Topic 12: Digestive System Disorders

Guest lecturer

Chang Pik Eu Jason

MBBS (Spore), MRCP(UK), MMed (Int Med), FAMS

Dr Chang is currently a Senior Consultant in the

Department of Gastroenterology and Hepatology,
Singapore General Hospital. His area of interest and
expertise is in liver cirrhosis and portal hypertension,
transient elastography (Fibroscan®), liver cancer, hepatitis
and liver transplantation. Dr Change is actively involved in
clinical education and he is an Adjunct Assistant Professor
at Duke-NUS Medical School.

Learning outcomes
Upon completing the pre-readings and the lecture, you should be able to
 Explain the function & physiology of gastrointestinal and hepatobiliary
system
 Describe the pathophysiology, diagnosis and management of patients with
hepatitis & liver cirrhosis
 Discuss the pathophysiology, diagnosis and management of common
upper GI conditions (e.g, GERD, peptic ulcers)
 Pathophysiology, diagnosis and management of colon cancer
 Relate the above to your professional practice and your roles in the
interdisciplinary care of patients with gastrointestinal and hepatobiliary
system disorders

Study resources
*VanMeter, K. C., & Hubert, R. J. (2014). Gould's Pathophysiology for the Health
Professions (5th Ed.). Philadelphia, PA: Saunders. Cp17: Digestive System Disorders

Hammer, G. D., & McPhee, S. J. (2014). Pathophysiology of Disease: An Introduction to

Clinical Medicine (7th Ed). McGraw Hill Professional. Cp 13. Gastrointestional Disease

Huether, S. E., & McCance, K. L. (2013). Understanding Pathophysiology (5th Ed.). New
York: Elsevier Health Sciences. Cp 33: Structure and function of the digestive system

Huether, S. E., & McCance, K. L. (2013). Understanding Pathophysiology (5th Ed.). New
York: Elsevier Health Sciences. Cp 34: Alterations of Digestive Function

Updated: 26 Jan 2018

Pre-readings
Structure & organization of digestive system (Fig 12-1)
 Organized into
upper & lower tract.
o Upper tract:
mouth,
esophagus,
stomach.
o The lower tract:
small intestine
(duodenum,
jejunum, ileum)
and large intestine
(ascending,
transverse,
descending &
sigmoid colon,
rectum)
 Accessory organs
of digestion:
o salivary glands,
o liver,
o gall bladder
o pancreas

Fig 12-1. Anatomy of the

digestive system with
associated events (Van
Meter, 2017 p.431)

 Peritoneum – serous
membrane in abdominal cavity
o Parietal & visceral
peritoneum- supports
abdominal organs and serves
as a conduit for blood vessels,
lymphatic vessels, and nerves
o Peritoneal cavity- space
between parietal and visceral
peritoneum
 Retroperitoneal cavity
 Mesentery- double fold of
the peritoneum. Serve to support
intestine
 Greater omentum- join
stomach to colon
 Lesser omentum- join
stomach to liver
Fig 12-2. Peritoneum and its organization (Source: http://www.stepwards.com/wp-
content/uploads/2016/05/serous_membranes-14B2E2B1A112F610CD6.png)

Updated: 26 Jan 2018

The purpose of the digestive system is to process ingested food and fluids & the
various secretions from glands.
 Digestive function: breakdown food into basic unit, via enzymatic activities
 Absorptive function: absorb the necessary nutrients through membrane
transport in small intestine

Stomach (Fig 12-3)

 Expansible muscular sac—acts as reservoir for food and fluid
 Three smooth muscle layers responsible for constant mixing and churning
of food
 Many types of gastric glands in mucosa
o Enteroendocrine cells
 Hormone gastrin: stimulate production of HCl & pepsinogen
when food enter stomach
o Parietal cells secrete
 HCl: as defensive mechanism to destroy microorganism
 intrinsic factor: Essential for absorption of vitamin B12 in the
ileum
o Chief cells secrete
 Pepsinogen Pepsin: initial digestion of proteins
 Formation of chyme
 Absorption of small and lipid-soluble molecules

Fig 12-3 Anatomy of stomach and its cross-sectional layers

(https://media1.britannica.com/eb-media/15/74315-004-B3A88818.jpg)

3 layers: Circular, longitudinal and oblique muscle layers

Liver
 Covered by fibrous capsule- distension will cause dull aching pain
 “Metabolic factory” of the body
o Synthesis of cholesterol, plasma proteins, clotting factors,
lipoproteins
o Hormone (aldosterone & estrogen) are inactivated in liver
o Glucose metabolism
 Glycogenesis: when high level of blood glucose. glucose 
glycogen (stored in liver)
Updated: 26 Jan 2018
 Glycogenolysis: when low blood glucose. Liver glycogen 
glucose
 Gluconeogenesis: when low blood glucose: protein & fat 
glucose
o Detoxification of drugs & alcohol
o Breakdown the old and damaged erythrocytes, recycling of iron &
protein from Hb
 A blood reservoir - able to release large volume of blood into general
circulation when blood volume is depleted
 Receives blood from hepatic portal vein: Transport of nutrients from
intestine to liver
 Hepatocytes (liver cells)
o Can regenerate
o Arranged in lobules (Fig 12-4) – functional unit of liver
o Store nutrients (mineral ions, copper, Vit A, B6,B12, D, K & folic
acid)
o Produce bile- important for emulsification of fats and fat soluble
vitamins before absorption in intestine
o Action site for carbohydrate, protein, fat metabolism
o Production of plasma proteins and clotting factors

Fig 12-4. Schematic drawing of hepatic lobules. Lobule is hexagon in shape and
comprise of rows of hepatocytes which radiate out from a central vein. The
hepatocytes (brown) are in close contact with blood filled sinusoids (blue) and bile
canaliculi (green) (source: Van Meter 2014, p 460)

Updated: 26 Jan 2018

  Blood supply (Fig 12-5)
o The liver has 2 sources of blood supply
 Hepatic artery – oxygenated blood from general circulation
 Hepatic portal vein- deoxygenated blood from small
intestines containing nutrients
o The blood drains out of the liver via hepatic vein

Fig 12-5. The blood supply of liver (source:

https://aholdencirm.files.wordpress.com/2013/12/05848-liver_large_1.jpg)

Pancreas
 Can be seen as 2 glands intimately woven into 1 organ
o Exocrine pancreas
o Endocrine pancreas
 Exocrine pancreas
o Make up of “exocrine” cells that secrete digestive enzymes to help
with digestion
 Trypsin
 Chymotrypsin
 Carboxypeptidase
 Ribonuclease
 Pancreatic amylase
 Bicarbonate ions – to neutralize HCl
o Content is released into pancreatic ducts that empty into duodenum
 Endocrine pancreas
o composed of small islands of cells, the islets of Langerhans.
o release hormones (insulin and glucagon) into the blood stream.

Small intestine (Duodenum, jejunum, ileum)

 Duodenum: digestions continue
 Ileum: absorption of nutrients.
 Site of production of mucus and many digestive enzymes (Enterokinase,
peptidases, nucleosidases, lipase, sucrase, maltase, lactase) and
hormone (cholecystokinin)

Updated: 26 Jan 2018

Large intestine / Colon
 Structure:
o Ascending colon
o Transverse colon
o Descending colon
o Sigmoid colon
o Rectum
o Anal canal
 Function
o Resident normal flora to
 Breakdown of certain food materials
 Vitamin K synthesis by bacteria
o Major fluid and electrolyte reabsorption  formation of solid feces

Neural & hormonal control of digestive systems

Source: Van Meter 2014, p 436

Common manifestations of digestive system disorders

 Anorexia, nausea, vomiting
o May be signs of digestive disorder or other condition elsewhere in
the body (e.g., Systemic infection, Uremia, Emotional responses,
Motion sickness, Pressure in the brain, Overindulgence of food,
drugs, Pain)
 Diarrhea
 Constipation
 Fluid & electrolyte imbalance: dehydration, hypovolemia, hyponatremia,
metabolic acidosis
 Pain
o Visceral pain
o Somatic pain
 Malnutrition

Updated: 26 Jan 2018

Common drugs used in digestive system disorders

(Source: Van Meter 2914, p 442)

Upper GI tract disorders

 Gastroesophageal reflux disease (GERD)
o Periodic reflux of gastric contents into distal esophagus causes
erosion and inflammation.
o Severity depends on competence of the lower esophageal
sphincter.
o Delayed gastric emptying may be a factor.
o Avoidance of: Caffeine, fatty and spicy foods, alcohol, smoking,
certain drugs
o Medication may reduce reflux and inflammation
 Gastritis - inflammation of the stomach lining
o Acute gastritis
o Chronic gastritis
o Gastroenteritis
 Peptic ulcer
o Most caused by H. pylori infection
o Usually occur in the proximal duodenum (duodenal ulcers) or the
antrum of the stomach (gastric ulcers)
o Development begins with breakdown of mucosal barrier
 Decreased mucosal defense
 Increased acid pepsin secretion
o Complications: hemorrhage, perforation, obstruction
o Treatment
 Antimicrobial and proton pump inhibitor to eliminate H. pylori
 Reduction of exacerbating factors

Updated: 26 Jan 2018

  Gastric cancer
o Arises primarily in mucous glands (adenocarcinoma)
o Mostly in the antrum or pyloric area, followed by lesser curvature of
stomach or cardia
o Risk factors
 Diet seems to be a key factor, particularly smoked foods,
nitrites, and nitrates.
 Genetic influences also play a role.
o Symptoms vague until cancer is advanced.
o Management: Surgery together with chemotherapy and radiation
may relieve symptoms.
 Dumping syndrome (Fig 12-6)– lost of control of gastric
emptying (in partial gastrectomy) where large quantity of
hyperosmolar chyme are rapidly dumped into intestine,
causing symptoms like abdominal cramps, diarrhea shortly
after meal. Also blood glucose swing- immediate
hyperglycemia followed by hypoglycemia 2-3 hr after meal.

Fig 12-6. Mechanism and effect of dumping syndrome (post gastrectomy)

(Van Meter 2014, p 458)

Updated: 26 Jan 2018

Disorders of the gall bladder & liver
 Gall stones
o Cholecystitis - Inflammation of gallbladder and cystic duct
o Cholangitis - Inflammation related to infection of bile ducts
o Choledocholithiasis - Obstruction of the biliary tract by gallstones
o Risk factors: High cholesterol, obesity, multiparity, oral
contraceptives or estrogen supplements, hemolytic anemia,
alcoholic cirrhosis, biliary tract infection
o Sudden wave of radiating pain, nausea & vomiting, jaundice

 Hepatitis
o Inflammation of the liver, many types classified by causes
 Alcoholic
 Idiopathic (Fatty liver)
 Local infection (Viral hepatitis)-HAV, HBV, HCV, HDV, HEV
 Infection elsewhere (infectious mononucleosis or amebiasis)
 Chemical or drug toxicity

 3 stages of hepatitis development (Fig

12-7)
o Preicteric (prodromal) stage
o Icteric (jaundice) stage
o Posticteric (recovery) stage

Fig 12-7 The course of Hepatitis viral

infection (Van Meter 2014, p 464)

Updated: 26 Jan 2018

  Jaundice (icterus)
o Yellowish color of the skin & other tissue results from high levels of
bilirubin in the blood
o Types of jaundice (Fig 12-8)
 Prehepatic jaundice: Result of excessive destruction of red
blood cells. Characteristic of hemolytic anemias or
transfusion reactions
 Intrahepatic jaundice: Occurs with disease or damage to
hepatocytes (e.g., Hepatitis or cirrhosis)
 Posthepatic jaundice: Caused by obstruction of bile flow into
gallbladder or duodenum (e.g, tumour, cholelithiasis)

Fig 12-8. Types of jaundice (Van Meter 2014, p 461)

 Cirrhosis
o Progressive destruction of the liver with resultant diffuse fibrosis
and loss of lobular organization.
o Causes:
 Alcoholic liver disease,
 Biliary cirrhosis (associated with immune disorders),
 Postnecrotic cirrhosis (linked with chronic hepatitis or long-
term exposure to toxic materials)

Updated: 26 Jan 2018

 
Metabolic (usually caused by genetic metabolic storage
disorders)
o Consequences of liver cirrhosis (Fig 12-9)
  removal and conjugation of bilirubin
  bile production  impairs digestion & absorption
 Impaired digestion and absorption of nutrients
  production of blood-clotting factors
 Impaired glucose and glycogen metabolism
 Impaired conversion of ammonia to urea
  inactivation of hormones and drugs (* Drug
dosages must be carefully monitored to avoid
toxicity.)
 Decreased removal of toxic substances
 Backup of bile in the liver (Leads to obstructive
jaundice)
 Blockage of blood flow through the liver  portal
hypertension
 Congestion in the spleen  Increases hemolysis
 Inadequate storage of iron and vitamin B12
 Development of esophageal varices 
Hemorrhage
Fig 12-9. Effects of advance  Development of ascites  abdominal distention
cirrhosis (Van Meter 2014, p469) and pressure (Fig 12-10)

Fig 12-10. Development of ascites with liver cirrhosis (Van Meter 2014,
p468)

Updated: 26 Jan 2018

  Liver cancer
o Primary Hepatocellular carcinoma is relatively rare
 Most common primary tumor of liver
 More common in cirrhotic livers
o Secondary or metastatic cancer to the liver (more common)
 Arises from areas served by the hepatic vein or spread along
the peritoneal membranes
o Diagnosis usually occurs with advanced stages
o Chemotherapy, possible lobectomy or radiofrequency ablation
(RFA) procedure

Disorders of the pancreas

 Acute pancreatitis
o Inflammation of the pancreas results in autodigestion of the tissue
o Acute form is considered a medical emergency
o Pancreas lacks a fibrous capsule, so destruction may progress into
tissue surrounding the pancreas
 Substances released by necrotic tissue lead to widespread
inflammation
 Hypovolemia and circulatory collapse may follow.
 Chemical peritonitis results in bacterial peritonitis.
 Septicemia, adult respiratory distress syndrome and acute
renal failure are possible complications.
o S&S:
 Severe epigastric or abdominal pain radiating to the back
 Signs of shock (due to hypovolemia)
 Low-grade fever until infection develops
 Abdominal distention and decreased bowel sounds

 Pancreatic tumour
o S&S depends on which pancreatic system is affected
 Ductal adenocarcinomas (most common
 Tumors block the exocrine system, patients can
develop pancreatitis and pain from the abnormal
release of digestive enzymes into the pancreas
instead of into the bowel, and they can develop
digestive problems, such as diarrhea,
 Pancreatic neuroendocrine tumors/ islet cell tumours
 When tumors destroy the endocrine function of the
pancreas, patients can develop sugar diabetes (abnormally
high blood sugar levels).

Updated: 26 Jan 2018

Lower gastrointestinal tract disorders – colorectal cancer
 Chronic inflammatory bowel disease
o Crohn’s disease and ulcerative colitis are chronic inflammatory bowel
diseases (IBDs).
 Crohn’s disease—often during adolescence
 Ulcerative colitis—second or third decade

(Source: Van Meter 2014, p472)

o Treatment approach
 Anti-inflammatory medications (Sulfasalazine,
Glucocorticoids)
 Antimotility agents
 Nutritional supplements
 Antimicrobials
 Immunotherapeutic agents
 Surgical resection (Usually ileostomy or colostomy)

 Intestinal obstruction - Lack of movement of intestinal contents through the

intestine
o 2 types
 Mechanical obstructions: Result from tumors, adhesions,
hernias, other tangible obstructions
 Functional or adynamic obstructions: Result from impairment of
peristalsis (e.g., spinal cord injury, Paralytic ileus caused by
toxins or electrolyte imbalance)
o Pathophysiology:

Updated: 26 Jan 2018

  Gases and fluids accumulate proximal to the blockage,
distending the intestine.
 Pressure increases in lumen  Compression of veins in wall &
Intestinal wall becomes edematous
 Prevention of absorption
 Intestinal distention leads to persistent vomiting  additional
loss of fluid and electrolytes  hypovolemia can result.
 Obstruction promotes rapid reproduction of intestinal bacteria.
Some produce endotoxins  Affected wall becomes necrotic
and more permeable
 Intestinal wall becomes ischemic and necrotic  gangrene
 Ischemia and necrosis  decreased innervation and cessation
of peristalsis  Paralytic ileus
 Perforation of the necrotic segment may occur  Generalized
peritonitis and septic shock

 Colorectal cancer
o Most colorectal cancer develops from adenomatous polyps.
o Cancer occurs primarily in persons older than 50 years.
o Risk factors
 Familial multiple polyposis
 Long-term ulcerative colitis
 Genetic factors
 Environmental factors
 Diet low in fiber
o General signs (Fig 12-11)
 Change in bowel habits
 Alternating diarrhea and constipation
 Bleeding
 Fatigue, weight loss, anemia
o Treatment
 Surgical removal
 Radiation and/or chemotherapy

Fig 12-11. Signs and symptoms of colorectal cancer by

location. Clinical manifestations are listed in order of frequency for
each region (Van Meter 2014, p 480)

Updated: 26 Jan 2018