Int-dx Ii_2001

1 09.01.2001

INTERNAL DIAGNOSTIC II EXAMINATION PROCEDURES Patient Evaluation  Exam procedures on Abdominal  Concentrate on chief complaint

A. History 1. 2. 3. 4. 5.

Weight loss: 6-10% body weight in 6 month w/o diet Vomiting blood Blood in stool: frank blood, black tarry Low back pain that is not relieved Abdominal pain acute  Abdominal rigidity  sign of Peritonitis, involuntary muscle spasm  Guarded Abd = belly pain = voluntary 6. Jaundice

B. Physical Examination 1. 2. 3. 4.

Inspection Auscultation Palpation Percussion

C. Radiographic Examination  Standard examination: KUB – kidney, ureter, bladder (Plain film radiographic evaluation of the abdomen). Upright or Supine. Look for air, fluid  1. 2. 3. 

In addition can add contrast: BOSO4 (Barium sulphate): Barium swallow (only esophagus) Swallow = upper GI (esophagus, duodenum, etc.) Barium upper GI w/ follow through (follow through the small intestine) Barium enema (other end)  single contrast or double contrast (barium and air)

 CT (for cavities - hollow)  Magnetic Resonance Imaging (for solid viscera)  Ultrasound (sonogram) – not particularly specific, best use in finding free fluid, stones in gallbladder  Endoscopy (fiberoptic scope)  Laparoscopy: form of endoscopy (go through the abdominal wall)  Manometry (measures pressure) - dx DES – diffuse esophageal syndrome

2  Laboratory evaluation (blood, urine, feces)

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A. HISTORY    

A good history is of extreme importance in obtaining an accurate diagnosis 80% of the diagnosis is made from history alone 90% of the diagnosis is made from history and physical examination Only 10% of the time are special diagnostic procedures required to establish the diagnosis 16.01.2001

HISTORY: General Considerations  Nutrition: food intake, weight gain (thyroid dz, endocrine dz, diabetes, etc.) or loss (malignancies) (5-10% of body weight w/in 6 months w/out trying to lose weight)  Medications (side effects, interfere w/ absorption of certain nutrients, can also be associated w/ aggressive GI infection)  Alcohol intake (prominent effect on GI, and GU dz)  Pregnancy (Gravida = how many times been pregnant, Para = # of live births, Aborta = # of elective or spontaneous abortions)  Stool characteristics (color, consistency, smell, frequency, blood, texture, bowel movement (BM), pain w/ defecation, frequency, food digested or not, buoyancy = fat in stool  floats)  Urinary characteristics (color, appearance: clear, cloudy, etc., frequency: pain?, smell  sweet  ketones, incontinence, dysuria = pain, oliguria = some)  Stressful like events  Recent infectious diseases  Trauma (seatbelt injuries, car accidents, etc.)

HISTORY: Chief Complaints  GI symptoms:  Abdominal pain (OPPQRST) • Crampy abdominal pain assoc w/ obstruction or poor peristalsis in a hollow tube, Distension causes the pain  Indigestion (aka Dyspepsia = Heartburn)  Nausea (Associated w/ every GI disorders • Nausea center located in …….. FIND OUT ! • Reversed peristalsis  Diarrhea (frequent liquid stools) • Viral gastroenteritis  Constipation (decrease in the volume of stools)  Fecal incontinence (cause: aging, stroke, spinal cord dz, cauda equina syndrome, etc.)  Jaundice (yellow skin, ↑ of bilirubin in the blood, Itching)

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HISTORY: Chief Complaints  GU symptoms:  Dysuria (painful urination)  Urinary frequency (increase – polyuria or decrease – oliguria)  Urinary incontinence (m/c cause = aging)  Hematuria (blood in the urine) • 2 types: 1. frank blood = macroscopic, 2. microscopic  Chyluria (milky urine) • Often sign of pus

B. PHYSICAL EXAMINATION  The abdomen is divided into four quadrants:  Right upper quadrant  Left upper quadrant  Right lower quadrant  Left lower quadrant  And nine regions: (best to use)  1. epigastric  2. umbilical  3. hypogastric (suprapubic)  4 & 5 right and left hypochondriac  6 & 7 right and left lumbar  8 & 9 right and left inguinal 4 6 8    

1 2 3

5 7 9

LLQ: m/c for abdominal pain because of constipation also ulcerative colitis, diverticulosis, irritable bowel syndrome RLQ: appendicitis m/c, Crohn’s dz, ulcerative, ovarian, genital LUQ: gastritis, splenic infarcts, hiatal hernia, kidney RUQ: liver, gallbladder, ulcerative colitis

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Parts of an abdominal exam (Should be done in this order – not to induce bowel sounds)

1.         

Inspection

Scars Striae (stretch marks: purple, blue, silver, brown) Lumps, bumps, moles Contusions (symmetry) Hernias Distension Visible Peristalsis Visible Pulsation Caput Medusa: radiating spicules of veins emanating from umbilical region

2. Auscultation    

Bowel sounds (5-30 / min) Borborygmus Bruits (turbulence inside a hollow tube, over arteries = bruit, veins obstructed = venous hum) Peritoneal Friction rubs (sound like hair rubbed b/w fingers)

3. Percussion  Percussion notes: Tympany (over hollow viscus), Hyper tympanic (abnormal, over distended area), Dull (over solid organs: liver, spleen, full bladder), Can also measure the organs (liver, spleen)

4.

Palpation      

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   

Masses (mobile, soft, hard, painful, pulsation) Rigidity (= involuntary spasm of the abdominal mm., sign of peritonitis) Guarding (= not a good sign, Pt doesn’t want you to touch the area) Fluid, Fluid wave Hepatomegaly, Splenomegaly Tenderness (Rebound tenderness --> peritonitis = inflammation of peritoneum). When report pain --> palpate diagonally! get rebound tenderness away from the area of tenderness Abdominal aorta (pulsation should come anterior – slight pulsation towards the front, if feel lateral pulsation --> need to check further, AAA --> can palpate it further lateral, 75% of aortic aneurysm are seen in lateral lumbar spine) Murphy’s = gallbladder inflammation Murphy’s kidney punch test Burney’s point = b/w ASIS + pubis Hernias

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C. Radiographic Exam  Plain film (aka KUB film --> Kidneys, ureter, bladder)  Upright + Supine (air, fluid bubble, obstruction, distension, masses, abnormal calcifications: m/c lymph nodes + abdominal aorta)  Phlebolith (= stone in the vein, calcification of renal valve)  Kidney stones, Gallstones (only 10-15% of the time, made of cholesterol)  Foreign bodies  Free air inside the peritoneum (sometimes seen after surgery)  Upper GI (with contrast media) 1. Esophagram 2. Standard upper GI (esophagus, stomach + duodenum), double contrast…., showing holes = ulcers 3. Upper GI follow through (???), single or double contrast. Single: just Barium, Double: barium & air, look at wall of gut  Use barium sulfate  Lower GI (with contrast media)  Catheter inserted into the rectum, use Barium sulfate  Can see ulcer, masses, polyps, etc.  Both of these have been replaced by endoscopy  IVP (intravenous pyelography)  Not done much anymore, now use more MRI, CT scans, etc.  Cystography: cystogram retrograde (indication = when kidneys are failing, checking for stones, etc.)  CT (computed tomography): IV (…) + Oro contrast: esophagus, small bowel, etc.  Nuclear Scan (reserved for bleeding, radiographic contrast attaching to red cells, etc.) 22.01.2001

1. Inspection, cont’d  Protuberant or Distended abdomen  Partial Bowel Obstruction: distended abdomen plus peristaltic movements heard over the distension is practically diagnostic (sound tinny, Complete obstruction: bowel is hyperactive, w/ time shuts down)  Increased air in bowel causing abdominal distension:  Mechanical factors, carcinoma or adhesions  Adynamic paralytic ileus (= not obstructive loss of bowel peristalsis, bowel is paralyzed, shuts down. Causes = trauma, surgery, also due to endocrinologic dz)

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Ascites: m/c cause is alcoholic cirrhosis leading to portal hypertension (IMP) (cirrhosis = fibrosis, hardening of the liver), (↑ of blood pressure in the portal system  causes blood to back up  fluid leaks to the abdomen  ascites) • Fluid Wave: press down abdomen and create a fluid wave is indicative of ascites • Puddle Sign: Have patient prone and then get on hands and knees, to get all ascites to a dependent position, then flick and auscultate the abdomen, listening for changes in intensity of sounds. Positive test indicates ascites • Ascites: can be assessed by shifting dullness when patient changes position • Chylous Ascites is milky (lipid) look to transudate, indicating lymphatic blockage. Occurs with intraabdominal lymphomas and Hodgkin’s disease. (milky lipid : transudate indicating lymphatic blockage  gets into 3rd space  into abdomen)

 Jaundice: most common causes  Viral Hepatitis (6 types: A,B,C,D,E, non A-non B)  Alcoholic Liver Disease (cirrhosis)  Drug-induced jaundice  Chronic active liver disease (liver, gallbladder, hemolysis)  Choledocholithiasis (stone in the gallbladder duct – small stones are worse)  Pancreatic carcinoma (the obstruction of the duct actually causes jaundice)  Metastatic liver disease (spread of a malignancy from some place else)  Grey Turner’s Sign: Ecchymoses on the abdomen, an unusual place for ecchymoses, It occurs in fulminant acute pancreatitis and carries a grave prognosis (Pt assumes in fetal position and doesn’t want to get out of it = classic sign of pancreatitis)  Abdominal Hernias A. Anatomical Types of Hernias: •

Inguinal Hernias: Most common hernia 1. Direct inguinal hernia: hernia directly penetrates the inguinal triangle. It creates a bulge right above (superior and medial to) the inguinal ligament) 2. Indirect Inguinal hernia: hernia passes through the inguinal canal, and creates a bulge directly over the inguinal ligament, as it passes through the inguinal ring. In men, often herniates into scrotum •

Femoral Hernia: Second most common. High risk of strangulation, 20% of cases.

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Umbilical Hernia: May occur in people with chronic increased intraabdominal pressure, multiparous women and COPD patients.

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8 Spigelian Hernia: occurs b/w umbilicus and pubic symphysis. Unusual.

9  Reducibility 2. Reducible: the contents of the hernia (= bowel) can be easily displaced 3. Irreducible, Incarcerated: The contents of the hernia cannot be displaced and are stuck there. 4. Strangulated: an incarcerated hernia that has cut off its blood supply, resulting in tissue necrosis and gangrene.

2. Auscultation  Peristaltic sounds:  Normal 3-30/minute  Absent bowel sounds adynamic ileus or late obstruction  Increased Bowel sounds: gastroenteritis or early obstruction  Borborygmi: High-pitched bowel sounds indicating small bowel obstruction. Can be normal “hunger pangs”  Succussion Splash: Audible presence of increased amount of fluid in stomach  Normal after a large meal  It is occurs after fasting, then it is indicative or pyloric obstruction  Abdominal Bruits  Caused by calcification of AA  AAA (75% are seen on lateral lumbar)  Renal aneurysm (heard in left + right hypochondriac area, best heard in the back over the costo…)  Splenic aneurysm (look like white circle over the spleen, splenic artery = most tortuous of body)  Peritoneal Friction Rubs: hearing a peritoneal friction rub over the liver is indicative of liver metastasis or primary hepatoma.(heard in people w/ surgery)

3.Percussion  Percuss for:  Ascites  Shifting dullness  Masses  Liver pan  10-12 cm in men, 8-11 cm in women  Splenic size (mononucleosis, leukemia, etc.)  Tympany

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4. Palpation  Tenderness  Palpate tender quadrant last  Rebound tenderness (not done over the area of complaint, done away from the area w/ pain  indicates peritonitis. Doesn’t indicate pain over an organ)  Guarding  Voluntary  Rigidity  Involuntary  Peritonitis    

Organomegaly Masses Aortic pulsations Hernia examination

 Liver:  Hepatomegaly: • Primary or metastatic Hepatoma (highly malignant, name seems to show that it’s benign, better name = hepatocellular carcinoma) • Alcoholic liver disease (fatty liver) • Severe CHF (at least the right side is involved) • Infiltrative diseases of liver like amyloidosis • Myeloproliferative disorders: CML (Chronic Myelogenous Leukemia), Myelofibrosis  Spleen  Splenomegaly • Infections • Leukemias • Portal hypertension  Gallbladder  Courvoisier’s Law: Gallbladder is palpable in 25% of cases of pancreatic carcinoma, due to painless distension  Murphy’s sign: RUQ pain aggravated by inspiration, indicative of acute cholecystitis  Kidney  Enlarged kidneys: Polycystic kidney disease (check for thoraco-lumbar anomalies, usually go together), hypernephroma (renal cell carcinoma), renal cysts, hydronephrosis

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Ptotic Kidney: Normal – sized kidney displaced inferiorly into abnormal position; pelvic kidney

12  Aorta  Pulsatile mass in midline (to left) is suggestive of Aortic Aneurysm  Masses and Bowel Loops  Femoral Pulses and Distal Aorta: decreased of absence femoral pulses can be found in several disorders  Dissecting Aortic aneurysm (hypotension)  Coarctation of Aorta (causing hypertension upper ext., hypotension in lower)  Severe atherosclerotic peripheral vascular disease  Leriche’s Syndrome: occlusion of the distal Aorta (can result from Saddle thrombus: obstruct the flow from the Aorta)  Symptom Tetrad: Absent femoral pulses, intermittent claudication, gluteal pain, impotence  Rectal Exam  25-50% of all malignant colonic polyps are w/in reach of your finger 23.01.2001

SYMPTOMS AND SIGNS OF GASTROINTESTINAL DISEASE A Clinical Primer

CONSTIPATION  Normal Defecation  3 to 7 stools per week  Gastro-colic reflex: “urge” to go after eating (in the morning f.ex.).  Gas = methane, sulfur Constipation  decrease volume of bowel movements  functional (ex: lack of peristalsis) / mechanical (ex: blockage) disorder  Functional = can be treated w/ chiropractic  Very subjective  females>males  > 40 y.o. alternating constipation and diarrhea could suggest a tumor Symptoms/Signs  Lack of consistent urgency  Smaller harder than normal stools (drink warm water)  Painful BMs  Abdominal “fullness”  Sense of incomplete emptying of bowels

13  Tenesmus (= persistent spasms of the rectum or bladder, accompanied by the desire to empty the bowel or bladder, but doesn’t do anything. Common w/ inflammatory bowel dz, Irritable bowel syndrome)

14 Most common causes of Constipation  Intestinal obstruction  Leads to alternating constipation and diarrhea except if it is total blockage  Low fiber diet  Poor bowel habits inadequate fluid intake  Ignoring the urgency (kids, elderly)  8-10 glasses of Water/day  Drug side-effect (anticholinergics, iron – pregnant women, babies, opiates)  Chronic laxative abuse  Stress  Constipation can be associated with:  any condition causing bowel obstruction (functional)  endocrine, metabolic, and neurologic disorders (mechanical)  Laboratory tests non-contributory  Diagnostic imaging non-contributory CONSTIPATION INVESTIGATION  Physical examination  Tenderness Left lower quadrant, decreased sounds, pain, fissures around the anus  Decreased bowel sounds  Masses  abdominal folds  tenderness (Left lower quadrant)  Plain film radiographs  Shows nothing  Digital rectal examination  Sigmoidoscopy  Shows nothing

Treatment of Constipation     

Manipulation Increase fluid intake Increase fiber in diet to >15 gm/day Enemas as a last resort Increase exercise

 Medications  Psyllium (Metamucil, etc..)  Laxatives (Milk of Magnesia, MagCit)  Stool softeners (Peri-Colace)  Do not use these in obstructed/inflamed patients (ex: Crohn’s etc.)

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ACUTE DIARRHEA  More than 3 BMs per day with liquidity of feces  Most commonly infectious  Acute viral diarrhea (self-limiting in 1-3 days) – aka stomach flue  Bacterial diarrhea (”food poisoning”, usually within 12 h of ingestion)  Protozoal diarrhea (travelers, Giardiasis m/c)  Traveler's diarrhea (begins 3-7 days after arrival, amoeba) – Entamoeba histolytica  Signs and Symptoms  loose liquidly stools +/- mucous or blood (blood tinged, not a lot)  cramping abdominal pain and distension (also get very gassy)  anorexia  nausea & vomiting  DDx      

UC (ulcerative colitis) – superficial inflammatory bowel of the large intestine Crohn's (distal) Pseudomembranous colitis (C. difficile) – (occurs after use of antibiotics, but doesn’t kill C. Difficile) Malabsorption Diverticulitis (occurs in Left Colon) Medications (cholinergic agents)

 Laboratory  Elevated WBC (mild 75,000-100,000 Leukemia)  Altered electrolytes  Occult blood  Diagnostic Imaging non-contributory ACUTE DIARRHEA INVESTIGATION  Physical examination  Tender abdominal area  Stool examination  Inflammatory cells (IBD, bacterial infection)  ova/parasites  Blood (IBD, bacterial infection)

17  Stool culture  Treat for specific bacteria if positive

18  Flexible Sigmoidoscopy  Abnormal mucosa (pseudomembranes, ulcerations) ACUTE DIARRHEA TREATMFNT  Rehydration  H2O, Pedialyte  Clear liquids  Avoid coffee, alcohol, dairy, fruits (because of fibers), seasoned foods  Medications  Loperamide, etc .....(Lomotil)  Anti-biotics, anti-protozoals

CHRONIC DIARRHEA  Passage of frequent loose stools for > 3 weeks  Five major types 1. Inflammatory diarrhea 2. Osmotic diarrhea (malabsorption syndromes) 3. Secretory diarrhea (carcinoid) 4. Intestinal dysmotility (IBD, IDDM, neurologic dzs) 5. Factitious diarrhea (laxative abuse, self-induced)  Signs and Symptoms  Frequent loose stools  Abdominal pain  Weight loss  Tenesmus  Dysmotility is m/c cause*

Chronic Inflammatory Diarrhea  Causes  Inflammatory bowel disease  Radiation enterocolitis  Eosinophilic gastroenteritis (assumed to be allergic in nature)  AIDS (mucosal inflammation/malabsorption)  Signs/Symptoms  Blood in stool  Weight loss  Abdominal pain

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Low grade fever Might have some nausea and vomiting (Reflex center in Area of Postrema)

20  Treatment  Fluid replenishment  Electrolyte supplementation  Abstain form lactose-containing products  Add hydrophilic products (psyllium)  Medications - decrease peristalsis  Lomotil  Imodium 29.01.2001

DYSPEPSIA (Commonly called Heartburn)  Describes various upper abdominal symptoms:  Pain (heartburn, epigastric pain)  Discomfort  Fullness  Bloating  Early satiety  Belching  Heartburn (pyrosis)  Regurgitation (Dr Wyatt’s expl:“Vurp” – ½ vomit, ½ burp)  Indigestion  Dyspepsia can occur from:  Drug intolerance (alcohol, caffeine, Aspirin, Ibuprofen)  Luminal dysfunction (esophageal spasm or reflux)  Pancreatic disease (lack of amylase, lipase, often Lactic acid)  Biliary tract disease  Diabetes mellitus (because of poor Insulin exchange, overindulgence of polydipsia, etc., Micro neuropathy, micro vasculopathy)?  Coronary ischemia  Collagen vascular diseases (scleroderma)  Intra-abdominal malignancy (metastatic dz)  Pregnancy  Psychosocial stresses

NAUSEA AND VOMITING  Vomiting is controlled by a medullary center which receives input from four areas: 1. Afferent vagal and splanchnic fibers from the gastrointestinal viscera (Vagal = parasympathetic, Splanchnic = innervation of the GI tract) 2. The vestibular system 3. Higher central nervous system centers triggered by sights, smells or emotional experiences

21 4. The chemoreceptor trigger zone (in the area of postrema) which maybe stimulated by hypoxia and chemo toxins in the blood

22  Complications of vomiting include:  Aspiration (aspiration pneumonia: aggressive sometimes lethal)  Malnutrition  Fluid & electrolyte imbalance  Gastroesophageal mucosal tear (Mallory-Weiss syndrome) – from prolonged wrenching  Post-emetic rupture of the esophagus (Boerhaave’s syndrome) – people w/ chronic esophageal conditions: scleroderma, Barrett’s, etc. Goes to the mediastinum --> leads to Mediastinitis

HICCUP (Singultus) (rapid spasms of the diaphragm)  Self limiting hiccups can be caused by:  Gastric distention  Sudden temperature changes  Alcohol ingestion  Hyperemotional states  Smoking  Recurrent or persistent hiccups have been associated with over 100 causes in the following categories:  Central nervous system disorders  Metabolic disorders  Irritation of the vagus or phrenic nerves  Surgical intervention  Psychogenic  Idiopathic

GASTROINTESTINAL GAS  Belching (eruptation)  Usually caused by swallowing air (aerophagia) – ex: eat too fast, chewing gums, carbonated drinks, smokers  With each swallow, 2 to 5 ml of air is ingested  Causes  Rapid eating  gum chewing  smoking  drinking carbonated beverages  mouth breathing

23  Bowel gas (flatus)  Usually caused by aerophagia (N2) and bacterial fermentation of undigested carbohydrates (typically odorless)  In contrast, putrefaction of undigested proteins release hydrogen sulfide (malodorous)

GASTROINTESTINAL BLEEDING  Upper GI  Bleeding from an area proximal to the stomach is usually regurgitated (hematemesis) as bright red blood – ligament of Treitz  If the area of bleeding is distal to the esophagus, the regurgitated blood is usually “coffee ground” type.  Gastric acid acts on blood  coagulates into granules  which are regurgitated. No distinct cut off b/w esophageal or stomach bleeding  Esophageal varices bleed chronically  regurgitation  Blood from upper GI hemorrhage that is not regurgitated, is digested and results in black tarry stools (melena).  Bleeding from upper GI does not come out bright red blood  If upper GI bleeding yields large amounts of defecated blood (hematochezia), then the blood loss was massive  Lower GI  Bleeding is from the small intestine or colon  95% of the cases from the colon  Hematochezia is usually present (Def. = BRBPR: bright red blood per rectum)  Stool streaked w/ blood: picking up blood off from some mass  Upper GI bleeding may result from:  Peptic ulcer disease (stomach or duodenum, “peptic” has to do w/ Pepsin)  Portal hypertension  Esophageal varices: dilation of esophageal veins  Mallory-Weiss tears (from harsh vomit, tear in lower esophagus)  Vascular anomalies  Neoplasm (esophageal carcinoma is a very aggressive tumor)  Erosive esophagitis  Erosive gastritis  Lower GI bleeding may result from:  Diverticulosis (older men, someone who doesn’t each much fibers)  Vascular ectasias (arteriovenous malformation)  Neoplasm  Inflammatory bowel disease (ulcerative colitis + Crohn’s disease-granulomatous)  Anorectal disease (hemorrhoids, fissure, fistulas)  Ischemic colitis (diabetics)

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THE PERITONEUM ASCITES  Healthy men have little or no intraperitoneal fluid. Healthy women, depending on the phase of their menstrual cycle, may have up to 20 ml of intraperitoneal fluid  Ascites may be of peritoneal origin (diseased peritoneum) or non-peritoneal origin (normal peritoneum)  The most common cause of ascites (about 80%) is portal hypertension secondary to chronic liver disease (non-peritoneal origin)  Peritoneal ascites is usually caused by infections, malignancy, and inflammation of the peritoneum. (Appendicitis could inflame the region of the peritoneum also)

MISCELLANEOUS ASCITES  Chylous ascites: a milky lipid-rich lymph with a high triglyceride level (> 1000 mg/dl) usually caused by lymphatic obstruction from malignancy  Pancreatic ascites: massive amounts of pancreatic secretions due to either a disruption of the pancreatic duct or a pancreatic pseudocyst. (fluid filled sack not lined w/ epithelium. Cyst is line w/ epithelium).  Bile ascites: most commonly caused from biliary tract surgery, liver biopsy, or abdominal trauma  Picture of Shinny, skin looks thin, bulges on the side, jaundice

SPONTANEOUS BACTERIAL PERITONITIS  A secondary or spontaneous bacterial infection of ascitic fluid (Pt w/ ascites that develops infection of ascitic fluid)  It is usually seen in ascites of chronic liver disease  Its occurrence may be as high as 40% in patients with chronic liver disease  80-90% of the patients with this condition do not have symptoms related to the peritonitis  Mortality rate exceeds 30%  70% of the patients that survive will have another episode within a year

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PERITONEAL CARCINOMATOSIS  Peritoneal carcinoma from metastasis is relatively common  The originating tumors are usually adenocarcinoma arising from the: ovary, uterus, pancreas, stomach, colon, lung, or breast  With the exception of ovarian origin, the prognosis is poor. Only 12% survival at 6 months

MESOTHELIOMA  Primary malignancies of the peritoneum are rare (Mesothelioma occurs in the lung, people exposed to asbestos)  When they occur, they are usually mesotheliomas  Over 70% of the cases have a history of asbestos exposure  The ascitic fluid is characteristically hemorrhagic  The prognosis is extremely poor

ESOPHAGUS THE NORMAL ESOPHAGUS  Its course and landmarks  It begins at the level of the cricoid cartilage and passes right of the transverse aortic arch  The right branch of the pulmonary artery passes anterior to it, the left main bronchus crosses it directly below the level of the aortic arch and may cause a slight, smooth indentation in a barium swallow  Its distal part lies to the right of and anterior to the descending thoracic aorta and directly behind the posterior surface of the heart in close relationship with the left atrium  Sometimes in the elderly, the aorta is elongated and tortuous, and may displace the lower part of the esophagus forward  The esophagus remains in close relationship to the right aortic border and will curve to the left and then back to the midline as it descends through the diaphragm  In elderly women, extrinsic compression of the distal esophagus by a dilated tortuous and rigid aorta may cause partial esophageal obstruction. The esophagus adjacent to the dilated aorta may exhibit a smooth, eccentric… missing end of sentence! (Dysphasia)  X-ray: Indentations produced by the transverse aortic arch (above) and the left atrium (below)

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NORMAL DEGLUTITION  The bolus of food is propelled into the esophagus by a powerful contraction of the pharyngeal muscles. (Parts of upper pharyngeal: nasopharynx, ….,check anatomy)  Contraction waves behind the advancing bolus are referred to as peristalsis  Contraction waves initiated by swallowing are termed primary peristaltic waves  Contraction waves not initiated by swallowing are called secondary peristaltic waves  Both 1st and 2nd waves are the effective waves of peristalsis  Peristalsis gets slower as you age

PRESBYESOPHAGUS  It is an abnormality of esophageal motility usually associated with aging  It involves the lower one-third to one-half of the esophagus  The primary peristaltic contraction is impaired and there is an increase in non-propulsive random contraction (there is also an increase of tertiary waves: ineffective nonpropulsive  ineffective = “curling”, results in dysphasia)  The non-propulsive random contractions are called tertiary contraction or curling  Radiographically these tertiary contractions are referred to as the “Curling Phenomenon” and look like multiple ring-like contractions that rapidly appear and disappear until the peristaltic wave moves the bolus into the stomach  Curling phenomenon is also known as “corkscrew esophagus” or “beaded esophagus” 05.02.2001 Test: Monday 12, 10 am

ACHALASIA  Achalasia is also known as cardiospasm (narrowing of distal esophagus near gastroesophageal junction)  It is a motor disorder caused from decrease or absence of the ganglion cells in the myenteric plexus (muscle in the gut) (aka Auerbach’s plexus)  There is loss of primary peristalsis, a failure of relaxation in the lower esophageal sphincter (prevents reflux), and lack or normal peristalsis in the rest of the esophagus  Pre-stenotic dilation  On x-ray there is a smooth tapering of the distal esophagus called a “bird’s beak”  Achalasia usually cause dysphagia with both solids and liquids (liquid dysphasia is worse)  In addition to dysphagia, substernal discomfort or fullness may be noted after eating  Regurgitation is common and may lead aspiration followed by recurrent bouts of pneumonia or chronic pulmonary inflammation (aspiration pneumonia)  Untreated, the esophagus may become markedly dilated (sigmoid esophagus)

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CHALASIA  This is the reverse of achalasia of the lower esophageal sphincter (sphincter doesn’t close)  It is usually discovered soon after delivery, as a cause of vomiting in infants  The esophagus is dilated and peristalsis is diminished resulting in free reflux of gastric contents.  The usual cause is an incomplete development of neuromuscular control in the lower esophagus

PROGRESSIVE SYSTEMIC SCLEROSIS (SCLERODERMA)  Collagen vascular dz: S/Sx related to the skin. Skin becomes waxy, hard, tight + very red, can slough off. Can get joint contractures, loss of ROM, periarticular soft tissue: like Myositis ossificans, particularly in the fingers.  A component of scleroderma is atrophy of smooth muscle, therefore, it can involve the lower 2/3 of the esophagus  The primary peristaltic wave does not continue into the lower half of the esophagus in a normal fashion (get achalasia)  The esophagus may be dilated and shortened. There may be gastroesophageal reflux and hiatus hernia (producing reflux)  Chest x-ray may show a dilated, air-filled esophagus  Systemic lupus erythematous and Raynaud’s disease can cause the same esophageal changes  Although Dermatomyositis usually causes abnormalities in the striated muscle of the pharynx and upper esophagus, it can also affect the smooth muscle of the lower esophagus

OTHER DEFECTS IN ESOPHAGEAL MOTILITY  Diabetes Mellitus – may cause a decrease in primary peristaltic contractions resulting in dilation, delay in emptying, tertiary contractions, and dysphagia  Trypanosomiasis (Chagas disease) – may cause esophageal changes similar to achalasia  Diffuse esophageal spasm (DES)– causes intermittent dysphagia and chest pain, repetitive contractions of the esophagus, and thickening of the esophageal wall. Dx is made w/ manometry.  Hypertensive lower esophageal sphincter – there is normal peristalsis with an increase in sphincter pressure which cause dysphagia and chest pain (like “pseudo-achalasia)

29 Congenital anomalies of the esophagus

ATRESIA of the Esophagus  The site of the defect is usually in the upper third of the esophagus just below the level of the sternal notch  Vogt’s classification:  Type I – complete absence of the esophagus (least common type)  Type II – incomplete esophagus with both upper and lower segments ending in a blind pouch (no fistula w/ the trachea). Fistula = abnormal tubular connection  Type III – incomplete esophagus with a tracheoesophageal fistula a. Fistula between the upper segment and the trachea b. Fistula between the lower segment and the trachea, the upper ending blindly (most common type) c. Fistula between the trachea and both esophageal  The most common is type III-b and the least common is type I  Aspiration pneumonia would occur w/III a, III b (no direct connection) + III c  Complications may include aspiration pneumonitis or atelectasis (collapse of subsection of the lung)  Other anomalies associated with esophageal atresia:  Skeletal (the most common) – butterfly vertebra, hemivertebra  Cardiovascular – atrial septal defect, ventricular septal defect, and tetralogy of Fallot (overriding aorta, VSP, right ventricular hypertrophy) X-ray: type III-b atresia of the esophagus

LARYNGOTRACHEOESOPHAGEAL CLEFTS  Clefts are formed as a result of a failure of normal separation of the fetal foregut into trachea and esophagus  Generally these clefts are limited to the larynx, cricoid area, and the upper trachea  Problems associated: breathing, …

CONGENITAL STRICTURE OF THE ESOPHAGUS  Half of all congenital strictures occur in the middle of the esophagus  Strictures are characterized by a smooth narrowing of the lumen resulting in an incomplete esophageal occlusion

30 06.02.2001

ESOPHAGEAL WEBS  Webs are thin, diaphragm like membranes of squamous mucosa (located inside the lumen of the esophagus)  They may be singular or multiple and usually occur in the mid or upper esophagus  Webs can cause obstruction with proximal esophageal dilation  When symptomatic they usually cause solid food dysphagia  They are usually diagnosed from a barium swallow (or EGD: Esopho Gastro Duodenoscopy= Flexible endoscope)  When symptomatic, they are usually treated with bougienage (passage of a dilating instrument called a bougie)

LOWER ESOPHAGEAL RING  Lower esophageal rings are also called Schatzki’s Ring  Rings are circumferential mucosal tissue that is characteristically symmetrical and thin (< 4 mm thick)  They usually occur in the distal esophagus at the squamocolumnar junction (Barrett’s esophagus also occurs there)  When they are not congenital, they are always associated with a hiatus hernia  They are best diagnosed by a barium esophagogram with a solid bolus (= glup)  When symptomatic, they can be treated with bougienage (Hamartoma = overgrowth of non-tumorous cells)

DUPLICATION OF THE ESOPHAGUS (last of congenital)  A closed duplication results in a cystic mass lined with esophageal epithelium and filled with fluid)  They are usually found in the central of posterior mediastinum (the esophagus is there)  The cysts may enlarge rapidly during infancy

31 07.02.2001

ESOPHAGITIS  Esophagitis is the most common disease affecting the esophagus  Types of esophagitis:  Chemical esophagitis  Acute ulcerative esophagitis  Reflux esophagitis  Peptic ulcer of the esophagus  Infectious esophagitis  Crohn’s disease  Mechanical esophagitis

CHEMICAL ESOPHAGITIS  Swallowing of caustic materials may cause necrosis and ulceration of the mucosa of the esophagus  The surface of the mucosa becomes irregular due to the edema, ulceration, and necrosis  As the inflammation subsides, fibrosis and scar-tissue develop, which may result in the formation of strictures (= Shrinking. Can be long or short)  The strictures are most frequent a the following levels  The thoracic inlet  The level of the aortic arch  At or above the level of the diaphragmatic hiatus (there are the most narrowing) – Clinically ends up in dysphasia

ACUTE ULCERATIVE ESOPHAGITIS  This condition is usually associated with frequent or recurrent vomiting in patients with a duodenal peptic ulcer  The ulceration is usually limited to the lower half to one third of the esophagus  Initially the esophagus goes into spasm. After a few weeks, this contracted state may become fixed of permanent due to fibrosis  The mucosal folds normally associated with a contracted esophagus are absent, leaving the surface with a relatively smooth appearance

REFLUX ESOPHAGITIS  Associated with Gastroesophageal Reflux Disease  This condition features reflux of gastric contents into the lower esophagus  Only when the gastric contents damage the esophageal mucosa is it “reflux esophagitis” (different from GERD)

32  The reflux may or may not have an associated hiatus hernia (approx 30-40%)

33  The major symptom is heartburn which occurs 30-60 minutes after meals and upon reclining  Patients with severe involvement generally have an incompetent lower esophageal sphincter  The amount of damage depends on the potency of the reflux and the amount of time that it is in contact with the mucosa

PEPTIC ULCER OF THE ESOPHAGUS  Peptic ulcer of the esophagus is frequently the end stage of reflux esophagitis  It is often associated with duodenal ulcer and hiatus hernia  Esophageal spasm may cause a diffuse narrowing of the lumen around the ulcer and for a short distance above the ulcer  Fibrosis from the ulcer and the narrowing from the spasm may result in esophageal obstruction  On endoscopic and radiographic examination, the ulcer will usually appear as a shallow crater

INFECTIOUS ESOPHAGITIS  Infection of the esophagus occurs most commonly in immunosuppressed patients  AIDS patients  Organ transplant patients (Cyclosporine, because of chemo)  Cancer patients  Diabetes mellitus (type I)  Patients on maintenance steroid or antibiotic therapy (Pt w/ Crohn’s, arthritis patients, etc.)  The most common pathogens are: candida albicans, herpes simplex, and cytomegalovirus  The most common symptoms are: dysphagia, odynophagia (painful swallowing), and substernal chest pain  The most frequent radiographic findings are: a shaggy mucosal outline, multiple ulcerations, segmental narrowing, and diminished peristalsis End material for midterm M/C, true false, short answers

34 20.02.2001

CROHN’S DISEASE  Crohn’s disease is also called Regional Enteritis  The esophagus is an uncommon location for Crohn’s disease, it is usually associated with the small bowel and colon  (“tongue to bongue”), typically found in distal ileum and proximal colon  When Crohn’s disease occurs in the esophagus, it usually presents as flat thickened mucosal folds which progress to a typical cobblestone pattern (affects transmural layer can get stenosis)  Stenosis may occur giving the radiographic appearance of a cone-like tapering and pre stenotic dilation. Stenosis may lead to complete obstruction requiring resection  Unlike in the small bowel and colon, esophageal fistulas are unusual

MECHANICAL ESOPHAGITIS  Mechanical esophagitis can be caused by anything that is swallowed and becomes lodged in the esophagus  Some common examples are metal objects like coins, bones, pills, etc.  The favorite site for a swallowed bone to become impacted is the cervical part of the esophagus at or just above the level of the thoracic inlet.  Impacted pills may lead to chemical ulceration due to prolonged mucosal contact. NSAID’s, iron, vitamin C, and some antibiotics are some of the more common medications involved  Complications of impacted esophageal foreign bodies may include: ulceration, infection, abscess formation (chronic), perforation, mediastinitis (need to have perforation first), and pleural effusion (build up of fluid in the pleural space. Get pleural effusion because of inflammation: mediastinum covered by …

LEIOMYOMA  Benign tumors of the esophagus are rare  Aka fibroid tumor  Leiomyoma is the most common benign tumor of the esophagus (smooth muscle)  It is usually a single intramural tumor that produces a sharp angular junction between the mass and the esophageal wall which results in a filling defect  Since the extramural portion of the tumor usually projects into the mediastinum, it rarely causes dysphagia and may be asymptomatic and remain undetected unless it is picked up incidentally on an endoscopic or radiographic examination.  Their clinical significance is that they must be differentiated from malignant lesions

35

ESOPHAGEAL CARCINOMA  Carcinoma may develop in any part of the esophagus  They are either squamous cell carcinomas or adenocarcinomas (because esophagus is lined w/ epithelium)  Half of the cases of squamous cell occur in the distal third of the esophagus and the other half occur in the proximal two thirds  Increased risk of squamous cell carcinoma is associated with chronic use of alcohol and tobacco  Adenocarcinoma usually occur in the distal third of the esophagus  The vast majority of adenocarcinomas develop as a complication of metaplasia due to chronic gastroesophageal reflux  They typically occur in the 50 to 70 age group and are 3 times more common in men  The major symptoms are progressive solid food dysphagia and weight loss. Other symptoms may present depending upon which tissues the tumor extends into. As an example: tracheoesophageal fistula may result in coughing on swallowing or pneumonia; laryngeal involvement may produce hoarseness (Coughing also caused by recurrent laryngeal nerve)  There is a wide variety of radiographic presentations from a simple filling defect to total esophageal obstruction  The diagnosis is confirmed by endoscopy with biopsy  The prognosis is poor in that most patients do not present in the physician’s office until the condition is advanced and incurable (poor because can be asymptomatic for a long time and lot of lymph nodes in the area)  The presence of supraclavicular (aka Virchow’s node) or cervical lymphadenopathy or of hepatomegaly implies metastatic disease 27.02.2001

STOMACH  6 parts: (Drawing)  1. Top = fundus (where “magenblase” is)  2. Body  3. Antrum  A. Anatomic Cardia  B. Incisura Angularis  C. Pyloric canal (peptic ulcers)  D. Duodenal Bulb  Fundoplication – fold fundus to make new esopheal sphincter

36

Gastritis & Gastropathy  The word “gastritis” is a very confusing term:  The endoscopists use it to denote mucosal changes such as erythema, hemorrhages, and erosions  The Pathologists use it to denote histologic inflammation  If there is epithelial or endothelial damage without inflammation, many specialists are using the term “gastropathy”  Gastritis is divided into 3 categories  Erosive and hemorrhagic  Non-erosive, non-specific  Specific  The typical gastritis symptoms are postprandial (= after eating) indigestion, fullness, bloating, nausea, early satiety, epigastric pain, and intolerance of fatty foods  Chronic abdominal, back, or chest pain that can be reproduced by pressure on a paraspinal trigger point is called “back-gut” syndrome.

Erosive & Hemorrhagic Gastritis  Erosive gastritis is usually caused by drugs (NSAID’s), alcohol, stress from critical illness, and portal hypertension  NSAID’s are associated with petechiae (= pin-point hemorrhage), erosions and ulcers of the gastric mucosa  Alcohol also leads to bleeding and erosion of the gastric mucosa (loose 5 cc of blood with non-coded NSAID’s)  Stress related mucosal disease can result from any severe medical or surgical illness. Curling’s ulcers are ulcers of the gastric mucosa that occur in burn patients. Cushing’s ulcers are gastric mucosal ulcers that occur with central nervous system disease, trauma or surgery. This gastric bleeding may double or triple the mortality rate of the underlying condition  2 big deal w/ burn victims = infection + hemorrhage  Portal Hypertension can cause congestion of the gastric mucosal and submucosal capillaries and venules which may lead to bleeding  Erosive gastritis is usually asymptomatic, but when symptoms occur, they are anorexia, epigastric pain, nausea and vomiting (hematemesis)  These conditions are diagnosed w/ endoscopy

37

Non-Erosive, Non-specific Gastritis  The diagnosis of non-erosive gastritis is usually based on histologic changes seen in biopsied mucosa. Gross endoscopic appearance many times is normal  There are two main types of non-erosive gastritis: Helicobacter pylori infection and mucosal changes associated with pernicious anemia 

H. Pylori: a spiral gram-negative rod that resides under the mucus layer next to the epithelial cells. Acute superficial infections may cause a transient clinical illness characterized by nausea and abdominal pain lasting for several days . If the inflammation extends deeper, into the gastric glands, gland atrophy and metaplasia of the epithelium may result. H. pylori infection is strongly associated with peptic ulcer disease, however, only 15% of patients with chronic H. pylori infection develop peptic ulcer. Several endoscopic and serologic test procedures can be used to detect H. pylori. Bu a positive serologic test does not necessarily mean that there is an active infection. Even after H. pylori has been eradicated, antibodies can remain for 6-12 months.

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Pernicious anemia gastritis: an autoimmune disorder resulting in achlorhydria and B12 malabsorption. There is gland atrophy and metaplasia. The inflammation and autoimmune reaction leads to the destruction of the acid-secreting cells and loss of intrinsic factor. The metaplasia results in an threefold increase in the risk of future adenocarcinoma. The achlorhydria causes a loss of the acid inhibition of the gastrin G cells, resulting in hypergastrinemia, which may lead to the development of carcinoid tumors Know which cells secrete acid (chief cells?)

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Specific Gastritis  There are a number of different conditions that fall under the classification of specific gastritis: phlegmonous, granulomatous, eosinophilic, lymphocytic, and Ménétrièr’s disease  Phlegmonous type is an abscess that can be the caused by bacterial, viral, fungal, or parasitic infections. It is considered to be a life-threatening medical emergency which requires gastric resection and antibiotic therapy  Granulomatous type consists of granulation tissue resulting from chronic inflammation caused such conditions as tuberculosis, syphilis, fungal infections, sarcoidosis, or Crohn’s disease  Increase of tuberculosis in metropolitans (loves the spine)  Eosinophilic type is characterized by infiltration of the mucosa, muscularis, or serosa layers with eosinophils. Corticosteroids help stop the eosinophilic infiltration  Lymphocytic type demonstrates a diffuse infiltration of lymphocytes on biopsy. On endoscopy, there are mucosal erosions and a varioliform (pox-like) appearance.

38  Ménétrièr’s disease is characterized by giant, thickened gastric folds. There is significant protein loss which may lead to severe hypoproteinemia anasarca (generalized massive edema). Idiopathic

39 05.03.2001

Peptic Ulcer Disease  Peptic ulcers are defects in the gastrointestinal mucosa that penetrate the muscularis layer  The two most important products of gastric secretion are hydrochloric acid and pepsin (secreted by the gastric mucosa, HCl = parietal cells)  Gastric acid secretion may be stimulated by acetylcholine, gastrin, and histamine  Other substances that can cause gastric ulceration are bile acids, lysolecithin, and pancreatic enzymes  Mucus, bicarbonate, good blood flow, and normal cell renewal help protect mucosa from injury by these aggressive agents  Peptic ulcer occur on the lesser curve  Some of the predisposing factors that may promote gastric ulceration  Duodenal reflux  Decreased or abnormal mucus  Diminished blood flow  Decreased bicarbonate secretion  Delayed gastric emptying (elderly, diabetics, pregnant women, etc.)  Cigarette smoking and NSAID use  Certain emotional states such as hostility, resentment, guilt, and frustration  There are three major causes for peptic ulcer disease: Helicobacter pylori, NSAID’s, and hypersecretory states such as Zollinger-Ellison syndrome  H. Pylori: some studies have indicated that 70-75% of gastric and duodenal ulcer patients have H. Pylori infections. H. Pylori is thought to increase gastric acid secretion. Studies have shown that after standard therapy, 70-85% of patients will have ulcer recurrence within 1 year. If H. pylori is successfully eradicated, the recurrence rate drops to about 20%  NSAID’s: Aspirin is the most ulcerogenic of the NSAID’s. NSAID’s cause decreased mucus and bicarbonate secretion, diminished mucosal blood flow, and possibly reduced cell renewal. Chronic NSAID users increase their risk for gastric ulcers 40-fold  Zollinger-Ellison syndrome: this condition is caused by gastrin-secreting neuroendocrine tumors called gastrinomas. This is the least common cause of peptic ulcer disease. In addition to the stomach, gastrinomas may occur in the pancreas, duodenum, and regional lymph nodes. Over two-thirds are malignant.  Characteristics of ulcer pain:  Usually epigastric in location and described as burning or gnawing (like chewing)  Some patients experience a cramping sensation not unlike “hunger pangs” which is relieved by ingestion of food or antacids  Episodes of pain usually occur in clusters lasting from days to weeks, interspersed with long symptom-free periods  Changes in the character of the ulcer pain may herald the onset of ulcer complications

40

41  Treatment:  Avoid those things that stimulate acid secretion such as smoking, alcohol, analgesics, and milk

Complications of Peptic Ulcer Disease  Gastrointestinal hemorrhage (perforation of the related blood vessels)  About 50% of all upper GI bleeding is due to gastric ulcer  Minor GI bleeding occurs in most ulcer patients with only 10-20% having clinically significant bleeding (black tarry streaks in the stools)  About 80% of ulcer patients stop bleeding spontaneously  The over-all mortality rate for bleeding ulcers is 6-10%  Ulcer perforation or penetration  Perforation occurs in only about 5% of ulcer patients and the ulcers are usually on the anterior wall. Perforations on the posterior wall may penetrate adjacent organs (and form a fistula)  Abuse of NSAID’s and use of crack cocaine may be causing the incidence to rise  Zollinger-Ellison syndrome should be considered in all cases of perforation  Gastric outlet obstruction  Obstruction can occur in the pylorus or duodenal bulb from edema or stenotic scarring, but this is a rare complication that only occurs in about 2% of ulcer patients

Differential Diagnosis of Peptic Ulcer disease  Common conditions that may produce epigastric pain simulating peptic ulcer  Myocardial infarction  Pericarditis (fluid production  fills around the heart  difficult for the heart to pump  cardiac tamponade)  Cholecystitis  Irritable bowel syndrome  Pleurisy (particularly adhesive pleuritis)  Esophagitis  Pancreatitis  Gastrica cancer  Tuberculosis (15-20% ↑ in metropolitan area)  Syphilis  Crohn’s disease (transmural inflammation)  Duodenal obstruction  Intestinal parasites

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Gastric Neoplasm  Most tumors of stomach are malignant. Reverse in colon (benign)  The most common primary malignancy of stomach is gastric adenocarcinoma. With its exception of skin cancer, it is the m/c cancer worldwide

Gastric Adenocarcinoma  Gastric ulcer dose not usually transform into cancer. Things that are thought to predispose one to gastric cancer:  Blood group A  Adenomatous polyps larger than 2 cm  Immunologic deficiencies  Poor diet (no direct proof  It is rare for gastric carcinoma to occur under age 30, with the majority occurring between the ages of 50 and 70  Men are affected twice as often as women and there is a higher incidence in Hispanics, American blacks, and American Asians.  Gastric carcinoma appears most often as a bulky mass with deep central ulceration. Less commonly, it may extend through out the entire stomach which is referred to as “linitis plastica” (a poor prognosis). It is difficult to distinguish polypoid carcinomas from the benign polyps that they may develop from  Three fourths of all gastric carcinomas occur in the distal third of the stomach  Gastric carcinoma may invade the lymph nodes, invade adjacent tissues by local extension, or under go hematogenous spread o Virchow’s nodes = Left supraclavicular fossa o 2 ways: hematogenous spread (vascular system) and lymphangitic spread (lymph vessels)  Common areas for metastasis are: lung, pleura, liver, brain, and bone  Some of the more common symptoms of gastric carcinoma are:  Anorexia, early satiety, weight loss, bloating, dysphagia, epigastric distress, vomiting. The epigastric pain usually occurs after meals, but is NOT relieved by foods or antacids. Boring pain radiating the back may indicate penetration of the tumor into the pancreas.  Early on, physical examination is often unremarkable. Later, weight loss, anemia, hepatomegaly, splenomegaly, jaundice and ascites may be present

43 

TNM system: tumor-node-metastasis: 4 general grades to cancers o Grade 0 = no malignancy o Grade 1 = localized tumor only o Grade 2 = direct local extension and ipsilateral lymphadenopathy o Grade 3 = local extension, ipsilateral and contralateral lymphadenopathy o Grade 4 = distant metastasis (chest, brain, etc.)

 Signs of metastases:  Enlarged left supraclavicular lymph node (Virchow’s Node)  An umbilical nodule (Sister Mary Joseph Nodule)  A rigid rectal shelf (Blumer’s Shelf)  Ovarian metastases (Krukenberg Tumor)  Possible Lab findings  Occult blood in stools  Iron deficiency anemia (hypochromic, microcytic)  Abnormal liver function tests  Endoscopic exam with biopsy is diagnostic  If detected early enough, surgical resection is the only therapy with curative potential  The long term survival of gastric carcinoma is less than 15%. In those cases in which surgical resection is successful, long term survival is greater than 50%

Other Malignant Tumors of the Stomach  Lymphoma  Only 5% of primary malignancies of the stomach  Divided into Hodgkin’s and non-Hodgkin’s type Non-Hodgkin’s is the most common of the two and has a better survival rate.  Leiomyosarcoma  Represents 1% of gastric cancers  Metastases to the liver and lymph nodes is common  Metastatic Carcinoma  Malignant melanoma, breast carcinoma, and lung carcinoma are the most frequent metastatic diseases to the stomach

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Benign Tumors of the Stomach  Leiomyomas (smooth muscle)  They are common but only rarely are they clinically significant  Bleeding and epigastric pain may stimulate a peptic ulcer  Adenomas (gland tumor)  Most polyps of the stomach are hyperplastic, not neoplastic and do not become malignant  Aka Hamartoma = benign, overgrowth of normal tissue  They are usually asymptomatic, but on occasion may cause bleeding, dyspepsia, and nausea  It is rare for a polyp under 2 cm to show malignant change  Other benign tumors of the stomach  Neurofibromas, neuromas (foot), lymphangiomas, ganglioneuromas, lipomas, carcinoids and hamartomas.

Hiatal Hernia  A hiatal hernia is protrusion of the stomach above the diaphragm  The etiology is usually unknown, it is thought to be either a congenital abnormality or occur secondary to trauma:  X-ray diagnosis divides them into 4 types 1.

Sliding hernia: the gastroesophageal junction and a portion of the stomach are above the diaphragm. This the most common type and is seen in greater than 40% of the population. It is usually asymptomatic, but when symptoms do occur they are those of gastroesophageal reflux (sliding - most common)

2.

Paraesophageal hernia – the gastroesophageal junctions is in the normal location, but the fundus of the stomach herniates through the diaphragm to lie adjacent to the distal part of the esophagus. It is usually asymptomatic, but if it is not surgically reduced there is a risk of strangulation (rolling – 2nd m/c)

3.

Short esophagus type – a variation of sliding type

4.

Intrathoracic stomach – the entire stomach is above the diaphragm

 The possible complications are bleeding, ulceration, obstruction and strangulation.

45 19.03.2001

Irritable Bowel Syndrome  Aka: mucous colitis, spastic colon  A subjective diagnosis based on the presence of a compatible profile and the exclusion of other organic disorders  It is a chronic idiopathic clinical entity characterized by  Abdominal pain that is relieved by defecation or is associated with a change in the frequency or consistency of the stool  Disturbed defecation evidenced by at least two of the following: o Altered frequency (more than 3 per day or less than 3 per week) o Altered form (lumpy-hard or watery) o Altered stool passage (straining, urgency, or incomplete evacuation) o Bloating or abdominal distention o Passage of mucus  The disorder is extremely common with up to 20% of the adult population having symptoms compatible with the diagnosis.  It is a life-long conditions that usually begins in the late teens to twenties, predominately in females  Symptoms should be present for at least 3 months before the diagnosis can be considered  A high fiber diet should be recommended  The following flatulogenic foods should be avoided:  Brown beans  Brussels sprouts  Cabbage  Cauliflower  Raw onions  Grapes  Plumbs  Raisins  Coffee  Red wine  Wine  Beer  Caffeine  Drug therapy should be reserved for patients with severe symptoms that do not respond to conservative measures

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47

Antibiotic Associated Colitis  Diarrhea occurs during the period of antibiotic exposure, is dose related, and resolves spontaneously after discontinuation of the antibiotic.  Stool examination usually reveals no fecal leukocytes and stool cultures reveal no pathogens.  This conditions is almost always caused by Clostridium difficile  The antibiotics disrupt the normal bowel flora and allow the bacterium to flourish.  C. difficile is the major cause of diarrhea in patients hospitalized for more than 3 days.  Most patients report mild to moderate greenish, foul-smelling watery diarrhea with lower abdominal cramps. (can go to pseudomembranous enterocolitis)  Complications  Dehydration  Electrolyte imbalance  Toxic megacolon  Perforation  Weight loss  Protein-losing enteropathy  In severe cases, death  If possible antibiotic therapy should be discontinued.

Inflammatory Bowel Disease  Ulcerative colitis – a chronic idiopathic inflammatory condition involving only the colon  Crohn’s disease – a chronic idiopathic inflammatory condition involving any segment of the gastrointestinal tract from the mouth ….. (missed the end!!)

Crohn’s Disease    

One-third of the cases involve only the distal small bowel (ileitis) Half the cases involve the distal small bowel and proximal colon (ileocolitis) In 20% of the cases only the colon is involved Crohn’s disease is a transmural process that can result in:  Inflammation  Ulceration  Stricturing (narrowing)  Fistula formation

48 

Abscess formation

49  Crohn’s disease presents with a wide variety of signs and symptoms because its involvement is variable in both location and severity of inflammation  Most commonly, there is one or a combination of the following clinical presentations: 

Chronic inflammatory disease o This is the most common presentation o Often seen in patients with ileitis or ileocolitis o Patients report low-grade ever, malaise, weight loss, and loss of energy o There may be diarrhea which is non-blood y and intermittent o Cramping or steady pain in the right lower quadrant or periumbilical area o Examination reveals focal tenderness in the right lower quadrant

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Intestinal obstruction o Narrowing of the small bowel may occur as a result of inflammation of fibrotic stenosis o Patients report postprandial bloating, cramping pains, and loud borborygmi

 Fistulization with or without infection  Some patient develop sinus tracts that penetrate through the bowel and form fistulas to other areas  Fistulas to the mesentery are usually asymptomatic (loose fatty CT that connect the bowel, organs)  Fistulas from the colon to the small intestine or stomach car result in bacterial overgrowth with diarrhea, weight loss and malnutrition  Fistulas to the bladder or vagina produce recurrent infections  Perianal disease (other presentation of Crohn’s): which usually includes anal fissures, perianal abscesses, and fistulas  Extraintestinal manifestations  Oral aphthous ulcers  Increased prevalence of gallstones due to malabsorption of bile salts  Nephrolithiasis with urate or calcium oxalate stones  Complications  Abscess  Obstruction  Fistulas  Perianal disease  Carcinoma – Patient’s with colonic disease are a t a greater risk of developing colonic carcinoma  Hemorrhage – unusual in Crohn’s disease (except for Crohn’s colitis)  Malabsorption – from bacterial over-growth in patients with fistulas

50  No specific treatment exists for Crohn’s disease, treatment is directed toward symptomatic improvement and controlling the disease process

51

Ulcerative Colitis  Like Crohn’s disease, ulcerative colitis has an idiopathic etiology  The inflammation involves the mucosal surface of the colon, resulting in diffuse friability and erosions with bleeding.  In 50% of the patients the disease is confined to the rectosigmoid region; 30% extend to the splenic flexure (left-sided colitis); less than 20% extend more proximally (extensive colitis)  The disease is characterized by periods of symptomatic flare-ups and remissions  Bloody diarrhea is the hallmark sign. (Ulcerative colitis tends to be pure diarrhea. Cancer = alternate b/w diarrhea and constipation)  Patients should be asked about stool frequency, the presence and amount of rectal bleeding, cramps, abdominal pain, fecal urgency, and tenesmus.  On abdominal examination, look for tenderness and evidence of peritoneal inflammation (peritonitis  rebound tenderness)  Patients are classified as having mild, moderate, or severe disease  Mild disease o Gradual onset of infrequent diarrhea (less than 5 episodes per day), intermittent rectal bleeding, and mucus o Rectal inflammation causes fecal urgency and tenesmus o Left lower quadrant cramps (no significant abdominal tenderness) relieved by defecation (just like IBS) 

Moderate disease o Most severe diarrhea with frequent bleeding o Abdominal pain and tenderness may be present but are not severe o Mild fever, anemia, and hypoalbuminemia

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Severe disease o More than six to ten bloody bowel movements per day o Severe anemia, hypovolemia, and hypoalbuminemia (get edema) o Impaired nutrition o Significant abdominal pain and tenderness

 Extracolonic manifestations (may occur in 25% of cases)  Erythremia nodosum (on the shin – leg)  Pyoderma gangrenosum  Episcleritis  Thromboembolic events  Oligoarticular, non deforming arthritis (oligoarticular = 2-6 joints, poly = >6)

52   

Anterior uveitis (eye) Ankylosing spondylitis Sclerosing cholangitis with an increased risk of developing cholangiocarcinoma

53  Endoscopic findings  The mucosal appearance is characterized by edema, friability, mucopus, and erosions  Colonoscopy should not be performed in “severe disease” patients because of the risk of colon perforation  Risk of colon cancer  In patients with the disease proximal to the sigmoid colon, there is an increased risk of developing colon carcinoma  In patients that have had the disease for longer than10 years, there is an increased risk of developing colon cancer  can develop inflammatory polyp, mega colon  (Any male > 40 y.o. w/anemia has a GI malignancy until proven otherwise)

Vascular Ectasias Vascular ectasias are also called angiodysplasia and arteriovenous malformation They most commonly occur in elderly individuals in the cecum and ascending colon They may be a cause of acute or chronic blood loss They may be congenital or related to autoimmune disorders such as scleroderma Most are thought to arise from chronic muscular contraction that obstructs the venous mucosal drainage  Over time, the mucosal capillaries dilate and become incompetent, and arteriovenous communication forms (incompetent = backflows)     

Colon Diverticular Disease  Colonic diverticular (= outpouching, as polyps = in) disease is prevalent in over onethird of patients over 60 years of age  Most are asymptomatic and are discovered incidentally at endoscopy or on a barium enema  They vary from a few millimeters to several centimeters in size and from one to several dozen in number  In most patients, diverticulosis is thought to arise from a fiber deficient diet of many years duration  Uncomplicated diverticulosis  More than two-thirds of patients with diverticulosis have no specific symptoms  The majority of these will never be aware of the diverticula

54  Diverticulitis (diverticula infection)  m/c cause of fever in an older patient = diverticulitis  Essentials of diagnosis: o Acute abdominal pain and fever o Left lower abdominal tenderness with a mass o Moderate leukocytosis (20 to 25 K blood cell count) o Constipation or loose stools o Nausea and vomiting o Stool occult blood is common but hematochezia is rare (m/c cause = blood red per rectum  hemorrhoids)  Complications:  perforation, fistula formation, colon stricturing, partial or complete bowel obstruction. check  Treatment  Most cases of diverticulitis will need to be hospitalized during the acute stage  Patients should be given nothing by mouth and should receive intravenous fluids  Antibiotics should be given for 7 to 10 days  Unless the diverticula is removed, diverticulitis will recur in one-third of the patients  Diverticular bleeding  Essential of diagnosis o Bleeding begins without warning in otherwise asymptomatic patients o Acute onset of abdominal cramping followed by a large amount of bright red or maroon blood mixed with clots (hematochezia) o If large amounts of blood are lost, signs of hypovolemia, orthostatic changes in vital signs, or shock may develop o (Exsanguinate: bleed to death) – (orthostatic change  ↓ BP) o Bleeding usually stops spontaneously, requiring no further treatment, in up to 90% of the cases o 80% of patients have only one episode of bleeding 20.03.2001

Polyps of the Colon and Small Intestine  Polyps are lesions of discrete mass that protrude into the intestinal lumen  Polyps may be divided into 3 major pathologic groups: 1. Mucosal neoplastic (adenomatous) polyps 2. Mucosal nonneoplastic polyps (hyperplastic; juvenile; hamartomas; inflammatory) 3. Submucosal lesions (lipomas; lymphoid aggregates; carcinoids; pneumatosis cystoids intestinalis)

55  The non-neoplastic mucosal polyps …missed the end

56

Adenomatous Polyps 1. Non-familial adenomatous polyps    

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Histologically, they are classified as tubular, villous, or tubulovillous They may be sessile (very broad base like a mountain) or pedunculated (has a stalk, like a cauliflower) They are present in 30% of adults over 50 years of age It is proposed that there is an adenoma to carcinoma sequence whereby colorectal cancer develops through a continuous process from normal mucosa to adenoma to carcinoma Malignant potential correlates with polyp size, villous features (for surface area), and degree of dysplasia o Steps Normal  to malignancy. Metaplasia, Dysplasia, Carcinoma in Situ, Neoplasia, Is has been estimated that it takes an average of 5 years for a medium-sized adenoma to develop from normal appearing mucosa and 10 years for a gross malignancy to arise o 25-50% of all colorectal malignancy are on finger reach on DRE (digital rectal exam) Most patients with adenomatous polyps are completely asymptomatic o “Occult blood” = can’t see it Chronic occult blood loss may lead to iron deficiency anemia Large polyps may ulcerate, resulting in hematochezia Because of the adenoma to cancer sequence, all polyps should be removed as soon as they are discovered

2. Familial adenomatous polyposis    

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Familial adenomatous polyposis is an autosomal dominant disease characterized by the development of hundreds to thousands of adenoma in the colon Polyps occur at a mean age of 16 years, and almost all affected individuals have adenomas by age 35 years Colon cancer is inevitable by age 50 unless prophylactic colectomy is performed Extraintestinal manifestations of this condition include o Osteomas o Soft tissue tumors of the skin o Dermoid tumors (in the pelvis, ovaries) o Congenital hypertrophy of the retina The combination of familial adenomatous polyposis and extraintestinal lesions used to be called Gardner’s syndrome When central nervous system tumors are found with familial adenomatous polyposis, the condition has been called Turcot’s syndrome

57 3. Other Polyposis syndromes 

Peutz-Jeghers syndrome o An autosomal dominant condition with hamartomatous polyps throughout the gastrointestinal tract and mucocutaneous pigmented macules on the lips, buccal mucosa and skin o The hamartomas may become quite large, leading to bleeding, intussusception (telescopes, folds on itself), or obstruction o Volvulus or intussusception o Although hamartomas are not premalignant, up to 50% of these patients develop malignancies of the gastrointestinal tract

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Familial Juvenile polyposis o Another autosomal dominant condition o Characterized by more than 10 juvenile hamartomatous polyps, located most commonly in the colon o There is an increased risk of adenocarcinoma

Colorectal Cancer  Colorectal cancer is the second leading cause of death due to malignancy in the United States (1st cause = lung cancer for men and women – breast = 2nd)  Colorectal cancers are almost all adenocarcinomas  Approximately half of these cancers are located within the rectosigmoid region  Risk factors:  90% of cases occur in patients over 50  A history of adenomatous polyps increases the risk of subsequent adenomas and carcinoma and requires periodic colonoscopic examination  A person with one family member with colon caner has a twofold to threefold increased risk; if the family member was under 55, the risk is much greater  Familial polyposis syndrome increases the risk of colorectal cancer  In hereditary nonpolyposis colorectal cancer syndrome, not only is there an increase in the risk of colorectal cancer, there is an increase in the risk of developing cancers in other areas such as: endometrial, ovarian, renal, gastric carcinoma  Pancreatic, and small intestinal  The risk of adenocarcinoma of the colon begins to rise about 7-10 years after the onset of ulcerative colitis

58  Clinical findings  Signs and symptoms o Adenocarcinomas grow slowly and may be present for several years before symptoms appear o Asymptomatic tumors may be detected by the presence of fecal occult blood o Chronic blood loss from right-sided colonic cancers may cause iron deficiency anemia with fatigue and weakness o The right colon has a large diameter and more liquid fecal mater, making obstruction uncommon in cancers in this area o Obstruction with colicky pain and a change in bowel habits may accompany cancers in the left colon because the diameter is smaller and the fecal matter is more solid o Constipation and diarrhea may alternate o The stool may be streaked with blood, although, marked bleeding is unusual o Patients may note tenesmus, urgency, and recurrent hematochezia 21.03.2001 video bypass of stomach = what is it called? 26.03.2001

Colorectal Cancer  Inspection  Cancers may be detected with a high degree of reliability with either barium enema or colonoscopy  The treatment of choice is surgical resection  The follow-up treatment and prognosis depend on the staging of the tumor  American Joint Committee Classification:  Stage 0: Carcinoma in situ  Stage 1: o Tumor invades submucosa and muscularis layers o 5-year survival rate 80-100% o No adjuvant therapy recommended  Stage II o Tumor invades subserosa and pericolonic or perirectal tissue. Negative for lymph node metastasis. 5 yrs survival rate 50-75%. Chemotherapy and radiation therapy recommended Negative for lymph node metastasis o 5-year survival rate 50-75% o Chemotherapy and radiation therapy recommended  Stage III o Bowel wall perforation with lymph node metastasis o 5-year survival rate 30-50%

59 o Chemotherapy and radiotherapy recommended

60 

Stage IV o Presence of distant metastasis o Long-term survival rate 5% o Systemic chemotherapy for palliation only, it does not prolong survival

Anorectal Disease  Hemorrhoids  Internal hemorrhoids are a plexus of superior hemorrhoidal veins located above the dentate line (circumferential line that divides the rectum in half) which are covered by mucosa o The principal problems attributable to internal hemorrhoids are bleeding and mucoid discharge o They are confined to the anal canal (stage I), prolapse during straining and reduce spontaneously (stage II), prolapse and require manual reduction after bowel movement (stage III), may remain chronically protruding (stage IV) 

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External hemorrhoids arise from the inferior hemorrhoidal veins located below the dentate line and are covered with squamous epithelium of the anal canal or perianal region Hemorrhoids may become symptomatic as a result of activities that increase venous pressure, resulting in distention and engorgement. Straining at stool, constipation, prolonged sitting, pregnancy, obesity, and low-fiber diets all may contribute They are usually treated with a high fiber diet and increased fluid intake. Stage III and IV hemorrhoids with chronic severe bleeding may require surgical excision

 Anorectal Infections  Proctitis is defined as inflammation of the distal 1.5 cm of rectum and is characterized by anorectal discomfort, tenesmus, constipation, and discharge (+ lots of itching)  Most cases of proctitis are sexually transmitted, especially by anal-receptive intercourse  Infectious proctitis can be caused by: o Neisseria gonorrhea o Treponema pallidum o Chlamydia trachomatis (m/c sexually transmitted disease) o Herpes simplex (type 2) o Condyloacuminata (venereal warts)  Rectal prolapse  Rectal prolapse is protrusion through the anus of some or all layers of the rectum  It is most commonly seen in the elderly  If the prolapse is chronic, its results in mucous discharge, bleeding, incontinence, and sphincter damage

61 

Patients with complete prolapse require surgical correction

62  Solitary rectal ulcer syndrome  This condition is characterized by anal pain, excessive straining at the stool, and passage of mucus and blood  It is most commonly seen in young adults, especially women  Proctoscopic examination reveals a shallow rectal ulcer  Treatment is directed at decreasing straining through patient education and the use of bulking agents  Fecal Incontinence  There are five general requirements for bowel continence (control) o Solid or semisolid stool o A distensible rectal reservoir o A sensation of rectal fullness o Intact pelvic nerves and muscles o The ability to reach a toilet in a timely fashion 

Minor incontinence o This consists of slight soilage of undergarments that tends to occur with straining or coughing o This may be due to local anal problems such as hemorrhoids and skin tags that make it difficult to form a tight anal seal, especially if the stools are somewhat loose

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Major incontinence o Any complete uncontrolled loss of stool reflects a significant problem with sphincter or neurologic damage o Causes of sphincter damage include traumatic childbirth, episiotomy, prolapse, prior anal surgery, and physical trauma o Neurologic disruption may be cause by obstetric trauma, aging, diabetes mellitus, multiple sclerosis, spinal cord injury, and cauda equina syndrome

 Other Anal conditions:  Anal fissures  These are linear ulcers that are usually less than 5 mm in length  They are believed to arise from trauma to the anal canal during defecation due to straining, constipation or high internal sphincter tone  Patients complain of severe , tearing pain during defecation followed by throbbing discomfort  Perianal abscess and fistula  The anal glands may become infected, leading to abscess formation  Other causes of abscess include anal fissure and Crohn’s disease  Symptoms of perianal abscess are throbbing, continuous perianal pain  Anal fistulas may be a component of Crohn’s disease, lymphogranuloma venereum, rectal tuberculosis, and cancer

63 

Fistulas are associated with purulent discharge that may lead to itching, tenderness, and pain

64  Pruritus ani  This condition is characterized by perianal itching and discomfort  It may be caused by poor anal hygiene associated with fistulas, fissures, prolapsed hemorrhoids, skin tags (hamartoma where a little tag of skin comes off), and minor incontinence  Overzealous cleaning with soaps may cause a contact dermatitis  Other causes of pruritus ani include pinworms, candidal infection, scabies, and venereal warts  Squamous cell carcinoma of the anus  Although rare, anal cancer is increased among people who practice receptive anal intercourse and in those with a history of …… check  In over 80% of cases, human papillomavirus may be detected  Bleeding, pain, and local tumor are the most common symptoms  The lesion is often confused with hemorrhoids and other common anal disorders

Malabsorption  Malabsorption generally denotes disorders in which there is a disruption of digestion and nutrient absorption  Normal digestion and absorption may be divided into three phases: 1. Intraluminal phase – Fats, proteins, and carbohydrates are hydrolyzed and solubilized by pancreatic and bile secretions o Fats – they are broken down by pancreatic lipase to monoglycerides and fatty acids that form micelles with bile salts. Micelles are important in the solubilization and absorption of fat-soluble vitamins o Proteins – these are hydrolyzed by pancreatic proteases to di- and tripeptide and amino acids 2. Mucosal phase – this phase requires a sufficient surface area of intact small intestinal epithelium. Brush border enzymes help in the hydrolysis of disaccharides and di-an tripeptide 3. Absorptive phase – Obstruction of the lymphatic system results in impaired absorption of chylomicrons and lipoproteins

Celiac Sprue  Sprue is also known as gluten enteropathy or celiac disease  This condition is thought to be a genetically predisposed sensitivity to gluten  The gluten incites a humoral or cell-mediated inflammatory response that results in mucosal inflammation and destruction leading to a malabsorption of most nutrients

65  The essentials of diagnosis are:  Weight loss  Distention, flatulence, greasy stools  Steatorrhea  Diarrhea  Increased fecal fat  Abnormal bowel biopsy  Clinical improvement on a gluten-free diet  In addition the patient may be anemic, bruise easily due to Vitamin K deficiency, have hyperkeratosis (thick skin) due to Vitamin A deficiency, and bone pain due to osteomalacia  10% of patient with celiac sprue have a skin condition called dermatitis herpetiformis.  Products containing wheat, rye, and barley must be eliminated from the patients diet. Products and flours made from rice, soybean, potato and corn are safe.

Whipple’s Disease  Whipple’s disease is a rare multisystemic illness caused by infection with Tropheryma whippelii. The source of the infection is unknown, but no cases of human-to-human spread have been documented  Most cases have gastrointestinal symptoms that include abdominal pain, diarrhea, and the signs of malabsorption (distension, flatulence, and steatorrhea)  Weight loss is the most common presenting symptom  Non-gastrointestinal symptoms may include low-grade fever, chronic cough, lymphadenopathy (because of infection), and arthralgias. Other systems that could be involved include cardiac, ocular, and central nervous system  Antibiotic therapy results in a dramatic clinical improvement within several weeks  If untreated, the disease is fatal.

66

Short Bowel Syndrome  This syndrome is a malabsorptive condition that arises secondary to the removal of significant segments of small intestine  The most common causes in adults are  Crohn’s disease  Mesenteric infarction (supposedly most painful condition in humans)  Radiation enteritis (cancer patient on radiation)  Trauma  The type and degree of malabsorption depend upon the length and site of the resection and the degree of adaptation of the remaining bowel

Lactase Deficiency  Lactase is a brush border enzyme that hydrolyzes the disaccharide lactose into glucose and galactose  Lactase deficiency is common in premature infants of less than 30 weeks’ gestation  Lactase levels are high at birth but decline steadily in non-Europeans during childhood, adolescence, and into adulthood.  With mild to moderate amounts of lactose malabsorption, patients may experience bloating, abdominal cramps, and flatulence. In more severe cases, diarrhea may result  Lactase supplementation or a limited lactose diet are the choices of treatment  Patients on a lactose-free diet should add calcium supplementation to prevent osteoporosis

Acute Small Intestinal Obstruction  The most common causes of obstruction are:  Adhesions (usually post-surgical)  External hernias (femoral, inguinal, umbilical)  Internal hernias  Volvulus (bowel twists on itself)  Crohn’s disease  Radiation enteritis  Intestinal wall hematomas (after trauma or anticoagulants)  Neoplasms (rare)

67  Most obstruction will cause simple occlusion of the intestinal lumen that results in distension and large losses of fluid into the gut  If the obstruction is proximal, the patient will develop cramping abdominal pain and vomiting within minutes of the obstruction and there will be minimal abdominal distention  If the obstruction is distal, it may take hours for the cramping abdominal pain and vomiting to appear and the abdominal distention is usually pronounced  Strangulation with necrosis of the bowel wall, which may lead to perforation, peritonitis, and sepsis are the major complications of obstruction  After the patient is stabilized, surgery is performed to remove the cause of obstruction 27.03.2001

History and Clinical Examination  In motility disturbances of the stomach, small intestine and colon, cramping abdominal pain occurs frequently, often after eating.  The location of pain usually indicates its source:  Epigastric for stomach  Periumbilical or generalized for small intestine  Lower quadrants for colon  Colonic pain resolves after a bowel movement or passing flatus  Early satiety or postprandial vomiting occurs in patients with conditions causing delayed transit through the stomach and upper small bowel.  Rapid gastric emptying causes of “dumping syndrome” which include: sweating, weakness, orthostasis, tachycardia, and diarrhea (= autonomic disorder)  Bowel sounds:  Obstruction causes high-pitched rushes (tiny)  In Pseudo-obstruction the bowel sounds are quiet but usually present (ileus)  Bowel habits:  Diarrhea or constipation are the cardinal symptoms of motor disorders  Diarrhea is more than three bowel movements a day  Constipation is less than three bowel movements a week  Vomiting and distention:  In proximal small bowel obstructions and pseudo-obstructions, vomiting is prominent and distention is not

68  

In distal obstruction distention is prominent and vomiting is not When vomiting occurs with a distal obstruction, it usually has a fecal odor

69

Delayed Gastric Emptying  Delayed gastric emptying occurs more often than rapid gastric emptying  Chronic delayed gastric emptying is called Gastroparesis (elderly, diabetics)  Acute gastroparesis is usually associated with  Electrolyte imbalance  Ketoacidosis  Systemic infection  Acute abdominal insult  Symptoms include:  Early satiety  Nausea  Vomiting  Phytobezoars (a concretion composed of the skin, seeds, and fibers of fruits and vegetables)  Delayed emptying can occur as a complication of surgery and diabetes  Rapid gastric emptying is seen in the following conditions:  Duodenal ulcer disease  Zollinger-Ellison syndrome  Pancreatic insufficiency  Celiac sprue

Decreased Intestinal Motility  Conditions that can cause a decrease in intestinal motility are:  Acute adynamic ileus (quits working, nothing is obstructing it)  Intestinal pseudo-obstruction  Progressive systemic sclerosis  Amyloidosis (may cause either a myopathy or a neuropathy)  Muscular dystrophy (through the affect on smooth muscle)  Hypothyroidism (decreases frequency and amplitude of intestinal contractions)  Intestinal diverticulosis

Acute Paralytic Ileus  This condition is also known as Adynamic Ileus  There is a neurogenic failure or loss of peristalsis in the intestine in the absence of any mechanical obstruction  It is frequently seen in patients hospitalized as a result of:  Abdominal surgery  Severe medical illness

70 

Medications

71  The essentials of diagnosis are:  Nausea  Vomiting  Obstipation (excessive constipation)  Distention  Minimal abdominal tenderness  Decreased bowel sounds (one of the hallmarks) o Differential = obstruction o Paralytic ileus = small bowel

Acute Colonic Pseudo-Obstruction  Also called Ogilvie Syndrome  This condition is often seen in hospitalized patients as a result of:  Severe medical illness  Postoperative states  There is severe abdominal distention with massive dilation of the cecum or right colon which may be precipitated by:  Electrolyte imbalances  Medications  The symptoms are usually mild abdominal pain and tenderness. However, the patients may be unable to …missed the end

Progressive Systemic Sclerosis  It is the most common “collagen vascular disease” to cause a decrease in intestinal motility  The defect is in both neural enervation and smooth muscle function  Patients become symptomatic only after there has been extensive replacement of the smooth muscle with collagen  Occasionally polymyositis …missed the end

Increased Motility Disorder  Visceral neuropathy  Causes a decrease of neural inhibition (of the bowel)  The hallmark findings of visceral neuropathy are: o A patchy loss of nerve tracts o A decreased number of neurons o Fragmentation and dropout axons

72

73  Irritable bowel syndrome  Diabetes mellitus  The primary symptom is diarrhea  Intestinal infections  Brain stem lesions  Hyperthyroidism

Tumors of the small Intestine Benign Tumors  Adenomatous polyps are the most common benign mucosal tumor  Although they are usually asymptomatic, because of the remote possibility of malignant transformation, surgical excision is usually recommended  Lipomas occur commonly in the ileum  They are not usually removed  Leiomyomas are found at all levels of the intestine  They are usually surgically excised because: o They may ulcerate o They may cause acute or chronic…missed the end

Malignant Tumors  Adenocarcinoma  They are very aggressive  They usually occur in the duodenum or proximal jejunum  Eighty percent have already metastasized at the time of diagnosis  Lymphoma  They most commonly occur in the distal small intestine  The majority are non-Hodgkin’s B cell lymphomas  Carcinonoids  They are the most common neuroendocrine tumors (particularly epinephrine)  The overall 5 year survival rate is 50%  Over 95% of all gastrointestinal Carcinoids occur in either the rectum, the appendix of the small intestine  Small intestinal carcinoids most commonly occur in the ileum  Kaposi’s Sarcoma in the intestine…missed the end

74

Appendicitis KNOW  Appendicitis is the most common abdominal surgical emergency  It occurs most commonly between the ages of 10 and 30 years  Signs and symptoms:  Early pain – periumbilical  Late pain – right lower quadrant  Anorexia  Nausea  Vomiting  Obstipation  Low-grade fever  Moderate neutrophilic leukocytosis (10,000-20,000 per microliter)  Psoas sign (pain on passive extension of the right hip)  Obturator sign (pain with passive flexion …)  The major complication of appendicitis is perforation. Some of the signs of perforation are:  Pain persisting for over 36 hours  High fever  Diffuse abdominal pain or tenderness  A palpable abdominal mass  Marked leukocytosis  A localized perforation results in a contained abscess, usually in the pelvis  A free perforation leads to suppurative peritonitis with toxicity  Uncomplicated appendicitis is treated with surgical appendectomy

Intestinal Tuberculosis  Previously rare in the USA, its incidence has been rising in immigrant groups and patients with AIDS  Increased 15-20% in last 10 years  Happens in upper lobes  The most frequent site of involvement is the ileocecal region  Intestinal tuberculosis may cause mucosal ulcerations or scarring and fibrosis with narrowing of the lumen  Patients may complain of chronic abdominal pain, obstructive symptoms, weight loss, and diarrhea. An abdominal mass may be palpable. Get febrile, night sweats

75  Complications include intestinal obstruction, hemorrhage, fistula formation, and bacterial overgrowth with malabsorption

76

Protein-Losing Enteropathy  Protein-losing enteropathy comprises a number of conditions that result in excessive loss of serum protein into the gastrointestinal tract  The essential diagnostic features are hypoalbuminemia and an elevated fecal alpha one antitrypsin level (found also in emphysema)  Proteins may be lost through one of three mechanisms  Mucosal disease with ulceration  Lymphatic obstruction  Idiopathic change in the permeability of mucosal capillaries  In most cases, protein-losing enteropathy is a component of other known gastrointestinal disorders