hyperplasia of mucosal epithelialof gastric rugal folds

Menetrierdisease

TGF- overexpression (?) Hypochlorydia Hypoproteinemia

Hyperplasia of surface mucous(foveolar) cells

Fundic gland atrophyHypertrophic-

hyper-

secretorygastropathy

Hyperchlorydia Hyperplasia of parietal and chiefcells (fundic glands)

Gastric Glandhyperplasia

Excessive gastrin secrxn Gastrinoma (Zollinger-

Ellison) Hyperchlorydia Parietal cell hyperplasia

Gastric Varices In portal hypertension Occurs near the gastroesophagealjunction

III. SMALL AND LARGE INTESTINESA. CONGENITAL ANOMALIES


MeckelDiverticulum

Blind pouch leading off thealimentary tract, lined by mucosaand communicating with the gutlumen

CongenitalAganglionicMegacolon\(HirschsprungDisease)

Arrested (proximal todistal) migration of neuralcrest cells into the gut

Assoc with Down syndrome

Male female ratio 4:1 Neonatal failure to pass

meconium or abdominaldistention

Risk: perforation, sepsis,enterocolitis

Absence of ganglion cells andganglia in muscle wall andsubmucosa of affected segment(usu. Rectum)

AcquiredMegacolon

Occur in Chagas disease, bowel obstruction, inflammatory bowel disease, and psychosomatic disordersB. ENTEROCOLITISDiarrhea >250 gm daily stool production with 70%-90% water Dysentery low volume painful diarrhea Secretory

diarrhea Net intestinal fluid secretion >500 mL/day; isotonic with plasma; persists during fasting

Osmoticdiarrhea >500 mL stool/day; osmotic gap

Malabsorption Voluminous, bulky stools w/ excess fat and osmolality Exudative

diseases Purulent bloody stools

Infectious Enterocolitis

Viral Entercolitis

Rotavirus; Calicivirus

(Norwalk/Norwalk-likevirus, Sapporo-likevirus);

Enteric adenoviruses; Astroviruses

Acute illness: 1-7 days Diarrhea, anorexia, fever,

headache

Shortened villi lamina propria inflammation enterocyte amage (brush border

loss & cytoplasmic vascuolization

crypt hyperplasia


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D. IDIOPATHIC INFLAMMATORY BOWEL DISEASEDISEASE ETIOLOGY CLINICAL MANIFESTATIONS MORPHOLOGY

Chron Disease

Genetic Infectious Mucosal integrity Abnormal host

immunoreactivity

Intermittent attacks of diarrhea,fever, abdominal pain, anorexia,weight loss

Migratory polyarthritis, sacroiliitis,ankylosing spondylitis, erythemanodosum, uveitis, cholangitis,

Non-caseating sarcoid-likegranulomas

Transmural inflammation Goblet cell population Maintenance of gladular architecture Skip lesions

BacterialEnterocolitis

Ingestion of preformed Infection w/ enteric

Explosive diarrhea & abdpain

Hrs-days incubation;diarrhea; dehydration;

dysentery

Yersinial & mycobacterialinfections

Antibiotic-Associated Colitis

(Pseudomem-branousColitis)

Clostridium difficile toxinovergrowth afterantibiotic therapy

Right colon plaquelike adhesionof fibrinopurulent necrotic, gray-yellow debris and mucus to thedamaged colonic mucosa

ParasiticEnterocolitis

Nematodes, Cestodes,Protozoa

NecrotizingEntercolitis

Immature gut immunity Onset of oral feeding Bacterial colonization Mucosal injury Impaired intestinal blood

flow

In low-birth-weight orpremature neonates

Mild diarrhea to fulminantillness with gangrene,perforation, sepsis, shock

Mucosal edema, hemorrhage,necrosis in terminal ileum andproximal colon or entire gut

Collagenous Colitis Chronic watery diarrhea

with abdominal pain

Patches of bandlike collagen underthe surface epithelium

Lymphocytic Colitis Autoimmune disease,sprue

Intraepithelial infiltrates oflymphocytes

Miscellaneous Intestinal Inflammatory Disorders

AIDS-associateddiarrheal illness

HIV In mucosal epithelium Transplantation Mild lymphocytic infiltrate

Crypt epithelial cell apoptosis Drug-induced

interstinal injury NSAID Focal ulceration

Mucosal inflammation Radiation

enterocolitis Inflammatory diarrhea

Neutropenic colitis(Typhlitis)

Bone marrow transplant Acute inflammatory destruction ofthe cecal region

Diversion colitis Enterostomy Inadequate nutrition

Chronic lymphoplasmacyticinflammation

Lymphoid follicular hyperplasia Colitis cystic

profunda solitaryrectal ulcersyndrome

Rectal bleeding Mucosal discharge

Acute angulation of anterior rectalshelf

Mechanical abrasion Distorted, cystically dilated glands

surrounded by proliferatingsmooth muscle cells

C. MALABSORPTION SYNDROME

MALABSORPTIONSYDROME

Defects in:

Intraluminal digestion Terminal digestion Transepithelial transport

Diarrhea, flatus, pain, weight loss, bulky,frothy,greasy stools Anemia, bleeding Ostopenia, tetany Amenorrhea, impotence, infertility, hyperparathyroidism Purpura and petechiae, edema, dermatitisPeripheral neuropathy

Celiac Disease

Gluten in wheat, oat,barley, rye

Diarrhea, flatulence, weightloss, fatgue

Antibodies to tissuetransglutaminase and

gliadin Dermatitis herpetiformis COMPLICATIONS: iron

and vitamin deficiencies;risk for GI lymphoma

marked atrophy of villi elongated regenerative crypts surface epithelial damage with

intraepithelial lymphocytes exuberant lamina propria chronic

inflammation

Tropical(Postinfectious) Sprue

Travel or habitationexposure

Villous blunting Abundant lymphocytes and

eosinophils in lamina propria

Whipple Disease Tropheryma whippelii Diarrhea, steatorrhea,

malabsorption, abdominalcramps, distention, fever,weight loss, migratoryarthritis, heart disease

In whites and males

mucosa becomes laden w/distended macrophages in thelamina propria

(+) PASLactase Deficiency Diarrhea; malabsorption No abnormalities of mucosaAbetalipo-proteinemia

Cannot synthesizeapolipoprotein B

Failure to thrive, diarrhea,steatorrea, neurologic andliver disorders, retinitispigmentosa

Lipid vacuolation Burr cells


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amyloidosis

COMPLICATIONS: fistulas,malabsorption, malnutrition,protein-losing enteropathy

Risk: bowel cancer

cobblestone appearance aphthous ulcers Chrronic mucosal damage; fibrosis;

dysplasia

UlcerativeColitis

Intermittent attacks of bloodymucoid diarrhea;abd pain

Toxic megacolon Migratory polyarthritis, , sacroiliitis,

ankylosing spondylitis, erythemanodosum, uveitis, cholangitis

Risk: carcinoma

Non-granulomatous No skip lesions Mucosa reddened, granular or friable

iwth inflammatory pseudopolyps andeasy bleeding

E. VASCULAR DISORDERSDISEASE ETIOLOGY CLINICAL MANIFESTATIONS MORPHOLOGY

Ischemic BowelDisease

Arterial thrombosis Arterial embolism Venous thrombosis Nonocclusive ischemia

Severe abdominal pain Bloody diarrhea Gross melena Nausea Vomiting Bloating Abdominal wall rigidity

Mucosal infarction: patchymucosal hemorrhage

Mural infarction: completemucosal necrosis

Transmural infarction: suddenand total occlusion of majorvasculature; gangrene, peforation

Venous thrombosis: acutemesenteric venous occlusion

Chronic ischemia: mucosalinflammation, ulceration, fibrosis,stricture

Angiodysplasia Tortuous abnormal dilations of

submucosal veins to lamina propriaof cecum or ascending colon

Hemorrhoids

Constipation Venous stasis during

pregnancy

Cirrhosis (portal HPN) Variceal dilations of anal and

perianal submucosal venous plexi

DiverticularDisease Focal bowel wall weakness

Usu asymptomatic Cramping, abd discomfort,

constipation COMPLICATION: pericolic

abscesses, sinus tracts,peritonitis

Multi flask-like outpouchings

F.INTESTINAL OBSTRUCTIONDISEASE ETIOLOGY CLINICAL MANIFESTATIONS MORPHOLOGY

Hernias Peritoneal wall weakness or

defect

Hernia sac

Incarceration

Adhesions Peritonitis following

surgery, infection,endometriosis, radiation

Complications: internalherniation; obstruction;strangulation

Fibrous bridging between viscera

Intussusception Children rotaviral

vaccination or infection

Adults tumor Telescoping of one intestinal

segment into immediately distalsegment

Volvolus Obstruction and infarction Twisting of a bowel loop about itsmesenteric vascular base

IV.APPENDIX

AcuteAppendicitis

Obstruction of appendiciallumen by fecalith, calculus,

intraluminal pressureischemia bacterialinvasion

Periumbilical pain migratingto RLQ

Nausea or vomiting Abdominal tenderness Mild fever Leukocytosis >15,000

cells/mm3

Early: scant appendicial wall neutrophil

exudates

congestion of subserosal vessels perivascular neutrophil emigration Advanced/Acute suppurative: Severe neutrophilic infiltration Fibrinopurulent serosal exudates Luminal abscess formation Ulceration Suppurative necrosis

Mucocele

Innocuous obstruction withinspissated mucus

Mucin secreting adenomas Adenocarcinoma

Dilation of appendiceal lumen bymucinous secretions

Pseudomyxomaperitonei

Peritoneum distended Tenaceious semisolid, mucin-

producing anaplastic


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adenocarcinoma cells

V.PERITONEUMA. INFLAMMATION


1. PeritonealInfection

Appendicitis, peptic ulcer,cholecystitis, diverticulitis,bowel strangulation, acutesalpingitis, abd trauma,peritoneal dialysis,nephritic syndrome,cirrhosis

Can resolve spontaneously orwith therapy

Peritoneal membranes dull andgray; exudates and franksuppuration

Localized abscesses Tuberculous peritonitis exudates

studded with minute palegranulomas

2. SclerosingRetroperitonitis

Methydergide use Fibrosing disorders

(carcinoid tumors,sclerosing cholangitis,Riedel fibrosing thyroiditis)

Hydronephrosis Dense infiltrative fibrosing

overgrowth of retroperitoneal tissues

Lymphocyte, plasma cell, neutrophilinfiltrate

3. MesentericCysts

Arise from sequestered lymphatic channels, pinched-off enteric diverticula of developing foregut orhindgut, developmental cysts of urogenital orgin, pancreatic pseudocyts, or walled-off infections

B. TUMORS

Primary tumors

MesotheliomaDesmoplastic small round cell tumor

Secondary tumors

TUMORS OF THE GASTROINTESTINAL TRACT

ESOPHAGUS

1. Benign Tumors:a. Intramural or submucosal: Leiomyoma, fibroma, lipoma, hemangioma, neurofibroma, lymphangiomab. Mucosal (larger than 3cm): Squamous papilloma, Fibrovascular polyp, Inflammatory polyp2. Malignant TumorsDISEASE ETIOLOGY CLINICAL MANIFESTATIONS MORPHOLOGY

Squamous CellCarcinoma

(SCC)

Dietary,Lifestyle,Esophageal

disorders,GeneticPredisposition

Adults older than 50 years More often in men and blacks Dysphagia Obstruction Weight loss Hemorrhage Sepsis Respiratory tree fistulas with

aspiration

Gross: lesions may be polypoid (60%),exhibit necrotizing excavation (25%), ordiffusely infiltrative (15%)

Microscopic: tumors well differentiated,with or w/o keratinisation

Begin as in situ gray-white, plaquelikelongitudinally/circumferential

Adenocarcinoma Barrett

esophagus

Patients older than 40, moreoften in men

Symptoms of GERD and SCC

Gross: exophytic nodules to excavated anddeeply infiltrative masses

Microscopic: mucin-producing glandulartumors with intestinal futures; Diffuselyinfiltrative signet ring cells

STOMACH

1. Benign Tumorsa.Non-Neoplastic Polyps


Hyper-plastic orinflammatorypolyps

Assoc with chronicgastritis

90% of gastric polyps Smooth, sessile or pedunculated Epithelial tubules and cysts

interspersed

Inflamed stroma Fundic gland

polyps Occur with FAP Fundic gland dilation

Inflammatoryfibroid polyps

Fibroblast proliferation insubmucosa with eosinophil infiltrate

Hamartomatouspolyps

Occur with Peutz-Jegherssyndrome or;

Juvenile polyposissyndrome


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II.1 The Gastrointestinal Tract (Robbins) - TransPage 7 of8

b. NeoplasticPolyps GastricAdenoma

Chronic gastritis Genetic polyposis

syndrome 40% harbour carcinoma Proliferative dysplastic epithelium Single, can be sessile or

pedunculated

2. Malignant

GastricCarcinoma

Environment; Diet;Smoking; chronic gastritis;autoimmune gastritis;

partial gastrectomy

Usu. Asymptomatic Weight loss, abdominal

painm, anorexia, vomiting,altered bowel habits,

dysphagia, anemia,hemorrhage

Gastric mucosa dysplasia Tumors are exophytic, flat, or

depressed or excavated

(See Lauren classification) Lymphoma

(MALT) H. pyloriinfection

Gastrointestinalstromal tumor(GIST)

c-KIT gene mutation Solid tumor of the gastric mucosa or

wall

Tumor cells are either epithelioid orspindle cell shaped

CarcinoidTumors

Enterochromaffin-like cell tumor Schwannomas Lipomas

TUMORS OF THE SMALL INTESTINEDISEASE ETIOLOGY CLINICAL MANIFESTATIONS MORPHOLOGY

Adenomas In Px with familial

polyposis syndromes

Clinically silent unless theyobstruct the intestinal lumenor CBD

Adenocarcinoma Obstruction (cramping pain,

nausea, vomiting), weightloss, bleeding

Metastatic spread to mesentery,regional lymph nodes, liver

TUMORS OF THE COLON AND RECTUM

1. Benigna. Non-neoplastic polyps

DISEASE ETIOLOGYCLINICAL

MANIFESTATIONSMORPHOLOGY

Hyperplasticpolyp

6th decade Nipple like hemispheric protrusions Well-formed mature glands with crowding

Juvenile polyp Children


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a. CarcinoidTumors

Asymptomatic butSx caused bytumor secretoryproducts

Tumors are small, firm, yellow-tan intramural orsubmucosal masses

Fibrosis of muscularis kinking and obstruction Microscopic: islands to sheets of uniform chohesive

cells with scant, granular cytoplasm and oval,stippled nuclei

(+) for chromogranin and synaptophysin

b. Gastro-intestinalLymphoma

Amenable tosurgical resection;chemoresponsive

Early lesions: plaquelike mucosal or submucosalexpansions

Advanced: full mural thickness or polypoidexophytic masses protruding to lumen Microscopic: atypical lymphocytes infiltrate

c. Mesenchymal Tumors Lipomas (Most common GImesenchymal

tumor) Asymptomatic Larger lesions:

mucosalulcerations withbleeding,obstruction, orintusseption

In SI or colon submucosa GIST Spindle shaped ore epitheloid; c-KIT positive Smooth muscle

tumors Spindle shaped lesions with smooth muscle

phenotype

Kaposi Sarcoma Visceral involvement

surgpath_2.1 the gastrointestinal tract (robbins) - table

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