1.

Peptic Ulcer disease (PUD):

Pathophysiology: Peptic ulcers are defects in the gastric or duodenal

mucosa that extent through the muscularis mucosa. Normally a
physiologic balance exists between peptic acid secretion and
gastroduodenal mucosa defense. PUD occurs when defense
mechanisms in the GI mucosa- i.e. intercellular junctions, mucus
production, mucosal blood flow, and cellular restoration- malfunction
and allow diffusion of H+ ions that injures the GI epithelium.

Etiology: M/C causes are Helicobacter pylori infection and NSAID

use. Less common causes are hypersecretion states such as Zollinger-
Ellison syndrome, G-cell hyperplasia, mastocytosis and basophilic
leukemias.

Risk Factors: Cirrhosis, chronic obstructive pulmonary dz (COPD), renal

failure, and organ transplantation as associated with an increased risk
of PUD.

Signs/Symptoms: M/C symptom is epigastric pain- a gnawing or

burning sensation that occurs 2-3 hrs. after meals and is relieved by
food or antacids. Pt. may also present with nausea, vomiting (possible
hematemesis), heartburn, and fatty food intolerance.

Complications: Perforation, penetration, obstruction, and perfuse

bleeding from PUD will require surgery.

Appropriate PE: Clinical finding are non-specific, and include epigastric

tenderness, guaiac (+) stool, melena (tar-like stool), and succussion
splash (a splashing sound heard over the stomach during auscultation,
as a result of gastric obstruction).

DDx: Upper GI endoscopy required to R/O gastric cancer.

Investigative Measures: Upper GI endoscopy M/C procedure, b/c it

allows you to visualize very small ulcers (<0.5 cm), obtain a biopsy of
the ulcer to R/O malignancy, and asses for H. pylori infection.
Detection of H. pylori infection is essential! Rapid urease endoscopic
test is the gold standard for confirming presence of H. pylori.
Antibodies to H. pylori can also be measured in patient’s serum or
stool.

Tx: Cure H. pylori infection with a triple-drug therapy of proton-

pump inhibitors (PPIs), amoxicillin and clarithromycin. Common PPIs
are omeprazole (Prilosec), lansoprazole (Prevacid), rabeprazole
(Aciphex), and esomeprazole (Nexium). Stop NSAID use. Surgery is
limited to patients with extensive bleeding or perforation, and usually
involves a vagotomy and pylorplasty.

Patient Ed.: Stop smoking, avoid NSAID use, and avoid heavy alcohol
use.
Acute Gastritis:

Pathophysiology: Acute gastritis covers a broad spectrum of entities

that induce inflammatory changes in the gastric mucosa. The common
mechanism of injury is an imbalance between the aggressive and
defensive factors that maintain the integrity of the gastric mucosa. In
erosive acute gastritis, gravity causes the irritating agents lie on the
greater curvature of the stomach and injure the mucosa in that area.
With nonerosive gastritis, H. pylori tends to infect the antrum of the
stomach.

Etiology: Acute gastritis has a number of causes- drugs, alcohol, bile,

ischemia, bacterial, viral or fungal infections, acute stress/shock,
radiation, allergy, food poisoning, and direct trauma.
There are 2 main categories:
• Erosive (superficial, deep, or hemorrhagic) M/C caused by
NSAIDs, stress, radiation, bile reflux, and ischemia. Erosive
agents reduce prostaglandin synthesis, making the gastric
mucosa vulnerable to injury from gastric acid.
• Nonerosive, M/C caused by H. pylori. The bacteria imbed
themselves in the protective mucous layer that coats the gastric
mucosa. It protects itself from the acidity by producing large
amounts of urase, and is able to adhere to mucosa cells. The
binding of H. pylori to gastric mucosa cells produces
inflammatory changes.

Risk Factors: Previous mucosal injury- peptic ulcer disease, endoscopic

injury or injury caused by surgery. Routine use to NSAIDs, esp. high
doses. History of eating raw fish.

Signs/Symptoms: Patient will present with a gnawing or burning feeling

in the epigastric region. Pain can improve or worsen with eating. Pain
is accompanied by nausea, vomiting, loss of appetite, belching, and
bloating. Fever, chills, and hiccups may be present.

Complications: Bleeding from an erosion or ulcer, gastric outlet

obstruction due to edema (food can’t get to small intestine),
dehydration from vomiting, or renal insufficiency as a result of
dehydration.
Appropriate PE: Physical exam findings are often normal. There may be
mild epigastric tenderness

Investigative Measures: There are 4 radiologic signs for acute

gastritis, regardless of the etiology: thick folds (> 5mm),
inflammatory nodules (bumpy appearance of gastric mucosa),
coarse area gastrica (enlarged areas of the stomach, indicates
swelling), and erosions (liner or serpiginous, found near greater
curvature of stomach). Can also test stool for H. pylori antigens (HpSA)
if bacterial infection is suspected.

Tx: Treatment is symptomatic, except for cases caused by H. pylori.

Administer fluids and electrolytes, antacids containing aluminum and
magnesium, and discontinue use of offending drugs i.e. NSAIDs and
alcohol. Proton-pump-inhibitors such as omeprazole (Prilosec) and
antidiarrheals such as bismuth subsalicylate (Pepto-Bismol) can also
help. For H. pylori infection, use H2-blockers such as cimetidine
(Tagamet) and antibiotics-amoxicillin, tetracycline, metronidazole, or
clarithromycin.

Chronic Gastritis:

Pathophysiology: Chronic gastritis is characterized by chronic

inflammation of the stomach mucosa. There are several common
forms:
• (M/C) H. pylori-associated chronic gastritis- these gram(-)
bacteria colonize the mucous layer of the stomach and infiltrate
into the underlying gastric mucosa, producing inflammation. H.
pylori is typically acquired during childhood, and complications
develop in late adulthood.
• Infectious granulomatous gastritis- tuberculosis may affect the
stomach, causing caseating granulomas and necrosis. Often
occurs in the immunosuppressed.
• Gastritis in immunusuppressed patients- caused by infection with
CMV, HSV, or Mycobacterium. Granuloma formation and necrosis
if the mucosa is observed.
• Autoimmune gastritis- associated with serum antiparietal and
anti-intrinsic factor antibodies that prevent the uptake of vitamin
B12. The gastric corpus (upper ½ of stomach) undergoes
progressive atrophy, and pernicious anemia develops.
• Chronic reactive chemical gastropathy- associated with long-
term use of NSAIDs, alcohol, or other drugs.
• Non-infectious granulomatous gastritis- Crohn’s dz and
sarcoidosis can produce non-infectious granulomas and
inflammation.
Etiology: Etiological agents depend on the type of chronic gastritis, and
include H. pylori (M/C), tuberculosis, CMV, HSV, Mycobacterium, serum
antiparietal and anti-intrinsic factor antibodies, NSAIDs, alcohol, drugs,
Crohn’s dz, sarcoidosis.

Risk Factors: Asian and Hispanic pts. are at a greater risk of developing
H. pylori associated chronic gastritis. Females of any race are 3x more
likely to be affected by autoimmune gastritis.

Signs/Symptoms: Depends on the form of chronic gastritis:

• H. pylori infection- epigastric pain, fullness, nausea, vomiting,
flatulence, malaise, (+/-) fever. Will see antral nodularity with
endoscope.
• Autoimmune gastritis- megaloblastic anemia, weakness,
lightheadedness, vertigo, sore tongue, diarrhea, numbness and
paresthesia in extremities.
• Granulomatous gastritis- gastric pain, nausea, vomiting,
granulomatous inflammation in other locations, esp. the lungs or
salivary glands. Will see gastric mucosal nodules with
cobblestoning, multiple apthous ulcers, and thick antral folds
with an endoscope.

Complications: Pts. with H.pylori associated chronic gastritis have a 12

to 16-fold increase of developing gastric carcinoma.

Appropriate PE: Physical exam findings are often normal, with possible
epigastric pain. Significant PE findings are only with autoimmune
gastritis- the patient is pale with jaundiced eyes and skin, the pulse is
rapid, the heart may be enlarged, and you may hear a systolic flow
murmur.

Investigative Measures: Definitive diagnosis of chronic gastritis can

only be done histologically (to ID H. pylori, viruses, granulomas, etc.).
Therefore, need an endoscopic biopsy. Diagnose autoimmune gastritis
by testing serum for antiparietal and anti-intrinsic factor antibodies.

Tx: Triple-drug therapy for H. pylori infection that includes a proton-

pump inhibitor, clarithromycin, and amoxicillin. Commonly used
proton-pump inhibitors are lansoprazole (Prevacid) and omeprazole
(Prilosec)

28.Fatty liver- NASH:

Pathophysiology: Non- alcoholic fatty liver disease (NASH) is a form of
steatohepatitis (fatty liver associated with inflammation). Excessive
accumulation of lipids within hepatocytes causes liver inflammation
and hepatocyte death. The excessive build-up of fats in the liver can
be caused by decreased mitochondrial fatty acid oxidation, increased
delivery of fatty acids to the liver, or deficient incorporation and/or
export of triglycerides in the body.

Etiology: Inflammation and necrosis of the liver is caused by excessive

accumulation of lipids within hepatocyes, WITHOUT the use of alcohol.

Risk Factors: Obesity, type II diabetes, and hypertriglyceridemia.

M/C in Caucasians. Can occur in ALL age groups!

Signs/Symptoms: Most pts. with NASH are asymptomatic. They could

complain of persistent fatigue or slight upper abdominal discomfort.
Symptoms of liver disease such as ascites, edema, and jaundice can
arise in pts. with cirrhosis due to NASH.

Complications: NASH can progress to cirrhosis and hepatocellular

carcinoma. Roughly 50% of pts. with NASH also have cirrhosis.

Appropriate PE: Hepatomegaly is commonly found. Splenomegaly and

signs of portal hypertension (ascites, spider angiomas, varices) can be
seen in patients who’ve progressed to cirrhosis. A liver biopsy will yield
specific histological findings- steatosis, inflammatory infiltrates,
ballooning degeneration, and fibrosis.

DDx: NASH diagnosis can only be established when excessive alcohol

and/or drug use can be excluded.

Investigative Measures: Test serum for elevated aspartate

aminotransferase (AST) and ALT levels, as well as elevated iron
levels. On ultrasound, the liver will appear to be hyperchogenic and
bright. A liver biopsy is essential in order for a definitive diagnosis
of NASH.

Tx: Weight loss and getting the patient’s diabetes and high cholesterol
under control can slow NASH and actually reverse some of the
damage. Lipid-lowering drugs such as metformin, gemfibozil,
atorvastatin, and glitazones can also help.

29. Gilbert’s Syndrome:

Pathophysiology: Gilbert’s syndrome causes mild

hyperbilirubinemia (less than 6mg/dL) due to underactivity of the
conjugating enzyme system bilirubin-UGT. Bilirubin-UGT is located in
the endoplasmic reticulum of hepatocytes, and is responsible for the
disposal of bilirubin, a chemical that results from the normal
breakdown of RBCs.

Etiology: Gilbert’s syndrome is the result of a genetic mutation on

chromosome 2, resulting in abnormal bilirubin-UGT enzymes. M/C
diagnosed after puberty, when alterations in sex hormone levels
cause the blood bilirubin to rise.

Risk Factors: Gilbert’s syndrome is an autosomal recessive disease;

both parents need to be carriers of the defective gene in order for their
children to get Gilbert’s syndrome.

Signs/Symptoms: Gilbert’s syndrome is often detected purely by

accident, in the course of routine blood screening. There will be mild
elevations of bilirubin in the blood, particularly after starvation,
dehydration, stress, or illness. Elevated bilirubin can sometimes cause
mild jaundice of the sclera.

Complications: None. Gilbert’s syndrome is a benign condition.

DDx: Order a CBC to R/O hemolysis. Also perform a liver function test
to R/O liver dz (people with Gilbert’s syndrome have completely normal
liver functioning).

Tx: No need for treatment, hyperbilirubinemia is a completely benign

condition. People with Gilbert’s syndrome are not at an increased risk
of morbidity.