GIT system Review

Mohamed Yahia
Esophageal Disease
• Dysphagia/Odyophagia Difficulty swallowing (dysphagia) or
pain with swallowing (odynophagia) due to abnormalities of the
oropharynx or esophagus
History/PE
• The presentation of dysphagia varies according to location: n n
Oropharyngeal dysphagia: Usually involves aspiration of food
into the lungs (liquids more than solids), leading to coughing or
choking.
• Causes can be neurologic or muscular and include stroke,
Parkinson’s disease, myasthenia gravis, prolonged intubation,
and Zenker’s diverticula.
• Esophageal dysphagia: If due to obstruction, usually involves
solids more than liquids (strictures, Schatzki rings, webs,
carcinoma) and is progressive.
• If due to a motility disorder (achalasia, scleroderma,
esophageal spasm), usually presents with both liquid and solid
dysphagia.
• Examine for masses (eg, goiter, tumor) and anatomic defects.
Diagnosis

Oropharyngeal dysphagia: Video fluoroscopy.

Esophageal dysphagia: Barium swallow (aka esophagram)
followed by endoscopy, manometry, and/or pH monitoring. If an
obstructive lesion is suspected, proceed directly to endoscopy
with biopsy. Odynophagia: Upper endoscopy. Etiology
dependent.
Clinical scenario (^_^)
• A 55-year-old white woman with a history of iron defi ciency anemia has had
intermittent trouble swallowing solids for the past few years. She denies alcohol
or tobacco use. Her vital signs are stable. Her iron level is 40 μg/dL and total iron
binding capacity is 500 μg/dL. Other laboratory tests are within normal limits.
Which of the following is the most likely diagnosis?
• (A) Achalasia
• (B) Barrett’s esophagus
• (C) Esophageal carcinoma
• (D) Mallory-Weiss syndrome
• (E) Plummer-Vinson syndrome
• (F) Refl ux esophagitis
• (G) Symptomatic diffuse esophageal spa
 Esophageal spasm
• A motility disorder in which normal peristalsis is periodically
interrupted by high-amplitude nonperistaltic contractions. Also known
as nutcracker esophagus
• Hx/PE: Presents with chest pain, dysphagia, and odynophagia. Often
precipitated by ingestion of hot or cold liquids; relieved by nitroglycerin.
• Dx: Barium swallow may show a corkscrew-shaped esophagus.
Esophageal manometry reveals high-amplitude, simultaneous
contractions.
• Tx: Nitrates and calcium channel blockers (CCBs) for symptomatic
relief; surgery (esophageal myotomy) for severe, incapacitating
symptoms.
Clinical scenario (^_^)
• . A 64-year-old white woman presents to her primary care
physician complaining of diffi culty and pain with swallowing, as
well as occasional chest pain. She has a history of breast
cancer treated with lumpectomy and radiation, hypertension,
high cholesterol, and ovarian polyps. She indicates that her
current problem started with liquids, but has progressed to
solids, and that the food “just gets stuck in my throat.” The chest
pain was once so bad that she took one of her husband’s
nitroglycerin pills and the pain subsided, but it has since
occurred many times. The physician orders an x-ray of the
chest, but it is not diagnostic. Manometry is conducted, and it
shows uncoordinated contractions. Which of the following is the
most likely diag
• (A) Breast cancer relapse
• (B) Diffuse esophageal spasm
• (C) Esophageal cancer
• (D) Myocardial infarction
• (E) Nutcracker esophagus
• The correct answer is B. Spasms of the esophagus are
characterized by both solids and liquids, causing odynophagia and
dysphagia, as well as noncardiac angina. Globus, or the feeling of
food stuck in one’s throat, is also very common. Nitroglycerin may
actually confuse the diagnosis because it acts to relax the smooth
muscle, thereby relieving the pain. X-rays may be helpful in
diagnosis by showing what is known as a corkscrew formation of
the esophagus. The anatomy of the esophagus may be divided
into three parts, and when these three do not contract in a uniform
manner as with spasms, then a food bolus may become trapped
and cause pain. Manometry establishes the diagnosis by showing
these uncoordinated contractions.
achalasia
• achalasia n A motility disorder of the esophagus characterized
by impaired relaxation of the lower esophageal sphincter (LES)
and loss of peristalsis in the distal two-thirds of the
esophagus. Results from degeneration of the inhibitory neurons
in the myenteric (Auerbach’s) plexus.
• Hx/PE: Common symptoms include progressive dysphagia, chest pain,
regurgitation of undigested food, weight loss, and nocturnal cough.
• nDx:nBarium swallow reveals esophageal dilation with a “bird’s beak”
ta-pering of the distal esophagus nManometry shows ↑ resting LES
pressure, incomplete LES relax-ation upon swallowing, and ↓
peristalsis in the body of the esophagus.nEndoscopy is indicated to
rule out mechanical causes of obstruction.
• nTx: Nitrates, CCBs, or endoscopic injection of botulinum toxin into the
LES may provide short-term relief of symptoms. Pneumatic balloon
dila-tion and surgical (Heller) myotomy are definitive treatment options.
Clinical scenario (^_^)
• The correct answer is D. This patient has achalasia, as confi
rmed by the narrowing of the gastroesophageal junction (the
“bird’s beak” appearance). Secondary causes include
malignancy and Chagas’ disease. Malignancies that can cause
achalasia include gastric carcinoma
• and lymphoma. Upper endoscopy and associated biopsies can
help to make the diagnosis of the secondary causes.
esophageal Diverticula
• Diverticula can be present in any location. Zenker’s diverticulum
is defined as cervical outpouching through the cricopharyngeus
muscle.
• Hx/PE: Presents with chest pain, dysphagia, halitosis, and
regurgitation of undigested food.nDx: Barium swallow will
demonstrate outpouchings.
• nTx: If symptomatic, treat with surgical excision of the
diverticulum. For Zenker’s diverticulum, myotomy of the
cricopharyngeus is required to relieve the high-pressure zone.
Esophageal cancer
• Squamous cell carcinoma (SCC) is the most common type of
esopha-geal cancer worldwide, whereas adenocarcinoma is
most prevalent in the United States, Europe, and Australia.
nRisk factors include the following:
• nSCC: Alcohol and tobacco use.nAdenocarcinoma: Barrett’s
esophagus (columnar metaplasia of the dis-tal esophagus 2° to
chronic GERD).
• Hx/PE: Progressive dysphagia, initially to solids and later to
liquids, is common. Weight loss, odynophagia, GERD, GI
bleeding, and vomiting are also seen. n n Dx: Barium study
shows narrowing of the esophagus with an irregular border
protruding into the lumen
• EGD with biopsy conf irms the diagnosis. CT and endoscopic
ultrasound are used for staging.
• Tx: Chemoradiation and surgical resection are first-line
treatment. Resection is also indicated in cases of high-
grade Barrett’s dysplasia. Has a poor prognosis.
Clinical scenario (^_^)
• A 66-year-old man presents to his primary care physician for
diffi culty swallowing. Approximately 8 months ago, he began
exclusively eating soft foods because of the sensation of solid
foods becoming “stuck” in his chest. He reports some anorexia
and an unintentional weight loss of 11.3 kg (25 lb) over the past
several months. He admits to smoking one pack of cigarettes
daily for the past 35 years and drinking two beers a day since
he was 18 years old. Physical examination reveals a
temperature of 37.0°C (98.6°F), pulse of 86/min, and blood
pressure of 136/86 mm Hg. He appears cachectic.
• What is the most likely diagnosis?
• Esophageal carcinoma, likely squamous. Squamous cell
carcinoma accounts for the majority of esophageal carcinomas
worldwide, although the incidence varies geographically. The
incidence in the United States is approximately 20 per 100,000.
In Western societies, smoking and alcohol consumption are
strongly linked with squamous cell carcinoma. Adenocarcinoma
of the esophagus, once an unusual malignancy, now accounts
for over 50% of esophageal cancer in Western countries. The
increased incidence of adenocarcinoma is the result of the well-
established association between gastroesophageal refl ux,
Barrett’s esophagus, and esophageal adenocarcinoma.
• What are the signs and symptoms of this condition?
 gastroesophageal reflux Disease
(GERD)
• Symptomatic reflux of gastric contents into the esophagus, most
commonly from transient LES relaxation. Can also result from an
incompetent LES, gastroparesis, or hiatal hernia.
• History/PE
Patients present with heartburn that commonly occurs 30–90
minutes after a meal, worsens with reclining, and often improves
with antacids, sitting, or standing. Sour taste (“water brash”), a
globus sensation (a sensation of a lump in the throat), unexplained
cough, and morning hoarseness are also common. Examination is
usually normal unless a systemic disease (eg, scleroderma) is
present.
• Diagnosis Primarily a clinical diagnosis. An empiric trial of
lifestyle modification and medical treatment is often attempted
first. Studies may include barium swallow (to look for hiatal
hernia and demonstrate reflUx
• esophageal manometry, and 24-hour pH monitoring. nEGD
with biopsies should be performed in patients whose symptoms
are unresponsive to initial empiric therapy, long standing (to rule
out Barrett’s
• esophagus and adenocarcinoma; associated with alarm
symptoms (eg, blood in the stool, weight loss,
dysphagia/odynophagia).
• Complications Erosive esophagitis, esophageal peptic stricture,
aspiration pneumonia, upper GI bleeding, Barrett’s esophagus.
 hiatal hernia
• Herniation of the stomach upward into the chest through the
diaphragm.
• There are 3 common types: nSliding hiatal hernia (95%):
The gastroesophageal junction and a portion of the stomach are
displaced above the diaphragm
. Paraesophageal hiatal hernia (5%): The gastroesophageal
junction remains below the diaphragm, while the fundus
herniates into the thorax .
Mixed hiatal hernias (rare).
hiatal hernia
• Hx/PE: May be asymptomatic. Patients with sliding hernias
may present with GERD. n n Dx: Commonly an incidental
finding on CXR; also frequently diagnosed by barium swallow or
EGD.
• Tx: n Sliding hernias: Medical therapy and lifestyle
modifParaesophageal hernias: Surgical gastropexy
(attachment of the stomach to the rectus sheath and closure of
the hiatus) is recommended to prevent gastric volvulus.ications
to ↓ GERD symptoms.
Disorders of the Stomach and Duodenum
• Inflammation of the gastric mucosa. Subtypes are as follows:
• Acute gastritis: Rapidly developing, superficial lesions that are
often due to NSAID use, alcohol, H pylori infection, and stress
from severe illness (eg, burns, CNS injury).
• Chronic gastritis: Type A (10%): Occurs in the fundus and is due
to autoantibodies to parietal cells. Causes pernicious anemia
and is associated with other autoimmune disorders. Associated
with an ↑ risk of gastric adenocarcinoma and carcinoid tumors.
Type B (90%): Occurs in the antrum and may be caused by NSAID
use or H pylori infection. Often asymptomatic, but associated with
an ↑ risk of PUD and gastric cancer.
• History/PE Patients may be asymptomatic or may complain of
epigastric pain, nausea, vomiting, hematemesis, or melena.
• Diagnosis n Upper endoscopy to visualize the gastric mucosa. A
double-contrast upper GI series can also be used but is less
sensitive than EGD. nH pylori infection can be detected by the
urease breath test, serum IgG antibodies (which point to a
history of exposure, not current infection), H pylori stool
antigen (indicates current infection), or endoscopic biopsy
• Treatment↓ intake of exacerbating agents. Antacids, sucralfate,
H2 blockers, and/or PPIs may help. Administer triple therapy
(amoxicillin, clarithromycin, omeprazole) to treat H pylori
infection unless the patient is penicillin allergic, in which case
metronidazole should be substituted for amoxicillin. Give
prophylactic PPIs to patients at risk for stress ulcers (eg, ICU
patients).
peptic ulcer Disease (PUD)
• Although commonly thought to result from stress, PUD is now
known to result from damage to the gastric or duodenal mucosa
caused by impaired mucosal defense and/or ↑ acidic gastric
contents. H pylori is the causative factor in > 90% of duodenal
ulcers and 70% of gastric ulcers. Other risk factors include
corticosteroid, NSAID, alcohol, and tobacco use. Males are
affected more often than females.
• History/PE
• Presents with chronic or periodic dull, burning epigastric pain
that is often related to meals and can radiate to the back.
Patients may also complain of nausea, hematemesis (“coffee-
ground” emesis), or blood in the stool.
• Examination is usually normal but may reveal epigastric
tenderness and  stool guaiac. Acute perforation presents with
a rigid abdomen, rebound tenderness, and/or guarding.
• Diagnosis
• Rule out perforation:
• Gastric ulcers: AXR reveals free air under the diaphragam.
Duodenal ulcers: CT scan with contrast shows air in the
retroperitoneal space.
• Order a CBC to detect GI bleeding!!!. Upper endoscopy with
biopsy to confirm and to rule out active bleeding or gastric
adenocarcinoma (10% of gastric ulcers).
• H pylori testing. In recurrent or refractory cases, check
serum gastrin levels to screen for Zollinger-Ellison syndrome.
 Acute management:
If perforation is suspected, CT with IV contrast is indicated. If the
diagnosis is confirmed, surgical laparotomy will likely be required.
Carefully monitor BP. Rule out active bleeding with rectal vault
examination, NG lavage, and serial hematocrits. Monitor BP and
treat with IV hydration, blood transfusion, and IV PPIs. Urgent
EGD should be performed to control suspected bleeding.
Long-term management: n Medical therapy is indicated to
protect the mucosa, ↓ acid production, and eradicate H pylori
infection. n n For mild disease, treat with antacids, PPIs, or H2
blockers. Patients with H pylori infection should receive triple
therapy. Discontinue use of exacerbating agents.
gastric cancer
• Gastric cancer n A malignant tumor with a poor prognosis that is
particularly common in Korea and Japan.
• Most are adenocarcinomas, which exhibit 2 morphologic types:
Intestinal type: Differentiated cancer that originates from the
intestinal metaplasia of gastric mucosal cells. Risk factors
include a diet high in nitrites and salt and low in fresh vegetables
(antioxidants), H pylori colonization, and chronic gastritis.
• Diffuse type: Undifferentiated cancer not associated with H pylori
infection or chronic gastritis. Risk factors are unknown; signet
ring cells on biopsy are characteristic.
• Hx/PE: Early-stage disease is usually asymptomatic but may be
associated with indigestion and loss of appetite. Late-stage disease
presents with abdominal pain, weight loss, and upper GI bleeding.
• Dx: Upper endoscopy with biopsy is necessary to rule out other
etiologies and confirm the diagnosis.
• Tx: If detected early, treatment is surgical resection. Most patients
present with late-stage, incurable disease. Five-year survival is <
10% for advanced disease.
ZOllinger-ellison synDrOme
• ZOllinger-ellisOn synDrOme n n n n n n A rare condition
characterized by gastrin-producing tumors in the duodenum
and/or pancreas that lead to oversecretion of gastrin.
Oversecretion of gastrin ↑ gastric acid production, leading to
recurrent or intractable ulcers in the stomach and
duodenum (may occur more distally). In 20% of cases,
gastrinomas are associated with multiple endocrine neoplasia
(MEN) type 1
• Hx/PE: Patients may present with unresponsive, recurrent
gnawing, burning abdominal pain as well as with diarrhea,
nausea, vomiting, fatigue, weakness, weight loss, and GI
bleeding.
• Dx: ↑ fasting serum gastrin levels and ↑ gastrin with the
administration of secretin are diagnostic; CT is indicated to
characterize and stage disease
• Tx: n n Moderate- to high-dose PPIs often control symptoms.
Surgical resection of the gastrinoma after localization by CT or
octreotide scan to identify suspected carcinoid tumors.
Hepatobiliary and panceritic disease
Biliary disease
Chronic liver disease
• Chronic liver disease:
Progressive destruction of the liver parenchyma
over period greater than 6 months leading to
fibrosis and cirrhosis
• Causes of chronic liver disease
1. Viral causes: hepatitis B , C,
cytomegalovirus ,epestian barr virus.
2. Al cohol
3. Metabolic : non alcoholic fatty liver,
haemochromatosis, Wilson disease
4. Autoimmune
5. Right heart failure
Cirrhosis is an irreversible inflammatory prograssive
, fibrotic liver disease
however, not all causes are clearly understood.
Structural
changes result from injury (alcoholism, viruses,
steatosis, chemicals) and fibrosis.
It,s complication of all types of liver diseases
Liver cirrhosis lead to two important complications
Intra hepatic portal hypertension , liver failure
• Portal hypertension
• is abnormally high blood pressure in the portal venous system
primarily caused by resistance to portal blood flow.
• normally 3 mmHg; portal hypertension is an increase to at least
10 mmHg.
It causes several pathophysiologic problems that are difficult to treat
and can be fatal.
• Clinical presenting of chronic liver diseases:
• Either due to portal hypertension and this include:
Manifestion of Increased pressure in peritoneal
capillaries
1. Ascites
2. Spontaneous bacterial peritonitis
• Manfestaion of Portosystemic shunting of blood
• Manifestion in GIT:
1. Esophageal varices.
2. Hemorrhoids.
3. Anemia , thrombocytopenia, leukopenia
• Manifestion in CNS :
1. Hepatic encephalopathy .
• Manifestion of pulmonary system :
Hepatopulmonary syndrome (pulmonary hypertenion,pulmonary
edema)
• Presentation due liver failure:
Hematological manifestion :
Anemia, bleeding, jaundice,
Endocrine Manifestion
Edema/ ascites(increase aldestrone)
Gynecomastia and testiculartrophy in men and irregularities
Menstrual in women (Increased androgens/ estrogens).
Renal manifestion:
Hepatorenal syndrome( renal failure)
Cns manifestion :
Hepatic Encephalopathy(mild tremor .confusion ,coma)
• Skin manifestion :
Liver failure brings on numerous skin disorders. These lesions, called
variously vascular spiders, telangiectases, spider angiomas, and
spider nevi.

Bone manifestion:
osteporosis
Signs of chronic liver disease
1.Palmar erythema
• Educational objective:
• Hyperestrinism In cirrhosis leads to gynecomastia, testicular
atrophy, decreased body hair, spider angiomas, and palmar
erythema.
2.Dupuytren’s contracture
3.Leuconychia
4. Koilonychia
5.Clubbing
6. Jaundice
7. Parotid enlargement
8.Spider neavi
9. Gynaecomastia
10.Scratch marks

11.Cyanosis

12.Loss of body hair

13.Testicular atrophy

14.Water hammer pulse

15.spleenomegaly
15.Signs of portal hypertension

1. Ascites
2. Dilated veins
3. Caput medusae
4. Rectal hemorrhoids
Signs of acute liver failure
 1. Hepatic encephalopathy
1.Mild confusion
2.Apraxia
3.Dysarthria
4.Drowsiness
5.Hyperreflexia or hyporeflexia
6.Decerebrate posturing
2.Cerebral edema

3. Jaundice

4.Fetor hepaticus

5.Flapping tremor (asterixis)

Management
General management:
• Good nutrition.
• Avoid alcohol.
• Avoid :
 NSAIDs → risk of renal impairment ,hepatorenal
syndrome and GI hemorrhage.
 Opioids → ↑risk of toxicity and hepatic
encephalopathy.
Cont.
• Colestyramine for pruritus.
• Ultrasound every 3-6 months to screen for
HCC.
Specific management:
HBV:
Antiviral:
• Interferon.
• Lamivudine.
• Adefovir.
“the aim is to clear HBsAg and prevent cirrhosis
and HCC”
Cont.
HCV:
Antiviral:
• Combined interferon and ribavirin.
Primary billiary cirrhosis "PBC":
Ursodeoxycholic acid
• May normalize LFT but may have no effect on the
disease progression.
Cont.
Primary sclerotic cholangitis "PCS":
Ursodeoxycholic acid:
• May protect against colon cancer and improve
LFT.
Wilson’s disease:
Penicillamine
• Binds to accumulated copper and elimination
through urine.
Cont.
Hereditary hemochromatosis:
Venesection “phlebotomy”:
• Needed for life.
A1AT deficiency:
No specific treatment.
Deal with the complication.
Management of cirrhosis complications:
Ascites:
Low salt diet.
Spironolactone.
Furosemide.
Spontaneous bacterial peritonitis:
Cefotaxime
Cont.
Esophageal varices:
ABCs.
Restore blood volume.
Endoscopy.
Octreotide.
Cont.
Hepatic encephalopathy:
Identify and remove possible precipitating
factors such as drugs
Purgation and enema “to empty the bowels of
nitrogenous substances”
Nutrition “increase protein”
Antibiotics “rifaximin and metronidazole”
Treat any infection
Cont
• End stage liver cirrhosis
• Liver transplantation.
Upper and lower GIT bleeding
Pancreatic diseases
CA PANCERAS
Risk factor
Smoking 3 risk, diabetes mellitus, heavy alcohol use, chronic
pancreatitis, diet high in fried meats,
male to female ratio 2:1
above 60
60% arise in the pancreatic head; 30% arise in the body and tail
the rest arise from the periampulary reigon
clinical presention :
depend on the location :
1)progressive jaundice in head tumor
intermittent jaundice periampulmpulary tumor
Weight loss
2)Pain in the right hypochondrium, epigastrium, or left hypochondrium
depending on location of the tumour. Back pain, when present, is due to
involve ment of retropancreatic nerves, or pancreatic duct obstruction or stasis,
disruption of nerve sheath by tumour.
Migratory superficial thrombophlebitis—Trousseau’s sign (10%) is due to
release of platelet aggregating factors from the tumour or its necrotic material
(Trousseau himself died of carcinoma pancreas who had migrating
thrombophlebitis).
Workup for ca pancreas

Hx

Final
Ex
decision

MDT invest
 Ca head
pancreas

No operable Operable

palliative Whipple
Abdominal wall defects
MANY THANKS FOR YOUR attention