Download Cm * gastro, block 5 exam 1, lectures 1-12

So far I finished lecture 1-7
Lectures 8-12 are coming.
Lecture 3 – I cut and pasted slides I thought might be important
There are __ total slides.
There are 74 title slides.
1.
2.
3.
4.
Bacteria responsible for caries
Vitamins and tooth growth / development
Cariogenic and non-cariogenic foods
Pathogenesis of caries with xerostomia
Question

A 4 year old presents with the findings seen in the
picture. Which bacteria would you expect to be most
responsible for these findings?
A.
B.
C.
D.
E.
Clostridium difficile
Streptococcus mutans
Lactobacillus casein
Actinomyces species
Peptostreptococcus mutans
Caries
Pathophysiology

Bacteria
 Steptococcus mutans most prevalent
 Streptococcus sanguis
 Streptococcus sobrinus
 Lactobacilus casein



Metabolize carbohydrates in the mouth producing organic
acids as a byproduct
Produce sticky polymers called fructans and glucans which
bind the bacteria to the smooth enamel surface and form the
bulk and matrix of the biofilm
Joined by thin, branched Actinomyces, gram-positive
bacteria, that add to the complex network of early plaque
Question

Which of the following supplements or vitamins is
required for development of the mineral component
of enamel and dentin?
A.
B.
C.
D.
E.
Fluoride
Vitamin A
Vitamin C
Vitamin D
Xylitol
Fluoride
Four primary actions on teeth
1. When incorporated into enamel and dentin along with calcium and
phosphorous it forms fluoroapatite which is more resistant to acid
challenge than hydroxyapatite
2. It promotes repair and remineralization of tooth surfaces with early
signs of decay
3. It helps to reverse the decay process while promoting the
development of a tooth surface that has increased resistance to
decay
4. Helps to deter the harmful effects of bacteria in the oral cavity by
interfering with the formation and function of the microorganisms
Can you answer the following?

A patient was asking about nutrition and dental health.
Which of the following breakfasts would you recommend
because of the least cariogenic properties?
A.
B.
C.
D.
E.
Aged cheddar cheese omelet
Oatmeal with brown sugar
A whole banana
Toast with a glass of skim milk
Waffle House #1 with orange juice
Anticariogenic Foods





Prevent plaque from recognizing a cariogenic food when it is
eaten first
Cheese particularly, aged cheddar, Monterey Jack and Swiss
cheeses (which contain casein, calcium and phosphate)
Xylitol (a 5-carbon sugar alcohol, sweetener in sugarless
gum) cannot be metabolized the same way as 6-carbon
sugars. It also replaces fermentable CHO in the diet. S.
mutans is actually inhibited by xylitol
May increase salivation or have antimicrobial activity
Casein phosphopeptide-amorphous calcium phosphate
(CPP-ACP; Recaldent) is a substance that promotes
remineralization of enamel surfaces
1. Bacteria responsible for caries
Caries
Pathophysiology

Bacteria
 Steptococcus mutans most prevalent
 Streptococcus sanguis
 Streptococcus sobrinus
 Lactobacilus casein



Metabolize carbohydrates in the mouth producing organic
acids as a byproduct
Produce sticky polymers called fructans and glucans which
bind the bacteria to the smooth enamel surface and form the
bulk and matrix of the biofilm
Joined by thin, branched Actinomyces, gram-positive
bacteria, that add to the complex network of early plaque
The Decay Process
Begins with the production of acids as a byproduct of
bacterial metabolism in plaque which is a sticky,
gelatinous mass that adheres to teeth and gingiva
 Composed of bacteria, salivary proteins, polysaccharides
and lipids
 Most common bacteria – S. mutans prefers sucrose, the
most common sugar consumed in the diets of children
and adults

2. Vitamins and tooth growth /
development
Introduction
Tooth development
During pregnancy, maternal nutrition must supply
preeruptive teeth with the appropriate building materials
 Primary tooth development begins at 2-3 months’
gestation. Mineralization begins at ~ 4 months’ gestation
thru preteen years
 Posteruption diet and nutrient intake continue to affect
tooth development, mineralization, enamel development
and strength

Introduction
Anatomy of a tooth

Enamel
 Keratin (requires Vit. A)

Dentin
 Collagen (requires Vit. C)

Mineral component of enamel and
dentin is hydroxyapatite (requires
Vit. D)
3. Cariogenic and non-cariogenic foods
3a. Cariogenic foods
Cariogenic Foods
 Refers
to the caries-promoting properties of a
diet, food or beverage
 Cariogenicity of a food is dependent on:
 the form in which it occurs,
 its nutrient composition,
 when it is eaten in relation to other foods and fluids,
 the duration of the exposure to the teeth,
 and the frequency with which it is eaten
Cariogenic foods
 Found
in 3 of the 5 MyPlate food groups
 Grains: crackers, chips, hot & cold cereals, breads, pretzels
 Fruits (fresh, dried, canned) and fruit juices
○ Fruit with high water content less cariogenic
○ Bananas and dried fruit more cariogenic
 Dairy products sweetened with fructose, sucrose or other sugar.
 However, dairy products are rich in calcium which has an alkaline
nature and may have a positive influence in reducing the
cariogenic potential of the food
Glucose, fructose and lactose, sucrose, maltose stimulate cariogenic bacterial activity
Cariogenic foods
All dietary forms of sugars including honey, molasses,
brown sugar, corn syrup solids, high-fructose corn syrup,
maple syrup have cariogenic potential and can be used
by bacteria to produce organic acid
 Be aware of hidden sugars!
 Learn and teach your patients how to identify them on
food labels

 E.g. agave nectar, dextrose, xylose, invert sugar, sorghum
Cariogenic foods
Cariostatic Foods
 Do
not contribute to decay, are not
metabolized by microorganisms
 Do not decrease salivary pH <5.5 within 30
minutes
 Include foods such as proteins,
meat, fish, eggs, poultry;
most vegetables, fats,
sugarless gums
3b. Non-cariogenic foods
Anticariogenic Foods





Prevent plaque from recognizing a cariogenic food when it is
eaten first
Cheese particularly, aged cheddar, Monterey Jack and Swiss
cheeses (which contain casein, calcium and phosphate)
Xylitol (a 5-carbon sugar alcohol, sweetener in sugarless
gum) cannot be metabolized the same way as 6-carbon
sugars. It also replaces fermentable CHO in the diet. S.
mutans is actually inhibited by xylitol
May increase salivation or have antimicrobial activity
Casein phosphopeptide-amorphous calcium phosphate
(CPP-ACP; Recaldent) is a substance that promotes
remineralization of enamel surfaces
4. Pathogenesis of caries with xerostomia
Roles of Saliva
Clears food from around teeth
 Provides buffering action to neutralize bacterial
metabolism

 via bicarbonate-carbonic acid and phosphate buffer systems

Supersaturated with calcium and phosphorus
 Once pH is restored, remineralization can occur
 If fluoride is present, minerals are deposited in the form of
fluoroapatite
Xerostomia (dry mouth)  pathogenesis of
caries
Flip-flop everything from the previous slide
Without saliva,
 Food cannot be cleared from the mouth
 Bacterial meteabolism cannot be buffed (i.e. bicarb,
phosphate buffering system) back to normal pH
 Abnormal pH prevents remineralization via calcium
and phosphorus

1.
2.
3.
4.
5.
Causes of PUD
Treatments for PUD
Uncomplicated vs. complicated ulcers
Treatment for perforated ulcers
ZE syndrome clinical findings
1. Causes of PUD
Etiology
Microbes - H. pylori (#1 risk factor)
 Drugs/toxins - NSAIDs, ASA, Biphosphonates,
corticosteroids, cocaine and alcohol
 Ischemia - Mesentaric vascular occlusion, P. Vera
 Hyperacidic syndromes - Zollinger-Ellison
 Systemic inflammation - Crohn’s disease
 Stress ulceration
 Radiation Gastritis

2. Treatments for PUD
Drugs to treat PUD

Antacids – Maalox, Mylanta, Tums, etc.
 Use for occ. dyspepsia

H-2 blockers – ranitidine, cimetidine, famotidine, etc.
 Use for chronic dyspepsia
PPI’s – pantoprazole, omeprazole, lansoprazole,
esomezole, etc.
 Mucosal protective agents –

 Sulcrafate – helpful adjunct esp., with smokers
 Misoprostol - Prostaglandin analog – use with NSAIDS, but
contraindicated with pregnancy.
 Bismuth subsalicylate (BSS) – use with H. pylori
Management
3. Uncomplicated vs. complicated ulcers
3a. Uncomplicated ulcers
Key Signs and Symptoms of PUD
UNCOMPLICATED ULCER





No symptoms (“silent ulcer” in up to 40% of cases)
Epigastric pain - Pain may radiate to the back, thorax,
other parts of abdomen (cephalad most likely, caudad
least likely)
Pain may be nocturnal (most specific), “painful hunger”
relieved by food, or continuous (least specific)
Nausea & Vomiting
Heartburn (mimics or associated with gastroesophageal
reflex)
3b. Complicated ulcers
Surgical Indications
Surgical Treatment Recommendations for Complications
Related to Peptic Duodenal Ulcer Disease
Intractable: Parietal cell vagotomy ± antrectomy
 Bleeding: Oversewing of bleeding vessel with treatment of
H. pylori
 Perforation: Patch closure with treatment of H. pylori
 Obstruction: Rule out malignancy and gastrojejunostomy
with treatment of H. pylori

4. Treatment for perforated ulcers
Surgical Indications
Surgical Treatment Recommendations for Complications
Related to Peptic Duodenal Ulcer Disease
 Intractable: Parietal cell vagotomy ± antrectomy
 Bleeding: Oversewing of bleeding vessel with treatment of
H. pylori
 Perforation: Patch closure with treatment of H. pylori
 Obstruction: Rule out malignancy and gastrojejunostomy
with treatment of H. pylori
5. ZE syndrome clinical findings

Zollinger-Ellison Syndrome: <1% of pts

Triad- gastric acid hypersecretion, severe PUD and
non-Beta cell tumor of the pancreas
 Caused by gastrin secreting endocrine tumor found usually in the




pancreas or proximal small bowel.
Associated with multiple endocrine neoplasias, esp.
hyperparathyroidism.
Pts will have elevated serum gastrin levels ( greater than 1000pg/ml is
diagnostic)and abnormal secretin testing.
CT or MRI will usually confirm the presence of the tumor (usually
benign)
Pts will frequently have a secretory diarrhea, as well.
Hypergastrinemic syndromes
I have cut and pasted some slides from Dr. Stewart’s lecture
She emphasized a few things
UMBILICAL HERNIA
Spontaneous closure
by age 1 year
 Large defects by 5-6 yo

 Size of the fascial
defect, NOT the
degree of protrusion,
is most indicative of
whether spontaneous
closure will occur
OMPHALOCELE




herniation of abdominal contents
into the base of the umbilical cord
abdominal cavity underdeveloped
defect may vary from <2-10 cm
sac is covered with peritoneum and
amnion without overlying skin
 + intestines
 + liver and intestines

embryologic etiology uncertain
 Persistent primitive body stalk
 Failure of retraction
 Failure of complete lateral folding
Omphalocele: Epidemiology
Occurs in approximately 1:4,000
live births
 + intestines 1/5,000
 + liver and intestines 1/10,000


High incidence of congenital
abnormalities (50 to 70 percent )
 Trisomy 13, 18, 21 most common
 Cardiac defects
 GI
Omphalocele: Diagnosis

Elevated maternal serum
alpha-fetoprotein
concentration (MSAFP) is
elevated in 70%

2nd trimester ultrasound
GASTROSCHISIS
Full thickness defect in the
abdominal wall
 Small defect
 Does not involve the umbilical
cord
 Contains small bowel, maybe
portions of stomach or colon
 Viscera are not protected by
the peritoneal sac
 Exact cause is uncertain

 defective formation or disruption
of the body wall in the embryonic
period, with subsequent
herniation of bowel
Gastroschisis: Treatment

Management in delivery room (same as omphalocele)
 Preserve heat and minimize insensible fluid loss – use sterile bowel
bag to reduce insensible fluid losses
 Orogastric tube to decompress the stomach
 Stabilize the airway
 IV access

Surgical repair EMERGENT (unlike omphalocele)
 Primary closure
 Staged closure
○ Dacron-reinforced silastic silo
 Prolonged TPN may be necessary
 “Gentle touch”
○ Slower process allowing gravity to reduce bowel before closure
Abdominal Wall Defects: Gastroschisis vs.
Omphalocele
GASTROSCHISIS
OMPHALOCELE
Defect
Open
Membrane covered
Defect Size
2-5 cm
1-15 cm
Umbilical Cord
Left of defect
Center of membrane
Bowel
Serositis, edema, matted
Normal
Assc Anomalies
10%
60%
Prognosis
70-90%
20-70%
IUGR (intrauterine growth
restriction)
Common
Less Common
Other organs
Rare (stomach, colon)
Liver often out
PRUNE BELLY SYNDROME

Absence of major abdominal
muscles
 Result of severe urethral
obstruction in early fetal life
or a genetic component
affecting mesodermal
development

Characteristic association
 deficient abdominal muscles
 undescended testes
 urinary tract abnormalities
Prune Belly Syndrome: Prognosis
1/3 are stillborn or die in the first few
months from pulmonary hypoplasia
 30% long term survivors develop end
stage renal disease from renal
dysplasia or complications of infection
and reflux
 depends on degree of pulmonary
hypoplasia and renal dysplasia

CONGENITAL DIPHRAGMATIC HERNIA





Developmental defect of the
diaphragm that allows abdominal
viscera to herniate into the chest
Incidence 1/ 2,000-5,000 live births
Females:male, 2:1
Etiology may be congenital or
traumatic
80-90% occur on the Left
BochdaLek type

2-6% occur on the Right side
MoRgani type
Congenital Diaphragmatic Hernia:
Pathology
Structural diaphragmatic defect
 Limiting factor for survival is the associated
pulmonary hypoplasia
 Lung hypoplasia was believed to be solely due to
compression by abdominal contents
 Pulmonary hypoplasia may precede the development of
the diaphragmatic defect

Congenital Diaphragmatic Hernia:
Presentation
 Respiratory
distress within the first several hours
after birth
 Level of distress consistent with the degree of pulmonary
hypoplasia and persistent pulmonary hypertension
 Increased
chest wall diameter with barrel-shaped chest
 Scaphoid abdomen
 Absence of breath sounds on the ipsilateral side
 Bowel sounds auscultated in the chest
 Heartbeat (PMI) displaced away from the hernia if there
is a shift in the mediastinum
Congenital Diaphragmatic Hernia:
Treatment
Management





Avoid blow-by oxygen and bag mask ventilation
Immediate endotracheal intubation
Ventilatory support with low airway pressure to minimize lung injury
May include ECMO
Nasogastric tube placed in the stomach connected to continuous suction for
decompression
 UAC and UVC (if possible)
 IVF and inotropes if necessary to support blood pressure
Surgical repair
 Delayed until resolution of early pulmonary insufficiency and acute pulmonary
hypertension
ESOPHAGEAL ATRESIA

Most frequent congenital anomaly of the esophagus
(1/
4,000)
> 90% present with a Tracheoesophageal fistula
> 90% survival rate
Exact cause unknown (defect of foregut septation)
Associated features include advanced maternal age,
European ethnicity, obesity, low socioeconomic status
and tobacco smoking.
 50% of infants are non-syndromic without other
anomalies, the rest have associated anomalies, most
frequently VATER/VACTERL or CHARGE.




Esophageal Atresia +/- TEF: Presentation





h/o polyhydramnios
Neonate presents with frothing or bubbling at the mouth and
nose after birth. Also, coughing, cyanosis and respiratory
distress.
Feeding exacerbates symptoms, causing regurgitation which may
lead to aspiration.
Aspiration of gastric contents via a distal fistula causes more severe
pneumonitis than aspiration of oropharyngeal secretions from the
blind upper pouch.
Infants with an isolated TEF in the absence of EA (H-type fistula)
may come to medical attention later in life with a history of
chronic respiratory problems, including refractory bronchospasm and
recurrent pneumonias.
DUODENAL ATRESIA
1/10,000 live births
 25-40% of all intestinal atresias
 30% associated chromosomal anomaly (primarily
Trisomy 21)

Causes
 Intrinsic defect of bowel formation
 failed recanalization of the intestinal lumen during
gestation
MALROTATION AND VOLVULUS
True incidence of malrotation
unknown as many cases
asymptomatic for life
 Symptomatic malrotation 1/6000
 90% present in the first 2
months
 75% < 1 month old
 can present at any age
 30 – 60% have an associated
anomaly

Malrotation: Diagnosis
Flat and upright x-ray:
 Bowel loops at the site of the liver
 Naso/orogastric tube located in an abnormally postioned duodenum
 “Double bubble” sign – showing distention of the stomach and duodenum
 With complete volvulus – dilated loops of bowel with air-fluid levels proximally and
absence of gas distally
Upper GI Series (gold standard):


abnormal duodenum with corkscrew appearance
Duodenal obstruction (classic “beak” appearance with volvulus)
Ultrasound
Barium enema
CT
1.
2.
3.
4.
Pyloric stenosis metabolic disorders
GE reflux treatments – non-medicinal
Treating dehydration/metabolic derangements in GI disorders
Normal course of GE reflux in infants
Key points
• Pyloric Stenosis
• Hypochloremic, hypokalemic, metabolic alkalosis
• Diagnostic modality of choice- US (ultrasound)
• Correct dehydration and metabolic derangements- 1.5
times the calculated maintenance rate
• GERD Treatment
• Adjust feeding volumes and frequency
• Thickening of feeds with rice cereal
• Usually resolves by age 12mo-18 mo
QUESTION
Which of the following results would you expect to
see in this infant with the diagnosis of pyloric
stenosis?
 A. Na+ 142, K+ 4.2, Cl- 108, CO2 27
 B. Na+ 128, K+ 6.8, Cl-98, CO2 13
 C. Na+ 137, K+ 5.2, Cl- 111, CO2 17
 D. Na+ 138, K+ 3.1, Cl- 89, C02 37
 E. Na+ 150, K+3.1, Cl- 99, CO2 17

Question?
 What
historical piece of information can be
considered normal infant behavior?
A. Regurgitation and vomiting 30-40 minutes after feedings
B. Arching and stiffening with vomiting
C. Aversion to feeding
D. Choking when vomiting/spitting
E. Increasing infant irritability
Question?

Which of the following is not an exacerbating factor
for GER in children?
○ A. Supine position
○ B. Secondary smoke exposure
○ C. Overfeeding
○ D. Breastfeeding
○ E. Increased respiratory effort (ie: cough)
1. Pyloric stenosis metabolic disorders
Pyloric Stenosis - Labs/Radiographs

Complete Metabolic Panel
 Hypochloremic, hypokalemic, metabolic alkalosis
 Hyperbilirubinemia (5%-14%) = icteropyloric syndrome

Ultrasound
 Diagnostic modality of choice
 Allows earlier diagnosis for those infants without palpable
olive on exam

Barium Studies – String sign
2. GE reflux treatments – non-medicinal
Key points
• Pyloric Stenosis
• Hypochloremic, hypokalemic, metabolic alkalosis
• Diagnostic modality of choice- US (ultrasound)
• Correct dehydration and metabolic derangements- 1.5
times the calculated maintenance rate
• GERD Treatment
• Adjust feeding volumes and frequency
• Thickening of feeds with rice cereal
• Usually resolves by age 12mo-18 mo
GERD Treatment - Infants
Most infants do not need any treatment for
“asymptomatic” GER
 Dietary changes

 Adjust feeding volumes and frequency
 Thickening of feeds with rice cereal
 Trial of hypoallergenic diet (exclude dairy or soy proteins)

Positioning
 Prone positions and upright carried positions can minimize
reflux

Pharmacology
GERD - older children and adolescents
Treatment

Conservative therapy and lifestyle changes
 Avoid tobacco smoke
 Avoid acidic or reflux inducing foods
 Weight reduction
 ? Left side position and head elevation during sleep

Pharmacology
 Acid suppression (see next slide)
3. Treating dehydration/metabolic
derangements in GI disorders
Key points
• Pyloric Stenosis
• Hypochloremic, hypokalemic, metabolic alkalosis
• Diagnostic modality of choice- US (ultrasound)
• Correct dehydration and metabolic
derangements - 1.5 times the calculated
maintenance rate
• GERD Treatment
• Adjust feeding volumes and frequency
• Thickening of feeds with rice cereal
• Usually resolves by age 12mo-18 mo
Pyloric Stenosis - Treatment

Correct dehydration and metabolic derangements
 Correction of alkalosis
 1.5 times the calculated maintenance rate

Pyloromyotomy
4. Normal course of GE reflux in infants
GERD
Peaks at 4 months
 Usually resolves by age 12mo-18 mo

 90% by 12 months
Likely genetic and environmental predispositions
 More common in:

 Premature infants
 Children with neuromuscular disorders
○ i.e. muscular dystrophy, cerebral palsy, and children with Down
syndrome
1.
2.
3.
4.
5.
Locations of salivary stones
Infectious causes of siladenitis
Illnesses associated with siladenitis
Complications of parotidectomy
Causes of bilateral parotid swelling in kids
1. Locations of salivary stones
Salivary Stones

Location
 Most are submandibular (80%)

Composition
 Most are calcium
○ Dr. Orr said this is a good EXAM Question:
 What distinguishes submandibular stones from salivary stones?
- Submandibular stones ARE calcified
- Salivary stones are NOT calcified
 Uric acid
2. Infectious causes of siladenitis
Sialadenitis – Infectious Etiology
Organisms involved
 S.
aureus - most common
Streptococcus
 Coliforms
 Anaerobes

3. Illnesses associated with siladenitis
Sialadenitis – Etiology
Usually after duct obstruction
 Hyposecretion states

 Sjogren’s Syndrome
 Prior radiation treatment to oral cavity
Most common in parotid gland
 Typical patient is 50-60 years old
 Can be seen in younger patients with anorexia

Sialadenitis – Atypical … DON’T MEMORIZE








Viral infections – paramyxovirus, influenza, coxsackie, adenovirus, HIV
Atypical bacteria – mycobacterium TB, non-TB mycobacterium,bartonella,
actinomycosis
Autoimmune – Sjorgen’s syndrome
Granulomatous – parotid gland sarcoidosis, Crohn’s disease
Radiation (I-131)
Endocrine – Acromegaly, alcoholism, diabetes insipidus, diabetes mellitus,
hypothyroidism, cirrhosis of the liver, uremia
Medications – Antihypertensives, Iodine, Isoprenaline, Lead, Mercury,
Naproxen, Oxyphenbutazone, Sulfisoxazole, Thiocyanate (from sodium
nitroprusside), Propylthiouracil, Valproic acid
Nutritional problems - Beriberi (B1 – thiamine deficiency), Bulimia, Malnutrition,
Pellagra (B3 – Niacin deficiency), Amylophagia, Vitamin A deficiency
4. Complications of parotidectomy
Salivary Gland Tumors – Benign

Treatment is excision (parotidectomy)
 Picking the right surgeon is critical

Complications of parotid surgery
 Facial nerve paralysis or paresis
 Greater auricular nerve damage
 Gustatory sweating (Frey’s syndrome)
 Salivary fistula (uncommon and usually subsides with
conservative treatment)
5. Causes of bilateral parotid swelling in
kids
Viral Sialadenitis
Typical case is mumps (paramyxovirus)
 Usually will see bilateral swelling and
tenderness
 Other viruses

 Influenza
 Coxsackie
 Adenovirus
 HIV – diffuse non-tender enlargement of all
glands

Treatment is supportive
1.
2.
3.
4.
Differentials for dysphagia
Surgical intervention for Zenkers
EGD findings for Plummer-Vinson
Gold standard for diagnosis and treatment procedures for achalasia
1. Differentials for dysphagia
Pathology
Zenker’s Diverticulum
 Eosinophilic Esophagitis
 Infectious Esophagitis
 Achalasia
 Diffuse Esophageal Spasm
 Plummer-Vinson Syndrome
 Boorhave’s Syndrome

2. Surgical intervention for Zenkers
Zenker’s Diverticulum

Barium Esophagram (Dx study of choice)

Therapy:
 Surgery – Zenker’s is a surgical disorder
Diverticulectomy + Myotomy
Myotomy + Diverticulopexy
Dohlman Procedure (Endoscopic Stapling and Division)
All Involve Division of the Cricopharyngeus Muscle for
Successful Treatment!!
1.
2.
3.
3. EGD findings for Plummer-Vinson
Plummer-Vinson Syndrome
Triad: Dysphagia, IDA, Esophageal Webs
 Typically in Postmenopausal Women
 Labs: hypochromic, microcytic anemia
 Endoscopy: Esophageal Webs (Cervical Esophagus)
 Tx: Oral Iron Supplements

PREMALIGNANT CONDITION
 SQUAMOUS CELL CA

4. Gold standard for diagnosis and
treatment procedures for achalasia
Achalasia
Greek Root: chalan = “to loosen”
 Etiology: Unknown
 Secondary Effect of Etiology:

 Loss of ganglionic cells in Myenteric Plexus
 Interruption of vagal n. innervation of LES, which
mediates relaxation
FAILURE OF LES RELXATION
INNEFFECTIVE PERISTALSIS
4a. Gold standard for diagnosis of
achalasia
Achalasia - Dx
Esophagram: “Bird’s Beak”
 Manometry (Gold Standard): Hypertensive LES
 EGD: Confirms Hypertensive LES, rules out
concomitant pathology

4b. Gold standard for treatment procedures
for achalasia.
Achalasia Tx
Treatment:


Not Curative
Endoscopic / Surgical Txs are
Palliative

 SL nitroglycerin
 Nitrates
 Calcium channel blocker

Relieve Obstruction
Prevent GERD
Achieve Long-Term Results
Endoscopic:
 Pneumatic dilation
 Botox injection
Principles of Tx:



Medical:

Surgical:
 Heller Myotomy with
Fundoplication (Standard)
 Esophagectomy
(Megaesophagus “sigmoid”, failed
myotomy, undilatable reflux
stricture)
1.
2.
3.
4.
5.
Most common risk factor for esophageal cancer
Treatment for H pylori
Treatments for esophageal cancer by stage
Best modality to diagnose esophageal cancer
Risk factors for gastric cancer (body or distal stomach)
1. Most common risk factor for esophageal
cancer
Risk Factor Summary - LEARN THIS
Factor
SCC
Adeno
Tobacco
+++
++
Alcohol
+++
-
Barrett’s
-
++++
Weekly reflux S’s
-
+++
Achalasia
+++
-
Obesity
-
++
Caustic injury
++++
-
Head/neck CA
++++
-
Poverty
++
-
Breast radiation
+++
+++
Risk Factors

Tobacco and Alcohol
 Per previous slide, if you have to pick one, I would
choose TOBACCO.
Achalasia
 Chronic Strictures
 Barrett’s Esophagus
 Environmental

2. Treatment for H pylori
Treatment of H Pylori
There are many schemes for treating H. pylori infection;
however, an optimal treatment has not been defined, and
there is not a single antibiotic treatment that can
eradicate it.
 Historically, a combination of various antibiotics has been
used to eradicate the infection. The antibiotics used
include clarithromycin, amoxicillin, metronidazole,
tetracycline, fluoroquinolones, tinidazole, and others.
These antibiotics are often used in combination with
antisecretory agents, such as PPIs, or with bismuth salts.

Up To Date guidelines – EXAM!!
TRIPLE THERAPY:
PPI + Clarithromycin + Amoxicillin
(substitute metro for PCN allergy)



The regimen most commonly recommended for first line treatment of
H. pylori is triple therapy with a proton pump inhibitor (PPI)
amoxicillin (1 g twice daily), and clarithromycin (500 mg twice daily)
for 7 to 14 days. We suggest treatment for 10 days to two weeks.
Metronidazole (500 mg twice daily) can be substituted for amoxicillin
in penicillin-allergic individuals.
A longer duration of treatment (14 versus 7 days) may be more
effective in curing infection but this remains controversial
EXAM!!!
QUADRUPLE THERAPY = PPI + Bismuth + metro + TCN

Quadruple therapy consists of a PPI, combined with bismuth (525
mg four times daily) and two antibiotics (eg, metronidazole 250
mg four times daily and tetracycline 500 mg four times daily)
given for 10 to 14 days. Quadruple therapy is appropriate as
initial therapy in areas in which the prevalence of resistance to
clarithromycin or metronidazole is ≥15 percent, or in patients with
recent or repeated exposure to clarithromycin or metronidazole
[18]. If tetracycline is not available, doxycycline (100 mg twice
daily) may be substituted
3. Treatments for esophageal cancer by
stage
Treatment

Treatment options vary according to stage, patient
performance status and local expertise
Treatment Stage 0-1
CA in situ or tumors limited to the
mucosa
 Esophageal Sparing Procedures

 Endoscopic mucosal resection
 Phototherapy
 RFA
No role for Chemo or XRT
 Conservative or Minimally
Invasive Resection

Treatment Stage 2-3
Higher potential for lymph node involvement
 Surgery alone is insufficient if N+ disease

 Neoadjuvant = Preoperative Treatment (SEE NEXT SLIDE)
T2N0 patients
 Definitive chemoradiation (no surgery) may be used
in selected patients – usually with SCC

What is adjuvant therapy?
Chemo +/- radiation given AFTER “curative” surgery
 Rationale: High risk patients with R0 resection might
have microscopic (undetected) metastases. Giving
chemo or radiation at this point is typically more
effective then waiting until metastases are manifest.
 Disadvantage: Some patients might have been cured
by surgery alone and are treated unnecessarily [Key:
Use guidelines for risk stratification to discuss options
with patients]

What is Neoadjuvant therapy?
Chemo +/- radiation BEFORE surgery
 Advantages:







Objective measurement of chemotherapy effectiveness
Possible organ preservation (rectum, breast…)
Patient has best functional state
XRT given to tissues that have not been devascularized
Possible survival advantage
Disadvantages:
 Delays surgery
 Possibly increased surgical complications
 Patients “want cancer out”
Treatment Stage 4
Non regional lymph node metastases (e.g. cervical or
celiac axis)
 Distant metastases
 Palliative chemotherapy
 Palliative resection - rarely
 Stenting
 Brachytherapy
 Photodynamic Therapy

4. Best modality to diagnose esophageal
cancer
Diagnosis
EGD with Biopsy
 Barium Swallow

EGD with Biopsy is the primary
diagnostic modality and allows
histologic evaluation as well as
anatomic evaluation of location,
position related to GE junction, and
evaluation of the stomach as potential
conduit or need for resection
Diagnosis
EGD with biopsy
 CT scan
 PET scan
 EUS

5. Risk factors for gastric cancer (body or
distal stomach)
Risk Factors

Environmental
 H.
Pylori
Diet – nitrosamines (smoked meat)
 Tobacco
 Genetic Predisposition
 Pernicious Anemia

 Vit B 12 deficiency
○ Due to cell change in stomach
 Low acid environments
Japan: Gastric cancer accounts for 50% of cancer
deaths – also high in Chile, Costa Rica, Hungary,
Portugal, and Romania (a very diverse group
geographically and ethnically)
 Migration to low risk areas decreases risk

H
pylori infection is probably the
biggest risk factor

Nitrosamine ingestion in animal models is
associated with gastric cancer
H pylori

Unequivocally linked to gastritis and gastric cancer

Associated with cancers
in the body and
distal stomach but not GE junction (these are
related to reflux)
 In North America 50% of adults older than 50 years
are seropositive for H pylori, but relatively few
develop gastric cancer
1.
2.
3.
4.
5.
First steps in treatment
Findings and chances of rebleeds
Rare causes of upper GI bleeds
Mortality in UGI bleeds
Steps to treatment of esophageal varices
1. First steps in treatment
2. Findings and chances of rebleeds
2a. Findings of rebleeds
2b. Chances of rebleeds
3. Rare causes of upper GI bleeds
4. Mortality in UGI bleeds
5. Steps to treatment of esophageal varices
1.
2.
3.
4.
Manometric findings with GERD
Stepwise treatment and workup of GERD
Define sliding hiatal hernias
Treatment options for Barrett’s
1. Manometric findings with GERD
2. Stepwise treatment and workup of GERD
2a. Stepwise treatment of GERD
2b. Stepwise workup of GERD
3. Define sliding hiatal hernias
4. Treatment options for Barrett’s
1.
2.
Presentation of intussusception / volvulus / necrotizing enterocolitis / malrotation
Long term complications of necrotizing enterocolitis
1. Presentation of intussusception /
volvulus / necrotizing enterocolitis /
malrotation
1a. Presentation of intussusception
1b. Presentation of volvulus
1c. Presentation of necrotizing enterocolitis
1d. Presentation of malrotation
2. Long term complications of necrotizing
enterocolitis
1.
2.
3.
4.
Location of Meckels diverticulum and presentation signs/symptoms
Define obturator sign
Management of appendicitis
Mesenteric lymphadenitis presentation
1. Location of Meckels diverticulum and
presentation signs/symptoms
2. Define obturator sign
3. Management of appendicitis
4. Mesenteric lymphadenitis presentation
1.
2.
3.
4.
5.
Metabolic abnormalities with SBO
Venous drainage to the small bowel
Anatomy of volvulus
Complications of SBO
Location of acute mesenteric ischemia
1. Metabolic abnormalities with SBO
2. Venous drainage to the small bowel
3. Anatomy of volvulus
4. Complications of SBO
5. Location of acute mesenteric ischemia