MEDICAL-SURGICAL
ACHALASIA
ACHALASIA
i.
About the disease
ii.
Pathophysiology/Pathogenesis
iii.
Clinical Presentation (Signs/Symptoms)
iv.
Assessment/Diagnostic Findings
v.
Classifications
vi.
Complications
vii.
Treatment/Management
ABOUT THE DISEASE
Achalasia is absent or ineffective peristalsis of the distal
esophagus accompanied by failure of the esophageal
sphincter to relax in response to swallowing.
Deglutition (swallowing) initiates a peristaltic wave down
the esophagus and also triggers the relaxation of the
LES (lower esophageal sphincter) allowing food to enter
the stomach.


Achalasia is Greek for “does not relax”
Patients primarily present with
regurgitation and dysphagia
Epidemiology:
 Affects males and females equally
 Presents ages 25-60
 progress slowly and occurs most often in people
40 years or older
CLINICAL PRESENTATION

The main symptom is dysphagia (solids and
liquids).

May also report non-cardiac chest or epigastric
pain

Pyrosis (heartburn) that may or may not be
associated with eating

Secondary pulmonary complications may result
from aspiration of gastric contents

Regurgitation (spitting food without force)

Difficult belching (expelling excess air from
upper digestive tract)

Chest pain (angina)

Heartburn

+/- weight loss (mild only)
ASSESSMENT/DIAGNOSTIC FINDINGS
PATHOPHYSIOLOGY/PATHOGENESIS


Loss of ganglion cells within the myenteric
(Auerbach's) plexus (longer the disease the
fewer ganglion cells present)
Loss of inhibitory (NO) ganglion function
resulting in impaired relaxation. Intact
cholinergic (excitatory)
 Use of CXR (chest radiograph)
Result:

Widened mediastinum and absence
of gastric bubble

shows esophageal dilation above
the
narrowing
at
the
gastroesophageal junction

CCK (cholecystokonin) octapeptide test

Possible autoimmune disease(viral insult)
involving latent HSV-1

Likely genetic component

Allgrove Syndrome(AAA): rare autosomal
recessive disorder associated with AchalasiaAddisonianism-Alacrimia
 Manometry (confirmatory test)
 Barium swallow (primary screening)
CLASSIFICATIONS
*BIRD-LIKE BEAK APPEARANCE

Type I: Classic achalasia

Type II: Achalasia with compartmentalized
panesophageal pressurization (>30mmHg)

Type III: Achalasia with spastic contractions
(with or without compartmentalized
pressurization)
*Type II and III=“vigorous achalasia”
Historical correlation: Chest pain more prevalent with
Type II and III

 EGD
(Esophagogastroduodenoscopy)




Recommended in all achalasia
patients to rule out malignancy
or “pseudoachalasia” (excessive
weight loss loss, symptoms <
6mos, >60 years old)
Examine cardia of stomach well
for malignancy
Dilated esophagus with retained
food
Esophageal stasis predisposes
to candida esophagitis

Type I- Heller myotomy

Type II- good response to all therapy

Type III- poor response to all therapy
*Felt that Type I represents progression from
Type II
 Esophageal decompensation after prolonged outlet
obstruction and continued destruction of myenteric
plexus
 Treat early to try to prevent progression to Type I
COMPLICATIONS
 Aspiration PNA (pneumonia)
 Epiphrenic diverticulum
In standard manometry,

Elevated LES pressure (usually >45mmHg)

Incomplete LES relaxation (normal <8mmHg)

Aperistalsis (there can still be contractions)
 SCC (squamous cell carcinoma) >
Adenocarcinoma


16 fold increase
Presents approximately 15
years after diagnosis of
achalasia
TREATMENTS
*The patient is instructed to eat slowly and to
drink fluids with meals.

VIGOROUS Achalasia:
most contractions in Achalasia are
low amplitude but some patient’s
have highamplitude contractions (3760mmHg)

Nitrates and CCB (Nifedipine);
relaxes the smooth muscle

Used for patient’s unwilling
or unable to undergo more
invasive therapy

Variable success

If standard manometry has 3-8 sensors at 3-5 cm apart,

HIGH RESOLUTION MANOMETRY
has 36 sensors at 1 cm apart
Medical Therapy
Botulinum Toxin
Injected into LES (25units in 4
quadrants)

Poisons the excitatory
(acetylcholine) neurons

Success rates of 80% however
relief wanes gradually to 41% at
12 mos. Requires repeat
injections

Increases intraoperative
perforation and myotomy failure
 Presence of low LES pressure or dilated
esophagus predicted higher rate of
failure with Heller
 High cost, longer recovery, GERD

Complication rate is higher if surgical
myotomy performed after endoscopic
therapy


Pneumatic dilation and Heller are
comparable
Dilation
1. Bougie

Temporary relief but lower risk
of perforation
2. Pneumatic



Forceful dilation, tears muscle
fibers
Stepwise approach: 3.0cm >3.5cm ->4.0cm
High success rate (85%)

1.6% perforation rate
 Gradual waning of success rate with repeat
dilations
 Consider additional therapy for persistent
dysphagia after 2-3 dilations

Consider PPI therapy
 The procedure can be painful; therefore,
moderate sedation in the form of an
analgesic or tranquilizer, or both, is given for
the treatment

Surgical Myotomy (Heller and
Open myotomy)

LES is cut
 Often partial wrap (Dor or Toupet
fundoplication) to prevent reflux (No
nissen, worse dysphagia)

High success rates (Open, 70%-85% at
10 years and 65-73% at 20-30 yrs) and
low recurrence
TREATMENT ALGORITHM
MEDICAL-SURGICAL
GASTROESOPHAGEAL REFLUX DISEASE (GERD)
GERD
i.
ii.
iii.
iv.
v.
vi.
vii.
viii.
About the disease
Epidemiology
Risk factors
Pathophysiology/Pathogenesis
Clinical Presentation (Signs/Symptoms)
Assessment/Diagnostic Findings
Complications
Treatment/Management
 Incidence in similar between men and women
 About 50% of pregnant women will experience
GERD; can also occur in infants
*Pregnancy causes enlargement of uterus
which causes changes in the LES through
stomach uplift
RISK FACTORS
ABOUT THE DISEASE

 A fairly common disorder marked by
backflow of gastric or duodenal contents
into the esophagus that causes
troublesome symptoms and/or mucosal
injury to the esophagus.




Pyrosis frequency of more than 2 times per week is
sometimes used as a criteria for GERD

Hydrochloric acid (which are produced by parietal
cells) has a pH level of or less than 4 which
damages the lumen of the stomach

Differential diagnosis of GERD chest pain: acute
myocardial infarction

Smoking
Excessive caffeine intake

Episodic pyrosis (heartburn) that is not
frequent enough or painful enough to be
considered bothersome by the patient is not
included in the above consensus GERD
definition
Alcohol use

 A condition that occurs when refluxed
stomach contents lead to troublesome
symptoms and/or complications

Obesity (BMI ≥ 30)
Fitting clothes
Respiratory diseases
gastric infection with Helicobacter pylori
PATHOPHYSIOLOGY/PATHOGENESIS

 Excessive reflux may occur because of an
incompetent lower esophageal sphincter,
pyloric stenosis, hiatal hernia, or a motility
disorder.
 Symptoms of GERD vary in severity, duration,
and frequency.
Key Factors in the Development of GERD
 When the esophagus is repeatedly
exposed to refluxed material for prolonged
periods of time, inflammation of the
esophagus (esophagitis) occurs, and in
some cases it can progress to erosion of
the squamous epithelium of the esophagus
(erosive esophagitis) and may lead to other
complications.
EPIDEMIOLOGY
 A decrease in lower esophageal
sphincter (LES) pressure
 Decreased clearance of gastric contents
from the esophagus
 Decreased mucosal resistance in the
esophagus
 Composition of reflux contents “extra acidic”
 The incidence of GERD seems to increase with
aging and is seen in patients with irritable
bowel syndrome and obstructive airway
disorders (asthma, COPD, cystic fibrosis)
 Heartburn is the most frequent clinical
complaint
 Most frequently occurs in adults over 40 years
of age
Gastric fluid that has a pH < 4 is
extremely caustic to the esophageal
mucosa.
 Decreased gastric emptying (increased
gastric emptying time)
 Certain anatomic features
 Most commonly a hiatal hernia
THIRD CATEGORY:
EXTRASOPHAGEAL/ATYPICAL
CLINICAL MANIFESTATIONS
Symptoms may include:
 pyrosis (heartburn, specifically more
commonly described as a burning
sensation in the esophagus)
 dyspepsia (indigestion)
 regurgitation
These symptoms have an association with GERD but
causality should only be considered if a concomitant
esophageal symptoms are present:



Chronic cough
Asthma-like symptoms
About 50% of those with asthma have
GERD
 dysphagia (difficulty swallowing) or
odynophagia (painful swallowing)

Laryngitis/Hoarseness

Recurrent sore throat

Dental enamel erosion
 hypersalivation
 esophagitis
*concomitant – associated to or of; occurring
*Symptoms may mimic those of a heart
attack.
*Angina present in GERD may have a
differential diagnosis as in acute
myocardial infarction
Aggravating Factors (makes condition
worse):
o
Recumbency (leaning, resting, or
reclining)
o
Increased intra-abdominal pressure
1. Typical or “CLASSIC” symptoms
o
Reduced gastric motility
2. ALARM (Complicated) symptoms
o
Decreased LES tone or pressure
3. EXTRASOPHAGEAL (ATYPICAL)
symptoms
o
Direct mucosal irritation
GERD symptoms are grouped in three
categories:
FIRST CATEGORY: TYPICAL OR CLASSIC

at the same time
Pyrosis (heartburn)
* Hallmark symptom
*A substernal feeling of warmth or burning rising
up from the abdomen that may radiate to the
neck
Foods that decrease LES pressure










fatty foods
peppermint
spearmint
chocolate
coffee
cola
tea
garlic
onions
chili peppers

Regurgitation/Belching
Medications that decrease LES pressure

Acid brash/hypersalivation

Chest pain (non-cardiac in nature)














SECOND CATEGORY: ALARM SYMPTOMS
*Any of these symptoms warrant immediate referral
for testing:

Dysphagia (difficulty swallowing)

Odynophagia (painful swallowing)

Bleeding

Unexplained weight loss

Choking (hand across the neck)

Chest pain (if could be cardiac in nature)
anticholinergics
barbiturates
benzodiazepines
caffeine
dihydropyridine
calcium channel blockers
dopamine
estrogen
ethanol
narcotics
nicotine
nitrates
progesterone
theophylline
Foods that are direct irritants to the
esophageal mucosa




Spicy foods
orange juice
tomato juice
coffee
Medications that are direct irritants to
esophageal mucosa






Oral bisphosphonates
Aspirin
Iron
NSAIDs
Quinidine
potassium
ASSESSMENT/DIAGNOSTIC FINDINGS
CLINICAL HISTORY
*The patient’s history aids in obtaining an
accurate diagnosis.
*Patients presenting with extraesophageal or atypical
symptoms should be reviewed on a case-by-case basis
to be considered for testing
*Alarm symptoms always warrant further testing
*Patient’s description of typical or classic GERD
symptoms such as pyrosis, is often enough to
consider GERD as an initial diagnosis
ENDOSCOPY

Endoscopy is the technique of choice
to identify complications of GERD such
as ulcerations, erosions, Barrett’s
esophagus, etc.

Biopsy of the esophageal tissue is
needed to identify and diagnose
Barrett’s esophagus and esophageal
adenocarcinoma

Many patients with GERD (presenting
with typical or atypical symptoms) will
have normal appearing esophageal
mucosa on endoscopy

Usually not part of the work-up except
in certain subsets of patients (alarm
symptoms,
those
refractory
to
treatment, etc.)
BARIUM SWALLOW/RADIOGRAPHY

Evaluates damage to the esophageal
mucosa

Not routinely used to diagnose GERD
due to a lack of sensitivity and specificity

Can detect hiatal hernia
COMPLICATIONS
GERD can result in:
 dental erosion
 ulcerations in the pharynx and esophagus
 laryngeal damage
 esophageal strictures
 adenocarcinoma
 pulmonary complications
BARRET’S ESOPHAGUS

Barrett’s esophagus occurs when the normal
squamous cell epithelium in the esophagus
converts to a columnar cell epithelium
(intestinal-type epithelium)

More common in men than women

Barrett’s esophagus does not cause specific
symptoms but the reflux does

Those with Barrett’s esophagus develop
adenocarcinoma of the esophagus at a rate of
0.12% per year

Gender ratio for esophageal adenocarcinoma is
8:1 (male:female)

Patients must be monitored via endoscopy to
evaluate changes in cell type and conversion to
adenocarcinoma

BE is a condition in which the lining of the
esophageal mucosa is altered.
AMBULATORY pH MONITORING
(12-36 HOURS)

Used to evaluate the degree of acid
reflux

Esophageal pH monitoring was
historically
an
uncomfortable
procedure, but the advent of wireless
capsule pH monitoring is better
tolerated and quite accurate.


Identifies patients with excessive
esophageal acid exposure and helps
determine if symptoms are acid related
Useful in patients not responding to
acid-suppression therapy
TREATMENT/MANAGEMENT
The initial treatment used is determined by the patient’s
condition:

Frequency of symptoms

Degree of symptoms

Presence and/or degree of esophagitis

Presence of complications
Goals of Treatment:
ANTACIDS

Alleviate or eliminate acute symptoms

Decrease frequency of recurrence

Promote healing if esophageal tissue injury is
present

Prevent complications
Mode of action:
Neutralizes hydrochloric acid in the
stomach, which results in an increase in
gastric pH
Agents:
1. Magnesium hydroxide
2. Aluminum hydroxide
NON-PHARMACOLOGIC THERAPIES
3. Calcium carbonate
Lifestyle modifications
 Should be incorporated into the management of
GERD regardless of the severity of disease

Monitoring:
Lifestyle modifications should be tailored to an
each individual patient’s needs
Periodic calcium and phosphate levels if on
chronic antacid therapy
Anti-reflux surgery

Patient interventions:
Used as a last resort option in select patients
 When long-term pharmacologic therapy is
undesirable

Antacids can decrease the levels of
numerous other drugs including
tetracycline,
digoxin,
iron
supplements, fluoroquinolones, and
ketoconazole.

Patients should separate antacids
and other medications by at least 2
hours

Patients with renal impairment
should not use aluminum or
magnesium containing antacids
unless directed by their physician

Onset of relief is less than 5 minutes
and duration of relief is 20 to 30
minutes
 Who have refractory GERD
 Have complications
Endoscopic therapies

Results have been disappointing and hence are
not usually recommended
LIFESTYLE MODIFICATIONS


Weight loss (if the patient is overweight or
obese)
Elevation of the head of the bed 6 to 8 inches or
30 degrees

ANTACIDS-ALGINIC ACID COMBINATION
Eat smaller, more frequent meals (as opposed
to larger meals less frequently)
Mode of action:

Include protein-rich meals in diet (increases LES
pressure)

The antacid neutralizes stomach acid and
the alginic acid is a foaming agent that
creates a viscous solution that floats on top
of the stomach contents and may be
protect the esophagus from refluxed
stomach acid.
Avoid eating 2-3 hours prior to sleeping or lying
down

Avoid foods or medications that exacerbate
GERD
Agents:

Avoid alcohol
1. Aluminum hydroxide

Tobacco cessation
2. Magnesium carbonate

The patient is instructed to eat a low-fat diet
3. Alginic acid (Gaviscon)
PHARMACOLOGIC MANAGEMENTS

Antacids and alginic acid products
H2-RECEPTOR ANTAGONISTS

H2-receptor antagonists (HRA)
Mode of action:

Proton pump inhibitors (PPIs)

Competitive inhibition of histamine at H2 receptors of
gastric parietal cells which inhibits gastric acid
secretion
Promotility agents
.
Agents:
Common adverse effects:
 headache
1. Cimetidine
(Tagamet)

dizziness
2. Famotidine (Pepcid)

somnolence
3. Nizatidine (Axid)

diarrhea
4. Ranitidine (Zantac)

constipation

flatulence

abdominal pain

nausea
(Possible) Adverse effects:

headache

somnolence (drowsiness)

fatigue

dizziness

Increased risk of Clostridium difficile infections

constipation

Increase risk of community-acquired pneumonia

diarrhea
Serious side effects:
Long-term adverse effects:
Monitoring:
Monitor for CNS effects (rare) in those over 50
years old or in those with renal or hepatic
impairment.
Patient interventions:

Hypomagnesemia

Bone fractures

Vitamin B12 deficiency
Monitoring:

If taking once a day, it is preferable to take the
dose at bedtime.

Appearance of diarrhea (frequency and type of
diarrhea episodes)

Onset of relief is 30 to 45 minutes and duration of
relief is 4 to 10 hours.

Periodic magnesium levels (if long-term therapy)

Routine bone density studies (DXA scans)
PROTON PUMP INHIBITORS (PPI)
*If other risk factors for osteoporosis or bone
fractures present
Mode of action:
Blocks acid secretion by inhibiting gastric H+/K+
adenosine triphosphates found on the secretory surface
of gastric parietal cells
Results in a long-lasting anti-secretory effect that can
maintain gastric pH levels above 4
Agents:
Patient interventions:

Preferable to take a PPI 30 to 60 minutes before
a meal (mainly breakfast)

If a second dose is needed, take prior to the
evening meal

Onset of relief is 2 to 3 hours and the duration of
relief is 12 to 24 hours
1. Dexlansoprazole (Dexilant) *most effective
2. Esomeprazole (Nexium)
PROMOTILITY AGENTS
3. Lansoprazole (Prevacid)

Promotility agents, such as metoclopramide and
bethanechol, have been used as adjunct therapy
to acid suppression agents such as PPIs in
patients who have a known motility defect.

However, they are not generally recommended to
be used for GERD treatment due to their limited
effectiveness and undesirable adverse effect
profiles.
4. Omeprazole (Prilosec)
5. Omeprazole/sodium bicarbonate (Zegerid)
6. Pantoprazole (Protonix)
*used to avoid interactions with
other drugs
7. Rabeprazole (Aciphex)
PPIs V. H2-RECEPTOR ANTAGONISTS

Symptomatic improvement as well as endoscopic
healing rates are higher for the PPIs compared to
the H2-receptor antagonists.

PPIs are therefore preferred over H2-receptor
antagonists in patients with erosive disease,
moderate to severe symptoms, or with
complications.
PPIs in Children greater than 1 year of age


15mg per day is recommended for children
weighing < 30kg

30mg per day is recommended for children
weighing > 30kg
MAINTENANCE THERAPY
Q: What patients should receive
maintenance therapy?
o Those with a history of complications (e.g.
Barrett’s esophagus, strictures, hemorrhage,
ulcerations, etc.)

Long-term maintenance therapy with
PPIs at the lowest possible dose


If NERD/uncomplicated GERD, try to
manage with on-demand or intermittent
PPI therapy or H2-receptor antagonists
Esomeprazole

Dosed 10 to 20mg a day for children 1 to 11 years
old

Dosed at 20 to 40mg a day for children 12 to 17
years old
*Can consider intermittent or on
demand PPI therapy in some
circumstances
o Those with symptomatic relapse following
discontinuation of the drug or a decrease in dose.
Lansoprazole

Omeprazole

5mg daily in children weighing between 5 and
10kg

10mg daily in children weighing between 10 and
20kg

20mg daily in children weighing ≥ 20kg
ELDERLY PATIENTS
PATIENTS WITH EXTRAESOPHAGEAL
(ATYPICAL) GERD
Patients with atypical symptoms may need higher
doses of acid suppression therapy with longer
treatment duration compared to those patients
with typical symptoms.
A PPI trial is recommended to treat
extraesophageal symptoms in patients who have
typical GERD symptoms as well
Reflux monitoring should be considered before a
PPI trial in patients with extraesophageal
symptoms who do not have typical GERD
symptoms.
1. Many elderly patients have decreased defense
mechanisms such as decreased saliva
production
2. PPI therapy may be warranted for those > 60
years of age with symptomatic GERD
3. They have superior efficacy and have once a day
dosing
4. Long-term risk of bone fractures is a concern and
elderly
patients
should
be
monitored
appropriately
5. Elderly are at higher risk of being sensitive to
possible CNS effects of H2-receptor antagonists
PEDIATRIC PATIENTS
1. A suspected cause of reflux in infants is
a developmentally immature LES
PATIENTS WITH REFRACTORY GERD
2. Many infants have reflux with little or no
clinical consequence
1. Refractory GERD should be considered in
patients who have not responded to a standard
course of twice a day PPI therapy
3. This uncomplicated reflux usually
manifests as regurgitation or spitting up
2. The majority of patients with refractory symptoms
experience nocturnal acid breakthrough
4. Usually responds to supportive therapy
3. Switching to a different PPI may be effective in
some patients
5. Chronic vomiting associated with GERD
must be carefully evaluated and
distinguished from other causes.
6. Careful consideration should be given before a
medication is recommended
7. When a medication is deemed necessary,
ranitidine dosed at 2 to 4mg/kg twice a day is
often used
8. PPIs are increasing being used in children older
than 1 year
9. Lansoprazole, esomeprazole, and omeprazole
are indicated for treating symptomatic and
erosive GERD in children greater than 1 year old
10. Omeprazole has been used off-label in children
less than 1 year old at a dose of 1mg/kg/day.
4. Adding an H2-receptor antagonist at bedtime for
nocturnal symptoms is reasonable but the effect
may decrease over time due to tachyphylaxis with
H2-receptor antagonists
MEDICAL-SURGICAL
HIATAL HERNIA
HIATAL HERNIA
i.
About the disease
ii.
Epidemiology
iii.
Risk factors
iv.
Pathophysiology/Pathogenesis
v.
Types
vi.
Clinical Presentation (Signs/Symptoms)
vii.
Assessment/Diagnostic Findings
viii.
Complications
ix.
Treatment/Management
x.
Gerontologic Considerations

Size of hiatus not fixed, narrows with
increase in intraabdominal pressure

Tear of the phrenoesophageal ligament
Phrenoesophageal ligament is a fibrous
layer of connective tissue and maintains
the LES within the abdominal cavity.
ABOUT THE DISEASE
Hiatal hernia is a condition where the opening in the
diaphragm through which the esophagus passes
becomes enlarged, and part of the upper stomach moves
up into the lower portion of the thorax.

Can be referred as:
Diaphragmatic hernia and esophageal
hernia
*Most common abnormality found on upper GI x-ray

A hiatal comprises reflux barrier

Reduces LES pressure

Reduced esophageal acid clearance

Transient
LES
relaxation
particularly at night time
episodes
TYPES
EPIDEMIOLOGY
*There are two major types of hiatal hernia.
*More common in older adults and in women
First type: SLIDING or type I
RISK FACTORS

Increasing age



Stomach slides through hiatal opening in
diaphragm when patient is supine, goes back
into abdominal cavity when patient is standing
upright.
Trauma
Poor nutrition
 The upper stomach and the gastroesophageal
junction are displaced upward and slide in and
out of the thorax.
Forced recumbent position

Congenital weakness
PATHOPHYSIOLOGY/PATHOGENESIS
Hiatal hernia can be due to:
 Structural changes which causes:
Weakening of muscles in diaphragm


Increased intraabdominal pressure which is
caused by:



Obesity
Pregnancy
Heavy lifting

Most common type; about 95% of patients with
esophageal hiatal hernia have a sliding hernia
MEDICAL-SURGICAL
HIATAL HERNIA
ASSESSMENT/DIAGNOSTIC FINDINGS
Second type: PARAESOPHAGEAL
or ROLLING

Esophagogastric junction remains in place, but
fundus and greater curvature of stomach roll up
through diaphragm

Acute paraesophageal hernia is a medical
emergency.

Occurs when all or part of the stomach pushes
through the diaphragm beside the esophagus

Paraesophageal hernias are further classified as
types II, III, or IV, depending on the extent of
herniation.
Diagnoses are typically confirmed by:

X-ray

Barium swallow

Esophagogastroduodenoscopy
(EGD)
…which is the passage of a fiber-optic
tube through the mouth and throat into the
digestive tract for visualization of the
esophagus, stomach, and small intestine
Type IV has the greatest herniation, with other intraabdominal viscera such as the colon, spleen, or small
bowel evidencing displacement into the chest along with
the stomach.
CLINICAL MANIFESTATIONS

Esophageal manometry

Chest CT scan
Symptoms may include:

May be asymptomatic

Heartburn or pyrosis (especially
after meal or when lying supine)

Dysphagia

Regurgitation
*The patient may present with vague
symptoms of intermittent epigastric pain or
fullness after eating.
*Large hiatal hernias may lead to
intolerance to food, nausea, and vomiting.
*Sliding hiatal hernias are commonly
associated with GERD.
*Hemorrhage,
obstruction,
and
strangulation can occur with any type of
hernia.
MEDICAL-SURGICAL
HIATAL HERNIA
3.
Prevent movement of gastroesophageal
junction
COMPLICATIONS
If left untreated, hiatal hernia can lead or cause:

GERD

Esophagitis

Hemorrhage from erosion

Stenosis (fixed narrowing of the esophagus)

Ulcerations of herniated portion

Strangulation of the hernia

Regurgitation with tracheal aspiration

Increased risk of respiratory problems
(shortness of breath or chronic cough)
o
Herniotomy
-
o
Herniorrhaphy
-
o
Excision of hernia sac
Closure of hiatal defect
Gastropexy
-
Attachment of stomach
subdiaphragmatically to prevent
reherniation
TREATMENT/MANAGEMENT

Includes frequent, small feedings that can
pass easily through the esophagus

Patient is advised not to recline for 1
hour after eating, to prevent reflux or
movement of the hernia, and to elevate
the head of the bed on 4- to 8-inch (10to 20-cm) blocks to prevent the hernia
from sliding upward
o
Current guidelines recommend a
laparoscopic approach, with an open
transabdominal or transthoracic
approach reserved for patients with
complications such as bleeding, dense
adhesions, or injury to the spleen.
o
Laparoscopically performed Nissen
and Toupet techniques are standard
anti-reflux surgeries.
Lifestyle modifications:

Eliminate alcohol

Stop smoking

Avoid lifting/straining

Reduce weight, if necessary

Use of anti-secretory agents and antacids as
prescribed by physician
SURGICAL MANAGEMENT
*Surgical hernia repair is indicated in patients who
are symptomatic, although the primary reason for
the surgery is typically to relieve GERD symptoms
and not repair the hernia.
* Surgical repair is often reserved for patients with
more extreme cases that involve gastric outlet
obstruction or suspected gastric strangulation, which
may result in ischemia, necrosis, or perforation of
the stomach
Goals of surgical therapy of hiatal hernia:
1.
2.
Reduce hernia
Provide acceptable lower esophageal
sphincter (LES) pressure
MEDICAL-SURGICAL
HIATAL HERNIA
o
Thoracic
or
open
abdominal
approach is used, depending on the
individual patient.
POST-SURGICAL CONSIDERATIONS
*Up to 50% of patients may experience early
postoperative dysphagia

Advances the diet slowly from liquids to
solids

Managing nausea and vomiting, tracking
nutritional intake, and monitoring weight

*Also
monitors
for
postoperative
belching, vomiting, gagging, abdominal
distension, and epigastric chest pain,
which may indicate the need for surgical
revision
*These
should
be
reported
immediately to the primary provider
GERONTOLOGIC CONSIDERATIONS

Higher Incidence with age

Medications commonly taken by older
patients can decrease LES pressure

LES may become less competent with
aging

First indication may be esophageal
bleeding or respiratory complications
MEDICAL-SURGICAL
NAUSEA AND VOMITING
NAUSEA AND VOMITING
i.
Important notes to follow
ii.
Epidemiology
iii.
General approach in managing nausea and vomiting
iv.
Pathophysiology/Pathogenesis
v.
Treatment/Management
▪ Aim for acceptable control < 3 days
▪ Consider whether dietary/ other factors may help.
✓ Avoiding triggers
IMPORTANT NOTES TO FOLLOW

Vomiting post chemo is much better controlled
than nausea

The evidence for use of anti-emetics is poor
✓ Parenteral fluids
✓ Limiting oral intake, protein meals, low fat diet
✓ Relaxation techniques
✓ Acupuncture point P6
✓ Ginger
✓ Surgery (stents, venting g-tubes)
Intractable nausea and vomiting
 “Nausea and vomiting that is not adequately
controlled after multiple anti-emetics are used in
series and/or in combination”
 Those with the most difficult N&V to manage
tend to be those with altered anatomy. Eg. due
to malignant bowel obstruction (dysfunction) or
stents/surgical interventions
PATHOPHYSIOLOGY/PATHOGENESIS
EPIDEMIOLOGY

Stomach – usually has slow wave contractions
(3/min)

Rate increases with ‘circular vection’

Vasopressin release

Nausea perception related to vasopressin
release

Primates – VP antagonists stop motion sickness

Humans – ginger reduces nausea, vasopressin
rise, reduced tachygastria in motion sickness
trials
GENERAL APPROACH IN MANAGING NAUSEA AND
VOMITING
1) Initially - identify and treat reversible causes
• This may not be appropriate if someone is imminently
dying
2) Assess severity – does the patient need rehydration?
3) Start anti-emetic treatment
a. Prescribe regularly
TREATMENT/MANAGEMENT
b. Review controls every 24-48 hours
A second line anti-emetic is required in 1/3 of patients
4) Consider route of administration
Oral route maybe ineffective as frequent vomiting means
poor absorption
Community options:
Dietary Management
• Protein meal – regulates gastrin release, which
reduces gastric dysrhythmia & nausea
Gastroparesis diet:
• Low fat – fat activates stretch receptors in stomach
fluids
Rectal route: domperidone suppositories
Buccal prochlorperazine
Hysoscine patch
(granisetron patch)
Drugs that help alleviate nausea and vomiting
• Maintains nutrition & hydration
Metoclopramide


Olanzapine orodispersible melt = 5mg strength

▪ Remember N&V is often multi-factorial
Prokinetic
Dopamine 2 antagonist, 5HT4 agonist, 5HT3
antagonist
Central (CTZ) and peripheral action (gut
mucosa)
MEDICAL-SURGICAL
NAUSEA AND VOMITING

Prokinetic effect antagonised by anticholinergic
drugs
Side effects:
 Extrapyramidal
symptoms
 Drowsiness,
restlessness,
depression,
diarrhea
 Max 30mg in 24
hours for up to 5 days – EU review 2013)

Drowsiness, urinary retention, dry mouth,
blurred vision, constipation, headache,
psychomotor impairment

Caution in severe liver disease, severe heart
failure, renal failure, glaucoma
Notes:
▪ Not advocated for use in heart failure
▪ Increases systemic & pulmonary arterial pressures
▪ Increases right & left ventricular filling pressures
▪ Counteract beneficial hemodynamic effects of opioids
in heart failure
Domperidone





Prokinetic
Dopamine 2 antagonist
Acts peripherally and at the CTZ
Does not readily cross the blood brain barrier
Oral only
Hyoscine Hydrobromide / Butylbromide
Side effects:
 Rarely
extrapyramidal
 Hyperprolactinaemia
 Cardiac arrhythmias
 Max dose 10mg TDS (for up to 7 days)
Ondansetron
Haloperidol




Dopamine 2 antagonist, 5HT2a and
α1antagonist
Acts predominantly at the CTZ but also
peripherally (gut mucosa)
First line for biochemical induced N&V
T½ 13 – 35 hours
Side effects:
 Extrapyramidal, hyperprolactinaemia
 Minimal sedation and hypotension
 NB - Prolongation of QT interval
Cyclizine

H1 antagonist and
cholinergic
muscarinic
antagonist

Acts at the
vestibular
apparatus (&
vomiting centre)

Plasma T½ 13 hours
Side effects:








5HT3 antagonist
Acts at CTZ and gut mucosa
Blocks amplifying effect of excess 5HT on vagus
Bowel wall enterochromaffin cells release 5HT
by various stimuli.
Sensitises the vagal afferent nerves
to emetogenic substances via 5HT3 receptors
Early N&V post chemo: First 24hrs after chemo
only
Useful where excessive 5HT released eg
chemotherapy or radiotherapy induced damage
of gut mucosa, bowel distension, renal failure
Side effects:
 Headache
 Flushing
 Constipation
MEDICAL-SURGICAL
NAUSEA AND VOMITING
Aprepitant







Neurokinin-1 receptor antagonist (NK1)
Substance P found widely in the CNS, including
CTZ, VC and GI tract
Chemotherapy increases substance P levels as
well as serotonin release
Antiemetic effects of NK1 antagonism is a
central effect
Effective for delayed Chemo Induced N&V
(>24hrs)
Given alongside 5HT3 antagonist and
dexamethasone
No evidence that it has much role in palliative
care
Side effects:
 Drowsiness, weight gain
 Dry mouth, constipation, hypotension, peripheral
edema
 Less movement disorders than with Haloperidol
Dexamethasone





Glucocorticoid
Reduces permeability of the CTZ and the blood
brain barrier to emetogenic substances
Reduces neuronal content of GABA in the brain
stem
Suggested that antagonism of PGs, release of
endorphins and depletion of tryptophan may
play a role
Central or peripheral effect
Levomepromazine



Dopamine 2 antagonist, Muscarinic cholinergic
antagonist, Histamine 1 antagonist, 5HT2A
antagonist, alpha-adrenergic antagonist
Acts at vomiting centre
Plasma T½ 15 – 30 hours
Side effects:
 Sedation, weakness
 Dry mouth, hypotension, extrapyramidal
symptoms
Summary
 Vomiting is unpleasant and debilitating

There are multiple causes

General measures and drug interventions are
usually successful

It is helpful to understand the receptor basis of

rational prescribing

But we cannot always control all associated
symptoms
Olanzapine





Atypical antipsychotic
Dopamine 1, 2, 3 and 4
antagonists
5HT2A, 5HT2C, 5HT3
and 5HT6 antagonist,
Alpha-adrenergic antagonist, Histamine-1
antagonist, Muscarinic cholinergic antagonist
Acts at the Vomiting Centre
T½ 34 hours (↑ 52 hours in the elderly)
How best to manage?
1. Surgical opinion & document time for audit
*Non-surgical: colic/ high risk perforation or no
colic
2. Antiemetic: Stimulant antiemetic/ Non stimulant
3. Laxative (nonstimulant)
4. Steroid s/c or IV (NNT 6)
5. NG/ antisecretory
6. Fluids
MEDICAL-SURGICAL
NAUSEA AND VOMITING
Medical management of bowel obstruction
Causes of bowel obstruction:
 Intraluminal

Extraluminal

Motility disorders (tumour infiltration, neuropathic
damage to GIT, drugs such as opioids,
NON-PHARMACOLOGICAL STRATEGIES:

Avoiding food with strong tastes and smells

Small but frequent meals

Control of malodour (strong unpleasant smell)
from wounds or ulcers

anticholinergics etc)

Constipation/ fecal impaction
Systematic review of surgery for malignant bowel
obstruction:
• Control of symptoms 42-80%
• Re-obstruction rates 10-50% (most studies did not
describe time scales)
• Wide range of post op morbidity & mortality
Gynaecological Oncology:
• Major surgical mobidity 22% - fistula/ abscess/ PE/
peritonitis/ sepsis
• Perioperative mortality 6%
BRISTOL TOOL CHART
Behavioural approaches (e.g. distraction,
relaxation)

Acupuncture/acupressure
MEDICAL-SURGICAL
GASTROINTESTINAL BLEEDING
GASTROINTESTINAL BLEEDING
i.
About the disease
ii.
Epidemiology
iii.
Risk factors
iv.
Pathophysiology/Pathogenesis
v.
Clinical Presentation (Signs/Symptoms)
vi.
Assessment/Diagnostic Findings
vii.
Treatment/Management
RISK FACTORS
Upper Gastrointestinal Bleeding

Variceal bleeding is UGIB caused by
esophageal or gastric varices. Non-variceal
bleeding is caused by any etiology of UGIB
other than varices.
ABOUT THE DISEASE

Gastrointestinal bleeding (GIB) common clinical
problem

GIB traditionally divided into either upper, lower
or acute and chronic
Can divide causes into: variceal and nonvariceal
Upper gastrointestinal bleeding (UGIB): bleeding from
any source proximal to ligament of Treitz

Despite advances in diagnosis and treatment,
mortality of UGIB remains from 5– 14%
Lower gastrointestinal bleeding (LGIB): bleeding from
any source distal to ligament of Treitz

Mortality higher in patients > 60 yrs old and in
patients with multiple comorbid conditions

20-30% of patients will have two or more
diagnoses of UGIB.

No disease is found in 10-15% of patients
(prognosis is excellent).

Bleeding peptic ulcer disease most common
etiology and is also the most widely studied
It was named after the Austrian physician and anatomist
Wenzel Treitz, who in 1853 first described the ligament as
a thin, triangular, fibromuscular band extending from the
upper, surface of the duodenojejunal junction. It is also
known as the suspensory ligament of the duodenum
because it suspends the duodenojejunal flexure from the
retroperitoneum.
EPIDEMIOLOGY
UGIB is more common than LGIB
UGIB approx. 67/100,000 population
LGIB approx. 36/100,000 population
LGIB:
More common with increasing age
More common in men
Other causes:
 Dieulafoy’s lesion (bleeding dilated vessel that
erodes through the gastrointestinal epithelium
but has no primary ulceration; can any location
along the GI tract).

Gastric Antral Vascular Ectasia (GAVE; also
known as watermelon stomach).

Cameron lesions (bleeding ulcers occurring at
the site of a hiatal hernia).

Post-surgical bleeds (post-anastomotic bleeding,
post-polypectomy bleeding, post-sphincterotomy
bleeding).

Hemobilia (bleeding from the biliary tract).
Mortality rate 2 - 4%
MEDICAL-SURGICAL
GASTROINTESTINAL BLEEDING
Lower Gastrointestinal Bleeding

Diverticulosis (colonic wall protrusion at the site
of penetrating vessels; over time mucosa
overlying the vessel can be injured and rupture
leading to bleeding).

Angiodysplasia (an abnormal condition of blood
vessels of the gastrointestinal tract and
especially the intestine in which vessels are thin,
fragile, and enlarged)

Infectious Colitis

Ischemic Colitis

Inflammatory Bowel Disease

Colon cancer
CLINICAL PRESENTATION

Hemorrhoids

Anal fissures (narrow opening or crack of
considerable length and depth usually occurring
from some breaking or parting)
Haematemesis
Vomiting of blood whether fresh and red or digested and
black.
Melaena
Passage of loose, black tarry stools with a characteristic
foul smell.

Rectal varices
Coffee ground vomiting
Blood clot in the vomitus.

Dieulafoy’s lesion (a medical condition
Hematochezia
Passage of bright red blood per rectum, usually indicates
bleeding from the lower GI tract, but can occasionally be
the presentation for a briskly bleeding upper GI source
characterized by a large tortuous arteriole most
commonly in the stomach wall (submucosal) that
erodes and bleeds)


Radiation colitis
Post-surgical (post-polypectomy bleeding, post
*The presence of frank bloody emesis suggests more
active and severe bleeding in comparison to coffeeground emesis.
*Lower GI bleeding classically presents with
hematochezia, however bleeding from the right colon or
the small intestine can present with melena.
biopsy bleeding)
PATHOPHYSIOLOGY/PATHOGENESIS
*Bleeding from the left side of the colon tends to present
bright red in color, whereas bleeding from the right side
of the colon often appears dark or maroon-colored and
may be mixed with stool.
*Majority of patients with UGIB will spontaneously cease.
*70-80% will stop within first 48 hrs of onset; of those 1020% will have recurrence of UGIB. At initial presentation
approximately 20% will continue to bleed.
*Mortality greatest in these patients and also patients
that have recurrent bleeding
DIFFERENTIAL DIAGNOSIS

Occasionally, hemoptysis may be confused
for hematemesis or vice versa.

Ingestion of bismuth containing products or
iron supplements may cause stools to
appear melanic.

Certain foods/dyes may turn emesis or stool
red, purple, or maroon
MEDICAL-SURGICAL
GASTROINTESTINAL BLEEDING
ASSESSMENT/DIAGNOSTIC FINDINGS
Initial Evaluations

Monitor hemodynamic status; look for signs of
hemodynamic instability
Resting tachycardia: associated with the loss of less
than 15% total blood volume
Orthostatic Hypotension: carries an association with
the loss of approximately 15% total blood volume
Supine Hypotension: associated with the loss of
approximately 40% total blood volume
Confirm UGI source of bleeding by:

history (hematemesis – fresh blood or coffee
ground emesis, melena)

Nasogastric aspiration is 80% sensitive for
actively bleeding UGI source
*False negative aspirates occur when the
tube is improperly positioned or when
reflux of blood from a duodenal source
prevented
by
pylorospasm
or
obstruction
Acute management of UGIB typically involves:

Assessment of the appropriate setting

Resuscitation

Supportive therapy

Investigating the underlying cause and
attempting to correct it.
Setting
Intensive Care Unit
*Patients with hemodynamic instability, continuous
bleeding, or those with a significant risk of
morbidity/mortality should undergo monitoring in an
intensive care unit to facilitate more frequent observation
of vital signs and more emergent therapeutic intervention.
*Most patients with GI bleeding will require
hospitalization. However, some young, healthy patients
with self-limited and asymptomatic bleeding may be
safely discharged and evaluated on an outpatient basis.
Resuscitation
Things to consider:
Laboratory Evaluations

Complete blood count

Hemoglobin/Hematocrit

INR, PT, PTT (International Normalized Ratio,
Prothrombin Time, Partial Thromboplastin Time)

Liver and renal function tests

Nothing by mouth

Adequate IV access - at least two large-bore
peripheral IVs or a centrally placed.

Provide supplemental oxygen if patient
hypoxic (typically via nasal cannula, but
patients with ongoing hematemesis or altered
mental status may require intubation).
Fluid/s:
TREATMENT/MANAGEMENT
Risk Stratification
Specific risk calculators attempt to help identify patients
who would benefit from ICU level of care; most stratify
based on mortality risk.
The Rockall Score calculate the mortality rate of upper
GI bleeds. There are two separate Rockall scores; one is
calculated before endoscopy and identifies preendoscopy mortality, whereas the second score is
calculated post-endoscopy and calculates overall
mortality and re-bleeding risks.
 IV fluid resuscitation (with Normal Saline
or Lactated Ringer’s solution)

Type and Cross matching
Transfusions:
RBC transfusion; typically started if hemoglobin is
< 7g/dL, including cardiac patients.
Platelet transfusion; started if platelet count <
50,000.
Prothrombin complex concentrate; if INR > 2
Medications:
PPIs: Bolus (80 mg), followed by maintenance (8
mg/kg/hr) 3-5 days-significant benefit in decreasing
recurrent bleeding.
Vasoactive medications: Somatostatin and its analog
octreotide can be used to treat variceal bleeding by
inhibiting vasodilatory hormone release.
Erythromycin: Given to improve visualization at the time
of endoscopy.
Antibiotics: Considered prophylactically in patients with
cirrhosis to prevent SBP, especially from endoscopy
MEDICAL-SURGICAL
GASTROINTESTINAL BLEEDING
Anticoagulant/antiplatelet agents: Should be stopped if
possible in acute bleeds. Consider the reversal of agents
on a case-by-case basis dependent on the severity of
bleeding and risks of reversal.
Thermal:
Multipolar
electrocautery
/
electrocautery and Argon plasma coagulation
Other procedures:
Placement of a sengestaken tube should be considered
in patients with hemodynamic instability/massive GI
bleeds in the setting of known varices, which should be
done only once the airway is secured.
Injection: Epinephrine
Mechanical: Band Ligation, Hemoclips (Endoclip)
This procedure carries a significant complication risk
(including arrhythmias, gastric or esophageal perforation)
and should only be done by an experienced provider.
Endoscopy

Can be diagnostic and therapeutic. It is the test of
choice for identifying and treating the bleeding
lesion

Allows visualization of the upper GI tract (typically
including from the oral cavity up to the
duodenum) and treatment with injection therapy,
thermal coagulation, hemostatic clips/bands or
band ligation.

No role for barium studies in acute UGIB

Greatest benefit in the ~20% of patients with
continued or recurrent bleeding

Improve morbidity and
decreased by nearly 30%.
mortality:
mortality

Active bleeding can be controlled in 85-90% of
patients, with less than 3% complication rate.

Should be done within 12-24 hrs.
Endoscopic Management:
Several endoscopic therapeutic techniques available
to attempt hemostasis in patients with UGIB
Algorithm
bipolar
MEDICAL-SURGICAL
GASTRITIS
GASTRITIS
i.
About the disease
ii.
Epidemiology
iii.
Risk factors
iv.
Pathophysiology/Pathogenesis
v.
Types
vi.
Clinical Presentation (Signs/Symptoms)
vii.
Assessment/Diagnostic Findings
viii.
Treatment/Management
PATHOPHYSIOLOGY/PATHOGENESIS

The impaired mucosal barrier allows corrosive
HCL, pepsin, and other irritating agents (e.g.,
NSAIDs and H. pylori) to come in contact with the
gastric mucosa, resulting in inflammation.

Described as a discontinuity in gastric and
duodenal mucosa exposed to acid or pepsin.

Loss of balance between mucosal protective
mechanism and aggressive factors of acid and
pepsin production.

In acute gastritis, this inflammation is usually
transient and self-limiting in nature. Inflammation
causes the gastric mucosa to become edematous
and hyperemic (congested with fluid and blood)
and to undergo superficial erosion. Superficial
ulceration may occur as a result of erosive
disease and may lead to hemorrhage

In chronic gastritis, persistent or repeated insults
lead to chronic inflammatory changes, and
eventually atrophy (or thinning) of the gastric
tissue.
ABOUT THE DISEASE
Microscopic evidence of inflammation affecting the
gastric mucosa
Gastritis is characterized by a disruption of the mucosal
barrier that normally protects the stomach tissue from
digestive juices (e.g., hydrochloric acid [HCl] and pepsin)
EPIDEMIOLOGY

It affects women and men about equally and is
more common in older adults
RISK FACTORS
Primary Gastritis:

10% occurrence in western Countries

Up to 100% in under developed countries

Primary duodenal ulcer almost always

Very rare in children below 1 year
TYPES

Gastritis may be acute, lasting several hours to a
few days, or chronic, resulting from repeated
exposure to irritating agents or recurring episodes
of acute gastritis.
Acute Gastritis
Secondary Gastritis:

Severe Stress (Systemic illness, Burns Head
injury)

NSAID (Ibuprofen, mefanamic acid)
*Inhibit HCo3 secretion
Acute Gastritis can be classified into two types:
EROSIVE and NON-EROSIVE
Erosive Gastritis
Often caused by irritants such as:



*5 folds High risk of massive bleeding

Cauresive gastritis mainly esophagus

Crohn’s disease
Aspirin or NSAIDs (ibuprofen [Motrin])
Alcohol consumption
Radiation therapy
Non-erosive gastritis

*30% ulcer
Often caused by Helicobacter pylori (H.
pylori)
*Can occur at any age
*Associated with high mortality

Severe form of acute gastritis
Others

Caused by the ingestion of strong acid or
alkali, which may cause the mucosa to
become gangrenous or to perforate

Scarring can occur, resulting in pyloric
stenosis (narrowing or tightening) or
obstruction.
*Iron, Kcl
*Antibiotics



Penicillin
Tetracyclin
Cephalosporin
Stress-related gastritis
Acute gastritis may also develop in acute illnesses:





Major traumatic injuries
Burns
Severe infection
Hepatic, kidney, or respiratory failure
Major surgery
MEDICAL-SURGICAL
GASTRITIS
Chronic Gastritis
CLINICAL MANIFESTATIONS
Chronic H. pylori gastritis is implicated in the
development of:
 Peptic ulcers
 Gastric adenocarcinoma
 Gastric mucosa-associated
tissue lymphoma







lymphoid
Chronic gastritis may also be caused by a
chemical injury (gastropathy)

ACUTE GASTRITIS
Epigastric pain or discomfort
Dyspepsia (indigestion)
Anorexia
Hiccups
Nausea and vomiting
Erosive gastritis may cause bleeding:



Long-term drug therapy—aspirin and
other NSAIDs
Reflux of duodenal contents into the
stomach
Often occurs after gastric surgery
Blood in vomit
Melena (black, tarry stools)
Hematochezia (bright red, bloody stools)
CHRONIC GASTRITIS
Autoimmune disorders are also associated with
the development of chronic gastritis:

Hashimoto thyroiditis
Chronic autoimmune thyroiditis that is
characterized by thyroid enlargement,
thyroid fibrosis, lymphatic infiltration of
thyroid tissue, and the production of
antibodies which attack the thyroid

Fatigue
Pyrosis (heartburn) after eating
Belching
Sour taste
Early satiety
Anorexia
Nausea and vomiting

Some patients may only have mild epigastric
discomfort relieved by eating or intolerance to
spicy or fatty foods.

Patients may not be able to absorb vitamin B12
which may lead to pernicious anemia.

Diminished production of intrinsic factor by the
parietal cells due to atrophy.

Some patients have no symptoms
Addison disease
Destructive disease marked by deficient
adrenocortical
secretion
and
characterized by extreme weakness,
loss of weight, low blood pressure,
gastrointestinal
disturbances,
and
brownish pigmentation of the skin and
mucous membranes








Graves’ disease
Common form of hyperthyroidism that is
an autoimmune disease characterized by
goiter, rapid and irregular heartbeat,
weight loss, irritability, anxiety, and often
a slight protrusion of the eyeballs
ASSESSMENT/DIAGNOSTIC FINDINGS

The definitive diagnosis of gastritis is
determined by an endoscopy and histologic
examination of a tissue specimen obtained
by biopsy.

A complete blood count (CBC) may be
drawn to assess for anemia as a result of
hemorrhage or pernicious anemia.

Diagnostic measures for detecting H.
pylori infection may be used.
MEDICAL-SURGICAL
GASTRITIS

Barium contrast study not sensitive about 40%
missed

Metronidazole (Flagyl)
*Assists with eradicating H. pylori
when given with other antibiotics and
proton pump inhibitors
TREATMENT/MANAGEMENT
ACUTE GASTRITIS

Should be given with meals to
decrease GI upset; may cause
anorexia and metallic taste

Patient
should
avoid
alcohol;
increases blood-thinning effects of
warfarin
*The gastric mucosa is capable of repairing itself.
• Patient recovers in 1 day.
• Appetite may be diminished for 2 or 3 days.






Instruct patient to refrain from alcohol and food
until symptoms subside.
A nonirritating diet is recommended.
If symptoms persist, IV fluids may be given.
Fiberoptic endoscopy.
Emergency surgery to remove gangrenous or
perforated tissue.
Gastric resection or gastrojejunostomy to treat
gastric outlet obstruction (pyloric obstruction).
CHRONIC GASTRITIS

Modify diet

Promote rest

Reduce stress

Avoid alcohol and NSAIDs

Medications—antacids, H2 blockers, or PPIs

H. pylori—PPI, antibiotics, and bismuth salts
 Tetracycline
*Exerts bacteriostatic effects to eradicate
H. pylori

May
cause
photosensitivity
reaction; advise patient to use
sunscreen

May cause GI upset

Must be used with caution in
patients with renal or hepatic
impairment

Milk or dairy products may reduce
effectiveness
ANTI-DIARRHEAL
 Bismuth subsalicylate (Pepto-Bismol)
*Suppresses H. pylori
PHARMACOTHERAPY
*Assists with healing of ulcers
ANTIBIOTICS

Amoxicillin (Amoxil)

*A bactericidal antibiotic that assists with
eradicating H. pylori
Given concurrently with
antibiotics
 Should be taken on empty stomach
 May cause diarrhea
 Should not be used in patients allergic
to penicillin
H2 RECEPTOR ANTAGONISTS
 Cimetidine (Tagamet)

Clarithromycin (Biaxin)
* Decreases amount of HCl produced
* Exerts bactericidal effects to
eradicate H. pylori
 May cause
altered taste
GI
upset,
by blocking action of histamine on
histamine receptors of parietal cells in
headache,
 Many drug-drug interactions
o
o
o
Colchicine [Colcrys]
Lovastatin [Mevacor]
Warfarin [Coumadin]
the stomach

Least expensive

May cause confusion, agitation, or
coma in older adults or those with
renal or hepatic insufficiency

Long-term use may cause diarrhea,
dizziness, and gynecomastia
MEDICAL-SURGICAL
GASTRITIS

and vomiting, or abdominal
Many drug-drug interactions
o Amiodarone [Cordarone]
discomfort.
o Amitriptyline [Elavil)
o Benzodiazepines
PROTON PUMP INHIBITORS
o Metoprolol (Lopressor)
 Esomeprazole (Nexium)
o Nifedipine (Procardia)
o Phenytoin [Dilantin]
*decreases gastric acid secretion by
o Warfarin
slowing H+, K+ ATPase pump on the
surface of the parietal cells of the
stomach

Famotidine (Pepcid)

*same action as Cimetidine
Used mainly for treatment of
duodenal ulcer
 Best for patient who is
and H. pylori
infection

critically ill because it is
To be swallowed whole and taken
known
before meals
 Having the least risk of
 Lansoprazole (Prevacid), Omeprazole
drug-drug interactions;
 Does
not
alter
(Prilosec), Pantoprazole (Protonix) and
liver
Rabeprazole (Aciphex)
metabolism
 Prolonged
in
*decreases gastric acid secretion by
renal
slowing H+, K+ ATPase pump on the
half-life
patients
with
surface of the parietal cells
insufficiency
 Short-term relief for GERD

To be swallowed whole and
taken before meals

 Nizatidine (Axid)
May cause diarrhea, nausea,
constipation, abdominal pain,
vomiting, headache, or
*same action Cimetidine
dizziness


Used for treatment of ulcers and
Drug-drug interactions
(Rabeprazole)
GERD


Prolonged half-life in patients
o
Digoxin
with renal insufficiency
o
Iron
May
o
Warfarin
cause
headache,
dizziness,
diarrhea,
nausea/vomiting, GI upset, and
PROSTAGLANDIN E1 ANALOG
urticaria

Misoprostol (Cytotec)
*Protects the gastric mucosa from
 Ranitidine
*same action as Cimetidine
ulcers
*Increases mucus production and

Prolonged half-life in patients
with
renal
and
hepatic

insufficiency

May
cause
headache,
dizziness, constipation, nausea
Used to prevent ulceration in
patients using
Causes fewer side effects than
cimetidine

bicarbonate levels

NSAIDs

Administer with food
MEDICAL-SURGICAL
GASTRITIS

May
cause
cramping
diarrhea
(including
and
uterine
cramping)

Used mainly for the treatment

Promoting fluid balance
• Minimal fluid intake – 1.5 L/day
of duodenal ulcers
• Minimal urine output – 0.5 mL/kg/h
• IV fluids – 3 L/day
• 1L D5W = 170 calories of carbohydrate
 Sucralfate (Carafate)
• Electrolyte values (sodium, potassium,
*Creates a viscous substance that
forms a protective barrier, binding
chloride) are assessed every 24 hours.
to the ulcer, and prevents digestion
• The nurse must always be alert to any
by pepsin
indicators of hemorrhagic gastritis:

 Should be taken without food
Hematemesis
(vomiting
of
blood)

Tachycardia
 Other medications should be

Hypotension
taken 2 hours before or after

Stool: frank or occult bleeding
this medication

Notify
but with water
 May
cause
constipation
primary
provider
and
monitor vital signs.
or
nausea

Relieving pain
• Instruct patient to avoid foods and
NURSING MANAGEMENT
beverages that may irritate the gastric

Reducing anxiety
mucosa.

Promoting optimal nutrition
• Medications to relieve chronic gastritis
• NPO until symptoms subside, allowing the
EDUCATING PATIENTS ABOUT SELF-CARE
gastric mucosa to heal.
• IV therapy
 Stress management
 Monitor I&O and electrolytes
• After symptoms subside, offer patient ice
 Diet
• Foods and substances to be avoided:
chips followed by clear liquids.


Introduce solid food as soon as possible.
Spicy, irritating, or highly seasoned
foods

Provides adequate nutrition

Decreases the need for IV therapy

Caffeine

Minimize

Nicotine

Alcohol
irritation
to
the
gastric
mucosa
• As food is introduced, report symptoms

Medications
that suggest a repeat episode.
• Reinforce the importance of completing the
• Discourage caffeinated beverages.
medication regimen to eradicate H. pylori.
 Caffeine is a CNS stimulant that
CONTINUING AND TRANSITIONAL CARE
increases pepsin secretion.

Discourage alcohol use.

Discourage smoking.

Nicotine
reduces
 Patients with vitamin B12 malabsorption need
information about lifelong vitamin B12 injections.
the
secretion
of
pancreatic bicarbonate, which inhibits the
neutralization of gastric acid in the
duodenum.
MEDICAL-SURGICAL
PEPTIC ULCER DISEASE
PEPTIC ULCER DISEASE
i.
About the disease
ii.
Epidemiology
iii.
Risk factors
iv.
Pathophysiology/Pathogenesis
v.
Types
vi.
Clinical Presentation (Signs/Symptoms)
vii.
Assessment/Diagnostic Findings
viii.
Complications
ix.
Treatment/Management
bacteria also occurs through close contact and
exposure to emesis

smoking and alcohol consumption may be
risks
*although the evidence is inconclusive

Familial tendency also may be a significant
predisposing factor.
*People with blood type O are more susceptible
to the development of peptic ulcers.
ABOUT THE DISEASE

Erosion of GI mucosa resulting from digestive
action of hydrochloric acid and pepsin

A peptic ulcer may be referred to as a gastric,
duodenal, or esophageal ulcer, depending on its
location.


A peptic ulcer is an excavation (hollowed-out
area) that forms in the mucosa of the stomach, in
the pylorus (the opening between the stomach
and duodenum), in the duodenum or in the
esophagus

There also is an association between peptic
ulcer
disease
and
chronic
obstructive
pulmonary disease, cirrhosis of the liver, and
chronic kidney disease.

Zollinger–Ellison syndrome
*a rare condition in which benign or malignant
tumors form in the pancreas and duodenum
that secrete excessive amounts of the hormone
Erosion of a circumscribed area of mucosa is the
cause
gastrin

Excessive amount of gastrin

An inherited, genetic condition called multiple
endocrine neoplasia, type 1 (MEN 1)
PATHOPHYSIOLOGY

This erosion may extend as deeply as the muscle
layers or through the muscle to the peritoneum
(thin membrane that lines the inside of the wall of
the abdomen)

Peptic ulcers are more likely to occur in the
duodenum than in the stomach.
EPIDEMIOLOGY

Women and men have about equivalent lifetime
risk of developing peptic ulcers.

The rates of peptic ulcer disease among middleaged adults have diminished over the past
several decades, whereas the rates among older
adults have increased.

Those who are 65 years and older present to both
outpatient and inpatient settings for treatment of
peptic ulcers more than any other age group.
RISK FACTORS

use of NSAIDs such as ibuprofen and aspirin

infection with the gram-negative bacteria H.
pylori
*which may be acquired through ingestion of food
and water; person-to-person transmission of the

The erosion is caused by the increased
concentration or activity of acid–pepsin or by
decreased resistance of the normally protective
mucosal barrier.

The use of NSAIDs inhibits prostaglandin
synthesis, which is associated with a disruption of
the normally protective mucosal barrier.

Person with a gastric ulcer has normal to less
than normal gastric acidity compared with person
with a duodenal ulcer.
MEDICAL-SURGICAL
PEPTIC ULCER DISEASE
TYPES
Acute

Superficial erosion

Minimal erosion
Chronic

Muscular wall erosion with
formation of fibrous tissue

Present continuously for many
months or intermittently
CLINICAL PRESENTATION

Common to have no pain or other symptoms
*These silent peptic ulcers most commonly
occur in older adults and those taking aspirin
and other NSAIDs
Stress ulcer is the term given to the acute
mucosal ulceration of the duodenal or gastric
area that occurs after physiologically stressful

Gastric and duodenal mucosa not rich in sensory
pain fibers

Duodenal ulcer pain (Burning, cramplike)

Gastric ulcer pain (Burning, gaseous)

Dull, gnawing pain or a burning sensation in the
mid-epigastrium or the back
events, such as burns, shock, sepsis, and
multiple organ dysfunction syndrome.
Specific types of ulcers that result from stressful
conditions include Curling ulcers and Cushing
ulcers.
DIFFERENCE
BETWEEN
GASTRIC ULCER
DUODENAL
AND
Association of pain:
GASTRIC ULCER: almost immediately after
eating
Curling ulcer is frequently
observed about 72 hours after
extensive burn injuries and
DUODENAL ULCER: commonly occurs 2 to 3
hours after meals
often involves the antrum of the
stomach or the duodenum.
Occurrence:
GASTRIC ULCER: 30% to 40% of patients
awake with pain during the night
Cushing ulcer is
common in patients
with
a
traumatic
DUODENAL ULCER: 50% to 80% of patients
voice the same type of complaint
head injury, stroke,
brain
tumor,
or
following
intracranial surgery.
Patients with duodenal ulcers are more likely to
express relief of pain after eating or after taking
an antacid than patients with gastric ulcers.
MEDICAL-SURGICAL
PEPTIC ULCER DISEASE
Other nonspecific symptoms of either gastric

Vomiting is rare in an uncomplicated peptic
ulcer, it may be a symptom of a complication
of an ulcer.

Peptic ulcer perforation

Bleeding peptic ulcers may present with
evidence of GI bleeding, such as hematemesis
(vomiting blood) or the passage of melena
(black, tarry stools)
ulcers or duodenal ulcers may include:
 pyrosis vomiting
 constipation or diarrhea
 bleeding
*These symptoms are often accompanied by sour
eructation (burping), which is common when the
patient’s stomach is empty
TREATMENT/MANAGEMENT
Pharmacologic Therapy
ASSESSMENT/DIAGNOSTIC FINDINGS

Physical examination may reveal pain,
epigastric tenderness, or abdominal distention.

Upper endoscopy is the preferred
diagnostic procedure because it allows direct
visualization of inflammatory changes, ulcers,
and lesions
The most commonly used therapy for peptic ulcers is
a combination of antibiotics, proton pump
inhibitors, and sometimes bismuth salts that
suppress or eradicate H. pylori.

Recommended combination drug therapy is
typically prescribed for 10 to 14 days and may
include triple therapy with two antibiotics plus
a proton pump.

Quadruple therapy with two antibiotics plus a
proton pump inhibitor and bismuth salts
Use of:


Antacids
o Used as adjunct therapy for peptic
ulcer disease
Serologic testing for antibodies against the H.
↑ gastric pH by neutralizing acid
pylori antigen, stool antigen test, and urea

breath test

Barium contrast studies
H2 receptor blockers
o
Used to manage peptic ulcer disease
o
Block action of histamine on H2
receptors
Widely used
↓ HCl acid secretion

X- ray studies
↓ conversion of pepsinogen to
pepsin
May be ineffective in differentiating a peptic
ulcer from a malignant tumor


↑ ulcer healing
Gastric analysis
Lab analysis
COMPLICATIONS
3 major complications:

Hemorrhage

Perforation

Gastric outlet obstruction
*Initially treated conservatively
*May require surgery at any time during course of
therapy

PPIs

Antibiotics

Anticholinergics

Cytoproctective therapy

The patient is advised to adhere to and complete the
medication regiment to ensure complete healing of
the ulcer.

The patient is advised to avoid the use of aspirin and
other NSAIDs.
Smoking Cessation

Smoking decreases the secretion of bicarbonate
from the pancreas into the duodenum, resulting
in increased acidity of the duodenum.
MEDICAL-SURGICAL
PEPTIC ULCER DISEASE

Continued smoking is also associated with
delayed healing of peptic ulcers.

Lifestyle changes to prevent recurrence
Surgical procedures
Dietary Modifications

The intent of dietary modification for patients with
peptic ulcers is to avoid oversecretion of acid and
hypermotility in the GI tract.

Dietary modifications may be necessary so that
foods and beverages irritating to patient can be
avoided or eliminated

Nonirritating or bland diet consisting of 6 small
meals a day during symptomatic phase

Protein considered best neutralizing food
*Stimulates gastric secretions

Carbohydrates and fats are least stimulating to

Vagotomy (severing of the vagus nerve)
*it decreases gastric acid by diminishing
cholinergic stimulation to the parietal cells,
making them less responsive to gastrin.

With or without pyroloplasty
*transecting nerves that stimulate acid secretion
and opening the pylorus)

Antrectomy
*removal of the lower portion of the antrum (which
contains cells of gastrin)
HCl acid secretion
*Do not neutralize well

Avoiding extremes of temperature in food and
beverages and overstimulation from the
consumption of alcohol, coffee (including
decaffeinated coffee, which also stimulates acid
secretion), and other caffeinated beverages.

An effort is made to neutralize acid by eating
three regular meals a day (small, frequent
feedings)
Surgical Management

Surgery is usually recommended for patients
with intractable ulcers (those failing to heal after
12 to 16 weeks of medical treatment), lifethreatening
hemorrhage,
perforation,
or
obstruction and for those with ZES that is
unresponsive to medications.
Remember the word: ANASTMOSIS (surgical
connection)
Indications for surgical interventions:
 Intractability
 History of hemorrhage, ↑ risk of bleeding
 Prepyloric or pyloric ulcers
 Drug-induced ulcers
 Possible existence of a malignant ulcer
 Obstruction
Goals of having surgery:
prescribed
therapeutic
 Experience a reduction or absence of
discomfort related to peptic ulcer disease
 Exhibits no signs of GI complications
 Have complete healing
Gastroduodenostomy or BILLROTH I
*The pylorus is removed and the
distal stomach is anastomosed
directly to the duodenum.
 Multiple ulcer sites
 Comply with
regimen

MEDICAL-SURGICAL
PEPTIC ULCER DISEASE

Gastrojejunostomy or BILLROTH II
*The pylorus is removed and the distal
stomach is anastomosed directly to the
jejunum.

Surgery may be performed using a traditional
open abdominal approach (requiring a long
abdominal incision) or through the use of
laparoscopy (only requiring small abdominal
incisions).
Follow-up care

Recurrence of peptic ulcer disease within 1 year
may be prevented with the prophylactic use of H2
blockers taken at a reduced dose.

. The likelihood of recurrence is reduced if the
patient avoids smoking, coffee (including
decaffeinated coffee) and other caffeinated
beverages, alcohol, and ulcerogenic medications
(e.g., NSAIDs).
MEDICAL-SURGICAL
MALABSORPTION
MALABSORPTION
i.
About the disease
ii.
Risk factors
iii.
Pathophysiology/Pathogenesis
iv.
Clinical Presentation (Signs/Symptoms)
v.
Assessment/Diagnostic Findings
vi.
Treatment/Management

ABOUT THE DISEASE

The inability of the digestive system to absorb one or
more of the major vitamins (especially A and B12), minerals (i.e.,
iron and calcium), and nutrients (i.e., carbohydrates, fats, and
proteins) occurs in disorders of malabsorption.
Interruptions in the complex digestive process may occur anywhere in the digestive system and cause decreased
absorption.
RISK FACTORS

Mucosal (transport) disorders causing generalized malabsorption (e.g., celiac disease, Crohn’s disease, radiation
enteritis)

Luminal disorders causing malabsorption (e.g., bile acid deficiency, Zollinger–Ellison syndrome, pancreatic
insufficiency, small bowel bacterial overgrowth, or chronic pancreatitis)

Lymphatic obstruction, interfering with transport of fat by products ofdigestion into the systemic circulation (e.g.,
neoplasms, surgical trauma).
*Characteristics of stools as recorded on the BSFS
are then used to determine category of irritable bowel
syndrome (IBS), where IBS-C (constipation), IBS-D
(diarrhea), IBS-M (mixed), and IBS-U (uncategorized).
*Table below shows the selected disorders of malabsorption
MEDICAL-SURGICAL
MALABSORPTION
PATHOPHYSIOLOGY
(3) impaired enterohepatic bile circulation, as seen
in small bowel resection or regional enteritis;
In general, the digestion and absorption of food materials
can be divided into 3 major phases:
1. The luminal phase where dietary fats, proteins,
and carbohydrates are hydrolyzed and
solubilized by secreted digestive enzymes and
bile.
(4) bile salt deconjugation due to small bowel
bacterial overgrowth.
.

Luminal availability and processing
Luminal bacterial overgrowth can cause a
decrease in the availability of substrates,
including carbohydrates, proteins, and
vitamins.
2. The mucosal phase relies on the integrity of the
brush-border membrane of intestinal epithelial
cells to transport digested products from the
lumen into the cells.
3. In the post absorptive phase, nutrients are
transported via lymphatics and portal circulation
from epithelial cells to others of the body.
MUCOSAL PHASE:

Impaired brush-border hydrolase activity
o
Disaccharidase deficiency
CAUSES:
o
Lactase deficiency
LUMINAL PHASE:
o
Immunoglobulin A (IgA) deficiency

Impaired nutrient hydrolysis
The most common cause is pancreatic
insufficiency due to chronic pancreatitis,
pancreatic resection, pancreatic cancer, or
cystic fibrosis.



Acquired disorders are far more common
and are caused by:
(1) Decreased absorptive surface area,
as seen in intestinal resection
Inactivation of pancreatic enzymes by gastric
hypersecretion, as seen in Zollinger-Ellison
syndrome
(2) Damaged absorbing surface, as seen
in celiac sprue, tropical sprue, giardiasis,
Crohn disease, AIDS enteropathy,
chemotherapy, or radiation therapy;
Impaired micelle formation
Impaired micelle formation causes lead to fat
malabsorption. This impairment is due to
different reasons, including
(1) decreased bile salt synthesis from severe
parenchymal liver disease (eg, cirrhosis);
(2) impaired bile secretion from biliary
obstruction or cholestatic jaundice (eg,
primary biliary cirrhosis, primary sclerosing
cholangitis);
Impaired nutrient absorption
(3) Infiltrating disease of the intestinal
wall, such as lymphoma and amyloidosis
POST ABSORPTIVE PHASE:

Obstruction of the lymphatic system, both
congenital (eg, intestinal lymphangiectasia)

Acquired
(eg,
Whipple
lymphoma, tuberculosis)
diseases
,
MEDICAL-SURGICAL
MALABSORPTION
ASSESSMENT/DIAGNOSTIC FINDINGS

Dermatitis herpetiformis, erythema
nodosum, and pyoderma gangrenosum
may be present.

Pellagra, alopecia, or seborrheic
dermatitis
History:

Diarrhea

Weight Loss

Steatorrhea (an excess of fat in the stools)

Flatulence and abdominal distention

Edema

Anemia

Metabolic defects of bones
Physical Manifestations:

Patients may have orthostatic hypotension.

Signs of weight loss, muscle wasting, or both
may be present.

Patients may have signs of loss of
subcutaneous fat

Cheilosis, glossitis, or aphthous ulcers of the
mouth.
Abdominal examination

The abdomen may be distended, and bowel
sounds may be hyperactive.

Ascites may be present in severe
hypoproteinemia.
Dermatological Manifestations:

Pale skin

Ecchymoses due to vitamin K deficiency
Neurological examination

Motor weakness, peripheral neuropathy,
or ataxia may be present.

The Chvostek sign or the Trousseau sign
may be evident due to hypocalcemia.
MEDICAL-SURGICAL
MALABSORPTION
Laboratory Findings:

Hematological tests
o CBC
o Serum iron, vitamin B-12, and folate
o Prothrombin time.



Electrolytes and chemistries
o
Hypokalemia, hypocalcemia,
hypomagnesemia, and metabolic
acidosis.
o
Protein malabsorption may cause
hypoproteinemia and
hypoalbuminemia.
o
Fat malabsorption can lead to low
serum levels of triglycerides,
cholesterol
o
ESR which is elevated in Crohn
disease and Whipple disease
Stool analysis
o
Stool pH may be assessed. Values of
<5.6 are consistent with carbohydrate
malabsorption
o
Pus cell in the stool e.g IBD
Schilling test
o
Malabsorption of vitamin B-12 may
occur as a consequence of deficiency
of intrinsic factor (eg, pernicious
anemia, gastric resection), pancreatic
insufficiency, bacterial overgrowth,
ileal resection, or disease.
TREATMENT/MANAGEMENT

A gluten-free diet helps treat celiac disease.

Similarly, a lactose-free diet for lactase

Protease and lipase supplements are the
therapy for pancreatic insufficiency

Antibiotics are the therapy for bacterial
overgrowth.

Corticosteroids, anti-inflammatory agents,
such as mesalamine, and other therapies are
used to treat celiac disease
Nutritional support:

Supplementing various minerals
calcium, magnesium, iron, and vitamins

Caloric and protein replacement also is
essential.

Medium-chain triglycerides can be used
for lymphatic obstruction.

In severe intestinal disease, such as
massive resection and extensive
regional enteritis, parenteral nutrition
may become necessary.
MEDICAL-SURGICAL
OSTEOPOROSIS
HIATAL HERNIA
i.
About the disease
ii.
Epidemiology
iii.
Risk factors
iv.
Pathophysiology/Pathogenesis
v.
Clinical Presentation (Signs/Symptoms)
vi.
Assessment/Diagnostic Findings
vii.
Treatment/Management
viii.
Gerontologic Considerations

Prescribed corticosteroids (e.g., prednisone) for
longer than 3 months
PATHOPHYSIOLOGY/PATHOGENESIS
ABOUT THE DISEASE

Osteoporosis is the most prevalent bone
disease in the world.

A disease that causes your bones to become
weak and brittle

Osteoporosis is important because of the
problems resulting from these fractures disability, loss of independence, and even
death.

Osteoporosis is silent because there are no
symptoms (what you feel).


Osteoporosis is characterized by reduced bone
mass, deterioration of bone matrix, and
diminished bone architectural strength.

Normal homeostatic bone turnover is altered; the
rate of bone resorption that is maintained by
osteoclasts (cells that degrade bone to initiate
normal bone) remodeling is greater than the rate
of bone formation that is maintained by
osteoblasts (cells that form bone tissue),
resulting in a reduced total bone mass.

The gradual collapse of a vertebra may be
asymptomatic.

Age-related loss begins soon after the peak bone
mass is achieved (i.e., in the fourth decade).

Calcitonin, which inhibits bone resorption and
promotes bone formation, is decreased.

Estrogen, which inhibits bone breakdown, also
decreases with aging.

Parathyroid hormone (PTH) increases with
aging, thus increasing bone turnover and
resorption.
Osteoporosis is not an inevitable part of aging,
but is a disease that can be prevented and
treated, provided it is detected early.

The main goal of treating osteoporosis is to
prevent such fractures in the first place.

EPIDEMIOLOGY
More than 1.5 million osteoporotic fractures
occur every year

Fractures requiring hospitalization have risen
significantly over the past two decades

It is estimated that a 50 year-old woman has a
40% chance of having an osteoporotic fracture
during her remaining lifetime.

It is projected that one of every two Caucasian
women and one of every five men will have an
osteoporosis-related fracture at some point in
their lives
RISK FACTORS

Alcohol intake of 3 or more drinks daily

Current use of tobacco products

Family history

History of bone fracture during adulthood

Inactive or sedentary lifestyle

Inadequate calcium and vitamin D intake

Low body mass index

Malabsorption disorders (e.g., eating disorder,
celiac disease, bariatric surgery)

Men older than 60 years of age

Women who are postmenopausal
MEDICAL-SURGICAL
OSTEOPOROSIS
CLINICAL PRESENTATION

Simple test that measures bone mineral density.

Often the measurements are at your spine and
your hip, including a part of the hip called the
femoral neck, at the top of the thighbone (femur).

The test is quick and painless.

The postural changes result in relaxation of the
abdominal muscles and a protruding abdomen.

It is similar to an X-ray, but uses much less
radiation.

Deformity may also produce pulmonary
insufficiency and increase the risk for falls related
to balance issues.

Even so, pregnant women should not have this
test, to avoid any risk of harming the fetus.
Question: Who needs bone densitometry?

Anyone who wants an accurate measurement of
bone density.

However, because of cost concerns, the test is
most often done for those with high risk of
developing osteoporosis, or to monitor the
effectiveness of treatment for osteoporosis.

Estrogen deficient women undecided about
taking hormones.
This is a way of measuring the amount of calcium
in a certain amount of bone.

Those with spinal abnormalities
evidence of bone loss.
This is important because the amount of calcium
in your bone determines how strong it is.

Anyone taking long-term corticosteroid treatment
(such as Prednisone).
If the bone density is very low, then you have
osteoporosis and a very high risk of fracturing
your bones.

Primary hyperparathyroidism with no symptoms.

Monitoring of therapy for osteoporosis.
ASSESSMENT/DIAGNOSTIC FINDINGS

Osteoporosis may be undetectable on routine xrays until there has been significant
demineralization, resulting in radiolucency of the
bones.
BONE DENSITOMETRY



or
X-ray
DUAL-ENERGY X-RAY ABSORPTIOMETRY
 Fracture risk can be estimated using the World
Health
Organization
(WHO)
Fracture
Risk
Assessment Tool (FRAX).
DEXA scan data are analyzed and reported as T-scores
(the number of standard deviations above or below the
average BMD value for a 30-year-old healthy Caucasian
woman).
MEDICAL-SURGICAL
OSTEOPOROSIS
Calcitonin
Other diagnostic tests used:

Laboratory studies

Serum calcium,

Serum phosphate,

Serum alkaline phosphatase [ALP],

Urine calcium excretion,

Urinary hydroxyproline excretion

Hematocrit

Erythrocyte sedimentation rate [ESR]

X-ray studies

This medication, a hormone made from the
thyroid gland, is given most often as a nasal
spray or as an injection (shot) under the skin.

Approved
for
the
management
of
postmenopausal osteoporosis and helps
prevent vertebral (spine) fractures.

It also is helpful in controlling pain after an
osteoporotic vertebral fracture.
Estrogen or hormone replacement therapy

Estrogen treatment alone or combined with
another hormone, progestin, has been shown to
decrease the risk of osteoporosis and
osteoporotic fractures in women.

Consult with your doctor about whether
hormone replacement therapy is right for you.
Differential diagnosis:

Multiple myeloma

Osteomalacia

Hyperparathyroidism

Malignancy
Selective estrogen receptor modulators

TREATMENT/MANAGEMENT



A diet rich in calcium and vitamin D throughout
life, with an increased calcium intake during
adolescence and the middle years, protects
against skeletal demineralization.
The recommended adequate intake level of
calcium for men 50 to 70 years is 1000 mg daily,
and for women aged 51 and older and men
aged 71 and older is 1200 mg daily.
The recommended vitamin D intake for adults up
to 70 years of age is 600 IU daily, and 800 IU
daily for those over the age of 70.

Regular weight-bearing exercise promotes bone
formation.

Recommendations include 20 to 30 minutes of
aerobic, bone-stressing exercise daily.
Pharmacologic Therapy

To ensure adequate calcium intake, a calcium
supplement (e.g., Caltrate, Citracal) with vitamin
D may be prescribed and taken with meals or
with a beverage high in vitamin C to promote
absorption
Bisphosphonates

This class of drugs (often called “antiresorptive”
drugs) helps slow bone loss.

Studies show they can decrease the risk of fractures.

With all of these medications, you should make sure
you are taking enough calcium and vitamin D, and
that the vitamin D levels in your body are not low.
These medications, often referred to as SERMs,
mimic estrogen’s good effects on bones without
some of the serious side effects such as breast
cancer.
Teriparatide

Teriparatide is a form of parathyroid hormone
that helps stimulate bone formation.

It is approved for use in postmenopausal women
and men at high risk of osteoporotic fracture.

It also is approved for treatment
glucocorticoid-induced osteoporosis.

It is given as a daily injection under the skin and
can be used for up to two years.
of
MEDICAL-SURGICAL
OSTEOPOROSIS
*Table that shows selected osteoporosis medications
GERONTOLOGIC CONSIDERATIONS

The prevalence of osteoporosis in
women older than 80 years is 50%.

The average 75-year-old woman has
lost 25% of her cortical bone and 40%
of her trabecular bone.

Older adults absorb dietary calcium less
efficiently and excrete it more readily
through their kidneys.

Postmenopausal women and older
adults need to consume approximately
1200 mg of daily calcium.

Quantities larger than this may place
patients at heightened risk of renal
calculi or cardiovascular disease.