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SYMPTOMATOLOGY GIT
DR MUZAMIL JAMIL
ASSOCIATE PROFESSOR
MEDICINE
♦ HAEMETEMESIS
♦ MALENA
♦ HEMATOCHEZIA
♦ NAUSEA &VOMITTING
♦ DYSPEPSIA
♦ DYSPHAGIA
♦ DIARRHEA
♦ ABDOMINAL PAIN
♦ JAUANDICE
♦ ASCITIS
Hemetemesis
♦ Vomiting of blood .
♦ Proximal to ligament of treitz.
♦ GI bleeding below duodenum rarely enters

stomach.
♦ Colour of vomited blood depends on
1.Concentration of HCL acid
♦ 2.Duration of contact with acid.

Short duration—red color
Long duration—dark red,brown
black or cofee ground appearance.
Melena
♦ Black tarry stools.
♦ Sticky,loose with characteristic odour.
♦ HCL acts on Hb to produce haemetin giving

black colour.
♦ Usaually follows hemetemesis.
♦ Both suggest proximal source.
♦ Bleeding from esophagus,stomach, small
gut and even ascending colon occasionally.
♦ 60 ml of blood –Single melena stool.
♦ More than this may lead melena upto 7

days.
♦ Occult blood in stools remains positive for
weeks with normal stool colour.
♦ Black or dark gray stools may occur with
use of iron, bismith or licorice.
♦ Occult blood in stool—potentially serious.
Hematochezia
♦ Passage of blood per rectum.
♦ Bleeding distal to ligament of treitz.
♦ Brisk proximal bleeding—rapid transit.
♦ Anal or rectal lesions like haemorrhoids or

anal fissure.
♦ Colonic lesions like growth ,IBD ,infections
and angiodysplasia.
Clinical manefestions
♦ Extent of bleeding.
♦ Rate of bleeding.
♦ Comorbid factors.
Extent of bleeding.
♦ Less than 500 ml of blood loss—rarely

associated with systemic signs.Exceptions
include elderly and anemic.
♦ Orthostatic hypotention—20% or greater
reduction in blood volume.
♦ Concomitant symptoms include
lightheadedness, syncope, nausea, sweating
and thirst.
♦ Blood loss upto 25-40%--Shock.
Common causes of upper GI
bleed.
♦ Varices
♦ Peptic ulcer
♦ Gastroduodenal erosions
♦ Mallory weiss tear
♦ Malignancy
Variceal bleeding.
♦ Varices—Bleed is abrupt and massive.
♦ Underlying cirrhosis and portal

hypertension
♦ 25% cases other sources like erosive
gastropathy and peptic ulcer.
♦ Stigma of CLD.
Peptic ulcer.
♦ Peptic ulcer—Break in gastric/duodenal

mucosa may extend through muscularis.
♦ 5 times more common in duodenum
♦ 95% in bulb or pyloric channel.
♦ NSAIDS ,H pylori, and acid hypersecretion.
♦ History suggestive.
Miscellaneous.
♦ Erosions—Asprin and NSAIDS.
♦ Mallory weiss—Mucosal tear with retching

and vomiting.
♦ Esophagititis—GERD ,infections and
malignancy.
Nausea and vomiting
♦ Nausea is a desire or feeling.
♦ Vomiting is forceful expulsion of gastric

contents.
♦ Retching is laboured rythmic contraction of
respiratory and abdominal musculature
precede or accompany vomiting.
Control of vomiting
♦ 2 distinct medullary centers.
♦ Vomiting center in dorsal part of lateral

reticular formation .
♦ CTZ area postrema of floor of fourth
ventricle.
♦ Vomiting center controls and integrates the
actual act of emesis.It receives inputs from
four different sources.
Impulses reaching vomiting
centre.
♦ Afferent vagal.
♦ Vestibular system.
♦ Higher centers.
♦ Area postrema.
Causes based on input
♦ Visceral afferent---Mechanical obstruction,

dysmotlity, peritonial irritation ,infection
,hepatobiliary or pancreatic and topical.
♦ CNS disorders(vestibular & higher centers)
middle ear diseases, increased ICP,CNS
infections,psychogenic.
♦ CTZ—irritation from drugs and systemic
disorders(DKA,uremia,adrenocortial crisis.
Associated features.
♦ Temporal relations like early morning

houres, relation with meals and psychogenic
♦ Associated symptoms are important.
♦ Vertigo and tinnitis—Meniers disease.
♦ Long standing history with out significant
sequel point psychogenic.
♦ Localizing symptoms like in abdomen or
CNS.
Character of vomitus.
Character of vomitus.
Large amount of acid.
Absence of acid.
Feculent or putrid odor.
Presence of blood.
EFFECTS OF VOMITING
Dyspepsia
♦ Upper abdominal or epigastric symptoms

including pain ,discomfort ,fulness ,bloating
early morning satiety,belching,heart burn,
regurgitation and indigestion.
♦ PREVALENCE
25% of adult population
3% of OPD patients in west.
Vast majority in our OPDs.
Etiolgy
♦ Drugs
♦ Luminal GIT dysfunction.

15-25%
1%
Miscellaneous
♦ Pancreatic diseases
♦ Biliary diseases
♦ Others

GERD
5-15%
Peptic Ulcer
Malignancy
Functial or non ulcer dyspepsia
♦ Most common.
♦ 70 % ------ no organic cause.
♦ Young age.
♦ Vague symptoms.
♦ Anxiety and depression.
♦ History of use of psychotropic drugs.
♦ Presence of more specific symptoms like weight

loss,dysphagia,hematemesis,malena and anemia
should be sought.
Underlying mechanisms.
♦ Increased visceral afferent sensitivity.
♦ Delayed gastric emptying.
♦ Impaired accomodation of food.
♦ Psychosocial stress.
Heart burn or pyrosis
♦ Sensation of warmth.
♦ Retrosternal burning.
♦ 90% with GERD.
♦ Relation with large meals.
♦ Presence of provocative factors.
Aerophagia
♦ Chronic repetitive eruction (belching) of

swallowed air.
♦ Anxiety.
♦ Rapid eating.
♦ Use of carbonated beverages.
♦ Use of chewing gums,smoking and with
post nasal drip.
Gaseousness,bloating and
flatulence
♦ Excessive sensetivity to normal impulses.
♦ Motility disorders.
♦ Foods like legumes, grain and beans.
♦ Infections like giardiasis.
Dysphagia
♦ Sensation of sticking or obstruction to the

passage of food through mouth ,pharynx or
esophagus.
♦ Other symptoms related to swallowing
include
♦ Aphagia: Complete obstruction.medical
emergency.
Causes.
♦ Difficulty in initiating swallowing.
♦ Disorders of voluntary phase.
♦ Paralysis of tongue.
♦ Oropharyngeal ansthesia
♦ Lack of salivation.
♦ Lesions of vagus and glossopharyngeal nerves.
♦ Lesions of swallowing centers.
♦ Once initiated------Completed.
Related symptoms.
♦ Odynophagia.
♦ Misdirection of food.

Characteristic of oropharyngial dysphagia.
Associated with nasal regurgitation,
laryngeal and pulmomary aspiration.
♦ Phagophobia
Fear of eating food.
Associated with Hysteria,Rabies and
tetnus.
♦ Globus pharyngeous.
Physiology of swallowing
♦ Oral phase.
♦ Pharyngeal phase.
♦ Deglutition reflex.
♦ Primary peristalsis.
♦ Deglutitive inhibition.
Pathophysiology of dysphagia.
♦ Size of ingested bolus.
♦ Luminal diametre.
♦ Peristaltic contractions.
♦ Relaxtion of upper and lower esophageal

sphincters.
Types
♦ Mechanical dysphagia.

Initially with solids and later with liquids.
♦ Motor dysphagia.
With both solids and liquids from onset.
Mechanical dysphagia
♦ Luminal—Size of bolus.

Normal esophageal distention upto 4cm.
No dilatation beyound 2.5cm---Solids
dilatation beyound 1.3cm---Semi solids and
liquids.
♦ Intrinsic narrowing.
Inflammatory condtions.
Webs and rings.
Strictures and growth.
♦ Extrinsic Compression.

No
Motor dysphagia
♦ Difficulty in initiating of swallowing.
♦ Abnormalities of peristalsis or deglutitive

inhibition due to diseases of esophageal
striated or smooth muscles.
♦ Important causes include pharyngeal
pralysis,cricopharyngeal
achlasia,scleroderma ,achalasia, esophageal
spasm and related motor disorders.
Symptoms associated with
dysphagia
♦ PAIN

Painless—denervation---tumors.
Pain------impaction---intact nerves.
Odynophagia:inflammatory state.
Peptic ulceration
Candidiasis.
Herpes simplex.
Progression
♦ Intermittent: Diffuse esophageal spasm.
♦ Progressive:
♦ Mild progression—Motor disorder—

months to years.
♦ Rapid progression—Over weeks is
dangerous as may be associated with
obstruction and malignancy.Needs urgent
evaluation.
Approach to patient.
♦ Duration.
♦ Past history of GERD.
♦ Association with solids and liquids.
♦ Level of obstruction:

High cricoid cartilage-Difficulty with ejection of bolus.
Takes many swallows to clear.
May be associated with cough
& aspiration. Tumor,stricture, pharyngeal
pouch or reflux
♦ Lower sternum:

After successful swallow food is held
up.
Tumors,achalasia,esophagitis.
Common causes
♦ Painful mouth or throat:

Recurrent aphthous ulcers,glandular
fever, tonsillitis and quinsy.
♦ Neurological involvement:
Bulbar or pseudobulbar palsy.
♦ Neuromuscular weakness:
Myasthenia gravis,achalsia,
scleroderma.
♦ Obstruction:Cacinoma esophagus,stomach
or extrinsic compression by bronchial Ca.
GIT Symptoms and Causes: A Guide to Gastrointestinal Symptomatology

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GIT Symptoms and Causes: A Guide to Gastrointestinal Symptomatology

  • 1. SYMPTOMATOLOGY GIT DR MUZAMIL JAMIL ASSOCIATE PROFESSOR MEDICINE
  • 2. ♦ HAEMETEMESIS ♦ MALENA ♦ HEMATOCHEZIA ♦ NAUSEA &VOMITTING ♦ DYSPEPSIA ♦ DYSPHAGIA ♦ DIARRHEA ♦ ABDOMINAL PAIN
  • 4. Hemetemesis ♦ Vomiting of blood . ♦ Proximal to ligament of treitz. ♦ GI bleeding below duodenum rarely enters stomach. ♦ Colour of vomited blood depends on 1.Concentration of HCL acid
  • 5. ♦ 2.Duration of contact with acid. Short duration—red color Long duration—dark red,brown black or cofee ground appearance.
  • 6. Melena ♦ Black tarry stools. ♦ Sticky,loose with characteristic odour. ♦ HCL acts on Hb to produce haemetin giving black colour. ♦ Usaually follows hemetemesis. ♦ Both suggest proximal source. ♦ Bleeding from esophagus,stomach, small gut and even ascending colon occasionally.
  • 7. ♦ 60 ml of blood –Single melena stool. ♦ More than this may lead melena upto 7 days. ♦ Occult blood in stools remains positive for weeks with normal stool colour. ♦ Black or dark gray stools may occur with use of iron, bismith or licorice. ♦ Occult blood in stool—potentially serious.
  • 8. Hematochezia ♦ Passage of blood per rectum. ♦ Bleeding distal to ligament of treitz. ♦ Brisk proximal bleeding—rapid transit. ♦ Anal or rectal lesions like haemorrhoids or anal fissure. ♦ Colonic lesions like growth ,IBD ,infections and angiodysplasia.
  • 9. Clinical manefestions ♦ Extent of bleeding. ♦ Rate of bleeding. ♦ Comorbid factors.
  • 10. Extent of bleeding. ♦ Less than 500 ml of blood loss—rarely associated with systemic signs.Exceptions include elderly and anemic. ♦ Orthostatic hypotention—20% or greater reduction in blood volume. ♦ Concomitant symptoms include lightheadedness, syncope, nausea, sweating and thirst. ♦ Blood loss upto 25-40%--Shock.
  • 11. Common causes of upper GI bleed. ♦ Varices ♦ Peptic ulcer ♦ Gastroduodenal erosions ♦ Mallory weiss tear ♦ Malignancy
  • 12. Variceal bleeding. ♦ Varices—Bleed is abrupt and massive. ♦ Underlying cirrhosis and portal hypertension ♦ 25% cases other sources like erosive gastropathy and peptic ulcer. ♦ Stigma of CLD.
  • 13. Peptic ulcer. ♦ Peptic ulcer—Break in gastric/duodenal mucosa may extend through muscularis. ♦ 5 times more common in duodenum ♦ 95% in bulb or pyloric channel. ♦ NSAIDS ,H pylori, and acid hypersecretion. ♦ History suggestive.
  • 14. Miscellaneous. ♦ Erosions—Asprin and NSAIDS. ♦ Mallory weiss—Mucosal tear with retching and vomiting. ♦ Esophagititis—GERD ,infections and malignancy.
  • 15. Nausea and vomiting ♦ Nausea is a desire or feeling. ♦ Vomiting is forceful expulsion of gastric contents. ♦ Retching is laboured rythmic contraction of respiratory and abdominal musculature precede or accompany vomiting.
  • 16. Control of vomiting ♦ 2 distinct medullary centers. ♦ Vomiting center in dorsal part of lateral reticular formation . ♦ CTZ area postrema of floor of fourth ventricle. ♦ Vomiting center controls and integrates the actual act of emesis.It receives inputs from four different sources.
  • 17. Impulses reaching vomiting centre. ♦ Afferent vagal. ♦ Vestibular system. ♦ Higher centers. ♦ Area postrema.
  • 18. Causes based on input ♦ Visceral afferent---Mechanical obstruction, dysmotlity, peritonial irritation ,infection ,hepatobiliary or pancreatic and topical. ♦ CNS disorders(vestibular & higher centers) middle ear diseases, increased ICP,CNS infections,psychogenic. ♦ CTZ—irritation from drugs and systemic disorders(DKA,uremia,adrenocortial crisis.
  • 19. Associated features. ♦ Temporal relations like early morning houres, relation with meals and psychogenic ♦ Associated symptoms are important. ♦ Vertigo and tinnitis—Meniers disease. ♦ Long standing history with out significant sequel point psychogenic. ♦ Localizing symptoms like in abdomen or CNS.
  • 20. Character of vomitus. Character of vomitus. Large amount of acid. Absence of acid. Feculent or putrid odor. Presence of blood. EFFECTS OF VOMITING
  • 21. Dyspepsia ♦ Upper abdominal or epigastric symptoms including pain ,discomfort ,fulness ,bloating early morning satiety,belching,heart burn, regurgitation and indigestion. ♦ PREVALENCE 25% of adult population 3% of OPD patients in west. Vast majority in our OPDs.
  • 22. Etiolgy ♦ Drugs ♦ Luminal GIT dysfunction. 15-25% 1% Miscellaneous ♦ Pancreatic diseases ♦ Biliary diseases ♦ Others GERD 5-15% Peptic Ulcer Malignancy
  • 23. Functial or non ulcer dyspepsia ♦ Most common. ♦ 70 % ------ no organic cause. ♦ Young age. ♦ Vague symptoms. ♦ Anxiety and depression. ♦ History of use of psychotropic drugs. ♦ Presence of more specific symptoms like weight loss,dysphagia,hematemesis,malena and anemia should be sought.
  • 24. Underlying mechanisms. ♦ Increased visceral afferent sensitivity. ♦ Delayed gastric emptying. ♦ Impaired accomodation of food. ♦ Psychosocial stress.
  • 25. Heart burn or pyrosis ♦ Sensation of warmth. ♦ Retrosternal burning. ♦ 90% with GERD. ♦ Relation with large meals. ♦ Presence of provocative factors.
  • 26. Aerophagia ♦ Chronic repetitive eruction (belching) of swallowed air. ♦ Anxiety. ♦ Rapid eating. ♦ Use of carbonated beverages. ♦ Use of chewing gums,smoking and with post nasal drip.
  • 27. Gaseousness,bloating and flatulence ♦ Excessive sensetivity to normal impulses. ♦ Motility disorders. ♦ Foods like legumes, grain and beans. ♦ Infections like giardiasis.
  • 28. Dysphagia ♦ Sensation of sticking or obstruction to the passage of food through mouth ,pharynx or esophagus. ♦ Other symptoms related to swallowing include ♦ Aphagia: Complete obstruction.medical emergency.
  • 29. Causes. ♦ Difficulty in initiating swallowing. ♦ Disorders of voluntary phase. ♦ Paralysis of tongue. ♦ Oropharyngeal ansthesia ♦ Lack of salivation. ♦ Lesions of vagus and glossopharyngeal nerves. ♦ Lesions of swallowing centers. ♦ Once initiated------Completed.
  • 30. Related symptoms. ♦ Odynophagia. ♦ Misdirection of food. Characteristic of oropharyngial dysphagia. Associated with nasal regurgitation, laryngeal and pulmomary aspiration. ♦ Phagophobia Fear of eating food. Associated with Hysteria,Rabies and tetnus. ♦ Globus pharyngeous.
  • 31. Physiology of swallowing ♦ Oral phase. ♦ Pharyngeal phase. ♦ Deglutition reflex. ♦ Primary peristalsis. ♦ Deglutitive inhibition.
  • 32. Pathophysiology of dysphagia. ♦ Size of ingested bolus. ♦ Luminal diametre. ♦ Peristaltic contractions. ♦ Relaxtion of upper and lower esophageal sphincters.
  • 33. Types ♦ Mechanical dysphagia. Initially with solids and later with liquids. ♦ Motor dysphagia. With both solids and liquids from onset.
  • 34. Mechanical dysphagia ♦ Luminal—Size of bolus. Normal esophageal distention upto 4cm. No dilatation beyound 2.5cm---Solids dilatation beyound 1.3cm---Semi solids and liquids. ♦ Intrinsic narrowing. Inflammatory condtions. Webs and rings. Strictures and growth. ♦ Extrinsic Compression. No
  • 35. Motor dysphagia ♦ Difficulty in initiating of swallowing. ♦ Abnormalities of peristalsis or deglutitive inhibition due to diseases of esophageal striated or smooth muscles. ♦ Important causes include pharyngeal pralysis,cricopharyngeal achlasia,scleroderma ,achalasia, esophageal spasm and related motor disorders.
  • 36. Symptoms associated with dysphagia ♦ PAIN Painless—denervation---tumors. Pain------impaction---intact nerves. Odynophagia:inflammatory state. Peptic ulceration Candidiasis. Herpes simplex.
  • 37. Progression ♦ Intermittent: Diffuse esophageal spasm. ♦ Progressive: ♦ Mild progression—Motor disorder— months to years. ♦ Rapid progression—Over weeks is dangerous as may be associated with obstruction and malignancy.Needs urgent evaluation.
  • 38. Approach to patient. ♦ Duration. ♦ Past history of GERD. ♦ Association with solids and liquids. ♦ Level of obstruction: High cricoid cartilage-Difficulty with ejection of bolus. Takes many swallows to clear. May be associated with cough & aspiration. Tumor,stricture, pharyngeal pouch or reflux
  • 39. ♦ Lower sternum: After successful swallow food is held up. Tumors,achalasia,esophagitis.
  • 40. Common causes ♦ Painful mouth or throat: Recurrent aphthous ulcers,glandular fever, tonsillitis and quinsy. ♦ Neurological involvement: Bulbar or pseudobulbar palsy. ♦ Neuromuscular weakness: Myasthenia gravis,achalsia, scleroderma. ♦ Obstruction:Cacinoma esophagus,stomach or extrinsic compression by bronchial Ca.