CH 16
Goodman
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Upper GI (mouth, esophagus, stomach and
duodenum) - ingestion and digestion
Lower GI: small intestines - digestion, absorption of
nutrients; large intestines – absorbs water and
electrolytes, stores waste products until elimination
Enteric nervous system - just as many nerves as the
spinal cord; can function completely independent of
the CNS; it is thought that the “brain in the bowel”
can have its own form of neuroses (such as functional
bowel syndromes)
PT needs to be aware of the clinical manifestations of
GI issues - many have implications on physical
activity tolerance and healing / recovery (dehydration,
malnutrition, anemia)
Gastrointestinal System
Mouth>pharynx>esophagus>stomach>small intestine
(duodenum, jejunum, ileum)>large intestine (cecum,
ascending, transverse, descending, sigmoid)
>rectum>anus
**liver, gallbladder and pancreas needed for digestion
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Liver
The liver has multiple functions, but two of
its main functions within the digestive system
are to make and secrete an important
substance called bile and to process the
blood coming from the small intestine
containing the nutrients just absorbed. The
liver purifies this blood of many impurities
before traveling to the rest of the body.
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Gallbladder
The gallbladder is a storage sac for excess
bile. Bile made in the liver travels to the small
intestine via the bile ducts. If the intestine
doesn't need it, the bile travels into the
gallbladder, where it awaits the signal from
the intestines that food is present. Bile serves
two main purposes. First, it helps absorb fats
in the diet, and secondly, it carries waste
from the liver that cannot go through the
kidneys.
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Pancreas
Among other functions, the pancreas is the
chief factory for digestive enzymes that are
secreted into the duodenum, the first
segment of the small intestine. These
enzymes break down protein, fats, and
carbohydrates.
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Aug. 21, 2009 — The lowly appendix, long-
regarded as a useless evolutionary artifact, won
newfound respect two years ago when
researchers at Duke University Medical Center
proposed that it actually serves a critical
function. The appendix, they said, is a safe haven
where good bacteria could hang out until they
were needed to repopulate the gut after a nasty
case of diarrhea, for example.
*Has been regarded as a vestigial structure (one
that has lost all or most of its original function
through evolution)
www.sciencedaily.com
Nausea (symptom)
 uneasy feeling - as if going to vomit - caused
by irritation in nerve ending of stomach
Vomiting (sign)
 Flow of stomach contents backwards through
upper GI......and either aspirated into lungs
or out the mouth (if back down the esophagus is
technically just reflux)
 Caused by anything that causes nausea
 Complications include fluid and electrolyte
imbalances, pulmonary aspiration --> aspiration
pneumonia; malnutrition; rupture of esophagus;
dental decay (if prolonged)
 If vomit is blood mixed with stomach acids looks
like “coffee-grounds” and is aptly referred to as
“coffee-ground vomit”
Diarrhea (sign)
 Abnormal fluid mixture, frequency and/or
volume of stool
 Results in poor absorption of fluid, nutritive
elements, and electrolytes
Anorexia (symptom vs. sign)
 Diminished appetite or aversion to food
Anorexia - Cachexia (sign)
 Anorexia that results in wasting of muscle; is
a common systemic response to cancer
 Associated with poor intake and high
metabolic rate
Constipation (sign)
 Fecal matter is too hard to pass easily; or
when bowel movements are so infrequent
that discomfort and other symptoms interfere
with daily activities
 May occur due to diet, dehydration, side
effect of medication, acute or chronic disease
of digestion system, inactivity or prolonged
bed rest, emotional stress
Dysphagia (sign vs. symptom)
 Difficulty swallowing that results in the
sensation that food is stuck somewhere in the
throat or chest; may be a symptom / sign of
many other disorders other than GI - such as
neurological conditions
Achalasia (sign vs. symptom)
 Rare disorder that makes it difficult for food
and liquid to pass from esophagus to
stomach.
 Due to loss of nerve cells in the esophagus so
that food is not propelled down the GI tract
 Also, the lower esophageal sphincter (LES)
which connects the esophagus and the
stomach doesn’t fully relax.
 This results in a feeling of “fullness” in the
sternal region that can progress to dysphagia
Heartburn (symptom)
 Pain or burning sensation in the esophagus,
can radiate to arms, jaw or back
Abdominal pain
 Inflammatory - due to inflammation
 Mechanical - stretching of the walls of GI
tract
 Ischemic - due to buildup of metabolites that
are released in an area of reduced blood flow
GI Bleeding
 Accumulation of blood in GI tract is irritating
and tends to cause discomfort; vomiting
(Coffee ground vomit), diarrhea (black, tarry),
or hematochezia (bleeding from rectum)
Fecal incontinence
 Inability to control bowel movements
 Psychological factors - confusion, anxiety,
disorientation
 Physiologic - neurological / motor
impairment
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Changes begin before 50 y/o
Oral changes (tooth decay) may lead to
difficulty with digestion
Sensory changes - decreased taste buds
which can contribute to depressed appetite
Salivary secretions decrease - dry mouth,
difficulty with digestion
Organs lose tone but manage to function well
enough
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Net effect of changes includes decreased
alimentary mobility (increased constipation),
decreased blood flow, decreased nutrient
absorption> slower digestion and emptying
There is a decline in “Intrinsic Factor” (IF) that
typically promotes vitamin B12 absorption
in the stomach; this frequently occurs after
middle age. In advanced age (90 y/o), prevalence
of problems associated with B12 deficiency is as
high as 90% (anemia, neurological symptoms,
constipation, weight loss)
Hiatal Hernia
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Definition & Incidence: lower esophageal sphincter gets
enlarged and stomach passes through the diaphragm into
the thoracic cavity
Estimated incidence of 5/1000 people / year
Prevalence estimated at 60% of people over 60 y/o
(symptomatic and asymptomatic)
Etiologic / risk factors - anything that weakens the
diaphragm muscle or alters the hiatus
Pathogenesis / Clinical Manifestations: heart burn - worse
when lying down or with increased abdominal pressure
Medical Management: diagnosed by ultrasound imaging or
barium swallow with fluoroscopy; treatment includes
symptomatic control
Gastroesophageal Reflux Disease (esophagitis)
(GERD)
 Definition & Incidence: inflammation of
esophagus; increasing incidence with aging;
 15% or more of the population may have
symptoms daily
 Types: reflux, chemical, infectious
 Etiologic / risk factors: backward flow of
stomach acids; irritation by nasogastric
intubation or radiation
GERD (continued)
 Pathogenesis / Clinical Manifestations: Heart
burn, belching, dysphagia; problem is that
 long term GERD can result in Barrett’s
esophagus (metaplasia - dysplasia) which
increases risk for neoplasia
GERD (continued)
 Medical Management: diagnosis with history,
endoscopy, barium radiography, H-pylori, esophageal
pH
 Can be confused with angina; Nitroglycerin can help
determine cardiac vs. GERD pain (but not without
error - some GERD goes away with nitroglycerin)
 Treatment includes acid suppression, lifestyle
modifications - drinking fluids between
 meals but not with meals, loose fitting clothes,
avoiding caffeine, nicotine, alcohol, aspirin,
NSAIDs, remaining upright for at least 3 hours after
meals, weight loss if obese
 Minimally invasive surgery is being developed
Mallory-Weiss Syndrome
 Mucosal laceration of the lower end of
esophagus accompanied by bleeding.
 It is commonly caused by retching and
vomiting due to alcohol abuse, eating
disorders or a viral syndrome
 Diagnosis is made with endoscopy
 Treatment with fluid replacement, blood
transfusion
 Endoscopic ligation may be required
Neoplasm
 Definition & Incidence
 Two types - squamous cell and
adenocarcinoma
 Adenocarcinoma is relatively uncommon but
incidence is rising (H-pylori treatment might
be reason)
 Etiologic / risk factors: irritation, any change
in function that keeps food in the esophagus
 longer than it should that results in ulceration
and metaplasia
Neoplasm (continued)
 Clinical Manifestations - dysphagia is the
primary sign / symptom, but it does not
present until the esophagus is blocked
between 30-50%; the only pain tends to be
heartburn with lying down
Neoplasm (continued)
 Medical Management - prevention by treatment
of irritation / GERD, etc.; diagnosis with
endoscopy
 Neoplasms are classified as resectable with
curative intent, resectable but not
curable, and not resectable/not curable;
(depends on metastases, lymph node
involvement)
 Prognosis is poor - 5 year survival is 10%, with a
median survival of less than 10 months
(related to the lack of symptoms / signs until
relatively late in the process)
Esophageal Varices
 Dilated veins in the lower third of esophagus
immediately beneath the mucosa due to
portal hypertension usually associated with
cirrhosis of the liver; usually painless but
significant bleeding that can result in anemia and
other low blood volume problems (in
extreme cases shock)
 About 1/2 cease without intervention; ligation
may be needed; in extreme cases a stent
may be required to relieve portal hypertension
Congenital Conditions
 Tracheoesophageal Fistula TEF - most
common congenital esophageal anomaly;
about 1 in 4000 live births; esophagus fails
to make connection to the stomach : might
go to trachea and then stomach; or trachea
alone; or just end blindly with or without
trachea making a connection to stomach requires surgical repair
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WHAT does this condition cause??
Depends on type
See page 840 in Goodman
Gastritis
 Definition & Incidence - inflammation of the lining of
the stomach; represents a group of the most
common stomach disorders; can be acute or chronic;
most common form of chronic gastritis is caused by a
bacterial infection: H-pylori
 Etiologic / risk factors: serious illness, medication use
(ASA, NSAID), stress, H-pylori
 Clinical Manifestations - epigastric pain; can lead to
GI bleeding
 Medical Management - Dx by history, endoscopy,
biopsy, tests of stool or blood for H-pylori;
 Rx, remove cause if possible, time to heal
Peptic Ulcer Disease PUD
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Definition & Incidence - break in protective mucosal lining
which exposes submucosal areas to gastric
contents/secretions
Two types – gastric (stomach) or duodenal (DUs are 2-3 x
more prevalent)
Etiologic / risk factors: anything that causes gastritis
Clinical Manifestations: epigastric pain - with burning,
gnawing, cramping, aching near xiphoid coming in waves;
can include nausea, loss of appetite and weight loss.
Perforation causes increased pain in thoracic spine area
T6-T11 with radiation to RUQ
Medical Management: Dx: same as gastritis; Rx - same as
gastritis; surgical intervention is required for perforation
Gastric Cancer
 1. Primary gastric lymphoma (relatively uncommon)
 2. Gastric Adenocarcinoma - malignant neoplasm
originating from gastric mucosa
 Etiologic / risk factors - chronic gastritis
 Clinical Manifestations - - depends on variety of
factors such as size of tumor, presence of gastric
outlet obstruction, metastatic versus nonmetastatic
disease
 Medical Management - Dx is usually delayed due to
symptomatic treatment of gastritis (early stages may
be asymptomatic)
 Surgery is treatment of choice; prognosis depends on
stage when discovered
Gastric cancer (continued)
 Prevention: presently best advice is to eat at
least 5 (1/2) cup servings of fruit and
vegetables/daily combined with exercise,
maintenance of healthy weight and reduced
intake of salt-preserved foods
Congenital Conditions
 Pyloric Stenosis (PS) - obstruction of pyloric
sphincter (stomach into duodenum)
 Clinical Manifestations - projectile vomiting is
the most common and dramatic early sign - and
may occur at birth
 Projectile vomiting requires vomit to eject 1 foot
or more when supine, or 3-4 feet when upright
 Medical Management - antispasmodic
medications (if effective) for 6-8 months to see if
stenosis loosens up; if it does not loosen up
surgical repair is required
Malabsorption Syndrome
 Definition & Incidence - group of disorders
(celiac disease, cystic fibrosis, Crohn’s
disease, chronic pancreatitis, pancreatic
carcinoma, pernicious anemia, short gut
syndrome, fibrotic changes due to
gastroenteritis) characterized by reduced
intestinal absorption
of dietary components and excessive loss of
nutrients in the stool
Malabsorption syndrome (continued)
 Traditionally classified as:
 Maldigestion- failure of chemical process of
digestion
 Malabsorption- failure of intestinal mucosa to
absorb nutrients
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Can occur separately or together
simultaneously
Malabsorption syndrome (continued)
 Etiologic / risk factors - most often in
therapy will see patients with gastroenteritis
due to NSAID use and resultant fibrotic
changes leading to malabsorption
Malabsorption syndrome (continued)
 Clinical Manifestations - Progressive - related to
nutrient deficiency
 General malaise - weakness, fatigue, muscle
wasting
 B12 - pernicious anemia
 Iron, vit A, D, K - osteomalacia
 Calcium, vit D, magnessium - tetany
 Vit B complex - Numbness and tingling
 Electrolytes - muscle spasms, palpitations
 Vit K - easy bruising / bleeding
 Protein - generalized swelling
Malabsorption syndrome (continued)
 Medical Management - treat underlying
condition; nutritional supplementation – may
need to bypass GI (parenteral nutrition - IV
feeding); prognosis depends on underlying
condition
Vascular Diseases
 Embolic occlusions of visceral branches of
abdominal aorta
 Intestinal Ischemia - caused by
atherosclerosis or emboli; pain, rapid onset
of cramping
 Rx - surgery
Bacterial Infections
 Food borne illnesses such as botulism are
caused by bacteria. Can be fatal. Appropriate
treatment depends on identifying pathogen.
Many episodes of acute gastroenteritis need
fluid replacement and supportive care.
Inflammatory Bowel Disease (IBD)
 Definition & Incidence  1. Crohn’s disease (CD) - chronic, life long
inflammatory disorder that can affect any
segment of the intestinal tract with “skips”
(sections of normal bowel with skips or
lesions)
 2. Ulcerative colitis (UC) - chronic
inflammatory disorder of the mucosa of the
colon in a continuous manner –chronic
diarrhea and rectal bleeding
IBD (continued)
 Etiologic / risk factors - both have unknown
etiologies
 Pathogenesis - both are considered autoimmune
 Clinical Manifestations - recurrent involvement of
intestinal segments resulting in a chronic,
unpredictable course
 Inflammatory process begins with low-grade
fever, malaise, weight loss, diarrhea and
abdominal cramping / pain; may be followed by
obstructive phase with persistent bloating
and distention from the movement of gas
through the system
IBD (continued)
 Medical Management - Dx only by history
and ruling out other conditions; monitoring
includes use of radiographs, colonoscopy,
barium enema x-ray, fecal occult blood tests,
blood testing
 Rx: symptom relief, anti inflammatory meds,
diet, surgery to resect parts of intestine may
be necessary
Antibiotic Associated Colitis
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Antibiotics can disrupt normal GI bacterial flora; common
for C - difficile (Clostridium difficile) to dominate; it is a
microorganism that can replace normal GI tract flora
It is not invasive, but can create toxins that damage the
colonic mucosa; signs start as a
lot of watery diarrhea - can occur early with antibiotic
treatment or within 4 weeks after the medications have
stopped.
Treatment is aimed at fluid and nutrition replacement, and
antimicrobials can be prescribed to treat the c-diff
Irritable Bowel Syndrome (IBS)
 Definition & Incidence - group of symptoms most common disorder of the GI system  Referred to as ‘nervous indigestion’, ‘spastic
colon’, ‘nervous colon’ and ‘irritable colon’
 There is absence of inflammation; it should
not be confused with Crohn’s or Ulcerative
colitis
 (It is not as severe - there are no structural or
biochemical defects identified)
IBS (continued)
 Etiologic / risk factors - three main functional
abnormalities: 1. altered GI motor activity;
2. visceral hypersensitivity; 3. altered
processing of information by the nervous
system
IBS (continued)
 Clinical Manifestations - Abdominal pain that
is relieved by a bowel movement, bloating,
distention, passage of mucus, changes in
stool form (hard or loose and watery),
alterations in stool frequency, or difficulty in
passing a movement
 Medical Management - Dx - history; no test.
 Rx aimed at symptoms, lifestyle changes
(dietary), stress reduction, behavior therapy
(to identify and reduce triggers)
Diverticular Disease
 Diverticulosis - outpouchings in intestinal wall,
uncomplicated
 Diverticulitis - inflammed outpouching,
complicated
 Asymptomatic in 80% of people with
diverticulosis; when inflammed - severe pain
 Treatment to relieve symptoms, prevent
diverticulitis; if diverticulitis may need antibiotics
and complete rest of colon with naso gastric tube
feedings and IV fluids until inflammatory process
has been resolved
Diverticular disease (clarified)
 *outpouching is called diverticula
 The presence of diverticula in wall of colon or
small intestine describes the herniation of
mucosa through the muscles of the colon
 It is when food particles or feces become
trapped in diverticula and become infected
and inflammed >>> diverticulitis
 Rarely reversible
Neoplasms
 Intestinal Polyps - growth or mass in wall of intestines
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Benign Tumors (most common adenomas, leiomyomas,
lipomas) - Rarely become malignant; only need to be
treated if causing symptoms
Malignant Tumors
Adenocarcinoma - (colorectal cancer) second leading
cause of cancer death in US men and women combined;
they have a long pre-invasive phase; few early warning
signs - rely on medical screening with colonoscopy;
persistent change in bowel habits is the single most
consistent symptom
Rx: surgical removal
Obstructive Disease
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Definition & Incidence - anything that reduces the
size of the gastric outlet, preventing normal flow of
chyme and delaying gastric emptying
Leads to: distention, cramping pain, tenderness that
progresses to point of being constant, vomiting due
to reflux, constipation, signs of dehydration,
hypovolemia
After ~ 24 hours of complete obstruction, impaired
blood supply can lead to necrosis and strangulation;
can cause fever, leukocytosis, peritoneal signs or
blood in feces
Obstructive Disease (continued)
 Three causes: Organic, mechanical, functional
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1. Organic: due to another condition
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2. Mechanical Obstruction
Adhesion - scar tissue from surgeries
Intussusception - telescoping of intestines on
itself (Figure 16-17)
Volvulus - twisting
Hernia - protrusion of intestines through the
groin, abdomen, navel (weakness in muscle
and connective tissue normally containing it)
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3. Functional Obstruction
Adynamic or Paralytic Ileus - neurologic or
muscular impairment of peristalsis
Oglvie’s Syndrome - Acute colonic pseudoobstruction early postoperatively
following trauma to hip, pelvis, or after
elective hip or pelvic surgery; etiology
unknown - but thought to be related to
disruption to sacral parasympathetic nerves
(S2-S4 supply colon and rectum)
Congenital Conditions
 Stenosis & Atresia - stenosis - narrowing of
small intestine; atresia is a defect
caused by incomplete formation of lumen
 Meckels Diverticulum - outpouching of the
bowel located at the ileum of small
intestine
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Definition & Incidence - inflammation of the
vermiform appendix that often results in necrosis and
perforation and subsequent peritonitis
Etiologic / risk factors - 1/2 no known cause; 1/3
due to obstruction of some type that prevents
drainage (what is the other 1/6 is caused by?)
Pathogenesis - obstruction -> infection; or just
infection
Clinical Manifestations - constant pain RLQ, n&v ;
children - fever; adults - mild fever; aggravated
by anything that increase abdominal pressure
Can present atypically
“Pinch an inch” test > rebound test
Medical Management - remove appendix
Peritonitis
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Definition & Incidence - inflammation of peritonium –
serous membrane lining the wall of abdominal cavity; if
spontaneous >primary; if due to trauma, surgery,
peritoneal contamination from a perforation > secondary.
Etiologic / risk factors - primary ?; secondary, trauma,
surgery, GI issue that leads to perforation
Clinical Manifestations - decreased GI motility and
distention with gas; vague generalized abdominal pain; as
progresses becomes severe pain and abdomen becomes
rigid (involuntary guarding), n&v, fever
Medical Management - infection control, and treat
consequences
Rectal (or anal) Fissure
 Ulceration or tear of lining of the anal canal usually caused by excessive tissue stretching
or tearing such as during childbirth or a
large, hard bowel movement; tends to reopen frequently
 Heal within a month or two - may need stool
softeners to help facilitate healing by
preventing re injury
Rectal Abscesses and Fistulas
 Abscesses (infection) or fistula (opening) can
occur as a result of an infected anal gland,
fissure or prolapsed hemorrhoid and are
most common in people with Crohn’s disease
Hemorrhoids “piles”
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Varicose veins of a pillow like cluster of veins
that lie just beneath the mucus membrane
at the lowest part of the rectum - associated with
anything that increases intra-abdominal
pressure (Box 16-1); internal hemorrhoids may
require ligation (tying up), sclerosing (shrinking
the vessels) , laser or cryosurgery to destroy the
tissue; external can be treated with local
applications of topical medications, high fiber
diet, avoidance of constipation
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1. The Digestive System Diagram, Organs, Function, and
More - WebMD
www.webmd.com/digestive-disorders/digestive-system
2. Upper GI Tract Anatomy - eMedicine World Medical
Library
emedicine.medscape.com/article/1899389-overview
3. Gut. 2004 February; 53(2): 310–311.
4. Evolution Of The Human Appendix: A Biological
'Remnant' No More
www.sciencedaily.com/releases/2009/08/090820175901.
htm
5. Achalasia — Diagnosis and treatment at Mayo Clinic
www.mayoclinic.org/achalasia/
Emotional Support Animals
Andrea C. Mendes PT, DPT
Sean M. Collins PT, ScD