Derivatives of pharyngeal tube

1. Parts of the floor of the mouth including the tongue

2. Pharynx
3. Derivatives of the pharyngeal pouches
4. Thyroid gland

Derivatives of foregut
1. Lower respiratory system (trachea, bronchial tree & lungs)
2. Esophagus
3. Stomach
4. Up to 2nd part of duodenum up to major duodenal papilla
5. Liver
6. Biliary apparatus (Hepatic duct, Gallbladder & Bile duct)
7. Pancreas
Derivatives of midgut
1. Duodenum below the opening of bile duct
2. Jejunum
3. Ileum
4. Caecum
5. Appendix
6. Ascending colon & right 2/3rd of the transverse colon

Derivatives of the hindgut

1. Left 1/3rd of the transverse colon
2. Descending colon & sigmoid colon
3. Rectum & anal canal upto pectinate line
4. Part of the urogenital system (urinary bladder & most of the urethra)
Gut arteries with territories of supply
1. External carotid artery: Supplies the supracardiac part of the foregut
2. Coeliac trunk: Supplies the infracardiac part of the foregut
3. Superior mesenteric artery: Supplies the midgut
4. Inferior mesenteric artery: Supplies the hindgut
5. Internal iliac artery: Supplies the proctodeum

Layers of anterior abdominal wall

1. Skin
2. Superficial fascia
3. External oblique muscle & its aponeurosis
4. Internal oblique muscle & its aponeurosis
5. Transversus abdominis muscle & its aponeurosis
6. Fascia transversalis
7. Extraperitoneal tissue
8. Parietal peritoneum
Muscles of anterior abdominal wall Contents of rectus sheath
1. External oblique A. Muscle : Rectus abdominis & Pyramidalis
2. Internal oblique B. Vessels: Superior & Inferior epigastric vessels
3. Transversus abdominis C. Nerve: Terminal part of the lower five intercoastal nerves &
4. Rectus abdominis the subcoastal nerve
5. Cremestar
6. Pyramidalis

Ligaments & tendons of anterior abdominal wall ❑ Organs having length of 25 cm

1. Inguinal ligament
1. Oesophagus
2. Lacunar ligament
3. Pectineal ligament 2. Stomach
4. Conjoint tendon 3. Duodenum
4. Descending colon
5. Ureter
Blood supply of different abdominal organs

Organ Artery supply

Oesophagus • Cervical part: Inferior thyroid artery > Thyrocervical trunk
• Thoracic part: Oesophageal branches of descending thoracic aorta
• Abdominal part: Oesophageal branches of left gastric artery
Stomach • Left gastric artery > Coeliac trunk
• Right gastric artery > Common hepatic art
• Right gastroepiploic > Gastroduodenal art
• Left gastroepiploic > Splenic art
• 5-7 short gastric art > Splenic art
Duodenum • Above major duodenal papilla: Superior pancreatico-duodenal art
• Below major duodenal papilla: Inferior pancreatico-duodenal art
Small Intestine Jejunal & Ileal branches of Superior Mesenteric artery
Appendix Appendicular artery > Ileocolic art > Sup mesenteric art
Colon Branches from Right colic & Ileocolic art > Sup mesenteric art
Rectum Superior Rectal Artery
Middle Rectal Artery
Median Sacral Artery
Anal canal • Above the pectinate line: Superior Rectal Artery
• Below the pectinate line: Inferior Rectal Artery > Internal pudendal artery
Pancreas • Pancreatic branches of splenic artery
• Superior pancreatico-duodenal art
• Inferior pancreatico-duodenal art
Spleen Splenic artery
Branches of abdominal aorta
A. Ventral branch
1. Coeliac trunk
2. Superior mesenteric artery
3. Inferior mesenteric artery

B. Lateral branch
1. Inferior phrenic arteries
2. Middle suprarenal arteries
3. Renal arteries
4. Gonadal arteries (testicular or ovarian)

C. Dorsal branch
1. Lumbar arteries (four pairs)
2. Median sacral artery

D. Terminal branches
1. Right & left common iliac arteries
 Nerve supply of gut
• Gut is supplied by CNS, ANS & enteric nervous system
• Parasympathetic pathways (vagal and sacral efferent), which are cholinergic, and increase
smooth muscle tone and promote sphincter relaxation
• Sympathetic pathways, which release noradrenaline (norepinephrine), reduce smooth
muscle tone and stimulate sphincter contraction.
• Autonomic para sympathetic part is stimulatory to the gut & increases smooth muscle tone
& promotes sphincter relaxation
• Autonomic sympathetic part is inhibitory to the gut & reduces smooth muscle tone &
stimulate sphincter contraction
• ENS comprises two major networks: Myenteric plexus/Auerbach’s plexus (Between inner
circular & outer longitudinal muscle layer) & Meissner’s plexus (in submucosal layer)
• Myenteric plexus regulates motor control of the gut
• Meissner’s plexus exerts secretory control over the epithelium, enteroendocrine cells and
submucosal vessels
Stomach
Histological structure of stomach

1. Serous coat: derived from peritoneum

2. Muscular coat: Outer longitudinal, Middle circular & Inner oblique
3. Submucous coat: consists of loose areolar tissue and contains plexuses of blood
vessels, lymphatics and nerves
4. Mucous membrane: lined by simple columnar epithelium

Cardinal features of large gut

1. Taenia coli
2. Sacculation or haustration
3. Appendices epiploicae
 Nerve supply of stomach
The stomach is innervated by sympathetic & parasympathetic fibres
A. Sympathetic innervation: originates from T6-T9 segments of the spinal cord and is mainly distributed to the
stomach via the greater and lesser splanchnic nerves via the coeliac plexus
Action:
1. Vasoconstrictor the gastric vasculature
2. Inhibitory to gastric musculature
3. Motor to the pylorus and thus constricts the pyloric sphincter
4. Convey painful sensations

B. Parasympathetic innervation: Derived from both the vagus nerves in the form of anterior and posterior vagal
trunks
Action:
1. Secretomotor to the gastric glands
2. Motor to the gastric musculature
3. Relaxes the pyloric sphincter
4. Convey the sensation of hunger and nausea
 Features Jejunum Ileum
1. Wall Thicker. More Thinner, Less
vascular vascular
1. Lumen Wider Narrower
1. Mesentery • Window present • No Window
• Arterial arcade 1 • Arterial arcade
or 2 3 or 6
• Vasa recta • Vasa recta
longer & fewer shorter &
numerous

1. Circular folds Larger, more closely Smaller, Sparse

set
1. Villi Larger, thick, more Shorter, thinner,
abundant less abundant

1. Peyer’s patches Absent Present

1. Solitary lymphatic Fewer Numerous

follicle
 Features Large intestine Small intestine
1. Taenia coli Present Absent
1. Appendices epiploicae Present Absent

1. Sacculation Present Absent

1. Calibre Larger Smaller

1. Fixity Greater part is fixed Greater part is mobile

1. Villi Absent Present

1. Peyer’s patches Absent Present
Abdominal tonsil
The submucous coat of appendix contains numerous lymphatic follicles, which is a source of lymphocyte
and strengthen the immunity of the body, like the tonsil. So, it is called abdominal tonsil

Mcburney’s point
It is represented by a point at the junction of medial two third & lateral one third of a line extending from
the umbilicus to the right anterior superior iliac spine. It corresponds roughly to the position of the base
of the appendix.
Peritoneal relations to the rectum

1. Upper 1/3rd: covered with peritoneum in front & on both sides

2. Middle 1/3rd: covered only the front
3. Lower 1/3rd: devoid of peritoneum
Blood supply of rectum

A. Arterial supply:
1. Superior rectal artery: continuation of inferior mesenteric artery
2. Middle rectal artery: anterior division of each internal iliac artery
3. Inferior rectal artery: branch of internal pudendal artery
4. In addition, it is supplied by Median sacral artery, Inferior gluteal artery & Internal pudendal
arteries

B. Venous supply:
1. Superior rectal vein: drains into inferior mesenteric vein (portal vein)
2. Middle rectal vein: drains into internal iliac vein (systemic vein)
3. Inferior rectal vein: drains into internal pudendal vein (systemic vein)
Development of anal canal
1. Above the pectinate line: from endodermal cloaca
2. Below the pectinate line: from ectodermal proctodeum

Tortuous arteries in the body

• Uterine artery
• Splenic artery
• Facial artery
• Nutrient arteries of bones involved in movement
Thoracic duct

• Arises from: Continuation of cisterna chyli which is situated in the level of

L1-L2 vertebra
• Ends in opening into the angle of the junction between left subclavian
vein & internal jugular vein
• Length: 38-45 cm
• Function: Lymphatic drainage
Cells present in gastric gland
Cells Secretion
1. Peptic / Chief cell 1. Pepsinogen
2. Parietal / Oxyntic cell 2. HCl, Intrinsic factor of Castle
3. Mucus neck cell 3. Mucus, Bicarbonate
4. Surface mucus cell 4. Mucus, Bicarbonate
5. G cell 5. Gastrin
6. Enterochromafin cell 6. Histamine
 Inguinal Canal
Structures passing through canal
1. Spermatic cord in male & Round ligament of the uterus in female
2. Ileoinguinal nerve

Constituents of spermatic cord: (Rule of 3: 3 artery, 3 nerves, 3 other things)

1. Vas deferens
2. Testicular & Cremasteric arteries, Artery of the vas deferens
3. Pampiniform plexus of veins
4. Lymph vessels from testes
5. Ileoinguinal nerve, Genital branch of genitofemoral nerve & plexus of sympathetic nerves around
the artery to the vas deferens
6. Remains of processus vaginalis
 Relation of peritoneum to various viscera

1. Intraperitoneal: Stomach, Jejunum, Ileum, Caecum, Appendix

2. Retroperitoneal: Duodenum, Pancreas, Kidney, Ureter, Suprarenal gland

3. Partially covered: Ascending colon, Descending colon, Rectum

** Unilateral absence of testes: Monorchism
** Bilateral absence of testes: Anorchism

** Undecsended testes: Cryptorchidism

• The testes may lie in lumbar, iliac, inguinal or upper scrotal region
• Spermatogenesis may fail to occur in it
• A malignant tumor is more prone to develop in it
• The condition can be corrected surgically
Weak areas of abdomen for hernia

1. Inguinal canal
2. Inguinal triangle of Hasselbach
3. Femoral ring
4. Umbilicus
5. Midline incision along the linea alba
6. Epigastric area along the linea alba
7. The diaphragm
Indirect / Oblique inguinal hernia Direct inguinal hernia
Hernia enters the inguinal canal through deep Hernia enters the inguinal canal through Triangle of
inguinal ring Hasselbach (Posterior wall of inguinal canal)

Usually it is unilateral & occurs in young patients Usually bilateral & occurs in old age

Neck of the hernial sac lies lateral to the inferior Neck of the hernial sac lies medial to the inferior
epigastric artery epigastric artery

Neck of the hernial sac is narrow Neck of the hernial sac is wide

Directed downwards, forward and medially Directed almost straight forward

Cause is congenital, due to persistence of processus Cause is acquired, due to weakness in conjoint
vaginalis of peritoneum tendon

It receives all the coverings of the spermatic cord It receives an additional covering from fascia
transversalis

Usually incomplete/complete Usually incomplete

Obstruction & strangulation is common Obstruction & strangulation is rare

 Hydrolytic type Echbolic type
1. Rich in HCO3-, but poor in 1. Rich in enzyme, poor in HCO3-
enzyme

1. Thin & watery 1. Thick

1. Secretion stimulated by Secretin 1. Secretion stimulated by CCK &
acetylcholine

1. Secreted in response to acid 1. Secreted in response to fatty acids

chime in the duodenum in the duodenum

1. Neutralizes the acidity of the 1. Digestive in function

chime
Factors affecting gastric emptying
Increased Reduced

Distension of stomach & antrum Fatty acids

Gastrin Hyperosmolar solution (amino acids and
Cold polypeptides)
Emotion Acid in Duodenum
Secretin, CCK-PZ
Heat and Emotion
Factors affecting small intestinal motility
Increased Reduced
Parasympathetic activity Sympathetic activity
Cholinergic agents Adrenargic agents
Gastrin, CCK-PZ, motilin Secretin
Prostaglandins
Serotonin

Factors affecting large intestinal motility

Increased Reduced
Parasympathetic activity Sympathetic activity Substance affecting HCl secretion
Cholinergic agents Adrenargic agents
Distension Inflammation Stimulated by Inhibited by
Emotion Emotion
• Acetylcholine • Amino Acid • Somatostatin
CCK-PZ
• Histamine • Hypoglycemia • Low pH
Laxatives
• Gastrin • Steroid • GIP
• Alcohol • PTH • Drugs (Prazoles, Ranitidine)
• Caffeine • ACTH • Serotonin
• Calcium • Insulin • Enterogastrone

**Cholecystokinine-Pancreazymine (CCK-PZ) reduces gastric motility but increases small and large intestinal motility.
Factors that favour Gallbladder emptying
1. Presence of fatty food in the duodenum
2. CCK
3. Acetylcholine

Electrolyte changes that occur after a heavy meal

• High serum HCO3-
• High blood pH
• Low serum Chloride
• Low serum [H+]
Digestive juice
1. Saliva
2. Gastric juice
Protective constituents in saliva
3. Pancreatic juice
1. Secretory IgA
4. Succus entericus
2. Lysozyme
5. Bile
3. Mucin
4. Bicarbonate
Salivary glands with their nature of secretion
1. Parotid – purely serous
2. Submandibular – mixed, predominantly serous
3. Sublingual – mixed, predominantly mucous
 Functions of gastric HCl

1. Converts inactive pepsinogen into active pepsin

2. Provides suitable environment for pepsin to start protein digestion
3. Kills many ingested bacteria
4. Stimulates the flow of bile and pancreatic juice
5. Keeps the iron in ferrous state for absorption
6. Hydrolyzes sucrose into glucose and fructose
Three basic stimuli for pancreatic secretion

1. Acetylcholine
2. Cholecystokinin
3. Secretin
 Classification of digestive enzymes
A. Carbohydrate splitting enzymes C. Lipolytic enzymes
1. Ptyaline 1. Gastric lipase
2. Pancreatic amylase 2. Lingual lipase
3. Sucrase 3. Pancreatic lipase
4. Maltase 4. Enteric lipase
5. Lactase 5. Lecithinase
6. Α Dextrinase 6. Phospholipase A2
7. Isomaltase 7. Cholesterol esterase
8. Trehalase 8. Co-lipase
E. Other enzymes
B. Proteolytic enzymes D. Nucleases 1. Carbonic anhydrase, Phosphatase, Isozymes
1. Pepsin 1. DNAase 2. Gastric renin
2. Trypsin, Chymotrypsin 2. RNAase 3. Enterokinase
3. Carboxypolypeptidase
4. Elastase
5. Aminopeptidase, Dipeptidase, Tripeptidase, Enteropeptidase, Endopeptidase
GI reflexes

1. Swallowing reflex
2. Conditioned reflex
3. Unconditioned reflex
4. Gastroileal reflex
5. Gastrocolic reflex
6. Reverse gastrocolic reflex
7. Duodenocolic reflex
8. Defecation reflex
Decreased peristalsis resulting in constipation

Decreased secretion

Impaired relaxation of sphincters of GIT.

 Digestion & Absorption

Carbohydrate

Starch is hydrolysed by salivary and pancreatic amylases to alpha-limit dextrins containing

4–8 glucose molecules; to the disaccharide, maltose; and to the trisaccharide, maltotriose.
Disaccharides are digested by enzymes fixed to the microvillous membrane to form the
monosaccharides, glucose, galactose and fructose. Glucose and galactose enter the cell by
an energy-requiring process involving a carrier protein, and fructose enters by simple
diffusion.
Protein

The Intragastric digestion by pepsin is quantitatively modest but important because the
resulting polypeptides and amino acids stimulate CCK release from the mucosa of the
proximal jejunum, which in turn stimulates release of pancreatic proteases, including
trypsinogen , chymotrypsinogen, pro-elastases and procarboxypeptidases, from the
pancreas. On exposure to brush border enterokinase, inert trypsinogen is converted to
the active proteolytic enzyme trypsin, which activates the other pancreatic proenzymes.
Trypsin digests proteins to produce oligopeptides, peptides and amino acids.
Oligopeptides are further hydrolysed by brush border enzymes to yield dipeptides,
tripeptides and amino acids. These small peptides and the amino acids are actively
transported into the enterocytes, where intracellular peptidases further digest peptides
to amino acids. Amino acids are then actively transported across the basal cell
membrane of the enterocyte into the portal circulation and the liver.
Fat

Dietary lipids comprise long-chain triglycerides, cholesterol esters and

lecithin. Lipids are insoluble in water and undergo lipolysis and
incorporation into mixed micelles before they can be absorbed into
enterocytes along with the fat-soluble vitamins A, D, K and E. The
lipids are processed within enterocytes and pass via lymphatics into
the systemic circulation.
Water and electrolytes
Absorption and secretion of electrolytes and water occur throughout the intestine. Electrolytes and water are
transported by two pathways: • the paracellular route, in which passive flow through tight junctions between
cells is a consequence of osmotic, electrical or hydrostatic gradients • the transcellular route across apical and
basolateral membranes by energy-requiring specific active transport carriers (pumps).

Gastric secretion
Gastrin, histamine and acetylcholine are the key stimulants of acid secretion. Hydrogen and chloride ions are
secreted from the apical membrane of gastric parietal cells into the lumen of the stomach by a hydrogen–
potassium adenosine triphosphatase (ATPase) (‘proton pump’). The hydrochloric acid sterilises the upper
gastrointestinal tract and converts pepsinogen – which is secreted by chief cells – to pepsin. The glycoprotein
intrinsic factor, secreted in parallel with acid, is necessary for vitamin B12 absorption.

Gastrin, somatostatin and ghrelin

The hormone gastrin is produced by G cells in the antrum, whereas somatostatin is secreted from D cells
throughout the stomach. Gastrin stimulates acid secretion and mucosal growth, whilst somatostatin
suppresses it. Ghrelin, secreted from oxyntic glands, stimulates acid secretion but also appetite and gastric
emptying.
CLINICAL
Upper GI Endoscopy
Colonoscopy
Dyspepsia
 Dysphagia
Dysphagia is defined as difficulty in swallowing.
Causes & Investigations of dysphagia
 Vomiting
Vomiting is the expulsion of gastric contents via the mouth.
 Gastrointestinal bleeding
Hematemesis: Vomiting out of blood.
Melaena: Passage of black tarry stools containing altered blood. This is usually due to bleeding from the
upper GIT.
Causes of upper GIT bleeding
 Diarrhoea
Passage of loose stool more than three times a day is called Diarrhoea.
Causes of Dysentery/Bloody diarrhoea
A. Infective cause Causes of watery diarrhoea
1. Bacillary dysentery: Shigella, E. Coli, Non typhoidal 1. Enterotoxigenic E. coli
Salmonella, Campylobacter, Clostridium difficile, Vibrio 2. V. cholera
parahemolyticus, Yersinia enterocolitica 3. Giardia lamblia
2. Amoebic dysentery: Entamoeba histolytica 4. Staphylococcus aureus
5. Bacillus cereus
B. Non infective cause 6. Norovirus
1. Inflammatory bowel disease 7. Rotavirus
2. Diverticular disease 8. Cryptosporidium hominis
3. Rectal or Colonic Malignancy
4. Ischemic colitis
5. Intussusception
Lower GIT bleeding
Malabsorption
Causes
1. Deficiency of bile or pancreatic enzymes. Fat and protein malabsorption results.
2. Bacterial overgrowth
3. Small bowel resection
4. Condition damaging the small intestinal epithelium:
o Coeliac disease
o Tropical sprue
o Dermatitis herpetiformis
o Whipple’s disease
o Radiation enteritis
o Parasitic infestation (e.g. Giardia intestinalis)
Abdominal pain
Gastro-Oesophageal Reflux Disease (GERD)
Gastro-oesophageal reflux disease develops when the oesophageal mucosa is exposed to gastro-
duodenal contents for prolonged periods of time, resulting in symptoms and in a proportion of cases,
oesophagitis.

Clinical features:
1. Heartburn & regurgitation provoked by bending, straining, lying down
2. Pt often overweight
3. Woken at night by choking as refluxed fluid irritates the larynx
4. Odynophagia or Dysphagia
5. Atypical chest pain, which may be severe that mimic angina and is probably due to reflux induced
oesophageal spasm
Complications:
1. Oesophagitis
2. Barret’s Oesophagus
3. Anaemia
4. Benign oesophageal stricture
5. Gastric volvulus
Investigation:
1. Endoscopy of upper GIT
2. 24 hours ph monitoring
Treatment:
1. Lifestyle modification
2. Antacids and Alginates
3. H2 receptor blocker. i.e. Ranitidine, Cimetidine, Famotidine
4. Proton Pump Inhibitor. i.e. Omeprazole, Esomeprazole, Pantoprazole, Rabiprazole, Lansoprazole
Factors responsible for GERD
 Barret’s Oesophagus

It is a pre malignant condition where glandular metaplasia of the lower oesophagus occurs, in which
the normal squamous lining is replaced by columnar mucosa composed of a cellular mosaic containing
areas of intestinal metaplasia. It is a major risk factor for oesophageal adenocarcinoma.

Diagnosis:
Multiple systematic biopsies to maximise the chance of detecting intestinal metaplasia and/or
dysplasia.
Achalasia Cardia
It is characterized by –
• Hypertonic lower oesophageal sphincter (LES) which fails to relax in response to
the swallowing waves.
• Failure of propagated oesophageal contraction, leading to progressive dilatation of
the gullet.

Clinical features:
1. Dysphagia
➢ Develops slowly
➢ Initially intermittent
➢ Worse for solids
➢ Eased by drinking liquids and by standing and moving around after eating.
2. Episodes of severe chest pain due to oesophageal spasm
Complications:
1. Achalasia predispose to Squamous cell carcinoma of the oesophagus
2. Dysphagia worsens, the oesophagus empties poorly and nocturnal pulmonary aspiration
develops

Investigations:
A. Barium swallow (Bird beak appearance)
B. Endoscopy
C. Manometry

Treatment:
A. Endoscopic: Forceful pneumatic dilatation. Endoscopically directed injection of botulinum
toxin into the LES.
B. Surgical myotomy (Heller’s operation)
 Peptic Ulcer Disease

Peptic ulcers are acute or chronic, most often solitary lesion that occur in any portion of the GIT exposed
to aggressive action of acid peptic juices.

Common sites of peptic ulcer

1. First part of duodenum
2. Stomach (usually antrum)
3. Lower oesophagus
4. Within the margins of a gastro-jejunostomy
5. Throughout in Zollinger Ellison syndrome
6. Within or adjacent to an ileal Meckel’s diverticulum that contains ectopic gastric mucosa.
Causes of PUD

1. Helicobacter pylori
2. Drugs: NSAIDs, Steroids
3. Smoking
4. Alcohol
5. Stress – Psychological, Burn, CVD
6. Reduced mucosal blood flow – Ischemia, Shock
7. Overproduction of gatric HCl: Gastrin producing tumor as in Zollinger Ellison
syndrome.
Consequences of H. pylori infection
1. Gastritis
2. Duodenal ulcer
3. Gastric ulcer
4. Gastric cancer

Complications of PUD
1. Perforation
2. Gastric outlet obstruction
3. Bleeding: Hematemesis & Melaena
 H. pylori eradication therapy

A. 1st line therapy (Triple therapy) for 7 days

➢ Proton Pump Inhibitor 12 hourly
➢ Clarithromycin 500mg 12 hourly
➢ Amoxicillin 1gm 12 hourly or Metronidazole 400 mg 12 hourly

B. 2nd line therapy (Quadruple therapy) for 7 days

➢ Proton Pump Inhibitor 12 hourly
➢ Bismuth 120mg 6 hourly
➢ Metronidazole 400 mg 12 hourly
➢ Tetracycline 500mg 6 hourly
Helicobacter pylori
H. pylori is a gram negative spiral bacillus and has multiple flagella at one end which makes it
motile, allowing it to burrow and live deep beneath the mucous layer closely adherent to the
epithelial surface.

Mode of transmission: By person to person contact via gastric refluxes or vomit.

Habitat:
• Exclusively gastric type epithelium
• Duodenum
• Patches of gastric metaplasia
Gastric carcinoma
Clinical features
• Asymptomatic
• Weight loss
• Anaemia
Investigations
• Ulcer like pain - Endoscopy of upper GIT
• Anorexia, Nausea - Multiple biopsies from the edge and base of a gastric ulcer
• Early satiety - Exfoliative brush cytology
• Haematemesis - Barium meal study
• Melaena
• Dyspepsia, Dysphagia
• Palpable Gastric mass
• Jaundice or ascites
• Tumor spread can cause :
o Supraclavicular lymphadenopathy (Troisier’s sign)
o Umbilicis (Sister Mary Joseph nodule)
o Ovaries (Krukenber tumour)
o Paraneoplastic phenomenon
o Acanthosis nigricans
o Thrombolphlebitis
o Deratomyositis
 Abdominal Tuberculosis
Organism: Mycobacterium tuberculosis

Sites:
• Ileo-Caecal junction (most common)
• Can affect any part of GIT
• Peritoneum (may result in peritonitis, exudative ascitis)
• Liver – Granulomatous hepatitis

Clinical features:
• Abdominal pain
• Low grade fever
• Night sweats
• Weight loss
• Features of anaemia (Tiredness, Palpitation)
• Alteration of bowel habit
• Features of intestinal obstruction (Constipation, vomiting)
• Abdominal swelling; if ascites due to peritoneal involvement
• Palpable abdominal mass
Investigations:
• ESR- raised
• Barium follow through: transverse ulceration, diffuse narrowing of
the bowel with shortening of caecal pole.
• USG or CT scan of abdomen shows mesenteric thickening and
lymph node enlargement
• S. ALP: Increased (suggests hepatic involvement)
• Confirmation is sought by endoscopy, laparoscopy or liver biopsy.

Treatment:
• Anti TB for 1 year
 Inflammatory Bowel Disease (IBD)
Two types:
• Ulcerative colitis
• Crohn’s disease

Investigations for IBD:

• Full blood count: Anaemia (resulting from bleeding or from malabsorption of iron, folic acid, vit B12)
• Serum Albumin: Low (because of protein loosing enteropathy)
• ESR & CRP: Raised
• Bacteriology: Blood culture, Stool culture
• Sigmoidoscopy with biopsies: Loss of vascular pattern, granularity, friability & ulceration.
• Barium follow through
• Other investigaions:
o Plain X-ray Abdomen: Dilatation of the colon, Mucosal oedema (thumb-printing), Evidence of perforation
o MRI
Treatment:
• Aims of treatment:
o Treat acute attacks
o Prevent relapses
o Detect carcinoma at an early stage
o Select patients for surgery

• Medical management:
o Aminosalicylates (mesalazine, olsalazine, sulfasalazine, balsalazine)
o Corticosteroids (Prednisolone, Hydrocortisone)
o Thiopurines (Azathioprine, 6-mercaptopurine)
o Methotrexate
o Ciclosporin
o Infliximab
o Antibiotics for proven infection
o Anti diarrhoeal agents (codeine phosphate, loperamide) – should be avoided in acute
severe attack
o Nutritional support
o Blood transfusion, if Hb < 10gm/dl
o Subcutaneous Heparin for prophylaxis of venous thromboembolism
• Surgical treatment:
o Panproctocolectomy with ileostomy, or
o Proctocolectomy with ileo anal pouch anastomosis
Complications of Inflammatory Bowel Disorder

Local/Intestinal:
• Severe life threatening inflammation of the colon
• Perforation
• Life threatening acute haemorrhage
• Fistula: Enteroenteric, Enterovesical, Enterovaginal
• Perianal abscess, fissure
• Cancer
Systemic Complication
Sign & Symptoms of Ulcerative colitis &
Crohn’s disease
Ulcerative colitis Crohn’s disease

✓ Bloody diarrhoea: the first attack is usually the most severe one.
Therefore the disease is followed by relapses and remissions. ✓ Abdominal pain
✓ Lower abdominal discomfort ✓ Diarrhoea
Symptoms ✓ Malaise, lethargy, anorexia, weight loss ✓ Weight loss
✓ Aphthous ulceration in mouth ✓ Subacute or acute intestinal obstruction – Vomiting,
✓ Tenesmus Constipation
✓ Fever

o Evidence of weight loss

o Anaemia
o No specific signs o Glossitis and Angular stomatitis
Signs o Abdomen may be slightly distended and tender o Abdominal tenderness
o Rectal examination will show the presence of blood. o Abdominal mass due to matted loops of thickened
bowel or an intra abdominal abscess may occur
o Perianal skin tags, fissures or fistulae
Irritable Bowel Syndrome
Protein losing enteropathy
Neuro-endocrine tumor
Acute Pancreatitis
Clinical features:
• Upper abdominal pain
• Nausea and Vomiting
• Marked epigastric tenderness
• Bowel sound: Quiet or Absent as paralytic ileus develops
• Shock, Oliguria
• Discoloration of the flanks (Grey Turner’s sign) or the periumbilical region (Cullen’s
sign)

D/D:
• Perforated viscus
• Acute cholecystitis
• MI
Investigations:
• S. Amylase & S. Lipase: Increased
• USG or CT scan: evidence of pancreatic swelling
• Plain X-ray abdomen to exclude other diagnosis
• Elevated urinary amylase:creatinine ratio
• Persistently elevated serum amylase concentration suggests pseudocyst formation
• CRP : elevated
• Blood urea & S. electrolytes
• Blood glucose level may be elevated
• S. Calcium: decreased
• CBC: Neutrophilia

Treatment:
• Analgesics: Pethidine
• Correction of hypovolemia
• Insulin (if hyperglycemia)
• Correction of hypocalcemia; by Inj. Calcium gluconate
• NG aspiration- if paralytic ileus develops
• Enteral feeding
• Prophylactic antibiotic by broad spectrum antibiotic
• Treatment of the cause
Chronic Pancreatitis