Gastric defence from acid + acid production + medication affecting acid production
- Mucous production
- prevents contact with acids - Bicarbonate (HCO3) production
- alkaline tide, pancreatic juices = protective layer along lamina propria (connective tissue outside of mucosal layer) to neutralises acid - Prostaglandin production
- promotes blood flow
- cell repair
- mucus production
- bicarbonate production - Tight junction between epithelial cells = keeps H+ in lumen
Acid is produced and release by H-K-ATPase at membrane along lumen.
Increased activity by histamines, gastrin, ACh.
Inhibited by prostaglandins, omeprazole.
Peptic Ulcer Disease
- Presentation
erosion in mucosa of GIT –> exposed to acid –> haemorrhage occurs when mucosa layer is completely breached
- esophagus
- stomach, along lesser curve of stomach, arise from gastritis (less common!)
- duodenum, first few cm (most common!)
Usually at single site, however may occur at multiple site (20%)
Smooth margins (unlike tumors)
PUD - pathophysiology, common risk factor
Normal defence and repair mechanism of GI lining are weakened –> erosion in mucosa –> exposed to acid, damaged –> complete breach of mucosa layer = haemorrhage
NSAIDS
Helicobacter Pylori
- Gram negative curved bacteria
- Affects 50% population
- Fecal-oral route
- chronic inflammatioon –> decrease mucosal defenses, stimulate gastrin secretion to stimulate gastric acid production by parietal cells
- treated with 2 types of abx + PPI
Smoking - atherosclerosis, vascular spasm, vascular insufficiency
Alcohol
Stress
Irregular eating pattern
Spicy food
PUD - clinical features
> Epigastric abdo pain, epigastric
Related to meal time:
- duodenal = relieved by food (closed pyloric sphincter during digestion)
- gastric - exacerbated by food
> Bloating, abdo fullness
> N/V
> GERD (gastroesophageal reflux disease), Heartburn
4 Complication of PUD + explanation
- Haemorrhage !
> Most common complication
> Erosion of ulcer into blood vessels
> Presents with haematemesis, melena
> urgent admission and treatment (surgical clipping) - Perforation
> 5% of PUD
> Mostly due to obstruction, ischemia, trauma, forceful vomitting, chronic inflammatory condition, NO HISTORY of ulcers
> erosion of GI walls = stomach content spill into abdo cavity = peritonitis, sepsis, death
> Sudden epigastric pain = generalised = shock
> Emergency surgery - Scarring and stenosis
> narrowing of duodenum or pyloric outlet
> Crampy abdominal pain
> Epigastric fullness
> Vomiting, dehydration - Malignant change
Malignant bleeding ulcers, rare
GI bleeding - local and systemic causes
Bleeding disorders
- anticoagulant therapy
- leukemia
- thrombocytopenia
Local GI disorders
- Oesophagitis
- Oesophageal varices
(cirrhosis –> portal htn –> varices)
- Gastric ulcer (50% duodenal ulcer)
- Acute erosive gastritis (20%)
- Mallory-Weiss syndrome
> Uncommon
> Longitudinal tears (2-3cm) in gastroesophageal junction –> bleeding, affects mucosa, submucosa
> After forceful retching (alcoholics, bulimia)
> usually does not perforate, not severe bleeding - Stomach CA
- Zollinger-Ellison syndrome
> Gastrinoma of pancreas –> excessive gastrin formed –> increased acid –> multiple recurrent ulcers
summary - causes of benign GI bleed along GIT
Oesophagus - erosive ulcers, varices
Stomach - erosive ulcers
Duodenum - erosive ulcers
Colon -
Diverticulosis (presence of submucosa herniation through muscle layer of the colon) .
Diverticulitis - inflammation of the pouches
SI - Meckel’s diverticulum at ileum
Diverticulosis / Diverticulitis - symptoms
Diverticulosis - asymptomatic, lower abdo crampy pain
Diverticulitis - fever, leukocytosis, lower abdo tenderness
Complication of diverticulitis - PR bleed, abscess, perforation
NOT TO BE CONFUSED W MECKEL’S DIVERTICULUM OF ILEUM SMALL INTESTINES, CONGENITAL!
Diverticulosis - risk factors
Risk factor: Older age, Low fibre diet, Lack of physical activity & obesity
Portal Venous System - where does it drain from
lower esophagus
intestines
rectum
pancreas
gall bladder
spleen
blood vessel network which drains blood into liver for filtration before entering systemic circulation via hepatic vein
portal hypertension - definition & 5 clinical feature
increase in pressure in network of blood vessels –> blood bypass the liver, via shunts?
features
- ascites
> Incr hydrostatic pressure + hypoalbuminemia
> intra-peritoneal collection of fluid –> distension
> complications: infection by GI bacteria, spontaneous bacteria peritonitis
- splenomegaly
> Prolonged congestion of spleen –> enlargement
> Sequestered blood cells (trapped) + increased destruction + (unable to recycle new, good ones) –> anemia, leukopenia, thrombocytopenia - porto-systemic shunts (esophageal varices –> bgit)
–> enlarged collateral veins> 1/3 liver cirrhosis pt develop haemorrhoids, less severe bleeding
Azygos veins, left gastric vein –> Esophageal varices> Posterior area of liver
Peri-umbilical region –> caput medusa
retroperitoneal region
…. - encephalopathy
- also affects liver filtration function
esophageal varices
- what is it
- how is it developed
- treatment
portal htn –> > Azygos veins, left gastric vein –> Esophageal varices
Engorged plexus of veins beneath esophageal mucosa (67% of cirrhosis), prone to rupture when vomitting
Rx: Surveillance endoscopy, medical therapy, B. blocker/Propanolol.
pre and post hepatic, hepatic causes of portal htn
Pre-hepatic
- congenital malformation of portal vein
- portal vein thrombosis
- tumor
- pancreatitis (presses on portal vein)
Hepatic - Liver obstruction (Liver cirrhosis / scarring & hardening)
Post-hepatic (rare)
- Congenital obliteration of hepatic vein
- Budd-Chiari syndrome (Thrombotic occlusion of hepatic vein, rare)
Pancreatitis pathophysiology
Acute inflammation of pancreas and surrounding tissues
due to premature activation of pancreatic enzyme
> Proteolytic destruction
> blood vessels necrosis
> Fats necrosis
> Assc inflammatory reactions from tissue damages
causes of pancreatitis
Causes:
- gallstones *
- middle-aged female likely to have gallstone pancreatitis, after buffet
- alcohol * (direct toxic effect on p. cells, sphincter inflammation)
- infection (mumps, salmonella, hep A)
- post-ercp *
- trauma, medications
Pancreatitis clinical features
Symptoms:
- severe epigastric pain, radiate to back
- profuse vomiting ++
- Tender, guarded abdomen
- Systemic inflammation Response Syndrome (SIRS) from necrotic pancreas, haemorrhage into retroperitoneal space
- Bluish discoloration of abdo wall
(Retroperitoneal haemorrhage, not specific to pancreatitis)
Turner’s sign - Flank
Cullen’s sign - Umbilicus
5 Pancreatitis invx, indicators of severe pancreatitis
Serum amylase
- Incr 10-20x / (x3 of upper limit of normal range)
- return to normal within 2-3 days
Serum lipase
- Incr x3 of upper limit of normal range
Leukocytosis, CRP
(WBC> 15 x 10^9/L, in severe cases)
Raised bilirubin (20%)
- obstruction of common bile duct
Glycosuria (insulin deficiency, 15% of cases)
Hyperglycemia (Blood glucose >11.1mmol/L without DM history –> severe pancreatitis)
Low calcium - poor prognosis
- between 3rd and 10th day
- reaction of calcium with fatty acids (digestion of fats) to form salts –> arrhythmias and complications
Colorectal carcinoma - epidemiology
Most common form of malignant GIT
95% adenocarcinoma
Age: 60-70yo
Increasing trend of young people with CRC, GI cancers have growing incidence amongst all early-onset cancers
