Anatomy and

Physiology

Elizabeth Co, Anatomy and Physiology, 1st Edition. © 2023 Cengage. All Rights Reserved. May not be scanned, copied or duplicated, or
posted to a publicly accessible website, in whole or in part. 1
Overview of the Digestive System

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 Functions of the Digestive System

1. Ingestion—intake of food and drink

2. Digestion—break down of ingested material
3. Secretion—production and release of fluids and enzymes associated with
digestive activity
4. Mixing and propulsion—mixing with secretions and moving through digestive
system
5. Absorption—absorbing nutrients in ingested material into the blood
6. Excretion—elimination of wastes via fecal material

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 Organs of the Digestive System (Figure
23.1)
• Digestive (GI) tract
• Series of organs through which ingested material
moves
• Breaks down and absorbs nutrients
• Accessory digestive organs
• Not part of GI tract
• Have function associated with digestive activity
• Liver, pancreas, gallbladder, salivary glands

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 Connections to Other Body Systems (Table
23.1)
• Digestive system works cooperatively
with other systems
• Cardiovascular system absorbs
nutrients and circulates them
following digestion
• Specific endocrine cells secrete
hormones that regulate digestive
activity
• Skin is involved in production of
vitamin D

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 Gastrointestinal (GI) Tract (Figure 23.2A)

• Continuous tube divided into different

organs
• Sections of GI tract:
1. Mouth
2. Pharynx
3. Esophagus
4. Stomach
5. Small intestine
6. Large intestine (colon)
7. Anus
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 Accessory Organs (Figure 23.2B)

• Aid in the break down of ingested

material
• Accessory organs include:
1. Teeth
2. Tongue
3. Salivary glands
4. Pancreas
5. Liver
6. Gallbladder
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General Gross and Microscopic
Anatomy of the Gastrointestinal
(GI) Tract
Section 23.2
Learning Objectives 23.2.1–23.2.9

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 Microscopic Structure of the GI Tract (Figure
23.3)
• Lumen = interior space of GI tract
• GI tract wall consists of four layers
• Mucosa—innermost layer; epithelial tissue,
lamina propria, muscularis mucosae
• Submucosa—connective tissue with blood
vessels, lymphatics, and nerves
• Muscularis—longitudinal and circular layers of
smooth muscle
• Stomach has additional oblique layer
• Serosa—outermost layer; thin layer of
connective tissue

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 Mucosa

• Non-keratinized stratified squamous epithelium lines mouth, pharynx, esophagus, and

anal canal
• Simple columnar epithelium lines stomach and intestines
• Epithelial tissue is supported by lamina propria
• Contains blood, lymphatic vessels, and mucosa-associated lymphoid tissue (MALT)
• Muscularis mucosa forms rugae in stomach and small intestine to increase surface area
• Goblet cells secrete mucus for lubrication
• Enteroendocrine cells secrete hormones in response of nutrients or pathogens

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 Submucosa

• Lies deep to the mucosal layer and connects the mucosa to muscularis layer
• Composed of dense connective tissue with blood and lymphatic vessels
• Contains submucosal glands that release digestive secretions
• Location of submucosal plexus
• Helps regulate digestive secretions and reacts to presence of food

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 Muscularis

• Most sections of the GI tract contain two layers in the muscularis

• Inner circular layer of muscularis
• Outer longitudinal layer of muscularis
• Stomach contains additional oblique layer of muscularis for a total of three
layers
• Contractions of muscularis propel food forward and mix and churn ingested
food
• Muscularis at ends of tract is made of skeletal muscle
• Gives voluntary control of swallowing and defecation
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 Serosa

• Superficial wall layer furthest from the lumen

• Composed of connective tissue
• Helps anchor arteries, veins, and nerves to GI tract wall
• Referred to as serosa only within abdominal cavity
• Referred to as adventitia for the mouth, pharynx, and esophagus

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 Mechanical versus Chemical Digestion

• Mechanical digestion—uses force generated by muscles to digest nutrients

• Begins with chewing (mastication) in the mouth
• Muscularis layer is involved in mechanical digestion
• Chemical digestion—utilizes enzymes and other secretions to break down
ingested material
• Other secretions come from salivary glands, stomach, liver, pancreas, and
gallbladder

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 Peristalsis (Figure 23.4)

• Sequential, alternating waves of contraction

and relaxation by layers of muscularis
• Propels food forward within tract
• Helps mix food with digestive juices

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 Nerve Supply

• Central nervous system initiates activities such as salivation

• Also responsible for sight, taste, smell, and feel of ingested materials
• Enteric nervous system innervates GI tract
• Myenteric plexus controls movements of muscularis
• Submucosal plexus controls digestive secretions
• Autonomic nervous system
• Sympathetic—decreases GI motility and secretion
• Parasympathetic—increases GI motility and secretion

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 Blood Supply

• Provides nutrients and removes wastes from GI tract and accessory organs
• Absorbs protein and carbohydrate nutrients
• Lipids absorbed by unique lymphatic capillaries called lacteals
• Hepatic portal system
• Veins that drain intestine carry absorbed nutrients to liver first
• Liver processes and detoxifies incoming nutrients before they enter general
circulation

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 The Peritoneum (Figure 23.5)

• Serous membrane that holds abdominal organs in

position
• Composed of parietal and visceral layers
• Peritoneal cavity contains peritoneal fluid to
reduce friction between the layers
• Intraperitoneal = organs within peritoneum
• Retroperitoneal = organs behind peritoneum
• Four major folds = lesser omentum, greater
omentum, transverse mesocolon, mesentery
proper

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 The Mesenteries (Figure 23.6A)

• Help hold abdominal organs in place

• Contains blood vessels, nerves, and lymphatics for
abdominal organs
• Lesser omentum = connects stomach to liver
• Greater omentum = hangs over abdominal organs
• Mesentery (proper) = anchors small intestine to
posterior abdominal wall
• Transverse mesocolon = anchors transverse colon to
posterior abdominal wall
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 The Mouth, Pharynx, and
Esophagus
Section 23.3
Learning Objectives 23.3.1–23.3.34

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 Mouth (Figure 23.7)

• Also known as oral cavity

• Framed by cheeks, tongue, and palate
• Entrance to GI tract bordered by lips (labia)
• Muscles involved in mastication (chewing) begin
mechanical digestion
• Hard palate made of bone provides hard surface to
push food during swallowing
• Soft palate made of skeletal muscle elevates during
swallowing
• Uvula directs ingested materials inferiorly

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 Tongue (Figure 23.8)

• Made of skeletal muscle

• Functions in ingestion, sensation,
swallowing, and speech
• Papillae contain taste buds
• Lingual frenulum anchors tongue

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 Salivary Glands (Figure 23.9)

• Secrete saliva into oral cavity

• Watery secretion that contains enzymes
• Three pairs of salivary glands:
1. Parotid glands
2. Submandibular glands
3. Sublingual glands

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 Saliva

• Begins chemical digestion and moistens food

• Secretion regulated by autonomic nervous system (ANS)
• Salivary amylase breaks down carbohydrates
• Infants secrete salivary lipase to break down lipids in breastmilk
• Bicarbonate and phosphate ions buffer acidic foods
• IgA and lysozyme prevent microbial infection in mouth
• Histostatin helps speed wound healing

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 Teeth (Figure 23.10)

• Organs similar to bones, used to tear, grind,

and mechanically break down food
• Deciduous teeth are replaced by permanent
teeth
• Eight incisors—used for biting and
cutting
• Four cuspids (canines)—used for
piercing
• Eight premolars—used for mashing and
grinding
• Twelve molars—used for crushing

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 Anatomy of a Tooth (Figure 23.11)

• Socket lined by gingivae (gums)

• Periodontal ligaments anchor teeth in sockets
• Crown above gumline; root embedded within
socket
• Pulp cavity contains nerves and blood vessels
that run through root canal to bone
• Bone-like dentin covers pulp cavity
• In crown, dentin is covered by enamel

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 Pharynx (Figure 23.12)

• Funnel-like passageway for food and air

• Sectioned into nasopharynx, oropharynx, and
laryngopharynx
• Oropharynx is lined by stratified squamous
epithelium

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 Swallowing (Figure 23.13)

• Voluntary phase—tongue moves up and back; pushes

bolus into oropharynx; can be consciously controlled
• Pharyngeal phase—uvula and soft palate reflexively
elevate to close nasopharynx
• Esophageal phase—bolus enters esophagus and
peristalsis begins
• Pharyngeal and esophageal phases are involuntarily
controlled

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 Esophagus (Figure 23.14)

• Flat, muscular tube that connects pharynx to

stomach
• Upper esophageal sphincter relaxes to allow
movement into esophagus
• Peristalsis moves bolus through esophagus
• Lower esophageal sphincter relaxes to allow
entry into stomach
• Fails when gastroesophageal reflux disease
(GERD) occurs

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 Histology of the Esophagus

• Mucosa contains non-keratinized stratified squamous epithelium

• Protects against friction from food moving through esophagus
• Muscularis varies in composition throughout the esophagus
• Upper third: skeletal muscle
• Middle third: combination of skeletal and smooth muscle
• Lower third: smooth muscle
• Outer adventitia due to esophagus located outside of abdominal cavity

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 Stomach (1 of 3) (Figure 23.15)

• Hollow, muscular organ that continues chemical

and mechanical digestion
• Very little absorption occurs in stomach
• Regions of stomach:
• Cardia, fundus, body, antrum, pylorus
• Pylorus divided into antrum and canal
• Pyloric sphincter regulates movement into
small intestine

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 Stomach (2 of 3) (Figure 23.16)

• Muscularis contains additional oblique layer

• Mixes food with gastric juice to become
chyme
• Cardia = region where food enters stomach
• Fundus = increases capacity of stomach
• Pylorus = connects stomach to duodenum
• Gastric rugae = allows stomach to expand when
full

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 Stomach (3 of 3) (Figure 23.17)

• Muscularis contains additional oblique

layer
• Mucosa contains gastric pits
• Gastric glands secrete gastric juice
• Parietal cells secrete hydrochloric acid
and intrinsic factor
• Chief cells secrete pepsinogen
• Mucous neck cells secrete mucus
• Enteroendocrine cells—secrete
hormones

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 Phases of Gastric Secretion (Figure 23.18)

• Cephalic phase—begins when body is alerted by the

smell, taste, sight, or thought of food
• Gastric phase—activated by nervous and endocrine
system when food enters stomach
• Results in increased gastric secretion and motility
• Intestinal phase
• Excitatory—duodenum increases gastric secretion
• Inhibitory enterogastric reflex inhibits gastric
secretion and movement when small intestine is full

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 Gastric Mucosa (Figure 23.19)

• Protects stomach from self-digestion due to

highly acidic conditions
• Mucous, bicarbonate, and stem cells rapidly
divide
• Helps regulate gastric emptying
• Acidic chyme slows gastric emptying to
prevent duodenum becoming overwhelmed
• Intrinsic factor—secretion that allows for vitamin
B12 absorption

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 Gastric Hormones

• Gastrin promotes GI tract motility and

gastric juice secretion
• Histamine promotes HCl secretion
into stomach
• Serotonin causes contraction of
stomach muscles for churning
• Somatostatin decreases GI tract
motility and secretion
• Ghrelin influences feelings of hunger
and satiety
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 Protein Digestion (Figure 23.2)

• Enzymes cannot easily access and break bonds of

highly folded proteins
• HCl in gastric juice denatures proteins making
peptide bonds accessible to enzymes
• Pepsin cuts proteins into shorter polypeptides
• Enzymes in small intestine break bonds to yield
individual amino acids

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 The Small Intestine (Figure 23.21)

• Chyme enters from stomach

• Site of most digestion and absorption of
nutrients
• Divided into three sections:
1. Duodenum—receives secretions from
biliary apparatus
2. Jejunum
3. Ileum
• Ileocecal sphincter regulates movement into
large intestine
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 The Duodenum

• Site of majority of chemical digestion

• Receives secretions from gallbladder, pancreas, and liver
• Liver produces bile that drains from hepatic ducts into common hepatic duct
• Common hepatic duct unites with cystic duct of gallbladder to form common
bile duct
• Common bile duct unites pancreatic duct to form hepatopancreatic ampulla
• Empties bile and pancreatic juice into duodenum
• Sphincter of Oddi regulates release into duodenum

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 The Biliary Apparatus (Figure 23.22)

• Liver and gallbladder contribute bile to

duodenum
• Head of pancreas is in curve of duodenum
• Secretions from all three accessory organs
empty into duodenum

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 Jejunum and Ileum (Figure 23.23)

• Jejunum is the middle segment of small

intestine
• No clear border separates it from ileum
• Ileum is longest, terminal segment of small
intestine
• Thicker and more vascular than other
segments
• Joins the cecum at the ileocecal junction /
sphincter

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 Histology of the Small Intestine

• Circular folds, villi, and microvilli increase surface area for absorption of nutrients
• Circular folds visible at gross level
• Villi (microscopic) contain capillaries and lacteals for absorption of nutrients
• Microvilli (microscopic) make up brush border on epithelial cell
• Contains enzymes for digestion
• Intestinal glands produce intestinal juice that help neutralize acidic chyme
• Duodenal glands secrete alkaline mucus to protect mucosa
• Intestinal MALT provides immune protection
• Aggregations of MALT seen in ileum

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Histology of the Small Intestine (Figure
23.24)

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 Mechanical Digestion in the Small Intestine
(Figure 23.25)
• Two motility patterns of small intestine:
• Peristalsis—pushes contents forward
• Segmentation—mixes contents locally
• Does not propel them forward
• Gastroileal reflex—increased stomach activity
leads to increased contraction of ileum
• Pushes intestinal contents forward into
cecum to allow further gastric emptying

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 Large Intestine (1 of 3) (Figure 23.26)

• Completes absorption of nutrients and water, forms fecal

material, and helps synthesize some vitamins
• Contains bacteria that aid in function
• Frames the small intestine within abdomen
• Regions of the large intestine:
• Cecum, ascending colon, transverse colon, descending
colon, sigmoid colon, rectum, and anus
• Appendix is attached to cecum

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 Large Intestine (2 of 3) (Figure 23.27)

• Flexures are bends in the large intestine

• Left colic and right splenic flexures
• Rectum holds fecal material until eliminated
• Internal and external anal sphincters
regulate release of feces
• Internal anal sphincter is smooth muscle;
external anal sphincter is skeletal muscle

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 Large Intestine (3 of 3) (Figure 23.29)

• Teniae coli extend the length of large intestine

• Contractions form haustra
• Motility in large intestine
• Haustral contractions—aid in water absorption
• Mass movement—forces contents toward rectum
•Gastrocolic reflex—gastric activity increases
colon activity
• Valsalva’s maneuver—increased abdominal pressure
aids in fecal elimination

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 Wall of the Large Intestine (Figure 23.28)

• Simple columnar epithelium primarily line the

mucosa
• Absorbs water, salts, and vitamins
• Mucosa contains deep intestinal glands
• Numerous goblet cells produce mucous to
reduce friction
• Each person contains unique bacterial
composition within large intestine

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Accessory Organs in Digestion:
The Liver, Pancreas, and
Gallbladder
Section 23.4
Learning Objectives 23.4.1–23.4.12

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 The Accessory Organs of Digestion (Figure
23.30)
• Accessory organs of digestion include the
liver, gallbladder, and pancreas
• Liver produces bile and filters blood
from intestines
• Gallbladder stores and concentrates
bile
• Pancreas produces pancreatic juice
that contains digestive enzymes

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 Functions of Liver

• Detoxifies nutrients brought to liver from absorbing digestive organs

• Processes drugs and toxins within body
• Stores iron
• Produces bile
• Produces plasma proteins
• Breaks down old red blood cells, decomposes hemoglobin, and excretes the
bilirubin waste in the bile

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 Liver (Figure 23.31)

• Located in right upper quadrant of abdomen

• 2nd largest organ of adult human body
• Divided into right, left, caudate, and quadrate
lobes
• Anchored to abdominal wall by ligamentum
teres and falciform, coronary, and lateral
ligaments
• Porta hepatis = site of hepatic artery, hepatic
portal vein, and common bile duct

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 Histology of the Liver (Figure 23.32)

• Liver is organized into lobules

• Microscopic lobules receive blood from hepatic portal
vein and hepatic artery
• Blood flows through sinusoids to the central veins
• Hepatic artery delivers oxygen and nutrients to
hepatocytes
• Hepatic portal vein delivers blood from intestinal
absorption for detoxification
• Central veins form hepatic veins and return blood to
inferior vena cava

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 Fat Emulsification (Figure 23.33)

• Hepatocytes produce bile in liver, which is stored in

the gallbladder
• Bile emulsifies large lipid globules
• Separates them into smaller globules
• Makes them more accessible to digestive
enzymes
• Bile canaliculi drain bile from liver lobules into bile
ducts
• Bile ducts and branches of hepatic artery and
hepatic portal vein form portal triads

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 Gallbladder (Figure 23.34)

• Located on posterior surface of liver

• Stores and concentrates bile
• Releases bile when necessary via cystic duct

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 Pancreas (Figure 23.35)

• Retroperitoneal organ at posterior of

abdomen
• Both endocrine and exocrine gland
• Head is nestled into
C-shaped duodenum
• Pancreatic acini secrete digestive enzymes
• Released via pancreatic and accessory
ducts

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 Biliary System

• Vessels that carry secretions of pancreas and bile from liver and gallbladder
• Right and left hepatic ducts of liver carry bile
• Unite to form common hepatic duct
• Common hepatic duct merges with cystic duct to form common bile duct
• Common bile duct unites with pancreatic duct to form hepatopancreatic
ampulla
• Release of bile and digestion enzymes occurs at major duodenal papilla

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 Pancreatic Juice

• Pancreatic juice—composed of water, sodium bicarbonate, digestive enzymes

• Sodium bicarbonate buffers chyme
• Protein-digesting enzymes produced in inactive form to prevent self-
digestion
• Activated by acidity of chyme in duodenum
• Pancreatic secretion stimulated by entry of chyme into the duodenum
• Leads to secretin and cholecystokinin (CCK) release that increases
secretion of pancreatic juice

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 Chemical Digestion and
Absorption: A Closer Look
Section 23.5
Learning Objectives 23.5.1–23.5.11

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 Digestion and Absorption (Figure 23.36)

• Digestion begins in the mouth

• Continues as food moves through GI tract
• Most absorption (~90%) occurs in the small intestine
• Indigestible food may be eliminated as feces or
metabolized by bacteria within GI tract
• Provides nutrients for both bacteria and human
body

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 Digestive Enzymes (Table 23.2)

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 Carbohydrate Digestion (Figure 23.37)

• Carbohydrates must be digested into monosaccharides for

absorption
• Common monosaccharides: Glucose, fructose, or
galactose
• Enzymes involved in carbohydrate digestion
• Amylases in saliva and pancreatic juice help digest
starches
 Cannot digest cellulose (fiber)
• Brush border enzymes in wall of small intestine
 Alpha-dextrinase, lactase, maltase, and sucrase

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 Protein Digestion (Figure 23.38)

• Begins with acid in stomach

• Most enzymes are produced in an
inactive state to prevent self-digestion
• Pepsin—produced by stomach
• Pancreatic enzymes:
• Trypsin, carboxypeptidase,
chymotrypsin, elastase
• Brush border enzymes

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 Lipid Digestion (Figure 23.39)

• Bile aids in lipid digestion by emulsifying lipids

• Breaks them up to allow faster digestion
• Enzymes involved in lipid digestion:
• Lingual lipase begins process in mouth
• Gastric lipase continues in stomach
• Pancreatic lipase accomplishes most lipid
digestion
• Breaks triglyceride into monoglyceride and two
fatty acids
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posted to a publicly accessible website, in whole or in part. 64
 Nucleic Acid Digestion

• Pancreatic enzymes involved in nucleic acid digestion:

• Deoxyribonuclease—digests DNA
• Ribonuclease—digests RNA
• Brush border enzymes involved:
• Nucleosidases, phosphatases

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posted to a publicly accessible website, in whole or in part. 65
Absorbable Food Substances (Table 23.3)

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posted to a publicly accessible website, in whole or in part. 66
 Absorption (1 of 2)

• Digestion converts ingested materials into molecules small enough for

absorption
• Absorption occurs through
• Active transport, simple diffusion, facilitated diffusion, secondary active
transport, and endocytosis
• Monomers of carbohydrates, proteins, and nucleic acids are absorbed via blood
capillaries
• Monomers of lipids are absorbed through lacteals (lymphatic systems)

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posted to a publicly accessible website, in whole or in part. 67
 Absorption (2 of 2)

• Minerals and electrolytes are absorbed almost completely

• Calcium absorption is regulated by PTH
• Iron absorption is dependent on the body’s need for iron
• Fat-soluble vitamins A, D, E, and K are absorbed by lacteals along with lipids
• Water-soluble vitamins absorbed by blood
• Water absorption occurs primarily in small intestine and remaining occurs in
large intestine
• Lack of water reabsorption leads to diarrhea

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posted to a publicly accessible website, in whole or in part. 68
 Inputs and Outputs of Digestive System (Figure
23.40)
• Digestive system takes in water and nutrients
• Digestive system secretes saliva, bile, gastric juice,
and pancreatic juice to digest nutrients
• Most of these secretions are reabsorbed in small and
large intestines
• Very little is lost in fecal material

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posted to a publicly accessible website, in whole or in part. 69
 Carbohydrate Absorption

• Carbohydrates are absorbed as monosaccharides

• Absorbed into mucosal cells by secondary active transport with sodium at
apical membrane
• Facilitated diffusion allows monosaccharides to enter blood capillaries (at
basement membrane)
• Indigestible carbohydrates (e.g., cellulose) eliminated in feces

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posted to a publicly accessible website, in whole or in part. 70
 Protein Absorption

• Proteins absorbed as amino acids

• Dipeptides and tripeptides enter mucosal cells via secondary active
transport with sodium at apical surface
• Broken down into individual amino acids within the epithelial cells
• Amino acids enter capillaries via diffusion

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posted to a publicly accessible website, in whole or in part. 71
 Lipid Absorption (Figure 23.41)

• Dietary fats broken down to long-chain fatty acids,

monoglycerides, and glycerol
• Bile salts encase them in micelles for absorption
through mucosal epithelium
• Fatty acids and monoglycerides reform
triglycerides within epithelial cells
• Mixed with phospholipids and cholesterol to
form chylomicrons
• Chylomicrons absorbed via lacteals

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posted to a publicly accessible website, in whole or in part. 72
 Nucleic Acid Absorption

• Nucleic acids broken down into pentose sugars, nitrogenous bases, and
phosphate ions
• Absorbed by mucosal cells via active transport at apical surface
• Enter capillaries to be absorbed by blood

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posted to a publicly accessible website, in whole or in part. 73
 Mineral Absorption

• Electrolytes are primarily absorbed by active transport

• Iron is absorbed by mucosal cells and bound to ferritin for storage
• Only enter blood when iron levels are low
• Calcium absorption is dependent on blood levels of calcium
• PTH stimulates absorption of calcium and production of
Vitamin D

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posted to a publicly accessible website, in whole or in part. 74
 Vitamin Absorption

• Fat-soluble vitamins (A, D, E, and K) are absorbed with dietary lipids via lacteals
• Water-soluble vitamins (B and C) are absorbed via blood capillaries
• Intrinsic factor is secreted by the stomach and aids in the absorption of
vitamin B12

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posted to a publicly accessible website, in whole or in part. 75
 Water Absorption

• ~7L of water are reabsorbed daily by digestive system

• Water absorption and reabsorption occurs via osmosis
• As nutrients and other solutes are absorbed, osmotic gradient is established
• Water moves in the direction of greater solute concentration
• Most water reabsorption occurs in small intestine (90%)
• Remainder occurs in large intestine (10%)

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posted to a publicly accessible website, in whole or in part. 76
Absorption in the GI Tract (Table 23.4)

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posted to a publicly accessible website, in whole or in part. 77
 Summary

• By the end of this chapter, you should be able to:

• Discuss the organization of the components of the digestive system.
• Describe the gross anatomy of the GI tract and accessory organs.
• Discuss the functions of the GI tract.
• Discuss the functions of the accessory organs.
• Discuss mechanical and chemical digestion.
• Discuss the absorption of nutrients.

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posted to a publicly accessible website, in whole or in part. 78
Disorders of the Mouth

1
Learning Objectives

By the end of the session learners will be able to:

1. Review the anatomy and physiology of gastrointestinal
system (GIT)
2. Discuss the causes, pathophysiology and manifestation of the
following GIT disorders
3. Discuss the diagnostic, medical and surgical management of
the below mentioned disorders
4. Apply nursing process including assessment, planning,
implementation and evaluation of care provided to the clients
with GIT disorders
5. Develop a teaching plan for a client experiencing disorders of
the GIT

2
A & P of Gastrointestinal Tract

3
 Disorders of mouth and esophagus

• Stomatitis
• Oral cancer/tumor
• Salivary gland disorders
• Gastro esophageal reflux disorder
• Hiatal hernia
• Achalasia
• Diverticula
• Esophageal cancer/tumor

4
 Disorders of mouth and esophagus
Stomatitis

Inflammation of the mucous membrane of the mouth.

It may be due to local lesion in the mouth, infection,
nutritional deficiency, chemotherapy, immune
suppression or a feature of a systemic disease.
OR
Stomatitis is inflammation of the mucosal tissue of
the mouth (inner cheeks, tongue, lips, throat and
gums etc.).

5
Sign and symptoms

• swelling,
• pain,
• ulcerations,
• excessive salivation,
• halitosis, (bad breath)
• sore mouth
• In ability to chewing
• bleeding
• Bad smell

6
 Causes of stomatitis
• Infection:
• Viruses: measles, primary herpes simplex.
• Bacteria: streptococcus, diphtheria.
• Fungus: .
• Eruption stomatitis: associated with eruption of teeth.
• Traumatic: cheek biters.
• Local reactions: due to sensitivity to contact
substances from foods.
• Immunological impairment: in leukemias.
• Drugs and poisons
• Chemotherapy
• Radiation therapy
7
 Investigations

• Oral swab culture

• Physical examination

• Learning Objectives

8
 Types of Stomatitis:

There are two main types of stomatitis

• Herpes simplex Stomatitis/cold sore

• Aphthous Stomatitis

9
Cont….

•Herpes simplex Stomatitis

• Herpes simplex Stomatitis (cold sore/fever blister):
• It is an externally common viral infection that produces
characteristic blisters commonly called cold sore or fever
blister.
• It is caused by herpes simplex virus type I (HSV-1)
predisposing factors of upper respiratory infections,
excessive exposure to sunlight, food allergies, emotional
stress and onset of menstruation.
• The virus is harbored in a dormant (inactive) state by cells in
the sensory nerve ganglia.
• Reactivation of the virus can occur with emotional stress,
fever, exposure to cold or ultraviolet rays.

10
Cold Sore

11
Cont…

• The lesions appear more common on the mucous

membranous border junction of the lips in the form of small
vesicles, which then erupt and form painful shallow ulcers.
• Vesicle formation may be single or clustered.
• Painful vesicles and ulceration of mouth, lips or edge of
nose; may have prodromal itching or burning, fever, malaise,
lymphadenopathy may occur.
• Prodromal: relating to or denoting the period between the
appearance of initial symptoms and the full development of a
rash or fever.
• Lymphadenopathy: A disease affecting the lymph nodes

12
/\Pathophysiology of HSS

• Etiology: HSV I (less commonly HSV II)

qTransmission:
• via mucous membranes or open skin
• Kissing
• Fomites (e.g. shared towels, utensils)
• Incubation: 2-20 days after contact.
• Shedding: 48-60 hour duration (not longer than 96 hours)

13
Aphthous Stomatitis

• Aphthous Stomatitis (cancer sore) it is recurrent and chronic form of

infection secondary to systemic disease, trauma, stress or unknown
causes. The cause remains unknown, an autoimmune base is
suspected. Self-limited, they usually resolve within a few weeks, but
they may recur in the same or a different location.
• It produces well-circumscribed ulcers on the soft tissues of the mouth,
including lips, tongue, insides of the cheeks, pharynx and soft palate.
• Ulcers of the mouth and lips causing extreme pain, ulcers surrounded
by erythematous base.
• Painful small ulceration on oral mucosa heals in 1 to 3 weeks.

14
Risk Factors
•Aging
•Nutritional deficiency
•Poor oral hygiene
•Smoking
•Alcohol
•Specific chemotherapeutic agents
•Bone marrow transplantation
•Radiotherapy

15
16
Pathophysiology

• Characterized by damage to the epithelium of the

oropharyngeal cavity .
• Rapidly dividing basal cells of the oral mucosa are
among the body cells vulnerable to damage by
chemotherapy and radiation therapies.

17
Treatment

• pain relief,
• removal of causative factor,
• oral hygiene with saline, Gentian violet, glycerin
• Broad spectrum antibiotic in sever case
• Anti fungal drugs i.e. Nystatin, Daktarin
• soft bland diet
• IV infusion in sever case

18
Nursing diagnosis

• Pain related to lesion of mouth.

• Alteration in nutrition less than body requirement
related to ulceration in the mouth and chewing
problem.
• Alter sleep pattern related to pain secondary to
stomatitis.
• Difficulty in talking (dysphasia) related to blisters
and sores on the tongue.

19
Nursing Intervention

• Check for oral burning, pain, or change in tolerance to

temperature.
• Do oral examination noting evidence of lesions within the
mouth and tongue.
• Administer the respective medication.
• Give analgesic to relieve from pain.
• Advice soft food and avoid spicy food.
• Do oral hygiene with soothing solution.
• Administer topical medication e.g. nylstate and bonjela to
relieve from pain to enhance sleep.

20
 Oral cancer

Oral cancer is a subtype of head and neck

cancer, is any cancerous tissue growth
located in the oral cavity.

21
Signs and symptoms

• lesion, lump, or ulcer that do not resolve in 14 days

located:
• On the tongue, lip, or other mouth areas
• Usually small
• Most often pale colored, be dark or discolored
• Early sign may be a white patch (leukoplakia) or a
red patch (erythroplakia) on the soft tissues of the
mouth
• Usually painless initially
• May develop a burning sensation or pain when the
tumor is advanced

22
Cont…

• Additional symptoms that may be associated with

this disease:
• Tongue problems
• Swallowing difficulty
• Mouth sores
• Pain and paresthesia are late symptoms.
• Feeling of something caught in the throat
• Difficulty or pain with chewing or swallowing
• Swelling in jaw
• Voice changes
• Pain in ear
23
Oral Cancer

• Occurs most often in people over age 40

Symptoms
• Sore that does not heal
• Lump on lip or mouth
• White or red patch on gum, tongue, or buccal
mucosa
• Unusual bleeding, numbness, or pain

24
Squamous Cell Carcinoma (SCC)

25
 Risk factors

• Uncommon (5% of all cancers) but has high rate of morbidity,

mortality
• Highest among males over age 40
• Risk factors include
• smoking and
• using oral tobacco,
• drinking alcohol,
• marijuana use,
• occupational exposure to chemicals,
• viruses (human papilloma virus)
• History of leukoplakia
• Erythroplakia
26
Pathophysiology

a. Squamous cell carcinomas

b. Begin as painless oral ulceration or lesion with irregular, ill-
defined borders
c. Lesions start in mucosa and may advance to involve tongue,
oropharynx, mandible, maxilla
d. Non-healing lesions should be evaluated for malignancy
after one week of treatment

27
Investigation

a. Elimination of causative agents

b. Determination of malignancy with biopsy
c. Determine staging with CT scans and MRI

28
Treatment

• Treatment usually involves surgery or radiation or both

• Chemotherapy primarily used as an adjunctive procedure in
advanced cases
• Advanced lesions < 30% 5-year survival rate
• 9 - 25% of patients develop additional mouth or throat cancer

• Several drugs currently being used include:

• Paclitaxel (Taxol, Bristol)
• Methotrexate
• Bleomycin
• Cisplatin
• 5-Fluorouracil
29
Nursing Diagnosis

• Pain related to oral lesion or treatment

• Imbalanced nutrition less than body requirements, related to
inability to ingest adequate nutrients secondary to oral
condition.
• Risk for infection related to disease or treatment
• Alter sleep pattern related to pain secondary to stomatitis.
• Impaired verbal communication related to treatment

30
Nursing Intervention

•Pain management
•Oral hygiene
•Preparation for surgery or radiation
•Nutritional management
•Post operative care and dressing
•Symptomatic treatment.
•Administration of chemotherapy
•Monitoring of client response to any treatment
•Emotional support to client and family
•Care of symptom associated with treatment

31
Cont….

qHealth promotion:
Teach risk of oral cancer associated with all tobacco use and
excessive alcohol use
Need to seek medical attention for all non-healing oral lesions
(may be discovered by dentists); early precancerous oral
lesions are very treatable
Work out for following possible Nursing Diagnoses
1. Risk for ineffective airway clearance
2. Imbalanced Nutrition: Less than body requirements
3. Impaired Verbal Communication: establishment of specific
communication plan and method should be done prior to any
surgery
4. Disturbed Body Image

32
 Salivary Glands disorder
• The salivary glands make saliva and release it into the mouth.
There are three pairs of relatively large, major salivary glands:
• Parotid glands: Located in the upper part of each cheek, close
to the ear. The duct of each parotid gland empties onto the
inside of the cheek, near the molars of the upper jaw.
• Submandibular glands: Under the jaw. They have ducts that
empty behind the lower front teeth.
• Sublingual glands: Beneath the tongue. They have ducts that
empty onto the floor of the mouth.
oIn addition to these major glands other minor salivary glands
are scattered throughout the mouth and throat.

33
Cont….

34
Classification of Salivary Glands disorder

1-Obstructions: this could be by calculi or cystic

type (stone, mucocele, ranula)
2-Infections: viral (Mumps), bacterial (acute &
chronic Sialadenitis)
3-Degenerative changes: Sjogren syndrome,
radiation.
4-Functional disorders.
5- Neoplasms.

35
Investigations for salivary glands

1- Sialometery: measures the amount of saliva

production in a certain time.
2- Sialochemistry: measures the composition of
saliva.
3- Sialography: by introducing the iodine containing
contrast media through the opening of the duct.
4- Sonography: Ultrasonic patterns when dealing
with minor salivary glands.
5- Cytology: by aspiration.
6- Biopsy.

36
Cont….

Some of the most common salivary gland disorders

include:
§Sialolithiasis
§Sialadenitis
§Viral infections
§Cysts
§Benign tumors
§Malignant tumors
§Sjogren's syndrome
§Sialadenosis

37
Sialolithiasis
§ Sialolithiasis (salivary gland stones) Tiny, calcium-rich stones
sometimes form inside the salivary glands. 70-90% of stones
occur in the submandibular gland due to long twisted path of the
duct & thick secretion of the gland. about 6% in parotid gland &
2% in sublingual gland & minor S.G.
• Etiology: The exact cause of these stones is unknown. Some
stones may be related to:
• Dehydration, which thickens the saliva.
• Decreased food intake, which lowers the demand for saliva.
• Medications that decrease saliva production, including
certain antihistamines, anti-hypertensive drugs and
psychiatric medications.
• Deposition of ca++ salt around a nidus of debris within the
duct lumen
38
Cont….

• Some stones sit inside the gland without causing any symptoms.
In other cases, a stone blocks the gland's duct, either partially or
completely. When this happens, the gland typically is painful
and swollen, and saliva flow is partially or completely blocked.
This can be followed by an infection called sialadenitis.
• Signs & Symptoms The most common symptom are dry
mouth and a painful lump, usually in the floor of the mouth.
Pain may worsen during eating.
• Treatments
• Gentle probing: If the stone is located near the end of the duct,
the doctor may be able to press it out gently.
• Therapeutic sialdenoscopy
• Surgery: If stone are in deeper part
• Shock wave treatment

39
40
Sialadenitis
§Sialadenitis: (infection of a salivary gland)
Sialadenitis is a painful infection. It is more common
among elderly adults with salivary gland stones.
Sialadenitis also can occur in infants during the first
few weeks of life.
• Etiology It is usually caused by bacteria.
• Sign and symptoms: Symptoms may include:
oA tender, painful lump in the cheek or under the
chin.
oIn severe cases, fever, chills and general weakness.

41
Cont….

Treatment

Treatment includes:
•Drinking fluids or receiving fluids intravenously
•Antibiotics
•Warm compresses on the infected gland
•Encouraging saliva flow by chewing gums,
sugarless candies or by drinking orange juice.
•If these methods do not cure the infection,
surgery can be done to drain the gland.

42
Viral infections
§Viral infections: Systemic (whole-body) viral
infections sometimes settle in the salivary glands. This
causes facial swelling, pain and difficulty in eating.
The most common example is mumps.
• Etiology These infections are caused by viruses.
• Sign and symptoms The first symptoms often
include:
• Fever and poor appetite
• Headache,
• Muscle aches
• Joint pain and malaise.

43
Cont….

• Treatment: These infections almost always go away

on their own. Treatment focuses on relieving
symptoms through:
• Rest
• Drinking fluids to prevent dehydration
• Taking acetaminophen (Tylenol) to relieve pain and
fever

44
Cysts
§ Cysts: (tiny fluid-filled sacs)
Babies sometimes are born with cysts in the parotid gland
because of problems related to ear development before birth.
Later in life, other types of cysts can form in the major or minor
salivary glands.
• Etiology They may result from traumatic injuries, infections, or
salivary gland stones or tumors.
• Sign and symptoms: A cyst causes a painless lump. It
sometimes grows large enough to interfere with eating.
• Treatment : A small cyst may drain on its own without
treatment. Larger cysts can be removed using traditional surgery
or laser surgery.

45
Benign tumors
§ Benign tumors: (noncancerous tumors)
Most salivary gland tumors occur in the parotid gland. The
majority are benign. The most common type of benign parotid
tumor usually appears as a slow-growing, painless lump at the
back of the jaw, just below the earlobe.
• Etiology Risk factors include radiation exposure and possibly
smoking.
• Sign and symptoms A slow-growing lump is the most
common symptom. The lump is sometimes painful. This lump
may be found in the cheek, under the chin, on the tongue or on
the roof of the mouth.
• Treatment Non cancerous tumors usually are removed
surgically. In some cases, radiation treatments are given after
surgery to prevent the tumor from returning.

46
Malignant tumors
• Malignant tumors: (cancerous tumors)
Salivary gland cancers are rare. They can be more or less
aggressive.
• Etiology The only known risk factors for salivary gland
cancers are Sjogren's syndrome and exposure to radiation.
Smoking also may play some role.
• Sign and symptoms A slow-growing lump is the most
common symptom. The lump is sometimes painful. This lump
may be found in the cheek, under the chin, on the tongue or on
the roof of the mouth.
• Treatment Smaller, early stage, low-grade tumors often can be
treated with surgery alone. However, larger, high-grade tumors
usually require radiation following surgery. Tumors that cannot
be operated are treated with radiation or chemotherapy.

47
Sjogren's syndrome
• Sjogren's syndrome Sjogren's syndrome is a chronic
autoimmune disorder. The body's immune defenses attack the
salivary glands, the lacrimal glands (glands that produce tears),
and occasionally the skin's sweat and oil glands.
• Classification:
ØPrimary: xerostomia + xerophthalmia
ØSecondary: xerostomia + xerophthalmia + C.T. disease usually
rheumatoid arthritis.
• Etiology Over activity of the immune system.
• Sign and symptoms The main features of Sjogren's syndrome
are swelling of the salivary glands, dry eyes and a dry mouth.
• Immune system attacks parts of your own body by mistake.
In Sjogren's syndrome, it attacks the glands that make tears
and saliva. This causes a dry mouth and dry eyes.

48
Cont….

Treatment

• The main symptom related to the salivary glands is a

dry mouth. Options include:
• Medication to stimulate more saliva secretion, such as
pilocarpine (Salagen) and cevimeline (Evoxac).
•Sugarless gum and candy to stimulate saliva
production.
• Avoiding medications that can make dry mouth worse.
• Avoid smoking.
• Good oral hygiene is must. People with Sjogren's have
teeth and gum problems because of low saliva
secretion.

49
Sialadenosis
§ Sialadenosis (nonspecific salivary gland enlargement)
Sometimes, the salivary glands become enlarged without
evidence of infection, inflammation or tumor. This nonspecific
enlargement is called sialadenosis. It most often affects the
parotid gland.
• Etiology Its cause remains unknown.
• Sign and symptoms This condition typically causes painless
swelling of the parotid glands on both sides of the face.
• Treatment: Treatment is aimed at correcting any underlying
medical problem. Once the medical problem improves, the
salivary glands should shrink to normal size.

50
Medical Diagnosis
• Medical history.
• Smoking history.
• Current medications.
• Blood tests.
• X-rays.
• Magnetic resonance imaging (MRI).
• Computed tomography (CT) scans.
• Sialography.
• Salivary gland biopsy.
• Salivary function test.

51
Complications
• Abscess of salivary gland.
• Infection returns.
• Spread of infection.
• Facial nerve injury (Sialorrhea).
• Hematoma.
• Deformity.
• Dry mouth (xerostomia).
• Mumps.

52
Prevention

• We can lower our risk of viral infections of the salivary glands.

To do so, get immunized against mumps and influenza.
• There are no specific guidelines to protect against other types of
salivary gland disorders. However, it is helpful to:
• Avoid smoking.
• Eat a healthy diet.
• Drink six to eight glasses of water daily to avoid dehydration.
• Practice good oral hygiene, with regular tooth brushing and
flossing.

53
Nursing Diagnosis

• Low secretion of saliva related to stone in the salivary gland.

• Dry mouth related to blockage of saliva.
• Pain related to tumor & inflammation in the mouth.
• Difficulty in eating related to painful lump in the mouth.
• Poor appetite related to disease.
• Fever related to infection of salivary gland.

54
Nursing Interventions
• Give medication to stimulate more saliva secretion, such as
pilocarpine (Salagen) and cevimeline (Evoxac).
• Give sugarless gum and candy to stimulate saliva production.
• Avoiding medications that can make dry mouth worse.
• Provide analgesic to relief pain.
• Administer tube feeding.
• Give acetaminophen (Tylenol) to relieve fever.
• Cold sponging to relieve from fever.

55
THANK YOU SO MUCH

56
ESOPHAGEAL
DISORDERS
1
 CONTENTS
ANATOMY PATHOLOGIES
• NERVE SUPPLY 1. DYSPHAGIA
• BLOOD SUPPY 2. ESOPHAGEAL
• VENOUS DRAINAGE MOTILITY DISORDERS
• POINTS OF 3. ESOPHAGEAL
CONSTRICTION INFECTION AND
• FUNCTION INFLAMMATION
4. BARRETT
ESOPHAGUS
5. ESOPHAGEAL
TUMORS
2
 ANATOMY
• Commonly known as the food pipe or gullet.
• Food passes thru it.
• The esophagus is one of the upper parts of the digestive
system.
• The esophagus is a fibromuscular tube, about
25 centimetres long in adults.
• Its travels behind the trachea and heart, passes through
the diaphragm and empties into the uppermost region of
the stomach.
• It has two muscular rings or sphincters in its wall, one at
the top and one at the bottom.
• The esophagus has a rich blood supply and venous
drainage.
3
4
 ENS
ENS being referred to as the "second brain”.

INTRINSIC-ENTERIC NEURAL PLEXUS

Myenteric
Plexus (Of
Auerobach)

SUBMUCOSAL
PLEXUS (OF
MEISSNER) 5
EXTRINSIC - VAGUS NERVE

6
 BLOOD SUPPLY
• Upper parts and the upper esophageal
sphincter inferior thyroid artery.
• Parts in the thorax bronchial
arteries and branches directly from
the thoracic aorta.
• Lower parts and the lower esophageal
sphincter left gastric artery and
the left inferior phrenic artery.

7
8
 VENOUS DRAINAGE
• Upper and middle parts of the esophagus
drain Azygos and hemiazygos
veins.
• Lower part drains left gastric
vein.
• All these veins drain into the superior
vena cava with the exception of the left
gastric vein, which is a branch of the portal
vein.
9
10
POINTS OF CONSTRICTION

11
 FUNCTIONS
• Swallowing: Peristaltic contractions of
the esophageal muscle push the food
down the esophagus.
• Reducing gastric reflux: Sphincters help
to prevent reflux (backflow) of gastric
contents and acid into the esophagus.

12
PATHOLOGIES

13
1. DYSPHAGIA
“DIFFICULTY IN SWALLOWING”.
ODYNOPHAGIA:
“PAIN ON SWALLOWING”.
TYPES:
A. OROPHAYNGEAL DYSPHAGIA
B. ESOPHAGEAL DYSPHAGIA
14
A. OROPHAYNGEAL
DYSPHAGIA
It’s characterized by:
• Difficulty “initiating” swallowing
movements.
• It’s associated with choking or aspiration
of food into the lungs or nasal
regurgitation.
• It’s more for liquids than for solids.
15
CAUSES
• Bulbar palsy
• Pseudobulbar
DIAGNOSIS
palsy
NEUROLOGICAL • Myasthenia
gravis • Video fluoroscopy.
• stroke

• Oral cancer
• Zenkers
diverticulum
STRUCTURAL

16
 B. ESOPHAGEAL
DYSPHAGIA
It’s characterized by:
• “Sticking sensation” of food after swallowing.
• Obstructive lesions caused dysphagia for solids
more than liquids.
• Motility disorders cause dysphagia for both
solids and liquids.
• Esophageal dysphagia+odynophagia=
esophagitis.
17
DIAGNOSIS CAUSES
• For obstruction: • Strictures;
endoscopy and OBSTRUC
esophageal
webs
biopsy. TION • Schatzki rings;
esophageal
• For motility carcinoma

disorders:
manometry and
• Achalasia
barium swallon. MOTILIT • Diffuse
Y esophageal
spasm
DISORD
ERS

18
 2. ESOPHAGEAL MOTILITY
DISORDERS
a. Achalasia
b. Diffuse esophageal spasm and nutcracker
esophagus
c. Zenker diverticulum

19
 A. ACHALASIA
DEFINITION:
It is esophageal disorder with 3 major
abnormalities.
• Failure of LES to relax with swallowing.
• Aperistalsis in distal 2/3.
• Increased resting tone of LES.

20
21
 CAUSES
• Idiopathic
• Chagas disease
• Diabetes autonomic neuropathy
• Amyloidosis
• Sarcoidosis
• Pseudo-achalasia=achalasia like
symptoms due to cancer of gastro-
esophageal junction.
22
 CLINICAL PRESENTATION
• Dysphagia for both solid and liquid.
• Age is mostly <50 years.
• Weight loss
• Nocturnal cough, regurgitation.
• Heartburn does not occur because the
closed esophageal sphincter prevents
reflux.

23
 DIAGNOSIS
Esophageal manometry
Barium swallow (confirms diagnosis):
• Birds beak appearance. • Increased resting
• Esophageal dilatation pressure in LES.
with uniform tapering of • Decreased peristalsis in
distal esophagus. the body of esophagus.

24
TREATMENT

25
 COMPLICATION
• Squamous cell carcinoma 5%(most
serious).
• Candida esophagitis
• Diverticulitis
• Aspiration pneumonia
• Airway obstruction

26
 B. DIFFUSE ESOPHAGEAL
SPASM
• It is a motility disorder in which normal peristalsis
is periodically interrupted by high-amplitude non-
peristaltic contractions.
CLINICAL FEATURES:
1. Episodic chest pain, mimicking an angina.
2. Transient dysphagia.

27
 DIAGNOSIS
Manometry
Barium swallow
• Repetitive high-amplitude
• “Corkscrew” apperance contraction(400-
due to dyscoordinated 500mmHg).
diffuse contraction.

28
 NUTCRACKER ESOPHAGUS
• It is a condition in which extremely forceful
peristaltic activity leads to episodic chest
pain and dysphagia.
• Manometry= very strong peristaltic waves
of >180 mmHg.

29
 TREATMENET
• Calcium channel blockers
• Nitrates
• Pneumatic dilatation
• Surgical myotomy

30
 C.ZENKER DIVERTICULUM
• Also known as pharyngoesophageal
diverticulum/pouch.
• It is the most common esophageal diverticulum.
• It is defined as outpouching through the
cricopharyngeus muscle, above the upper
esophageal sphincter.
• It protrudes through the natural weak point i.e.
killian’s dehiscence between inferior
pharyngeal constriction and cricopharyngeus
muscle.
31
32
 CLINICAL FEATURES
• Dysphagia, regurgitation.
• Mass in neck.
• Halitosis-due to entrapped food.
• When diverticulum is small= pharyngeal
dysphagia.
• When diverticulum is large= esophageal
dysphagia.

33
 MANAGEMENT
DIAGNOSIS TREATMENT
• Barium swallow will • Surgery is the treatment
demonstrate of choice in symptomatic
outpouchings. patients.
• Endoscopy maybe • It involves myotomy and
hazardous; as it can resection of the pouch.
perforate the pouch.

34
 3.ESOPHAGEAL INFECTION
AND INFLAMMATION
a. Gastroesophageal reflux disease
b. Hiatal hernia
c. Infectious esophagitis

35
 A. GASTROESOPHAGEAL
REFLUX DISEASE(GERD)
• Also known as “reflux esophagitis”.
• It refers to reflux of gastric contents into
the lower esophagus, resulting in
esophagus irritation and inflammation.
PATHOGENESIS:
• Transient LES relaxation.
• Incompetent LES.

36
 RISK FACTORS
• Sliding hiatal hernia.
• Delayed gastric emptying.
• Reduction in reparative capacity of mucosa.
• Decreased LES tone due to:
1. Hypothyroidism
2. CNS depressants
3. Pregnancy
4. Alcohol
5. Tobacco
37
 CLINICAL FEATURES
Esophageal: Extra- esophageal
• Heartburn and • Atypical chest
regurgitation are the pain(mimicking angina).
major symptoms. • Chronic cough, asthma
• Heartburn is provoked (often poorly controlled).
by bending, straining, or • Laryngitis, dental
lying down. erosion.
• Dysphagia, water brash • Recurrent chest
(salivation due to reflux infection.
salivary gland
stimulation as acid
enters the gullet). 38
 DIAGNOSIS
• Based on history and empiric trial of PPI
e.g. omeprazole.
• Endoscopy is the investigation of choice. It
is done when:
1. Failure to respond to PPI.
2. Alarm symptoms>55years, dysphagia,
anemia, weight loss, positive fecal occult
blood test(FOBT).
39
• If diagnosis uncertain and endoscopy is
normal, then:
1. Manometry = decreased LES pressure.
2. 24-hour pH monitoring is the most
accurate investigation.

40
 TREATMENT
LIFE STYLE MODIFICATIONS

Avoid large and late night meals Elevate head of bed

PHARMACOLOGIC
PPI e.g. omeprazole, esomeprazole.
H2 RECEPTOR ANATGONIST e.g. ranitidine, famotidine.
PPI are treatment of choice.

SURGERY
INDICATIONS:
1. Failure of medical therapy.
2. Unwilling to take long-term PPIs.

41
 COMPLICATIONS OF GERD
• Esophagitis.
• Barrett’s esophagus.
• Anemia.
• Benign esophageal stricture.
• Gastric volvulus(if hiatal hernia present).

42
 B. HIATAL HERNIA
• It is defined as “ Herniation of stomach
upward into the chest through esophageal
hiatus of diaphragm.”

43
 TYPES
1. SLIDING HERNIA 2. ROLLING HERNIA
(AXIAL) (NON-AXIAL)
• Most common type;95% • Also known as
of cases. paraesophageal hernia.
• It is refers to Herniation of • It is refers to Herniation of
proximal stomach through portion of stomach
a widened diaphragmatic (greater curvature)
hiatus. alongside the distal
• The gastro-esophageal esophagus.
junction is displaced • The gastro-esophageal
above the diaphragm. junction remains at the
level of diaphragm.
44
45
 CLINICAL FEATURES
• Often asymptomatic.
• Commonly and incidental finding on CXR.
• Heartburn & regurgitation can occur.
• Para-esophageal hernia can cause gastric
volvulus.

46
 C. INFECTIOUS
ESOPHAGITIS
• It usually occur in immunocompromised
individuals.
• It presents with odynophagia.
• Commonly caused by:

Herpes Candida
Cytomegalovirus
simplex virus Albicans

47
1. Herpes simplex virus:
• It typically produces “punched-out” ulcers; ulcers are small, but
deep.
• It forms multinucleated giant cells with intra-nuclear inclusions in
epithelial cells at the margin of ulcer.
• Tx : IV acyclovir
2. Cytomegalovirus:
• It typically produces “linear” ulcers; ulcers are large, superficial.
• It forms intra-nuclear and intra-cytoplasmic inclusions.
• Tx: IV gancyclovir
3. Candida Albicans:
• It forms patchy gray-white pseudomembrane.
• It produces yeast and densely matted fungal hyphae.
• Tx: oral fluconazole or nystatin.

48
49
 4.BARRETT ESOPHAGUS
• It is a pre-malignant condition.
• It is characterized by the replacement of
the normal squamous epithelium by the
more resistant columnar epithelium
containing areas of intestinal metaplasia.
• It occur as a complication of long-standing
GERD (10% cases).

50
 RISK FACTORS
• Men(especially white).
• Age>50years.
• Weakly associated with smoking.
• No association with alcohol.

51
 TYPES
• <3cm of columnar epithelium
SHORT
extending cephalad from GE-
SEGMENT
BARRETT
junction.

• >3cm of columnar epithelium

extending cephalad from GE-
LONG SEGMENT
BARRETT junction.(classic barrett)

52
53
DIAGNOSIS MANAGEMENT
• Endoscopic biopsy- • Barrett metaplasia
investigation of choice. without dysplasia=PPIs
and endoscopy 2-3 years.
• Low-grade
dysplasia=PPIs and
endoscopy 6-12months.
• High-grade dysplasia=
esophagectomy (surgical
resection)

54
 5. ESOPHAGEAL TUMORS
A. Benign tumors
B. Esophageal carcinoma

55
 A. BENIGN TUMORS
• It is most common gastrointestinal stromal
tumor(GIST).
• Other types:
1. Leiomyomas
2. Fibromas
3. Lipomas

56
 B. ESOPHAGEAL
CARCINOMA
1. SQUAMOUS CELL CARCINOMA
• Most common type of esophageal carcinoma.
• It is male-dominant, mostly in over 50years of age.
• Most common in upper and middle thirds of esophagus.
RISK FACTORS:
• Betel chewing
• Tobacco use
• Alcohol
• Achalasia
• Celiac disease
57
2. ADENOCARCINOMA
• It is malignant epithelial tumor with
glandular differentiation.
• It is more prevalent in west.
• Most common in lower thirds of
esophagus.
RISK FACTOR:
• Tobacco
• Obesity
• Barrett esophagus; most common. 58
 CLINICAL FEATURES
• Weight loss
• Anorexia
• Bleeding
• Chest pain
• Hematogenous spread:
Liver; lungs.
Brain; bones.

59
 MANAGEMENT
DIAGNOSIS TREATMENT
• Endoscopy & biopsy- • Surgical resection is choice of
investigation of choice. tx.
• CT scan (thoracic & • Surgery is combined with
abdominal)- to identify chemo-therapy.
metastatic spread & local • However, 70% of patient have
invasion. extensive disease at
• Endoscopic ultrasound (EUS) presentation, & therefore tx is
is the most sensitive method mainly palliative.
for determining: • Stent placement to keep
• Depth of penetration of tumor esophagus patent & relieve
into the esophageal wall. dysphagia.
• Detecting involved regional • Nutritional support &
lymph nodes. analgesia. 60
61
 Chapter 48

Management of Patients With

Intestinal and Rectal Disorders

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

Constipation
 Abnormal infrequency or irregularity of defecation; any variation
from normal habits may be a problem
 Causes include medications, chronic laxative use, weakness,
immobility, fatigue, inability to increase intra-abdominal pressure, diet,
ignoring urge to defecate, and lack of regular exercise
• Increased risk in older age (Chart 48-1:“Ten Ds of Constipation”)
• Perceived constipation: a subjective problem in which the person’s
elimination pattern is not consistent with what he or she believes is
normal
 Manifestation:
– Fewer than three bowel movements per week; Abdominal
distention
– Decreased appetite; Headache; Fatigue; Indigestion
– A sensation of incomplete evacuation; Straining at stool
– Elimination of small-volume, hard, dry stools
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Constipation
• Complications:
– Hypertension; Fecal impaction
– Hemorrhoids; Fissures; Megacolon

• Patient Learning Needs (see chart 48-2)

– Normal variations of bowel patterns
– Establishment of normal pattern
– Dietary fiber and fluid intake
– Responding to the urge to defecate
– Exercise and activity
– Laxative use (see table 48-1)

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 Diarrhea
 Increased frequency of bowel movements (more than three per
day), increased amount of stool (>200 g per day), and altered
consistency (i.e., looseness) of stool
• Usually associated with urgency, perianal discomfort, incontinence, or a
combination of these factors
• May be acute or chronic
 Causes include infections (*Clostridium difficile), medications, tube
feeding formulas, metabolic and endocrine disorders, and various
disease processes
 Manifestations
– Increased frequency and fluid content of stools
– Abdominal cramps, Distention, Borborygmus
– Painful spasmodic contractions of the anus, Tenesmus

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Diarrhea
 Complications
– Dehydration
– Fluid and electrolyte imbalances
• Cardiac dysrhythmias due to loss of potassium
• Patient Learning Needs
– Recognition of need for medical treatment
– Rest, Diet and fluid intake
– Avoid irritating foods, including caffeine, carbonated beverages,
very hot and cold foods
– Perianal skin care- Witch hazel, Medications
– May need to avoid milk, fat, whole grains, fresh fruit, and
vegetables
– Lactose intolerance (see * chart 48-3; p.1295)
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Fecal Incontinence
 Causes :
– Trauma, Neurologic disorders; Inflammation and infection
– Chemotherapy, Radiation treatment, Fecal impaction
– Pelvic floor relaxation, Laxative abuse, Medications
– Advancing age (loss of anal or rectal muscle tone)
 Manifestations
– Minor soiling
– Occasional urgency
– Loss of control
– Complete incontinence Flexi-Seal Fecal Management System
• Patient Learning Needs
– Bowel training program, Skin care, Emotional support
Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
Irritable Bowel Syndrome
• 12% to 14% of adults in the United States report symptoms of IBS
• “Spastic colon”
• More common in women than men
• Factors of triggers include heredity, psychological stress, depression,
anxiety, high-fat diet, irritating foods, alcohol and smoking use
 Clinical Manifestations
– Alteration in bowel patterns
– Pain, Bloating, Abdominal distention
• Patient Learning Needs
– Medication management, Complimentary medicine (Probiotic)
– Dietary changes (↑ fiber), Adequate fluid intake
– Avoid alcohol and smoking, Relaxation techniques
Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
 Malabsorption
• The inability of the digestive system to absorb one or more of the major
vitamins, minerals, or nutrients
 Conditions (Table 48-2)
– Mucosal (transport) disorders (celiac disease, regional enteritis)
– Infectious disease (topical sprue)
– Luminal disorders (bile acid deficiency, chronic pancreatitis)
– Postoperative malabsorption
– Disorders that cause malabsorption of specific nutrients (food
allergies)
 Clinical Manifestations
– Hallmark finding is diarrhea or frequent, loose, bulky, foul-smelling
stools, high fat content and often grayish
– Symptoms similar to irritable bowel syndrome
– Manifested by weight loss and vitamin and mineral deficiency
Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
Malabsorption (cont’ d)
• Diagnostic Findings
– Fat analysis, Lactose tolerance tests
– D-xylose absorption tests, Schilling tests
– Hydrogen breath test, Endoscopy with biopsy
– Ultrasound, CT, radiography
– CBC, pancreatic function tests
• Patient Learning Needs
– Treat underlying causes
– Vitamin replacement –VitB12, folic acid, calcium, vit A, D, & K
– Dietary therapy (i.e.; avoid gluten), Probiotics
– Consider fluid and electrolyte imbalance
– Risk of osteoporosis (due to mineral deficiency –Calcium)
Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
Diverticular Disease
 Diverticulum: sac-like herniation of the lining of the bowel that extends
through a defect in the muscle layer
• May occur anywhere in the intestine but most common in the sigmoid
colon
 Diverticulosis: multiple diverticula without inflammation
 Diverticulitis: infection and inflammation of diverticula
• Diverticular disease increases with age and is associated with a low-fiber
diet
 Diagnosis is usually by colonoscopy or BE
 Patients may have chronic constipation preceding development of
diverticulosis, frequently asymptomatic but may include bowel
irregularities, nausea, anorexia, bloating, and abdominal distention.
 Prevention of constipation: ↑ fluids, exercise, ↑ soft fiber (bulk-
forming laxative: Metamucil). No stimulants laxatives (Ducolax, senna)
or mineral oil routinely
 No nuts, corn, popcorn/seeds (tomatoes, cucumber, squash, berries)

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

The Care of the Patient With Diverticulitis
 * With acute diverticulitis, symptoms include mild or severe pain in
lower left quadrant, nausea, vomiting, fever, chills, and leukocytosis
 Treatment
– Outpatient:
• clear liquids until inflammation subsides, then high-fiber, low-
fat diet/ Antibiotics 7- 10days
– *Acute diverticulitis
• IV antibiotics
• NPO, Rest, IV, NG tube suctioning
 *Complications: Perforation, hemorrhage,
peritonitis, obstruction, fistula (colovesical)
– Surgical management
Hartmann’s procedure for
diverticulitis
Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
Inflammatory Bowel Disease (See Table 48-4 )
 Onset peaks between ages 15 and 25 years; Second peak in sixth
decade; Equally affects both sexes; Exact cause is unknown
• Patients suffer mild to severe acute exacerbations that occur at
unpredictable intervals over their lifetimes with periods of remission
 Crohn’s disease (regional enteritis): Inflammation of any segment of
the GI tract from mouth to anus; most common in ileum; diarrhea and
bleeding less severe; Weight loss (more severe due to decreased
absorption), abd pain, fatigue
 Ulcerative colitis: Inflammation and ulceration of the colon
(descending colon) and rectum(100%), bleeding & diarrhea with
mucus, pus are severe; dehydration; “cured” by colectomy
 Complications: hemorrhage, bowel perforation, peritonitis,
fistula (b/t bowel & bladder), Toxic megacolon (total or segmental
nonobstructive colonic dilatation plus systemic toxicity); *High risk
for colorectal cancer
– Surgical intervention
Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
 • Usually starts in the
• Segments of normal bowel
rectum and moves in a
that are present between
continual manner
diseased portions
toward the cecum
Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
Maintaining Normal Elimination Pattern
• Identify relationship between diarrhea and food, activities, or
emotional stressors
• Provide ready access to bathroom or commode
• Encourage bed rest to reduce peristalsis
• Record frequency, consistency, character, and amounts of stools
• Patient Education
– Understanding of disease process/ Nutrition and diet
– Medications: Sulfasalazine (Azulfidine), Corticosteroids,
Immunosuppressants, biologic therapy [anti-TNF (tumor necrosis
factor) - Infliximab (Remicade); Adalimumab (Humira);
Certolizumab pegol (Cimzia)] to maintain remission
– Information sources: National Foundation for Ileitis and Colitis
– Ileostomy care if applicable

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

Other Interventions
• Assessment and treatment of pain or discomfort, anticholinergic
medications before meals, analgesics, positioning, diversional
activities, and prevention of fatigue
• Fluid deficit, I&O, daily weight, assessment of symptoms of
dehydration or fluid loss, encourage oral intake, measures to decrease
diarrhea
• Optimal nutrition; elemental feedings that are high in protein and
low residue or PN may be needed; avoid high fiber diet
• High in calories and nutrients
• Reduce anxiety, use a calm manner, allow patient to express feelings,
listening, patient education
• Smoking and coffee should be avoided (increases motility and
secretion)

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

Surgical intervention: Ileostomy
care if applicable
 Total colectomy with ileostomy:
• excision of the entire colon and surgical creation of an opening into the
ileum by a means of an ileal stoma on the abdominal wall /liquid to
unformed drainage
 Preoperative care: thorough explanation regarding ileostomy-location,
care (WOC: wound-ostomy-continence nurse) - RLQ 2cm below the
waist
 Postoperative care: accurate record of I&O d/t loss of large
volume(continuous liquid drainage), NG suction, rectal packing removal
in 1 wk
 Skin and stoma care: 1” pink to bright red, shiny, fecal drainage
(continuous liquids form) begin in 24-48 hrs. appliance empty q 4-
6hrs, change bags 5-10 days -disposable, odor-proof pouch
 Diet and fluid intake: low-residue diet x 6-8 wks, avoid hard to
digest food (i.e: corn) – *obstruction risk
Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
Continent ileostomy (Kock pouch)
 Use distal ileum (30 cm) to create a reservoir with a nipple valve –
remove fecal content by a catheter
• No external fecal collection bag
• Irrigating Continent ileostomy –
– Postoperatively, a catheter is extends from the stoma and is
attached to a closed drainage system
– Every 3 hrs, 10 -20 ml of N/S is instilled into the pouch gently;
return is allowed to drain by gravity
– After 2 weeks, the catheter is removed
– Then, pt learns how to drain the pouch
• Drainage by inserting a catheter thru
the nipple valve – (Chart 48-7)

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

Restorative proctocolectomy with ileal pouch
anal anastomosis (IPAA) : (Fig 48-6)
 IPAA: Most commonly used surgical
procedure for ulcerative colitis

*Connect the ileum to the anal pouch

(made from a small intestinal segment) –
connect the pouch to the anus (removing
diseased colon and rectum) /temporary
diverting loop ileostomy (x 3mo) to allow
healing
voluntary defecation is maintained
*Perianal skin care due to leakage of fecal anal sphincter control
content- use of skin barrier (Vaseline) after
each bowel movement
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 Intestinal Obstructions
• Mechanical obstruction (Table 48-5)- adhesion, intussusception, hernia,
tumor, volvulus
• Functional obstruction: neurological disorder, DM, muscular dystrophy
 Small bowel: vigorous vomiting with fecal content if obstruction is
complete. Decompression with NG tube or surgery if tissue necrosis
 Large bowel: less dramatic symptoms, progression slower than small
bowel obstruction. Abdominal distention
o Adenocarcinoma tumor accounts for the majority of obstruction.
Colonoscopy to decompress the bowel or surgical intervention
Intussusception

Volvulus of sigmoid colon

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
Colorectal Cancer (CRC)
• The third most common site of new cancer cases in the United States
 *Risk factors (*chart 48-9)
– Diet: High in red or processed meat; Low in fruits and vegetables
• High fat diet, low fiber diet
– Lifestyle factors: Obesity; Physical inactivity; Alcohol; smoking
– Family history: FAP (Familial adenomatous polyposis), colon
cancer
– Previous colorectal polyps or inflammatory bowel disease
(IBD)
– Age >50
• Adenocarcinoma is the most common type of CRC
– About 85% arise from adenomatous polyps
 Manifestations may include change in bowel habits; blood in stool
—occult, tarry, bleeding; tenesmus; symptoms of obstruction; pain,
either abdominal or rectal; feeling of incomplete evacuation; Change
in stool caliber; Iron-deficiency anemia and occult bleeding
Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
CRC
• Staging of CRC: Dukes’ Classification (Chart 48-10)
• Importance of screening procedures
– Fecal occult blood test (FOBT)
– Fecal immunochemical test (FIT) -positive result indicates
abnormal bleeding in the lower digestive tract
– Flexible sigmoidoscopy every 5 years
– Colonoscopy every 10 years
– Double-contrast barium enema study every 5 years
• Treatment depends on the stage of the disease
– Adjuvant –radiation/chemotherapy
– Surgical intervention/colostomy

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

Colorectal Cancer/Colostomy

Stoma skin barrier

• Nature of discharge varies with the
site
• Begins to function in 3-6 days after
surgery
•Chart 48-6: Guidelines for changing
an ostomy appliance

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

The Care of the Patient With Cancer of the
Colon or Rectum
• Preparing the patient for surgery/Emotional support: Consult a
wound, ostomy, and continence nurse specialist- Select the ostomy
site; Provide follow-up care and teaching
• Providing postoperative care: Sterile dressing changes, care of
drains, and patient and caregiver teaching about the stoma
• Maintaining optimal nutrition/Providing wound care: Wound should be
examined regularly; Record bleeding, excessive drainage, and odor
• Monitoring and managing complications (*Table 48-6)
• Removing and applying the colostomy appliance/Irrigating the
colostomy
• Supporting a positive body image
• Discussing sexuality issues
• Promoting home and community-based care
Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
Irrigating colostomy
 Irrigating the colostomy (see Chart 48-12): to regulate the passage
of fecal materials/ done at a regular time/less fear of fecal drainage
during social or business activities
– Irrigating reservoir contain 500 -1500 ml lukewarm tap water
– Hang it 18 in (45-50 cm) above the stoma (shoulder height)
– Insert cath 3-4 “
– Perform irrigation 1 hr after a meal

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Anorectal Conditions
• Anorectal abscess
• Anal fistula
• Anal fissure
• Hemorrhoids
– Internal hemorrhoids
– External hemorrhoids
• Sexually transmitted anorectal diseases
– Proctitis, proctocolitis, enteritis
• Pilonidal (a nest of hair) sinus or cyst: penetration of hairs into
epithelium or subcutaneous tissue

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

Anal Lesions

Pilonidal Sinus
(nest of hair)

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Interventions
• Encourage intake of at least 2 L of water a day
• Recommend high-fiber foods
• Bulk laxatives, stool softeners, and topical medications
• Promote urinary elimination
• Hygiene and sitz baths
• Monitor for complications
• Educate on self-care

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

Question

What is an example of a laxative osmotic agent?

A. Bisacodyl (Dulcolax)
B. Dioctyl sodium sulfosuccinate (Colace)
C. Magnesium hydroxide (Milk of Magnesia)
D. Polyethylene glycol and electrolytes (Colyte)

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

Question

Is the following statement true or false?

The most common site for diverticulitis is the ileum.

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Question

Is the following statement true or false?

Regular bowel habits can be established for a patient with

an ileostomy.

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Question

Is the following statement true or false?

Abdominal pain and constipation are common clinical

manifestations of Crohn’s disease.

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Question

After teaching D.B. about dietary modifications for inflammaory

bowel disease, you determine that teaching was effective when
he chooses which menu?

a. Baked cod, baked sweet potato, and canned pears

b. Barbecued brisket, coleslaw, baked beans, and angel food
cake
c. Fried shrimp with cocktail sauce, corn on the cob, and a fruit
roll-up
d. Turkey burger with cheese on a whole wheat bun, french fries,
and an orange

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Question

D.B. must undergo surgical intervention. Which comment

indicates that additional instruction about the care of his
new ileostomy is needed?

1. “I should change the appliance daily to prevent odors.”

2. “When I change the appliance, I should check the skin for
irritation.”
3. “I should clean around the stoma with mild soap and water
and pat dry.”
4. “I’ll need to alter the appliance opening when the stoma
becomes smaller as the area heals.”

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