Symptomatology-GIT-1
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Symptomatology-GIT-1 Symptomatology-GIT-1 Presentation Transcript

  • SYMPTOMATOLOGY IN GIT PART-11 DR.MUZAMIL JAMIL ASSOCIATE PROFESSOR MEDICINE
  • JAUNDICE ♦ Accumulation of bilirubin. ♦ Yellowish pigmentation of plasma. ♦ Discolouration of heavily perfused tissues likeskin,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.
  • Pathological terms. ♦ Hemolytic. ♦ Hepatocellular. ♦ Obtructive.
  • Classification ♦ Predominantly unconjugated 1-Over production A)Hemolysis B)Ineffective erythropoises. 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 Drugs inhibition –Choramphenical
  • ♦ Breast milk jaundice. ♦ Hepatocellular disease. ♦ 4-Sepsis.
  • Predominantly conjugated hyperbilirubinema. ♦ 1.Impaired hepatic excreation A.Familial or hereditary. Dubin jhonson &Rotor syndromes, Recurrent benign intrahepatic cholestasis, Cholestatic jaundice of pregnancy. B.Acquired disorders. 1)Hepatocellular diseases Hepatitis,cirrhosis. 2)Drugs. OCP, Androgens,Chloramphenical.
  • ♦ 3)Alcohol 4)Sepsis 5)Post operative 6)Biliary cirrhosis. ♦ Extrahepatic Biliary obstruction. Intraductal Compression of biliary duct. –
  • Evalution of jaundice. Hyperbilirubinemia. ♦ Hemolysis—In direct Bilirubin. ♦ Hepatobiliary –Direct Bilirubin.
  • Unconjugated Hyperbilirubinia. ♦ Hemolysis. ♦ Resorbtion of large hematoma. ♦ 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. ♦ Acholic stools. ♦ 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.
  • Diarrhea. ♦ Increase in daily stool weight of more than 250gm/24 hours. ♦ Normal bowel frequency ranges between 3times/day to3times/week.
  • Factors influencing stool weight ,consistency and frequency. in diet. ♦ 1.fiber content ♦ 2.Gender. ♦ 3.Ingested medicines. ♦ 4.Exercise. ♦ 5.Stress.
  • ♦ Pseudodiarrhea: Increased frequency with normal weight. IBS ,Proctitis and Hyperthyroidism. ♦ Incontinence: Involuntary release of rectal contents.
  • Acute and choronic. ♦ Acute: 7---14 days. occasionally less than 6 week. ♦ Chronic: More than 4 weeks. Occasionally more than 6 weeks. ♦ Persistent:2—4 weeks. ♦ Acute infectious causes are commonest. ♦ Acute GI diseases are second only to URTI.
  • Epidemiology. ♦ In less than 5 years of age. 2—3 illnesses per child per year.Developed countries. 10— 18 illnesses per child per year in developing countries. One Billion cases world wide. 4—6 million deaths. 12600 Deaths/Day.
  • Acute infectious diarrhea. ♦ Non-inflammotry. ♦ Inflammotry. . 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(non-inflammatory) ♦ Viral:Norwalk,Nor walk like and Rota virus ♦ Protozoal: Giardia,cryptosporidium. ♦ Bactrial: 1.Preformed toxins:Styphylococcus aures, bacellius cereus and clostridium perfringens 2.Enterotoxin production:Ecoli,vibrio cholera.
  • Food poisoning ♦ Staphylococcus aureus. ♦ Shortest incubation period.1—6 hours. Lasts 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. ♦ Short incubation period. 1—6 hours emetic form. Long incubation period. upto 18 hours diarrheal form. ♦ 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 upto 24 hours.
  • Etiology for infllammatory diarrhea. ♦ Viral:CMV. ♦ Protozoal:Entamoeba histolytica. ♦ Bacterial:Shigella,salmonella,compylopacte r jejuni,entero invasive E-coli and vibrio parahemolytic.
  • 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. ♦ 8.Common source. ♦ 9.Antibiotic use. ♦ 10.Travel.
  • Physical examination. ♦ Signs of dehydration—Severity of illness. ♦ MILD. -Thirst. -Dry mouth. -Decreased axillary sweat. -Decreased urine out put. -Slight weight loss.
  • Moderate dehyderation. ♦ Orthostatic hypotension ♦ Skin tenting. ♦ Sunken eye balls.
  • Severe dehydration. ♦ Hypotension. ♦ Tachycardia. ♦ Confusion. ♦ Frank coma.
  • Prompt medical evaluation. ♦ Inflammatory diarrhea. ♦ High fever. ♦ Bloody diarrhea. ♦ Abdominal pain. ♦ 6 or more unformed stools/24 hours. ♦ Profuse watery diarrhea. ♦ Severe dehyderatuon. ♦ Elderly or immunocompromised patients.
  • Chronic diarrhea. Diarrhea which persists for more than 4 weeks Needs evaluation to exclude serious pathology Most of the causes are noninfectious.
  • Classification. ♦ 1-Osmotic. ♦ 2-Secreatary. ♦ 3-Inflammatory. ♦ 4.Motility disorders. ♦ 5.Fectitious. ♦ 6.Malabsorptive conditions. ♦ 7.chronic infections.
  • Osmotic diarrhea. ♦ 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, drugs like laxatives etc.
  • Steatorrheal causes. ♦ Intraluminal maldigestion. .Chronic pancreatitis. .Decreased bile salts. .Bacterial over growth. ♦ Mucosal malabsorption. .Celiiac disease. .Tropical sprue.
  • Secreatary diarrhea. ♦ Excreation of large ammount more than 1 litre/day. ♦ No effect with fasting. ♦ Abnormal fluid and electrolyte transport. ♦ Harmones mediated. ♦ Causes may include Carcinoid, Zollinger ellison syndrome, Medullary carcinoma of thyroid and extensive gut recsection.
  • 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. ♦ FECTITIOUS 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.
  • Common causes ♦ Abdominal tuberculosis. ♦ Coeliac disease. ♦ Inflammatory bowel disease. ♦ Giardiasis. ♦ Tropical sprue. ♦ Colonic malignancy.