Professional Documents
Culture Documents
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Gastro-Intestinal Tract
Mouth
Esophagus
Stomach
Small intestine
Large intestine
Rectum
Anus
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Gastro-Intestinal Tract (Cont.)
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Gastro-Intestinal Tract (Cont.)
Ingestion of food
Propulsion of food and wastes from the mouth to
the anus
Secretion of mucus, water, and enzymes
Mechanical digestion of food particles
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Gastro-Intestinal Tract (Cont.)
Chemical digestion of food particles
Absorption of digested food
Elimination of waste products by defecation
Immune and microbial protection against
infection
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Gastro-Intestinal Tract (Cont.)
Histology
Mucosa
Submucosa
Muscularis
Serosa or adventitia
Enteric plexus
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Gastro-Intestinal Tract (Cont.)
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Mouth
Reservoir for chewing and mixing of food with
saliva
Taste buds
Salty, sour, bitter, and sweet and savoury (umami)
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Salivary Glands
Three pairs:
Submandibular
Sublingual
Parotid
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Salivary Glands (Cont.)
Saliva
Water with mucus, sodium, bicarbonate, chloride,
potassium, and salivary α-amylase (carbohydrate
digestion)
Controlled by sympathetic and parasympathetic fibres
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Swallowing
Esophagus
Peristalsis
Coordinated sequential contraction and relaxation of outer
longitudinal and inner circular layers of muscles
Primary and secondary
Upper esophageal sphincter
Keeps air from entering the esophagus during respiration
Lower esophageal sphincter
Prevents regurgitation from the stomach and caustic injury to the
esophagus
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Swallowing (Cont.)
Phases
Oropharyngeal
• Food formed into bolus and forced toward pharynx
• Pharynx contracts
• Respiration inhibited and epiglottis slides down
Esophageal
• Food bolus enters esophagus
• Esophagus relaxes
• Peristalsis occurs to move food down to lower esophageal
sphincter
• Food bolus enters stomach
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Stomach
A hollow, muscular organ that stores food,
secretes digestive juices, mixes food with the
juices, and propels partially digested food
(chyme)
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Stomach (Cont.)
Boundaries:
Cardiac orifice
Pyloric sphincter
Pylorus
Functional areas:
Fundus
Body
Antrum
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Stomach (Cont.)
Three layers of smooth muscle:
Longitudinal (outer)
Circular (middle)
Oblique (inner)
Blood supplied from celiac artery
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Stomach (Cont.)
Modified from Patton, K.T., & Thibodeau, G.A. (2014). The human body in health & disease (6th ed.). St Louis, MO: Mosby.
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Gastric Motility
Swallowing
Causes relaxation
Facilitated by gastrin and cholecystokinin
Motilin
Increases peristalsis
Secretin
Decreases peristalsis
Gastric mixing and emptying
Retropulsion
Rate dependent on volume, osmotic pressure, and chemical
composition
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Gastric Secretion
Phases
Cephalic phase
• Stimulated by the thought, smell, and taste of food
Gastric phase
• Stimulated by distension of the stomach
Intestinal phase
• Stimulated by histamine and digested protein
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Gastric Secretion (Cont.)
Stimulation of gastric secretion
Eating
Gastrin
Paracrine pathways
Acetylcholine
Chemicals
• Ethanol, coffee, protein
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Gastric Secretion (Cont.)
Stomach secretes large volumes of gastric
juices
Mucus
Acid
Enzymes
Hormones
Intrinsic factor
Gastroferrin
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Gastric Secretion (Cont.)
Acid
Secreted by parietal cells
Dissolves food fibres, acts as a bactericide against
swallowed micro-organisms, and converts
pepsinogen to pepsin
Pepsin
Secreted by chief cells
Proteolytic enzyme
• Breaks down protein and forms polypeptides in the stomach
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Gastric Secretion (Cont.)
Mucus
Stimulated by prostaglandins
Mucosal barrier
Gastric mucosal blood flow
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Gastric Pits and Gastric Glands
From Patton, K.T., Thibodeau, G.A., & Douglas, M.M. (2012). Essentials of anatomy and physiology. St Louis, MO: Mosby.
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Small Intestine
5 to 6 m long
Three segments
Duodenum
Jejunum
Ileum
• Ileocecal valve
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Small Intestine (Cont.)
Peritoneum
Membrane surrounding the organs of the abdomen
and pelvic cavity
Visceral
Parietal
Peritoneal cavity
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Small Intestine (Cont.)
Duodenum
Supplied by gastroduodenal artery
Jejunum and ilium
Supplied by superior mesenteric artery
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Small Intestine (Cont.)
Innervated by enteric nerves
Myenteric (Auerbach) plexus
Submucosal (Meissner) plexus
Two layers of smooth muscle
Longitudinal (outer)
Circular (inner)
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Small Intestine (Cont.)
Absorption through villi
Microvilli
Brush border
Lamina propria
Lacteal
Crypts of Lieberkühn
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Small Intestine (Cont.)
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Intestinal Digestion and Absorption
Initiated in stomach
Actions of gastric hydrochloric acid and pepsin
Continues in proximal portion of small intestine
Action of pancreatic enzymes, intestinal enzymes,
and bile salts
• Carbohydrate breakdown
• Proteins degraded
• Fats emulsified
Nutrients absorbed by active transport, diffusion,
or facilitated diffusion
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Intestinal Motility
Movements of the small intestine facilitate both
digestion and absorption
Haustral segmentation
Peristalsis
Ileogastric reflex
Intestinointestinal reflex
Gastroileal reflex
Ileocecal valve
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Large Intestine
Cecum
Pouch that receives chyme from the ileum
Vermiform appendix
Colon
Ascending
Transverse
Descending
Sigmoid
Rectum
Anus
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Large Intestine (Cont.)
Modified rom Patton, K.T., & Thibodeau, G.A. (2014). The human body in health and disease (6th ed.). St Louis, MO:
Mosby.
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Large Intestine (Cont.)
Ileocecal valve
O’Beirne (rectosigmoid) sphincter
Internal anal sphincter
External anal sphincter
Teniae coli
Three longitudinal bands in the longitudinal muscle
layer of the cecum and colon
Shorter than the colon and gives it a gathered
appearance
Haustra
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Large Intestine (Cont.)
Motor and secretory activity regulated by enteric
nervous system
Vagal stimulation increases rhythmic contraction
of the proximal colon
Blood supply is derived primarily from branches
of the superior and inferior mesenteric arteries
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Large Intestine (Cont.)
Colonic movement primarily segmental
Fecal mass massaged
Water absorbed
Peristaltic movements promote the emptying of the
colon
Gastrocolic reflex
• Causes the fecal mass to pass rapidly into the sigmoid colon
and rectum
Defecation reflex
• Stimulated by the movement of feces into the sigmoid colon
and rectum
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Gastro-Intestinal Absorption
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Immunity and the GI System
Major role in immune defences by killing many
micro-organisms
Mucosal secretions produce antibodies (IgA).
Paneth cells produce defensins and other antibiotic
peptides and lysozymes important to mucosal
immunity.
Peyer patches (collections of lymphocytes, plasma
cells, and macrophages) produce immunoglobulin A
as a component of the gut-associated lymph tissue in
the small intestine.
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Intestinal Microbiome
Numbers of bacteria increase from proximal to
distal GI tract
Highest in colon
Multiple factors affect normal composition of
bacterial flora
Genetics, diet, environmental, medications
Alert immune system to protect against infection
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Intestinal Microbiome (Cont.)
Intestinal tract
Sterile at birth but colonized within a few hours
Number and diversity of bacteria decrease with aging
Bacteria in stomach are relatively sparse
• Acid kills ingested pathogens and inhibits bacterial growth
Low concentration of aerobes in duodenum and
jejunum
• Suppressed by bile acid, intestinal motility, and antibodies
Anaerobes found distal to ileocecal valve but not
proximal to the ileum
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Splanchnic Blood Flow
Provides blood flow to:
Esophagus
Stomach
Small and large intestine
Liver
Gallbladder
Pancreas
Spleen
Important reservoir of blood volume
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Accessory Organs of Digestion
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Accessory Organs
of Digestion (Cont.)
Liver
Divided into right and left lobes
• Right lobe further divided into the caudate and quadrate
lobes
Falciform ligament
Round ligament
Coronary ligament
Glisson capsule
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Liver
From Applegate, E. (2011). The anatomy and physiology learning system (4th ed.). St Louis, MO: Saunders.
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Accessory Organs of Digestion
Liver
Hepatic artery
Hepatic portal vein
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Hepatic Portal Circulation
From Herlihy, B. (2015). The human body in health and illness (5th ed.). St Louis, MO:
Saunders
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Liver
Liver lobules
Hepatocytes
• Functional cells of the liver
Sinusoids
Bile canaliculi
Common bile duct
Ampulla of Vater
Major duodenal papilla (sphincter of Oddi)
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Liver (Cont.)
Kupffer cells
Tissue macrophages important for healing of liver injury
Stellate cells
Contractile in liver injury, contain retinoids, remove foreign
substances from blood
Natural killer cells
Produce interferon-γ and are important in tumour defence
Disse space
Drains interstitial fluid into the hepatic lymph system
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Secretion of Bile
Bile is an alkaline, bitter-tasting, yellowish green
fluid that contains bile salts, cholesterol,
bilirubin, electrolytes, and water
Formed by hepatocytes and secreted into the
bile canaliculi
Enterohepatic circulation
Recycling of bile salts
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Enterohepatic Circulation
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Bile
Two fractional components
Acid dependent
Acid independent
Primary bile acids
Cholic
Chenic (chenodeoxycholic)
Secondary bile acids
Deoxycholic
Lithocholic
Primary and secondary bile acids together form the bile
acid pool
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Metabolism of Bilirubin
Bilirubin is a by-product of the destruction of
aged red blood cells
Bilirubin gives bile a greenish black colour and
produces the yellow tinge of jaundice
Unconjugated bilirubin
Conjugated bilirubin
Urobilinogen
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Metabolism of Bilirubin (Cont.)
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Vascular and
Hematological Liver Functions
Stores blood
Hemostatic functions
Synthesizes clotting factors
• Because bile salts are needed for reabsorption of fats,
vitamin K absorption depends on adequate bile production in
the liver
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Liver Functions
Metabolism of nutrients
Fats
Proteins
Carbohydrates
Metabolic detoxification
Storage of minerals and vitamins
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1. Which assists in the removal of foreign
substances and traps bacteria in the liver
sinusoids?
A. Hepatocytes
B. Liver lobules
C. Kupffer cells
D. Disse space
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Gallbladder
Saclike organ that lies on the inferior surface of
the liver
Function is to store and concentrate bile
between meals
Holds about 90 mL of bile
Begins to contract 30 minutes after eating under
the influence of the vagus nerve and
cholecystokinin
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Exocrine Pancreas
Exocrine pancreas is composed of acinar cells
that secrete enzymes and networks of ducts that
secrete alkaline fluids to assist in digestion
Pancreatic duct (Wirsung duct)
Ampulla of Vater
Arterial blood is supplied by branches of the celiac
and superior mesenteric arteries
Venous blood leaves through tributaries to the portal
vein and through the splenic vein
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Exocrine Pancreas (Cont.)
Secretions
Isotonic
Contain potassium, sodium, bicarbonate, and chloride
Enzymes
Hydrolyze proteins, carbohydrates, and fats
Include trypsin, chymotrypsin, carboxypeptidase, and
elastase
Secreted in inactive forms
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Exocrine Pancreas (Cont.)
Trypsin inhibitor
Prevents the activation of proteolytic enzymes while
they are in the pancreas
Enterokinase
Secreted by the duodenal mucosa
Activates inactive enzymes
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2. Bile is produced by which organ?
A. Liver
B. Pancreas
C. Gallbladder
D. Small intestine
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Case Study
A 28-year-old pregnant woman is seen in her obstetrician’s office
for a routine appointment during her 30th week of gestation. This
is her second pregnancy, and she has been feeling tired. The
baby is measuring large for gestational age, and she states that
the baby has been giving her heartburn. She is craving spicy,
Mexican food and cannot get enough of chips and salsa. The
obstetrician reminds the young woman that she still has
approximately 10 weeks until delivery. He reminds her to
continue to take her vitamins and iron supplements and to cut
back on the spicy foods, especially before bedtime, to decrease
the incidence of heartburn or gastroesophageal reflux.
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Case Study:
Discussion Questions
In the digestive system, the stomach is stimulated by eating to
produce large volumes of gastric secretions.
A. Gastroferrin
B. Hydrochloric acid
C. Intrinsic factor
D. Chymotrypsin
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Case Study:
Discussion Questions (Cont.)
2. The enteric nervous system regulates intestinal
motility. Of the two movements that promote
motility, what one occurs more frequently?
A. Segmentation
B. Peristalsis
C. Vagal stimulation
D. Neural reflex
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Chapter 36
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Clinical Manifestations of
Gastro-Intestinal Dysfunction
Anorexia
Lack of a desire to eat despite physiological stimuli
that would normally produce hunger
Vomiting
Forceful emptying of the stomach and intestinal
contents through the mouth
Several types of stimuli initiate the vomiting reflex
Common symptoms of vomiting are hypersalivation
and tachycardia
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Clinical Manifestations of Gastro-
Intestinal Dysfunction (Cont.)
Nausea
Subjective experience that is associated with a
number of conditions
Retching
Nonproductive vomiting
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Clinical Manifestations of Gastro-
Intestinal Dysfunction (Cont.)
Projectile vomiting
Spontaneous vomiting that does not follow nausea or
retching
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Clinical Manifestations of Gastro-
Intestinal Dysfunction (Cont.)
Constipation
Infrequent or difficult defecation
Primary condition
• Normal transit (functional)
• Slow transit
• Pelvic floor or outlet dysfunction
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Clinical Manifestations of Gastro-
Intestinal Dysfunction (Cont.)
Secondary condition
• Caused by many different factors such as diet, medications,
various disorders, aging
Manifestations
• Straining with defecation
• Hard stools
• Sensation of incomplete emptying
• Manual manoeuvres to facilitate stool evacuation
• Fewer than three bowel movements per week
Manage underlying disease
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Clinical Manifestations of Gastro-
Intestinal Dysfunction (Cont.)
Diarrhea
Presence of loose, watery stools
• Acute or persistent
Large-volume diarrhea
• Caused by excessive amounts of water or secretions or both
in the intestines
Small-volume diarrhea
• Volume of feces is not increased, usually results from
excessive intestinal motility
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Clinical Manifestations of Gastro-
Intestinal Dysfunction (Cont.)
Major mechanisms of diarrhea
• Osmotic diarrhea
• Secretory diarrhea
• Motility diarrhea
Systemic effects
• Dehydration
• Electrolyte imbalance
• Weight loss
Associated with malabsorption syndromes
Treated with fluid restoration, antimotility or water-
absorbent medications, treatment of causal factors
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Clinical Manifestations of Gastro-
Intestinal Dysfunction (Cont.)
Abdominal pain
Mechanical, inflammatory, or ischemic
Usually associated with tissue injury and inflammation
Parietal
Visceral
Referred
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Clinical Manifestations of Gastro-
Intestinal Dysfunction (Cont.)
Gastro-intestinal bleeding
Upper gastro-intestinal bleeding
• Esophagus, stomach, or duodenum
Lower gastro-intestinal bleeding
• Jejunum, ileum, colon, or rectum
Occult bleeding
Physiological response depends on rate and amount
of blood loss
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Clinical Manifestations of Gastro-
Intestinal Dysfunction (Cont.)
GI bleeding
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Disorders of Motility
Dysphagia
Difficulty swallowing
• Mechanical obstructions
• Functional disorders
Achalasia
• Related to loss of inhibitory neurons in the myenteric plexus
with smooth muscle atrophy in the middle and lower portions
of the esophagus
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Achalasia
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Disorders of Motility
Dysphagia
Manifestations
• Stabbing pain at the level of obstruction
• Discomfort after swallowing
• Regurgitation of undigested food
• Unpleasant taste sensation
• Vomiting
• Aspiration
• Weight loss
Symptoms managed by eating small meals slowly, taking
fluid with meals, and sleeping with the head elevated to
prevent regurgitation and aspiration
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Disorders of Motility (Cont.)
Gastroesophageal reflux disease (GERD)
Reflux of acid and pepsin from the stomach to the
esophagus that causes esophagitis
Resting tone of the LES tends to be lower than
normal
Conditions that increase abdominal pressure or delay
gastric emptying can contribute to the development of
reflux esophagitis
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Disorders of Motility (Cont.)
Manifestations
• Heartburn
• Acid regurgitation
• Dysphagia
• Chronic cough
• Asthma attacks
• Laryngitis
• Upper abdominal pain within 1 hour of eating
Proton pump inhibitors are the agents of choice for
controlling symptoms and healing esophagitis
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Disorders of Motility (Cont.)
Hiatal hernia
Diaphragmatic hernia with protrusion of the upper part
of the stomach through the diaphragm and into the
thorax
• Sliding
• Paraesophageal
• Mixed
Conservative treatment
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Hiatal Hernia
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Disorders of Motility
Gastroparesis
Delayed gastric emptying in the absence of
mechanical gastric outlet obstruction
Associated with diabetes mellitus, surgical vagotomy,
or fundoplication
Symptoms include nausea, vomiting, abdominal pain,
and postprandial fullness or bloating
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Disorders of Motility (Cont.)
Pyloric obstruction
Blocking or narrowing of the opening between the stomach
and the duodenum
Acquired or congenital
Manifestations
• Epigastric pain and fullness
• Nausea
• Succussion splash
• Vomiting
• With a prolonged obstruction: malnutrition, dehydration, and
extreme debilitation
Usually conservative management
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Disorders of Motility (Cont.)
Intestinal obstruction and paralytic ileus
Intestinal obstruction is any condition that prevents
the flow of chyme through the intestinal lumen
• Simple obstruction
Mechanical blockage of the lumen
• Functional obstruction (paralytic ileus)
Failure of intestinal motility
Often occurs after intestinal or abdominal surgery, pancreatitis,
or hypokalemia
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Intestinal Obstruction
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Disorders of Motility
Intestinal obstruction and paralytic ileus
Signs of small intestinal obstruction
• Colicky pains
• Nausea and vomiting
Signs of large intestinal obstruction
• Hypogastric pain and abdominal distension
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Gastritis
Inflammatory disorder of the gastric mucosa
Acute gastritis
Caused by injury of the protective mucosal barrier
Chronic gastritis
Chronic fundal gastritis (type A, immune)
Chronic antral gastritis (type B, nonimmune)
Symptoms vague
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Peptic Ulcer Disease
Break or ulceration in the protective mucosal
lining of the lower esophagus, stomach, or
duodenum
Acute and chronic ulcers
Superficial
Erosions
Deep
Zollinger-Ellison syndrome
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Peptic Ulcer Disease (Cont.)
Duodenal ulcers
Most common of the peptic ulcers
Developmental factors:
• Helicobacter pylori infection
• Hypersecretion of stomach acid and pepsin
• Use of NSAIDs
Characterized by intermittent pain in the epigastric
area
• Relieved rapidly by ingestion of food or antacids
Management aimed at relieving the causes and
effects of hyperacidity and preventing complications
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Duodenal Ulcer
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Gastric Ulcer
Gastric ulcers tend to develop in the antral
region of the stomach, adjacent to the acid-
secreting mucosa of the body
Pathophysiology
Primary defect is an increased mucosal permeability
to hydrogen ions
Gastric secretion tends to be normal or less than
normal
Manifestations and treatment similar to duodenal
ulcers except food causes pain
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Gastric Ulcer (Cont.)
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Stress-Related Mucosal Disease
Acute form of peptic ulcer that is related to
severe illness or major trauma
Ischemic ulcers
• Within hours of trauma, burns, hemorrhage, heart failure, or
sepsis
Curling ulcers
• Develop as a result of burn injury
Cushing ulcers
• Develop as a result of a brain injury or brain surgery
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Surgical Treatment of Ulcer
Most common indications are recurrent or
uncontrolled bleeding and perforation of the
stomach or duodenum.
Objectives are to reduce stimuli for acid
secretion, decrease the number of acid-
secreting cells in the stomach, and correct
complications of ulcer disease.
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Postgastrectomy Syndromes
Dumping syndrome
Alkaline reflux gastritis
Afferent loop obstruction
Diarrhea
Weight loss
Anemia
Bone and mineral disorders
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1. A patient undergoes gastric resection. Following
surgery, she experiences intermittent severe pain
and epigastric fullness after eating. Which factor is
the most likely reason for her symptoms?
A. Diarrhea
B. Dumping syndrome
C. Alkaline reflux gastritis
D. Afferent loop obstruction
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Malabsorption Syndromes
Maldigestion
Failure of the chemical processes of digestion
Malabsorption
Failure of the intestinal mucosa to absorb digested
nutrients
Maldigestion and malabsorption frequently occur
together
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Malabsorption Syndromes (Cont.)
Pancreatic exocrine insufficiency
Insufficient pancreatic enzyme production
• Lipase, amylase, trypsin, or chymotrypsin
Causes
• Pancreatitis
• Pancreatic carcinoma
• Pancreatic resection
• Cystic fibrosis
Fat maldigestion is the main problem, so the patient
will exhibit fatty stools and weight loss
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Malabsorption Syndromes (Cont.)
Lactase deficiency
Inability to break down lactose into monosaccharides
and therefore prevents lactose digestion and
absorption
Fermentation of lactose by bacteria causes gas
(cramping pain, flatulence, etc.) and osmotic diarrhea
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Malabsorption Syndromes (Cont.)
Bile salt deficiency
Conjugated bile salts needed to emulsify and absorb
fats
Bile salts are conjugated in the bile that is secreted
from the liver
Can result from liver disease and bile obstructions
Poor intestinal absorption of lipids causes fatty stools
(steatorrhea), diarrhea, and loss of fat-soluble
vitamins (A, D, E, K)
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Malabsorption Syndromes (Cont.)
Fat-soluble vitamin deficiencies:
Vitamin A
• Night blindness
Vitamin D
• Decreased calcium absorption
• Bone pain
• Osteoporosis
• Fractures
Vitamin K
• Prolonged prothrombin time
• Purpura
• Petechiae
Vitamin E
• Uncertain
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Inflammatory Bowel Disease
Ulcerative colitis (UC) and Crohn’s disease (CD)
Chronic, relapsing inflammatory bowel disorders
• Genetics
• Environmental factors
• Alterations of epithelial barrier functions
• Altered immune reactions to intestinal flora
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Ulcerative Colitis
Chronic inflammatory disease that causes
ulceration of the colonic mucosa
Sigmoid colon and rectum
Begins in the rectum and may extend proximally to
the entire colon
Intermittent periods of remission and exacerbation
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Ulcerative Colitis (Cont.)
Symptoms:
Diarrhea (10 to 20/day)
Urgency
Bloody stools
Cramping
Treatment
Mild to moderate disease treated with 5-aminosalicyclate
therapy followed by steroids
Thioprine and immunomodulatory agents or vedolizumab
used for serious disease
Surgery for severe disease
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Crohn’s Disease
Granulomatous colitis, ileocolitis, or regional
enteritis
Idiopathic inflammatory disorder; affects any part
of the digestive tract, from mouth to anus
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Crohn’s Disease (Cont.)
Causes “skip lesions”
One side of the intestinal wall may be affected
and not the other
Ulcerations can produce fissures that extend
into the lymphatics
Symptoms similar to ulcerative colitis
Anemia may result from malabsorption of
vitamin B12 and folic acid
Treatment similar to ulcerative colitis
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Microscopic Colitis
Relatively common cause of diarrhea
Primarily in females and older adults
Two forms
Lymphocytic
Collagenous
Cause unknown
Results in chronic daily watery diarrhea
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Irritable Bowel Syndrome (IBS)
Symptom-based disease characterized by
recurrent abdominal pain with altered bowel
habits
More common in females
Associated with anxiety, depression, and
reduced quality of life
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Irritable Bowel
Syndrome (IBS) (Cont.)
Cause unknown but mechanisms proposed:
Visceral hypersensitivity
Abnormal intestinal permeability, motility, and
secretion
Postinflammatory
Alteration in gut microbiota
Food allergy/intolerance
Psychosocial factors
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Irritable Bowel
Syndrome (IBS) (Cont.)
Manifestations
Lower abdominal pain or discomfort and bloating
Symptoms are usually relieved with defecation
and do not interfere with sleep
No cure, and treatment is individualized
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Diverticular Disease of the Colon
Diverticula
Herniations of mucosa through the muscle layers of
the colon wall, especially the sigmoid colon
Diverticulosis
Asymptomatic diverticular disease
Diverticulitis
Inflammatory stage of diverticulosis
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Diverticular Disease
of the Colon (Cont.)
Diverticula can occur anywhere in the gastro-
intestinal tract, particularly at weak points in the
colon wall.
Complicated diverticulitis includes abscess,
fistula, obstruction, bleeding, or perforation.
Symptoms of uncomplicated diverticular disease
may be vague or absent.
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Appendicitis
Inflammation of the vermiform appendix
Possible causes:
Obstruction, foreign bodies, infection
Gastric or periumbilical pain
Rebound tenderness to RLQ
Perforation, peritonitis, and abscess formation
are the most serious complications
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Mesenteric Vascular Insufficiency
Blood supply to the stomach and intestine
Celiac artery
Superior and inferior mesenteric arteries
Mesenteric venous thrombosis
Acute mesenteric artery insufficiency
Chronic mesenteric ischemia
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Obesity
Increase in body fat mass
Body mass index (BMI) >30 kg/m2
Associated with higher all-cause mortality
Generally develops when caloric intake exceeds
caloric expenditure
Major risk factor for morbidity, death, and high
health care costs
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Obesity (Cont.)
Interaction of peripheral and central pathways
and numerous cytokines, hormones, and
neurotransmitters
Signalling mediators act on hypothalamus and
brainstem to regulate hunger and satiety
Leptin
Ghrelin
Adiponectin
Peptide YY
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Obesity (Cont.)
Two different forms of adipose tissue distribution
Visceral obesity
• Distribution of body fat is localized around the abdomen and
upper body
• “Apple shape”
Peripheral obesity
• Distribution of body fat is extraperitoneal and distributed
around the thighs and buttocks
• “Pear shape”
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Obesity (Cont.)
Normal weight obesity (NWO)
Normal body weight and BMI with percent of body fat
>30%
Metabolically healthy obesity (MHO)
Obese but have no metabolic-obesity associated
complications and decreased risk for morbidity and
mortality
Weight loss (bariatric) surgery is the most
effective treatment for decreasing obesity-
related morbidity
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Malnutrition and Starvation
Malnutrition
Lack of nourishment from inadequate amounts of
calories, protein, vitamins, or minerals
Starvation
Decreased energy intake leading to weight loss
Short-term starvation
• Glycogenolysis
• Gluconeogenesis
Long-term starvation
• Refeeding syndrome
Cachexia
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Liver Disorders
Portal hypertension
Abnormally high blood pressure in the portal venous
system caused by resistance to portal blood flow
• Intrahepatic
• Posthepatic
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Liver Disorders (Cont.)
Varices
• Lower esophagus
• Stomach
• Abdominal wall
• Rectum
Splenomegaly
• Hepatopulmonary syndrome
• Portopulmonary syndrome
Vomiting of blood from bleeding esophageal varices is
the most common clinical manifestation
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Varices
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Liver Disorders
Ascites
Accumulation of fluid in the peritoneal cavity
Most common cause is cirrhosis
Development associated with:
• Portal hypertension
• Decreased synthesis of albumin by the liver
• Splanchnic vasodilation
• Renal sodium and water retention
25% mortality in 1 year if associated with cirrhosis
Causes abdominal distention and increased abdominal girth and
weight gain
Paracentesis
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Liver Disorders (Cont.)
Hepatic encephalopathy
Neurological syndrome of impaired behavioural,
cognitive, and motor function
Develops rapidly during fulminant hepatitis or slowly
during course of liver disease
Cells in the nervous system are vulnerable to
neurotoxins absorbed from the GI tract that, because
of liver dysfunction, circulate to the brain
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Liver Disorders (Cont.)
Early symptoms
• Subtle changes in personality, memory loss, irritability,
disinhibition, lethargy, and sleep disturbances
Later symptoms
• Confusion, disorientation to time and space, flapping tremor
of the hands (asterixis), slow speech, bradykinesia, stupor,
convulsions, and coma
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Liver Disorders (Cont.)
Jaundice (icterus)
Caused by hyperbilirubinemia
Obstructive jaundice
• Extrahepatic
• Intrahepatic
Hemolytic jaundice
• Prehepatic jaundice
• Excessive hemolysis of red blood cells
Characterized by dark urine, yellow discolouration of
sclera and skin, and light-coloured stools
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Jaundice
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Hepatorenal Syndrome
Functional kidney failure that develops as a
complication of advanced liver disease
Type 1
Type 2
Manifestations include oliguria and
complications of advanced liver disease
May be acute or gradual onset
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Acute Liver Failure
Rare clinical syndrome resulting in severe
impairment or necrosis of liver cells without pre-
existing liver disease or cirrhosis
Acetaminophen overdose is common cause
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Cirrhosis
Irreversible inflammatory, fibrotic liver disease
Biliary channels become obstructed and cause
portal hypertension
Severity and rate of progression depend on the
cause
Many causes
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Cirrhosis (Cont.)
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Alcoholic Liver Disease
Related to toxic effects of alcohol and coexisting
liver disease
Alcoholic fatty liver
Alcoholic steatohepatitis
Alcoholic cirrhosis
Anorexia, nausea, jaundice, and edema develop
with advanced fatty infiltration or the onset of
alcoholic steatohepatitis
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Nonalcoholic Fatty Liver Disease
and Nonalcoholic Steatohepatitis
Nonalcoholic fatty liver disease (NAFLD)
Infiltration of hepatocytes with fat occurring in the
absence of alcohol intake
May progress to nonalcoholic steatohepatitis (NASH),
which may progress to cirrhosis and end-stage liver
disease
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Biliary Cirrhosis
Damage and inflammation leading to cirrhosis
begin in bile canaliculi and bile ducts
Primary
Secondary
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Viral Hepatitis
Systemic viral disease that primarily affects the
liver
Five types (A, B, C, D, and E)
Can cause acute, icteric illness
Spectrum of manifestations ranges from
absence of symptoms to fulminating hepatitis,
with rapid onset of liver failure and coma
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Viral Hepatitis (Cont.)
Phases
Incubation
Prodromal
Icteric
Recovery
Chronic active hepatitis
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Disorders of the Gallbladder
Obstruction or inflammation (cholecystitis) most
common cause of gallbladder problems
Cholelithiasis—gallstone formation
Risks
• Obesity
• Middle age
• Female
• Oral contraceptive use
• Rapid weight loss
• First Nations ancestry
• Genetic predisposition
• Gallbladder, pancreas, or ileal disease
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Disorders of the Gallbladder (Cont.)
Gallstones
Formed from impaired metabolism of cholesterol, bilirubin,
and bile acids
Type depends on chemical composition
• Cholesterol
Formed from bile that is supersaturated with cholesterol
produced by the liver
• Pigmented brown
Formed from calcium bilirubinate and fatty acid soaps that bind
with calcium
• Black
Composed of calcium bilirubinate with mucin glycoproteins
Associated with chronic liver disease and hemolytic disease
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Disorders of the Gallbladder (Cont.)
Often asymptomatic or vague
Epigastric and right hypochondrium pain
Intolerance to fatty foods
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Gallstones
From Kissane, J.M. (Ed.). (1990). Anderson’s pathology (9th ed.). St Louis, MO: Mosby.
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Disorders of the Gallbladder
Cholecystitis
Almost always caused by a gallstone lodged in the
cystic duct
Pain is similar to that caused by gallstones
Fever, leukocytosis, rebound tenderness, and
abdominal muscle guarding are common findings
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2. Which is TRUE regarding cholelithiasis?
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Disorders of the Pancreas
Pancreatitis
Inflammation of the pancreas
Develops because of obstruction to the outflow of
pancreatic digestive enzymes caused by bile and
pancreatic duct obstruction
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Disorders of the Pancreas (Cont.)
Acute pancreatitis Chronic pancreatitis
Usually mild and resolves Process of progressive
spontaneously fibrotic destruction of the
May result from direct pancreas
cellular injury from alcohol, Related to chronic alcohol
medications, or viral abuse
infection Continuous or intermittent
Cardinal manifestation is abdominal pain and weight
constant epigastric or loss are common
midabdominal pain Risk factor for pancreatic
cancer
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Cancer of the
Gastro-Intestinal Tract
Esophagus
Squamous cell carcinoma
Adenocarcinoma
Risk factors include chronic alcohol use combined
with smoking or chewing tobacco, hot and irritant
(alcohol) drinks, food containing nitrosamines, and
achalasia
Frequent symptoms are chest pain and dysphagia
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Cancer of the Gastro-
Intestinal Tract (Cont.)
Stomach
Associated with atrophic gastritis and Helicobacter
pylori
Sporadic and associated with consumption of heavily
salted and preserved foods, low intake of fruits and
vegetables, and use of tobacco and alcohol
Vague symptoms early such as loss of appetite,
malaise, and indigestion
Later symptoms of unexplained weight loss, upper
abdominal pain, vomiting, change in bowel habits,
and anemia
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Cancer of the Gastro-
Intestinal Tract (Cont.)
Colon and rectum
Most are sporadic or associated with a family history
of colorectal cancer
Caused by multiple gene alterations and
environmental interactions
• Familial adenomatous polyposis
• Hereditary nonpolyposis
Colorectal polyps
Neoplastic polyps
Symptoms depend on the location, size, and shape of
the lesion and are silent in the early stages
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Colon Cancer
Signs and symptoms
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Cancer of the Accessory
Organs of Digestion
Liver
Usually caused by metastatic spread from a primary
site elsewhere in the body
Hepatocellular carcinoma
• Usually asymptomatic
Cholangiocellular carcinoma
• Commonly presents insidiously as pain, loss of appetite,
weight loss, and gradual onset of jaundice
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Cancer of the Accessory
Organs of Digestion (Cont.)
Gallbladder
Usually caused by metastasis
Chronic inflammation may trigger dysplasia and
progress to metaplasia
Early stages usually asymptomatic
Usually caught in late stages
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Cancer of the Accessory
Organs of Digestion (Cont.)
Pancreas
Ductal adenocarcinomas
• Pancreatic tumours from metaplastic exocrine cells in the
ducts
Chronic pancreatitis and inflammatory cytokines
support tumour growth
When symptoms occur, there usually has been a
malignant transformation
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Case Study
A 31-year-old woman visits a gastroenterologist’s
office with complaints of diarrhea. She reports that she
has at least four loose stools per day. An extensive
history is obtained, and the woman is able to provide a
stool sample that day. The stool is bloody with mucus.
Although the sample will be sent to a laboratory for
analysis, the gastroenterologist suggests an
endoscopy and histological studies of biopsied tissue.
She discusses the possible diagnoses, among them
Crohn’s disease and ulcerative colitis.
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Case Study:
Discussion Questions
3. What type of diarrhea is caused by an
inflammatory disorder of the intestine?
A. Secretory
B. Small-volume
C. Motility
D. Large-volume
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Case Study:
Discussion Questions (Cont.)
4. Patients who suffer from ulcerative colitis and
Crohn’s disease have abdominal pain, which is
the result of distension and inflammation. What
type of pain does this describe?
A. Visceral
B. Referred
C. Parietal
D. Somatic
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Chapter 37
Alterations of Digestive
Function in Children
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Cleft Lip and Cleft Palate
Syndromic
Occurs as part of chromosomal, mendelian, or
teratogenic syndromes
Nonsyndromic
Cleft palate occurring alone
Embryonic developmental anomalies that vary in
severity
May be caused by genetic or environmental
influences
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Cleft Lip and Cleft Palate (Cont.)
Cleft lip
Caused by the incomplete fusion of the nasomedial or
intermaxillary process during the fourth week of
embryonic development
Commonly occurs under one nostril, but the defect
can be bilateral and symmetrical or asymmetrical
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Cleft Lip and Cleft Palate (Cont.)
Cleft palate
Commonly associated with cleft lip but can occur
without it
May affect only the uvula and soft palate or may
extend forward to the nostril and involve the hard
palate and the maxillary alveolar ridge
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Cleft Lip and Cleft Palate (Cont.)
Clinical manifestations
Immediately recognizable disruptions of normal facial
structure
Feeding difficulties
Evaluation and treatment
Ultrasound and postnatal imaging
Surgical correction
Speech training
Prosthodontist and orthodontist follow-up
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Cleft Lip and Cleft Palate (Cont.)
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Esophageal Atresia
Esophagus ends in a blind pouch
Usually accompanied by a tracheoesophageal fistula
Associated with many anomalies and syndromes
Environmental and genetic risk factors
Antenatal diagnosis increases with finding of
polyhydramnios, confirmed by inability to pass gastric
tube after birth
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Esophageal Atresia and
Tracheoesophageal Fistula
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Infantile Hypertrophic
Pyloric Stenosis
Acquired narrowing and distal obstruction of the
pylorus
Unclear etiology—likely genetic and
environmental factors
Forceful, nonbilious vomiting starting 2 to 8
weeks after birth
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Infantile Hypertrophic
Pyloric Stenosis (Cont.)
Vomiting causes weight loss, electrolyte
imbalances, and dehydration
Infant irritable as a result of hunger and
esophageal discomfort
Evaluation and treatment
Hypertrophic pylorus is palpable in the RUQ
Standard treatment is pyloromyotomy
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Obstructions of the Duodenum,
Jejunum, and Ileum
Duodenal obstruction
Upper abdominal distension, visible peristaltic waves,
decrease in meconium stools, weight loss, persistent
vomiting, and dehydration
Obstruction may be partial or complete
“Double bubble” sign
Jejunal and ilial obstruction
Atresia, stenosis, megacolon, intussusception, Meckel
diverticulum, intestinal duplication, or strangulated
hernia
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Malrotation
Small intestine lacks normal posterior
attachment
Intestine twists upon itself (volvulus)
Most cases develop during neonatal period
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Malrotation (Cont.)
Clinical manifestations
Intermittent or persistent bile-stained vomiting
Dehydration and electrolyte imbalances
Fever, pain, scanty stools, diarrhea, and bloody stools
Evaluation and treatment
Clinical manifestations and x-rays
Laparoscopic or open surgery to reduce volvulus
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Meckel Diverticulum
Outpocketing of all layers of the small intestinal
wall (usually in the ileum)
“Rule of 2s”
Most asymptomatic
Most common symptom is painless rectal
bleeding
Intestinal obstruction, intussusception, and
volvulus can occur
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Meconium Syndromes
Meconium is a substance that fills the intestine
before birth
Meconium ileus (MI)
Meconium-caused intestinal obstruction in a newborn
Two types
• Simple
• Complex
Complex MI is a surgical emergency
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Meconium Syndromes (Cont.)
Meconium plug syndrome
Transient
Characterized by delayed passage of meconium and
intestinal dilatation
Meconium disease
Associated with severe prematurity and low birth
weight
Bowel obstruction from highly sticky meconium and
poor intestinal motility
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Meconium Syndromes (Cont.)
Distal intestinal obstruction syndrome
Characterized by complete or incomplete intestinal
obstruction of viscid fecal accumulation in the terminal
ileum and proximal colon
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Meconium Syndromes (Cont.)
Pathophysiology
Terminal ileum plugged with thick, viscous meconium
resulting from the formation of an insoluble, calcium-
glycoprotein compound in abnormal mucus
Peristalsis fails to propel this viscous material through
the ileum, and it becomes impacted
Manifested by abdominal distension shortly after
birth, followed by vomiting
Diagnosed by radiographical examination
Usually relieved by intestinal lavage and laxatives
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Idiopathic Intestinal
Pseudo-obstruction
Disorder of impaired intestinal motility
Pseudo-obstruction is caused by nerve or
peristaltic muscle dysfunction
Manifested by abdominal swelling or bloating,
crampy abdominal pain, nausea, vomiting,
constipation, or diarrhea
Treated with intestinal decompression,
nutritional support, symptom management
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Hirschsprung’s Disease
Also referred to as aganglionic megacolon
Caused by the failure of the parasympathetic
nervous system to form intramural ganglion cells
in the enteric nerve plexuses
Abnormally innervated colon impairs fecal
movements
Causes colon distension
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Hirschsprung’s Disease (Cont.)
Clinical manifestations
Mild to severe constipation
Diarrhea
Enterocolitis, sepsis, death
Surgery is the definitive treatment
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Congenital Aganglionic
Megacolon
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Anorectal Malformations
Anorectal stenosis, imperforate anus, anorectal
atresia, and rectal atresia
40% of infants born with anorectal malformations
have other developmental anomalies
Most identified in routine physical examination
Treated with dilations for stenosis or surgery for
other malformations
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Anorectal Malformations (Cont.)
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Gastroesophageal Reflux (GER)
Related to dilation of the esophagus and reflux
of stomach contents
In newborns reflux is normal because
neuromuscular control of the gastroesophageal
sphincter is not fully developed
Contributing cause of sudden unexpected infant
death (SUID)
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Gastroesophageal
Reflux (GER) (Cont.)
Clinical manifestations
Excessive vomiting, food refusal, unexplained crying,
choking, gagging
Complications include esophagitis, hemorrhage,
stricture, Barrett esophagus
Evaluation and treatment
Often diagnosed by clinical manifestations
Normal physiological GER resolves without treatment
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Intussusception
Telescoping of a proximal segment of intestine
into a distal segment, causing an obstruction
Most common scenario is the ileum telescopes into
the cecum and part of the ascending colon by
collapsing through the ileocecal valve
Causes ischemia and necrosis if not treated
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Intussusception (Cont.)
Clinical manifestations
Abdominal pain, irritability, vomiting, and “currant jelly”
stools
Evaluation and treatment
Clinical manifestations and ultrasonography
Reduction with enema
Surgical reduction
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Intussusception (Cont.)
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Cystic Fibrosis
Autosomal recessive disease that involves many
organs
In the digestive tract it causes a blockage of
pancreatic enzymes
Triad
Obstruction
Infection
Inflammation
Maldigestion of proteins, carbohydrates, fats, and
fat-soluble vitamins occurs
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Celiac Disease
Gluten is the protein component in cereal grains
(wheat, rye, barley, malt)
Appears to be caused by dietary, genetic, and
immunological factors
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Celiac Disease (Cont.)
Onset of manifestations depends on the age of
the infant when gluten-containing substances
are added to the diet
Usually by 18 months
Severity of symptoms varies tremendously
Celiac crisis
Diagnosis confirmed with serological
autoantibody measurement
Gluten-free diet for life
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Celiac Disease (Cont.)
Treatment is a gluten-restrictive diet, and vitamin
D, iron, and folic acid supplements
Celiac crisis results in severe diarrhea,
dehydration, malabsorption, and protein loss
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Celiac Disease (Cont.)
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Kwashiorkor and Marasmus
Types of malnutrition associated with long-term
starvation
Known collectively as protein-energy
malnutrition (PEM)
Kwashiorkor is a severe protein deficiency
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Kwashiorkor and Marasmus (Cont.)
Marasmus is a deficiency of all nutrients
Stunted physical and mental development of
children
Liver function
In kwashiorkor, the lack of proteins causes the liver to
swell because of the inability to produce lipoproteins.
In marasmus, liver function continues, but the overall
caloric intake is too low to support cellular protein
synthesis.
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Kwashiorkor and Marasmus (Cont.)
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Failure to Thrive (FTT)
Also called growth faltering
Characterized by inadequate physical development
of an infant or child
Deceleration in weight gain
Low weight/height ratio or BMI ratio
Low weight/height/head circumference ratio
Multifactorial
Biological
Psychosocial
Environmental
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Necrotizing Enterocolitis
Ischemic, inflammatory condition that causes
bowel necrosis and perforation
Most common severe neonatal gastro-intestinal
emergency
Primarily affects smallest and most premature
infants
Etiology unclear
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Necrotizing Enterocolitis (Cont.)
Contributing factors
Infections
Abnormal bacterial colonization
Intestinal ischemia
Immature immunity
Exaggerated inflammatory responses
Immature intestinal motility and barrier function
Perinatal stress
Effects of medications and feeding practices
Genetic predisposition
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Necrotizing Enterocolitis (Cont.)
Clinical manifestations
Mild abdominal distension to bowel perforation
Bloody stools and septicemia
Evaluation and treatment
Clinical manifestations, laboratory results, and plain
films of abdomen
Cessation of feeding, gastric suction, antibiotics, and
surgery
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Diarrhea
Prolonged diarrhea in children is very dangerous
Leading cause of death in young children
Children have lower fluid reserves than adults
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Diarrhea (Cont.)
Infant diarrhea
Infectious diarrhea
Acute infectious diarrhea
Rotavirus
Chronic diarrhea
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Primary Lactose Intolerance
Inability to digest milk sugar
Caused by the inadequate production of lactase,
the enzyme that catabolizes lactose
Lactose malabsorption causes
Osmotic diarrhea
Abdominal pain
Bloating
Flatulence
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Neonatal Jaundice
Yellow pigmentation of the skin caused by an
increased level of bilirubin in the bloodstream
Usually becomes clinically apparent when the
serum bilirubin concentration is >34 mcmol/L
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Neonatal Jaundice (Cont.)
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1. Which is TRUE regarding physiological
jaundice of the newborn?
A. Generally chronic
B. Caused by increased red blood cell breakdown
C. Occurs during the first week of life in full-term
infants
D. Caused by indirect bilirubin reading of >200
mcmol/L
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Biliary Atresia
Congenital malformation characterized by the
absence or obstruction of the intrahepatic or
extrahepatic bile ducts
Plugging, inflammation, and fibrosis of the bile
canaliculi, and cholestasis
Jaundice is the primary clinical manifestation
Liver transplant long-term therapy
80% die before 3 years of age if untreated
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Hepatitis
Hepatitis A
30 to 50% of hepatitis A infections occur in children
Hepatitis B
90% of newborns are infected by their mothers
Hepatitis D infection depends on active infection of HBV
Hepatitis C
Associated primarily with blood transfusions
Chronic hepatitis
May develop because the infant’s immune system is
immature
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Cirrhosis
Chronic liver diseases in children can progress
to cirrhosis, but it is infrequent.
Complications for cirrhosis in children are the
same as adults.
Children may also experience
Growth failure
Nutritional deficits
Developmental delay
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Portal Hypertension
Extrahepatic portal hypertension
Intrahepatic portal hypertension
Clinical manifestations
Splenomegaly
Upper GI bleeding
Ascites
Hepatic encephalopathy
Evaluation and treatment
Examination, laboratory tests, imaging, and biopsy
Treatment is same as for adults
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Metabolic Disorders
Wilson’s disease
Autosomal recessive defect of copper metabolism
Causes toxic levels of copper to accumulate in the
liver, brain, kidneys, and corneas
Galactosemia
Autosomal recessive trait of deficient galactose-1-
phosphate uridyl transferase
Causes toxic levels of galactose in body tissues, liver,
and brain
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Metabolic Disorders (Cont.)
Fructosemia
Autosomal recessive trait of deficient fructose-1-
phosphate aldolase
Causes toxic levels of fructose to accumulate in body
tissues
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2. What is an inherited disease associated with
pancreatic enzyme deficiency?
A. Cystic fibrosis
B. Celiac disease
C. Kwashiorkor
D. Biliary atresia
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