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# Colonic polyps and diverticular disease Colonic polyps and diverticular disease involve the study of abnormal growths in the colon and outpouchings of the colon wall, respectively, with significant implications for patient health and disease management. ## 1. Colonic polyps Colonic polyps are growths projecting from the lining of the colon. They are broadly classified into nonneoplastic and neoplastic types [1](#page=1). ### 1.1 Nonneoplastic polyps These polyps are benign and do not possess malignant potential [1](#page=1). * **Hyperplastic polyps**: Constitute approximately 90% of nonneoplastic polyps. They are typically small and asymptomatic [1](#page=1). * **Juvenile polyps**: Most commonly found in children under 10 years of age. They are vascular and usually require removal [1](#page=1). * **Inflammatory/pseudopolyps**: These are associated with ulcerative colitis [1](#page=1). ### 1.2 Adenomatous polyps These are precancerous lesions that carry a risk of developing into adenocarcinoma [1](#page=1). * **Types**: * **Tubular**: The most common type, associated with the least malignant potential [1](#page=1). * **Tubulovillous**: Present an intermediate risk for malignancy [1](#page=1). * **Villous**: Carry the highest risk of malignant transformation, often described with the mnemonic "villainous" [1](#page=1). * **Malignant potential factors**: The risk of malignancy in adenomatous polyps increases with: * **Size**: Polyps larger than 1 centimeter are considered higher risk [1](#page=1). * **Histology**: Villous histology carries the worst prognosis [1](#page=1). * **Atypia (dysplasia)**: The presence and severity of dysplasia are significant risk factors [1](#page=1). * **Shape**: Sessile polyps are associated with a higher cancer risk compared to pedunculated ones, described with the mnemonic "sessile = sneaky" [1](#page=1). ### 1.3 Clinical notes on polyps Colonic polyps are most frequently found in the rectosigmoid region of the colon. They are often asymptomatic, with rectal bleeding being the most common presenting symptom [1](#page=1). ### 1.4 Treatment of polyps The standard treatment for colonic polyps is complete removal, a procedure known as polypectomy [1](#page=1). ### 1.5 Exam tip for polyps Remember "villous = villainous," "sessile = sneaky" (higher cancer risk), and "bigger = badder" for polyps [1](#page=1). ## 2. Diverticular disease Diverticular disease encompasses diverticulosis, the presence of diverticula, and diverticulitis, the inflammation of these diverticula [2](#page=2). ### 2.1 Diverticulosis This refers to the presence of outpouchings of the colonic mucosa [2](#page=2). #### 2.1.1 Definition Diverticulosis involves the formation of "pouches" in the colon wall [2](#page=2). #### 2.1.2 Etiology and pathophysiology These outpouchings occur when increased intraluminal pressure forces the colonic mucosa through weak spots in the colon wall. A low-fiber diet contributes to constipation, which in turn elevates intraluminal pressure. The colon wall also weakens with age [2](#page=2). #### 2.1.3 Risk factors Key risk factors include advanced age, a diet low in fiber, and a positive family history of diverticular disease [2](#page=2). #### 2.1.4 Most common site Diverticula are most frequently found in the sigmoid colon, which experiences the highest intraluminal pressure [2](#page=2). #### 2.1.5 Clinical features Diverticulosis is usually asymptomatic. When symptoms occur, they can include vague left lower quadrant discomfort, bloating, and changes in bowel habits, such as constipation or diarrhea [2](#page=2). #### 2.1.6 Diagnosis The barium enema is considered the test of choice for diagnosing diverticulosis. An abdominal X-ray typically appears normal in cases of uncomplicated diverticulosis [2](#page=2). #### 2.1.7 Treatment Management focuses on dietary modifications, including a high-fiber diet (e.g., bran) and psyllium supplementation [2](#page=2). #### 2.1.8 Complications of diverticulosis * **Painless rectal bleeding**: Occurs in approximately 40% of cases [2](#page=2). * **Diverticulitis**: Develops in 15%–25% of individuals with diverticulosis [2](#page=2). ### 2.2 Diverticulitis This is an inflammatory complication of diverticulosis, often resulting from fecal impaction within a diverticulum [2](#page=2). #### 2.2.1 Definition Diverticulitis is the inflammation of a diverticulum, which can lead to microperforation [2](#page=2). #### 2.2.2 Pathophysiology The process typically begins with a fecalith obstructing a diverticulum, leading to bacterial invasion and subsequent microperforation, which triggers inflammation [2](#page=2). #### 2.2.3 Clinical features Classic symptoms include left lower quadrant pain, fever, and leukocytosis. Patients may also experience changes in bowel habits and, occasionally, a tender mass on rectal examination [2](#page=2). #### 2.2.4 Diagnosis The gold standard for diagnosing diverticulitis is a CT scan performed with oral and intravenous contrast. An abdominal X-ray may be used to rule out obstruction or perforation. It is crucial to avoid colonoscopy and barium enema in patients with suspected diverticulitis due to the risk of perforation [2](#page=2). #### 2.2.5 Treatment * **Uncomplicated diverticulitis**: Managed with intravenous antibiotics, bowel rest (NPO), and intravenous fluids. Outpatient management is possible for stable patients [2](#page=2). * **Persistent symptoms**: If symptoms do not improve after 3–4 days, surgical intervention should be considered [2](#page=2). * **Complicated diverticulitis**: This includes conditions such as abscess, fistula, obstruction, or perforation, and invariably indicates surgery [2](#page=2). #### 2.2.6 Complications of diverticulitis * **Abscess**: May require drainage [2](#page=2). * **Colovesical fistula**: Characterized by the presence of air in the urine [2](#page=2). * **Obstruction**: Can occur due to chronic inflammation [2](#page=2). * **Free perforation**: Leading to peritonitis, a life-threatening condition [2](#page=2). ### 2.3 High-yield exam markers for diverticular disease * **Key symptom triad**: Left lower quadrant pain, fever, and leukocytosis strongly suggest diverticulitis [2](#page=2). * **Diagnostic imaging**: Barium enema is appropriate for diverticulosis but not for diverticulitis. CT scan is the preferred diagnostic tool for diverticulitis [2](#page=2). * **Bleeding**: Painless bleeding is a hallmark of diverticulosis [2](#page=2). * **Recurrence**: Recurrent episodes of diverticulitis typically warrant surgical consideration [2](#page=2). --- # Mesenteric ischemia and bowel obstruction This section covers acute and chronic mesenteric ischemia, and small bowel obstruction, detailing their causes, clinical presentations, diagnostic approaches, and management strategies. ### 2.1 Mesenteric ischemia Mesenteric ischemia refers to the acute compromise of intestinal blood flow, leading to ischemia and potentially infarction. Chronic mesenteric ischemia, primarily caused by atherosclerotic occlusive disease, presents with symptoms of abdominal angina and significant weight loss [3](#page=3). #### 2.1.1 Acute mesenteric ischemia (AMI) AMI is characterized by the sudden compromise of intestinal blood flow [3](#page=3). ##### 2.1.1.1 Causes of AMI The causes of AMI are multifactorial and can be categorized as follows [3](#page=3): * **Arterial embolism (~50%):** This is the most common cause, typically arising suddenly from a cardiac source such as atrial fibrillation (AF), myocardial infarction (MI), or valve disease [3](#page=3). * **Arterial thrombosis (~25%):** This cause is generally more gradual and is associated with underlying atherosclerosis [3](#page=3). * **Nonocclusive (~20%):** This type is often seen in critically ill patients and is due to low flow states or vasospasm [3](#page=3). * **Venous thrombosis (<10%):** This less common cause is associated with hypercoagulable states or pancreatitis [3](#page=3). ##### 2.1.1.2 Clinical hallmark of AMI The classic clinical presentation of AMI is severe abdominal pain that is disproportionate to the physical examination findings. Patients may also experience nausea, vomiting, and mild gastrointestinal bleeding. As the condition progresses, signs of peritonitis and sepsis can develop [3](#page=3). ##### 2.1.1.3 Diagnosis of AMI The definitive diagnostic tool for AMI is mesenteric angiography, which can also be therapeutic. CT angiography is a rapid and modern diagnostic method used to identify occlusion and assess bowel wall enhancement. Laboratory findings may include elevated lactate levels (a late sign), leukocytosis, and metabolic acidosis. An imaging sign suggestive of mucosal edema is "thumbprinting" seen on contrast studies [3](#page=3). > **Tip:** The "pain out of proportion to exam" is a critical clue for suspecting AMI. ##### 2.1.1.4 Urgent treatment for AMI Treatment for AMI is urgent and involves several key steps: * **Resuscitation:** This includes aggressive intravenous fluid resuscitation, oxygen administration, and broad-spectrum antibiotics [3](#page=3). * **Anticoagulation:** Heparin is administered unless contraindicated [3](#page=3). * **Angiographic intervention:** Mesenteric angiography can be used for therapeutic interventions such as papaverine infusion, thrombolysis, or embolectomy [3](#page=3). * **Surgery:** Laparotomy and resection of nonviable bowel are indicated if peritonitis is present or if the bowel is deemed not viable [3](#page=3). > **High-Yield Point:** Mortality for AMI is high, ranging from 60–70%, and increases to over 90% if bowel infarction occurs. Time is critical in managing AMI [3](#page=3). #### 2.1.2 Chronic mesenteric ischemia Chronic mesenteric ischemia (CMI) is typically caused by atherosclerotic occlusive disease affecting the celiac artery, superior mesenteric artery (SMA), or inferior mesenteric artery [3](#page=3). ##### 2.1.2.1 Symptoms of CMI The primary symptom of CMI is **abdominal angina**, characterized by dull, typically postprandial abdominal pain. This pain occurs because the increased demand for splanchnic blood flow during digestion cannot be met due to the stenotic vessels, analogous to angina in coronary artery disease. Significant weight loss is also a common symptom, often due to the abdominal pain and subsequent reduced oral intake [3](#page=3). ##### 2.1.2.2 Diagnosis of CMI Mesenteric arteriography is considered the confirmatory diagnostic test for CMI [3](#page=3). ##### 2.1.2.3 Treatment of CMI The definitive treatment for CMI is **surgical revascularization**, which provides pain relief in approximately 90% of cases [3](#page=3). ### 2.2 Small bowel obstruction (SBO) Small bowel obstruction (SBO) is a mechanical or functional blockage of the small intestine that leads to dilation, vomiting, fluid loss, and increased intraluminal pressure. SBO carries a significant risk of ischemia, necrosis, and perforation, particularly in cases of closed-loop obstruction [17](#page=17) [18](#page=18). #### 2.2.1 Classifications of SBO SBO can be classified based on several criteria: * **Partial vs. Complete:** * **Partial SBO:** Patients may still be able to pass gas or stool [17](#page=17) [18](#page=18). * **Complete SBO:** Characterized by obstipation (inability to pass gas or stool) [17](#page=17) [18](#page=18). * **Closed-loop vs. Open-loop:** * **Closed-loop SBO:** The lumen is blocked at two points, significantly increasing the risk of strangulation and requiring emergency management [17](#page=17) [18](#page=18). * **Open-loop SBO:** The obstruction occurs at a single point. * **Proximal vs. Distal SBO:** * **Proximal SBO:** Leads to earlier vomiting and less abdominal distension [17](#page=17) [18](#page=18). * **Distal SBO:** Is associated with marked abdominal distension and later onset of vomiting [17](#page=17) [18](#page=18). #### 2.2.2 Pathophysiology of SBO The primary event in SBO is the obstruction, which causes dilation of the bowel proximal to the blockage due to accumulation of gas and fluid. Vomiting and fluid sequestration lead to dehydration, hypochloremia, hypokalemia, and metabolic alkalosis. Significant hypovolemia can result in tachycardia and hypotension. If strangulation occurs, it compromises blood supply, leading to ischemia, necrosis, and potentially perforation and peritonitis [17](#page=17) [18](#page=18). #### 2.2.3 Causes of SBO The mnemonic "A HINT" is useful for remembering the common causes of SBO [17](#page=17) [18](#page=18): * **A — Adhesions:** The most common cause of SBO in adults, often a sequela of prior abdominal surgery [17](#page=17) [18](#page=18). * **H — Hernias:** Specifically, incarcerated hernias can cause obstruction [17](#page=17) [18](#page=18). * **I — Intussusception:** A telescoping of one segment of the intestine into another [17](#page=17) [18](#page=18). * **N — Neoplasm / Carcinomatosis:** Malignancies can cause luminal or extrinsic compression [17](#page=17) [18](#page=18). * **T — Twisting/Volvulus:** Twisting of the bowel on its mesentery; strictures (e.g., from Crohn's disease); SMA syndrome (compression of the duodenum by the SMA) [17](#page=17) [18](#page=18). #### 2.2.4 Clinical features of SBO Key clinical features of SBO include: * **Abdominal pain:** Typically crampy and colicky [17](#page=17) [18](#page=18). * **Severe continuous pain:** This is a red flag and strongly suggests strangulation [17](#page=17) [18](#page=18). * **Nausea and vomiting:** Vomiting may become feculent if the obstruction is distal [17](#page=17) [18](#page=18). * **Obstipation:** Inability to pass gas or stool, characteristic of complete SBO [17](#page=17) [18](#page=18). * **Abdominal distension:** More pronounced in distal SBO [17](#page=17) [18](#page=18). * **Red flags:** Fever, tachycardia, peritonitis, and leukocytosis indicate a more severe or complicated obstruction [17](#page=17) [18](#page=18). > **High-Yield Pearl:** Severe continuous pain is a critical indicator of bowel ischemia in SBO [17](#page=17) [18](#page=18). #### 2.2.5 Diagnosis of SBO A multi-modal approach is used for diagnosing SBO: * **Abdominal X-ray:** May show dilated small bowel loops, air-fluid levels, and minimal colonic gas if the SBO is complete. The valvulae conniventes, which cross the entire lumen, are a characteristic finding of small bowel dilation [17](#page=17) [18](#page=18). * **CT abdomen with contrast:** Considered the **best diagnostic test** for SBO. It can identify the transition point of the obstruction, detect closed-loop obstructions, assess for ischemia, visualize mesenteric swirl, and identify free fluid [17](#page=17) [18](#page=18). * **Barium enema:** Useful in differentiating between small and large bowel obstruction [17](#page=17) [18](#page=18). * **Upper GI series with follow-through:** May be used if other imaging modalities are inconclusive [17](#page=17) [18](#page=18). #### 2.2.6 Management of SBO Management of SBO is tailored to the severity and type of obstruction: * **Initial management (for all patients):** * **NPO:** Nil per os (nothing by mouth) [17](#page=17) [18](#page=18). * **Aggressive IV fluids:** Essential for correcting dehydration and electrolyte imbalances [17](#page=17) [18](#page=18). * **Nasogastric (NG) tube:** For gastric decompression to relieve distension and reduce vomiting [17](#page=17) [18](#page=18). * **Broad-spectrum antibiotics:** Administered if strangulation is suspected [17](#page=17) [18](#page=18). * **Monitoring:** Serial abdominal examinations, vital signs, and urine output are crucial [17](#page=17) [18](#page=18). * **Nonoperative management (for incomplete and stable SBO):** * This involves continued fluid resuscitation, NG decompression, and observation. Adhesive partial SBOs often resolve conservatively [17](#page=17) [18](#page=18). * **Operative management:** * Indicated for complete obstruction, signs of strangulation or peritonitis, or failure of conservative management [17](#page=17) [18](#page=18). * Procedures may include lysis of adhesions, hernia repair, or resection of necrotic bowel segments [17](#page=17) [18](#page=18). > **Tip:** Early recognition and management of SBO are critical to prevent complications like strangulation and perforation [17](#page=17) [18](#page=18). #### 2.2.7 Complications of SBO Potential complications of SBO include: * **Strangulation, ischemia, and necrosis:** Due to compromised blood supply [17](#page=17) [18](#page=18). * **Perforation:** Leading to peritonitis and sepsis [17](#page=17) [18](#page=18). * **Severe dehydration and electrolyte imbalance:** Resulting from vomiting and fluid sequestration [17](#page=17) [18](#page=18). * **Short bowel syndrome:** A consequence of extensive bowel resection [17](#page=17) [18](#page=18). > **High-Yield Pearls:** > * Adhesions are the most common cause of SBO in adults [17](#page=17) [18](#page=18). > * Closed-loop obstruction is a surgical emergency [17](#page=17) [18](#page=18). > * Vomiting that occurs early suggests proximal SBO, while early distension points to distal SBO [17](#page=17) [18](#page=18). > * CT scan is the preferred imaging modality for SBO [17](#page=17) [18](#page=18). --- # Esophageal and gastric pathologies This section details various conditions affecting the esophagus and stomach, ranging from motility disorders and structural abnormalities to inflammatory processes, precancerous lesions, and malignancies. ### 3.1 Esophageal pathologies Esophageal pathologies encompass a spectrum of conditions affecting the tube that connects the pharynx to the stomach, including motility disorders, structural abnormalities, and injury-related issues. #### 3.1.1 Achalasia Achalasia is a primary esophageal motor disorder characterized by the failure of the lower esophageal sphincter (LES) to relax and aperistalsis of the esophageal body [6](#page=6). * **General Characteristics:** It involves impaired LES relaxation and absent peristalsis in the esophageal body [6](#page=6). * **Causes:** Most commonly idiopathic, it can also be secondary to adenocarcinoma of the proximal stomach (pseudoachalasia) or Chagas disease [6](#page=6). * **Clinical Features:** Patients experience dysphagia for both solids and liquids, often requiring water to chase food and postural adjustments for swallowing. Regurgitation, chest pain, and weight loss are also common. Pulmonary complications such as aspiration, lung abscess, and bronchiectasis can occur due to aspiration [6](#page=6). * **Diagnosis:** A barium swallow may show a characteristic "bird's beak" appearance. Upper GI endoscopy is crucial to rule out carcinoma, and esophageal manometry is the gold standard, confirming incomplete LES relaxation and aperistalsis [6](#page=6). * **Complications:** There is an increased risk (7-fold) of squamous cell carcinoma (SCC) after 15-25 years [6](#page=6). * **Treatment:** Management includes lifestyle modifications (soft food, elevating the trunk), medical therapies (antimuscarinics, nitrates, calcium channel blockers), botulinum toxin injection, and forceful dilation with a pneumatic balloon (with a 5% perforation risk). Surgical options include Heller myotomy, providing good short-term relief but not a cure [6](#page=6). #### 3.1.2 Diffuse esophageal spasm (DES) Diffuse esophageal spasm is a motility disorder characterized by nonperistaltic, simultaneous contractions of the esophageal body [7](#page=7). * **General Characteristics:** Multiple esophageal segments contract simultaneously, impeding bolus advancement. The LES function remains normal [7](#page=7). * **Clinical Features:** The hallmark symptom is noncardiac chest pain that can mimic angina and radiate to the jaw, arms, or back. Dysphagia is common, while regurgitation is less frequent [7](#page=7). * **Diagnosis:** Esophageal manometry is diagnostic, revealing simultaneous, multiphasic, and repetitive contractions after swallowing, with a normal sphincter response. A barium swallow may show a "corkscrew esophagus" in approximately 50% of cases [7](#page=7). * **Treatment:** There is no completely effective therapy, and treatment failure rates are high. Medical options include nitrates, calcium channel blockers (to reduce contraction amplitude), and tricyclic antidepressants for symptomatic relief. Esophagomyotomy is usually not performed due to controversial efficacy and is considered only if symptoms are incapacitating [7](#page=7). #### 3.1.3 Esophageal hiatal hernias Esophageal hiatal hernias involve the protrusion of the stomach or gastroesophageal junction through the diaphragm [7](#page=7). * **General Characteristics:** * **Sliding (Type 1):** The gastroesophageal junction and a portion of the stomach herniate above the diaphragm. This is the most common type (>90%), often benign, and associated with GERD [7](#page=7). * **Paraesophageal (Type 2; Types 2-4 include paraesophageal elements):** The stomach herniates into the thorax while the gastroesophageal junction remains below the diaphragm. This type is less common (<5%) but can be serious [7](#page=7). * **Clinical Features:** The majority of hiatal hernias are asymptomatic and found incidentally. Possible symptoms include heartburn, chest pain, and dysphagia. Complications of sliding hernias include GERD, reflux esophagitis, and an increased risk of Barrett esophagus and cancer. Paraesophageal hernias carry risks of obstruction, hemorrhage, incarceration, and strangulation, which can be life-threatening [7](#page=7). * **Diagnosis:** A barium upper GI series and upper endoscopy are used for diagnosis [7](#page=7). * **Treatment:** Type 1 hernias are managed medically with antacids, small meals, and head elevation after meals. Surgery (Nissen fundoplication) may be required in 15% of cases if symptoms are refractory or esophagitis is present. Type 2-4 hernias warrant elective surgical repair due to the risk of severe complications [7](#page=7). #### 3.1.4 Mallory-Weiss syndrome Mallory-Weiss syndrome is defined as a mucosal tear at or just below the gastroesophageal junction, typically following forceful vomiting or retching [9](#page=9). * **Definition:** Mucosal tear at/just below the gastroesophageal junction after forceful vomiting/retching [9](#page=9). * **Pathophysiology:** Increased intra-abdominal pressure during vomiting causes a mucosal tear at the GE junction. A transmural tear in this context is known as Boerhaave syndrome [9](#page=9). * **Risk/Setting:** It is commonly associated with binge drinking and severe vomiting from any cause [9](#page=9). * **Clinical Features:** Patients present with hematemesis, which can range from streaks to massive bright red blood, and a history of recent forceful vomiting or retching [9](#page=9). * **Diagnosis:** Upper GI endoscopy (OGD) is diagnostic [9](#page=9). * **Treatment:** Treatment involves supportive resuscitation and proton pump inhibitors (PPIs) for healing. Endoscopic therapy (clips, coagulation) is used for ongoing bleeding, and angiographic embolization or surgery may be considered for refractory cases [9](#page=9). #### 3.1.5 Plummer-Vinson syndrome Plummer-Vinson syndrome, also known as Paterson-Kelly syndrome or sideropenic dysphagia, is characterized by upper esophageal webs associated with iron deficiency anemia [9](#page=9). * **Key Features:** Upper esophageal web(s) causing dysphagia, iron deficiency anemia (leading to fatigue and pallor), koilonychia (spoon-shaped nails), and atrophic oral mucosa [9](#page=9). * **Risk:** This condition is considered premalignant, with an increased risk of squamous cell carcinoma in the oral cavity, hypopharynx, and esophagus [9](#page=9). * **Diagnosis:** A barium swallow or upper endoscopy can visualize the web. A complete blood count (CBC) will reveal iron deficiency [9](#page=9). * **Treatment:** Esophageal dilatation and correction of nutritional iron deficiency are the mainstays of treatment. Surveillance is important due to the premalignant nature of the condition [9](#page=9). #### 3.1.6 Schatzki ring A Schatzki ring is a thin, circumferential mucosal ring located in the distal esophagus, always associated with a sliding hiatal hernia [9](#page=9). * **Definition:** A thin circumferential mucosal ring in the lower esophagus, invariably associated with a sliding hiatal hernia [9](#page=9). * **Clinical Features:** Most patients are asymptomatic. If the ring is tight, intermittent dysphagia to solids may occur [9](#page=9). * **Causes/Risk:** Chronic reflux from a hiatal hernia is a primary cause. Caustic ingestion (alkali being worse than acid) is also a risk factor [9](#page=9). * **Complications:** Potential complications include esophageal stricture and an increased risk of esophageal cancer [9](#page=9). * **Treatment:** Asymptomatic rings require no treatment. Symptomatic rings are managed with dilatation. Associated reflux may necessitate anti-reflux surgery. Full-thickness caustic damage may require esophagectomy, and strictures are managed with bougienage, potentially with steroids and antibiotics if there is injury [9](#page=9). #### 3.1.7 Esophageal diverticula Esophageal diverticula are outpouchings of the esophageal wall, typically caused by underlying esophageal motility disorders [10](#page=10). * **General:** Caused by underlying motility disorders [10](#page=10). * **Zenker Diverticulum (Upper):** Occurs due to failure of cricopharyngeal muscle relaxation. Symptoms include dysphagia, regurgitation, halitosis, and cough. It is seen in individuals over 50 years old. Diagnosis is by barium swallow, and treatment is cricopharyngeal myotomy [10](#page=10). * **Traction Diverticulum (Mid-esophagus):** Caused by mediastinal inflammation, such as from tuberculosis. It is usually asymptomatic, and treatment is typically not required [10](#page=10). * **Epiphrenic Diverticulum (Lower):** Associated with spastic motility disorders like achalasia and DES. Symptoms include dysphagia and regurgitation. Treatment may involve esophagomyotomy, sometimes with diverticulectomy [10](#page=10). #### 3.1.8 Esophageal perforation Esophageal perforation is a full-thickness tear of the esophagus, leading to mediastinal or pleural contamination [10](#page=10). * **Definition:** Full-thickness tear of the esophagus resulting in mediastinal or pleural contamination [10](#page=10). * **Etiology:** The most common cause is iatrogenic (endoscopy, tubes). Other causes include Boerhaave syndrome (forceful vomiting/retching), blunt trauma, foreign bodies, and caustic ingestion [10](#page=10). * **Clinical Features:** Patients present with severe retrosternal, chest, or shoulder pain, tachycardia, hypotension, fever, tachypnea, and dyspnea. Subcutaneous emphysema and Hamman sign (mediastinal crunch) may be present. Chest X-ray can show mediastinal air, pneumothorax, or pleural effusion [10](#page=10). * **Diagnosis:** A contrast esophagogram using water-soluble contrast (e.g., Gastrografin) is definitive. CT chest with oral contrast is sensitive. CXR may show mediastinal air, and pleural fluid analysis (low pH, high amylase) is useful if an effusion is present [10](#page=10). * **Management:** Immediate management includes ABCs, NPO, IV fluids, broad-spectrum IV antibiotics, IV PPIs, and an urgent surgical consult. Conservative management (NPO, antibiotics, drainage) is for stable patients with contained leaks. Unstable patients, large leaks, pleural communication, or sepsis require surgery within 24 hours for primary repair and drainage. Pleural or mediastinal collections should be drained via tube thoracostomy or percutaneously [10](#page=10). * **Key Points:** Boerhaave syndrome is a transmural tear, distinct from Mallory-Weiss. A Gastrografin study is diagnostic, and time to surgery less than 24 hours improves survival [10](#page=10). #### 3.1.9 Esophageal cancer Esophageal cancer is a malignant neoplasm of the esophagus, with the two main types being squamous cell carcinoma and adenocarcinoma [11](#page=11). * **Types:** * **Squamous Cell Carcinoma (SCC):** Typically found in the upper and mid-esophagus. It is more common in African American men and associated with risk factors such as alcohol, tobacco, nitrosamines, hot beverages, HPV, achalasia, Plummer-Vinson syndrome, caustic ingestion, and nasopharyngeal carcinoma [11](#page=11). * **Adenocarcinoma:** Occurs in the distal esophagus and gastroesophageal junction. Its incidence is increasing, accounting for about 50% of cases. Key risk factors include GERD, Barrett esophagus, obesity, and smoking (less important than for SCC) [11](#page=11). * **Pathogenesis:** SCC arises from chronic irritation leading to dysplasia and carcinoma. Adenocarcinoma develops from GERD, leading to Barrett esophagus (columnar metaplasia), dysplasia, and subsequent carcinoma [11](#page=11). * **Clinical Features:** Dysphagia, starting with solids and progressing to liquids, is the most important symptom. Other signs include unexplained weight loss, anorexia, odynophagia (late stage), hematemesis, hoarseness (due to recurrent laryngeal nerve involvement), aspiration pneumonia, tracheoesophageal fistula, and chest pain [11](#page=11). * **Diagnosis:** A barium swallow can be the initial diagnostic test, followed by upper endoscopy with biopsy for definitive diagnosis. Endoscopic ultrasound is used for local staging. CT scans of the chest and abdomen, CXR, and bone scans are used to assess for metastases [11](#page=11). * **Staging:** Staging systems (e.g., TNM) classify the depth of invasion, nodal involvement, and distant metastasis [11](#page=11). * **Treatment:** Palliation is common due to late presentation. Surgery is indicated for stage 0, I, and some stage IIa disease. Chemoradiotherapy is often used pre-operatively. Palliative stenting, feeding tubes, and complication management are also part of treatment [11](#page=11). ### 3.2 Gastric pathologies Gastric pathologies encompass a range of conditions affecting the stomach, from inflammatory and ulcerative diseases to malignancies. #### 3.2.1 Peptic ulcer disease (PUD) Peptic ulcer disease is characterized by mucosal ulcerations in the stomach or duodenum caused by an imbalance between aggressive factors (acid, pepsin, H. pylori, NSAIDs) and mucosal defenses [12](#page=12). * **Definition:** Mucosal ulceration in the stomach or duodenum due to an imbalance between aggressive factors and mucosal defenses [12](#page=12). * **Causes:** The most common causes are *H. pylori* infection and NSAIDs/aspirin use, which reduce prostaglandins, mucus, bicarbonate, and blood flow. Acid hypersecretion states like Zollinger-Ellison syndrome (ZES) are also a cause. Smoking and alcohol are contributing risks [12](#page=12). * **Pathogenesis:** *H. pylori* leads to mucosal inflammation, increasing acid (duodenal) or reducing defenses (gastric). NSAIDs inhibit COX, reducing prostaglandins and impairing mucosal protection. Gastrinomas in ZES cause massive acid secretion, leading to refractory or multiple ulcers [12](#page=12). * **Clinical Features:** Epigastric pain, often described as aching or gnawing. Duodenal ulcers are typically relieved by meals and may cause nocturnal pain. Gastric ulcers may worsen with eating, and weight loss is more common. Complications include upper GI bleeding, perforation (leading to acute abdomen), and gastric outlet obstruction. Nausea, vomiting, and early satiety can also occur [12](#page=12). * **Diagnosis:** Endoscopy is the gold standard, with biopsies taken of all gastric ulcers to rule out malignancy. Duodenal ulcers are usually benign and do not require biopsy. *H. pylori* can be detected via urea breath test, stool antigen test, or endoscopic biopsy. Barium swallows are less accurate, and serum gastrin levels are measured if ZES is suspected [12](#page=12). * **Treatment:** Supportive measures include stopping NSAIDs, switching to acetaminophen, and avoiding alcohol, smoking, and late meals. *H. pylori* eradication is achieved with triple therapy (PPI + amoxicillin + clarithromycin) or quadruple therapy (PPI + bismuth + metronidazole + tetracycline) for 14 days. Acid suppression is primarily achieved with PPIs; H2 blockers are less potent. Antacids provide symptomatic relief. Cytoprotective agents like sucralfate promote healing, and misoprostol can prevent NSAID-induced ulcers. Surgery is rare and reserved for complications [12](#page=12). * **Duodenal vs. Gastric Ulcers:** Duodenal ulcers are associated with increased acid, 70-90% *H. pylori* rates, pain relief with eating, nocturnal pain, younger patients, and are rarely malignant. Gastric ulcers are associated with reduced defenses, 60-70% *H. pylori* rates, pain that doesn't improve with eating, older patients, and have a 5-10% malignancy risk, necessitating biopsy [12](#page=12). * **Complications:** Upper GI bleeding, perforation (a surgical emergency), gastric outlet obstruction, and malignancy risk (for gastric ulcers) [12](#page=12). #### 3.2.2 Acute gastritis Acute gastritis is a sudden inflammation of the gastric mucosa, often transient [13](#page=13). * **Definition:** Sudden inflammation of the gastric mucosa, often transient [13](#page=13). * **Causes:** NSAIDs/aspirin (due to reduced prostaglandins and mucus), *H. pylori* infection, alcohol, heavy smoking, caffeine, severe physiologic stress (shock, sepsis, burns), caustic ingestion, and certain medications [13](#page=13). * **Pathogenesis:** An imbalance between mucosal defenses and aggressive factors underlies acute gastritis. NSAIDs impair protection, *H. pylori* causes acute inflammation, and stress leads to mucosal ischemia and acid injury [13](#page=13). * **Clinical Features:** May be asymptomatic or present with epigastric pain (variable with food), nausea, vomiting, and upper GI bleeding if erosions form [13](#page=13). * **Diagnosis:** Upper GI endoscopy is the best test. *H. pylori* testing (urea breath test, stool antigen, biopsy) is also performed [13](#page=13). * **Treatment:** Treatment involves stopping NSAIDs and irritants (alcohol, smoking), acid suppression with PPIs (first-line) or H2 blockers, and eradicating *H. pylori* if positive. ICU stress prophylaxis with IV PPIs or H2 blockers is standard [13](#page=13). * **Complications:** Acute erosions leading to bleeding and, rarely, progression to chronic gastritis [13](#page=13). #### 3.2.3 Chronic gastritis Chronic gastritis is a long-standing inflammation of the gastric mucosa, primarily divided into *H. pylori*-associated (Type B) and autoimmune (Type A) forms [14](#page=14). * **Definition:** Long-standing inflammation of the gastric mucosa, with two major types: *H. pylori* (Type B) and Autoimmune (Type A) [14](#page=14). * **Causes:** *H. pylori* infection (>80%, predominantly in the antrum) and autoimmune gastritis (characterized by antiparietal cell and anti-intrinsic factor antibodies) [14](#page=14). * **Pathogenesis:** * ***H. pylori:*** Chronic inflammation leads to mucosal atrophy, increasing the risk of PUD, gastric carcinoma, and MALT lymphoma [14](#page=14). * **Autoimmune:** Autoantibodies destroy parietal cells, resulting in reduced acid (achlorhydria) and intrinsic factor, leading to pernicious anemia (Vitamin B12 deficiency) [14](#page=14). * **Clinical Features:** Often asymptomatic, but can cause epigastric discomfort, nausea, vomiting, and early satiety. Autoimmune gastritis may manifest with signs of B12 deficiency, such as anemia and neuropathy [14](#page=14). * **Diagnosis:** Upper GI endoscopy with biopsy is the gold standard. *H. pylori* testing (breath, stool antigen, biopsy urease) and autoimmune labs (parietal cell and IF antibodies, low B12) are performed [14](#page=14). * **Treatment:** For *H. pylori* type, eradication therapy (triple or quadruple) and PPIs for symptom control are used. For autoimmune type, parenteral Vitamin B12 replacement is essential, and monitoring for gastric carcinoma and MALT lymphoma is recommended [14](#page=14). * **Complications:** Peptic ulcer disease, gastric adenocarcinoma, MALT lymphoma, and pernicious anemia (in the autoimmune type) [14](#page=14). #### 3.2.4 Gastric cancer Gastric cancer, predominantly adenocarcinoma, is a malignancy of the stomach, with a lower incidence in the U.S. compared to East Asian countries [15](#page=15). * **General:** Majority are adenocarcinomas. Rare in the U.S.; common in Japan/Asia [15](#page=15). * **Morphology:** Can present as ulcerative carcinoma (deep ulcer), polypoid carcinoma (intraluminal mass), superficial spreading (best prognosis), or linitis plastica (diffuse infiltration, thick/rigid stomach, signet-ring cells, poor prognosis) [15](#page=15). * **Risk Factors:** *H. pylori* infection (3-6x risk), chronic atrophic gastritis with intestinal metaplasia and dysplasia, adenomatous gastric polyps, pernicious anemia, postgastrectomy (Billroth II) decades later, Ménétrier disease, high intake of preserved/salted/smoked foods (nitrates/nitrites), and blood type A [15](#page=15). * **Clinical Features:** Abdominal pain, unexplained weight loss, anorexia, dyspepsia, early satiety, nausea/vomiting, anemia, melena, and positive FOBT. Metastatic signs include Virchow node (left supraclavicular), Sister Mary Joseph nodule (periumbilical), Krukenberg tumor (ovary), and Blumer shelf (rectal shelf metastasis) [15](#page=15). * **Diagnosis:** Upper endoscopy (EGD) with multiple biopsies is the most accurate method. Barium upper GI series is an adjunct. CT abdomen/pelvis is used for staging and metastasis assessment, and FOBT for occult bleeding [15](#page=15). * **Treatment:** Surgical resection with wide margins (subtotal/total gastrectomy) and extended lymph node dissection is the primary treatment. Chemotherapy may be used for selected cases (neoadjuvant/adjuvant) [15](#page=15). * **Prognosis:** Depends on the stage; early detection significantly improves survival [15](#page=15). #### 3.2.5 Gastric lymphoma Gastric lymphoma is a non-Hodgkin lymphoma primarily originating in the stomach, most commonly MALT lymphoma associated with *H. pylori* [16](#page=16). * **General:** Primary gastric lymphoma (non-Hodgkin type). Most commonly MALT lymphoma (*H. pylori*-associated) [16](#page=16). * **Pathogenesis:** Chronic *H. pylori* infection can lead to lymphoid proliferation and the development of MALT lymphoma, which may progress to diffuse large B-cell lymphoma (DLBCL) [16](#page=16). * **Clinical Features:** Symptoms include abdominal pain, weight loss, and anorexia, similar to gastric adenocarcinoma. Complications can include bleeding, obstruction, or perforation, which may present as an emergency [16](#page=16). * **Diagnosis:** EGD with biopsy is the gold standard. Histology and immunophenotyping confirm the diagnosis. CT/PET scans are used for staging, and bone marrow biopsy may be necessary [16](#page=16). * **Treatment:** For MALT lymphoma with positive *H. pylori*, eradication therapy is the first-line treatment, as it can lead to regression. For persistent MALT or DLBCL, chemotherapy (e.g., CHOP ± rituximab) and radiation therapy are used. Surgery is typically reserved for complications [16](#page=16). * **Key Points:** *H. pylori* eradication can cure early MALT lymphoma. All suspicious gastric lesions should be biopsied to differentiate from gastric cancer [16](#page=16). --- # Inflammatory bowel diseases and appendiceal conditions This section details inflammatory bowel diseases, specifically Crohn disease and ulcerative colitis, alongside conditions of the appendix, namely acute appendicitis and appendiceal carcinoid tumors [23](#page=23) [24](#page=24) [25](#page=25) [26](#page=26) [27](#page=27) [28](#page=28). ### 4.1 Crohn disease Crohn disease is a chronic transmural inflammatory disease that can affect any part of the gastrointestinal tract, from the mouth to the anus, with the terminal ileum being a hallmark site [23](#page=23) [24](#page=24). #### 4.1.1 Distribution The disease commonly affects the ileum and cecum (40% of cases), followed by the small bowel only (30%), and the colon only (25%). Rarely, it can affect the stomach, mouth, and esophagus [23](#page=23) [24](#page=24). #### 4.1.2 Pathology Key pathological features of Crohn disease include skip lesions (discontinuous involvement), full-thickness (transmural) inflammation, the formation of fistulae (enteroenteric, enterovesical, enterovaginal), and strictures that can lead to chronic small bowel obstruction (SBO). Noncaseating granulomas are supportive findings, though not always present. "Fat creeping" over the bowel surface is also characteristic [23](#page=23) [24](#page=24). #### 4.1.3 Clinical features Patients typically present with diarrhea, usually non-bloody, and right lower quadrant (RLQ) abdominal pain. Other symptoms include weight loss, malabsorption, fever, malaise, nausea, and vomiting. Extraintestinal manifestations are common and can affect the eyes (uveitis, episcleritis), skin (erythema nodosum, pyoderma gangrenosum), joints (arthritis, ankylosing spondylitis), mouth (aphthous ulcers), and hepatobiliary/renal systems (gallstones, oxalate stones) [23](#page=23) [24](#page=24). #### 4.1.4 Diagnosis The gold standard for diagnosis is colonoscopy with biopsy, which may reveal cobblestone mucosa, aphthous ulcers, pseudopolyps, and patchy skip lesions. CT or MR enterography is also valuable, as is a small bowel follow-through which can show a "string sign". Laboratory findings may include elevated ESR/CRP, anemia, and low albumin. Fecal calprotectin is a useful marker for active inflammation [23](#page=23) [24](#page=24). #### 4.1.5 Complications Complications of Crohn disease include fistulae, strictures leading to SBO, perianal disease, abscesses, malabsorption (particularly of B12 and bile salts), gallstones, kidney stones, and growth retardation in children. There is also an increased risk of small bowel and colon cancer [23](#page=23) [24](#page=24). #### 4.1.6 Treatment Treatment aims to induce and maintain remission. Induction therapy often involves corticosteroids (prednisone) or budesonide for ileocecal disease. Maintenance therapy includes thiopurines (azathioprine, 6-mercaptopurine), methotrexate, and biologics such as anti-TNF agents (infliximab, adalimumab). Antibiotics, particularly ciprofloxacin and metronidazole, are used for perianal disease. Nutritional support is crucial, including B12 injections for ileal disease and supplementation of Vitamin D, calcium, and iron. Surgery is reserved for complications like SBO, fistulae, abscesses, or perforation, and may involve segmental resection or stricturoplasty. It is not curative, with recurrence rates around 50% at 10 years [23](#page=23) [24](#page=24). ### 4.2 Ulcerative colitis Ulcerative colitis is a chronic inflammatory disease confined to the colon and rectum, always involving the rectum and characterized by continuous mucosal inflammation without skip lesions, limited to the mucosa and submucosa [25](#page=25) [26](#page=26). #### 4.2.1 Distribution The disease distribution varies: proctitis (rectum only) accounts for 10%, involvement of the rectum and left colon for 40%, rectum, left, and right colon for 30%, and pancolitis (involving the entire colon) for 30% [25](#page=25) [26](#page=26). #### 4.2.2 Pathology Pathologically, ulcerative colitis presents as continuous inflammation without skip lesions. Crypt abscesses formed by neutrophils (PMNs) are a classic finding, along with mucosal ulceration and friability. Backwash ileitis, affecting the terminal ileum, occurs in about 10% of pancolitis cases [25](#page=25) [26](#page=26). #### 4.2.3 Clinical features The hallmark clinical feature is hematochezia (bloody diarrhea). Patients also experience frequent small-volume stools, tenesmus (rectal urgency), abdominal pain, cramping, and in severe flares, fever and weight loss. Extraintestinal manifestations are similar to Crohn disease and include uveitis, arthritis, erythema nodosum, and a strong association with primary sclerosing cholangitis (PSC) [25](#page=25) [26](#page=26). #### 4.2.4 Diagnosis Diagnosis begins with stool cultures and testing for *C. difficile*. Fecal leukocytes and calprotectin are measured, and colonoscopy with biopsy is the gold standard. Colonoscopic findings include continuous inflammation, loss of the vascular pattern, superficial ulcers, and crypt abscesses. Imaging may be used to assess complications like toxic megacolon [25](#page=25) [26](#page=26). #### 4.2.5 Complications Serious complications include toxic megacolon, which is the leading cause of death, and an increased risk of colorectal cancer, which rises with the duration and extent of the disease. Other complications include hemorrhage, strictures (less common than in Crohn disease), increased risk of PSC and cholangiocarcinoma, growth failure in children, and fulminant colitis [25](#page=25) [26](#page=26). #### 4.2.6 Treatment Treatment depends on disease severity. Mild to moderate cases are treated with 5-aminosalicylic acid (5-ASA) medications like mesalamine or sulfasalazine, with topical 5-ASA for proctitis and enemas for left-sided disease. Moderate to severe cases require oral steroids (prednisone), anti-TNF agents (infliximab, adalimumab), or thiopurines (azathioprine, 6-MP). Supportive care includes fluid and electrolyte correction, anemia treatment, and nutritional support [25](#page=25) [26](#page=26). Surgical intervention, primarily total colectomy, is curative and indicated for toxic megacolon, massive hemorrhage, perforation, failure of medical therapy, or the presence of dysplasia or cancer [25](#page=25) [26](#page=26). > **High-Yield Pearls for Ulcerative Colitis:** > * The rectum is **always** involved. > * Inflammation is **continuous** and mucosal. > * There is a strong association with **PSC**. > * A colectomy is **curative**. > * **Toxic megacolon** is an emergency. ### 4.3 Diseases of the appendix #### 4.3.1 Acute appendicitis Acute appendicitis is a common surgical emergency [27](#page=27) [28](#page=28). ##### 4.3.1.1 Pathogenesis The primary cause is lumen obstruction, most commonly due to lymphoid hyperplasia (60%) or a fecalith (35%). Less common causes include foreign bodies, parasites, or tumors. Obstruction leads to stasis and bacterial overgrowth, increasing intraluminal pressure, venous congestion, and ischemia. This can progress to necrosis and perforation, leading to peritonitis [27](#page=27) [28](#page=28). ##### 4.3.1.2 Clinical features The classic presentation involves pain that begins in the epigastric or periumbilical region and then migrates to the RLQ. Anorexia is very common, and nausea/vomiting typically follows the onset of pain. A low-grade fever is usually present, which can be higher if perforation has occurred. Physical examination reveals RLQ tenderness at McBurney’s point, rebound tenderness, guarding, and decreased bowel sounds. Special signs include Rovsing's sign, psoas sign, and obturator sign [27](#page=27) [28](#page=28). ##### 4.3.1.3 Diagnosis The diagnosis is primarily clinical. Laboratory findings may show mild leukocytosis. CT scans offer high sensitivity and specificity (98–100%) for diagnosis, while ultrasound is used in children and pregnant women, with approximately 90% sensitivity [27](#page=27) [28](#page=28). ##### 4.3.1.4 Treatment The standard treatment is appendectomy, often performed laparoscopically. Perioperative antibiotics are administered. In cases of perforation, surgery is combined with broad-spectrum antibiotics, and any abscess is drained. Nonoperative management with antibiotics may be considered in select low-risk cases [27](#page=27) [28](#page=28). ##### 4.3.1.5 Complications Complications include perforation (occurring in about 20% of cases), peritonitis, abscess formation, and sepsis [27](#page=27) [28](#page=28). > **High-Yield Pearls for Acute Appendicitis:** > * **Pain migration** from the umbilicus to the RLQ is a classic sign. > * **Anorexia** is almost always present. > * **CT scan** is the imaging modality of choice for uncertain cases. > * Appendectomy is **curative** for appendicitis. #### 4.3.2 Appendiceal carcinoid (neuroendocrine tumor) Appendiceal carcinoid tumors are neuroendocrine tumors originating from neuroendocrine cells, with the appendix being their most common site [27](#page=27) [28](#page=28). ##### 4.3.2.1 Features These tumors often present incidentally during surgery for presumed appendicitis. They secrete serotonin [27](#page=27) [28](#page=28). ##### 4.3.2.2 Carcinoid syndrome Carcinoid syndrome, characterized by cutaneous flushing, diarrhea, and wheezing or bronchospasm, occurs only when the tumor metastasizes, typically to the liver. Right-sided valvular lesions can also develop with metastatic disease [27](#page=27) [28](#page=28). ##### 4.3.2.3 Diagnosis Diagnosis is confirmed by histology from an appendectomy specimen. If carcinoid syndrome is suspected, a 24-hour urine collection for 5-hydroxyindoleacetic acid (5-HIAA) may be performed. Imaging is used to assess for metastasis in larger tumors [27](#page=27) [28](#page=28). ##### 4.3.2.4 Treatment Treatment depends on tumor size and location. Tumors less than 2 centimeters typically require an appendectomy. For tumors larger than 2 centimeters or located at the base of the appendix, a right hemicolectomy is indicated. For metastatic disease, treatment options include somatostatin analogs (e.g., octreotide) and surgical cytoreduction or hepatic therapies [27](#page=27) [28](#page=28). > **High-Yield Pearls for Appendiceal Carcinoid Tumors:** > * Carcinoid syndrome is indicative of **metastasis**. > * Appendectomy is curative for small carcinoid tumors. --- # Liver diseases and disorders This section provides a detailed overview of various liver diseases and disorders, their causes, clinical presentations, diagnostic methods, and management strategies, along with an in-depth look at gallbladder and biliary tract conditions [36](#page=36) [37](#page=37) [38](#page=38) [39](#page=39) [40](#page=40) [41](#page=41) [42](#page=42) [43](#page=43) [44](#page=44) [45](#page=45) [46](#page=46) [47](#page=47) [48](#page=48) [49](#page=49) [50](#page=50) [51](#page=51) [52](#page=52) [53](#page=53) [54](#page=54) [55](#page=55) [56](#page=56) [57](#page=57) [58](#page=58) [59](#page=59) [60](#page=60). ### 5.1 Acute liver failure Acute liver failure (ALF) is defined as severe liver injury with encephalopathy and impaired synthetic function (INR > 1.5) occurring within 26 weeks in individuals without pre-existing cirrhosis [36](#page=36) [37](#page=37). #### 5.1.1 Causes of acute liver failure The most common cause of ALF is acetaminophen toxicity. Other causes include [36](#page=36) [37](#page=37): * Viral hepatitis (A, B, C, D, E) [36](#page=36) [37](#page=37). * Autoimmune hepatitis [36](#page=36) [37](#page=37). * Ischemic hepatopathy ("shock liver") [36](#page=36) [37](#page=37). * Budd–Chiari syndrome [36](#page=36) [37](#page=37). * Acute fatty liver of pregnancy / HELLP syndrome [36](#page=36) [37](#page=37). * Wilson disease [36](#page=36) [37](#page=37). * Sepsis, toxins, and malignancy [36](#page=36) [37](#page=37). * Other drugs and mushroom poisoning [36](#page=36) [37](#page=37). #### 5.1.2 Clinical features of acute liver failure Key clinical features include: * Encephalopathy (confusion, asterixis, altered level of consciousness) [36](#page=36) [37](#page=37). * Coagulopathy (INR > 1.5) [36](#page=36) [37](#page=37). * Jaundice [36](#page=36) [37](#page=37). * Hepatomegaly or a tender liver [36](#page=36) [37](#page=37). * Thrombocytopenia [36](#page=36) [37](#page=37). * Hypoglycemia (due to impaired glycogen storage) [36](#page=36) [37](#page=37). #### 5.1.3 Diagnosis of acute liver failure Diagnosis requires encephalopathy, INR > 1.5, and elevated liver function tests. Investigations include [36](#page=36) [37](#page=37): * Labs: LFTs, PT/INR, ammonia, glucose, viral serologies, autoimmune markers [36](#page=36) [37](#page=37). * Imaging: CT abdomen/pelvis, MRI, abdominal ultrasound [36](#page=36) [37](#page=37). * A liver biopsy may be considered if the cause is unclear [36](#page=36) [37](#page=37). #### 5.1.4 Management of acute liver failure Management is primarily supportive and requires ICU monitoring [36](#page=36) [37](#page=37). * Treat the underlying cause: N-acetylcysteine for acetaminophen toxicity, steroids for autoimmune hepatitis, delivery for AFLP/HELLP, antivirals for HBV, anticoagulation for Budd-Chiari syndrome [36](#page=36) [37](#page=37). * Encephalopathy: Lactulose and potentially Rifaximin [36](#page=36) [37](#page=37). * Prevent cerebral edema: Monitor ICP, elevate head, consider mannitol [36](#page=36) [37](#page=37). * Supportive care: Nutritional support, correct hypoglycemia, manage infections [36](#page=36) [37](#page=37). * Liver transplantation should be considered early, offering an 80% 1-year survival rate [36](#page=36) [37](#page=37). #### 5.1.5 Prognosis of acute liver failure ALF has high mortality without transplantation. Cerebral edema is a major cause of death [36](#page=36) [37](#page=37). ### 5.2 Cirrhosis Cirrhosis is a chronic liver disease characterized by irreversible fibrosis and nodular regeneration, leading to disrupted liver architecture, portal hypertension, and liver failure [38](#page=38) [39](#page=39) [40](#page=40). #### 5.2.1 General characteristics of cirrhosis Key features include irreversible fibrosis, disrupted architecture, and two major consequences: portal hypertension and hepatocellular failure. Severity is assessed using the Child-Pugh score and MELD score (which predicts 3-month survival) [38](#page=38) [39](#page=39) [40](#page=40). #### 5.2.2 Causes of cirrhosis The most common causes, in descending order, are: 1. Alcoholic liver disease [38](#page=38) [39](#page=39) [40](#page=40). 2. Chronic Hepatitis B & C [38](#page=38) [39](#page=39) [40](#page=40). 3. NASH (Nonalcoholic Steatohepatitis) [38](#page=38) [39](#page=39) [40](#page=40). 4. Autoimmune hepatitis [38](#page=38) [39](#page=39) [40](#page=40). 5. Drugs (e.g., acetaminophen, methotrexate) [38](#page=38) [39](#page=39) [40](#page=40). 6. Primary Biliary Cholangitis (PBC) / Primary Sclerosing Cholangitis (PSC) [38](#page=38) [39](#page=39) [40](#page=40). 7. Metabolic diseases (Hemochromatosis, Wilson disease, α1-antitrypsin deficiency) [38](#page=38) [39](#page=39) [40](#page=40). 8. Cardiac cirrhosis (right-sided heart failure) [38](#page=38) [39](#page=39) [40](#page=40). 9. Post-liver transplant vascular disease [38](#page=38) [39](#page=39) [40](#page=40). #### 5.2.3 Clinical features of cirrhosis * **Early:** Fatigue, anorexia, weight loss, hepatomegaly or a small shrunken liver. May be asymptomatic [38](#page=38) [39](#page=39) [40](#page=40). * **Stigmata of Chronic Liver Disease:** Spider angiomas, palmar erythema, gynecomastia, testicular atrophy, caput medusae, hemorrhoids, ascites, splenomegaly [38](#page=38) [39](#page=39) [40](#page=40). * **Lab Abnormalities:** Elevated bilirubin, elevated INR/PT, decreased albumin, thrombocytopenia [38](#page=38) [39](#page=39) [40](#page=40). #### 5.2.4 Major complications of cirrhosis * **Portal Hypertension:** * **Varices (esophageal/gastric):** Massive hematemesis, melena. Management includes hemodynamic stabilization, octreotide, antibiotics, endoscopic ligation, beta-blockers, and TIPS [38](#page=38) [39](#page=39) [40](#page=40). * **Ascites:** Caused by portal hypertension and hypoalbuminemia. Diagnosis via ultrasound, paracentesis (SAAG > 1.1 g/dL indicates portal hypertension). Treatment includes sodium restriction, spironolactone, furosemide, and therapeutic paracentesis [38](#page=38) [39](#page=39) [40](#page=40). * **Splenomegaly:** Leads to thrombocytopenia [38](#page=38) [39](#page=39) [40](#page=40). * **Hepatic Encephalopathy:** Triggered by elevated ammonia. Symptoms include confusion, asterixis, and fetor hepaticus. Treatment involves lactulose and rifaximin [38](#page=38) [39](#page=39) [40](#page=40). * **Hepatorenal Syndrome (HRS):** Functional renal failure with azotemia, oliguria, hyponatremia, and low urine sodium (<10 mEq/L). Not improved by fluids. Liver transplantation is the only cure [38](#page=38) [39](#page=39) [40](#page=40). * **Spontaneous Bacterial Peritonitis (SBP):** Infection of ascitic fluid. Diagnosis requires PMN > 250. Treatment with 3rd-generation cephalosporins and prophylaxis for recurrence [38](#page=38) [39](#page=39) [40](#page=40). * **Coagulopathy:** Elevated PT/INR due to decreased clotting factor synthesis. Vitamin K is ineffective; treat with FFP [38](#page=38) [39](#page=39) [40](#page=40). * **Hyperestrinism:** Spider angiomas, palmar erythema, gynecomastia, testicular atrophy [38](#page=38) [39](#page=39) [40](#page=40). * **Hepatocellular Carcinoma (HCC):** Occurs in 10–25% of cirrhotics. Screen every 6 months with ultrasound and AFP [38](#page=38) [39](#page=39) [40](#page=40). #### 5.2.5 Treatment overview for cirrhosis * Treat the underlying cause (e.g., stop alcohol, treat viral hepatitis) [38](#page=38) [39](#page=39) [40](#page=40). * Manage complications (e.g., HE, ascites, varices, SBP, coagulopathy) [38](#page=38) [39](#page=39) [40](#page=40). * Liver transplantation is the definitive cure, requiring alcohol abstinence ≥ 6 months and based on MELD score [38](#page=38) [39](#page=39) [40](#page=40). ### 5.3 Wilson's disease Wilson's disease is an autosomal recessive disorder of copper metabolism caused by a mutation in the ATP7B gene, leading to impaired copper excretion into bile and incorporation into ceruloplasmin. Copper accumulates in the liver, brain, cornea, and kidneys, typically presenting between ages 5–35 [41](#page=41) [42](#page=42). #### 5.3.1 Clinical features of Wilson's disease * **Hepatic involvement:** Acute hepatitis, chronic hepatitis, cirrhosis, or fulminant liver failure [41](#page=41) [42](#page=42). * **Kayser–Fleischer rings:** Copper deposits in the cornea, appearing as yellow-brown rings, without vision impairment [41](#page=41) [42](#page=42). * **Neurologic signs:** Parkinsonism, chorea, dysarthria, incoordination, tremor, and drooling [41](#page=41) [42](#page=42). * **Psychiatric manifestations:** Depression, personality changes, and psychosis [41](#page=41) [42](#page=42). * **Renal involvement:** Aminoaciduria and nephrocalcinosis [41](#page=41) [42](#page=42). #### 5.3.2 Diagnosis of Wilson's disease * **Labs:** Elevated AST/ALT, coagulopathy [41](#page=41) [42](#page=42). * **Copper markers:** Low ceruloplasmin (in 90%), elevated free serum copper, elevated 24-hour urinary copper [41](#page=41) [42](#page=42). * **Liver biopsy:** Elevated hepatic copper concentration [41](#page=41) [42](#page=42). * Screening of first-degree relatives is recommended [41](#page=41) [42](#page=42). #### 5.3.3 Treatment of Wilson's disease * **Chelation therapy:** D-Penicillamine or Trientine [41](#page=41) [42](#page=42). * **Zinc therapy:** Reduces dietary copper absorption [41](#page=41) [42](#page=42). * **Liver transplantation:** For fulminant failure or drug-resistant disease [41](#page=41) [42](#page=42). * Monitoring involves serum and urinary copper, ceruloplasmin, and liver function tests [41](#page=41) [42](#page=42). ### 5.4 Hemochromatosis Hemochromatosis is an autosomal recessive disease of iron metabolism characterized by excessive dietary iron absorption, leading to iron deposition (ferritin and hemosiderin) in organs and damage from free radicals. Siblings should be screened due to its inherited nature [43](#page=43). #### 5.4.1 Affected organs in hemochromatosis The primary affected organ is the liver, but also the pancreas, heart, joints, skin, and endocrine organs [43](#page=43). #### 5.4.2 Clinical features of hemochromatosis Initially asymptomatic, clinical manifestations include fatigue, abdominal pain, arthritis (especially in the 2nd and 3rd MCP joints), arrhythmias, impotence/amenorrhea, and signs of liver disease [43](#page=43). #### 5.4.3 Complications of hemochromatosis * Cirrhosis with a 200-fold increased risk of HCC [43](#page=43). * Cardiomyopathy (CHF, arrhythmias) [43](#page=43). * Diabetes mellitus ("Bronze diabetes") [43](#page=43). * Arthritis (MCP joints) [43](#page=43). * Hypogonadism and hypothyroidism [43](#page=43). * Skin hyperpigmentation ("bronze skin") [43](#page=43). #### 5.4.4 Diagnosis of hemochromatosis * Elevated serum iron, elevated ferritin, and elevated transferrin saturation (most sensitive) [43](#page=43). * Decreased TIBC [43](#page=43). * HFE gene mutation testing is the gold standard [43](#page=43). #### 5.4.5 Treatment of hemochromatosis * Repeated phlebotomy is the first-line treatment [43](#page=43). * Treat complications such as CHF, diabetes, and thyroid issues [43](#page=43). * Liver transplant for advanced cases [43](#page=43). ### 5.5 Benign liver tumors Benign liver tumors include hepatocellular adenoma, cavernous hemangioma, and focal nodular hyperplasia (FNH) [44](#page=44) [45](#page=45). #### 5.5.1 Hepatocellular adenoma * **Epidemiology:** Young women (15–40 years), strongly associated with oral contraceptive pills (OCPs) and anabolic steroids [44](#page=44) [45](#page=45). * **Pathophysiology:** Hormone-driven proliferation of hepatocytes, which can enlarge and increase the risk of rupture and hemorrhage [44](#page=44) [45](#page=45). * **Clinical Features:** Often asymptomatic, but can cause RUQ pain or fullness. A significant risk is hemoperitoneum due to rupture [44](#page=44) [45](#page=45). * **Diagnosis:** CT or MRI are best; hepatic arteriography is most accurate but invasive [44](#page=44) [45](#page=45). * **Treatment:** Stop oral contraceptives. Resection is indicated if the adenoma is > 5 cm or does not regress, to prevent rupture [44](#page=44) [45](#page=45). #### 5.5.2 Cavernous hemangioma * **Epidemiology:** The most common benign liver tumor, usually asymptomatic [44](#page=44) [45](#page=45). * **Pathophysiology:** A vascular malformation consisting of blood-filled spaces. Can enlarge with pregnancy or OCP use [44](#page=44) [45](#page=45). * **Clinical Features:** Typically silent. Large tumors can cause RUQ pain or fullness. Rare complications include rupture, jaundice, coagulopathy, and CHF (due to large arteriovenous shunts) [44](#page=44) [45](#page=45). * **Diagnosis:** Ultrasound or CT with contrast. **Biopsy is contraindicated due to the risk of massive bleeding** [44](#page=44) [45](#page=45). * **Treatment:** Observe small, asymptomatic lesions. Resection is reserved for symptomatic or very large tumors [44](#page=44) [45](#page=45). #### 5.5.3 Focal nodular hyperplasia (FNH) * **Epidemiology:** More common in women of reproductive age, **not associated with OCPs** [44](#page=44) [45](#page=45). * **Pathophysiology:** A hyperplastic reaction to abnormal vascular flow. Characteristically has a central stellate scar visible on imaging [44](#page=44) [45](#page=45). * **Clinical Features:** Usually asymptomatic, though hepatomegaly may occur [44](#page=44) [45](#page=45). * **Diagnosis:** MRI/CT revealing a central scar. Biopsy is rarely needed [44](#page=44) [45](#page=45). * **Treatment:** None required as FNH is benign and has no malignant potential [44](#page=44) [45](#page=45). ### 5.6 Hepatocellular carcinoma (HCC) HCC accounts for over 80% of primary liver cancers and is a highly lethal cancer worldwide, with higher incidence in Africa and Asia [45](#page=45) [46](#page=46). #### 5.6.1 Pathologic types of HCC * **Nonfibrolamellar (most common):** Associated with HBV, HCV, and cirrhosis. Typically has a poor prognosis and is unresectable [45](#page=45) [46](#page=46). * **Fibrolamellar:** Not associated with hepatitis or cirrhosis. Seen in adolescents and young adults, often more resectable with better survival [45](#page=45) [46](#page=46). #### 5.6.2 Risk factors for HCC * Cirrhosis (the most important risk factor) [45](#page=45) [46](#page=46). * Chemical carcinogens (aflatoxin, vinyl chloride, thorotrast) [45](#page=45) [46](#page=46). * Hemochromatosis [45](#page=45) [46](#page=46). * Wilson disease [45](#page=45) [46](#page=46). * Schistosomiasis [45](#page=45) [46](#page=46). * Hepatic adenoma (10% can become malignant) [45](#page=45) [46](#page=46). * Cigarette smoking [45](#page=45) [46](#page=46). * Glycogen storage disease (type 1) [45](#page=45) [46](#page=46). #### 5.6.3 Clinical features of HCC * Abdominal pain (often due to painful hepatomegaly) [45](#page=45) [46](#page=46). * Weight loss, anorexia, fatigue [45](#page=45) [46](#page=46). * Signs of chronic liver disease: portal hypertension, ascites, jaundice, splenomegaly [45](#page=45) [46](#page=46). * **Paraneoplastic Syndromes:** Erythrocytosis, thrombocytosis, hypercalcemia, carcinoid syndrome, hypoglycemia, high cholesterol [45](#page=45) [46](#page=46). #### 5.6.4 Diagnosis of HCC * **Liver biopsy:** Definitive diagnosis [45](#page=45) [46](#page=46). * **Labs:** HBV/HCV serology, LFTs, INR [45](#page=45) [46](#page=46). * **Imaging:** Ultrasound (US), CT, MRI [45](#page=45) [46](#page=46). * **AFP (alpha-fetoprotein):** Elevated in 40–70% of cases; used for screening and monitoring therapy [45](#page=45) [46](#page=46). #### 5.6.5 Treatment of HCC * **Surgical resection:** Only eligible for about 10% of patients [45](#page=45) [46](#page=46). * **Liver transplantation:** For early-stage HCC [45](#page=45) [46](#page=46). * For unresectable tumors: * TACE (transarterial chemoembolization) [45](#page=45) [46](#page=46). * Radiofrequency ablation [45](#page=45) [46](#page=46). * Selective internal radiation therapy [45](#page=45) [46](#page=46). ### 5.7 Other liver conditions #### 5.7.1 Nonalcoholic steatohepatitis (NASH) NASH has histology identical to alcoholic hepatitis but occurs without alcohol use. It is associated with obesity, hyperlipidemia, and diabetes mellitus. While usually asymptomatic with mild elevations in ALT/AST, 10–15% can develop cirrhosis. Treatment is not clearly established but may involve weight loss and metabolic control [47](#page=47). #### 5.7.2 Hemobilia Hemobilia is the presence of blood entering the duodenum via the common bile duct (CBD). Common causes include trauma (most frequent), thyroid carcinoma, surgery (cholecystectomy, CBD exploration), tumors, and infection. Clinical features include GI bleeding (melena/hematemesis), RUQ pain, and jaundice. Diagnosis is made via arteriogram (gold standard) or endoscopy showing blood from the ampulla of Vater. Treatment involves resuscitation, transfusion if needed, and surgical or arterial embolization for severe bleeding [47](#page=47). #### 5.7.3 Liver cysts * **Polycystic Liver Cysts:** Autosomal dominant inheritance, associated with autosomal dominant polycystic kidney disease (ADPKD). Usually asymptomatic, treated only if symptomatic [48](#page=48). * **Hydatid (Echinococcus) Cysts:** Caused by *E. granulosus* or *multilocularis*. Usually in the right lobe. Small cysts are asymptomatic; large ones cause RUQ pain or rupture, risking anaphylaxis. Treatment is surgical resection with antihelminthics (albendazole/mebendazole) [48](#page=48). #### 5.7.4 Liver abscesses * **Pyogenic Liver Abscess:** Caused by biliary obstruction (most common), portal spread, trauma, or surgery. Organisms include *E. coli*, Klebsiella, Proteus, Enterococcus, and anaerobes. Features include fever, RUQ pain, anorexia, and jaundice. Diagnosis by US/CT, elevated LFTs, and blood cultures. Treatment involves IV broad-spectrum antibiotics and percutaneous drainage, or surgery if necessary [48](#page=48). * **Amebic Liver Abscess:** Caused by *Entamoeba histolytica* via fecal-oral transmission. More common in men, often with portal seeding from the colon. Features include fever, RUQ pain, hepatomegaly, and sometimes diarrhea. Diagnosis by serology (IgG EIA), imaging (US/CT), and stool tests. Treatment is metronidazole, with percutaneous aspiration for large or unresponsive abscesses [48](#page=48). #### 5.7.5 Budd–Chiari syndrome Budd-Chiari syndrome is characterized by hepatic venous outflow obstruction, leading to hepatic congestion, ischemia, and portal hypertension. It can be acute, subacute, or chronic [49](#page=49). ##### 5.7.5.1 Causes of Budd–Chiari syndrome * **Hypercoagulable states:** Polycythemia vera, myeloproliferative disorders, pregnancy, oral contraceptives, antiphospholipid syndrome, protein C/S deficiency [49](#page=49). * Chronic inflammatory disease, malignancy, infection, trauma [49](#page=49). * Idiopathic (approximately 40%) [49](#page=49). ##### 5.7.5.2 Clinical features of Budd–Chiari syndrome * Hepatomegaly (often tender) [49](#page=49). * RUQ abdominal pain [49](#page=49). * Ascites (often rapid onset) [49](#page=49). * Variable jaundice [49](#page=49). * Variceal bleeding due to portal hypertension [49](#page=49). * Can progress to acute liver failure [49](#page=49). ##### 5.7.5.3 Diagnosis of Budd–Chiari syndrome * **Doppler ultrasound** is the first-line investigation [49](#page=49). * CT/MRI confirm reduced venous flow [49](#page=49). * Hepatic venography is the gold standard [49](#page=49). * Ascitic fluid analysis shows SAAG > 1.1 g/dL, indicating portal hypertension [49](#page=49). ##### 5.7.5.4 Treatment of Budd–Chiari syndrome * **Medical:** Anticoagulation, diuretics for ascites, thrombolytics in selected cases [49](#page=49). * **Interventional:** Balloon angioplasty with stenting, TIPS to decompress the portal system [49](#page=49). * **Surgical:** Portacaval shunt if interventional therapy fails [49](#page=49). * **Liver transplantation:** For cirrhosis or acute liver failure [49](#page=49). #### 5.7.6 Jaundice Jaundice is the yellowing of the skin, sclera, and mucous membranes due to elevated bilirubin, visible when levels exceed approximately 2 mg/dL [50](#page=50). ##### 5.7.6.1 Bilirubin pathway Red blood cells break down into heme, which is converted to unconjugated (indirect) bilirubin. This is bound to albumin and transported to the liver for conjugation. Conjugated (direct) bilirubin is then excreted into the gut [50](#page=50). ##### 5.7.6.2 Types of jaundice * **Conjugated (direct) jaundice:** Characterized by urine positive for bilirubin and pale stools. It results from impaired excretion or cholestasis. Causes include extrahepatic obstruction (gallstones, pancreatic cancer), intrahepatic cholestasis (PBC, PSC, drugs), hepatocellular damage (viral hepatitis, cirrhosis), and genetic disorders (Dubin-Johnson, Rotor). Key indicators are dark urine, pale stools, and elevated ALP/GGT [50](#page=50). * **Unconjugated (indirect) jaundice:** Characterized by a negative urine bilirubin test. It arises from increased bilirubin production (hemolysis) or impaired uptake/conjugation. Causes include hemolytic anemias, Gilbert syndrome (benign, exacerbated by fasting/stress), and Crigler-Najjar syndrome. Clues include anemia, elevated reticulocyte count, high LDH, and low haptoglobin [50](#page=50). ##### 5.7.6.3 Clinical features and red flags * Dark urine with pale stools suggests obstruction (conjugated) [50](#page=50). * Pruritus indicates cholestasis [50](#page=50). * Fever, RUQ pain, and jaundice suggest ascending cholangitis, which is an emergency [50](#page=50). * Signs of hemolysis include pallor, splenomegaly, and a high reticulocyte count [50](#page=50). ##### 5.7.6.4 Initial investigations for jaundice * Serum: total and direct bilirubin [50](#page=50). * LFTs: AST/ALT, ALP, GGT, albumin, INR [50](#page=50). * CBC, reticulocyte count, LDH, haptoglobin (if hemolysis is suspected) [50](#page=50). * Urine dipstick for bilirubin and urobilinogen [50](#page=50). * Abdominal ultrasound to look for ductal dilatation, stones, or masses [50](#page=50). ##### 5.7.6.5 Further imaging and procedures * If obstruction is suspected: MRCP, CT, or ERCP (which is also therapeutic) [50](#page=50). * If hepatocellular and the cause is unclear: viral serologies, autoimmune markers, and potentially a liver biopsy [50](#page=50). ##### 5.7.6.6 Management of jaundice Management principle is to treat the underlying cause [50](#page=50). * Hemolysis: Treat the underlying cause (e.g., steroids for autoimmune), transfuse if necessary [50](#page=50). * Obstruction: Biliary decompression via ERCP, stenting, or surgery. Cholangitis requires emergency IV antibiotics and urgent decompression [50](#page=50). * Viral hepatitis: Antivirals or supportive care as indicated [50](#page=50). * Drug-induced jaundice: Discontinue the offending drug [50](#page=50). * Symptomatic control: Cholestyramine or rifampicin for pruritus; phototherapy or exchange transfusion for severe neonatal indirect hyperbilirubinemia [50](#page=50). > **Exam Tip:** Remember that "Dark urine = Direct (D for Dark + Direct)" [50](#page=50). > **Exam Tip:** Gilbert syndrome is benign and worsens with fasting/stress [50](#page=50). > **Exam Tip:** Reynolds' pentad for severe cholangitis includes Fever + Jaundice + RUQ pain + Hypotension + Altered mental status [50](#page=50). ### 5.8 Liver function tests (LFTs) Liver function tests (LFTs) provide insights into liver health, encompassing aminotransferases, alkaline phosphatase, GGT, bilirubin, albumin, and prothrombin time [51](#page=51). #### 5.8.1 Aminotransferases (ALT/AST) * **ALT:** More specific to the liver than AST [51](#page=51). * **Patterns of elevation:** * Mild elevation (low hundreds): Chronic viral hepatitis, alcoholic hepatitis [51](#page=51). * Moderate elevation (high hundreds to 1000s): Acute viral hepatitis [51](#page=51). * Severe elevation (>10,000): Ischemic (shock) liver, acetaminophen toxicity, severe viral hepatitis [51](#page=51). * **Alcoholic hepatitis:** AST:ALT ratio > 2:1 [51](#page=51). * **Late cirrhosis/metastasis:** Transaminases may be normal due to few remaining hepatocytes [51](#page=51). * **Mnemonic for causes (A B C D E F G H I):** Autoimmune, HepB, HepC, Drugs, Ethanol, Fatty liver, Growths, Hemodynamic, Iron/Copper/AAT [51](#page=51). #### 5.8.2 Alkaline Phosphatase (ALP) * Not liver-specific; also found in bone, gut, and placenta [51](#page=51). * Elevated with cholestasis or bile duct obstruction [51](#page=51). * Very high levels (≈10x normal) suggest extrahepatic obstruction or severe intrahepatic cholestasis (e.g., PBC, drugs) [51](#page=51). * Checking GGT confirms a hepatic source for ALP elevation: * ALP ⇧ + GGT ⇧ => Hepatic origin [51](#page=51). * ALP ⇧ + GGT normal => Bone disease or pregnancy [51](#page=51). #### 5.8.3 Gamma-GT (GGT) Used to confirm the hepatic origin of an ALP rise. Alcohol and many drugs can also raise GGT [51](#page=51). #### 5.8.4 Bilirubin * **Conjugated (direct):** Water-soluble, leads to dark urine. Indicates cholestasis or hepatocellular excretion failure [51](#page=51). * **Unconjugated (indirect):** Not water-soluble, urine is negative. Indicates overproduction or impaired uptake/conjugation [51](#page=51). * **Patterns:** * Cholestatic LFTs: Very elevated ALP and GGT; ALT/AST slightly elevated [51](#page=51). * Hepatocellular necrosis: Very elevated ALT/AST; ALP normal or slightly elevated [51](#page=51). #### 5.8.5 Albumin A marker of chronic synthetic function. Decreased in chronic liver disease, nephrotic syndrome, malnutrition, and inflammation [51](#page=51). #### 5.8.6 Prothrombin Time (PT) Reflects hepatic synthesis of clotting factors. Prolonged PT indicates a loss of synthetic capacity and advanced liver disease [51](#page=51). #### 5.8.7 Quick interpretation cheat sheet * **Hepatocellular pattern:** ALT/AST ⇧⇧⇧ >> ALP [51](#page=51). * **Cholestatic pattern:** ALP & GGT ⇧⇧ >> ALT/AST [51](#page=51). * **Synthetic failure:** Low albumin + prolonged PT (INR) [51](#page=51). #### 5.8.8 Most useful tests for: * **Acute hepatocellular injury:** ALT, AST [51](#page=51). * **Cholestasis/obstruction:** ALP + GGT (along with imaging/ERCP) [51](#page=51). * **Chronic liver reserve:** Albumin + PT (INR) [51](#page=51). > **Memo Mnemonic:** "AST from A-Side too" means AST is found in many tissues, not just the liver [51](#page=51). > **Memo Mnemonic:** "GGT proves ALP's story" indicates GGT confirms the hepatic source of elevated ALP [51](#page=51). > **Memo Mnemonic:** "Shock, Tylenol, Virus = >10k" are common causes of very high transaminases [51](#page=51). ### 5.9 Gallbladder and biliary tract diseases #### 5.9.1 Cholelithiasis (Gallstones) Cholelithiasis refers to stones in the gallbladder, often found incidentally [52](#page=52). * **Types:** * **Cholesterol stones:** Most common, yellow/green. Risks include obesity, diabetes, hyperlipidemia, multiple pregnancies, OCPs, Crohn's disease, ileal resection, age, and cirrhosis. Mnemonic: FAT, FERTILE, FORTY (+Crohn/Cirrhosis) [52](#page=52). * **Pigment stones:** Black (gallbladder) associated with hemolysis and alcoholic cirrhosis. Brown (bile ducts) associated with biliary infection [52](#page=52). * **Mixed stones:** A combination of cholesterol and pigment stones [52](#page=52). * **Clinical Features:** * **Asymptomatic:** Most patients [52](#page=52). * **Symptomatic (Biliary Colic):** Caused by temporary cystic duct obstruction during gallbladder contraction. Pain is RUQ/epigastric, may radiate to the right scapula (Boas sign). Often occurs after fatty meals or at night, lasting minutes to hours. If symptoms persist for days, consider cholecystitis [52](#page=52). * **Complications:** Acute/chronic cholecystitis, choledocholithiasis (CBD stone leading to jaundice and cholangitis risk), gallstone ileus, and gallbladder carcinoma (rare) [52](#page=52). * **Diagnosis:** RUQ ultrasound is the best test (>95% sensitivity for stones > 2 mm). CT or MRI can be used if ultrasound is inconclusive [52](#page=52). * **Treatment:** Conservative management for asymptomatic stones. Elective cholecystectomy for symptomatic patients or those with recurrent biliary colic [52](#page=52). #### 5.9.2 Acute cholecystitis Acute cholecystitis is an inflammation of the gallbladder wall, typically initiated by cystic duct obstruction rather than infection. It occurs in about 10% of patients with gallstones and can progress to chronic cholecystitis [53](#page=53). * **Clinical Features:** * Symptoms: Constant RUQ or epigastric pain (may radiate to the right shoulder/scapula), nausea, vomiting, anorexia [53](#page=53). * Signs: RUQ tenderness, rebound tenderness, positive Murphy sign (inspiratory arrest on palpation), hypoactive bowel sounds, low-grade fever, leukocytosis [53](#page=53). * **Diagnosis:** * RUQ ultrasound is the test of choice, showing a thickened gallbladder wall, pericholecystic fluid, a distended gallbladder, and stones [53](#page=53). * CT scan for complications [53](#page=53). * HIDA scan can confirm cystic duct obstruction if the gallbladder is not visualized [53](#page=53). * **Complications:** Gangrenous cholecystitis, perforation, emphysematous cholecystitis, cholecystoenteric fistula (leading to gallstone ileus), and empyema of the gallbladder [53](#page=53). * **Treatment:** Admission for IV fluids, NPO status, IV antibiotics, analgesics, and electrolyte correction. Early cholecystectomy (within 24–48 hours) is preferred. For critically ill patients, percutaneous cholecystostomy may be performed [53](#page=53). #### 5.9.3 Acalculous cholecystitis Acalculous cholecystitis is acute cholecystitis occurring *without* gallstones. It is seen in critically ill patients and is caused by dehydration, ischemia, burns, trauma, or the postoperative state. Symptoms are similar to acute cholecystitis (RUQ pain, fever, leukocytosis) but may be subtle due to the patient's critical condition. Diagnosis is made via ultrasound (showing inflammation but no stones) and CT scan for complications. Treatment involves emergent cholecystectomy or, if the patient is too unstable, percutaneous drainage (cholecystostomy) [54](#page=54). #### 5.9.4 Choledocholithiasis Choledocholithiasis is the presence of stones in the common bile duct (CBD) [55](#page=55). * **Types of Stones:** * **Primary stones:** Originate in the CBD, usually pigmented [55](#page=55). * **Secondary stones (95%):** Originate in the gallbladder and migrate to the CBD [55](#page=55). * **Major Complications:** Cholangitis, obstructive jaundice, acute pancreatitis, biliary colic, and biliary cirrhosis [55](#page=55). * **Clinical Features:** Can be asymptomatic for years. The symptomatic phase includes RUQ or epigastric pain and jaundice [55](#page=55). * **Diagnosis:** * Labs: Elevated total and direct bilirubin, elevated ALP [55](#page=55). * RUQ ultrasound: Initial test, but only detects about 50% of CBD stones [55](#page=55). * ERCP: Gold standard for diagnosis and therapy (stone removal) [55](#page=55). * PTC (percutaneous transhepatic cholangiography): An alternative when ERCP is not feasible [55](#page=55). * **Treatment:** ERCP with sphincterotomy and stone extraction is the preferred treatment. Stent placement is common. Laparoscopic choledocholithotomy is reserved for select cases [55](#page=55). #### 5.9.5 Cholangitis Cholangitis is an infection of the biliary tract secondary to obstruction, leading to bile stasis and bacterial overgrowth [56](#page=56). * **Common Causes:** Choledocholithiasis (60%), post-operative strictures, ERCP/PTC injury, pancreatic/biliary neoplasm, choledochal cysts [56](#page=56). * **Pathophysiology:** Obstruction leads to increased ductal pressure, stasis, bacterial translocation, and systemic infection [56](#page=56). * **Clinical Features:** Charcot's triad: RUQ pain, jaundice, and fever. Reynolds' pentad includes Charcot's triad plus septic shock and altered mental status (AMS). Patients may be acutely ill but lack significant abdominal signs [56](#page=56). * **Diagnosis:** * Labs: Elevated conjugated bilirubin, leukocytosis, mild LFT elevations [56](#page=56). * RUQ Ultrasound: First-line, shows duct dilation and stones, but has limited sensitivity for CBD stones [56](#page=56). * Cholangiography (ERCP or PTC): Definitive diagnostic and therapeutic tool [56](#page=56). * **Management:** * **Initial:** Resuscitation with IV fluids, vital sign monitoring, and broad-spectrum IV antibiotics [56](#page=56). * **Definitive Drainage (if stable after ≈48 hours):** ERCP with sphincterotomy and stone extraction is preferred. PTC is an option if ERCP is not possible or the duct is dilated. Surgical drainage may be required [56](#page=56). * **Urgent Decompression:** For unstable patients or those with Reynolds' pentad, requiring ICU care [56](#page=56). * **Complications:** Hepatic abscess, sepsis, and multi-organ failure, all associated with high mortality [56](#page=56). > **Mnemonic:** "C H O L A N G I T I S" can be an exam hint: **C**harcot triad = **C**linical clue [56](#page=56). > **Exam Pointer:** If Charcot's triad is present along with shock or AMS, it signifies Reynolds' pentad and requires emergency drainage, not just antibiotics [56](#page=56). #### 5.9.6 Primary Sclerosing Cholangitis (PSC) PSC is a chronic, idiopathic, progressive disease of intrahepatic and extrahepatic bile ducts, leading to inflammation, fibrosis, strictures, cholestasis, cirrhosis, and liver failure [57](#page=57). * **Associations:** Strong association with Ulcerative Colitis (50–70%), and less so with Crohn disease [57](#page=57). * **Complications:** Cholangiocarcinoma (20–30% risk), recurrent cholangitis (~15%), and secondary biliary cirrhosis leading to liver failure and portal hypertension [57](#page=57). * **Clinical Features:** Insidious onset with jaundice, pruritus, fatigue, malaise, and weight loss [57](#page=57). * **Diagnosis:** * Imaging: ERCP shows "beading" of bile ducts; PTC reveals strictures and dilatations [57](#page=57). * Labs: Cholestatic pattern (elevated ALP, elevated GGT), later elevated bilirubin [57](#page=57). * **Treatment:** No curative therapy other than liver transplantation. Dominant strictures can be managed with ERCP and stent placement or balloon dilatation. Symptomatic relief for pruritus can be achieved with cholestyramine [57](#page=57). > **Differential Pearl:** PSC typically affects men more than women, is associated with UC, and diagnosed via ERCP. PBC affects women more than men, is AMA-positive, primarily intrahepatic, and responds to ursodeoxycholic acid [57](#page=57). > **High-Yield Notes:** The course of PSC is not improved by colectomy for UC. PSC patients require lifelong monitoring for cholangiocarcinoma; abrupt deterioration may indicate malignancy [57](#page=57). #### 5.9.7 Primary Biliary Cholangitis (PBC) PBC is a chronic, progressive cholestatic liver disease involving the autoimmune destruction of intrahepatic bile ducts, leading to cholestasis, fibrosis, and cirrhosis [58](#page=58). * **General:** Autoimmune in nature, associated with other autoimmune diseases. Primarily affects middle-aged women [58](#page=58). * **Pathophysiology:** Autoimmune attack on small intrahepatic bile ducts causes bile retention, cholestasis, hepatocyte injury, fibrosis, and eventually portal hypertension and cirrhosis in the long term [58](#page=58). * **Clinical Features:** Early symptoms include fatigue and pruritus (cholestatic itch). Later, jaundice may develop. RUQ discomfort, xanthomas/xanthelasmata (due to elevated cholesterol), and osteoporosis (due to fat malabsorption and Vitamin D deficiency) are also seen. Signs of portal hypertension appear in advanced stages [58](#page=58). * **Diagnosis:** * LFT pattern: Cholestatic (elevated ALP, elevated GGT) [58](#page=58). * **AMA (anti-mitochondrial antibodies) are positive in 90–95%**, serving as a hallmark [58](#page=58). * Elevated IgM and elevated cholesterol (specifically HDL) [58](#page=58). * Imaging (US/CT) is used to exclude obstruction, but not diagnostic for PBC itself [58](#page=58). * Liver biopsy may be performed for staging if needed [58](#page=58). * **Complications:** Cirrhosis with portal hypertension, hepatic failure, and cholestatic complications like fat malabsorption and bone disease [58](#page=58). * **Treatment:** First-line therapy is Ursodeoxycholic Acid (UDCA), which slows disease progression. Symptomatic treatment includes cholestyramine for pruritus and calcium/Vitamin D/bisphosphonates for osteoporosis. Liver transplantation is the definitive treatment for progressive or end-stage disease [58](#page=58). #### 5.9.8 Gallbladder & Biliary Tract Carcinoma and Choledochal Cysts * **Gallbladder Carcinoma:** Mostly adenocarcinoma. Risk factors include chronic gallstones and porcelain gallbladder (calcified), which carries a high cancer risk. Clinical presentation includes RUQ pain, weight loss, anorexia, and late-stage jaundice or a palpable RUQ mass. Diagnosis is via imaging (US/CT) and biopsy. Most present late, leading to a poor prognosis (median survival < 1 year). Radical resection is curative if early-stage [59](#page=59). * **Cholangiocarcinoma (bile-duct cancer):** Can be proximal (Klatskin tumor - most common, poor prognosis), distal (best chance for resection), or intrahepatic (least common). Risk factors include PSC (primary), UC, choledochal cysts, and *Clonorchis* infection. Clinical features include obstructive jaundice, pruritus, and weight loss. Diagnosis is via cholangiography (ERCP/PTC). Resection is possible in rare early cases; otherwise, stenting is used for palliation. Overall survival is poor [59](#page=59). * **Choledochal Cysts (congenital biliary dilatation):** Cystic dilatation of extra- and intrahepatic ducts. More common in females. The classic triad (though not always present) is RUQ/epigastric pain, jaundice, and fever. Major complications include cholangiocarcinoma (≈20% long-term risk), recurrent cholangitis, hepatic abscess, pancreatitis, and cirrhosis. Diagnosis can be made via US or ERCP. Treatment involves complete surgical resection and biliary-enteric reconstruction to remove cancer risk and restore drainage [59](#page=59). > **Quick Mnemonics & Exam Bait:** "PUCC" mnemonic for cholangiocarcinoma risks: **P**SC, **U**C, **C**holedochal cysts, **C**lonorchis infection [59](#page=59). > **Exam Bait:** Porcelain gallbladder suggests prophylactic cholecystectomy due to high cancer risk [59](#page=59). > **Exam Bait:** Choledochal cysts carry a high long-term risk of cholangiocarcinoma, necessitating surgery [59](#page=59). > **Clinical Pearl:** Any chronic biliary stasis or dilation raises suspicion for malignant transformation. PSC patients require surveillance for cholangiocarcinoma. ERCP is both diagnostic and therapeutic for stone extraction and stenting [59](#page=59). #### 5.9.9 Bile duct stricture Bile duct stricture is the narrowing of a bile duct, leading to obstructive jaundice [60](#page=60). * **Causes:** Iatrogenic injury (most common, e.g., post-cholecystectomy, liver transplant), recurrent choledocholithiasis, chronic pancreatitis, and PSC [60](#page=60). * **Clinical Features:** Obstructive jaundice, pruritus, dark urine, and pale (clay-colored) stools [60](#page=60). * **Complications:** Secondary biliary cirrhosis, liver abscess, and ascending cholangitis [60](#page=60). * **Treatment:** Endoscopic stenting is preferred. Surgical bypass may be necessary if stenting fails [60](#page=60). #### 5.9.10 Biliary dyskinesia Biliary dyskinesia is a motor dysfunction of the sphincter of Oddi, causing biliary colic *without* gallstones [60](#page=60). * **Clinical Features:** Recurrent RUQ pain and symptoms of biliary colic, with imaging showing no stones [60](#page=60). * **Diagnosis:** HIDA scan with CCK administration. A low ejection fraction indicates dyskinesia [60](#page=60). * **Treatment:** Laparoscopic cholecystectomy is the treatment; endoscopic sphincterotomy is an alternative [60](#page=60). --- # Pancreatic diseases This topic covers inflammatory conditions of the pancreas, including acute and chronic pancreatitis, and malignant neoplasms, specifically pancreatic cancer [31](#page=31) [32](#page=32) [33](#page=33) [34](#page=34) [35](#page=35). ### 6.1 Acute pancreatitis Acute pancreatitis is characterized by the premature activation of pancreatic enzymes, leading to pancreatic autodigestion [31](#page=31) [32](#page=32). #### 6.1.1 Causes of acute pancreatitis The mnemonic "GET SMASHED" is helpful for recalling the major causes: * **G**allstones (approximately 40%) [31](#page=31) [32](#page=32). * **E**thanol (alcohol) (approximately 30%) [31](#page=31) [32](#page=32). * **T**rauma [31](#page=31) [32](#page=32). * **S**teroids [31](#page=31) [32](#page=32). * **M**umps (viral) [31](#page=31) [32](#page=32). * **A**utoimmune pancreatitis [31](#page=31) [32](#page=32). * **S**corpion sting [31](#page=31) [32](#page=32). * **H**ypertriglyceridemia / Hypercalcemia [31](#page=31) [32](#page=32). * **E**RCP (Endoscopic Retrograde Cholangiopancreatography) [31](#page=31) [32](#page=32). * **D**rugs (e.g., sulfonamides, thiazides, HIV medications) [31](#page=31) [32](#page=32). #### 6.1.2 Clinical features of acute pancreatitis * **Pain:** Severe epigastric pain that typically radiates to the back in a belt-like fashion [31](#page=31) [32](#page=32). * **Gastrointestinal symptoms:** Nausea, vomiting, and anorexia are common [31](#page=31) [32](#page=32). * **Systemic signs:** Low-grade fever, tachycardia, hypotension, and leukocytosis may be present [31](#page=31) [32](#page=32). * **Abdominal findings:** Decreased bowel sounds and signs of ileus can occur [31](#page=31) [32](#page=32). * **Hemorrhagic signs (severe cases):** * Cullen's sign: Periumbilical ecchymosis [31](#page=31) [32](#page=32). * Grey-Turner's sign: Flank ecchymosis [31](#page=31) [32](#page=32). * Fox's sign: Inguinal ecchymosis [31](#page=31) [32](#page=32). #### 6.1.3 Diagnosis of acute pancreatitis The diagnosis is typically made using the "2 of 3 rule": 1. Typical abdominal pain [31](#page=31) [32](#page=32). 2. Serum lipase (or amylase) elevated at least three times the upper limit of normal. Lipase is more specific than amylase [31](#page=31) [32](#page=32). 3. Imaging (e.g., CT scan) consistent with pancreatitis [31](#page=31) [32](#page=32). #### 6.1.4 Laboratory and imaging findings * **Laboratory tests:** * Serum lipase and amylase levels [31](#page=31) [32](#page=32). * Liver function tests (LFTs) to assess for gallstone etiology [31](#page=31) [32](#page=32). * Glucose levels may be elevated [31](#page=31) [32](#page=32). * Calcium levels may be decreased due to fat saponification [31](#page=31) [32](#page=32). * Leukocytosis is common [31](#page=31) [32](#page=32). * **Imaging:** * Abdominal ultrasound can identify gallstones or biliary obstruction [31](#page=31) [32](#page=32). * CT scan of the abdomen is the best modality for assessing severity and complications [31](#page=31) [32](#page=32). #### 6.1.5 Complications of acute pancreatitis * **Pancreatic necrosis:** Can be sterile or infected, with infected necrosis carrying a high mortality rate [31](#page=31) [32](#page=32). * **Pancreatic pseudocyst:** A collection of pancreatic fluid that typically forms 2–3 weeks after an attack. Cysts less than 5 cm are usually observed, while those greater than 5 cm may require drainage [31](#page=31) [32](#page=32). * **Hemorrhagic pancreatitis** [31](#page=31) [32](#page=32). * **Acute Respiratory Distress Syndrome (ARDS)** [31](#page=31) [32](#page=32). * **Ascites and pleural effusion** [31](#page=31) [32](#page=32). * **Ascending cholangitis**, particularly if the etiology is gallstones [31](#page=31) [32](#page=32). #### 6.1.6 Treatment of acute pancreatitis Treatment priorities focus on supportive care and addressing the underlying cause: * **Supportive care (for most patients):** * NPO (Nil Per Os): Bowel rest is crucial [31](#page=31) [32](#page=32). * Aggressive intravenous fluid resuscitation, with Lactated Ringer's solution being preferred [31](#page=31) [32](#page=32). * Analgesia, with fentanyl often preferred over morphine [31](#page=31) [32](#page=32). * Electrolyte correction [31](#page=31) [32](#page=32). * Nasogastric (NG) tube placement if persistent vomiting or ileus occurs [31](#page=31) [32](#page=32). * **Cause-directed therapy:** * For gallstone pancreatitis, cholecystectomy after recovery is recommended. ERCP is indicated if there is biliary obstruction [31](#page=31) [32](#page=32). * **Management of severe or necrotizing disease:** * Admission to the Intensive Care Unit (ICU) [31](#page=31) [32](#page=32). * Early enteral nutrition (within 72 hours) is recommended [31](#page=31) [32](#page=32). * Antibiotics may be considered if necrosis exceeds 30%, but caution is advised [31](#page=31) [32](#page=32). * Percutaneous or surgical debridement for infected necrosis [31](#page=31) [32](#page=32). * Drainage of pseudocysts larger than 5 cm or those causing symptoms [31](#page=31) [32](#page=32). #### 6.1.7 Prognosis and severity assessment * **Ranson criteria:** A severity assessment tool using admission and 48-hour criteria to predict mortality. * 0–2 criteria: Low mortality (approximately 1%) [31](#page=31) [32](#page=32). * 3–4 criteria: Moderate mortality (approximately 15%) [31](#page=31) [32](#page=32). * ≥5 criteria: High mortality (up to 40%+) [31](#page=31) [32](#page=32). * **High-yield pearls:** * Hypocalcemia is a poor prognostic sign due to fat saponification [31](#page=31) [32](#page=32). * Aggressive early IV fluid administration reduces complications [31](#page=31) [32](#page=32). * Hemorrhagic signs (Cullen's/Grey-Turner's) indicate severe disease [31](#page=31) [32](#page=32). > **Tip:** While amylase and lipase are key for acute pancreatitis diagnosis, they are often normal in chronic pancreatitis. ### 6.2 Chronic pancreatitis Chronic pancreatitis is defined by persistent inflammation leading to fibrosis of the pancreas, resulting in irreversible destruction of both exocrine and endocrine functions [33](#page=33). #### 6.2.1 Main causes of chronic pancreatitis * **Alcoholism:** The most common cause, accounting for over 80% of cases [33](#page=33). * Hereditary pancreatitis [33](#page=33). * Tropical pancreatitis [33](#page=33). * Autoimmune pancreatitis [33](#page=33). * Idiopathic causes, duct anomalies, and toxins [33](#page=33). #### 6.2.2 Clinical features of chronic pancreatitis * **Pain:** Chronic epigastric pain, often radiating to the back, occurring in about 50% of patients. Pain may be recurrent or persistent and is often worse after alcohol consumption or eating [33](#page=33). * **Weight loss:** Significant due to malabsorption and anorexia [33](#page=33). * **Steatorrhea:** Fatty, bulky stools, a late sign indicating exocrine insufficiency [33](#page=33). * **Diabetes mellitus:** Resulting from the loss of pancreatic islets [33](#page=33). #### 6.2.3 Diagnosis of chronic pancreatitis * **CT scan:** The study of choice, useful for identifying calcifications, ductal changes, and pseudocysts [33](#page=33). * **Abdominal radiograph:** Highly specific for detecting pancreatic calcifications [33](#page=33). * **ERCP (Endoscopic Retrograde Cholangiopancreatography):** Considered the gold standard for visualizing ductal anatomy, revealing strictures and the characteristic "chain of lakes" appearance [33](#page=33). * **Laboratory tests:** Serum amylase and lipase levels are often normal, which is a key diagnostic differentiator from acute pancreatitis [33](#page=33). #### 6.2.4 Complications of chronic pancreatitis * Narcotic dependence due to chronic pain [33](#page=33). * Diabetes mellitus, affecting up to approximately 70% of patients [33](#page=33). * Malabsorption and steatorrhea, leading to nutritional deficiencies [33](#page=33). * Pancreatic pseudocysts, which may necessitate drainage [33](#page=33). * Biliary (common bile duct) obstruction, leading to obstructive jaundice [33](#page=33). * Effusions (pleural, pericardial, peritoneal) [33](#page=33). * Increased risk of pancreatic carcinoma [33](#page=33). #### 6.2.5 Treatment of chronic pancreatitis Treatment principles focus on conservative management and surgical intervention for refractory cases: * **Nonoperative management (mainstay):** * Pain control, with careful use of narcotics [33](#page=33). * Bowel rest (NPO) during acute flares [33](#page=33). * Pancreatic enzyme replacement therapy combined with H2 blockers [33](#page=33). * Dietary recommendations: small, frequent, low-fat meals, and strict alcohol abstinence [33](#page=33). * Insulin therapy for endocrine failure (diabetes) [33](#page=33). * **Surgical management:** Indicated for refractory pain, ductal obstruction, or complications. Procedures may include: * Pancreaticojejunostomy (duct drainage) [33](#page=33). * Resection (distal pancreatectomy or Whipple procedure) in selected patients [33](#page=33). > **Tip:** The classic triad of chronic pancreatitis is steatorrhea, pancreatic calcifications, and diabetes mellitus. ### 6.3 Pancreatic cancer Pancreatic cancer is a malignant neoplasm of the pancreas with a generally poor prognosis. #### 6.3.1 General characteristics * **Age:** Most commonly diagnosed in elderly patients, with 75% occurring in individuals over 60 years old. It is rare before age 40 [34](#page=34) [35](#page=35). * **Demographics:** More common in African Americans [34](#page=34) [35](#page=35). * **Anatomic location:** * Head of the pancreas (75%) - most common site [34](#page=34) [35](#page=35). * Body (20%) [34](#page=34) [35](#page=35). * Tail (5–10%) [34](#page=34) [35](#page=35). #### 6.3.2 Risk factors * **Cigarette smoking:** The strongest and most high-yield risk factor [34](#page=34) [35](#page=35). * Chronic pancreatitis [34](#page=34) [35](#page=35). * Diabetes mellitus (especially new-onset) [34](#page=34) [35](#page=35). * Heavy alcohol use [34](#page=34) [35](#page=35). * Chemical exposure (e.g., benzidine, β-naphthylamine) [34](#page=34) [35](#page=35). #### 6.3.3 Prognosis The prognosis for pancreatic cancer is very poor, with most patients dying within months of diagnosis [34](#page=34) [35](#page=35). #### 6.3.4 Clinical features * **Abdominal pain:** A vague, dull ache present in approximately 90% of cases [34](#page=34) [35](#page=35). * **Jaundice:** Particularly common with tumors in the head of the pancreas, indicating common bile duct obstruction and advanced disease [34](#page=34) [35](#page=35). * **Constitutional symptoms:** Weight loss, anorexia, and fatigue [34](#page=34) [35](#page=35). * **Glucose intolerance/new diabetes:** Recent mild glucose intolerance or new onset of diabetes can be an early sign [34](#page=34) [35](#page=35). * **Migratory thrombophlebitis (Trousseau syndrome):** Occurs in about 10% of patients [34](#page=34) [35](#page=35). * **Courvoisier sign:** A palpable, non-tender gallbladder accompanied by jaundice [34](#page=34) [35](#page=35). #### 6.3.5 Diagnosis Pancreatic cancer is often diagnosed late due to vague early symptoms. * **CT scan:** The preferred imaging modality for diagnosis and staging [34](#page=34) [35](#page=35). * **ERCP:** Most sensitive for pancreatic head tumors and can distinguish lesions of the common bile duct, ampulla, or duodenum. It also allows for palliative stent placement [34](#page=34) [35](#page=35). * **Tumor markers:** * CA 19-9: Exhibits 83% sensitivity and 82% specificity [34](#page=34) [35](#page=35). * CEA (carcinoembryonic antigen): Less sensitive than CA 19-9 [34](#page=34) [35](#page=35). #### 6.3.6 Treatment * **Surgical resection:** The only chance for cure. * The Whipple procedure (pancreaticoduodenectomy) is the standard surgical approach [34](#page=34) [35](#page=35). * Approximately only 10% of patients are resectable at the time of diagnosis [34](#page=34) [35](#page=35). * The 5-year survival rate after resection is approximately 10% [34](#page=34) [35](#page=35). * **Management of unresectable disease:** * ERCP with biliary stenting for palliation of jaundice [34](#page=34) [35](#page=35). * Chemotherapy, potentially combined with radiation therapy [34](#page=34) [35](#page=35). * Symptom control, including nutrition and analgesia [34](#page=34) [35](#page=35). * End-of-life support is often required [34](#page=34) [35](#page=35). --- ## Common mistakes to avoid - Review all topics thoroughly before exams - Pay attention to formulas and key definitions - Practice with examples provided in each section - Don't memorize without understanding the underlying concepts

| Term | Definition | |------|------------| | Colonic Polyps | Growths that project from the lining of the colon. They are broadly classified into non-neoplastic (benign) and adenomatous (precancerous) types, requiring identification and often removal. | | Hyperplastic Polyps | A common type of non-neoplastic colonic polyp, accounting for about 90% of these growths. They are typically small, asymptomatic, and have no malignant potential. | | Juvenile Polyps | Non-neoplastic polyps found predominantly in children under 10 years old. These polyps are often vascular and are typically removed as a precautionary measure. | | Adenomatous Polyps | Precancerous growths in the colon that carry a risk of developing into adenocarcinoma. Their malignant potential increases with size, specific histology (villous being worst), presence of atypia, and shape. | | Tubular Adenoma | The most common type of adenomatous polyp, characterized by a predominantly tubular structure and generally considered to have the least malignant potential among adenomatous types. | | Tubulovillous Adenoma| An adenomatous polyp that exhibits a mix of tubular and villous architecture. These polyps represent an intermediate risk for malignant transformation compared to pure tubular or villous adenomas. | | Villous Adenoma | A type of adenomatous polyp with a predominantly villous (finger-like projections) structure. These polyps have the highest risk of malignant transformation among adenomatous types. | | Polypectomy | The surgical removal of a colonic polyp. This procedure is the standard treatment for most colonic polyps to prevent potential malignant progression. | | Diverticulosis | A condition characterized by the presence of multiple small outpouchings (diverticula) in the wall of the colon, typically caused by increased intraluminal pressure pushing the mucosa through weak spots. | | Diverticulitis | Inflammation of a colonic diverticulum, usually occurring when fecal matter obstructs a pouch, leading to bacterial invasion and microperforation, resulting in inflammation and potential complications. | | Fecalith | A hardened mass of stool that can obstruct a colonic diverticulum, serving as a common trigger for the development of diverticulitis. | | Colovesical Fistula | A rare but serious complication of diverticulitis, characterized by an abnormal connection between the colon and the bladder, often presenting with air in the urine. | | Peritonitis | Inflammation of the peritoneum, the membrane lining the abdominal cavity. This life-threatening condition can result from the free perforation of a colonic diverticulum during severe diverticulitis. | | Acute Mesenteric Ischemia | A condition characterized by the sudden and severe compromise of blood flow to the intestines, potentially leading to ischemia and infarction of bowel tissue. | | Chronic Mesenteric Ischemia | A condition resulting from long-term atherosclerotic occlusive disease affecting the mesenteric arteries, causing reduced blood flow to the intestines, typically presenting as postprandial abdominal pain. | | Small Bowel Obstruction | A mechanical or functional blockage within the small intestine, leading to dilation, vomiting, fluid loss, and increased intraluminal pressure, with a significant risk of ischemia, necrosis, and perforation. | | Abdominal Angina | A symptom of chronic mesenteric ischemia, characterized by dull, crampy abdominal pain that typically occurs after eating, due to the increased demand for splanchnic blood flow during digestion. | | Mesenteric Angiography | An imaging technique that visualizes the blood vessels of the mesentery, used as the definitive diagnostic and sometimes therapeutic tool for mesenteric ischemia by identifying occlusions and allowing intervention. | | CT Angiography | A rapid, modern diagnostic imaging test that uses computed tomography and contrast dye to visualize the mesenteric arteries, helping to detect occlusions and assess for bowel wall hypoenhancement indicative of ischemia. | | Nonocclusive Ischemia | A form of acute mesenteric ischemia occurring in critically ill patients due to low systemic blood flow or vasospasm, rather than a direct blockage of the mesenteric arteries. | | Closed-Loop Obstruction | A type of small bowel obstruction where the intestinal lumen is blocked at two distinct points, creating a high risk of strangulation and requiring urgent surgical intervention. | | Adhesions | Bands of scar tissue that can form in the abdomen after surgery or inflammation, representing the most common cause of small bowel obstruction in adults by mechanically kinking or compressing the bowel. | | Valvulae Conniventes | Folds of the intestinal mucosa that extend across the entire lumen of the small bowel, visible on X-rays and indicative of the small intestine. Their presence in dilated loops can suggest obstruction. | | Strangulation | A severe complication of bowel obstruction where blood supply to the obstructed segment of intestine is compromised, leading to ischemia, necrosis, and potentially perforation. | | Obstipation | The complete absence of bowel movements (gas or stool), a key clinical feature of complete small bowel obstruction. | | Mesenteric Swirl Sign | An imaging finding on CT scans suggestive of mesenteric ischemia, characterized by the twisting of mesenteric vessels around a blocked artery or vein. | | Lysis of Adhesions | A surgical procedure to cut or release adhesions within the abdominal cavity, commonly performed to relieve small bowel obstruction caused by these fibrous bands. | | Necrotic Bowel | Intestinal tissue that has died due to a lack of blood supply (ischemia), a critical consequence of untreated mesenteric ischemia or severe bowel obstruction with strangulation. | | Volvulus | A twisting of a segment of the intestine upon itself, which can lead to obstruction and compromise of its blood supply, representing a surgical emergency. | | SMA Syndrome | Superior Mesenteric Artery Syndrome, a rare cause of intestinal obstruction where the third portion of the duodenum is compressed between the superior mesenteric artery and the aorta, often due to weight loss. | | Postprandial Pain | Pain that occurs after eating, a hallmark symptom of chronic mesenteric ischemia due to the increased metabolic demands of digestion exceeding the compromised blood supply to the intestines. | | Ischemia | A condition in which an inadequate blood supply damages cells or tissues. In the context of mesenteric ischemia, it refers to insufficient blood flow to the intestines. | | Infarction | Tissue death caused by a lack of blood supply, a severe outcome of prolonged or acute mesenteric ischemia where bowel tissue undergoes irreversible damage. | | Hypercoagulable State | A condition where the blood has an increased tendency to clot, which can be a predisposing factor for venous mesenteric ischemia or thrombosis in other mesenteric vessels. | | Metabolic Alkalosis | An electrolyte imbalance characterized by an excess of bicarbonate or loss of acid from the body, often seen in patients with small bowel obstruction due to vomiting and fluid loss. | | Hypochloremia | An abnormally low level of chloride in the blood, frequently occurring in patients with significant vomiting due to small bowel obstruction, contributing to electrolyte disturbances. | | Hypokalemia | An abnormally low level of potassium in the blood, a common consequence of fluid and electrolyte losses from vomiting in small bowel obstruction, which can lead to cardiac and muscular issues. | | Leukocytosis | An elevated white blood cell count, often indicative of inflammation or infection, and can be a red flag for complications like peritonitis or strangulation in cases of bowel obstruction. | | Lactic Acidosis | A buildup of lactic acid in the bloodstream, often a late indicator of severe tissue hypoperfusion and ischemia, and a sign of poor prognosis in acute mesenteric ischemia. | | Thumbprinting | An imaging sign on contrast studies of the bowel where thickened mucosal folds resemble thumbprints, indicating mucosal edema and submucosal hemorrhage, often seen in mesenteric ischemia. | | Embolectomy | A surgical procedure to remove a blood clot (embolus) from a blood vessel, used as a treatment for acute mesenteric ischemia caused by arterial embolism. | | Thrombolysis | The process of dissolving blood clots, often administered via angiography for acute mesenteric ischemia to restore blood flow to the affected part of the intestine. | | Revascularization | Surgical restoration of blood flow to an organ or tissue, typically performed for chronic mesenteric ischemia to bypass or open blocked mesenteric arteries, often providing significant symptom relief. | | NPO | An abbreviation for "nil per os," meaning nothing by mouth. It is a standard initial management step for patients with bowel obstruction to rest the gastrointestinal tract. | | Nasogastric Tube (NG Tube) | A tube inserted through the nose into the stomach, used for gastric decompression in bowel obstruction by removing accumulated air and fluid, relieving pressure and reducing vomiting. | | Short Bowel Syndrome | A malabsorption disorder resulting from extensive surgical resection of the small intestine, leading to reduced surface area for nutrient absorption and potential for dehydration and malnutrition. | | Intussusception | A condition where one segment of the intestine telescopes into another, causing obstruction and potentially compromising blood supply. It is a cause of small bowel obstruction, particularly in children. | | Hernia (Incarcerated) | A condition where a portion of the intestine or other organ protrudes through a weak spot in the abdominal wall and becomes trapped, leading to obstruction and potential strangulation. | | Neoplasm / Carcinomatosis | A tumor or widespread cancer within the abdomen, which can cause obstruction by compressing or invading the small bowel, leading to a mechanical blockage. | | Atherosclerosis | A disease characterized by the buildup of plaque within arteries, leading to hardening and narrowing of the vessels. It is the primary cause of chronic mesenteric ischemia and can also contribute to arterial thrombosis. | | Splanchnic Blood Flow | The blood flow to the organs of the digestive system, including the intestines, stomach, liver, spleen, and pancreas. Increased demand during digestion can exacerbate issues in reduced flow states. | | Mesenteric Vein Thrombosis | A blood clot forming in the veins that drain blood from the intestines, which can impede blood outflow and lead to bowel swelling and ischemia. | | Arterial Embolism | A sudden blockage of an artery by a traveling blood clot or other substance, often originating from the heart, that can lead to acute mesenteric ischemia. | | Arterial Thrombosis | The formation of a blood clot within an artery, usually due to atherosclerosis, which can lead to acute or chronic occlusion of mesenteric arteries and resultant ischemia. | | Occlusive Disease | A condition characterized by the blockage or narrowing of blood vessels, specifically referring to atherosclerotic occlusive disease affecting the celiac, superior mesenteric, or inferior mesenteric arteries. | | Sepsis | A life-threatening complication caused by the body's overwhelming response to infection, which can develop from bowel infarction or perforation related to mesenteric ischemia or obstruction. | | Dehydration | A state where the body loses more fluid than it takes in, often occurring with vomiting and poor oral intake in small bowel obstruction, leading to electrolyte imbalances and hypovolemia. | | Hypovolemia | Low blood volume, often a consequence of severe dehydration and fluid sequestration in the bowel lumen during obstruction, leading to reduced blood pressure and increased heart rate. | | Achalasia | A motor disorder of the esophagus characterized by the failure of the lower esophageal sphincter (LES) to relax and aperistalsis of the esophageal body. | | Adenocarcinoma | A type of cancer that originates in glandular cells, commonly found in the distal esophagus and gastric junction, often associated with GERD and Barrett esophagus. | | Aperistalsis | The absence of normal peristaltic muscular contractions in the esophagus, leading to impaired movement of food down the digestive tract. | | Autoimmune Gastritis | A chronic inflammation of the gastric mucosa caused by autoantibodies that destroy parietal cells, leading to decreased acid and intrinsic factor production. | | Barrett Esophagus | A condition where the normal squamous epithelium of the esophagus is replaced by columnar epithelium, often a consequence of chronic gastroesophageal reflux disease (GERD). | | Barium Swallow | An imaging technique using barium contrast to visualize the esophagus, stomach, and duodenum, helpful in diagnosing structural abnormalities and motility disorders. | | Boerhaave Syndrome | A transmural tear or rupture of the esophagus, typically occurring after forceful vomiting or retching, leading to mediastinal contamination and a surgical emergency. | | Bronchiectasis | A chronic condition where the lung airways become damaged and widened, often a complication of aspiration due to esophageal pathologies. | | Cancer | A malignant tumor characterized by uncontrolled cell growth that can invade surrounding tissues and spread to distant parts of the body. | | Chest Pain | Discomfort or pain felt in the chest area, which can be a symptom of various esophageal and gastric pathologies, sometimes mimicking angina. | | Chronic Gastritis | Long-standing inflammation of the gastric mucosa, most commonly caused by *H. pylori* infection or autoimmune processes, potentially leading to atrophy and increased cancer risk. | | Cricopharyngeal Myotomy | A surgical procedure involving the cutting of the cricopharyngeal muscle to improve relaxation and facilitate swallowing, often used for Zenker diverticulum. | | Cytoprotection | Measures or substances that protect the gastric mucosa from damage by aggressive factors, such as sucralfate and misoprostol. | | Dysphagia | Difficulty or discomfort in swallowing, a common symptom across various esophageal disorders, often described as a sensation of food sticking in the throat or chest. | | Diffuse Esophageal Spasm | A motility disorder characterized by uncoordinated, simultaneous contractions of multiple segments of the esophageal body, leading to chest pain and dysphagia. | | Epiphrenic Diverticulum | A pouch that protrudes from the wall of the lower esophagus, often associated with esophageal motility disorders like achalasia or diffuse esophageal spasm. | | Esophageal Cancer | Malignant tumors arising from the lining of the esophagus, primarily squamous cell carcinoma and adenocarcinoma, with varying risk factors and locations. | | Esophageal Diverticula | Outpouchings or sacs that form in the wall of the esophagus, categorized by location (Zenker, traction, epiphrenic) and often related to motility issues or inflammation. | | Esophageal Perforation | A full-thickness tear in the esophageal wall, leading to leakage of contents into the mediastinum or pleural space, a potentially life-threatening condition. | | Esophageal Stricture | A narrowing of the esophagus, often caused by inflammation, scarring, or tumors, leading to dysphagia. | | Esophagitis | Inflammation of the esophageal lining, commonly caused by gastroesophageal reflux disease (GERD), infections, or irritants. | | Esophagomyotomy | A surgical procedure where the muscular layer of the esophagus is cut to relieve spasms or strictures, often performed for achalasia or diffuse esophageal spasm. | | Forceful Dilation | A therapeutic technique using pneumatic balloons to stretch and open narrowed or non-relaxing areas of the esophagus, such as the LES in achalasia. | | Gastric Adenocarcinoma | The most common type of gastric cancer, originating from the glandular cells of the stomach lining, influenced by factors like *H. pylori* and chronic gastritis. | | Gastric Cancer | Malignant tumors originating in the stomach, most commonly adenocarcinoma, with a significant association with *H. pylori* infection and chronic atrophic gastritis. | | Gastric Diverticulum | A pouch that protrudes from the wall of the stomach, a rare condition typically asymptomatic but can lead to complications like inflammation or bleeding. | | Gastric Empties | The process by which the stomach contents are moved into the small intestine, which can be delayed in certain gastric pathologies leading to obstruction. | | Gastric Hiatal Hernias | A condition where a portion of the stomach protrudes through the diaphragm into the chest cavity, categorized into sliding and paraesophageal types. | | Gastric Lymphoma | A non-Hodgkin lymphoma that primarily affects the stomach, most commonly MALT lymphoma associated with *H. pylori* infection. | | Gastric Outlet Obstruction | A blockage at the exit of the stomach, preventing food from passing into the small intestine, often caused by ulcers, tumors, or inflammation. | | Gastric Ulcer | An open sore that develops on the lining of the stomach, usually caused by *H. pylori* infection or NSAID use, characterized by pain that may worsen with eating. | | Gastritis | Inflammation of the gastric mucosa, which can be acute (sudden onset) or chronic (long-standing), caused by various irritants, infections, or autoimmune processes. | | Gastroesophageal Junction (GEJ) | The anatomical area where the esophagus meets the stomach. | | Haematemesis | Vomiting of blood, which can range from streaks to large amounts of bright red blood, often indicative of bleeding in the upper gastrointestinal tract. | | Hamman Sign | A crunching or crackling sound heard over the heart during systole, caused by air in the mediastinum, indicative of esophageal perforation. | | *H. pylori* Infection | Infection with the bacterium *Helicobacter pylori*, a major cause of peptic ulcer disease and chronic gastritis, and a risk factor for gastric cancer. | | Heller Myotomy | A surgical procedure that involves cutting the muscle of the lower esophageal sphincter to relieve the pressure and allow for easier passage of food, used for achalasia. | | Hiatal Hernia | A condition where the upper part of the stomach bulges through the diaphragm into the chest cavity. | | Hoarseness | A raspy or rough sound to the voice, which can be a symptom of esophageal cancer if the recurrent laryngeal nerve is involved. | | Idiopathic | A condition where the cause is unknown or spontaneous. | | Incarceration | A complication of a hernia where the herniated organ becomes trapped and cannot be reduced back into its normal position. | | Intestinal Metaplasia | A precancerous change where the normal lining of the stomach is replaced by cells similar to those found in the intestine, often a precursor to gastric cancer. | | Iron Deficiency Anemia | A condition characterized by a lack of sufficient iron in the body, leading to a reduced number of red blood cells and symptoms like fatigue and pallor, associated with Plummer-Vinson syndrome. | | Kölonychia | Spoon-shaped fingernails, a sign that can be associated with iron deficiency anemia, often seen in Plummer-Vinson syndrome. | | Linitis Plastica | A type of gastric cancer characterized by diffuse infiltration of the stomach wall, causing it to become thick and rigid, with a poor prognosis. | | Lower Esophageal Sphincter (LES) | The muscular ring at the bottom of the esophagus that relaxes to allow food into the stomach and contracts to prevent reflux. | | Mallory-Weiss Syndrome | A condition characterized by a mucosal tear at or just below the gastroesophageal junction, typically occurring after forceful vomiting or retching, leading to bleeding. | | Manometry | A diagnostic test that measures the pressure and contractions of the esophagus and its sphincters to assess motility disorders. | | Mediastinal Air | The presence of air in the mediastinum, the space between the lungs, often seen on imaging as a sign of esophageal perforation. | | Metaplasia | The transformation of one mature cell type into another, often occurring in response to chronic irritation or inflammation, such as in Barrett esophagus. | | MALT Lymphoma | Mucosa-Associated Lymphoid Tissue lymphoma, a type of non-Hodgkin lymphoma that arises in the tissues of the digestive tract, often linked to *H. pylori* infection. | | Nasopharyngeal Carcinoma | Cancer that develops in the nasopharynx, the upper part of the throat behind the nose, and is a risk factor for esophageal squamous cell carcinoma. | | Nissen Fundoplication | A surgical procedure to treat severe GERD or hiatal hernias, where the top part of the stomach is wrapped around the lower esophagus to strengthen the valve. | | Noncardiac Chest Pain | Chest pain that is not related to the heart, often caused by esophageal motility disorders like diffuse esophageal spasm or GERD. | | NSAIDs | Nonsteroidal anti-inflammatory drugs, commonly used for pain relief and inflammation, but can cause gastric irritation and ulceration. | | Odynophagia | Painful swallowing, often a late symptom of esophageal cancer indicating invasion into surrounding tissues. | | Oesophageal Diverticulum | A pouch or sac that protrudes from the esophagus wall. | | Oesophageal Diverticulosis | The presence of multiple esophageal diverticula. | | Oesophageal Perforation | A full-thickness tear through the esophageal wall. | | Oesophageal Spasm | Involuntary contractions of the esophagus muscles, which can cause chest pain and difficulty swallowing. | | Oesophagitis | Inflammation of the esophagus. | | Oesophagogastric Junction | The point where the esophagus joins the stomach. | | Oesophagus | The muscular tube connecting the pharynx (throat) with the stomach. | | Palliative Stenting | The placement of a tube (stent) into a narrowed or obstructed area to relieve symptoms and improve quality of life, often used in advanced cancer. | | Paraesophageal Hernia | A type of hiatal hernia where the gastroesophageal junction remains below the diaphragm, but a portion of the stomach bulges into the chest. | | Pathogenesis | The mechanism by which a disease develops. | | Peptic Ulcer Disease (PUD) | A condition characterized by the formation of ulcers in the lining of the stomach or duodenum, primarily caused by *H. pylori* infection or NSAID use. | | Pernicious Anemia | A type of anemia caused by the body's inability to absorb vitamin B12 due to a lack of intrinsic factor, often associated with autoimmune gastritis. | | Polypoid Carcinoma | A type of cancer that forms a mushroom-shaped growth projecting into the lumen of an organ. | | Postgastrectomy | The period following surgical removal of part or all of the stomach, which can lead to specific complications and increased risks for certain conditions. | | Regurgitation | The backward flow of undigested food from the stomach or esophagus into the mouth, often without nausea or forceful expulsion. | | Reflux Esophagitis | Inflammation of the esophagus caused by the backflow of stomach acid into the esophagus, a common complication of GERD and sliding hiatal hernias. | | Risk Factors | Factors that increase the likelihood of developing a particular disease or condition. | | Schatzki Ring | A thin, circumferential mucosal ring located in the distal esophagus, typically associated with sliding hiatal hernias and causing intermittent dysphagia to solids. | | Screw Esophagus | A radiographic finding on barium swallow characterized by multiple simultaneous contractions of the esophagus, seen in diffuse esophageal spasm. | | Serology | The study of serum and its components, often used to detect antibodies in the blood as an indicator of infection or autoimmune disease. | | Signet-Ring Cells | Cells with a characteristic appearance under a microscope, containing a large amount of mucin that pushes the nucleus to the periphery, often found in linitis plastica gastric cancer. | | Sliding Hernia | The most common type of hiatal hernia, where the gastroesophageal junction and a portion of the stomach slide upward into the chest. | | Squamous Cell Carcinoma (SCC) | A type of cancer that arises from squamous cells, commonly found in the upper and mid-esophagus, with risk factors including alcohol and tobacco use. | | Stricture | A narrowing of a duct or tube, such as the esophagus, which can impede the passage of food or other substances. | | Subcutaneous Emphysema | The presence of air trapped under the skin, which can occur with esophageal perforation due to air escaping from the mediastinum. | | Superficial Spreading Cancer | A form of cancer that is confined to the superficial layers of the tissue, often associated with a better prognosis. | | Surgical Resection | The removal of diseased tissue or organs through surgery, a primary treatment for many cancers. | | Traction Diverticulum | An esophageal diverticulum caused by the pulling effect of scar tissue from adjacent inflammation, typically located in the mid-esophagus. | | Treatment Failure Rates | The percentage of patients for whom a particular treatment does not achieve the desired therapeutic outcome. | | Triple Therapy | A common treatment regimen for *H. pylori* infection, typically consisting of a proton pump inhibitor (PPI) and two antibiotics (e.g., amoxicillin and clarithromycin). | | Ulcerative Carcinoma | A type of cancer that presents as a deep ulcer with irregular edges, often invading through the layers of the organ wall. | | Upper GI Endoscopy | A procedure using a flexible tube with a camera to visualize the esophagus, stomach, and duodenum, used for diagnosis and treatment. | | Weight Loss | An unintentional decrease in body weight, which can be a symptom of various gastrointestinal pathologies, including cancers and severe motility disorders. | | Zenker Diverticulum | A pouch that forms in the upper part of the esophagus, just above the cricopharyngeal muscle, caused by a failure of this muscle to relax properly during swallowing. | | Zollinger–Ellison Syndrome | A rare condition characterized by the development of one or more tumors (gastrinomas) that produce excessive amounts of gastrin, leading to severe acid hypersecretion and multiple peptic ulcers. | | Crohn Disease | A chronic inflammatory disease characterized by transmural inflammation affecting any part of the gastrointestinal tract, with the terminal ileum being a common site. | | Ulcerative Colitis | A chronic inflammatory disease limited to the colon and rectum, characterized by continuous mucosal inflammation and ulceration. | | Transmural Inflammation | Inflammation that extends through all layers of the bowel wall, from the mucosa to the serosa. | | Skip Lesions | Patches of inflammation in the gastrointestinal tract that are separated by areas of healthy tissue; a characteristic feature of Crohn disease. | | Noncaseating Granulomas | Collections of activated macrophages, typically found in the inflamed tissue of Crohn disease, which do not undergo caseous necrosis. | | Fistula | An abnormal connection or passageway between two organs or between an organ and the body surface, often occurring in Crohn disease. | | Aphthous Ulcers | Small, painful sores that can occur in the mouth, often seen as an extraintestinal manifestation of inflammatory bowel disease. | | Cobblestone Mucosa | A rough, nodular appearance of the intestinal lining, resembling cobblestones, which can be seen during endoscopy in Crohn disease. | | Pseudopolyps | Projections of inflamed or hyperplastic mucosa that resemble polyps but are not neoplastic; can be seen in both Crohn disease and ulcerative colitis. | | Fecal Calprotectin | A protein released by neutrophils in the gut; elevated levels in stool indicate intestinal inflammation, commonly used to monitor IBD activity. | | Toxic Megacolon | A severe complication of inflammatory bowel disease characterized by rapid dilation of the colon, often associated with severe inflammation and risk of perforation. | | Primary Sclerosing Cholangitis (PSC) | A chronic liver disease involving inflammation and scarring of the bile ducts, strongly associated with ulcerative colitis. | | Backwash Ileitis | Inflammation of the terminal ileum that occurs in some cases of extensive ulcerative colitis (pancolitis) due to reflux of colonic contents. | | Acute Appendicitis | Inflammation of the appendix, typically caused by obstruction of its lumen, leading to pain, fever, and potential perforation. | | Lymphoid Hyperplasia | An increase in the number of lymphoid cells, which can be a cause of appendiceal obstruction in children and young adults. | | McBurney's Point | A specific location on the abdomen (typically one-third the distance from the anterior superior iliac spine to the umbilicus) where tenderness is indicative of appendicitis. | | Rovsing Sign | Pain felt in the right lower quadrant of the abdomen when the left lower quadrant is palpated, suggestive of appendicitis. | | Psoas Sign | Pain elicited when the patient's hip is extended, indicating irritation of the psoas muscle, often associated with retrocecal appendicitis. | | Obturator Sign | Pain experienced upon internal rotation of the flexed hip, suggesting inflammation of the obturator internus muscle, indicative of pelvic appendicitis. | | Appendiceal Carcinoid Tumor | A neuroendocrine tumor arising from the appendix, often discovered incidentally and capable of secreting serotonin. | | Carcinoid Syndrome | A paraneoplastic syndrome caused by serotonin-secreting neuroendocrine tumors, characterized by flushing, diarrhea, wheezing, and cardiac valve lesions. | | 5-HIAA | 5-hydroxyindoleacetic acid, the main metabolite of serotonin excreted in the urine; measured to diagnose carcinoid syndrome. | | Acute Liver Failure (ALF) | A sudden, severe liver injury characterized by hepatic encephalopathy and impaired synthetic function (INR > 1.5), occurring within 26 weeks in individuals without pre-existing cirrhosis. | | Cirrhosis | A chronic liver disease marked by irreversible fibrosis and nodular regeneration, leading to disrupted liver architecture, portal hypertension, and eventual hepatocellular failure. | | Portal Hypertension | Elevated pressure within the portal venous system, a major consequence of cirrhosis, leading to complications such as varices, ascites, and splenomegaly. | | Hepatic Encephalopathy | A neuropsychiatric complication of liver dysfunction characterized by confusion, altered consciousness, asterixis, and fetor hepaticus, often triggered by elevated ammonia levels. | | Hepatocellular Carcinoma (HCC) | The most common type of primary liver cancer, often arising in the context of cirrhosis, with risk factors including chronic viral hepatitis (HBV/HCV) and chemical carcinogens. | | Wilson's Disease | An autosomal recessive disorder of copper metabolism caused by an ATP7B gene mutation, leading to excessive copper accumulation in the liver, brain, cornea, and kidneys, presenting with hepatic, neurologic, and psychiatric symptoms. | | Hemochromatosis | An autosomal recessive disorder characterized by excessive iron absorption and deposition in organs like the liver, pancreas, and heart, leading to fibrosis, organ damage, and complications such as cirrhosis and diabetes. | | Hepatocellular Adenoma | A benign liver tumor predominantly affecting young women, strongly associated with oral contraceptive use and anabolic steroid use, characterized by hormone-driven proliferation of hepatocytes with a risk of rupture and hemorrhage. | | Cavernous Hemangioma | The most common benign liver tumor, a vascular malformation characterized by blood-filled spaces, typically asymptomatic but can cause pain if large or lead to rare complications like rupture. | | Focal Nodular Hyperplasia (FNH) | A benign liver lesion representing a hyperplastic reaction to abnormal vascular flow, characterized by a central stellate scar on imaging, and not associated with malignant potential. | | Nonalcoholic Steatohepatitis (NASH) | A histological condition identical to alcoholic hepatitis but occurring in individuals without alcohol consumption, associated with obesity, hyperlipidemia, and diabetes, with a potential to progress to cirrhosis. | | Hemobilia | The presence of blood within the common bile duct, leading to its passage into the duodenum, most commonly caused by trauma, surgery, or tumors, presenting with gastrointestinal bleeding, abdominal pain, and jaundice. | | Liver Cysts | Benign fluid-filled sacs within the liver; Polycystic Liver Cysts are inherited and associated with ADPKD, while Hydatid Cysts are caused by Echinococcus infection. | | Liver Abscess | A collection of pus within the liver, which can be pyogenic (bacterial) or amebic, presenting with fever, abdominal pain, and elevated liver enzymes, requiring antibiotics and drainage. | | Budd-Chiari Syndrome | A condition resulting from hepatic venous outflow obstruction, leading to hepatic congestion, ischemia, portal hypertension, and potentially acute liver failure, caused by hypercoagulable states, malignancy, or idiopathic factors. | | Jaundice | The yellowing of the skin, sclera, and mucous membranes due to elevated bilirubin levels (visible when bilirubin exceeds approximately 2 mg/dL), classified as conjugated (direct) or unconjugated (indirect) based on the type of bilirubin elevated and its underlying cause. | | Cholelithiasis (Gallstones) | The formation of stones within the gallbladder, most commonly cholesterol stones, which are often asymptomatic but can lead to biliary colic or complications like cholecystitis and choledocholithiasis. | | Acute Cholecystitis | Inflammation of the gallbladder wall, typically caused by cystic duct obstruction by gallstones, presenting with constant right upper quadrant pain, fever, and tenderness, requiring prompt treatment with antibiotics and cholecystectomy. | | Acalculous Cholecystitis | Acute inflammation of the gallbladder occurring in the absence of gallstones, often seen in critically ill patients due to factors like dehydration and ischemia, presenting with similar symptoms to calculous cholecystitis but with subtle presentations. | | Choledocholithiasis | The presence of gallstones within the common bile duct (CBD), which can cause obstructive jaundice, acute pancreatitis, cholangitis, or biliary colic, requiring endoscopic retrograde cholangiopancreatography (ERCP) for diagnosis and treatment. | | Cholangitis | Infection of the biliary tract, typically secondary to obstruction and bile stasis, characterized by Charcot's triad (RUQ pain, jaundice, fever) and potentially Reynolds' pentad (including septic shock and altered mental status), requiring urgent resuscitation, antibiotics, and biliary drainage. | | Primary Biliary Cholangitis (PBC) | A chronic, progressive cholestatic liver disease characterized by autoimmune destruction of intrahepatic bile ducts, leading to cholestasis, fibrosis, and cirrhosis, typically affecting middle-aged women and marked by the presence of anti-mitochondrial antibodies (AMA). | | Bile Duct Stricture | A narrowing of the bile duct, most commonly caused by iatrogenic injury after surgery, which can lead to obstructive jaundice, pruritus, secondary biliary cirrhosis, and ascending cholangitis; preferred treatment involves endoscopic stenting. | | Biliary Dyskinesia | A motor dysfunction of the sphincter of Oddi causing biliary colic-like symptoms in the absence of gallstones, diagnosed using HIDA scan with CCK administration, and treated with laparoscopic cholecystectomy or endoscopic sphincterotomy. | | Aminotransferases (ALT/AST) | Liver enzymes that are released into the bloodstream when hepatocytes are damaged; ALT is more specific to the liver. Elevated levels can indicate various types of liver injury, with levels above 10,000 suggesting ischemic hepatitis, acetaminophen toxicity, or severe viral hepatitis. | | Alkaline Phosphatase (ALK-P) | An enzyme found in the liver, bone, and placenta; elevated levels, especially when accompanied by elevated GGT, are indicative of cholestasis or bile duct obstruction. | | Gamma-Glutamyl Transferase (GGT) | An enzyme used to confirm the hepatic origin of elevated alkaline phosphatase; elevated GGT can also be indicative of alcohol consumption or certain drug effects. | | Albumin | A protein synthesized by the liver that serves as a marker of chronic liver synthetic function; low levels can indicate chronic liver disease, malnutrition, or inflammation. | | Prothrombin Time (PT) | A measure of the time it takes for blood to clot, reflecting the liver's synthesis of clotting factors; a prolonged PT indicates advanced liver disease and impaired synthetic capacity. | | Hepatic Vein Outflow Obstruction | A blockage in the veins that drain blood from the liver, leading to congestion and potentially Budd-Chiari syndrome. | | Stercobilin | A brown pigment produced in the intestine from the breakdown of bilirubin, responsible for the color of feces; alterations in its production or excretion can indicate gastrointestinal or liver issues. | | Urobilinogen | A colorless compound formed in the intestine by the action of gut bacteria on bilirubin; part of it is reabsorbed and excreted in the urine, and elevated levels can indicate hemolysis or hepatic disease. | | Cholecystoenteric Fistula | An abnormal connection between the gallbladder and the intestine, often a complication of severe cholecystitis or gallstones, which can lead to gallstone ileus. | | Cholangiocarcinoma | Cancer of the bile ducts, with risk factors including primary sclerosing cholangitis (PSC), ulcerative colitis (UC), and choledochal cysts; it often presents with obstructive jaundice and has a poor prognosis. | | Choledochal Cysts | Congenital cystic dilatations of the bile ducts, which can lead to recurrent cholangitis, pancreatitis, and a significantly increased long-term risk of developing cholangiocarcinoma. | | Porcelain Gallbladder | Calcification of the gallbladder wall, considered a precancerous condition that warrants prophylactic cholecystectomy due to its high association with gallbladder carcinoma. | | Gallstone Ileus | An intestinal obstruction caused by a gallstone that has migrated from the gallbladder into the intestine, typically through a cholecystoenteric fistula. | | Hepatic Arteriography | An invasive imaging technique that involves injecting contrast dye into the hepatic artery to visualize blood vessels, used for diagnosing and sometimes treating liver tumors or bleeding. | | Percutaneous Transhepatic Cholangiography (PTC) | An invasive procedure where a needle is inserted through the skin and liver into a bile duct to inject contrast and visualize the biliary tree, used for diagnosis and drainage when ERCP is not feasible. | | Endoscopic Retrograde Cholangiopancreatography (ERCP) | A procedure combining endoscopy and X-rays to visualize and treat problems in the bile and pancreatic ducts, commonly used for stone removal, stenting, and obtaining biopsies. | | Laparoscopic Cholecystectomy | A minimally invasive surgical procedure to remove the gallbladder using a laparoscope and small incisions, commonly performed for symptomatic gallstones or cholecystitis. | | TACE (Transarterial Chemoembolization) | A procedure for treating unresectable liver tumors where chemotherapy drugs are delivered directly to the tumor via an artery, followed by embolization to block blood supply. | | Radiofrequency Ablation | A minimally invasive procedure used to treat liver tumors by applying heat generated by radiofrequency energy to destroy cancer cells. | | Selective Internal Radiation Therapy (SIRT) | A treatment for liver cancer that involves delivering radioactive microspheres directly to the tumor via the hepatic artery. | | SAAG (Serum-Ascites Albumin Gradient) | A calculation used to differentiate between portal hypertensive ascites (SAAG > 1.1 g/dL) and ascites due to other causes (SAAG ≤ 1.1 g/dL), aiding in diagnosis. | | Child-Pugh Score | A scoring system used to assess the severity of cirrhosis and predict prognosis, based on bilirubin levels, albumin levels, INR, ascites, and hepatic encephalopathy. | | MELD Score (Model for End-Stage Liver Disease) | A scoring system used to prioritize patients for liver transplantation, predicting short-term mortality risk based on bilirubin, creatinine, and INR. | | Hepatitis | Inflammation of the liver, which can be caused by viral infections (hepatitis A, B, C, D, E), autoimmune disorders, toxins, or metabolic conditions. | | Steatosis | The accumulation of fat within liver cells, commonly seen in alcoholic liver disease and nonalcoholic fatty liver disease (NAFLD). | | Fibrosis | The development of excessive fibrous connective tissue in an organ, a hallmark of chronic liver injury that can progress to cirrhosis. | | Nodular Regeneration | The formation of nodules of regenerating liver cells surrounded by fibrous tissue, a characteristic feature of cirrhosis. | | Alcoholic Hepatitis | Liver inflammation caused by excessive alcohol consumption, which can range from mild steatosis to severe liver injury and failure. | | Autoimmune Hepatitis | A chronic liver disease where the body's immune system attacks its own liver cells, leading to inflammation and damage. | | Ischemic Hepatopathy ("Shock Liver") | Liver injury caused by reduced blood flow to the liver, often occurring in critically ill patients with severe hypotension or shock. | | Acute Fatty Liver of Pregnancy (AFLP) | A rare but serious complication of pregnancy characterized by the rapid accumulation of fat in the liver, potentially leading to acute liver failure. | | HELLP Syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) | A severe pregnancy complication that involves the liver, often associated with preeclampsia, and can lead to liver damage and failure. | | Malignancy | The presence of cancerous tumors, which can affect the liver directly (primary liver cancer) or spread from other parts of the body (metastatic liver cancer). | | Mushroom Poisoning | Ingestion of toxic mushrooms that can cause severe liver damage and acute liver failure. | | Encephalopathy | Impaired brain function due to liver failure, characterized by confusion, altered consciousness, and neurological signs. | | Coagulopathy | A disorder of blood clotting, often seen in liver disease due to impaired synthesis of clotting factors. | | INR (International Normalized Ratio) | A standardized measure of blood clotting time, used to assess the severity of coagulopathy in liver disease. | | Thrombocytopenia | A low platelet count, which can occur in liver disease due to hypersplenism or impaired platelet production. | | Hypoglycemia | Low blood sugar, which can occur in severe liver failure due to the liver's impaired ability to store and release glucose. | | N-acetylcysteine | An antidote used to treat acetaminophen overdose, which is a common cause of acute liver failure. | | Steroids | Medications used to suppress the immune system, often prescribed for autoimmune hepatitis. | | Antivirals | Medications used to treat viral infections, such as hepatitis B and C. | | Anticoagulate | The use of medications to prevent blood clotting, used in conditions like Budd-Chiari syndrome. | | Lactulose | A medication used to treat hepatic encephalopathy by reducing ammonia levels in the gut. | | Rifaximin | An antibiotic used to treat hepatic encephalopathy by reducing ammonia-producing bacteria in the gut. | | Cerebral Edema | Swelling of the brain, a life-threatening complication of acute liver failure. | | ICP (Intracranial Pressure) | The pressure inside the skull, which needs to be monitored in patients with acute liver failure to prevent or manage cerebral edema. | | Mannitol | A medication used to reduce intracranial pressure in cases of cerebral edema. | | Nutritional Support | Providing adequate nutrition to patients with liver disease, often through enteral or parenteral feeding. | | Liver Transplantation | Surgical replacement of a diseased liver with a healthy donor liver, often the only curative treatment for end-stage liver disease. | | Ascites | Accumulation of fluid in the abdominal cavity, a common complication of cirrhosis and portal hypertension. | | Splenomegaly | Enlargement of the spleen, often seen in portal hypertension. | | Spider Angiomas | Small, red, spider-like blood vessels on the skin, a sign of chronic liver disease. | | Palmar Erythema | Reddening of the palms of the hands, another sign of chronic liver disease. | | Gynecomastia | Enlargement of breast tissue in men, associated with hyperestrinism in liver disease. | | Testicular Atrophy | Shrinkage of the testicles, associated with hyperestrinism in liver disease. | | Caput Medusae | Dilated superficial veins radiating from the umbilicus, a sign of portal hypertension. | | Hemorrhoids | Swollen veins in the rectum or anus, often associated with portal hypertension. | | Hematemesis | Vomiting blood, a sign of upper gastrointestinal bleeding, often from esophageal varices. | | Melena | Black, tarry stools indicating bleeding in the upper gastrointestinal tract. | | Octreotide | A medication used to reduce portal pressure and control bleeding from varices. | | Antibiotic Prophylaxis | The use of antibiotics to prevent infection, such as in patients with varices to prevent spontaneous bacterial peritonitis. | | Endoscopic Ligation/Banding | A procedure to tie off varices to prevent bleeding. | | Nonselective β-blockers | Medications used for long-term management of varices to reduce portal pressure. | | TIPS (Transjugular Intrahepatic Portosystemic Shunt) | A procedure to create a channel between the hepatic vein and portal vein to reduce portal pressure. | | Sodium Restriction | Limiting salt intake to help manage ascites. | | Spironolactone | A diuretic used to treat ascites by blocking aldosterone. | | Furosemide | A diuretic used in combination with spironolactone to treat ascites. | | Therapeutic Paracentesis | The removal of ascitic fluid using a needle. | | SBP (Spontaneous Bacterial Peritonitis) | Infection of ascitic fluid. | | PMN (Polymorphonuclear leukocytes) | A type of white blood cell; a count of >250 in ascitic fluid is diagnostic for SBP. | | 3rd-gen cephalosporin | A class of antibiotics commonly used to treat SBP. | | FFP (Fresh Frozen Plasma) | A blood product used to correct coagulopathy in liver disease. | | Hyperestrinism | Elevated levels of estrogen, often seen in chronic liver disease. | | AFP (Alpha-fetoprotein) | A tumor marker that can be elevated in hepatocellular carcinoma. | | ATP7B mutation | A genetic mutation in the ATP7B gene, responsible for Wilson's disease. | | Ceruloplasmin | A protein that binds copper; its levels are often low in Wilson's disease. | | Kayser-Fleischer rings | Yellow-brown rings around the cornea of the eye, pathognomonic for Wilson's disease. | | Parkinsonism | A group of neurological symptoms resembling Parkinson's disease, which can be a feature of Wilson's disease. | | Chorea | Involuntary, purposeless, rapid movements, a neurological sign of Wilson's disease. | | Dysarthria | Difficulty speaking due to problems with the muscles that control speech. | | Aminoaciduria | The presence of excess amino acids in the urine, a potential sign of kidney damage in Wilson's disease. | | Nephrocalcinosis | Calcification within the kidney tissue. | | Chelation therapy | Treatment that uses chelating agents to remove excess metals, such as copper, from the body. | | D-Penicillamine | A chelating agent used to treat Wilson's disease. | | Trientine | Another chelating agent used to treat Wilson's disease. | | Zinc therapy | Treatment with zinc, which reduces dietary copper absorption, used in Wilson's disease. | | Transferrin saturation | A measure of the amount of iron bound to transferrin, a key indicator in diagnosing hemochromatosis. | | TIBC (Total Iron-Binding Capacity) | The total amount of iron that can be bound by proteins in the blood; it is often decreased in hemochromatosis. | | HFE gene mutation testing | Genetic testing to identify mutations in the HFE gene, the gold standard for diagnosing hereditary hemochromatosis. | | Phlebotomy | The process of drawing blood, used as the primary treatment for hemochromatosis to remove excess iron. | | Oral Contraceptives (OCPs) | Birth control pills, which are associated with an increased risk of hepatocellular adenoma and cavernous hemangioma. | | Anabolic steroids | Performance-enhancing drugs that are also associated with hepatocellular adenoma. | | Hemoperitoneum | Bleeding into the abdominal cavity, a serious complication of ruptured liver tumors. | | Central Stellate Scar | A characteristic finding on imaging for Focal Nodular Hyperplasia (FNH). | | Paraneoplastic Syndromes | A group of diseases or symptoms that are the indirect results of a cancer, occurring distant from the actual tumor. | | Erythrocytosis | An abnormally high red blood cell count, a paraneoplastic syndrome seen in HCC. | | Thrombocytosis | An abnormally high platelet count, a paraneoplastic syndrome seen in HCC. | | Hypercalcemia | High calcium levels in the blood, a paraneoplastic syndrome seen in HCC. | | High cholesterol | Elevated cholesterol levels, a paraneoplastic syndrome seen in HCC. | | Gallbladder Carcinoma | Cancer of the gallbladder, often associated with chronic gallstones and porcelain gallbladder. | | Klatskin Tumor | A type of cholangiocarcinoma that occurs at the junction of the right and left hepatic ducts. | | Clonorchis infection | Infection with a liver fluke, a risk factor for cholangiocarcinoma. | | Obstructive Jaundice | Yellowing of the skin and eyes due to blockage of the bile ducts, preventing bilirubin from being excreted. | | Pruritus | Itching, a common symptom of cholestasis. | | Pale (clay-colored) stools | Stools lacking the normal brown color due to a lack of bile pigments, indicating biliary obstruction. | | Secondary Biliary Cirrhosis | Cirrhosis of the liver that develops as a result of prolonged bile duct obstruction. | | Ascending Cholangitis | A serious infection of the bile ducts that spreads upwards from the intestine. | | Sphincter of Oddi | A muscular valve that controls the flow of bile and pancreatic juice into the duodenum. | | HIDA Scan | A nuclear medicine test that visualizes bile flow and gallbladder function. | | CCK (Cholecystokinin) | A hormone that stimulates gallbladder contraction and secretion of pancreatic enzymes. | | Ejection Fraction | A measure of how much blood is pumped out of the heart or gallbladder with each contraction. | | Endoscopic Sphincterotomy | A procedure to cut the sphincter of Oddi to relieve obstruction or improve bile flow. | | Hepatic Venography | An imaging technique that visualizes the hepatic veins. | | Balloon Angioplasty + Stent | Procedures used to open narrowed or blocked blood vessels, including hepatic veins in Budd-Chiari syndrome. | | Portacaval Shunt | A surgical procedure to connect the portal vein to the vena cava to decompress the portal system. | | Reynolds Pentad | A severe clinical presentation of cholangitis including Charcot's triad plus septic shock and altered mental status. | | Charcot Triad | A classic presentation of cholangitis consisting of right upper quadrant pain, jaundice, and fever. | | Cholestyramine | A bile acid sequestrant used to relieve pruritus associated with cholestasis. | | Ursodeoxycholic Acid (UDCA) | A bile acid used to treat primary biliary cholangitis by slowing disease progression. | | Bisphosphonates | Medications used to treat osteoporosis by slowing bone loss. | | Anti-mitochondrial Antibody (AMA) | An autoantibody that is a hallmark diagnostic marker for Primary Biliary Cholangitis (PBC). | | IgM (Immunoglobulin M) | A type of antibody; elevated IgM levels are often seen in PBC. | | HDL (High-Density Lipoprotein) | Considered "good" cholesterol; HDL levels can be elevated in PBC. | | Xanthomas/Xanthelasmata | Skin deposits of cholesterol, which can occur in cholestatic liver diseases like PBC. | | Osteoporosis | A condition characterized by weakened bones, a complication of malabsorption of Vitamin D in cholestatic liver diseases. | | Autoimmune Disease Association | The co-occurrence of certain conditions with autoimmune liver diseases, such as Ulcerative Colitis with PSC and other autoimmune disorders with PBC. | | Colectomy | Surgical removal of all or part of the colon, performed for Ulcerative Colitis; it does not improve the course of PSC. | | Cholangiocarcinoma Surveillance | Regular monitoring of patients with PSC for the development of bile duct cancer. | | Post-cholecystectomy | Occurring after the surgical removal of the gallbladder. | | Liver Transplant | Surgical replacement of a diseased liver with a healthy donor liver. | | Bile Stasis | The slowing or stopping of bile flow. | | Bacterial Translocation | The movement of bacteria from the gut into the bloodstream or other tissues. | | Septic Shock | A life-threatening condition caused by the body's overwhelming response to infection, leading to dangerously low blood pressure. | | Altered Mental Status (AMS) | A state of confusion or disorientation, a sign of severe illness. | | ERCP (Endoscopic Retrograde Cholangiopancreatography) | A procedure to diagnose and treat conditions of the bile and pancreatic ducts. | | PTC (Percutaneous Transhepatic Cholangiography) | An imaging technique to visualize the bile ducts by inserting a needle through the skin and liver. | | T-tube | A temporary drainage tube inserted into the common bile duct after surgery. | | Laparotomy | Open surgical abdominal surgery. | | Hepatic Abscess | A collection of pus within the liver. | | Multi-organ Failure | The failure of two or more organ systems. | | Post-operative Stricture | A narrowing that develops after surgery. | | Chronic Pancreatitis | Long-term inflammation of the pancreas. | | Endoscopic Stenting | Placing a tube (stent) in a bile duct to keep it open. | | Surgical Bypass | Creating a new pathway for bile to flow around a blockage. | | Motor Dysfunction of Sphincter of Oddi | Abnormal functioning of the muscular valve that controls bile and pancreatic juice flow. | | Biliary Colic | Severe pain in the upper right abdomen caused by temporary blockage of a bile duct, usually by a gallstone. | | HIDA + CCK | A diagnostic test involving a radionuclide scan of the gallbladder followed by administration of cholecystokinin to assess gallbladder ejection fraction. | | Gallbladder Ejection Fraction | The percentage of bile released from the gallbladder when stimulated by CCK. | | Acute Pancreatitis | Inflammation of the pancreas characterized by the premature activation of pancreatic enzymes, leading to pancreatic autodigestion. It is commonly caused by gallstones or excessive alcohol consumption. | | Autodigestion | The process by which an organism digests itself, in the context of pancreatitis, this refers to the self-destruction of pancreatic tissue by its own enzymes when they are prematurely activated. | | Cullen's Sign | Periumbilical ecchymosis (bruising around the navel) that can be a sign of hemorrhagic pancreatitis, indicating bleeding into the abdominal wall. | | Grey-Turner's Sign | Flank ecchymosis (bruising on the sides of the abdomen) that can be a sign of hemorrhagic pancreatitis, suggesting retroperitoneal bleeding. | | Pancreatic Necrosis | Death of pancreatic tissue, which can occur in severe cases of acute pancreatitis. It may be sterile or infected, with infected necrosis carrying a high mortality rate. | | Pancreatic Pseudocyst | A collection of fluid that forms outside the pancreas, typically 2-3 weeks after an episode of acute pancreatitis. Cysts larger than 5 cm often require drainage. | | Steatorrhea | The presence of excess fat in the feces, characterized by fatty, bulky, and foul-smelling stools. It is a late finding in chronic pancreatitis due to malabsorption of fats from impaired exocrine function. | | Pancreatic Calcifications | The presence of calcium deposits within the pancreas, which is a hallmark finding of chronic pancreatitis and can be visualized on imaging studies like CT scans or abdominal radiographs. | | Pancreatic Cancer | Malignant neoplasm of the pancreas, most commonly occurring in the head of the pancreas. Risk factors include smoking, chronic pancreatitis, and new-onset diabetes. Prognosis is generally very poor. | | Whipple Procedure | Also known as pancreaticoduodenectomy, this is a major surgical procedure to remove the head of the pancreas, the duodenum, the gallbladder, and part of the bile duct. It is the primary treatment for resectable pancreatic cancer. | | CA 19-9 | A tumor marker that is elevated in many cases of pancreatic cancer. It is used in conjunction with imaging and clinical assessment for diagnosis and monitoring, although it is not solely diagnostic. | | Migratory Thrombophlebitis | Inflammation of veins with clot formation that appears in different locations at different times. In pancreatic cancer, it is known as Trousseau syndrome and can be an early presenting sign. | | Courvoisier's Sign | The presence of a palpable, non-tender gallbladder in a jaundiced patient. It suggests obstruction of the common bile duct, often due to pancreatic cancer. |