Diarrhea Pain: Lactose Intolerance Hydrogen Breath Test

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1-patient presents with a history of diarrhea, abdominal pain, bloating, and flatulence following consumption of dairy

products.>>>> This patient's presentation suggests lactose intolerance (LI), for which a trial lactose-free diet is often
the first diagnostic step. A diagnosis of LI is then confirmed using a validated symptom questionnaire and if symptoms
subside within 5–7 days without consumption of lactose-containing products. A hydrogen breath test can also be used
in the diagnostic workup; this test is considered positive if breath hydrogen levels increase to > 20 ppm following the
ingestion of a lactose-loaded drink. Other conditions with a similar manifestation (celiac disease, inflammatory bowel
disease, gastroenteritis, other food intolerances) should be considered in patients with severe gastrointestinal
symptoms or in those who show no improvement despite a lactose-free diet. Treatment of LI consists of lactase enzyme
supplements as needed and avoidance of products that contain lactose.

2- 1. **Lifestyle Modifications

- Focus on preventing complications in asymptomatic cholelithiasis.

- Minimize modifiable risk factors, such as obesity, smoking, and lithogenic drugs.

- Implement a low-fat diet, promote weight loss, and encourage regular exercise.

2. **Ursodeoxycholic Acid Therapy

- Indicated for symptomatic cholelithiasis in patients unfit for surgery.

- Not recommended for asymptomatic cases.

3. **ERCP-Guided Extraction

- Reserved for patients with suspected cholangitis or choledocholithiasis.

5. **Elective Cholecystectomy

- Mainstay for symptomatic cholelithiasis.

- Considered in asymptomatic cases with specific risks (e.g., gallbladder cancer, complications, or symptomatic
potential).

- Not indicated for prophylactic cholecystectomy in diabetes mellitus with asymptomatic cholelithiasis.

3-combination of recurrent episodes of abdominal pain with varying location and intensity that are exacerbated by
emotional stress, altered bowel habits (change in stool frequency and form), and normal physical examination and
laboratory studies (e.g., hemoglobin, ESR) are suggestive of irritable bowel syndrome (IBS), which is most commonly
seen in individuals aged 20–39 years.

4-This patient likely has intrahepatic cholestasis of pregnancy as evidenced by her elevated bile acid (the
most sensitive and specific measure of intrahepatic cholestasis of pregnancy) and elevated direct bilirubin
levels. Importantly, the presence of pruritus (due to elevated bile salts) helps differentiate intrahepatic
cholestasis of pregnancy from other liver diseases of pregnancy (e.g., HELLP). First-line treatment is
ursodeoxycholic acid to increase bile flow.
Maternal complications during pregnancy

2-
5-Serological testing for IgA tissue transglutaminase antibodies is the preferred initial test for diagnosing celiac disease.
The exact role of the antibody in the pathophysiology of celiac disease is unknown; in addition to the initial diagnosis, an
antibody test is also useful for follow-up. Antibody levels start to decline and usually normalize within 3–12 months
following the introduction of a gluten-free diet. Other antibodies that are often present in patients with celiac disease
include deamidated gliadin peptide antibodies and anti-endomysial antibodies. Confirmatory testing consists of upper
endoscopy with duodenal biopsy, which would show intraepithelial lymphocytic infiltration, crypt hyperplasia, and
villous atrophy.

6-If left untreated, CVF predisposes the patient to recurrent urinary tract infections. Diverticulitis is the most
common cause of CVF (65–80% of cases); localized inflammation of the peridiverticular tissue can result in the
formation of a phlegmon or a diverticular abscess that can rupture into adjacent organs, creating a fistula. An
abdominal CT scan with oral contrast is typically performed to confirm the diagnosis. In most patients with
CVF, surgical repair is indicated.

7-CT scan of the chest is used to confirm the diagnosis of Boerhaave syndrome in patients who are hemodynamically
unstable or otherwise not suited to undergo contrast esophagography. CT findings of Boerhaave syndrome include
pneumomediastinum, esophageal wall thickening, pneumothorax, pneumoperitoneum, subcutaneous emphysema,
and pleural effusion. While bedside testing is usually preferred over CT scan for unstable patients (e.g., TEE to confirm
aortic dissection), there is no bedside imaging available to reliably confirm the diagnosis of esophageal rupture. In this
hemodynamically unstable patient (low systolic pressure, high pulse) with inconclusive x-ray findings, a CT scan of the
chest should be performed to confirm the diagnosis and aid in procedure planning. In patients who are
hemodynamically stable, contrast esophagography with gastrografin is the preferred confirmatory test.
8-Intestinal amebiasis

 Stool analysis
o Microscopic identification of cysts or trophozoites in fresh stool

 Trophozoites often contain ingested erythrocytes Cysts contain up to four nuclei The following tests
confirm the microscopic findings (important since E. histolytica and Entamoeba dispar are morphologically
identical

o EIA or coproantigen ELISA


o Molecular methods: e.g., PCR
 Stool microscopy is not sensitive, especially in later phases, so at least three stool samples should be
examined before reporting a negative result.

 Colonoscopy with biopsy: flask-shaped ulcers

Metronidazole (or tinidazole) is considered the first-line treatment to eradicate invasive trophozoites in patients with
symptomatic intestinal amebiasis (amebic dysentery) and extraintestinal amebiasis (e.g., amebic liver abscess).
Following treatment with metronidazole or tinidazole, patients should also receive an intraluminal amebicide (e.g.,
paromomycin) to eradicate intestinal cysts and prevent relapse.

In travelers with asymptomatic infection, treatment with luminal agents is usually sufficient. Individuals from endemic
areas with asymptomatic infection do not require treatment.

9-anal fissure treatment :

Conservative

 First-line treatment for most anal fissures


 Includes:
o Dietary improvement (e.g., adequate ingestion of dietary fiber and water)
o Stool softeners (e.g., docusate)
o Anti-inflammatory and analgesic creams and/or suppositories (e.g., 2% lidocaine jelly)
o Sitz baths
o Local anesthetic injection
o Topical vasodilator therapy: calcium channel blocker gel (e.g., nifedipine) or glyceryl trinitrate
ointment (GTN)


o

Interim

 Persistent symptoms despite > 8 weeks of conservative therapy → endoscopy to exclude IBD
 If IBD is excluded, then the patient should receive definitive surgical treatment.

Outpatient procedures
 Botulinum toxin A (BTX) injection into the internal anal sphincter

Surgical

 Indicated when conservative treatment is unsuccessful


 The risk of fecal incontinence (e.g., high in multiparous or elderly patients) determines the type of
surgical intervention.
o Low risk
 Sphincterotomy (e.g., lateral internal sphincterotomy)

  Anal dilatation (although there is a high risk of fecal incontinence with this procedure)

 High risk

 Anal advancement flap


 Fissurectomy (excision of the fissure)

10-
10-
11-Colonoscopy with biopsy is the test of choice to confirm the diagnosis of IBD. In contrast to CD, which may affect
the entire gastrointestinal tract but typically spares the rectum, UC usually affects only the colon and rectum in a
continuous pattern. Typical macroscopic findings in UC include an inflamed, reddened mucosa, bleeding on contact with
the endoscope, fibrin-covered ulcers, and loss of vascular markings. Histological findings include granulocyte infiltration
to the mucosa and submucosa, crypt abscesses, and, in advanced disease, mucosal atrophy and epithelial dysplasia.

Colonoscopy is contraindicated in patients with features of acute severe disease, defined as > 6 bloody stools per day
and/or signs of systemic toxicity (fever, tachycardia, anemia, elevated erythrocyte sedimentation rate), because of an
increased risk of bowel perforation. Instead, a lower endoscopy (sigmoidoscopy) may be attempted to confirm the
diagnosis and determine the appropriate treatment. In these patients, a full colonoscopy should be performed once
their condition has improved.

12-

A combination of symmetric oligoarthritis, loose stools, features of malabsorption (weight loss, iron deficiency
anemia), cardiac symptoms (valve insufficiency), hyperpigmentation, and generalized lymphadenopathy
indicates Whipple's disease.

PAS-positive macrophages in gastrointestinal biopsy specimens are a hallmark finding in Whipple's disease. Apart from
the features in this patient, Whipple's disease may also manifest with various neurological symptoms (e.g., ataxia,
myoclonus, impairment of oculomotor function). If gastrointestinal complaints are absent, biopsies may be taken from
other sites with disease activity. Whipple's disease is treated with IV ceftriaxone for 2 weeks followed by maintenance
treatment with oral trimethoprim-sulfamethoxazole for 1 year.

13-Albendazole is the first-line treatment for echinococcosis and should be administered daily for 1–6 months
depending on the size of the cyst. Because long-term albendazole use is associated with an increased risk of leukopenia,
a CBC should be conducted before initiating therapy and every 2 weeks thereafter during treatment.

Cysts larger than 5 cm and those associated with complications (e.g., rupture, pulmonary cysts, biliary fistulae) may
require surgical excision or PAIR (Puncture, Aspiration, Injection, Re-aspiration) in addition to medical therapy.

14-Stool softeners (e.g., docusate and topical/suppository lidocaine if painful) are used for the conservative
treatment of hemorrhoids. Further appropriate interventions include Sitz baths and lifestyle modifications (e.g.,
weight loss, exercise, high fiber diet, avoidance of fatty and spicy foods). Conservative therapy is the first-line
management of external as well as grade I and grade II internal hemorrhoids.
15-Gastroesophageal endoscopy is indicated in this patient to rule out malignancy (e.g., cancer of the esophagus or
the gastroesophageal junction) as a cause of secondary achalasia (pseudoachalasia). Distal esophageal cancer and
achalasia can present similarly, which is why it is important to maintain a high index of suspicion for esophageal cancer.
Additionally, achalasia itself predisposes to esophageal cancer, although cancer is unlikely to arise within a period of just
6 months. But in this particular patient, significant weight loss and a history of smoking are findings that would support
the diagnosis of esophageal cancer, making endoscopic inspection necessary.

16-Acute-onset nausea, vomiting, abdominal cramps, and moderate watery, nonbloody diarrhea are consistent with
norovirus infection, which is the most common cause of adult gastroenteritis (see “Overview of pathogens causing
watery and bloody diarrhea” table). Symptoms typically develop after an incubation period of 12–48 hours. Norovirus is
transmitted fecal-orally; the patient might have contracted the illness from consuming contaminated food or water or
from contact with contaminated surfaces. Person-to-person or airborne-droplet transmission is also possible. Because
the virus is highly virulent, infected individuals are highly contagious during the acute phase and up to 72 hours
following the onset of symptoms.

Diagnosis of a suspected norovirus infection should be confirmed with reverse transcription PCR to determine isolation
measures and whether the condition needs to be reported. Treatment is supportive because symptoms typically resolve
spontaneously within 48–72 hours.

17-PCR for hepatitis C virus RNA is the confirmatory test for a chronic hepatitis C infection. The hepatitis C
antibody test is a screening test and is positive in cases of active, chronic, or previous infection. This patient last
used IV illicit drugs 5 years ago and has been symptomatic for 3 months with clinical features of cirrhosis and
portal hypertension, which suggests a chronic hepatitis C infection. The cutaneous erosions and blistering on the
dorsum of this patient's hands are likely due to porphyria cutanea tarda, a common extrahepatic manifestation
of chronic hepatitis C. Chronic HCV infection is treated with a combination of two direct-acting antivirals (e.g.,
ledipasvir and sofosbuvir).

18-The initial management of hypertrophic pyloric stenosis involves intravenous fluid therapy with 0.9% NaCl to
correct the extracellular volume loss and replete chloride, thereby ensuring adequate chloride delivery to the distal
convoluted tubule (DCT). Adequate chloride delivery to the DCT is necessary for the activity of the pendrin exchanger,
which reabsorbs chloride in exchange for excreting bicarbonate into the lumen of the DCT. Correction of the volume
status usually also corrects any mild electrolyte disturbances, but for moderate to severe electrolyte disturbances, it
may be necessary to take further measures (e.g., repletion with potassium chloride for severe hypokalemia).

19-This 8-month-old patient, who has recently started eating solid foods, presents with abdominal pain,
infrequent, hard bowel movements, hyperactive bowel sounds, a normal ultrasound, and no alarm symptoms
(e.g., fever, vomiting, diarrhea), all of which suggests primary constipation.

Recommend apple juice diluted with water

26%

Infants who are transitioning from breastmilk to solid foods often present with primary constipation due to
insufficient intake of fiber and fluid from the transitional diet. Primary constipation typically manifests with
abdominal pain and infrequent, hard, and/or painful bowel movements. Sorbitol, which is commonly found in
juice (e.g., apple, prune, pear), is a nonabsorbable disaccharide that draws water into the intestinal lumen and
softens the stool. Early treatment with sorbitol-containing juices may prevent the development and
exacerbation of fecal impaction. Glycerine suppositories may be used to assist in management.

Primary constipation accounts for approximately 95% of cases of constipation in children. Chronic constipation
that persists despite treatment may be a sign of an underlying condition (e.g., celiac disease, hypothyroidism,
spinal defects) and therefore requires further investigation.
20-The presence of blood-tinged stools in an otherwise active and healthy infant raises concern for food
protein-induced proctocolitis.

Perform an upper gastrointestinal series

6%

Assess for IgA anti-tissue transglutaminase antibodies

4%

Continue breastfeeding and advise mother to avoid dairy and soy products

49%

This child presents with new-onset passage of blood and mucus with no signs of obstruction (e.g., abdominal
distention) or systemic illness (e.g., vomiting, diarrhea, fever, hypotension). This constellation of symptoms in
an exclusively breastfed infant suggests food protein-induced proctocolitis due to a non-IgE-mediated immune
response to food antigens in the mother's milk. Diagnosis of this condition is clinical and management should
begin with elimination of all dairy and soy products from the mother's diet. If symptoms continue, egg
products should then be eliminated. Continued breastfeeding is encouraged as long as the offending proteins
can be avoided. Formula-fed infants with food protein-induced proctocolitis should be switched to hydrolyzed
formulas (e.g., hydrolyzed casein).

Rectal bleeding usually improves within 3 days of removal of the offending food antigen. Most infants will be
able to tolerate reintroduction of the offending food antigen to their diet by the time they are 1 year old.

21-Candiada ttt :

Treatment of local mucocutaneous candidiasis : all local except esophegeal

 Topical antifungal agents: e.g., clotrimazole, miconazole, ketoconazole, nystatin for 7–14 days
 Vaginal yeast infection: either topical antifungal agents (e.g., clotrimazole cream) 3–14 days or a single
dose of oral fluconazole
 Oral candidiasis
o First line
 Newborns: topical nystatin (preferred due to easy administration)
 Children and adults: topical nystatin or oral fluconazole
o Alternatives if treatment fails: other azoles (e.g., itraconazole, voriconazole) or echinocandins
(e.g., caspofungin)
 Esophageal candidiasis
o First line: oral or IV fluconazole for 14–21 days
o Alternatives if treatment fails: IV echinocandins (e.g., caspofungin or micafungin), topical or IV
amphotericin B, or oral or IV voriconazole

Treatment of systemic candidiasis


 Indications: systemic treatment is preferred in the following
o Immunocompromised patients
o Hematological infiltration or organ involvement
 Drug of choice: IV caspofungin or micafungin (echinocandins) for 2 weeks after resolution of symptoms
and documented clearance of C. albicans
 Alternatives
o Fluconazole: in patients that are not critically ill and in the case that resistance is unlikely

 Amphotericin B: because of toxicity, only indicated if there is intolerance, limited availability, or resistance
to alternatives

22-Rota virus inves : nzyme immunoassay of the stool is a highly sensitive test for diagnosing rotavirus.

23-Determining the fasting serum gastrin level after discontinuation of proton pump inhibitor (PPI) therapy is the best
initial test for diagnosing gastrinoma (Zollinger-Ellison syndrome). A 10-fold increase in gastrin levels is conclusive
evidence of a gastrinoma. A gastrin-producing tumor is suggested by the patient's extended course of symptoms and
multiple peptic ulcers that have been refractory to PPI therapy. Even though gastrinomas are a rare cause of PUD, more
than 95% of patients with gastrinoma present with PUD. More frequent causes of PUD, such as infection with
Helicobacter pylori or long-term use of NSAIDs can be ruled out based on patient history.

In addition to determining the fasting serum gastrin level, this patient's gastric pH should also be measured. Elevated
serum gastrin and a pH of < 2 are indicative of a gastrinoma. When pH is > 2, other etiologies of elevated gastrin should
be ruled out (e.g., PPI ingestion).

gastrinomas arising from the pancreas are often difficult to visualize on a CT scan.

24-
21-
25-Perianal cellophane-tape examination (i.e., a tape test) is the diagnostic test for Enterobius
vermicularis infection. At night, female worms migrate from the colon to the anal opening,
where they deposit eggs, which cause perianal and vulvar irritation and pruritus. The test is
conducted by applying a transparent piece of cellophane tape to the anal opening early in the
morning; any ova of Enterobius vermicularis will then stick to the tape. By pressing the sticky
side of the tape against a slide, anything picked up by the tape can be examined for the
presence of eggs. If the tape test confirms pinworm infection, treatment of the entire
household with albendazole or mebendazole is indicated to prevent reinfection.

26-HAV prophylaxis :

- Hepatitis A Preexposure Prophylaxis:


- Advise all travelers to adhere to primary preventive measures, including food and water
safety.
- Hepatitis A Vaccine:**
- Refer to the "ACIP immunization schedule" for scheduling details.
- Recommend routine active immunization for:
- All children > 12 months of age.
- Individuals at increased risk of HAV infection, such as those traveling to endemic countries,
in close contact with adoptees from endemic countries, having potential occupational
exposure, men who have sex with men, use injection or noninjection drugs, and those with
unstable housing.
- Individuals at increased risk of severe disease, including those with chronic liver disease,
adults, and children > 12 months of age with HIV, and any individual requesting vaccination.
- Hepatitis A vaccination is considered suitable during pregnancy in previously unvaccinated
individuals with an increased risk of infection or severe disease.

- Hepatitis A Postexposure Prophylaxis:


- Postexposure prophylaxis is indicated for all previously unvaccinated individuals in contact
with someone with serologically confirmed hepatitis A within the past two weeks (Hepatitis A
is a notifiable disease).
- **Recommended Regimens for Postexposure Prophylaxis:**
- **Active Immunization:**
- Healthy individuals aged 1–40 years.
- **Passive Immunization with Immune Globulin:**
- Individuals with contraindications for vaccination.
- Infants < 12 months of age.
- **Both Active and Passive Immunization:**
- Individuals with chronic liver disease.
- Immunocompromised individuals.
- Consideration in adults > 40 years of age with an increased risk of infection (refer to
"Hepatitis A preexposure prophylaxis").

27-The patient most likely has inflammatory diarrhea (bloody stools with PMNs) caused by Salmonella enteritidis
This patient developed inflammatory diarrhea one day following the food festival, which is consistent with the
incubation period of S. enteritidis (1–3 days). Omelets may contain undercooked eggs, which can be contaminated with
S. enteritidis. S. enteritidis is the 2nd most common pathogen responsible for bacterial foodborne gastroenteritis (the
most common in the US being Campylobacter). Typical diagnostic findings are fever as well as leukocytes, blood, and/or
mucus in stool due to destruction of the enteric mucosa by invasive Salmonella.

28-hepatits b &c antiviral drugs vvviiip

29-ttt of bacterial siadleintis :

 Treatment

 Hydration
 Stimulation of salivation (chewing gum, lemon drops)
 Intravenous antibiotics: nafcillin + metronidazole OR clindamycin (1st choice).
o Immunocompromised patients: vancomycin OR linezolid + one of the following:
 Cefepime + metronidazole
 Imipenem
 Meropenem
 Piperacillin-tazobactam
o Poor response to 48 hours of antibiotics or an abscess: surgical drainage and decompression
 Recurrent infections: parotidectomy

 Complications: deep neck infections


30-Options for antiviral therapy against hepatitis B include tenofovir, entecavir, and pegylated interferon alpha (IFN-α).
IFN-α is, however, contraindicated among pregnant women or patients with any of the following conditions:
autoimmune disease (e.g., systemic lupus erythematosus), uncontrolled psychiatric disease, cytopenias, severe cardiac
disease, or uncontrolled seizures.

Acute hbv -------supportive ttt

31-Liver transplantation is the only definitive treatment option in patients with fulminant hepatic failure

32-Pancreatic abscess (walled-off necrosis) is a late complication of acute necrotizing pancreatitis. This condition most
commonly manifests more than 4 weeks after an episode of acute pancreatitis with fever and a tender abdomen. The
complex cystic collection on ultrasound is most likely necrotic material within a fibrous capsule. Drainage is required for
symptomatic

Pancreatic pseudocyst:

A pancreatic pseudocyst is a complication of acute or chronic pancreatitis. While pancreatic pseudocysts can manifest
with a tender abdomen and fever if they become infected, they are most commonly asymptomatic. Moreover,
ultrasound usually shows a well-defined anechoic or hypoechoic mass rather than a complex cystic mass.

33-CT scan of the abdomen with contrast (oral and intravenous) is the test of choice for diagnosing diverticulitis. Typical
CT findings include bowel wall thickening (> 4 mm) and inflammation of the pericolonic fat with fat stranding (visible
traces of fluid in the fat). A CT scan is also helpful in ruling out complications such as abscess (fluid collections
surrounded by inflammatory changes), obstruction (dilated intestinal loops, air-fluid levels), perforation (free air in the
abdominal cavity), and fistula (air in organs other than the bowel).

The treatment of uncomplicated diverticulitis can usually occur in an outpatient setting. It includes a restricted, clear
liquid diet and bowel rest until pain improves, broad-spectrum oral antibiotics for 7–10 days (e.g., ciprofloxacin plus
metronidazole), and pain management, if necessary (e.g., acetaminophen, ibuprofen).

34-Iatrogenic trauma is the most common etiology of esophageal perforation (e.g., following upper endoscopy). While
this patient's x-ray findings and Hamman sign already suggest pneumomediastinum, gastrografin contrast
esophagography is indicated as a confirmatory test to visualize the potential defect and assess its size and exact
location. Gastrografin is preferred over barium as a contrast agent because it is water-soluble and less irritating;
extravasation of barium may cause mediastinitis and subsequent fibrosis. There is no free air under the diaphragms on
CXR, thus gastric perforation is unlikely.

If Boerhaave syndrome is suspected, a chest x-ray is conducted first, which may show lucency from mediastinal and/or
subcutaneous air. While gastrografin contrast esophagography is usually the preferred confirmatory test, there may be
false negatives in up to 20% of cases. The ease of a CT scan has made CT a popular alternative in hemodynamically
unstable patients and/or if x-ray and contrast esophagogram are inconclusive. In a patient with esophageal perforation,
the CT may demonstrate intramural swelling/hematoma and periesophageal air collections tracking into the surrounding
tissues.

35-Esophagogastroduodenoscopy is the best initial and confirmatory test for suspected esophageal cancer and can also
be used to classify reflux esophagitis as well as to detect a peptic ulcer. It should be conducted in all patients presenting
with symptoms of gastroesophageal reflux disease (e.g., retrosternal burning pain, regurgitation) and additional alarm
symptoms (e.g., weight loss, anemia, melena, dysphagia). If a biopsy confirms esophageal cancer in this patient, further
staging of the disease will include an endoscopic ultrasound to determine the infiltration depth and register regional
lymph node disease as well as a chest and abdominal PET-CT. Treatment depends on the exact location of the tumor,
histopathologic type (adenocarcinoma or squamous cell carcinoma), and the stage.

36-This patient's history of constipation and left lower quadrant pain together with CT findings of segmental colonic wall
thickening with multiple diverticula and surrounding fat stranding suggest acute diverticulitis. The > 4.0-cm low-
attenuating fluid collection is consistent with a large pelvic abscess, which has developed as a complication of
diverticulitis. There are no signs that suggest peritonitis (e.g., guarding, rebound tenderness, rigid abdomen).
Intravenous antibiotics alone are highly unlikely to resolve this patient's condition.

CT-guided percutaneous drainage is the treatment of choice for patients, like this one, with acute diverticulitis
complicated by large abscesses and no indications for emergent surgery (e.g., signs of peritonitis). CT-guided drainage
enables resolution of the abscess while minimizing the risk of complications from open surgery (e.g., colostomy,
adhesions). Patients who respond to initial management but subsequently develop recurrent episodes of diverticulitis or
chronic complications (e.g., fistulas) may be considered for elective colonic resection.

37- Angiography is the recommended procedure in patients with active hematochezia, hemodynamic instability
despite resuscitation efforts, and a normal EGD. The source of bleeding can be localized fast (does not require bowel
preparation) and reliably if the bleeding rate is more than 0.5–1 mL/min. Some centers opt to conduct CT angiography
for visualization of the bleed and analysis of anatomic detail before proceeding with invasive catheter angiography for
directed therapeutic intervention (e.g., embolization, vasopressin injection). If angiography fails to locate the source of
bleeding, a colonoscopy is the next step in management. Angiography is also used in stable patients when other
diagnostic methods are inconclusive.

38-Severe cytomegalovirus (CMV) infection (including CMV colitis) may occur in HIV-infected patients with a CD4 count
< 50 cells/mm3. CMV colitis typically presents with watery and explosive diarrhea, but if the distal colon becomes
involved, diarrhea may become bloody. Suspected CMV colitis can be confirmed via the detection of characteristic linear
lesions on colonoscopy and owl eye inclusions on biopsy. Options for empiric treatment of CMV infection include
foscarnet, ganciclovir, and cidofovir.

39-This patient's postprandial dull and constant abdominal pain in the RUQ, nausea, and vomiting suggest biliary colic.
This condition is caused by increased intraluminal gallbladder pressure as a result of gallbladder contraction against an
occluded cystic duct, most commonly due to gallstones. Referred pain to the shoulder and interscapular region, as seen
here, can also occur secondary to diaphragmatic irritation via the phrenic nerve. Patients with uncomplicated
cholelithiasis usually have normal laboratory values, as seen here; fever and leukocytosis should raise concern for acute
cholecystitis or acute cholangitis, and jaundice and hyperbilirubinemia suggest choledocholithiasis (see “Disorders
caused by gallstones” table).

Contrary to the name, the pain in biliary colic is not colicky but usually dull and constant.

40-
41-A trial of conservative management is recommended for all patients with mechanical SBO who show no signs of
bowel compromise (e.g., bowel ischemia, perforation, necrosis) and are hemodynamically stable. Although this patient
presents with vomiting and abdominal distention, he has no fever, abdominal guarding, or rebound tenderness, and is
hemodynamically stable, making conservative treatment the best next step in management. Nonoperative management
includes fluid resuscitation with electrolyte correction, nasogastric tube placement for gastrointestinal decompression,
and bowel rest. Serial abdominal examinations and laboratory studies are also required for patient monitoring. If
symptoms worsen during or do not improve after a 3- to 5-day trial of conservative management, surgical
decompression is indicated.

42-In patients with acute pancreatitis, the release of inflammatory cytokines and vascular injury by pancreatic enzymes
leads to vasodilation and increased vascular permeability, which can result in significant third-space fluid loss and
hemoconcentration. Patients with significant third-space fluid loss usually have a more severe disease course and a
worse prognosis. Blood urea nitrogen (BUN) and hematocrit are indicators of the severity of third-space fluid loss and
an increase in these is associated with a poor prognosis. Several scoring systems (e.g., Ranson criteria, BISAP) use these
indicators to assess the severity and prognosis of patients with acute pancreatitis.

43-Appenditis
complications :
44-
44- In addition to supportive care and correction of precipitating causes, the first-line treatment for acute HE consists
of lactulose because of its efficacy, availability, and relatively low cost. Lactulose improves HE by decreasing the
absorption of ammonia in the bowel. This effect occurs via multiple mechanisms, including a laxative effect that may
help resolve constipation (a trigger for HE, as seen in this patient), reduction of the pH in the lumen of the bowel, which
decreases the amount of ammonia absorbed into the plasma, and displacement of ammonia-producing bacteria.
Rifaximin is used as a second-line or adjunct treatment for HE that has not improved after 48 hours on first-line therapy.

45- Anal Cancer :

 Treatment of choice: radiochemotherapy

Recurrent cancers are treated surgically.

46-A history of multiparity is a significant risk factor for gallstones, which account for 90–95% of cases of acute
cholecystitis. The risk of gallstone disease is about 10 times greater among multiparous women than nulliparous women.
Higher estrogen levels during pregnancy increase the secretion of cholesterol into bile, while higher progesterone levels
decrease the production of hydrophilic bile acids, resulting in a decreased ability of bile to sequester cholesterol. The
combination of these effects leads to the supersaturation of bile with cholesterol, which in turn predisposes the patient
to gallstone disease.

47-ascites fluid analysis

48-n an individual with a significant history of heavy alcohol use, the combination of acute epigastric pain and
hematemesis following multiple episodes of vomiting raises concern for Mallory-Weiss syndrome.

49-Clinically, ischemic colitis typically manifests in three phases: a hyperactive phase of crampy abdominal pain with
bloody, loose stools; a paralytic phase with diffuse pain, bloating, absent bowel sounds, and cessation of stools; and,
finally, a shock phase with signs of peritonitis and septic shock. These phases can be clearly identified in this patient's
clinical course, as her vital signs indicate early signs of developing shock.

50-The risk for malignant transformation of BE with high-grade dysplasia to esophageal adenocarcinoma is approx. 7%
per year. Therefore, endoscopic eradication of dysplasia via mucosal resection and/or radiofrequency ablation is the
treatment of choice in patients with high-grade dysplasia. Concurrent eradication of intestinal metaplasia also reduces
the risk of dysplasia recurrence. In BE with low-grade dysplasia, the risk for malignant transformation is approx. 0.7%
per year. Endoscopic eradication is also preferred for BE with low-grade dysplasia but surveillance endoscopy every 12
months is an acceptable alternative.

Endoscopic eradication therapy is also indicated in the management of certain patients with stage T1a esophageal
adenocarcinoma (i.e., with intact muscularis propria).
48-
53- Boheeve s :

Conservative therapy is indicated for generally healthy patients in a stable medical condition with a small, contained
perforation and no signs of sepsis. Components of conservative therapy for Boerhaave syndrome include nothing by
mouth with parenteral nutrition if required, IV proton pump inhibitors, analgesia, broad-spectrum antibiotic
prophylaxis (e.g., ampicillin/sulbactam), percutaneous drainage of any fluid collections, and cardiopulmonary
monitoring. Prior to restarting oral intake, a contrast esophagogram with gastrografin is indicated to confirm healing of
the perforation.

Surgical repair of a ruptured esophagus is indicated for Boerhaave syndrome patients who either fail conservative
treatment or do not satisfy the criteria for it. This patient has a small perforation contained to the mediastinum, no
major comorbidities, and no signs of sepsis. Therefore, she is eligible for a trial of conservative therapy prior to more
invasive measures.

54- This patient has spontaneous bacterial peritonitis (SBP), which is defined as > 250 polymorphonuclear
leukocytes/mm3 in ascites fluid. SBP is caused by bacterial translocation (usually gram-negative rods such as E. coli or
Klebsiella spp.), including migration of bacteria through the intestinal wall to the peritoneal space and possible
colonization of the mesenteric lymph nodes. This condition occurs most commonly in patients with portal hypertension
and resulting ascites secondary to advanced liver cirrhosis. This patient's liver failure is evident from his spider
angiomata, scleral icterus, and confusion. Patients with SBP may be asymptomatic but often present with fever,
abdominal pain, and a change in mental status, as seen here.

Empiric antibiotic treatment for SBP with a third-generation cephalosporin (e.g., cefotaxime) or a fluoroquinolone (e.g.,
levofloxacin) should be initiated immediately. Coverage may be narrowed when culture sensitivities are available, but
determination of the causative pathogen is often unsuccessful. After the first episode of SBP, this patient should start
antibacterial prophylaxis with ciprofloxacin or TMP-SMX.

55-The first step in managing HAs is to stop oral contraceptives (OCPs) and anabolic steroids and remove any hormone-
containing IUDs, all of which can increase the size of the tumor. In female patients, an asymptomatic HA < 5 cm in
diameter, as seen here, can be managed conservatively because it is unlikely to undergo rupture or malignant
transformation. However, some HAs have been known to increase in size following discontinuation of OCPs or steroids;
thus, follow-up CT/MRI with contrast at 6-month intervals for 2 years is strongly recommended. Once serial monitoring
over this period has shown that the HA size is stable, imaging may be conducted annually. Surgical resection is
recommended in female patients who present with symptoms (e.g., upper abdominal pain, fullness, nausea) and/or a
tumor size of > 5 cm as well as in male patients irrespective of tumor size because of an increased risk of malignant
transformation.

56-Mechanical dilation with a bougie or balloon dilator is the first-line treatment for an obstructing Schatzki ring. This
procedure provides immediate symptom relief. However, recurrence of strictures is possible and subsequent dilations
may be needed. Esophageal rings are thought to arise secondary to chronic damage from gastroesophageal reflux
disease.

. After treatment of the Schatzki ring, Nissen fundoplication may be considered for treating his sliding hiatal hernia.
57-colon polyps

58-An air enema is both diagnostic and therapeutic for intussusception. An air enema or an enema with water-soluble
contrast would show an interruption of contrast at the site of invagination and would likely reduce the intussusception.
An abdominal ultrasound may be performed prior to air enema if the diagnosis is unclear. However, if there is a high
clinical suspicion of intussusception, radiographic imaging may not be necessary and should not delay management.

Infectious gastroenteritis can also be considered as a possible cause of this patient's symptoms, but it is less likely
because of the episodic nature of the abdominal pain, the mass on physical exam, and the lack of feve

59-This young boy presents with painless lower gastrointestinal bleeding, which is the characteristic
presentation of Meckel diverticulum.

Technetium-99m pertechnetate scan is the ideal diagnostic test when there is a high suspicion for Meckel diverticulum
in children. This scan uses a radioactive tracer that has a high affinity for gastric mucosa and is, therefore, able to
identify Meckel diverticulum with high sensitivity and specificity. Ectopic gastric mucosa can secrete gastric acid within
the diverticulum, possibly resulting in ileal ulceration and subsequent bleeding.

The sensitivity of technetium-99m pertechnetate scan is lower in adults because the adult population tends to have a
higher percentage of Meckel diverticulum that lack ectopic gastric mucosa. False positives may be seen in
intussusception and inflammatory bowel disease.

60- Blind loop syndrome is a type of small intestinal bacterial overgrowth (SIBO) that develops in patients who have a
blind intestinal loop following abdominal surgery (e.g., subtotal gastrectomy with Roux-en-Y, Billroth II). A blind pouch
that is no longer connected to the stomach results in locally decreased intestinal motility and a relative lack of acidity,
both of which result in excessive growth and colonization of the intestinal flora. This overgrowth of bacteria results in
the formation of loose and/or fatty stools and, in some cases, malabsorption. Vitamin B12 deficiency is a common
manifestation of SIBO and is a result of both malabsorption and increased uptake of the vitamin by the bacteria.

SIBO can be diagnosed with endoscopic cultures from the jejunum (gold standard) or a positive lactulose breath test.
Treatment options include an elemental diet, correction of nutrient or micronutrient deficiencies, antibiotics, or
probiotics. In rare cases, surgical correction of the reconstruction may be necessary.

61-Rectal biopsy is the gold standard confirmatory test for suspected HD. It can be performed either as a full-thickness
biopsy, carried out under general anesthesia, or as a rectal suction biopsy, directly at the bedside, sparing the patient
the need to undergo general anesthesia. If the biopsy shows an absence of ganglion cells in an adequate tissue sample,
HD is confirmed. A normal biopsy result taken from a correct site (i.e., 2 cm proximal to the dentate line) virtually rules
out HD.

If HD is confirmed, the aganglionic segment of the colon is resected and anastomosed, either in a one-stage operation
or, less commonly, as a two-stage surgery in which a diverting colostomy is performed to decompress the dilated bowel,
followed by definitive anastomosis of the bowel loops.
62-The combination of epigastric tenderness, bloating, early satiety, persistent nonbilious emesis, gastric dilation
(tympanitic epigastric mass), and a succussion splash on abdominal auscultation should raise concern for gastric outlet
obstruction (GOO). This patient's heartburn, severe episodic epigastric pain that is relieved with food but worsens hours
after eating, and features of gastrointestinal bleeding (positive fecal occult blood test, hematemesis) suggest a duodenal
ulcer as the most likely underlying cause of GOO.

GOO can be caused by acute or chronic peptic ulcer disease (PUD). This patient has had episodic epigastric pain and
heartburn for only one week, suggesting acute PUD, which can cause obstruction via inflammation-induced edema and
tissue deformation of the gastroduodenal junction. In patients with chronic PUD, which is most commonly seen in
individuals with long-term NSAID use or those with Helicobacter pylori infection, GOO can result from scarring and tissue
fibrosis. Other causes of GOO include malignancy (most common) and strictures in the pyloric channel (e.g., due to
Crohn disease, ingestion of a caustic substance, or chronic pancreatitis).

In patients with GOO, persistent vomiting can lead to hypokalemic hypochloremic metabolic alkalosis and decreased
fluid uptake, the latter of which can result in prerenal acute kidney injury evidenced in this patient by elevated serum
urea nitrogen and creatinine. In cases of suspected GOO, upper endoscopy is used to confirm the diagnosis. Initial
management includes nasogastric suction, electrolyte and fluid replacement, and parenteral nutrition. Further
treatment should target the underlying cause (e.g., proton pump inhibitor therapy in patients with PUD). If conservative
measures fail, endoscopic dilation or surgery can be considered for definitive treatment.

63-**Neonatal Jaundice: Physiological and Pathological Aspects**

**Physiological Neonatal Jaundice:**

- Asymptomatic, except for transient icterus.

- Manifests after the 1st day of life, usually resolving without treatment in 1 week (term infants) or 2 weeks (preterm
infants).

- Typically most severe on the 5th day.

**Pathological Neonatal Jaundice:**

- Jaundice can appear < 24 hours after birth and persist > 1 week in term infants and > 2 weeks in preterm infants.

- Clinical features of the underlying cause should be investigated.

**Diagnostics:**

- Regular assessment for icterus recommended every 8–12 hours.

- Bilirubin Tests:

- Transcutaneous bilirubin measurement (TcB): Levels > 95th percentile indicate high-risk neonates.

- Serum bilirubin measurement: Differentiation of direct and indirect bilirubin; assessment based on nomogram.

- Additional laboratory tests for comprehensive evaluation.


**Treatment:

Phototherapy:

- Primary treatment for neonates with unconjugated hyperbilirubinemia.

- Indications based on AAP phototherapy nomogram, considering gestational age and risk factors.

- Procedure involves exposure to blue light, promoting photoisomerization and photooxidation of bilirubin.

- Continued until total bilirubin levels < 15 mg/dL.

- Adequate fluid supplementation, eye protection, and precautions for contraindications and side effects.

**Side Effects and Complications:

- Diarrhea, dehydration, changes in skin hue, separation from the mother, increased risk of AML, and rare bronze baby
syndrome.

- Newborns with TSB levels below the phototherapy threshold usually do not require treatment.

**Exchange Transfusion:

- Most rapid method for lowering serum bilirubin concentrations.

- Indications:

- Threshold in a 24-hour-old term baby: Total serum bilirubin > 20 mg/dL.

- Inadequate response to phototherapy, rapid rise in bilirubin (> 1 mg/dL/hour in less than 6 hours), acute bilirubin
encephalopathy, hemolytic disease, severe anemia.

- Procedure:

- Use ABO-matched and Rh-negative erythrocyte concentrate.

- Exchange blood in quantities of 5–20 mL via an umbilical venous catheter until total serum bilirubin is < 95th
percentile on nomogram.

- Side Effects:

- Higher mortality and morbidity from infections, acidosis, thrombosis, hypotension, electrolyte imbalances.

**IV Immunoglobulin:

- Indications: Used in cases with immunologically mediated conditions or significant neonatal jaundice due to Rh, ABO,
or other blood group incompatibilities.

- Dose Range: 500–1000 mg/kg.


64-hcc or mets ????

Hepatocellular carcinoma (HCC) may manifest with weight loss, abdominal distention, and deranged liver function tests.
However, HCC does not cause lower gastrointestinal symptoms or occult blood in stool. On contrast-enhanced CT scan,
HCC appears as a solitary hepatic lesion that characteristically enhances brightly in the arterial phase and appears
hypodense in the venous phase due to the rapid contrast washout. Although this patient's CT scan also shows
hypodense lesions, the presence of multiple lesions and only minimal rim enhancement in the arterial phase makes HCC
an unlikely diagnosis.

weight loss, low-grade fever, lower gastrointestinal complaints (i.e., constipation), and evidence of blood in stool
(positive stool occult blood test). This contrast-enhanced CT scan shows multiple hypodense solitary lesions with
peripheral rim enhancement in both lobes of the liver, characteristic of hepatic metastases. These features are highly
suggestive of a primary colorectal malignancy that has metastasized to the liver, the most frequent metastatic site for
this condition. The palpable hepatomegaly with a hard nodule and mildly deranged liver function tests are caused by the
metastatic deposits.

65- lynch ss from amboss library

66-
67-

68-Necrotizing enterocolitis (NEC) is the most common cause of acute abdomen in premature infants with low birth
weight. It typically occurs 2–4 weeks after birth, once oral feeding has begun. Infants present with poor feeding,
lethargy, vomiting, diarrhea, hematochezia, thrombocytopenia, and/or a distended abdomen with decreased bowel
sounds.

If uncomplicated NEC (i.e., without perforation/peritonitis) is diagnosed, blood cultures, broad-spectrum IV antibiotics,
and supportive care (i.e., bowel rest, total parenteral nutrition, fluid replacement, and cardiovascular/respiratory
support) are the management of choice. Surgical treatment is warranted when there is evidence of perforation (e.g.,
pneumomediastinum) or no response to optimal medical therapy.

69-medication of ulcerative colitis.

70- Biliary cysts (i.e., choledochal cysts) are most commonly seen in patients of Asian descent and appear as saccular or
fusiform dilations of the biliary tree or as dilated masses that communicate with the biliary tree. A biliary cyst can result
in cholestatic jaundice, abdominal pain, and a palpable right upper quadrant mass and, if left untreated, increases the
risk of cholangitis and malignancy (e.g., cholangiocarcinoma, pancreatic cancer, gallbladder cancer). In rare cases, a
biliary cyst may involve the cystic duct and result in gallbladder dilation. The recommended treatment for a biliary cyst is
surgical excision of the cyst, followed by the creation of a biliary-enteric anastomosis with a Roux-en-Y
hepaticojejunostomy.
69-

71-Infants who are breastfed have a lower incidence of pyloric stenosis compared to infants who are bottle-fed. Infants
who are bottle-fed (whether breastmilk or formula) tend to consume a larger volume in less time compared to infants
who are breastfed, which may lead to pylorus muscle hypertrophy via overstimulation. In addition, higher levels of
vasoactive intestinal peptide (VIP) in breast milk may help mediate pyloric relaxation, facilitating gastric emptying
compared to infants who are formula-fed.

72-This patient with postcholecystectomy syndrome has elevated cholestatic parameters and a dilated
common bile duct (> 10 mm). These findings can be due either to residual gallstones within the biliary tree or sphincter
of Oddi dysfunction (SOD). Although there were no gallstones seen in the common bile duct on abdominal ultrasound,
this does not exclude choledocholithiasis because intraductal stones and microliths may be difficult to visualize. An ERCP
with sphincterotomy should be performed as ERCP is highly sensitive for most causes of biliary dysfunction and
sphincterotomy is indicated for this patient with biliary-type pain, abnormal liver function tests, and a dilated common
bile duct. ERCP with sphincter of Oddi manometry is indicated prior to sphincterotomy in patients with less distinct
features of SOD (i.e., biliary-type pain but normal common bile duct or cholestatic parameters). While magnetic
resonance cholangiopancreatography (MRCP) is an acceptable alternative test for the evaluation of
postcholecystectomy syndrome, ERCP is preferred when an intervention is planned, as in this patient.

73-Acalculous cholecystitis has high risk of gallbladder perforation and rapid deterioration.

Apart from fluid resuscitation, he should be started on broad-spectrum antibiotics such as piperacillin-tazobactam
immediately,

cholecystostomy should be performed to decompress his distended gallbladder. Cholecystectomy is the definitive
treatment for acalculous cholecystitis.

A percutaneous cholecystostomy, on the other hand, is a less invasive temporizing alternative for severely ill patients
(such as this patient, who has several severe diseases and has recently undergone a major surgical procedure) or
patients too unstable to be under general anesthesia.

If the patient does not improve within 24 hours, a cholecystectomy should be performed.

74- Acute colonic pseudo-obstruction (Ogilvie syndrome).

history of multiple medical conditions presents with abdominal distention and pain as well as radiographic evidence of
colonic dilation with haustral preservation. In the absence of an obstructing lesion indicating mechanical bowel
obstruction.

Tttt : -supportive . for 2 days if no improve then ..

- Intravenous neostigmine therapy is a highly effective treatment option for acute colonic pseudo-obstruction (Ogilvie
syndrome) that is indicated if supportive therapy (i.e., bowel rest, intravenous fluids with correction of any electrolyte
abnormalities, bowel decompression) does not relieve symptoms within 24–48 hours. As Ogilvie syndrome is thought to
arise from an imbalance between adrenergic and cholinergic signaling, an increase in acetylcholine from neostigmine
administration should stimulate bowel peristalsis and relieve symptoms in most patients.

In patients presenting with cecal dilatation > 12 cm, neostigmine therapy can also be used as initial therapy, if there
are no signs of colonic ischemia, perforation, or peritonitis (e.g., fever, abdominal guarding or rebound) that necessitate
surgery. Patients undergoing neostigmine therapy should be monitored for bradycardia, which is a common side effect.

Laparotomy is indicated in patients with acute colonic pseudo-obstruction that show signs and symptoms of acute
abdomen indicating impending or current colonic ischemia and/or perforation, such as fever, rigid abdomen, guarding,
or rebound tenderness. However, this patient is afebrile and his physical exam reveals a distended abdomen with only
mild tenderness to palpation. A less aggressive treatment option is more appropriate in this case.

75- he 5 Ps: Peritonitis, Postoperative, low Potassium, oPioids, and Pelvic/spinal fractures are among the most common
causes of paralytic ileus.

76- The vast majority of congenital umbilical hernias close spontaneously by age 5. Because the patient is asymptomatic
and the hernia is small, the most appropriate management at this time is reassurance and observation. The risk of
complications (e.g., incarceration, strangulation) is low in comparison to other types of hernias.
If the patient develops features of bowel obstruction, such as constipation, vomiting, or incessant crying, or if the hernia
does not decrease with time, surgical repair may be indicated.

77-

77-

78- Following fluid and electrolyte resuscitation, endoscopic detorsion (via sigmoidoscopy) is the best initial treatment
for patients with sigmoid volvulus and no signs of peritonitis (e.g., abdominal rigidity/rebound tenderness). Endoscopic
detorsion successfully reduces sigmoid volvuli in 90% of cases and allows colonic mucosa inspection for signs of ischemia
(e.g., hemorrhage or bluish discoloration of the colon wall). It is recommended to perform sigmoid colectomy ∼ 72
hours after reduction to reduce the high risk of recurrence. A rectal tube should be placed following endoscopic
detorsion to allow for continued decompression of the colon until surgery. If a patient has peritonitis (suggesting bowel
strangulation/infarction), signs of ischemia on endoscopy, or fails endoscopic detorsion, intravenous antibiotics and
emergency sigmoid colectomy are required.

79-MALT lymphoma :

\H. pylori eradication therapy (e.g., amoxicillin, clarithromycin, and omeprazole) for 10–14 days is the first-line
treatment for gastric MALT lymphomas. Because of the strong association between MALT lymphomas and H. pylori
infection, eradication therapy should be performed even if the patient tests negative. In 60–80% of patients with H.
pylori-associated gastric MALT lymphoma, eradication therapy results in complete regression of the tumor.

A urea breath test or stool antigen test, as well as an endoscopic biopsy, should be performed three months after
therapy to confirm H. pylori eradication and histological response.

\ If there is no or only a partial histological response, radiotherapy or chemotherapy should be initiated.

80- Biopsy of the lesions is the next best step in the management of leukoplakia, which most commonly affects the oral
cavity. While leukoplakia is by itself a benign lesion, it predisposes to squamous cell carcinoma. Up to 20% of leukoplakia
lesions progress to carcinoma within 10 years. Because of this, it is important to biopsy leukoplakia lesions to check for
signs of dysplasia.

Treatment consists of smoking cessation, cryotherapy, laser ablation, or surgical excision if the lesion persists.

81- This patient most likely has chronic intestinal bleeding due to angiodysplasia (an arteriovenous malformation) in the
colonic wall. Angiodysplasia is associated with older age (> 60 years) and ESRD. In patients with ESRD, ∼ 30% of cases of
lower GI bleeding are due to angiodysplasia. However, the association between gastrointestinal angiodysplasia and ESRD
is not fully understood. Other conditions associated with angiodysplasia include von Willebrand disease and aortic
stenosis.

In hemodynamically stable patients, colonoscopy is the best next step in management for suspected lower
gastrointestinal bleeding and can be followed by upper endoscopy if the diagnosis remains unclear. Although
angiography is the gold-standard method for diagnosing angiodysplasia, endoscopy is frequently the first modality used,
as it can be both diagnostic and therapeutic; however, angiodysplasia is not always detected during routine endoscopy.
Patients with active bleeding and/or those with iron deficiency anemia should undergo endoscopic coagulation (e.g.,
using cautery, electrocoagulation, or clipping).

hyperplastic polyps, which are of low malignant potential and were removed.

82-
82-

83- A videofluoroscopic modified barium swallow is considered the test of choice for evaluating oropharyngeal
dysphagia. It involves direct visualization of the entire swallowing process using continuous x-rays and barium contrast.
This diagnostic test evaluates the patient's risk of aspiration and determines whether the patient might benefit from
supervised feedings, swallow rehabilitation therapy, and/or enteral nutrition.

Dysphagia causes dd amboss

84-calssification of diahhrea

85-
86- **Complications of Peptic Ulcer Disease (PUD):**

**1. Bleeding:
- *Definition:* Bleeding and/or hemorrhage of a peptic ulcer (duodenal or gastric), the most common
complication of PUD.
- *Etiology:*
- Posterior duodenal ulcers are more likely to bleed.
- Gastric ulcers of the lesser curvature may cause bleeding from the left gastric artery.
- Duodenal ulcers of the posterior wall may cause bleeding from the gastroduodenal artery.
- *Clinical Features:*
- Hematemesis (coffee-grounds emesis)
- Melena
- Anemia
- Hematochezia (less common)
- Orthostatic hypotension
- *Treatment:* NPO, volume resuscitation, transfusion, endoscopy. See “Initial management of an overt GI
bleed” for more details.

**2. Peptic Ulcer Perforation:


- *Definition:* Full-thickness injury and loss of bowel wall integrity leading to leakage of gastrointestinal
contents.
- *Etiology:*
- Prepyloric gastric ulcers are the most common cause.
- Duodenal ulcers of the anterior wall are more likely to perforate than ulcers of the posterior wall.
- *Clinical Features:*
- Sudden, diffuse abdominal pain and rigidity
- Fever, tachycardia, tachypnea, hypotension
- Pneumoperitoneum
- Shoulder pain (irritation of the phrenic nerve)
- *Treatment:* NPO, volume resuscitation, supportive care. Graham patch for small perforated duodenal
ulcers. See “Treatment” in “Gastrointestinal perforation” for more details.

*Note: Posterior ulcers are more likely to bleed, and anterior ulcers are more likely to perforate.*

**3. Ulcer Penetration and Fistula Formation:


- *Definition:* Penetration of a peptic ulcer through the gastric/duodenal wall into adjacent organs without
leaking into the peritoneal cavity.
- *Etiology:* Duodenal ulcers are the most common cause.
- *Clinical Features:*
- Change in symptoms related to affected neighboring organs.
- Colon: Gastrocolic or duodenocolic fistulas may manifest with copremesis and postprandial diarrhea.
- Liver, spleen, or diaphragm: Penetration may result in visceral abscesses (fever, abdominal tenderness, and
sepsis).
- Gastroduodenal artery or aorta: Vascular fistulas may result in severe hemorrhage.
- Biliary tree: Choledochoduodenal fistulas may manifest with biliary tract obstruction.
- Pancreas: Increased epigastric pain and peritonitis.
- *Treatment:* Conservative management for spontaneous closure. Surgical resection in unresponsive cases.

**4. Gastric Outlet Obstruction (GOO):


- *Pathophysiology:*
- Acute PUD → inflammation and edema.
- Chronic PUD → scarring and fibrosis.
- *Clinical Features:*
- Postprandial, nonbilious vomiting
- Succussion splash
- Early satiety
- Progressive gastric dilation
- Weight loss
- *Diagnostics:* Imaging (e.g., barium swallow, CT abdomen), EGD (confirmatory test). Laboratory studies may
show hypokalemic hypochloremic metabolic alkalosis.
- *Management:* Symptomatic (nasogastric suction, electrolyte/fluid replacement). Definitive (surgery or
endoscopic dilation).

**5. Malignant Transformation:


- *Gastric Ulcers:*
- High malignant potential (5–10% progression to cancer).
- *Etiology:* Malignancy ruled out with biopsy.
- *Duodenal Ulcers:*
- Usually benign.
- *Etiology:* Routine biopsy not required.
88- Cigarette smoking significantly increases the risk of pancreatic cancer. Smoking accounts for about 25% of all cases
and it is considered the most significant environmental contributing factor. This patient's history of 50 pack years is
likely to have been the main risk factor for developing pancreatic cancer. Further risk factors for pancreatic cancer
include chronic pancreatitis (esp. > 20 years), age > 50 years, and hereditary genetic syndromes.
87-

89- A gastrinoma (Zollinger-Ellison syndrome) causes a large volume of gastric acid to be produced, which decreases
intestinal pH. Pancreatic lipases, which require an alkaline environment to function, are inactivated and can no longer
emulsify fats. This may result in a deficiency of fat-soluble vitamins (e.g., vitamin E), causing neuromuscular disorders,
such as ataxia. In addition, increased gastric acid leads to the development of PUD. Finally, gastrin acts directly on the
intestine and prevents sodium and water reabsorption, resulting in secretory diarrhea. Treatment of gastrinoma
(Zollinger-Ellison syndrome) includes proton pump inhibitors (e.g., omeprazole) and H2 antagonists (e.g., ranitidine) in
order to reduce acid production. Octreotide (a somatostatin analog) may be used in refractory cases.

90- Plain abdominal x-ray and/or CT scan with contrast are used to diagnose toxic megacolon and should be ordered in
patients who present with bloody diarrhea, abdominal distention, and signs of systemic inflammation. Radiographic
evidence of colonic dilation (transverse colon > 6 cm in diameter) is needed to confirm the diagnosis. Multiple air-fluid
levels and loss of colonic haustration further indicate colonic dilation and paralytic ileus. Patients with inflammatory
bowel diseases such as ulcerative colitis are at risk of developing toxic megacolon, especially early in the disease course.

Initial treatment is usually conservative and includes IV antibiotics, fluid resuscitation, complete bowel rest, nasogastric
decompression, and IV steroids (for inflammatory bowel disease). If the patient does not improve within 24–72 hours,
surgery may be required.

Indications for exploratory laparotomy for toxic megacolon include features of bowel perforation or ischemia
(abdominal guarding, rebound tenderness, air under the diaphragm on radiography), massive gastrointestinal
hemorrhage, and no improvement of symptoms after 24–72 hours of conservative therapy. This patient has no clinical
signs of bowel ischemia or perforation and requires a confirmatory diagnostic test for toxic megacolon before initiating
treatment.
91- A history of hematochezia, anal pruritus, painful defecation, and weight loss in a patient with an exophytic, friable,
ulcerated mass above the anal verge is suggestive of anal canal cancer. Squamous cell carcinoma is the most common
histological type of anal canal cancer and typically arises below the dentate line (see “Characteristics of the anal canal
above and below the dentate line” table). Patients must undergo a biopsy of the tumor to confirm the diagnosis.
Women diagnosed with anal canal squamous cell carcinoma should also undergo a gynecological examination for
cervical cancer screening.

Condylomata acuminata of the anus is caused by HPV infection, which this patient has a history of, and can manifest as
an exophytic lesion. However, although condylomata acuminata are pruritic, tender, and friable in a small percentage of
cases, they are more commonly asymptomatic; weight loss is not expected. Moreover, when present in the anal canal,
condylomata acuminata usually appear as small papules rather than large, ulcerated lesions.

No weight loss with condyloma accuminata

92- All individuals ≥ 18 years of age should be screened for hepatitis C virus (HCV) infection at least once in their
lifetime. More frequent screening is recommended for individuals with risk factors for HCV infection, such as a history of
injection drug use, solid-organ transplantation, long-term hemodialysis, or HIV infection. Screening is performed by
testing the serum for anti-HCV antibodies; if screening is positive, the diagnosis can be confirmed with polymerase chain
reaction testing for HCV RNA. With direct-acting antiviral treatment, the rate of complete cure with sustained virological
response is over > 90%.

93- Widening of the femoral ring occurs with increasing age and may result in femoral hernia, which has a higher
incidence in women, who have a wider pelvis compared to men and, therefore, a larger vascular lacuna. Typical
symptoms include painless groin swelling. They manifest as a palpable mass below the inguinal ligament, medial to the
femoral vein; an expansive cough impulse is a common finding. In addition to obesity, chronic cough resulting from
chronic obstructive pulmonary disease increases intraabdominal pressure, consequently increasing the risk of
developing a femoral hernia.

94- Abdominal ultrasound with Doppler [10][18]

 Indications
o Suspected cirrhosis: best initial test
o Established cirrhosis: for HCC screening and detecting complications

95- Indications for primary prophylaxis against esophageal variceal hemorrhage include size and appearance of varices,
and severity of cirrhosis. Red signs on endoscopy (i.e., red patches on the variceal surface), as seen in this patient,
indicate an increased risk for bleeding. Nonselective beta blockers (e.g., nadolol, propranolol) are the first-line
pharmacotherapy for primary prophylaxis in patients with nonbleeding varices. These agents cause splanchnic
vasoconstriction, which decreases portal blood flow and portal pressure, thereby preventing further enlargement of
varices and reducing the risk of hemorrhage. Endoscopic band ligation is an alternative measure for primary prophylaxis
that can be considered in individuals with medium or large varices and/or in those who do not respond well to
treatment with beta blockers.

Beta blockers should not be used in patients with acute variceal bleeding, as these drugs decrease blood pressure and
suppress the physiological increase in heart rate.
96- Paracentesis with ascitic fluid analysis is the next best step in the management of patients with suspected SBP, and
it is the gold standard for confirming the diagnosis before the initiation of antibiotics. Ascitic fluid analysis should
include measuring albumin, total protein, cell count, and bacterial cultures. A polymorphonuclear cell count ≥ 250
cells/mm3, with or without positive bacterial cultures, in the ascitic fluid is consistent with SBP.

Diagnostic paracentesis is also indicated in all cases of new-onset ascites.

Any Ascites ,,,next step …..paracentsis .

97- Patient-controlled analgesia (PCA) with intravenous opioids (e.g., hydromorphone, fentanyl) is indicated in patients
with severe acute pain (e.g., postoperative pain, malignancy pain, or pain resulting from acute pancreatitis, sickle cell
crisis, or burn injuries). With PCAs, patients press a button that releases additional intravenous medication, allowing
them to control the amount of analgesic they receive and minimizing the risk of underdosing. The pumps include a
lockout period during which no further analgesic can be administered in order to avoid inappropriately high doses and
reduce the risk of respiratory depression. Although opioids are known to cause sphincter of Oddi dysfunction, there is no
evidence showing that opioids aggravate pancreatitis or worsen clinical outcomes.

98- Esophageal strictures are common sequelae of untreated GERD and/or esophagitis. Reflux esophagitis (erosive
esophagitis), the most common complication of GERD, is characterized by inflammation of the esophageal mucosa.
Esophageal strictures are formed via fibrosis as the inflamed esophageal mucosa heals. Treatment of both reflux
esophagitis and GERD consists of lifestyle modifications (e.g., elevation of the head of the bed when sleeping, avoidance
of dietary triggers such as spicy food) and acid suppression with proton pump inhibitors.

The most important risk factors for esophageal squamous cell carcinoma (SCC) are cigarette smoking and chronic alcohol
use. However, GERD with reflux esophagitis does not increase the risk of developing esophageal SCC. Moreover,
esophageal SCC typically occurs in the upper two-thirds of the esophagus, whereas this patient has endoscopic evidence
of distal esophageal disease

99-dehydrayion amboss library

100- Endoscopic small bowel biopsy should be performed in patients with suspected tropical sprue following blood
tests, serological antibody testing, and stool analysis. Histological findings include villous atrophy, elongated crypts, and
inflammatory cells (plasma cells, lymphocytes, eosinophils). However, these findings are not specific to tropical sprue;
they may also be seen in celiac disease. Therefore, the diagnosis is ultimately confirmed by a response to treatment,
which usually consists of tetracycline in combination with folic acid for 3–6 months.

Endoscopic small bowel biopsy is also indicated as a confirmatory test for celiac disease and as an initial diagnostic step
for Whipple disease, both of which can cause malabsorption syndrome. However, this patient's negative IgA anti-tissue
transglutaminase antibody almost certainly rules out celiac disease. Whipple disease, on the other hand, is a rare but
lethal condition if left untreated, and it often manifests initially with weight loss and extraintestinal symptoms (e.g.,
fever, arthralgias arthritis, cardiac, and neurological symptoms) before diarrhea occurs; the characteristic histological
finding of this condition is PAS-positive foamy macrophages in the lamina propria.
101- This patient has cannabinoid hyperemesis syndrome (CHS), a condition characterized by cyclic episodes of colicky
abdominal discomfort, nausea, and vomiting in a patient with a history of chronic cannabis use. The symptoms of
nausea and vomiting associated with CHS are classically relieved with hot showers, as seen in this patient. The
pathophysiology of this condition remains incompletely understood. The only known effective long-term treatment for
CHS is cannabis cessation. Other therapies that may have limited benefit include topical capsaicin, benzodiazepines, and
antiemetics (e.g., ondansetron).

102- A urea breath test is indicated to confirm H. pylori eradication 4–6 weeks after completing treatment. Proton
pump inhibitors (e.g., omeprazole) should be stopped at least 2 weeks before testing because they increase the risk of
false negative results. Other tests for confirming eradication include stool antigen testing and rapid urease testing of
biopsy samples. The latter is only considered in patients who require follow-up endoscopy (e.g., those with persistent
symptoms, dysplasia on biopsy, new onset of symptoms after successful eradication). Acid suppression medications can
be discontinued after eradication is confirmed.

103- This man has nonbilious emesis following food intake, early satiety, weight loss, epigastric tenderness, and a
succussion splash, all of which indicate gastric outlet obstruction (GOO). In adults, GOO is caused by a malignant
obstruction in the majority of cases.

104- The strongest predisposing factor for malignant transformation is the histological subtype of the lesion, followed
by its size, location, and gross appearance. Adenomatous polyps (tubular adenoma, tubulovillous adenoma, villous
adenoma) carry the highest risk of malignant transformation of all types of colonic polyps. A villous adenomatous polyp
has the highest risk (∼ 50%) of malignant transformation of the three types of adenomatous polyps. The larger the
villous polyp, the higher the risk.

105- after management of acute pancreatitis search for the most common cause which is biliary : In patients with acute
pancreatitis, following initial management with intravenous fluid resuscitation and analgesia, the next step is to evaluate
the underlying cause in order to plan further treatment and prevent recurrence. The most common cause of acute
pancreatitis in the United States is biliary obstruction. Abdominal ultrasonography is a highly sensitive
imaging modality for detecting gallstones in the biliary and pancreatic duct and should be performed in all patients with
acute pancreatitis. It is important to distinguish biliary pancreatitis from a nonbiliary etiology to guide treatment; biliary
pancreatitis is managed with cholecystectomy with or without a preceding ERCP.

106- Amiodarone can have several adverse effects, including hepatotoxicity, pulmonary fibrosis, hypothyroidism and
hyperthyroidism, corneal microdeposits, photosensitivity, and peripheral neuropathy. Amiodarone-associated
hepatotoxicity often manifests with an asymptomatic and transient rise in AST and ALT. If patients have more than a
twofold increase in AST and ALT, amiodarone should be discontinued and another rhythm or rate control medication
should be considered.

Before initiating amiodarone therapy, patients should receive a baseline ECG, chest x-ray, and tests for thyroid, liver, and
pulmonary function. Thyroid and liver function should be monitored every six months, and an ECG should be performed
annually.
107- infectious gastroenteriris

108- Biliary cysts are associated with an increased risk of inflammatory (e.g., cholangitis, cholelithiasis, pancreatitis) and
malignant complications (e.g., cholangiocarcinoma, gallbladder cancer, pancreatic cancer). This patient's cyst was most
likely complicated by acute cholangitis, which would explain her symptoms and increased cholestatic parameters (i.e., ↑
ALP, ↑ bilirubin).

Complete surgical excision of biliary cysts followed by biliary-enteric anastomosis is recommended to reduce the risk of
developing complications, especially malignancy (e.g., cholangiocarcinoma). Biliary cysts are most commonly found in
children, but can also develop in adults. Although the exact etiology of biliary cysts remains unknown, one possible
mechanism of biliary cyst formation is pancreatobiliary reflux (PBR), which induces biliary tree inflammation and damage
with consequent deformation and dilation. PBR in combination with biliary stasis can also explain the high risk of
inflammatory and malignant complications associated with this condition.

109--

This patient presents with recurrent abdominal pain, vomiting, and a palpable epigastric mass, while his vital
signs and physical examination are otherwise unremarkable. His history of alcohol use suggests an underlying
condition that is often caused by chronic alcohol use.

A pancreatic pseudocyst, which is a complication of acute or chronic pancreatitis, is caused by leakage of


pancreatic exocrine secretions from damaged ducts. This patient's history of recurrent epigastric pain,
vomiting, and chronic alcohol consumption makes a diagnosis of pancreatitis highly likely. Patients with
chronic pancreatitis and heavy alcohol use are often cachectic due to malnutrition. Pancreatic pseudocysts,
when large enough, can manifest with a palpable epigastric mass and bilious vomiting (due to extrinsic
compression of the distal duodenum) or nonbilious vomiting (due to gastric outlet obstruction). The diagnosis
can be confirmed by imaging; a well-defined fluid collection would be seen in the vicinity of the pancreas.

111- Obesity is an important risk factor for esophageal adenocarcinoma. Although the exact mechanism is
unknown, it is hypothesized that obesity increases the risk of adenocarcinoma by increasing the risk of reflux
and via mechanisms independent of reflux. Gastroesophageal reflux disease induces metaplasia (Barrett
esophagus), which can progress to adenocarcinoma. In addition, excessive visceral fat increases the risk of
inflammation, the production of cytokines and growth factors, and insulin resistance, all of which are risk
factors for carcinoma. Other risk factors for esophageal adenocarcinoma include smoking, achalasia, and certain
diets (high in animal protein or cholesterol, low in fiber). Smoking and achalasia furthermore increase the risk
of esophageal squamous cell carcinoma.

112- Curling ulcers are a subtype of stress gastritis seen in patients with extensive burns and occur due to
hypovolemia and subsequent hypoperfusion of the stomach. The resultant ischemic tissue injury to the
stomach epithelium results in an interruption in the normal mucosal barrier of the stomach, and ulcer formation.
Proton pump inhibitors should be administered in patients with extensive burns to prevent the formation of
Curling ulcers.
113-

110-

Autoimmune metaplastic atrophic gastritis (AMAG) can lead to intestinal metaplasia, which increases the risk
of gastric adenocarcinoma. Patients with AMAG are also at increased risk for carcinoid tumors because of the
presence of autoantibodies against parietal cells, which normally produce gastric acid. The resulting
achlorhydria stimulates the release of gastrin and antral G-cell hyperplasia, resulting in hypergastrinemia.
Hypergastrinemia, in turn, is associated with enterochromaffin-like cell hyperplasia, which may progress to
gastric carcinoid tumor.

114- A Cushing ulcer is a type of stress ulcer that occurs in patients with brain injuries. Increased ICP directly
stimulates the vagal nuclei, which leads to increased release of acetylcholine (ACh) by the vagal nerve
endings. This release of ACh, in turn, stimulates the muscarinic-3 receptors expressed by gastric parietal cells,
which leads to the production of excess gastric acid and eventually results in the ulceration of the gastric
mucosa.

115- This patient presents with dyspeptic symptoms (i.e., abdominal pain, nausea, vomiting, and diarrhea),
weight loss, and possible hypoproteinemia (as evidenced by bilateral pedal edema). In combination with
prominent gastric rugae on endoscopy and atrophic parietal cells on histology, these features are diagnostic of
Ménétrier disease.

(protein-losing hyperplastic gastropathy), which is a result of the proliferation of gastric mucus-producing


cells. The pathogenesis involves increased signaling of EGFR, which results in the proliferation of epithelial
cells of the mucous cell compartment.
116- Salmonella enterica serotype Typhi causes typhoid fever, which is characterized by three distinct stages,
all of which typically last approximately one week. After the incubation period, patients usually develop a
prodrome of fluctuating fever and malaise, relative bradycardia, and a change in bowel habits (e.g., constipation
or diarrhea). The prodrome is then followed by the onset of persistently high fever, profuse diarrhea (pea-soup
diarrhea), a salmon-colored maculopapular rash (rose spots), and hepatosplenomegaly. This patient also
recently returned from an S. Typhi endemic region.

S. Typhi is transmitted via the fecal-oral route, with the bacteria initially entering the host through intestinal
Peyer patches. After a period of incubation (5–30 days), the organism enters the bloodstream and can seed
several organs (e.g., the liver and spleen). Diagnosis is established based on blood and stool cultures, which
become positive 1 and 2–3 weeks after the onset of symptoms, respectively. Treatment comprises a third-
generation cephalosporin (e.g., ceftriaxone) or a fluoroquinolone. If left untreated, patients can develop
gastrointestinal ulceration and/or perforation. Vaccination is recommended for those traveling to high-risk areas
(East and Southeast Asia, Latin America, Africa).

117- This patient presents with biliary colic (postprandial, abdominal pain, nausea, vomiting). The prolonged
episode of pain, signs of extrahepatic cholestasis (scleral icterus, elevated parameters of cholestasis), and
absence of fever indicate choledocholithiasis.

118- In combination with a large gastric bubble on the CT scan, this patient's acute onset of nausea, bilious
vomiting, upper abdominal pain, and abdominal distention suggest an upper small bowel obstruction. In a child
with a history of recent blunt abdominal trauma (e.g., handlebar injury during a fall from a bicycle), duodenal
hematoma is the most likely diagnosis. Duodenal hematoma is a common injury in children following blunt
abdominal trauma because the abdominal wall is thinner and less developed, making hollow viscus more prone
to injury. The hematoma typically resolves spontaneously in days to weeks. Hemodynamically stable patients
can be managed conservatively with nasogastric intubation and total parenteral nutrition. Laparotomy may be
indicated in hemodynamically unstable children and/or in those with suspected duodenal perforation.

119- Dysphagia for solid foods, episodic food impaction, and epigastric pain in a boy with atopy (i.e., asthma,
food allergy) and linear furrows and circumferential lesions on upper endoscopy are highly suggestive of
eosinophilic esophagitis (EoE). An endoscopic biopsy will typically show an increased number of eosinophils
(≥ 15/HPF).

120- The first-line pharmacological treatment for uncomplicated chemotherapy-induced diarrhea (CTID) is oral
loperamide, an antidiarrheal opioid that acts on μ-receptors. CTID often occurs due to chemotherapy,
particularly with fluoropyrimidines or irinotecan, affecting rapidly dividing cells in the gastrointestinal tract.
Initial evaluation includes CBC, electrolyte panel, C. difficile toxin assay, and blood and stool cultures.
Management for uncomplicated CTID involves loperamide, oral rehydration, temporary discontinuation or dose
reduction of chemotherapy, and diet modification.

Complicated CTID presents with severe symptoms like abdominal cramping, nausea, vomiting, bloody stools,
high-grade fever, sepsis, acute kidney injury, and neutropenia. Treatment for complicated CTID includes
intravenous hydration, electrolyte repletion, oral loperamide plus intravenous octreotide, and continuous
monitoring of hemodynamic status.
121- Oral vancomycin is a first-line therapy used to treat C. difficile infection (see “Antibiotic therapy for CDI
in adults” table.). This condition typically manifests following antibiotic therapy (e.g., ciprofloxacin, as in this
case), which destroys many gastrointestinal bacteria except for C. difficile, which is resistant to the most
frequently used antibiotics. This selective advantage allows it to proliferate and cause infection. In addition to
discontinuing the inciting antibiotic, management includes correction of fluid loss and electrolyte
imbalances if needed, and contact precautions to prevent transmission. Oral fidaxomicin is another
appropriate first-line therapy for C. difficile infection. Recent guidelines suggest fidaxomicin over vancomycin
in patients with nonfulminant C. difficile infection. Metronidazole is a second-line therapy recommended when
vancomycin and fidaxomicin are unavailable or contraindicated (e.g., due to allergy).

C. difficile infection can be confirmed either by nucleic acid amplification testing for C. difficile toxin-
producing genes alone or by enzyme immunoassays for both glutamate dehydrogenase and C. difficile toxin A
and toxin B. Empiric antibiotic therapy can be started before laboratory confirmation of C. difficile infection.

`122-

C difficile infection amboss library

123- Ulcerative colitis (UC) is a risk factor for developing colorectal cancer and the risk increases with increased
duration and/or extent of disease. This patient's features (i.e., blood in stool, unintentional weight loss, change in stool
consistency, anemia) in conjunction with the results of his barium enema are consistent with malignant transformation.
The CT scan suggests no lymph node involvement and no metastases. As UC is restricted to the colon and rectum, a
proctocolectomy with an ileal pouch-anal anastomosis or ileostomy is a potentially curative treatment for both UC and
colorectal carcinoma.

124- Early oral feeding reduces the risk of infectious complications by decreasing gastrointestinal dysmotility, gut
permeability, and the likelihood of bacterial translocation. Therefore, oral feeding should be initiated as soon as
tolerated (i.e. not causing pain, nausea, or vomiting), ideally within 24 hours. Complete bowel rest, which was previously
recommended, is unnecessary in most patients. Enteral feeding can be delivered orally or via an enteral tube, and
success has been demonstrated with various diets (e.g., liquid, low-fat, full-solid).

125- Bacterial mesenteric lymphadenitis is the underlying etiology of pseudoappendicitis. The disease manifests with
right lower quadrant pain, fever, vomiting, and leukocytosis, identical to the findings observed in this patient. However,
pseudoappendicitis primarily affects children under 5 years of age.

126-

127- Radiation damage to the rectal mucosa causes acute radiation proctitis (ARP), which manifests with pelvic and
rectal pain, mucus in diarrhea, tenesmus, and/or fecal urgency within 6 weeks of radiation therapy (see “Radiation
proctitis” table). The risk of ARP depends on the radiation dose to the rectum and how much of the rectum receives
radiation. Evaluation of patients with suspected ARP consists of a detailed history, laboratory tests with stool cultures to
exclude infection, and, if there is diagnostic uncertainty, endoscopy with biopsies. Supportive treatment with
antidiarrheals, hydration, and sodium butyrate enemas is usually sufficient.
128- HH is the most common benign liver tumor in women between the ages of 30–50 and is usually an incidental
finding on imaging. This patient has a small (≤ 5 cm), asymptomatic HH that can be treated conservatively with
observation and regular follow-up. Patients with larger lesions (> 5 cm) should undergo contrast-enhanced imaging 6–
12 months after diagnosis to confirm the stability of the lesion. Surgical intervention may be considered for those with
fast-growing or large HHs (> 10 cm) or lesions that cause persistent symptoms such as abdominal discomfort, early
satiety, and nausea.

129- Postcholecystectomy diarrhea is a type of secretory diarrhea that has an onset of several weeks after the
procedure and affects up to 10% of patients. This complication is most frequently seen in obese individuals < 50 years of
age. Because the gall bladder is a reservoir for bile, its removal results in constant drainage of bile acids into the bowel,
which induces fluid secretion and increases mucosal permeability in the colon. Bile acid resins (e.g., cholestyramine),
which bind the excess bile acids, are the treatment of choice.

130- Cholangiography is the most accurate imaging modality to confirm the diagnosis of BA (gold standard). The
investigation is usually only performed intraoperatively after other diagnoses have been ruled out and findings from
other imaging modalities have supported the diagnosis of BA. In patients with suspected BA following clinical and
laboratory evaluation, abdominal ultrasound is initially indicated to rule out other causes of biliary obstruction (e.g.,
choledochal cysts). Supportive findings of BA include the absence of a gallbladder and no dilation of the biliary tree.
Hepatobiliary scintigraphy can also be considered to assess the patency of the biliary tree. Liver biopsy is usually
performed to exclude other causes of intrahepatic cholestasis (e.g., Alagille syndrome) and to identify changes
consistent with BA, such as active inflammation with bile duct degeneration and fibrosis, portal stromal edema, and bile
duct proliferation. Patients with supportive findings should undergo intraoperative cholangiography; if the diagnosis is
confirmed, Kasai procedure is performed.

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