SYMPTOMATOLOGY GIT

DR MUZAMIL JAMIL

ASSOCIATE PROFESSORMEDICINE

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.

GERD 5-15% Peptic Ulcer 15-25% Malignancy 1 % Miscellaneous

Pancreatic diseases Biliary diseases Others

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 No dilatation beyound 1.3cm---Semi solids and liquids.

Intrinsic narrowing. Inflammatory condtions. Webs and rings. Strictures and growth.

Extrinsic Compression.

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.