Achalasia

Achalasia is a rare swallowing disorder that affects the esophagus (the tube between
the throat and the stomach). In people with achalasia, the esophagus muscles do not
contract properly and do not help propel food down toward the stomach.
1. Acquired motor disorder of esophageal smooth muscle in which the lower esophageal
sphincter (LES) fails to completely relax with swallowing, and abnormal peristalsis of esophageal
body replaces normal peristalsis.
2. Absolute criteria for diagnosis
a. Incomplete relaxation of the LES
b. Aperistalsis of esophagus

Etiology
Loss of nerve cells in the ganglion of the myenteric plexus.
Fagal fiber de-generation.
Autoimmune or autoantibodies to the myenteric neurons. Chagas disease.

S+S
1. Progressive dysphagia (food and liquid).
2. Regurgitation a. Food gets “stuck” in the esophagus and then comes back up. b.
Regurgitation may lead to aspiration.
3. Chest pain
4. Weight loss
5. Recurrent pulmonary complications secondary to aspiration, which may cause lung abscess,
bronchiectasis, or hemoptysis.

Diagnosis
1. Barium swallow (Figure down below)— “bird’s beak”—beak-like narrowing of distal esophagus and a
large, dilated esophagus proximal to the narrowing.

2. Upper GI endoscopy—to rule out secondary causes of achalasia (gastric carcinoma) and retention
esophagitis or esophageal cancer.
3. Manometry—to confirm the diagnosis; reveals failure of LES relaxation and aperistalsis of esophageal
body.

Treatment
1. Start off with nitrates (relief for 90 min), then calcium channel blockers (60 min), both
are for symptomatic relief.
2. Inject Botulinum toxin in the lower esophagus (inject endoscopically) (blocks cholinergic
activity), should be repeated every 2 years.
3. Forceful dilatation—mechanical, pneumatic, or hydrostatic.
a. Pneumatic balloon dilatation is most effective.
b. Lowers basal LES tone by disrupting the muscular ring.

If super severe, heller extra-mucosal myotomy. Is a surgical treatment where there is an incision
of the circular muscle of the esophagus forcing it to relax.
Diffuse esophageal spasm.
Diffuse esophageal spasm (DES), also known as distal esophageal spasm, is a
condition characterized by uncoordinated contractions of the esophagus, which may
cause difficulty swallowing (dysphagia) or regurgitation. In some cases, it may cause
symptoms such as chest pain, similar to heart disease.

If a patient is 50+ and has this disease, first you do an ECG to rule out heart disease.

Etiology
Degeneration of inhibitory neurons associated with mental issues (stress, anxiety).

S+S
1. There is noncardiac chest pain that mimics angina and may radiate to the jaw, arms, and
back.
2. Dysphagia is common; however, regurgitation of food is uncommon.
3. Pain starts at rest and provoked by cold drinks.

Diagnosis
1. Esophageal manometry is diagnostic—simultaneous, multiphasic, repetitive contractions that occur
after a swallow; sphincter response is normal. (Picture below)

2. Upper GI barium swallow (“corkscrew esophagus”)—in 50%, which represents multiple simultaneous
contractions. (This isn’t gold standard because you can’t see it every time, attacks are episodic).

Why not endoscope? Because you don’t see anything, Dr said it’s useless.
Treatment
1. In general there is no completely effective therapy—treatment failure rates are high.

2. Medical treatment involves nitrates and calcium channel blockers (decreases amplitude of
contractions). Tricyclic antidepressants may provide symptomatic relief.

3. Esophagus myotomy is usually not performed, and its efficacy is controversial. Some support its use,
whereas others only recommend it when a patient is incapacitated by symptoms.
Gastroesophageal reflux disease (GERD)
occurs when stomach acid repeatedly flows back into the tube connecting your mouth
and stomach (esophagus). This backwash (acid reflux) can irritate the lining of your
esophagus. Many people experience acid reflux from time to time.

Etiology
a. Decreased esophageal motility to clear refluxed fluid.
b. A gastric outlet obstruction
c. A hiatal hernia (common finding in patients with GERD)
d. Dietary factors (e.g., alcohol, tobacco, chocolate, high-fat foods, coffee)—may decrease LES
pressure and exacerbate the condition.
e. pregnancy, obesity.

S+S
1. Heartburn, dyspepsia.
a. Retrosternal pain/burning shortly after eating (especially after large meals).
b. Exacerbated by lying down after meals.
c. May mimic cardiac chest pain (which may lead to unnecessary workup for ischemic heart
disease).
2. Regurgitation.
3. Waterbrash—reflex salivary hypersecretion.
4. Cough—due to either aspiration of refluxed material or a reflex triggered by acid reflux into
the lower esophagus.
5. Hoarseness, sore throat, feeling a lump in the throat.
6. Early satiety, postprandial nausea/vomiting.

Diagnosis
1. Endoscopy with biopsy—the test of choice but not necessary for typical uncomplicated cases.
a. Indicated if heartburn is refractory to treatment, or is accompanied by dysphagia,
odynophagia, or GI bleeding. b. A biopsy should also be performed to assess changes in
esophageal mucosa.
2. Upper GI series (barium contrast study)—this is only helpful in identifying complications of
GERD (strictures/ulcerations) but cannot diagnose GERD itself.
3. Twenty-four–hour pH monitoring in the lower esophagus—this is the most sensitive and
specific test for GERD. It is the gold standard but is usually unnecessary. (Normal esophageal
pH is close to pH 7.0. The most accepted definition of gastroesophageal reflux during
pH monitoring is a sudden decrease in intraesophageally pH to below 4.0, with the nadir
pH being reached within 30 seconds from the beginning of the drop.)
4. Esophageal manometry—use if a motility disorder is suspected
Complications
1. Erosive esophagitis—these patients are at high risk of developing complications such as
stricture, ulcer, or Barrett esophagus. These patients are candidates for long-term PPI therapy.
2. Peptic stricture
a. Consists of fibrotic rings that narrow the lumen and obstruct the passage of food.
b. Presents with dysphagia; may mimic esophageal cancer.
c. EGD can confirm the diagnosis. Dilation should be performed.
3. Esophageal ulcer—possible cause of upper GI bleeding
4. Barrett esophagus—occurs in 10% of patients with chronic reflux.
a. The normal stratified squamous epithelium of the distal esophagus is replaced by columnar
epithelium. Dysplastic changes may occur, with risk of adenocarcinoma.
b. Patients who have had symptomatic GERD for at least 5 years (and can undergo surgery if
cancer is found) should be screened for the possibility of Barrett esophagus.
c. Endoscopy with biopsy is required. If the patient has documented Barrett esophagus without
any dysplastic changes, periodic surveillance is appropriate (every 3 years)
d. medical treatment—long-term PPIs.
5. Recurrent pneumonia (due to recurrent pulmonary aspiration)—the cytologic aspirate
finding on bronchoscopy that can diagnose aspiration of gastric contents is lipid-laden
macrophages (from phagocytosis of fat)
6. Pitting of dental enamel (dental erosion); gingivitis
7. Laryngitis, pharyngitis.
Treatment

1. Initial treatment: a. Behavior modification—diet (avoid fatty foods, coffee, alcohol, orange juice,
chocolate; avoid large meals before bedtime); sleep with trunk of body elevated; stop smoking b.
Antacids—after meals and at bedtime

2. Add an H2 blocker—can be used instead of or in addition to antacids for mild and intermittent
symptoms

3. If above treatment fails or patient has severe GERD (e.g., erosive esophagitis), switch to a PPI

4. Anti-reflux surgery for severe or resistant cases. (Laparoscopic Nissan fundoplication)

a. Indications for surgery Intractability (failure of medical treatment) Respiratory problems due to reflux
and aspiration of gastric contents Severe esophageal injury (ulcer, hemorrhage, stricture, Barrett
esophagus)

b. Types of surgery Nissen fundoplication (may be done open or laparoscopically)—procedure of choice

for a patient with normal esophageal motility Partial fundoplication—when esophageal motility is poor.

c. Outcome of surgery—excellent results have been reported.

Plummer–Vinson Syndrome
(Upper Esophageal Webs) Key features:
upper esophageal web (causes dysphagia), iron deficiency anemia, koilonychia (spoon-shaped
fingernails), and atrophic oral mucosa.
Ten percent of patients develop SCC of the oral cavity, hypopharynx, or esophagus; therefore,
this is considered a premalignant lesion. Treatment: esophageal dilatation; correct nutritional
deficiency.

If there is a complete web formation the web should be semi-circular, in ring formation the
whole esophageal mucosa comes out/loosens.

Schatzki Ring (Distal Esophageal Webs)

A circumferential ring in the lower esophagus that is always accompanied by a sliding hiatal
hernia. It is usually asymptomatic, but mild to moderate dysphagia may be present.
If the patient is symptomatic (but has no reflux), consider esophageal dilatation. If the patient
has reflux, consider anti-reflux surgery.
Usually due to ingestion of alkali, acids, bleach, or detergents (e.g., in suicide attempts).
Ingesting alkali is more dangerous than ingesting acid because it may lead to liquefactive
necrosis of the esophagus with full-thickness perforation.
Acid ingestion does not cause full-thickness damage (only causes necrosis of esophageal
mucosa). Complications: stricture formation and risk of esophageal cancer. Treatment is
esophagectomy if full-thickness necrosis has occurred.
Patients should avoid vomiting, gastric lavage, and all oral intake (can compound the original
injury). Give the patient steroids and antibiotics as well. Perform bougienage (dilation) for
esophageal stricture.

This ring happens at the gastroesophageal junction.

Infectious esophagitis
Infectious esophagitis is an infection of the esophagus from viruses, bacteria, fungi, or
yeast. This can occur in people with a weak immune system. Cytomegalovirus is a large
herpes-type virus commonly found in humans that can cause serious infections in
people with impaired immunity.

Etiology
1. Candida
2. Herpes simplex virus type 1 and 2
3. Cytomegalovirus (CMV)

S+S
Odynophagia (painful swallowing), dysphagia, weight loss.
Bleeding in upper esophagus which can lead to hemoptysis, anemia (iron deficiency), melena
(black stool).

Look for odynophagia + immune suppressed (HIV) think of esophagitis.

Diagnosis + treatment
Candida, endoscopy - you can see multiple small white-yellowish plaque lesions. If severe you
can see cottage-cheese appearance. Biopsy you can see candida pseudo hyphae.
Treatment
For non-immunosuppressed, give oral nystatin and clotrimazole.
If immune-suppressed, do oral/iv fluconazole.
HSV, endoscopy - you see numerous vesicles that ulcerate (size <2cm), described as volcano-
shaped ulcers. Biopsy you can see eosinophilic intranuclear occlusions.
Treatment
Acyclovir + all cyclovir drugs, if this doesn’t work give them IV foscarnet.
CMV, endoscopy – deep ulcers (size >2cm) and often linear. Biopsy you can see basophilic
intranuclear inclusions.
Treatment
Ganciclovir, if resistance give them IV foscarnet.
Eosinophilic esophagitis
Eosinophilic esophagitis is an allergic condition that happens in the esophagus. The
esophagus becomes inflamed and does not contract properly. It can get narrowed and
develop rings or abscesses. The symptoms happen when your immune system makes
white blood cells in reaction to an allergen.

Etiology
Allergic reactions, affects young males.
Faizan hella cute still.

S+S
Dysphagia to solid foods and reflux.

Diagnosis
Endoscopy – you see multiple rings in the esophagus.
Biopsy you see >15 eosinophils per HPF in mucus (make of that what you will).

Treatment
Anti-allergy medication, anti-reflux medication (PPI and anti-histamines2).
Rings can be treated by dilation therapy.
Zenker diverticulum
is the most common type; found in upper third of the esophagus. Failure of the cricopharyngeal
muscle to relax during swallowing leads to increased intraluminal pressure. This causes
outpouching of mucosa through an area of weakness in the pharyngeal constrictors.
It is typically seen in patients >50 years old.

S+S
Dysphagia, regurgitation, halitosis (bad breath), weight loss, and chronic cough.

Diagnosis
Barium-swallow, you see an outpouching shown by the arrow.
Upper endoscopy (be careful because of risk of perforation).

Treatment
Surgery, cricopharyngeal muscle myectomy (take out the
muscle).
If the tear is mucosal and at the gastroesophageal junction, it is referred to as Mallory–Weiss
syndrome. If a tear is transmural (causing esophageal perforation), it is referred to as
Boerhaave syndrome.
Mallory can lead to Boerhaave.
Etiology
Heavy alcohol, aggressive vomiting.

S+S
Hematemesis (blood in vomit), Melena, cough prior to hematemesis.

Diagnosis
Upper endoscopy, look for the lacerative tears.

Treatment
Epinephrin to reduce blood leakage, then endoscopic suturing.
Esophageal cancer
Esophageal cancer is a disease in which malignant (cancer) cells form in the tissues of
the esophagus. Smoking, heavy alcohol use, and Barrett esophagus can increase the
risk of esophageal cancer. Signs and symptoms of esophageal cancer are weight loss
and painful or difficult swallowing.

Etiology
a.
SCC Incidence is higher in African American men than in other groups.
Most common locations are the upper and midthoracic esophagus. About one-third may be in
distal 10 cm of esophagus.
Risk factors are alcohol and tobacco use, diet (nitrosamines, betel nuts, chronic ingestion of hot
foods and beverages such as tea), human papillomavirus, achalasia, Plummer–Vinson
syndrome, caustic ingestion, and nasopharyngeal carcinoma.
b.
Adenocarcinoma More common in Caucasians and men (5:1 over women).
Most common in distal third of the esophagus/gastroesophageal junction (in 80% of cases).
Risk factors: GERD and Barrett esophagus are main risk factors.

S+S
1. Dysphagia—most common symptom (initially solids only, then progression to liquids).

2. Weight loss—second most common symptom.

3. Anorexia.

4. Odynophagia (pain with swallowing)—a late finding that suggests extraesophageal involvement
(mediastinal invasion).

5. Hematemesis, hoarseness of voice (recurrent laryngeal nerve involvement).

6. Aspiration pneumonia, respiratory symptoms due to involvement of tracheobronchial tree.

7. Tracheoesophageal or broncho esophageal fistula.

8. Chest pain.

Diagnosis
CT, you look for metastasis.
Endoscopy – look for any mass or lesions in the esophageal lining.
Biopsy – Check the malignant cells.
Ultrasonography – to check the depth of the tumor.
Blood tests – (anemia could indicate that there is recurring bleeding).

Treatment
Use immunotherapy (TNF inhibitors -UMAB drugs) + chemotherapy (mitomycin and cisplatin)
(to suppress the cell cycle PDL1 overexpression) the and surgical resection (stage 0.1.2A).
Preoperative neoadjuvant chemotherapy (helps in reducing tumor size), then surgery (stage 2.b
and 3).
Palliative care without surgery (too late), reduce esophageal obstruction (reduce tumor size),
then dilation method (bougienage method), esophagostomy or jejunostomy, then use metal
mash stent to dilate esophagus. (Stage 4)
If the cancer is around the gastroesophageal junction, you use a valvular stent. (To not allow
regurgitation or to not let anything out).
Peptic ulcer disease
Ulcers are caused when there is an imbalance between the digestive juices produced
by the stomach and the various factors that protect the lining of the stomach.

Causes 1. Most common causes

a. Helicobacter pylori infection
b. NSAIDs—inhibit prostaglandin production, which leads to impaired mucosal defenses.
c. Acid hypersecretory states, such as Zollinger–Ellison syndrome.
2. Other risk factors associated with higher risk of PUD (have not been shown to be causative)
a. Smoking
b. Alcohol use
c. Emotional stress and dietary factors (such as coffee and spice intake) have not been shown to
be associated with higher risk of PUD.

Symptoms
Burning stomach pain.
Feeling of fullness, bloating, or belching.
Intolerance to fatty foods.
Heartburn.
Nausea.
Epigastric pain.
Aching or gnawing in nature.
Nocturnal symptoms and the effect of food on symptoms are variable.

Diagnosis
Endoscopy - examine the mucous lining of your upper gastrointestinal tract.
Lab’s test – to diagnose H Pylori.
Treatment
If by H Pylori, do triple therapy. 2 antibiotics (amoxicillin and clarithromycin) and then a
PPI (omeprazole).
If this fails, then do quadruple therapy. 2 antibiotics (tetracycline and metronidazole) and
then a PPI (omeprazole) + bismuth.

If it’s due to NSAIDs, stop NSAIDs and then treat with H2 blockers. If you can’t stop the
NSAIDs you add misoprostol.
Ellison-Zollinger syndrome

Zollinger-Ellison syndrome is a condition that occurs when one or

more tumors link—called gastrinomas link, which are located mainly in
your pancreas or duodenum—cause your stomach to make too much
acid.

Type 1: Gastrinoma
Type 2: MENS1 (multiple endocrine neoplasia) which targets the pancreas, pituitary
gland and parathyroid.

Etiology
Hypersecretion of acid, pancreatic tumors (gastrinoma).

S+S
Multiple peptic ulcers in unusual sites (duodenum or esophagus).
Diarrhea (which is not normal for ulcers).
Abdominal pain. Nausea, vomiting, weight loss, fatty stools, bloating in the abdomen.

Diagnosis
If normal peptic ulcer treatment doesn’t work, then you suspect this.
Check for fasting gastrin level >150.
Basal acid output >15.
Secretin stimulation test, to confirm. When you inject secretin normally gastrin should
decrease, but in ZES gastrin remains elevated.
CT-scan, endoscopy ultrasound to identify the tumor.

Treatment
High dose of PPI 80mg (40 is normal for ulcers), surgery for tumor.
Acute gastritis
Acute gastritis refers to a sudden onset inflammation of the stomach lining that results
from a disruption to the gastric mucosa that allows for further damage and inflammation
from stomach acids.

Etiology
NSAIDS and corticosteroids, H Pylori, excessive alcohol, gastric ischemia.

S+S

loss of appetite, indigestion, black stools, nausea, vomiting.

bloody vomit that looks like used coffee grounds.

pain in the upper part of the abdomen.

a full feeling in the upper abdomen after eating.

Gnawing, burning diffuse pain around the epigastric (MUQ).

Diagnosis

A complete blood count (for overall health).

Blood, breath, or saliva test – to check for H Pylori.

Endoscopy – to check the damage.

Fecal test – Again H Pylori if the other one doesn’t find it.

Treatment
If NSAIDS induced, empiric therapy with acid suppression (H2 antagonist or PPI omeprazole).
If H Pylori, do triple therapy. 2 antibiotics (amoxicillin and clarithromycin) and then a PPI
(omeprazole).

If this fails, then do quadruple therapy. 2 antibiotics (tetracycline and metronidazole) and then
a PPI (omeprazole) + bismuth.

Chronic gastritis
Chronic gastritis is a condition that occurs when your stomach lining becomes inflamed.
Unlike acute gastritis, in which irritation appears quickly in the stomach lining, chronic
gastritis develops gradually and can be more difficult to get rid of.
Etiology

Type A is autoimmune mediated. Caused by your immune system destroying stomach

cells. And it can increase your risk of vitamin deficiencies, anemia, and cancer.
pernicious anemia (B12 deficiency).

Type B is infectious (H Pylori).

S+S

If H Pylori usually you are asymptomatic. The condition may manifest as epigastric pain like
PUD. Other associated symptoms such as nausea/vomiting and anorexia are rare.

Diagnosis

Upper GI endoscopy.

Blood, breath, or saliva test for H Pylori.

Treatment Triple or quadruple therapy, look above if you want to see it.

Inflammatory bowel disease

Crohn’s and ulcerative colitis

Inflammatory bowel disease (IBD) is a term for two conditions (Crohn's disease and
ulcerative colitis) that are characterized by chronic inflammation of the gastrointestinal
(GI) tract. Prolonged inflammation results in damage to the GI tract.
Crohn Disease (“Regional Enteritis”)
Crohn's disease is an inflammatory bowel disease that causes chronic
inflammation of the GI tract, which extends from your stomach all the way down
to your anus. Different areas of the GI tract can be affected in different people,
and it often spreads into the deeper layers of the bowel.

1. Crohn disease is a chronic transmural inflammatory disease that can affect any part of the GI
tract (mouth to anus) but most commonly involves the small bowel (terminal ileum).
2. Distribution: usually in the terminal ileum.

Pathology

a. Terminal ileum is the hallmark location, but other sites of GI tract may also be involved.

b. Skip lesions—discontinuous involvement

c. Fistulae d. Luminal strictures e. Noncaseating granulomas.

f. Transmural thickening and inflammation (full-thickness wall involvement)— results in

narrowing of the lumen.

g. Mesenteric “fat creeping” onto the antimesenteric border of small bowel.

S+S

1. Hematochezia (bloody diarrhea). Crohn's disease in the colon (large intestine) or rectum
is more likely to cause blood in or on the stool.

2. Abdominal pain RLQ or MLQ.

3. Bowel movements are frequent but small.

4. Fever, anorexia, and weight loss (severe cases).

5. Tenesmus (rectal dry heaves).

6. Extraintestinal symptoms (e.g., jaundice, uveitis, arthritis, skin lesions).

7. Pernicious or iron deficiency anemia.

8. Oral mucosal lesions.

Diagnosis
perform the following initial studies.
1. Stool cultures for Clostridium difficile, ova, and parasites to rule out infectious diarrhea.
2. Fecal leukocytes
a. WBCs can appear in UC, ischemic colitis, or infectious diarrhea.
3. Colonoscopy (cobble stone appearance) to assess the extent of disease and the presence of
any complications.
4. Ultrasound.
5. Barium enema

Treatment
1. Medical
a. Systemic corticosteroids (prednisone)—used as initial therapy for low-risk patients with
diffuse disease or left-sided colon disease.
b. Budesonide—used in low-risk patients with mild disease in ileum or right colon.
c. Biologic agent (TNF inhibitor) or methotrexate in patients with moderate to severe disease.
d. Amino salicylate
d. Probiotics
2. Surgical (eventually required in most patients)
a. Reserved for complications of Crohn disease or for those who have persistent symptoms
despite best medical management.
b. Involves segmental resection of involved bowel.
3. Nutritional supplementation and support—parenteral nutrition is sometimes necessary.

Complications
1. Fistulae—between colon and other segments of intestine (enteroenteral), bladder
(enterovesical), vagina (enterovaginal), and skin (enterocutaneous).
2. Anorectal disease (in 30% of patients)—fissures, abscesses, perianal fistulas.
4. Malignancy—increased risk of colonic and small bowel tumors (but less common than risk of
malignancy in UC).
5. Malabsorption of vitamin B12 and bile acids (both occur in terminal ileum). And iron
deficiency.
6. Cholelithiasis may occur secondary to decreased bile acid absorption.
7. Nephrolithiasis—increased colonic absorption of dietary oxalate can lead to calcium oxalate
kidney stones.
8. Aphthous ulcers of lips, gingiva, and buccal mucosa (common).

Ulcerative colitis
Ulcerative colitis is a chronic inflammatory bowel disease (IBD) in which abnormal
reactions of the immune system cause inflammation and ulcers on the inner lining of
your large intestine.

UC is a chronic inflammatory disease of the colon or rectal mucosa.

5. Pathology
a. Uninterrupted involvement of rectum and/or colon
b. Inflammation is not transmural (as it is in Crohn disease). It is limited to the mucosa and
submucosa.
c. PMNs accumulate in the crypts of the colon causing crypt abscesses.
d. Pancolitis (in 30% of cases)
e. The small bowel is not usually involved in UC, but it may reach the distal ileum in a small
percentage of patients (“backwash ileitis” in 10% of cases)

Etiology
Norovirus, Rotavirus, Adenovirus, and Cytomegalovirus.
Parasitic infestation, such as Entamoeba histolytica, a protozoan parasite, can invade the
colonic mucosa and cause colitis.

S+S
1.Hematochezia (bloody diarrhea), Tenesmus (rectal dry heaves) frequent small volume
shitting.
2. Abdominal pain LLQ or left iliac fossa. (tenderness)
3. Bowel movements are frequent but small
4. Fever, anorexia, and weight loss (severe cases)
6. Extraintestinal symptoms (e.g., jaundice, uveitis, arthritis, skin lesions)
7. Iron deficiency anemia.

Diagnosis
1. Stool cultures for Clostridium difficile, ova, and parasites to rule out infectious diarrhea.
2. Fecal leukocytes
a. WBCs can appear in UC, ischemic colitis, or infectious diarrhea.
3. Colonoscopy (pseudo polyps)
4. Barium enema, you see loss of haustration. (Intestine becomes smooth)
5. HRCT to assess colonic inflammation, if this doesn’t work then do capsule imaging of the gut.

Treatment
1. Medical
a. Sulfasalazine (topical application as a suppository)—the mainstay of treatment.
b. Oral glucocorticoids—used when patients fail to respond to topical and oral 5- ASA therapy
(above).
c. TNF inhibitors (infliximab, adalimumab) and thiopurines (6-mercaptopurine, azathioprine)
can be used in patients who do not respond to corticosteroids or for severe disease.
d. Antidiarrheal agents.
e. Amino salicylate

Complications
1. Iron deficiency anemia, pernicious anemia.
2. Hemorrhage
3. Electrolyte disturbances and dehydration secondary to diarrhea
4. Strictures, benign and malignant (usually malignant)
5. Colon cancer—The risk correlates with extent and duration of colitis. In distal proctitis there
is no increased risk of CRC.
6. Sclerosing cholangitis (SC)—Does not correlate with bowel disease and is not prevented by
colectomy.
7. Cholangiocarcinoma—Half of all bile duct cancers are associated with UC.
8. Toxic megacolon is the leading cause of death in UC and affects.
Diverticulosis
occurs when small defects in the muscle of the wall of the large
intestine or colon allow small pockets or pouches (diverticula) to form.

Etiology
Peristalsis abnormalities (e.g., intestinal spasms)
intestinal dyskinesia, or high segmental intraluminal pressures.

S+S
• Low fiber diet
• Old age • LLQ pain
• Palpable abdominal mass
• Diarrhea
• Constipation
• GI bleeding
Anemia from bleeding.
Painless bleeding.

Diagnosis

• Barium enema • Abdominal CT • Abdominal Xray

Treatment
For a person with diverticulosis, there is no proven way to prevent the formation of new
diverticula. Treatment revolves around the settling of symptoms.
 ● A gradual switch to a diet with increased soluble fibre (green vegetables, oat
bran and fiber supplements such as psyllium) usually leads to an improvement in
bowel habit and mild symptoms.
● Some foods may make symptoms worse or even lead to diverticulitis. Nuts,
seeds, and pips are best avoided, while some people find avoiding legumes
(peas and beans) and sweet corn also helps.
● Short-term use of laxatives to treat and prevent constipation may be advised.

● Rarely, elective surgery is performed to remove seriously affected bowel

segments when symptoms are disabling.

Complications

Abscess – untreated, diverticulitis may lead to an abscess (a ball of pus).

Perforation – a weakened pocket of bowel wall may rupture. The contents of the bowel
can then seep into the abdominal cavity. Symptoms include pain, high fever and chills.
A perforated bowel is a medical emergency.

Peritonitis – perforation can lead to peritonitis (infection of the membranes that line the
abdominal cavity and abdominal organs). This complication is potentially life
threatening.

Hemorrhage – diverticula can be the source of hemorrhage. When bleeding occurs, it is

important to exclude other causes. A person with diverticulosis can also get cancer.
Diverticulitis
Diverticular disease and diverticulitis are related digestive conditions that affect the
large intestine (colon). In diverticular disease, small bulges, or pockets (diverticula)
develop in the lining of the intestine. Diverticulitis is when these pockets become
inflamed or infected.

Etiology
fecal impaction, diarrhea, appendicitis, or obstruction by colon cancer.

S+S

Pain, LLQ.

Nausea and vomiting.

Fever.

Abdominal tenderness.

Constipation or, less commonly, diarrhea.

Painful mass on rectal examination if inflammation is near the rectum.

Physical findings

fever and localized abdominal tenderness in the affected diverticula.

Diagnosis

CT scan (abdomen and pelvis) with oral and IV contrast is the test of choice; it may reveal a
swollen, edematous bowel wall or an abscess.

Abdominal radiographs help in excluding other potential causes of LLQ pain and can rule out
ileus or obstruction (indicated by air–fluid levels, distention), and perforation (indicated by free
air).

Barium enema and colonoscopy are contraindicated in acute diverticulitis due to the risk of
perforation.

Treatment

Uncomplicated diverticulitis is managed with IV antibiotics, bowel rest (NPO), IV fluids.

Mild episodes can be treated on an outpatient basis if the patient is reliable and has few or no
comorbid conditions.

If symptoms persist after 3 to 4 days, surgery, resection of the involved segment, may be
necessary. Antibiotics continued for 7 to 10 days. After successful treatment, about one-third
has recurrence. Surgery recommended for recurrent episodes.

Complicated diverticulitis (you see abscesses, fistula and perforation on CT) - surgery indicated.
Adenomatous polyposis syndrome
Classic familial adenomatous polyposis, called FAP or classic FAP, is
a genetic condition. It is diagnosed when a person develops more
than 100 adenomatous colon polyps. An adenomatous polyp is an
area where normal cells that line the inside of a person's colon form a
mass on the inside of the intestinal tract.

Etiology
Genetic, FAP-gene mutation, autosomal dominant.
Associated with congenital hypertrophy with retinal pigmentation which can cause
multiple lesions of both eyes of an infant.

S+S
Altered bowel habits.
Abdominal pain, bloody diarrhea.

Diagnosis
Colonoscopy – over 100 polyps. The risk for colon cancer is 100% after age of 45.
Genetic testing.
Biopsy of polyps, to identify type of polyps.
Treatment
Surgery.
NSAIDS, corticosteroids, celecoxib, all for suppressing inflammation.
Preventive measurement
If family history has this, do colonoscopy at age of 10 and then again at age of 21 (at
age of 21 do upper endoscopy, and then some patients can take colon out).

Turcot syndrome – mutation in the FAP gene with colonic polyps + brain tumors.
Gardeners’ syndrome – mutation in the FAP gene with colonic polyps + bony or soft
tissue tumors (osteoma, fibroma, lipoma).
Peutz–Jeghers Autosomal dominant. Single or multiple hamartomas that may be scattered
through the entire GI tract: in small bowel (78%), colon (60%), stomach (30%).
Hyperpigmentation around the oral cavity or lips.
Familial juvenile polyposis coli Rare; presents in childhood.
Only a small risk of CRC.
Between 10 and hundreds of juvenile colon polyps.
Cowden syndrome – mutation in gene PTEN, multiple polyps + skin manifestations (papules,
hyperkeratosis).
Linn syndrome – Cancer formed in early 20’s, caused by DNA mismatch gene (MMR), or
mutation. Commonly associated with endometrial cancer and ovarian cancer.
Diagnosis = Immunohistochemistry testing and genetics.
Treatment = subtotal colectomy with ileorectal anastomosis.
Celiac sprue (disease).
Celiac disease, sometimes called celiac sprue or gluten-sensitive enteropathy, is an
immune reaction to eating gluten, a protein found in wheat, barley, and rye. If you have
celiac disease, eating gluten triggers an immune response in your small intestine.
This disease increases intraepithelial lymphocytes.

Etiology
Genetic HLA/DQ2.
You can have this with systemic diseases such as diabetes, SLE, Addison, autoimmune
liver disease.

S+S
Malabsorption, fatty stool, abdominal pain, can cause deficiency in iron.
Dermatitis herpetiform (herpes like rash), you’ll see papulovesicular rash. (Could be
something like mouth ulcers or elbow rash or leg just anywhere)

Diagnosis
Serology, IGA/IGG for anti-gliadin, IGA for endomysia antibodies. IGG/IGA for
transglutaminase.
Biopsy, check for villous atrophy and crypt hyperplasia.
Treatment
Stop gluten eating, diet.
Electrolytes correcting. IF you see any complication, give corticosteroids.

Complication
Anemias, iron B12 folic acid.
Malabsorption, osteoporosis.

Tropical sprue
Also known as “environmental enteropathy,” occurs in people who live in or visit tropical areas.
Unknown etiology, believed to be caused by overgrowth of bacteria.
Similar symptoms to celiac sprue include weight loss, diarrhea, cramps, fatigue, malabsorption.
Abnormal flattening of villi can be observed during endoscopy.
Treat with antibiotics and folic acid for 6 months or longer.

In the cases, if you see celiac disease symptoms which are not associated to gluten, and the
patient has a travelling history, specifically not too long ago, think of this little fucker.
Whipple disease
Whipple disease is a rare bacterial infection that most often affects your joints and
digestive system. Whipple disease interferes with normal digestion by impairing the
breakdown of foods, and hampering your body's ability to absorb nutrients, such as fats
and carbohydrates.

Etiology
Tropheryma whipplei (bacteria).
Risk factors – farmers (agricultural workers), genetic HLAB27 antigen.

S+S
Diarrhea, malabsorption (anemias come with this).
Affects the heart, and joints.

Diagnosis
Microscope, visualization of periodic acid-Schiff stain (PAS)–positive macrophages in the lamina
propria containing non–acid-fast gram-positive bacilli.
Labs, look for low albumin and anemia.

Treatment
trimethoprim/sulfamethoxazole (TMP/SMX), long term therapy.
The next 3 are all congenital (gilberts, crigler Najjar, dubin johnson).
Gilbert’s syndrome
Gilbert's syndrome is characterized by the liver's inability to process the yellowish-brown
pigment in bile (bilirubin). Too much bilirubin can cause yellowing of the skin and eyes
(jaundice). Gilbert's syndrome is considered harmless and typically doesn't need
medical treatment.

Etiology
Genetic mutated UGT1A1 gene. (UGT absorbs bilirubin).

S+S
Mild unconjugated bilirubin elevation. You’ll see jaundice symptoms during starvation or
infection.

Diagnosis
Genetic test.
Crigler-Najjar
Crigler-Najjar syndrome is a rare genetic condition that occurs when your liver can't
break down bilirubin (a substance created by red blood cells). Children with this
condition have jaundice, where their skin appears yellow. Some symptoms are life-
threatening and cause irreversible brain damage if left untreated.

Type 1 – Total absence of UGT (protein). Lifespan 1 year.

Type 2 – partial absence of UGT.

Etiology
Genetics

S+S
Unconjugated hyperbilirubinemia, bilirubin in the brain (crosses the BBB – kernicterus).
Jaundice symptoms. (Yellowing of eyes (scleral icterus), yellowing of skin, clay colored
stool, dark urine).
Unconjugated bilirubin more than 20mg/dl. (Avg is 1)

Diagnosis
Genetic test.
Dubin-Johnson syndrome
Dubin-Johnson syndrome is a rare condition that affects the liver. A genetic mutation
causes a yellow substance (bilirubin) to collect in your liver instead of moving through
your digestive tract (bile). People diagnosed with Dubin-Johnson syndrome have
lifelong, mild symptoms of jaundice.

Etiology
Genetics MOAT protein. (This does not stand for Moataz).

S+S
Conjugated bilirubin which is elevated (avg is 0.3).
Jaundice symptoms. Hyperpigmentation of the liver (black liver jaundice).

Diagnosis
Biopsy and genetic testing.
Alcoholic fatty liver disease
Drinking a large amount of alcohol, even for just a few days, can lead to a build-up of fat
in the liver. This is called alcoholic fatty liver disease and is the first stage of ARLD.
Fatty liver disease rarely causes any symptoms, but it's an important warning sign that
you're drinking at a harmful level.

Etiology
Alcohol

S+S
Begins asymptomatically, then develops into alcoholic hepatitis.
Stage 1 steatosis (fat accumulation in liver), Asymptomatic, only hepatomegaly.
Stage 2 alcoholic hepatitis, malaise, jaundice, tender hepatomegaly, fever, weight loss,
abdominal discomfort RUQ.
Stage 3 cirrhosis, hepatomegaly, splenomegaly, malaise, jaundice, weight loss, signs of
chronic liver disease (gynecomastia, ascites, spider-angioma, palmar erythema,
esophageal varices, hepatic encephalopathy).

Diagnosis
History of alcohol, liver function test (AST/ALT) to diagnose should be >2.
GGT (elevated in this disease), ultrasound/CT.

Treatment
Stop alcohol, give nutritional supplements.
For mild alcohol hepatitis, give albumin, antioxidants (vitamin E, omega 3 and
colchicine).
For severe, naltrexone, corticosteroids.
End stage, liver transplant.
Non-alcoholic fatty liver disease
(Cryptogenic cirrhosis – because it’s hidden cirrhosis, as in you’ll have no symptoms till
you reach cirrhosis).
Non-alcoholic fatty liver disease (NAFLD) is the term for a range of conditions caused
by a build-up of fat in the liver. It's usually seen in people who are overweight or obese.
Early-stage NAFLD does not usually cause any harm, but it can lead to serious liver
damage, including cirrhosis, if it gets worse.

Type 1, steatosis.
Type 2, steatosis + nonspecific globular inflammation.
Type 3, steatosis + inflammation with or without fibrosis.
Type 4, fibrosis + liver degeneration (cirrhosis).

Etiology
Obesity, type 2 diabetes associated with metabolic syndrome.
Genetics, PNL gene mutation and PLA3 mutation.

S+S
Asymptomatic, enlarged liver, pain in RUQ, fatigue, malaise.

How to suspect?
Chronic elevation of AST/ALT, if the patient has insulin resistance, obstructive sleep
apnea,
metabolic syndrome (Metabolic syndrome is a group of conditions that together raise
your risk of coronary heart disease, diabetes, stroke, and other serious health problems.
Metabolic syndrome is also called insulin resistance syndrome.

Diagnosis
Liver function test AST/ALT (ratio is <7).
Abnormal ferritin level in the presence of normal transferrin level.
Ultrasound/CT, liver biopsy.

Treatment
Correct all the metabolic issues (for instance, diabetes 2, give them metformin and
pioglitazone).
Lifestyle changes, weight loss, increase coffee use for decreasing of chronic liver
disease.
Also give Vaso deoxycholic acid, helps in decreasing elevated liver enzymes.
Ace-inhibitors for hypertension, diuretics for hypertension (and for ascites if it’s there).
Lipid lowering drugs -statins.

Complications
Sepsis, cardiovascular disease, hepatocellular carcinoma (liver cancer).
Viral hepatitis (LIVER)
Viral hepatitis is an infection that causes liver inflammation and damage. Several
different viruses cause hepatitis, including hepatitis A, B, C, D, and E.

Hepatitis B and C is chronic. B is sexual and blood, C is blood.

Hepatitis A and E are acute. Water and stool (fecal oral route).
Hepatitis D needs another form of hepatitis to affect the patient (super-infection).
S+S hepatitis A and E (acute).

Hepatitis B and C (chronic). (These 2 can lead to cancer/carcinoma).

There is no
treatment,
supportive
treatment will be
the correct
answer.
Hep A goes
away Hep E
goes away.
Hepatitis B,
prophylaxis vaccine 2 types.
1 – live-attenuated vaccine (do not give to immune-compromised).
2 – attenuated vaccine (contains the antigen).
3 – if you’re just infected (under 48 hours) give them hep B immunoglobulins (inject it).
4 – interferon alfa and lamivudine and adefovir.
Hepatitis C
No vaccine.
Interferon alfa and ribavirin.

Liver cirrhosis
Cirrhosis is a condition in which your liver is scarred and permanently damaged. Scar
tissue replaces healthy liver tissue and prevents your liver from working normally. As
cirrhosis gets worse, your liver begins to fail.

Etiology
1. Alcoholic liver disease/Nonalcoholic liver disease.

2. Chronic hepatitis B and C infections—next most common causes

4. Drugs (e.g., acetaminophen toxicity, methotrexate)

5. Autoimmune hepatitis

6. Primary biliary cirrhosis (PBC), secondary biliary cirrhosis

7. Inherited metabolic diseases (e.g., hemochromatosis, Wilson disease)

8. Hepatic congestion secondary to right-sided heart failure, constrictive pericarditis

9. α1-Antitrypsin (AAT) deficiency

S+S

Fatigue. Easily bleeding or bruising. Loss of appetite. Nausea. Pain RUQ.

Edema of extremities (lower), Weight loss. Itchy skin. jaundice.

Ascites (uh-SAHY-teez just in case). Spider angioma.

Redness in the palms of the hands (palmar erythema).

Pale fingernails, especially the thumb and index finger. Clubbing of the fingers.

For women, absence of or loss of periods not related to menopause.

For men, loss of sex drive, testicular shrinkage, or breast enlargement, known as
gynecomastia. Liver cirrhosis leads to high levels of estrogen.

Hepatic encephalopathy.

Diagnosis

Diagnosis
Cirrhosis can be diagnosed by radiology testing such as computed tomography (CT),
ultrasound or magnetic resonance imaging (MRI) or via a needle biopsy of the liver.
A new imaging technique called elastography, which can be performed with ultrasound
or MRI, can also diagnosis cirrhosis. When liver is fibrotic, it loses its elasticity.

Treatment
Teleport someone’s liver in your own. You can also use Hashirama cells for treatment
since they are highly effective against injury as stated by Dr. Tsunade in her medical
internal research notebook (Ambassing).
Treat complications.
Complications
Portal hypertension, which can lead to esophageal varices (if it starts to bleed you can
hardly stop it so use endoscopic band ligation and if that fails), treat with trans jugular
intrahepatic portosystemic shunt (TIPS).
Ascites, if mild stop eating salt. If milder use diuretics (spironolactone + furosemide). If severe
then do Paracentesis.
Hepatic encephalopathy. Treatment is lactulose, a synthetic or man-made sugar, and
certain antibiotics.

Primary sclerosing cholangitis

Primary sclerosing cholangitis (PSC) is a chronic liver disease in which the bile ducts
inside and outside the liver become inflamed and scarred, and eventually narrowed or
blocked. When this happens, bile builds up in the liver and causes further liver damage.

There is a strong association with UC (less so with Crohn disease). UC is present in 50%
to 70% of patients with PSC; often the UC may dominate the clinical picture.
No etiology

S+S
1. Signs and symptoms begin insidiously.
2. Chronic cholestasis findings, including jaundice and
Pruritus (Itchy skin) if you see jaundice + itching, think of this.
All patients eventually present with chronic obstructive jaundice.
3.Other symptoms: fatigue, malaise, weight loss.
This is pre-hepatic jaundice.

Diagnosis
 1. ERCP (endoscopic retrograde cholangio pancreatography) and PTC (Percutaneous
Transhepatic Cholangiography) are diagnostic studies of choice—see multiple areas of
bead-like structuring and bead-like dilatations of intra- and extrahepatic ducts.
2. If you can’t do ERCP the reason is that ERCP can be complicated by pancreatitis and
ascending cholangitis.
2. Laboratory tests show cholestatic LFTs. (Liver enzymes are going to be abnormal).
3. Primary sclerosing cholangitis antibody – ANCA. (In cases you can see pANCA as
well).

Treatment
1. There is no curative treatment other than liver transplantation.

2. When a dominant stricture causes cholestasis, ERCP with stent placement for biliary drainage and bile
duct dilatation may relieve symptoms.

3. Use cholestyramine for symptomatic relief (to decrease pruritus)

Complication

● Liver disease and failure. Chronic inflammation of the bile ducts

throughout your liver can lead to tissue scarring (cirrhosis), liver cell death
and, eventually, loss of liver function.

● Repeated infections. If scarring of the bile ducts slows or stops the flow of
bile out of the liver, you may experience frequent infections in the bile ducts.
The risk of infection is particularly high after you've had a surgical procedure
to expand a badly scarred bile duct or remove a stone blocking a bile duct.

● Portal hypertension. Your portal vein is the major route for blood flowing
from your digestive system into your liver. Portal hypertension refers to high
blood pressure in this vein.

Portal hypertension can cause fluid from the liver to leak into your
abdominal cavity (ascites). It can also divert blood from the portal vein to
other veins, causing these veins to become swollen (varices). Varices are
weak veins and tend to bleed easily, which can be life-threatening.
 ● Thinning bones. People with primary sclerosing cholangitis may
experience thinning bones (osteoporosis). Your doctor may recommend a
bone density exam to test for osteoporosis every few years. Calcium and
vitamin D supplements may be prescribed to help prevent bone loss.

● Bile duct cancer. If you have primary sclerosing cholangitis, you have an
increased risk of developing cancer in the bile ducts or gallbladder.

● Colon cancer. People with primary sclerosing cholangitis associated with

inflammatory bowel disease have an increased risk of colon cancer. If
you've been diagnosed with primary sclerosing cholangitis, your doctor may
recommend testing for inflammatory bowel disease, even if you have no
signs or symptoms, since the risk of colon cancer is elevated if you have
both diseases.

Primary biliary cholangitis (cirrhosis)

Primary biliary cholangitis, previously called primary biliary cirrhosis, is a chronic
disease in which the bile ducts in your liver are slowly destroyed. Bile is a fluid made in
your liver. It aids with digestion and helps you absorb certain vitamins.
Is associated with Sjogren’s syndrome, thyroid dysfunction, rheumatoid arthritis and
crushed syndrome.
Etiology
Autoimmune associated with SNPs.
T-lymphocyte mediated attack on small interlobar bile duct

S+S
1. Fatigue
2. Pruritus (early in course of disease)
3. Jaundice (late in course of disease)
4. RUQ discomfort
5. Xanthomata (patchy yellowing around the body look google) and xanthelasmas (yellowish
growing around the eyes next to the nose).
6. Osteoporosis
7. Portal HTN (with resultant sequelae)

Diagnosis
1. Laboratory findings
a. Cholestatic LFTs (elevated ALK-P)
b. Positive antimitochondrial antibodies (AMAs) found in 90% to 95% of patients. This is the
hallmark of the disease (specificity of 98%). If serum is positive for AMAs, perform a liver biopsy
to confirm diagnosis.
c. Elevated cholesterol, HDL.
d. Elevated immunoglobulin M.
2. Liver biopsy (percutaneous or laparoscopic) to confirm the diagnosis.
3. Abdominal ultrasound or CT scan to rule out biliary obstruction.
Treatment
1. Treatment is symptomatic for pruritus (cholestyramine) and osteoporosis (calcium,
bisphosphonates, vitamin D).
2. Urso deoxycholic acid (a hydrophilic bile acid) to slow down the disease.
3. Liver transplantation is the only curative treatment available
Cholangitis
Cholangitis is inflammation of the bile duct system. The bile duct system carries bile
from the liver and gallbladder to the first part of your small intestine (the duodenum). In
most cases cholangitis is caused by a bacterial infection. People who have gallstones
are at greater risk for cholangitis.

Etiology
Gallstones (choledocholithiasis), postoperative strictures.
Invasive procedure (ERCP, PTC), Biliary & pancreatic neoplasm.

S+S
1. Charcot triad: RUQ pain, jaundice, and fever
2. Reynolds pentad: Charcot triad plus septic shock and altered mental status (CNS depression
—e.g., coma, disorientation).
3. Patient is acutely ill, and abdominal symptoms may be lacking or may go unrecognized.

Diagnosis
1. RUQ ultrasound is the initial study.
2. Laboratory findings—hyperbilirubinemia, leukocytosis, mild elevation in serum
transaminases.
3. Cholangiography (PTC or ERCP).
a. This is the definitive test, but it should not be performed during the acute phase of illness.
Once cholangitis resolves, proceed with PTC or ERCP to identify the underlying problem and
plan treatment.
b. Perform PTC when the duct system is dilated (per ultrasound) and ERCP when the duct
system is normal.

Treatment
1. IV antibiotics and IV fluids

a. Close monitoring of hemodynamics, BP, and urine output is important.

b. Most patients respond rapidly. Once the patient has been afebrile for 48 hours, cholangiography (PTC
or ERCP) can be performed for evaluation of the underlying condition.

2. Decompress CBD via PTC (catheter drainage); ERCP (sphincterotomy), or laparotomy (T-tube
insertion) once the patient is stabilized, or emergently if the condition does not respond to antibiotics.
Cholelithiasis
Cholelithiasis or gallstones are hardened deposits of digestive fluid that can form in your
gallbladder. The gallbladder is a small organ located just beneath the liver.

1. Cholelithiasis refers to stones in the gallbladder (i.e., gallstones).

a. Cholesterol stones (yellow to green)—associated with the following:
Obesity, diabetes, hyperlipidemia, Multiple pregnancies, oral contraceptive use, Crohn disease,
ileal resection, Cirrhosis, Cystic fibrosis.
b. Pigment stones
Black stones are usually found in the gallbladder and are associated with either hemolysis (e.g.,
sickle cell disease, thalassemia, hereditary spherocytosis, artificial cardiac valves) or alcoholic
cirrhosis.
Brown stones are usually found in bile ducts and are associated with biliary tract infection.
c. Mixed stones have components of both cholesterol and pigment stones, and account for the
majority of stones.

S+S
1. Most cases are asymptomatic. Most patients who are found to have incidental gallstones will
remain asymptomatic.
2. Biliary colic is the cardinal symptom of gallstones and is due to temporary obstruction of the
cystic duct by a gallstone. Pain occurs as the gallbladder contracts against this obstruction.
a. Pain is typically located in the RUQ or epigastrium and may be mild, moderate, or severe.
b. Patients classically report pain after eating and at night.
c. Boa’s sign—referred right subscapular pain of biliary colic.
Diagnosis
1. RUQ ultrasound has high sensitivity and specificity (>95%) for stones >2 mm.
2. CT scan and MRI are alternatives.
Treatment
1. No treatment if the patient is asymptomatic. 2. Elective cholecystectomy for patients with
recurrent bouts of biliary colic.

Complications
1. Cholecystitis (chronic or acute) with prolonged obstruction of cystic duct.

2. Choledocholithiasis.

3. Gallstone ileus

4. Malignancy
Cholecystitis
Acute cholecystitis is swelling (inflammation) of the gallbladder. It is a potentially serious
condition that usually needs to be treated in hospital.
1. Obstruction of the cystic duct (not infection) induces acute inflammation of the gallbladder
wall.
2. Chronic cholecystitis may develop with recurrent bouts of acute cholecystitis.
3. Ten percent of patients with gallstones develop acute cholecystitis.

S+S
Pain in the RUQ or epigastrium; it may radiate to the right shoulder or scapula.
Nausea and vomiting, anorexia
Murphy’s sign RUQ tenderness, rebound tenderness in RUQ.
Hypoactive bowel sounds.
Low-grade fever, leukocytosis. (WBC count high).

Diagnosis
1. RUQ ultrasound is the test of choice.

a. High sensitivity and specificity b. Findings include thickened gallbladder wall, pericholecystic fluid,
distended gallbladder, and presence of stone(s).

2. CT scan is as accurate as ultrasound but is more sensitive in identifying complications of acute

cholecystitis (e.g., perforation, abscess, pancreatitis).

3. Radionuclide scan (hepatoiminodiacetic acid [HIDA])

a. Used when ultrasound is inconclusive. Its sem x Isensitivity and specificity parallel that of ultrasound.
If HIDA scan is normal, acute cholecystitis can be ruled out.

b. A positive HIDA scan means the gallbladder is not visualized.

c. If gallbladder is not visualized 4 hours after injection, diagnosis of acute cholecystitis is confirmed.

Treatment
1. Hydration with IV fluids, bowel rest (NPO), IV antibiotics, analgesics, correction of electrolyte
abnormalities.

2. Surgery—cholecystectomy is indicated in most patients with symptomatic gallstones. Early

cholecystectomy is preferred (first 24 to 48 hours). Recurrence rate with nonsurgical treatment is as
high as 70%. In most patients, early cholecystectomy is preferred.

3. In critically ill patients with high surgical risk, percutaneous cholecystostomy tube placement for
drainage of the gallbladder is an alternative to immediate surgery.

IF you want to read this

Acute cholecystitis without stones obstructing the cystic duct (up to 10% of patients with acute
cholecystitis).
Usually idiopathic and seen in patients with severe underlying illness; possibly associated with
dehydration, ischemia, burns, severe trauma, and a postoperative state.

Signs and symptoms are the same as for acute cholecystitis. Diagnosis may be difficult because patients
with this condition are often severely ill and have other medical problems; so clinical features are less
apparent.

Emergent cholecystectomy is the treatment of choice. For patients who are too ill for surgery, perform
percutaneous drainage of the gallbladder with cholecystostomy.

Choledocholithiasis
General Characteristics
1. Refers to gallstones in the CBD
2. Primary versus secondary stones
a. Primary stones originate in the CBD (usually pigmented stones).
b. Secondary stones originate in the gallbladder and then pass into the CBD (usually cholesterol
or mixed stones). These account for 95% of all cases.

S+S
1. Patients may be asymptomatic for years.
2. Symptoms, when present, include RUQ or epigastric pain and jaundice.
Diagnosis
1. Laboratory tests—total and direct bilirubin levels are elevated, as well as ALK-P. If ALK is
higher than AST/ALT then think this.
2. RUQ ultrasound is usually the initial study but is not a sensitive study for choledocholithiasis.
It detects CBD in only 50% of cases, so it cannot be used to rule out this diagnosis.
3. ERCP is the gold standard (sensitivity and specificity of 95%) and should follow ultrasound.
ERCP is diagnostic and therapeutic.
4. PTC is an alternative to ERCP.

Treatment
1. ERCP with sphincterotomy and stone extraction with stent placement (successful in 90% of
patients).
2. Laparoscopic choledocholithotomy (in select cases).
Acute pancreatitis
Acute pancreatitis is a condition where the pancreas becomes inflamed (swollen) over a
short period of time. Most people with acute pancreatitis start to feel better within about
a week and have no further problems.

Etiology
1. Gallstones (40%)—the gallstone passes into the bile duct and blocks the ampulla of Vater
2. Alcohol abuse (30%) (SID) (Recurrence is common)
3. post-ERCP—pancreatitis occurs in up to 10% of patients undergoing ERCP
4. Viral infections (e.g., mumps, Coxsackievirus B)
5. Drugs—sulfonamides, thiazide diuretics, furosemide, estrogens, HIV medications, and many
other drugs have been implicated
6. Postoperative complications (high mortality rate)
7. Autoimmune pancreatitis (But akhiii)
8. Scorpion bites (Faizan)
9. Hypertriglyceridemia, hypercalcemia
10. Uremia (Wagner Fernandes)
11. Blunt abdominal trauma (most common cause of pancreatitis in children) (Makhkhkhomed)
12. Infectious insects (scorpion, spider) (You are not spiderman, you have pancreatitis).

S+S
Symptoms
a. Abdominal pain, usually in the epigastric region May radiate to back (50% of patients) Often
steady, dull, and severe, worse when supine and after meals.
b. Nausea and vomiting, anorexia.
2. Signs
a. Low-grade fever, tachycardia, hypotension, leukocytosis.
b. Epigastric tenderness, abdominal distention.
c. Decreased or absent bowel sounds indicate partial ileus.
d. The following signs are seen with hemorrhagic pancreatitis as blood tracks along fascial
planes:
Grey Turner sign (flank ecchymoses).
Cullen sign (periumbilical ecchymoses).
Fox sign (ecchymosis of inguinal ligament).

Diagnosis
1. Must fulfill two of three criteria: classical clinical presentation (epigastric pain that radiates to
the back), lab findings, and imaging findings.
2. Laboratory studies
a. Serum lipase and amylase. Lipase is more specific.
b. LFTs—to identify cause (gallstone pancreatitis).
c. Hyperglycemia, hypoxemia, and leukocytosis may also be present.
d. Order the following for assessment of prognosis (Ranson criteria): glucose, calcium,
hematocrit, BUN, arterial blood gas (PaO2, base deficit), LDH, AST, WBC count.
3. Abdominal radiograph
a. More helpful in ruling out other diagnoses, such as intestinal perforation (free air). The
presence of calcifications can suggest chronic pancreatitis.
4. Abdominal ultrasound
a. Can help in identifying the cause of pancreatitis (e.g., gallstones).
b. Useful for following up pseudocysts or abscesses.
5. CT scan of the abdomen
a. Most accurate test for diagnosis of acute pancreatitis and for identifying complications of the
disease.
b. Indicated in patients with severe acute pancreatitis.
6. Indications for ERCP:
a. Severe gallstone pancreatitis with biliary obstruction.
b. To identify uncommon causes of acute pancreatitis if disease is recurrent.
Treatment
1. Patients with mild acute pancreatitis:
a. Bowel rest (NPO)—goal is to rest the pancreas.
b. IV fluids—patients may have severe intravascular volume depletion. Correct electrolyte
abnormalities. Balanced crystalloids (lactated Ringer solution) are superior to normal saline, as
normal saline can cause hyperchloremic metabolic acidosis. Acidosis will increase pancreatic
zymogen activity which will then worsen autodigestion.
c. Pain control, but be cautious in giving narcotics. Fentanyl and meperidine preferred over
morphine which causes an increase in sphincter of Oddi pressure.
d. Nasogastric tube, if severe nausea/vomiting or ileus present; routine use is controversial.
e. All patients with gallstone pancreatitis should have cholecystectomy after recovery from
pancreatitis. These patients may benefit from early ERCP.
2. Patients with severe pancreatitis:
a. Admit to the ICU.
b. Early enteral nutrition in the first 72 hours is recommended through a nasojejunal tube.
c. If the severe acute pancreatitis has not resolved in a few days, supplemental parenteral
nutrition should be started. d. If more than 30% of the pancreas is necrosed, prophylactic
antibiotics (imipenem) should be considered to prevent infection (which has high morbidity and
mortality).

Complications
Pancreatic necrosis, pancreatic pseudocysts, hemorrhagic pancreatitis.
Chronic pancreatitis
is a condition where the pancreas has become permanently damaged from
inflammation and stops working properly.
1. Persistent or continuing inflammation of the pancreas, with fibrotic tissue replacing
pancreatic parenchyma, and alteration of pancreatic ducts (areas of stricture/dilation);
eventually results in irreversible destruction of the pancreas.
2. The endocrine and exocrine functions of the pancreas are impaired.

Etiology
a. Chronic alcoholism is the most common cause (>80% of cases).
b. other causes include hereditary pancreatitis, tropical pancreatitis, and idiopathic chronic
pancreatitis.

S+S

The classical triad of TCP consists of abdominal pain, steatorrhea,

and diabetes.
1. Severe pain in the epigastrium; recurrent or persistent abdominal pain. RUQ

a. Often accompanied by nausea and vomiting.

b. May be aggravated by an episode of binge drinking alcohol, or by eating.

c. Radiates to the back in 50% of cases.

2. Weight loss, due to malabsorption, alcohol abuse, and diabetes; steatorrhea secondary to
malabsorption.

Diagnosis
1. CT scan is the initial study of choice. It may show calcifications not seen on plain films. So a normal CT
scan does not necessarily rule out chronic pancreatitis.

2. Abdominal radiograph—the presence of pancreatic calcifications is 95% specific but is found in only
30% of cases.

3. ERCP is the gold standard but is not done routinely because it is invasive.
4. Laboratory studies are not helpful in diagnosis. Serum amylase and lipase levels are not elevated in
chronic pancreatitis.

They are elevated in acute pancreatitis.

Treatment
1. Nonoperative management

a. Narcotic analgesics for pain

b. Bowel rest (NPO)

c. Pancreatic enzymes and H2 blockers given simultaneously.

d. Insulin—may be necessary due to severe pancreatic endocrine insufficiency.

e. Alcohol abstinence

f. Frequent, small-volume, low-fat meals—may improve abdominal pain.

2. Surgery—main goal is relief of incapacitating abdominal pain.

a. Pancreatojejunostomy (pancreatic duct drainage procedure to decompress the dilated pancreatic

duct)—most common procedure.

b. Pancreatic resection (distal pancreatectomy, Whipple procedure).

Complication
1. Narcotic addiction—probably the most common complication.

2. Diabetes mellitus/impaired glucose tolerance a. Caused by progressive loss of islets of Langerhans b.

Eventually appears in up to 70% of patients

3. Malabsorption/steatorrhea

a. Caused by pancreatic exocrine insufficiency—occurs when pancreatic enzyme secretion decreases

significantly.

b. A late manifestation of chronic pancreatitis

4. Pseudocyst formation

5. Pancreatic ductal dilation

6. CBD obstruction (may occur secondary to fibrosis in head of gland)

7. Vitamin B12 malabsorption

8. Effusions (e.g., pleural, pericardial, peritoneal)

9. Pancreatic carcinoma—patients with chronic pancreatitis have an increased risk.

Pancreatic cancer
Anatomic location

a. Pancreatic head (75% of cases) (leads to obstructive jaundice).

b. Pancreatic body (20% of cases)

c. Pancreatic tail (5% to 10% of cases)

Risk factors

a. Cigarette smoking (most clearly established risk)

b. Chronic pancreatitis

c. Diabetes

d. Heavy alcohol use e. Exposure to chemicals—benzidine and β-naphthylamine

4. The prognosis is dismal: most patients die within months of diagnosis.

S+S

Abdominal pain

Jaundice

a. Most common with carcinoma of head of pancreas—less than 10% of patients with cancer involving
body and tail of pancreas have jaundice.

b. Indicates obstruction of intrapancreatic CBD and is a sign of advanced disease.

3. Weight loss (common due to decreased food intake and malabsorption); anorexia

4. Recent onset of glucose intolerance, but diabetes is mild.

5. Depression, weakness, fatigue

6. Migratory thrombophlebitis—develops in 10% of cases

7. Courvoisier sign (palpable gallbladder)—present in 30% of patients with cancer involving head of
pancreas; presents without pain.

Diagnosis
1. ERCP is the most sensitive test for diagnosing pancreatic cancer. It can also distinguish cancer of the
head of the pancreas from tumors of the CBD, duodenum, ampulla, and lymphomas, which have more
favorable prognosis.
2. CT scan is the preferred test for diagnosis and assessment of disease spread.

3. Tumor markers.

a. CA 19-9

b. CEA

Treatment

1. Surgical resection (Whipple procedure) is the only hope for a cure; however, only a minority of tumors
are resectable (roughly 10%). The prognosis is grim even after resection, with a 5-year survival rate of
10%.

2. If the tumor is unresectable and biliary obstruction is present, perform PTC or ERCP with stent
placement across the obstruction for palliation.