1. SYMPTOMATOLOGY IN
GIT PART-11
DR.MUZAMIL JAMIL
ASSOCIATE PROFESSOR
MEDICINE

2. 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

3. ♦ 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.

4. 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.

5. ♦ 80% of Bilirubin –RBCs break down.
♦ 15-20%-Ineffective erythropoises and
metabolism of other heme containing
protiens

6. Metabolism
♦ Hepatic uptake.
♦ Conjugation.
♦ Excretion into bile.

7. Derangement of bilirubin
metabolism
♦ Over production .
♦ Decreased hepatic uptake.
♦ Decreased hepatic conjugation.
♦ Decreased excretion.

8. Pathological terms.
♦ Hemolytic.
♦ Hepatocellular.
♦ Obtructive.

9. Classification
♦ Predominantly unconjugated
1-Over production
A)Hemolysis
B)Ineffective erythropoises.
2-Decreased hepatic uptake.
A)Prolonged fasting.
B)Sepsis.

10. ♦ 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

11. ♦ Breast milk jaundice.
♦ Hepatocellular disease.
♦ 4-Sepsis.

12. 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.

13. ♦ 3)Alcohol
4)Sepsis
5)Post operative
6)Biliary
cirrhosis.
♦ Extrahepatic Biliary obstruction.
Intraductal
Compression of biliary
duct.
–

14. Evalution of jaundice.
Hyperbilirubinemia.
♦ Hemolysis—In direct Bilirubin.
♦ Hepatobiliary –Direct Bilirubin.

15. 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.

16. Conjugated Hyperbilirubinia
Hepatocellular.
Intrahepatic obstruction.
Extra hepatic obstruction.

17. 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.

18. ♦ Transfusion.(hepatitis B&C).
♦ Use of intravenous drugs.
♦ Sexual contact.
♦ Ethanol.
♦ Travel and immunization.
♦ Drugs.
Cholestsis.Anabolic steroids and chlorpromazine.
Heepatocellular
necrosis. Acetoaminophen,ATT.

19. ♦ Sore throat and rash—
Infectious mononucleosis.
♦ Pruritis—Chronic cholestasis.
Hepatic: Primary Biliary cirrhosis.
.
Sclerosing cholangitis.
Extra hepatic obstruction.
♦ Acholic stools.
♦ Pregnancy.

20. ♦ 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.

21. Physical examination.
♦ Excoriation.
♦ Fever and epigastric/RUQ tenderness.
♦ Painless jaundice.
♦ Enlarged tender liver.
♦ Rapidly enlarging liver.
♦ Palpable gall bladder.
♦ Spleenomegaly.

22. ♦ Peripheral stigmas of liver diasease.
♦ Wasting and lymphoadenopathy.
♦ History pointing to malignancy.
Primary tomours in abdomen ,breast
and thyroid should be looked for.

23. Diarrhea.
♦ Increase in daily stool weight of more than
250gm/24 hours.
♦ Normal bowel frequency ranges between
3times/day to3times/week.

24. Factors influencing stool
weight ,consistency and
frequency. in diet.
♦ 1.fiber content
♦ 2.Gender.
♦ 3.Ingested medicines.
♦ 4.Exercise.
♦ 5.Stress.

25. ♦ Pseudodiarrhea:
Increased frequency with normal
weight.
IBS ,Proctitis and
Hyperthyroidism.
♦ Incontinence:
Involuntary release of rectal contents.

26. 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.

27. 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.

28. Acute infectious diarrhea.
♦ Non-inflammotry.
♦ Inflammotry.
.
NON-INFLAMMOTRY
♦ Watery.
♦ Non bloody.
♦ Periumblical cramps.
♦ Bloating.
♦ Nausea and vomitting .
♦ Single or in combition.

29. Inflammatory diarrhea
♦ Fever.
♦ Bloody.
♦ Small in volume.
♦ Left lower quadrant cramps.
♦ Urgency and tenesmus.

30. 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.

31. 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.

32. 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.

33. Clostridium perferingens
♦ Incubation period 8—14 hours.
♦ Heat resistant spores.
♦ Inadequately cooked meat, poultry or
legumes.
♦ self limiting upto 24 hours.

34. Etiology for infllammatory
diarrhea.
♦ Viral:CMV.
♦ Protozoal:Entamoeba histolytica.
♦ Bacterial:Shigella,salmonella,compylopacte
r jejuni,entero invasive E-coli and vibrio
parahemolytic.

35. 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.

36. ♦ 5.Vomiting.
-Acute illness
-Toxin.
-Systemic disease.
-Obstruction.
♦ 6.Tenesmes:shigellosis.
♦ 7.Appearance of stools.
-Blood—Shigellosis.

37. ♦ -Rice watery—Vibrio cholera.
-Bulky white—small intestine.
♦ 8.Common source.
♦ 9.Antibiotic use.
♦ 10.Travel.

38. Physical examination.
♦ Signs of dehydration—Severity of illness.
♦ MILD.
-Thirst.
-Dry mouth.
-Decreased axillary sweat.
-Decreased urine out put.
-Slight weight loss.

39. Moderate dehyderation.
♦ Orthostatic hypotension
♦ Skin tenting.
♦ Sunken eye balls.

40. Severe dehydration.
♦ Hypotension.
♦ Tachycardia.
♦ Confusion.
♦ Frank coma.

41. 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.

42. Chronic diarrhea.
Diarrhea which persists for more than 4
weeks
Needs evaluation to exclude serious
pathology
Most of the causes are noninfectious.

43. Classification.
♦ 1-Osmotic.
♦ 2-Secreatary.
♦ 3-Inflammatory.
♦ 4.Motility disorders.
♦ 5.Fectitious.
♦ 6.Malabsorptive conditions.
♦ 7.chronic infections.

44. 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.

45. Steatorrheal causes.
♦ Intraluminal maldigestion.
.Chronic pancreatitis.
.Decreased bile salts.
.Bacterial over
growth.
♦ Mucosal malabsorption.
.Celiiac
disease.
.Tropical sprue.

46. 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.

47. 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.

48. Motility disorders
♦ Systemic disorders like diabetes and
hyperthyroidism.
♦ Previous gut surgery.
♦ Irritable bowel.
♦ Fecal impaction.
♦ Neurological disorders.
♦ FECTITIOUS DIARRHEA:Laxative abuse

49. Approach to patients.
♦ History.
♦ Symptoms and signs of inflammation.
♦ Extra intestinal manefestations.
♦ Perepheral edema or ascitis.
♦ Type of stools-intestinal malabsoption.
♦ Flatulence.
♦ Weight loss.

50. ♦ 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.

51. Common causes
♦ Abdominal tuberculosis.
♦ Coeliac disease.
♦ Inflammatory bowel disease.
♦ Giardiasis.
♦ Tropical sprue.
♦ Colonic malignancy.