Gastrointestinal Disease Part II Lecture Notes PDF

Presenting problems in gastrointestinal disease part II Dr. Bahaa Aldin Adnan FIBMS MED ONC  Diarrhea.  Increase in daily stool weight of more than 200gm/24 hours.  Normal bowel frequency ranges between 3times/day to 3times/week. Pseudodiarrhea: Increased frequency with normal...

Presenting problems in gastrointestinal disease part II Dr. Bahaa Aldin Adnan FIBMS MED ONC  Diarrhea.  Increase in daily stool weight of more than 200gm/24 hours.  Normal bowel frequency ranges between 3times/day to 3times/week. Pseudodiarrhea: Increased frequency with normal weight. IBS ,Proctitis and Hyperthyroidism. Incontinence: Involuntary release of rectal contents. Constipation refers to infrequent defecation (less than two bowel movements weekly) Patients may also complain of sensation of incomplete evacuation and either perianal or abdominal discomfort Diarrhea Acute & chronic  Acute:7-14 days. occasionally less than 6 week.  Persistent: 2-4 weeks  Chronic: More than 4 weeks. Occasionally more than 6 weeks.  Acute infectious causes are commonest. Acute infectious diarrhea.  Non-inflammotry.  Inflammatory. NON-INFLAMMOTRY  Watery.  Non bloody.  Periumblical cramps.  Bloating.  Nausea and vomitting.  Single or in combition. Inflammatory diarrhea  Fever.  Bloody.  Small in volume.  Left lower quadrant cramps.  Urgency and tenesmus. Etiology Food poisoning  Staphylococcus aureus.  Shortest incubation period. 1-6 hours. Last for less than 12 houres.  Infected human carriers are the source.  If food is left to cool slowly and remains at room temperature organisms have opportunity to form toxins.  Out breaks after picnics.  Potatos,salads,mayonnise,cream pastries.  Bacillus cereus.  Two types of illness Emetic form: within 6 hours (stereotypically due to rice) Diarrheal form: after 6 hours  If cooked rice is not refrigerated,heat resistant spores which have escaped boiling germinate and produce toxin.Frying before serving may not destroy these preformed heat stable toxins. Clostridium perferingens  Incubation period 8-14 hours.  Heat resistant spores.  Inadequately cooked meat, poultry or legumes.  Self limiting up to 24 hours. Etiology of inflammatory diarrhea  Viral: Noro virus ( diarrhea & vomiting same time), Rota virus ( workers in nursery care), watery  Protozoal: Entamoeba histolytica (Gradual onset bloody diarrhea, abdominal pain and tenderness that may last several weeks. Cryptosporidium (common in patients with HIV/ AIDS) Giardiasis (prolonged non bloody leads to malabsorption)  Bacterial: Shigella (Bloody diarrhea, vomiting, abdominal pain), Compylobacter jejuni (A flu-like prodrome is usually followed by crampy abdominal pain, fever and diarrhea which may be bloody), E-coli (Commonest infectious agent amongst travelers, watery diarrhea with abdominal cramps and nausea  Approach to patient.  HISTORY: 1.Duration. 2.Fever.Infections out side the gut like malaria. 3.Frequency.May correlate with dehydration. 4.Abdominal pain. -Inflammatory nature. -RIF Pain with yersina. -Bloating with Giardiasis. 5.Vomiting. -Acute illness -Toxin. -Systemic disease. -Obstruction. 6. Tenesmes: shigellosis. 7. Appearance of stools. -Blood--Shigellosis -Rice watery--Vibrio cholera. -Bulky white--small intestine  Chronic diarrhea. Diarrhea which persists for more than 4 weeks Needs evaluation to exclude serious pathology Most of the causes are noninfectious. Classification of chronic diarrhea  Osmotic.  Secretary.  Inflammatory.  Motility disorders.  Factitious.  Malabsorptive conditions.  Chronic infections. Osmotic diarrhea.  Large volume stool results from lack of absorption of orally ingested solutes (food).Osmotic effect.  Relieved with fasting.  Clinical symptoms are usually becauses of malabsorption of fat or carbohyderates.  Osmotic causes include lactase deficiency intolerant to dairy products, drugs like laxatives etc.  Secreatary diarrhea.  Watery painless excretion of large ammount more than 1 litre/day.  No effect with fasting (persist).  Abnormal fluid and electrolyte transport. no pus, mucus or blood in stool.  Hormones mediated.  Causes may include Carcinoid, Zollinger ellison syndrome, Medullary carcinoma of thyroid and extensive gut recsection. Steatorrheal causes.  Intraluminal maldigestion. Chronic pancreatitis. Decreased bile salts. Bacterial over growth.  Mucosal malabsorption. Celiac disease. Tropical sprue.  The stools are large volume.  Fatty or greasy, pale yellow to grey colored, extremely smelly, sometimes frothy and float in the toilet bowl (lavatory pan) and are difficult to flush away. Quantitatively, steatorrhea is defined as stool fat exceeding the normal 7 g/d; rapid-transit diarrhea may result in fecal fat up to 14 g/d; daily fecal fat averages 15–25 g with small intestinal diseases and is often >32 g with pancreatic exocrine insufficiency. Inflammatory diarrhea.  Fever  Abdominal pain and tenderness.  Hematochezia.  Patients may have toxic looks.  Extra intestinal manefestation may be present.  Causes include IBD,malignancy,radiation enterits. Motility disorders  Systemic disorders like diabetes and hyperthyroidism.  Previous gut surgery.  Irritable bowel.  Fecal impaction.  Neurological disorders.  FACTITIOUS DIARRHEA:Laxative abuse Approach to patients.  History.  Symptoms and signs of inflammation.  Extra intestinal manefestations.  Perepheral edema or ascitis.  Type of stools-intestinal malabsoption.  Flatulence.  Weight loss.  Systemic manifestations like flushing.  Autonomic dysfunctions like postural drop and disordered sweating in diabetes.  Diarrhea alternating with constipation-IBS.  Effects of malabsorption like anemia, bleeding tendency,osteopenia,amenorrhea and infertility should be looked for. JAUNDICE  Accumulation of bilirubin.  Yellowish pigmentation of plasma.  Discolouration of heavily perfused tissues like skin,sclera and mucous membranes.  Clinically hyperbilrubinemia manifests as icterus or jaundice.  Serum bilrubin > 34-43 micro mol/l  2.6-2.5 mg/dl  Jaundice manifestes even at lower levels in people with fair skin and anemia  Obscured in dark skin individuals or with edema.  Need to be observed in sun light.  Needs to be differentiated from Carotenemia charecterised by yellow brown pigmentation of palms ,soles and nasolabial folds with normal sclera ,mucosal membrane and urine color. Production and metabolism  Normal serum Bilirubin Conc. 5-17 micro mol/l.3-1 mg/l  More than 90% is unconjugated circulating as albumin bound complex.  Remainder conjugated(primarily glucuronide) to polar group which is water soluble and excreted in urine.  80% of Bilirubin –RBCs break down.  15-20%Ineffective erythropoises and metabolism of other heme containing protiens Metabolism  Hepatic uptake.  Conjugation.  Excretion into bile Derangement of bilirubin metabolism  Over production.  Decreased hepatic uptake.  Decreased hepatic conjugation.  Decreased excretion.  Classification Predominantly unconjugated 1- Over production A)Hemolysis B)Ineffective erythropoiesis. 2- Decreased hepatic uptake. A)Prolonged fasting. B)Sepsis 3-Decreased conjugation. (decreased glucoronyl transferase) A)Hereditary Transferase deficiency Gilbert syndrome. Crigler Najjar syndrome. B) Neonatal jaundice. C) Acquired transferase deficiency.  Predominantly conjugated hyperbilirubinema.  1-Impaired hepatic excretion A.Familial or hereditary. Dubin jhonson &Rotor syndromes, Recurrent benign intrahepatic cholestasis, Cholestatic jaundice of pregnancy. B.Acquired disorders. Hepatocellular diseases Hepatitis, cirrhosis. Drugs like:- OCP, Anabolic steroids, Chloramphenicol, Chlorpromazine, Erythromycin, Augmentin, TMT/SMX, Antifungals, Tricyclic antidepressant, Azathioprim, Antiretrovirals, Tetracyclins, Fluoroquinolones  Alcohol Sepsis Post operative Biliary cirrhosis. 2-Extrahepatic: Biliary obstruction. Compression of biliary duct. – Evalution of jaundice. Hyperbilirubinemia.  Hemolysis—Indirect Bilirubin.  Hepatobiliary –Direct Bilirubin. Unconjugated Hyperbilirubinia.  Hemolysis.  Bil. Rarely above 5mg%.  Gilbert syndrone is an exception.  Reticulocyte count is high.  Hb is low.  LDH is high. Conjugated Hyperbilirubinia Hepatocellular. Intrahepatic obstruction. Extra hepatic obstruction. Approach to patient with jaundice.  Age. Young------- Hepatitis. Old -------Malignancy.  Duration of symptoms.  Abdominal pain.  Fever and other symptoms of active inflammation.  Appitite change,weight loss or altered bowels—Malignancy.  Transfusion.(hepatitis B&C).  Use of intravenous drugs.  Sexual contact.  Ethanol.  Travel and immunization.  Drugs. Cholestsis.Anabolic steroids and chlorpromazine. Heepatocellular necrosis. Acetoaminophen,ATT.  Sore throat and rash— Infectious mononucleosis.  Pruritis—Chronic cholestasis. Hepatic: Primary Biliary cirrhosis. Sclerosing cholangitis. Extra hepatic obstruction.  Pregnancy.  Past history of jaundice, hepatitis,arthralgias Prodromal symptoms. Viral hepatitis.  Previous surgery:Biliary procedures. Stones, strictures.  Pre existing IBD.  Right heart failure.  Skin tatooing.  History of GI bleeding.  Family history.Congenital spherocytosis. Physical examination.  Excoriation.  Fever and epigastric/RUQ tenderness.  Painless jaundice.  Enlarged tender liver.  Rapidly enlarging liver.  Palpable gall bladder.  Spleenomegaly.  Peripheral stigmas of liver diasease.  Wasting and lymphoadenopathy.  History pointing to malignancy. Primary tomours in abdomen ,breast and thyroid should be looked for.