1. colovesical fistula
    • Defn: connection between the colon and bladder, which can be a complication of acute diverticulitis.
    • Etiology:
    • • Diverticular disease (sigmoid most common)
    • • Crohn disease
    • • Malignancy (colon, bladder, pelvic organs)
    • Pathogenesis: is usually due to direct extension of a ruptured diverticulum or erosion of a diverticular abscess into the bladder.
    • Clinical Features: Patients typically develop fecaluria (stool in the urine) or pneumaturia (air In the urine) that usually occurs at the end of urination as the gas collects at the top of the bladder. Patients can also develop recurrent urinary tract infections (sometimes due to mixed flora with coliform organisms) or other nonspecific symptoms that can sometimes delay the diagnosis.
    • Diagnosis: Abdominal CT scan with oral or rectal (not intravenous) contrast can confirm the diagnosis by showing contrast material in the bladder with thickened colonic and vesicular walls.
    • Colonoscopy is usually recommended in patients diagnosed with colovesical fistula to exclude colonic malignancy.
    • Treatment: is typically surgical after resolution of the Infection.
  2. Diverticula
    • Definition: are outpouchlngs of the colonic wall that form at points of weakness
    • Most common location: in the sigmoid colon. Incidence: increases with age.
    • C/F: usually asymptomatic
    • Complications: diverticular hemorrhage , diverticulitis (acute fever, abdominal pain, and possible perforation with abscess formation).
    • Diverticulosis is associated with chronic constipation : increased colonic pressures seen in constipation may promote formation of diverticula, and conversely, altered motility seen in diverticulosis may contribute to constipation.
    • Impact of dietary fiber on formation of diverticulosis: unclear.
    • However,incidence of acute diverticular complications is lower in individuals with a high intake of fruit and vegetable fiber.
    • Physical activity is also inversely correlated with the risk of complications.
    • Factors associated with an increased risk of complications:
    • Include heavy meat consumption, aspirin or non steroidal anti-inflammatory drug use, obesity, and possibly smoking.
  3. Drugs and toxins typically cause hepatic Injury
    • Mechanism: either through direct toxic effects or through Idiosyncratic reactions.
    • Direct toxic effects : are dose-dependent and have short latent periods. Some examples of direct toxins include carbon tetrachloride, acetaminophen. tetracycline, and substances found in the Amanita phalloides mushroom.
    • Idiosyncratic reactions : are not dose-dependent and have variable latent periods. Some examples of pharmacological agents that cause idiosyncratic reactions include isoniazid, chlorpromazine, halothane, and antiretroviral therapy.
  4. Drug-induced fiver disease
    • can also be broadly categorized according to morphology:
    • 1)cholestasis: which is caused by medications such as chlorpromazine, nitrofurantoin, erythromycin, and anabolic steroids
    • 2) fatty liver: which is caused by medications such as tetracycline, valproate, and antl-retrovirals
    • 3) hepatitis: which is caused by medications such as halothane, phenytoin, isoniazid, and alpha methyldopa
    • 4) toxic or fulminant liver failure: which Is caused by medications such as carbon tetrachloride and acetaminophen
    • 5) granulomatous: which is caused by medications such as allopurinol and phenylbutazone.
  5. Dyspepsia
    • Clinical Features: chronic, intermittent epigastric pain and postprandial discomfort typical of dyspepsia.
    • causes of dyspepsia: include nonsteroidal anti inflammatory drugs, gastric or esophageal cancer, functional dyspepsia, gastroesophageal reflux disease (GERD), and symptomatic Infection (eg, peptic ulcer disease (PUD)) with Helicobacter pylori (a urease producing organism).
    • Definitive diagnosis of dyspepsia: often requires endoscopy.
    • Indication of Endoscopy: patients age >55 or with alarm symptoms (eg, weight loss, bleeding, anemia, dysphagia, persistent vomiting).
    • In those without alarm symptoms: evaluation for H pylori infection (eg, urea breath testing, stool antigen testing) can be performed.
    • Patients who fall to improve after initial management (eg, antibiotics if positive for H pylori, proton pump inhibitor) should undergo endoscopy.
  6. Esophageal cancer
    • Subtypes
    • • Adenocarcinoma: Distal esophagus, arises from Barrett esophagus
    • • Squamous cell carcinoma: Anywhere in the esophagus
    • Risk factors:
    • • Acid reflux, obesity, Smoking (adenocarcinoma)
    • • Smoking, Heavy alcohol consumption , caustic injury (squamous cell)
    • Symptoms:
    • • Chest pain
    • • Weight loss
    • • Dysphagia (solids)
    • Diagnosis: Young, low-risk patients with undetermined esophageal symptoms may start with barium esophagram, but those who are age >55 as well as those with alarm symptoms (eg, weight loss. gross or occult bleeding, early satiety) will usually proceed directly to endoscopy
    • • Endoscopy with biopsy
    • • CT (PET/CT) for staging
  7. Clinical features of esophageal perforation
    • Etiology:
    • • Spontaneous rupture (Boerhaave syndrome due to severe retching)
    • • Instrumentation (eg, endoscopy : MC cause of rupture esp. if dilation of strictures is being done)
    • • Esophagitis (infectious/pills/caustic)
    • • Esophageal ulcer
    • Penetrating trauma
    • Clinical Presentation: Tachypnea
    • • Chest & abdominal pain, systemic findings (eg, fever)
    • • Subcutaneous emphysema in the neck, left sided pleural effusion:
    • • Hamman sign (crunching sound on chest auscultation)
    • Diagnosis:
    • • CXR or CT scan: Wide mediastinum, pneumomediastinum, pneumothorax, air around paraspinal muscles, pleural effusion (late)
    • • CT scan: Esophageal wall thickening, mediastinal air fluid level
    • • Water -soluble contrast esophagogram: Leak at perforation site
    • Management:
    • • Antibiotics & supportive care for all patients
    • • Surgical repair for significant leakage with systemic Inflammatory response
    • If perforation is confirmed, primary closure of esophagus and drainage of mediastinum must be attempted urgently to prevent the development of mediastinitis.
  8. Management of esophageal Perforation
    • EP is a surgical emergency and requires immediate surgical consultation. Management Involves:
    • • Making patients nil per oral (NPO)
    • • Administering Intravenous proton pump inhibitors, broad-spectrum antibiotics, and nutrition
    • • Performing surgical drainage and debridement of infected or necrotic areas
    • Some patients - Including those with minimal symptoms without signs of sepsis, those with a imited perforation, or those In a hospital with immediate thoracic surgery backup - can be considered for nonoperatlve management.
  9. Esophageal Perforation
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  10. Hepatitis B Serology
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  11. Mallory Weiss tear
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  12. Esophageal Stricture
    • Clinical Features: Strictures typically cause slowly progressive dysphagia to solid foods without anorexia or weight loss. As they progress, they can actually block reflux, leading to improvement of heartburn symptoms.
    • chronic gastroesophageal reflux with new dysphagia and symmetric lower esophageal narrowing- suggests esophageal (peptic) stricture.
    • Pathophysiology: Chronic gastroesophageal reflux disease (GERD) predisposes to Barrett's esophagus (intestinal metaplasia of the lower esophagus) and esophageal strictures. Both conditions are consequences of the body's reparative response to chronic gastric acid exposure and can occur simultaneously.
    • Benign strictures affect 5% - 15% of patients with GERD.
    • Causes of peptic strictures:
    • GERD
    • radiation
    • systemic sclerosis
    • caustic ingestions.
    • Investigation: Barium Swallow: appear as symmetric, circumferential narrowing on barium swallow. Nonetheless, in any case of stricture in the setting of Barrett's esophagus, biopsy is necessary to rule out adenocarcinoma.
    • This is usually accomplished via endoscopy which may be diagnostic and therapeutic (dilation is performed if no malignancy is detected).
  13. Primary Prophylaxis of esophageal Varices
    • In most patients with nonbleeding varices, prophylactic treatment with nonselective beta blockers (eg, propranolol. nadolol) is recommended to reduce the likelihood of progression to large varices as well as the risk of variceal hemorrhage.
    • They are thought to act by decreasing adrenergic tone in mesenteric arterioles, which results in unopposed alpha-mediated vasoconstriction and decreased portal venous flow
    • Endoscopic variceal ligation can be used as an alternate primary preventive therapy in patients with contraindications to beta blocker therapy.
  14. Management of Variceal Hemorrhage
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    • Initial treatment of suspected variceal bleeding includes volume resuscitation, through 2 to 3 large bore peripheral intravenous lines.
    • Prophylactic antibiotics (eg. ceftriaxone) should be given to cirrhotic patients with gastrointestinal bleeding to decrease infectious complications, recurrent bleeding, and mortality.
    • Somatostatin analogues (eg, octreotide) inhibit the release of vasodilator hormones, which leads indirectly to splanchnic vasoconstriction and decreased portal flow.
    • Urgent endoscopy (within 12 hours) can diagnose and treat (eg, endoscopic band ligation, sclerotherapy) active bleeding.
    • Patients with uncontrollable bleeding require temporary balloon tamponade (eg, Sengstaken-Biakemore, Minnesota, Unton-Nachtas tubes) as a short-term measure until more definitive therapy, including transjugutar intrahepatic portosystemic shunt (TIPS) or shunt surgery.
    • Patients without further bleeding after endoscopy can be monitored and receive secondary prophylaxis (beta blocker) with repeat endoscopic band ligation 1-2 weeks later.
    • Current guidelines suggest keeping the hemoglobin >9 g/dl in variceal hemorrhage:
  15. Association With Hepatitis C
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  16. Association of Hepatitis C
    • Hepatitis C (HCV) has a strong correlation with Porphyria Cutanea Tarda (PCT), and all patients with PCT should be screened for HCV.
    • HCV also has a strong correlation with essential mixed cryoglobulinemia; nearly 90% of patients with his condition have HCV, and nearly 50% of patients with HCV have cryoglobulinemia.
    • Essential mixed cryoglobulinemia is due to circulating immune complexes that deposit in small to medium vessels and may be associated with low serum complement levels. Patients can develop palpable purpura, arthralgias and renal complications (usually membranoproliferative glomerulonephritis).
  17. Folic Acid Deficiency
    • Patient's pale skin, nail beds and conjunctiva suggest anemia. His diet shows an obvious lack of folate, a nutrient typically found in foods like fresh green leafy vegetables and liver. Furthermore, folate is heat sensitive, so cooked foods are typically lacking.
    • In the setting of dietary deficiency, folic acid stores can become depleted within 4-5 months, leading to decreased RBC production and macrocytic anemia.
  18. Carcinoma Stomach
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  19. H pylori and malignancies
    • Helicobacter pylori infection is a significant risk factor for gastric adenocarcinoma and lymphoma (mucosa associated lymphoid tissue (MALT) lymphoma).
    • Eradication is recommended for patients with resectable disease to reduce the risk of developing a second cancer.
    • Eradication of H pylori causes remission in some patients with gastric MALT lymphoma, but it is not curative for adenocarcinoma.
  20. Acute erosive gastropathy
    • is characterized by the development of severe hemorrhagic lesions after the exposure of gastric mucosa to various injurious agents or after a substantial reduction in blood now.
    • Aspirin decreases the protective prostaglandin production, and cocaine results in vasoconstriction, significantly reducing gastric blood now.
    • In addition, aspirin and alcohol cause direct mucosal injury, which decreases the normal protective barriers (eg, secreted mucins, bicarbonate), thereby permitting acid and other luminal substances (eg, proteases, bile acids) to penetrate into the lamina propria. This results in additional injury to the vasculature and subsequent hemorrhage.
  21. GERD : Management
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    • Patients with typical GERD require upper gastrointestinal (GI) endoscopy if they have alarm symptoms: (dysphagia, odynophagia, weight loss, anemia, Gl bleeding, or recurrent vomiting) or are men age >50 with chronic (>5 years) symptoms and cancer risk factors (eg, tobacco use).
    • Patients with esophagitis on endoscopy can receive treatment depending on the diagnosis (eg, autoimmune disease, Barrett's esophagus}.
    • Patients without esophagitis on endoscopy usually require further evaluation (eg, esophageal manometry).
    • Patients with typical GERD symptoms: who do not meet initial endoscopy criteria can receive an initial trial of dally proton pump Inhibitor (PPI).
    • Patients with refractory symptoms should try another PPI or increase the use of PPI to twice daily.
    • Patients with persistent symptoms likely require further testing such as endoscopy or esophageal pH monitoring.
  22. Diverticulosis
    • Diverticulosis is the most common cause of gross lower gastrointestinal (GI) bleeding in adults.
    • Diverticula are outpouchings of the colonic wall that form at points of weakness. The deformation in the colonic wall can cause weakness in the associated arterial supply and lead to bleeding Into the diverticular lumen.
    • Diverticulosis is most common in the sigmoid colon. but diverticular bleeding is more common in the right colon.
    • Clinical Features: Diverticular bleeding is typically painless, but large-volume bleeding may be associated with lightheadedness and hemodynamic instability, low- or moderate-volume bleeding from the right colon will mix with stool and pass as dark or maroon-colored hematochezia. Large-volume hemorrhage can lead to passage of frank red blood.
    • Investigation: The diagnosis is confimed on colonoscopy.
    • Treatment: Most cases of diverticular hemorrhage will resolve spontaneously, but a minority of patients will require endoscopic or surgical intervention.
  23. Hemorrhoids
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  24. Evaluation of BRBPR
    • depends on the patient's presentation and risk factors.
    • Clinical factors associated with increased risk of serious disease: include blood mixed with stool, systemic symptoms (eg, fever, weight loss), diarrhea, anemia, change in bowel habits, and abdominal pain.
    • Age: also correlates strongly with risk of malignancy in patients with BRBPR. Patients age more than 50: are at elevated risk for colorectal cancer and should undergo colonoscopy unless they have had a normal colonoscopy within the last 2-3 years.
    • Patients age 40-49 : are at Intermediate risk and could be considered for sigmoidoscopy as an alternative to colonoscopy.
    • If the patient is age <40: and has no other risk factors for colon cancer, office-based anoscopy or proctoscopy should be performed first.
    • If no etiology is found, colonoscopy or sigmoidoscopy is then considered.
    • Anoscopy is also useful in older patients to visualize a palpable abnormality found on physical examination.
  25. Angiodysplasia
    • Def: is characterized by dilated submucosal veins and arteriovenous malformations, and has an increased incidence after age 60.
    • Location: It may occur anywhere in the Gl tract but is most common in the right colon.
    • Risk Factors: Angiodysplasia is more frequently diagnosed in patients with advanced renal disease and von Willebrand (vW) disease, possibly due to the bleeding tendency associated with these disorders. Angiodysplasla may also be more common in patients with aortic stenosis (AS), possibly due to acquired vW factor deficiency (from disruption of the vW multimers as they traverse the turbulent valve space induced by AS). Angiodysplastic bleeding has been reported to remit following aortic valve replacement.
    • Diagnosis: of anglodysplasla is usually made on endoscopic evaluation (eg, upper Gl endoscopy, colonoscopy). However, it is not uncommon for angiodysplasia to be missed on colonoscopy due to poor bowel preparation or location behind a haustral fold.
    • Treatment: Asymptomatic patients do not require treatment. Patients with anemia or gross or occult bleeding can be treated endoscopically, usually with cautery.
  26. Why is there increased BUN in UGI Bleeding?
    • Patients with upper (but not lower) Gl bleeding often have an elevated blood urea nitrogen (BUN) and elevated BUN/creatinine ratio.
    • Possible causes include increased urea production from intestinal breakdown of hemoglobin and increased urea reabsorption in the proximal tubule due to associated hypovolemia.
  27. RBC Transfusion Index:
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    • Packed red blood cell transfusions are recommended in acute gastrointestinal bleeding for patients with hemoglobin <7 g/dl.
    • A higher threshold of hemoglobin <9 g/dl is considered for unstable patients with acute coronary syndrome or with active bleeding and hypovolemia.
  28. Indication of FFP Transfusion
    • Fresh frozen plasma contains all clotting factors and plasma proteins from one unit of blood.
    • It Is usually indicated for severe coagulopathy (eg, liver disease, disseminated Intravascular coagulation) with active bleeding.
    • Fresh frozen plasma is generally not needed to correct a minimally abnormal INR (<1.6), which is a common finding in gastrointestinal bleeding.
  29. Indication of platelet Transfusion:
    Platelet transfusions are typically given for a platelet count <10,000/mm) (increased risk of spontaneous hemorrhage) or for a platelet count <50,000/mm) with active bleeding.
  30. Giardia Lamblia
    • Typical features of giardiasis, includes diarrhea acquired during international travel, abdominal cramps, foul-smelling stools, bloating, and benign findings on abdominal examination.
    • Location: Giardia duodenalis (sometimes noted as G ambiia or G intestinalis) is common in rural areas and developing countries and has an incubation period of 1-2 weeks.
    • Mode Of Transmission : It is most commonly transmitted by contaminated water but can be foodbome or transmitted person-to-person via a fecal-oral route.
    • C/F: Most patients are asymptomatic; however, a significant minority of those who do develop clinical illness may go on to develop chronic giardiasis characterized by malabsorption, weight loss, or persistent gastrointestinal distress.
    • Inv: The preferred confirmatory test for giardiasis is a stool antigen assay: (direct immunofluorescence or ELISA). Stool microscopy: for oocysts and trophozoltes can also identify the organism and is useful in resource-poor settings or if other parasitic organisms are suspected. Some facilities also offer a nucleic acid amplification assay.
    • Tx: Metronidazole Is the preferred treatment. Asymptomatic carriers do not usually need treatment.
  31. Gilbert Syndrome:
    • Epidemiology:
    • • More common in males
    • • Most common inherited disorder of bilirubin glucuronidation
    • Pathogenesis:
    • • AR or AD mutation in UGT1A1 gene
    • • Decrease UDP-glucuronosyltransferase activity -
    • • Increased unconjugated bilirubin
    • Clinical findings:
    • • lntemittent episodes of mild jaundice
    • • Provoked by stress (eg, infection, fasting, vigorous exercise, surgery)
    • Jaundice may be triggered by fasting or consumption of a fat-free diet, physical exertion, febrile illness, stress, or menstruation
    • Diagnosis:
    • • Unconjugated hyperbilirubinemia (<3 mg/dl) on repeat testing
    • • Normal CBC, blood smear, reticulocyte count (Normal haptoglobin)
    • • Normal AST, ALT, alkaline phosphatase
    • Treatment:
    • • No specific treatment
  32. Immunization in patient with Cirrhosis
    • All patients with chronic liver disease should be immunized against hepatitis A and B unless they are already immune, as they are at high risk for acute hepatic failure or cirrhosis upon infection with viral hepatitis.
    • Patients with risk factors for hepatitis B virus should be vaccinated, which is especially important in patients already infected with hepatitis C virus who are continuing their highrisk behaviors.
  33. D/D of solid liver mass
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  34. Hepatic Adenoma
    • Hepatic adenomas are benign epithelial tumors that are most common in young and middle-age women.
    • Risk factors: OCP Use, anabolic androgen use and pregnancy.
    • Ultrasound: shows well-demarcated, hyperechoic lesions
    • contrast-enhanced CT: can show early peripheral enhancement.
    • Needle biopsy: is not recommended for suspected hepatic adenoma due to the risk of bleeding, and surgical excision is preferred.
    • Long-term complications : progressive growth, rupture, and malignant transformation.
    • D/D: Hepatic adenoma can clinically resemble focal nodular hyperplasia (FNH), a common mass lesion In young women caused by hyperperfusion from anomalous arteries.
    • However, FNH Is not associated with oral contraceptives, and imaging will show evidence of Increased arterial flow and sometimes a central scar.
  35. Hepatic encephalopathy
    • HE refers to impaired central nervous system (CNS) function in patients with cirrhosis and is due in part to the neurotoxicity from ammonia (NH3) in the setting of impaired liver function.
    • Precipitating factors:
    • • Drugs (eg, sedatives, narcotics, Diuretics)
    • • Hypovolemia (eg, diarrhea)
    • • Electrolyte changes (eg, hypokalemia)
    • • Increased nitrogen load (eg, Gl bleeding)
    • • Infection (eg, pneumonia, UTI, SSP)
    • • Portosystemic shunting (eg, TIPS)
    • Clinical presentation:
    • • Sleep pattern changes
    • • Altered mental status
    • • Ataxia
    • • Asterixis
    • Treatment:
    • • Correct precipitating causes (eg, fluids, antibiotics)
    • • Decrease blood ammonia concentration (eg, lactulose, rifaximin)
  36. Precipitants of HE
    • Patients with hepatic encephalopathy on diuretics can develop low intravascular volume despite having total volume overload leading to a metabolic alkalosis with associated hypokalemia.
    • Treatment: Includes volume resuscitation and repletion of hypokalemia in addition to serum ammonia-lowering medications (eg. lactulose).
    • Hypokalemia: which can exacerbate HE as the resultant intracellular acidosis (excreted Intracellular potassium replaced by hydrogen ions to maintain electroneutrallty) causes increased NH3 production (glutamine conversion) in renal tubular cells
    • Metabolic alkalosis (elevated bicarbonate): which an also exacerbate HE as It promotes conversion of ammonium (NH4), which cannot enter the CNS.
  37. Why Lactulose in Hepatic Encephalopathy?
    • Nonabsorbable dlsaccharides (eg, lactulose, lactitol) are preferred for lowering serum ammonia.
    • Colonic bacteria metabolize lactulose to short-chain fatty acids (eg, lactic acid, acetic acid). This acidifies the colon to stimulate conversion of the absorbable ammonia to the nonabsorbable ammonium (an ammonia trap) and causes bowel movements (which facilitates fecal nitrogen excretion).
    • The medication is titrated to produce 2 or 3 semlformed stools daily
  38. Pathogenesis of Hepatitis B
    • The first serologic marker to appear in the serum with acute hepatitis B is HBsAg, which appears usually 4-8 weeks after infection.
    • lgM anti-HBc appears shortly thereafter, which is around the time clinical symptoms occur and patients develop elevations in hepatic aminotransferase levels (often >25 times the normal limit).
    • There can be a time lag (weeks to months) between the disappearance of HBsAg and the appearance of anti-HBs, which Is termed the window period. lgM anti-HBc may be the only detectable marker for acute hepatitis B infection during this period.
    • As such, HBsAg and anti-HBc IgM: are the most appropriate diagnostic tests for acute hepatitis B infection as these are both elevated during initial infection and anti-HBc IgM: will remain elevated during the window period.
    • HBeAg: Is a good Indicator of Infectivity but is a poor test for acute hepatitis B infection as levels typically fall early in the course of the disease.
  39. Serological markers for the hepatitis B virus include the following:
    • HBsAg: The first serologic marker detected in the serum after inoculation. It precedes the onset of clinical symptoms and elevation of serum aminotransferases. It also remains detectable during the entire symptomatic phase of acute hepatitis B and suggests infectivity.
    • Anti-HBs: Appears in the serum after either successful HBV vaccination or clearance of HBsAg, and remains detectable for life in most patients. It indicates non-infectivity and immunity. However, there is a time lag between the disappearance of HBsAg and the appearance of anti-HBs; this is termed the "window period."
    • HBcAg: This marker is not detectable in serum as it is normally sequestered within the HBsAg coat.
    • Anti-HBc: lgM appears shortly after the emergence of HBsAg and may be the only diagnostic marker for acute HBV infection during the "window period." lgG remains detectable during recovery from acute HBV infection or progression to chronic infection.
    • HBeAg: This antigen is detectable shortly after the appearance of HBsAg and indicates active viral replication infectivity. It is associated with the presence of HBV DNA. HBeAg tends to disappear shortly after aminotransferase levels peak and before HBsAg is eliminated; It is followed by the appearance of anti-HBe.
    • Anti-HBe: This marker suggests cessation of active viral replication and low infectivity.
  40. Shingles
    • may occur at any age, but it is most common after age 50 and the risk increases with age.
    • It is frequently triggered by severe physical stress (such as cancer treatment) or immunosuppressed states, but many cases are spontaneous.
    • Shingles develops when there is reactivation of the varicella zoster virus in a dorsal root ganglion, where it has remained dormant since a past chickenpox infection.
    • This results in pain and a vesicular rash in a dermatomal distribution along the course of the nerve.
    • In some cases, patients may develop persistent hypersensitivity of afferent pain fibers leading to chronic pain known as post-herpetic neuralgia.
    • Treatment: with antiviral medications (acyclovir, valacyclovir, or famciclovir) in the first few days of a shingles outbreak can shorten the duration of symptoms and decrease the risk of post-herpetic neuralgia.
  41. Peripheral Signs of Liver Disease
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  42. Mechanism Of Hypogonadism and Hypothyroidism in Pregnancy
    • Erectile dysfunction and testicular atrophy are most likely due to hypogonadism, which is a common complication of chronic liver disease with cirrhosis.
    • Cirrhosis (especially due to alcoholic liver disease or hemochromatosis) can cause hypogonadism due to primary gonadal injury or hypothalamic-pituitary dysfunction.
    • Cirrhosis is also associated with elevated circulating levels of estradiol due to increased conversion from androgens. Findings due to excess estrogen include telangiectasias, palmar erythema, testicular atrophy, and gynecomastia (usually bilateral but can be unilateral).
    • In addition, the liver produces serum binding proteins for thyroid hormones (eg, thyroxine-binding globulin, transthyretin, albumin, lipoproteins). Cirrhosis leads to decreased synthesis of these proteins, which lowers the total triiodothyronine (T3) and thyroxine (T4) in circulation; however, free T3 and T41evels are unchanged, and TSH will be normal, reflecting a euthyroid status.
  43. Crohn disease
    • Clinical findings: can involve any part of the gastrointestinal tract from mouth to anus, apthus ulcers in mouth, rectal sparing, fistula formation
    • • Gl: Abdominal pain, nonbloody diarrhea, oral ulcers,
    • malabsorption, weight loss, fistula/abscess formation
    • • Extraintestinal: MSK (arthritis), eye (eg, uveitis, sdentis, episcleritis), skin (eg, erythema nodosum, pyoderma gangrenosum)
    • Perianal Disease : Anal tags, fissures, fistulas
    • Diagnosis:
    • • Increased WBC,Reactive Thrombocytosis, iron deficiency anemia, lncreased inflammatory markers ( Increased ESR)
    • • Endoscopy: Focal ulcerations adjacent to normal mucosa (cobblestoning), skip areas of disease
    • • Radiography: Strictures, bowel wall thickening
    • Biopsy: Noncaseating granuloma
    • Treatment:
    • • 5-ASA drugs, corticosteroids, antibiotics
    • • Azathioprine
    • • Anti-TNF therapies
  44. Ulcerative Colitis
    • Symptoms:
    • • Bloody diarrhea, abdominal pain, tenesmus, fecal incontinence
    • • Weight loss, fever
    • Endoscopic findings:
    • • Erythema, friable mucosa with ulcers
    • • Pseudopolyps, exudates, edema, and spontaneous bleeding
    • • Involvement of rectosigmoid
    • • Continuous and circumferential colonic involvement (no skip lesions)
    • Extraintestinal Manifestations: arthritis, uveitis, episcleritls, erythema nodosum, and primary sclerosing cholangitis.
    • Laboratory findings: leukocytosis, iron deficiency anemia, reactive thrombocytosis, and elevated inflammatory markers (eg, erythrocyte sedimentation rate [ESR]).
    • Biopsy:
    • • Mucosal & submucosal inflammation
    • • Crypt abscesses and crypt distortion.
    • Complications:
    • • Toxic megacolon
    • • Primary sclerosing cholangitis
    • • Colorectal cancer
    • • Erythema nodosum, pyoderma gangrenosum
    • • Spondyloarthritis
  45. Colon cancer Screening:
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    • A screening colonoscopy interval of 5 years is appropriate for patients without inflammatory bowel disease who are found to have 1 or 2 small adenomatous polyps. Five years is also an appropriate interval for patients with a first-degree family history of CRC or adenomatous polyps
  46. Toxic megacolon
    • C/F: typically presents with total or segmental nonobstructive colonic dilation, severe bloody diarrhea, and systemic findings ( eg, fever, tachycardia).
    • causes of toxic megacolon: IBD (within 3 years), Ischemic colitis, volvulus, diverticulitis, Infections (eg, Clostridia difficile), and obstructive colon cancer (less common).
    • Diagnosis: is confirmed by plain abdominal x-rays and more than or equal to 3 of the following:
    • fever >38 C (100.4 F),
    • pulse >120/min,
    • white blood cells >10,500/mL, and
    • anemia.
    • Other findings: can include volume depletion, altered mental status, hypotension, and electrolyte abnormalities.
    • Plain films: usually reveal dilated right or transverse colon (>6 em), possible multiple air-fluid levels, and thick haustral markings that do not extend across the entire lumen.
    • Tx: Toxic megacolon is a medical emergency that can progress rapidly and result In colonic perforation.
    • Treatment Includes: Intravenous fluids, broad spectrum antibiotics, and bowel rest.
    • Intravenous corticosteroids: are preferred for treating IBD-induced toxic megacolon.
    • Emergency surgery (subtotal colectomy with end-ileostomy as the procedure of choice) may be required if the colitis does not resolve.
  47. Difference between Crohn's Disease and Ulcerative ColitisImage Upload 13
  48. Iron Deficiency Anemia in Elderly
    • New IDA in elderly patients should be considered to be from gastrointestinal (GI) blood loss (eg, polyps, cancer, angiodysplasia) until proven otherwise.
    • In the clinical setting fecal occult blood tests (FOBTs) are frequently performed in patients before a diagnosis of iron deficiency is established with laboratory testing.
    • When positive, FOBTs may guide the decision to perform colonoscopy and endoscopy in elderly patients, regardless of iron levels.
    • However, a single negative FOBT is not sufficient to exclude occult Gl bleeding.
    • Elderly patients with IDA should be evaluated with colonoscopy and endoscopy despite a single negative FOBT, especially if no other obvious source of chronic blood loss is identified.
  49. Drug Induced Gastritis
    Both NSAIDs and aspirin can cause gastritis and/or gastric ulcers leading to chronic gastrointestinal blood loss and depletion of iron stores. Evaluation of this patient would likely include blood counts, iron studies, and fecal occult blood testing. If iron deficiency is confirmed, especially if there is evidence of ongoing blood loss, definitive diagnosis can be obtained with upper (and usually lower) gastrointestinal endoscopy.
  50. Clinical features of irritable bowel syndrome
    • Rome diagnostic criteria:
    • Recurrent abdominal pain/discomfort more than or equal to 3 days/month for the past 3 months & more than or equal to 2 of the following:
    • • Symptom Improvement with bowel movement
    • • Change in frequency of stool
    • • Change in form of stool
    • Warning sign or symptoms:
    • Signs/symptoms suggesting etiologies other than IBS
    • • Rectal bleeding
    • • Nocturnal (awakens from or prevents sleep) or worsening abdominal pain
    • • Weight loss
    • • Abnormal laboratory findings (eg, anemia & electrolyte disorders)
    • IBS presents most commonly: in young women as chronic, crampy abdominal pain with alternating episodes of constipation and diarrhea.
    • Passage of stool often relieves the pain.
    • It can also present with nonspecific symptoms such as gastroesophageal reflux, dysphagia, early satiety, and chest pain.
    • IBS is further subclassified: as diarrhea-predominant, constipation-predominant or mixed.
    • IBS was previously considered a diagnosis of exclusion.
    • However, patients With ISS symptoms based on the ROME criteria, no alarm features and no family history of inflammatory bowel disease or colorectal cancer do not require extensive workup.
    • Colonoscopy: performed on IBS patients typically shows normal colonic mucosa.
Card Set
colovesical fistula