Various common Symptoms of GIT are discussed with possible causes. I tried to cover the topic in second presentation as it is extensive enough to cover in single presentation. I hope it will help you somehow.

1. SYMPTOMATOLOGY IN
GIT PART-11
Ahsan Sajjad
RMU-43

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
- Pregnanediol

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.
 1.fiber content in diet.
 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:E-coli,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.