Gastrointestinal system Flashcards

Question

What are the factors predictive of disease progression in HBV?

Answer 1

 IgG anti-HBc * Yet to rise in acute hepatitis B * +ve in exacerbation (flare) of chronic hepatitis B

Answer 2

 HBeAg can cross the placenta from HBeAg +ve mothers as they are low molecular weight and water-soluble proteins  Immuno-incompetence in infants * Excessive suppression of immune system * Relative cytokine deficiency such as IFN-γ * NK and cytotoxic T-cells deficiency  Failure of host to recognize infected hepatocytes * Covering of HBcAg by maternal anti-HBc

Answer 3

 Hepatitis B virus contains glucocorticoid responsive element that regulates enhancer * Steroids stimulate glucocorticoid responsive element and enhance viral replication and leads to an increase in HBV DNA viral load o Enhancer I stimulates protein expression especially core protein o Enhancer II stimulates surface gene promoters * Steroids withdrawal will lead to immune rebound with increase in cytotoxic suppressor T- cell that increase immune attack on hepatocytes o ↑ AST and ALT level o ↓ HBV DNA level

Answer 4

 Anti-CD20 and anti-CD52 is known to reactivate chronic hepatitis B and occult hepatitis B * Occult hepatitis B is defined as HBsAg -ve but HBV DNA +ve in blood or liver  Mechanism of reactivation * Profound depletion of B cells * HBcAg-binding B cells prime specific cytotoxic T cells

Answer 5

Goal of treatment =cure Eradication of HCV RNA is prediced by achievement of sustained virologic response Traget patients: patient with acute HCV without spontaneous clearance at 12-16 weeks. All patients with chronic HCV should be treated including those with end stage liver disease, except those with short life expectancy due to non HCV disease

Answer 6

 Contact with contaminated food and water * Consumption of raw or undercooked meat or meat products derived from infected animal * Consumption of raw or undercooked shellfish  Blood transfusion  Poor sanitation

Answer 7

Acute - Supportive - No antiviral - Transplant for fulminant Chronic - Ribavirin 12w - Check Sustained Virological Response in 12w via HEV RNA - Lower immunusuppressants

Answer 8

 Peptic ulcer disease  Choledocholithiasis/ Cholangitis/ Cholecystitis  Hepatitis  Mesenteric ischemia  Intestinal obstruction  Myocardial infarction*

Answer 9

 Diagnosis of acute pancreatitis required 2/3 of the following * Acute onset of persistent, severe, epigastric pain often radiating to the back (Clinical) * Elevation of serum amylase or lipase to ≥ 3x upper limit of normal (Biochemical) * Characteristic findings of acute pancreatitis on imaging including transabdominal USG, contrast-enhanced CT and MRI (Radiological)

Answer 10

* CBC with DC: leukocytosis, haematocriti ncreased: haemoconcentration due to extravasation of intravascular fluid into 3rd space (Sequestration of edematous fluid in retroperitoneum) * Serum inflammatory markers: increased CRP levels * LFT: increased conjugated bilirubin, increased AST, ALT and ALP in gallstone pancreatitis * RFT: increased creatinine and blood urea nitrogen * Serum BG level: hyperglycemia/hypoglycemia * Serum Ca2+: hypocalcemia as a result of complexing with fatty acids (saponification or fat necrosis) produced by activated lipases as well as hypoalbuminemia * Serum and urine amylase level: serum amylase >3x ULN to dx acute pancreatitis --> rises within 6-12 hours and peaks at 24 hours after onset --> returns to normal within 3-5 days. FP results (intestinal diseases: perforated bowel, intestinal osbtruction, bowel ischemia. Pancreatic didsease (pseudocyst, post ERCP/acute cholecytisis/alcoholism) * Serum lipase level: >3x ULN to dx acute pancreatitis. More sensitive marker in patients with acloholic pancreatitis. Rises earlier (4-8 hours) and lasts longer than serum amylase thus useful in patients with delayed presentation who present>24hours after onset of pain. Other conditions with elevated serum amylase: post ERCP/pancreatic tumors/acute cholecystitis * Cardiac markers and ECG to exclude MI (must do)

Answer 11

 Resolve spontaneously within 7 – 10 days without the need for drainage

Answer 12

 Angiography is the definitive diagnostic test and has been used increasingly to manage pseudoaneurysms by embolization with radiological coils  Pseudoaneurysms are an ABSOLUTE contraindication to endoscopic drainage unless arterial embolization is performed first * Severe and fatal hemorrhage can occurring following endoscopic drainage in patients with an unsuspected pseudoaneurysm

Answer 13

PE General exam: jaundice Abd exam: hepatomegaly, RUQ tenderness, rebound tenderness, guarding Biochemical tests CBC with DC: normochromic normocytic anemia, leukocytosis Serum inflammatory markers: increased ESR and CRP LFT: hypoalbuminemia Blood culture Aspirate smear, culture and microscopy: CT or USG guided fine needle aspiration. Smear and culture for both aerobic and anaerobic organisms. Microscopy for trophozoites Serology and antigen detection for amebiasis: presence of anti-amebic antibodies. Detection of E.histolytica antigens CXR Ultrasound abd: guide fine needle aspiration for microbial culture CT abdomen: diagnostic modality of choice. Findings of liver abscess include fluid collection with surrounding edema with/without stranding and loculated subcollections. Must be distinguished from cysts and tumors. * Cysts appear as fluid collections without surround stranding or hyperemia * Tumor has a solid radiographic appearance and may contain areas of calcification with fluid filled appearance due to necrosis and bleeding * Cannot differentiate between pyogenic and amoebic liver abscess

Answer 14

* Alcoholic fatty liver disease * Alcoholic hepatitis * Alcoholic cirrhosis

Answer 15

* CBC with DC **Macrocytic anemia: vit b12/folate deficiency, alcohol toxicity or increased lipid deposition** in RBC membranes Hemolytic anemia --> **Zieves syndrome** = hemolytic anemai + jaundice +abd pain + hyperlipidemia. Occurs in patients with severe alcoholic hepatitis or during withdrawal from prolonged alcohol use (alcohol related hemolysis). Haemolytic anemia with spur cells/acanthocytes due to alteration of red cell metabolism namely pyruate kinase instability leaving them susceptible to circulating haemolysin. **Leukopenia**: leucocytosis with neutrophil predominance in alcoholic hepatitis **Thrombocytopenia**: **bone marrow hypoplasia** due to alcohol. Splenic sequestration due to portal hypertension and hypersplenism. * **Clotting profile**: increased PT and INR * LFT: **increased AST and ALT**: to 2x-7x but <400-500IU/L in AFLD and alcoholic hepatitis (never sky high >500IU/L unlike acute viral hepatitis, autoimmune hepatitis and wilsons disease). **AST>ALT** (often ratio>2) due to hepatic deficiency of P5P in alcoholics which is a cofactor for ALT enzymatic activity. Generally ALT>AST in most liver diseases except in alcoholic liver disease, liver cirrhosis and HCC **Increased ALPT and GGT:** GGT elevated in all forms of fatty liver such as non alcoholic steatohepatitis **Hyperbilirubinemia** **Hypoalbuminemia**: impaired hepatic function or malnutrition * RFT: increased creatinine level in patients who develop **hepatorenal syndrome** * Iron profile: serum ferritin and transferrin saturation for hemochromatosis screening. Ferritin and transferrin level may be high in alcoholic liver diseases, acute or subacute hepatitis and hence suspected individuals should undergo further testing for haemochromatosis * **Lipid profile**: hypertriglyceridemia in alcholic fatty liver disease Ddx * **HBV and HCV** serology * **Autoantibodies** for autoimmune hepatitis: total IgG or gamma globulin level, antinuclear antibody (ANA), antismooth muscle antibody, antiliver/kidney microsomal 1 antibody (Anti-LKM-1) Unclear dx * **Liver biopsy**: may be necessary in patients with suspected alcoholic liver disease when dx if unclear due to atypical features of possible concomitant disease

Answer 16

Generally ALT>AST in most liver diseases except in alcoholic liver disease, liver cirrhosis and HCC AST/ALT (ratio >2) in alcoholic liver disease due to hepatic deficiency of P5P in alcoholics which is a cofactor for ALT enzymatic activity

Answer 17

 Alcoholic liver disease  Hepatocellular carcinoma (HCC) complicating post-viral cirrhosis  Wilsons disease

Answer 18

 Advice on total abstinence of alcohol  Liver transplantation * At least 6 months of total abstinence is considered imperative * Indicated for poor liver synthetic function, ascites and variceal bleeding

Answer 19

 Bleeding  Dehydration  Infection  Obesity  Alcoholism  Medications

Answer 20

Place a balloon catheter in the hepatic vein and measure free hepatic venous pressure when balloon is deflated and wedged hepatic venous pressure when balloon is inflated. Hepatic venous pressure gradient = WHVP- FHVP which represents Normal HVPG = 1-5mmHg, portal hypertension is HVPG>6mmHg. Clinically significant when HVPG is ascites >10mmHg, variceal bleeding occurs when >12mmHg

Answer 21

* CBC with DC Anemia: anemia of chronic liver disease. Leukopenia: result of hypersplenism. Thrombocytopenia (common): decreased hepatic synthesis of thrombopoietin and impaired platelet production --> platelet sequestration in spleen in hypersplenism * Clotting profile Increased PT/INR and APTT. Isolated prolonged PT in mild liver disease. Prolonged PT and aPTT in severe liver disease. Deranged clotting profile due to decreased synthetic function is not the most common cause. Usually due to vit K deficiency from decreased absorption of fat soluble vits due to obstructive jaundice (intrahepatic cholestasis) which reduces bile secretion by hepatocytes and bile excretion into intrahepatic bile ducts * Iron profile: increased iron/ferritin/transfferin (TIBC) * Serum protein level Reversed A/G ratio (increased globulin/decreased albumin): globulin increased secondary to portosystemic shunting of bacterial antigens in portal venous blood from liver to lymphoid tissue inducing Ig production. Gut antigens entering liver is not well handled due to cirrhosis. * Hep virus serology: HBV and HCV serology * LFT Increased AST/ALT: AST>ALT but not 2x in liver cirrhosis. Generally ALT>AST in most liver diseases except alcoholic liver disease (except fatty liver), liver cirrhosis sand HCC * RFT: increased creatinine due to hepatorenal syndrome. Hyponatremia due to RAAS stimulation * Serum AFP level: screen for HCC

Answer 22

* Ascites and edema: most common * Spontaneous bacterial peritonitis * Portal hypertensive gastropathy * Variceal hemorrhage * Hepatic encephalopathy * Hepatorenal syndrome * Hepatic hydrothorax * Hepatopulmonary syndrome * Portopulmonary hypertension * Cirrhotic cardiomyopathy

Answer 23

Liver cirrhosis leads to portal hypertension --> splanchnic arterial vasodilation leadas to decreased total systemic vascular resistance --> arterial underfilling leads to decrease effective arterial blood volume. Stimulation of RAAS and sympathetic nervous system --> increased Na+ and H2O retentin + hypoalbuminemia. Ascites and edema formation. Diagnostic paracentesis should be 1st step of management Therapeutic paracentesis for tense ascites sand symptomatic retlief Give IV 6-8g albumin per L tapped if 5L/day of fluid is removed: decreases risk for post paracentesis circulatory dysfunction and hypoNa Exclusion of SBP before large volume paracentesis. Increases risk of acute kidney injury for large volume paracentesis Complications of paracentesis Shock and sepsis Bleeding from puncture sites Perforation of caecum: always do paracentesis in LLQ. Sigmoid colon is mobile with its mesentery whereas caecum is fixed Acute kidney injury: intravascular depletion with large volume paracentesis, excessive paracentesis with inadequate albumin replacement hepatic encephalopathy: excessive paracentesis with inadequate albumin replacement Conservative management Bed rest Salt restriction for 0.5-2g/day Fluid restriction for 0.8-1L/day: indicated in patients with dilutional hyponatremia, monitor input and output, body weight and urine Na+ Diuretics: target weight loss = 1kg/day (1L of diuresis): spironolactone is preferred Precaution: Depletion of fluid into 3rd space and depletion of intravascular volume (diuretics) can lead to hypotensiosn and thus albumin is required to increase oncotic pressure. Other treatment: TIPS and liver transplantation but only for refractory cases that are not responsive to previous treatment

Answer 24

Shunting from portal venous system to caval system: left gastric veins collateralizes to esophageal veins Risk of esophageal varices when HVPG>12mmHg Clinical manifestation: haematemesis, melena, shock Endoscopic grading F1= compression with air insufflation. F2 = Failure of compression with air insufflation. F3 = can occlude the whole lumen Initial manageement **Fluid** replacement for treatment of shock: 2D1S Q6-8H, maintain systolic BP at 90-100Mg **Restrictive blood transfusion** Correction of thrombocytopenia and coagulopathy: **FFP and platelet infusion** **NPO** except for medication **Do not insert NG** tube since it will worsen variceal bleeding (unless there is perforation alreadY) **ET** intubation if coma Close monitoring of vitals including BP/P Q1H Medical treatment **Terlipressin** and ntrioglycerin (1st line treatment) **Octreotide**/somatostatin: inhibits release of vasodilator hormones such as glucagon --> indirectly causing splanchnic vasoconstriction and decreased portal inflow. Surgical management OGD management: endoscopic **band ligation, balloon tamponade**(last line if repeated band ligation fails) can be done for max 1 day Last line is **TIPS** and surgical shunting if refractory to treatment Prevention of further complications - Prevention of hepatic encephalopathy: **lactulose** and titrate until 2-4 soft stools/day. Rationale: blood is high in protein content (increased ammonia digesting the blood) - Prevention of sepsis:**prophylactic antibiotic** for 7 days. Ciprofloxacin in patientd with preserved lung function. Ceftriaxone in patients with advanced cirirhosis or fluoroquinolone resistance. Ertapenem in patients with ESBL enterobacteriaceae infection. - Prevention of rebleeding: **EVL and NSBB** in secondary prevention. EVL repeated Q1-2 weeks until complete obliteration with FU OGD at 3 months and then every 6-12 months to monitor for recurence

Answer 25

 Post-hepatitis cirrhosis of liver * History of chronic hepatitis B * Stigmata of chronic liver disease * Shrunken liver * Splenomegaly * Ascites  Ascites * Secondary to cirrhosis of liver due to chronic hepatitis B infection

Answer 26

 From his mother at birth or through close post natal contact * Maternal uncle’s death due to HCC further confirms that his mother’s family had the infection * Typically not all siblings are infected and theoretically the younger children are less likely to be infected o Mother might have undergone HBeAg seroconversion resulting in a lower viral load as she grows older  Sexual transmission due to multiple sexual partners * Infection in adulthood is unlikely to give rise to chronic infection

Answer 27

 Concomitant ankle swelling is indicative of fluid retention in patient * Making ascites a likely cause of his simultaneous abdominal swelling  Cirrhotic patients are prone to develop ascites early due to portal HT * Portal HT will localize retained fluid in the peritoneum

Answer 28

* CBC: degree of hypersplenism (seqeustration) * Hep B serology: HBsAg (tested annually since there is 0.1-1% annual rate of spontaneous HBsAg seroclearance. HBeAg, HBV DNA (needs checking to determine whether the patient requires treatment * LFT Increased AST and ALT level Increased ALP and GGT level Decreased serum albumin level Increased serum globulin level Increased AFP (routine measurement for HCC) Increased PT * RFT: baseline for diuretic therapy * Paracentesis of ascites fluid: decreased protein level * USG liver and spleen: performed every 6 months to detect early HCC <3cm in diameter

Answer 29

* Autoimmine thyroiditis * Graves disease * Ulcerative colitis * Immune thrombocytopenia

Answer 30

 Acute hepatitis  Chronic hepatitis  Primary biliary cholangitis  Primary sclerosing cholangitis  Wilson’s disease  Hepatic hemochromatosis

Answer 31

Liver biopsy only indicated if dx is unclear. Findings: * Presence of interface hepatitis * Presence of lymphocytic or lymphoplasmacytic infiltrates in the portal tracts and extending into lobules * Fibrosis is present in all forms of autoimmune hepatitis which connects portal and central areas (bridging) and ultimately leads to cirrhosis by arhictectural distortion of the hepatic lobule and appearance of regenerative nodules

Answer 32

 Stasis + Stricturing + Recurrent infection * Stone formation lead to a cycle of persistent obstruction predisposing to stasis and recurrent infection with additional stone formation * Stricture formation is the result of repeated episodes of inflammation and healing

Answer 33

 Causes of secondary sclerosing cholangitis * Chronic bacterial cholangitis * Recurrent pyogenic cholangitis * Choledocholithiasis * Cholangiocarcinoma * Recurrent pancreatitis * Surgical biliary trauma  Autoimmune pancreatitis/ IgG4-associated cholangitis  Autoimmune hepatitis-PSC overlap syndrome

Answer 34

P- ANCA most common, above IgM and AMA

Answer 35

* Pruritis * Fatigue * Steatorrhea: decreased bile acid production * RUQ discomfort

Answer 36

Radiological ix: USG abdomen and MRCP (exclude extrahepatic biliary obstruction)

Answer 37

 Factors associated with a poorer prognosis * Unresponsive to ursodeoxycholic acid (UDCA) * Presence of symptoms at the time of diagnosis * Elevated ALP and bilirubin levels * Advanced histological stage * Presence of anti-nuclear antibodies (ANA)

Answer 38

 Ursodeoxycholic acid * Affects biliary composition and flow by unknown mechanism * Results o Decreases pruritus o Improves liver function o Improves survival and delay liver transplantation

Answer 39

 Medications * (IV) Dextrose drip o Provide adequate calorie intake to prevent protein breakdown * (Oral) Lactulose o As an enema with the aim of inducing bowel movements 2 – 4 times per day  Remarks * No protein diet * Any treatable precipitating factor should be identified and treated

Answer 40

 Mechanism * Non-absorbable disaccharide * Acts as an osmotic diarrheal agent * Acted upon by lactobacilli in colon to form H2 and CO2 * Acidic pH buffers NH3 from gut-derived bacteria and in blood to form NH4+  Side effects * Flatulence * Dehydration (From excessive diarrhea) * Aversion to sweet taste

Answer 41

 MELD is superior because * It has a continuous scale for all 3 parameters in the formula whereas the Childs-Pugh score is discontinuous * It eliminates subjective elements (presence and degree of encephalopathy or ascites) and parameters that are often variable in different laboratories o Serum albumin o Prothrombin time

Answer 42

 Bimodal distribution * Affects young patients in 20 – 30 years old * Affects older patients in 50 – 60 years old  Female predominance * In contrast with no gender predominance in ulcerative colitis (UC) * Male predominance is observed in East Asia

Answer 43

* Antibiotics indication (concomitant infection): active luminal disease, perianal diseases such as fistula, septic complications of IBD such as abscess and wound infection e.g. ciprofloxacin/metronifazole * 5-ASA (mesalamine) Clinical role = induction agent (induction of remission Mesalamine = 2-4g/da, sulfasalazine (being phased out due to AE) = 3-6g/day (AE: agranulocytosis, SJS, pancreatitis, fever, headache) Sulfasalazine is used for colitis as increased bioavailability since colonic bacteria cleaves the sulphur bond to release the 5-ASA moiety * Glucocorticoids (indicated in patients who do not respond to 5-ASA and antibiotics): calcium and vit D supplements required for osteoporotive effect if prescribed for more than 12 weeks Prednisolone =40mg/day reducing by 5mg/day at weekly intervals, 20mg/day for 4 weeks reducing by 5mg/day at weekly intervals Budesonide (preferred for UC as it has high 1st pass effect --> very little will escape into systemic circulation --> stay in colon) * Immunomodulators (indicated in patients with refractory disease Clinical role: maintenance agent (maintenance of remission) + steroid sparing check TPMT level if available. AZA (azathioprine) --> 6-MP --> 6TG and 6MMP 6TG levels predict bone marrow toxicity and therapeutic efficacy. 6MMP levels predicts hepatotoxicity. High TPMT activity: higher 6-MMP and increase risk of hepatotoxicity Low TPMT activity (homozygous mutation of TPMT): higher 6-TG and increase risk of myelosuppression Dsoage: azathioprine 1.5-2.5mg/kg/day 6-mercaptopurine = 0.75-1.5mg/kg/day Methotrexate (IM/SC) = 25mg/week x 16 weeks for induction, 15mg/week for maintenance AE of AZA: myelosuppression, hepatotoxicity, pancreatitis * Biologic therapies Must screen for TB with CXR/quantiFERON TB Gold + HBV infection with HBsAg. Requires TB prophylaxis with isoniazid/rifampicin, requires HBV prophylaxis with entecavir Contraindications: latent untreated or active TB, lymphoma, heart failure of NYHA class III-IV Infliximab (1st line), adalimumab Infliximab induction IV 5mg/kg at 0,26 weeks. Maintenance = IV 5mg/kg Adalimumab induction = SC 160 mg at 0 week and 80 mg at 2 weeks; Maintenance = SC 40 mg Q2 weeks

Answer 44

Avoid surgery until absolute necessary Surgical treatment is not curative in crohns disease and is mainly used to treat compications only. Bowel preserving surgery performed to avoid short gut syndrome Indications for surgery * Persistent symptoms refractory to medical treatment * Presence of complications including severe bleeding, strictures, abscess, fistula, perforation, malignancy

Answer 45

Montreal classification

Answer 46

* Antibiotics indication (concomitant infection): active luminal disease, perianal diseases such as fistula, septic complications of IBD such as abscess and wound infection e.g. ciprofloxacin/metronifazole * 5-ASA (mesalamine): topical 5-ASA is 1st line treatment in mild to moderate UC in those willing to use rectal therapy including suppositories or enemas Clinical role = induction agent (induction of remission Mesalamine = 2-4g/da, sulfasalazine (being phased out due to AE) = 3-6g/day (AE: agranulocytosis, SJS, pancreatitis, fever, headache) Sulfasalazine is used for colitis as increased bioavailability since colonic bacteria cleaves the sulphur bond to release the 5-ASA moiety * Glucocorticoids (indicated in patients who do not respond to 5-ASA and antibiotics): calcium and vit D supplements required for osteoporotive effect if prescribed for more than 12 weeks Budesonide (preferred for UC as it has high 1st pass effect --> very little will escape into systemic circulation --> stay in colon) or prednisolone enema or suppository is used for distal colitis Oral budenoside or prednisolone is used for mild to moderate disease IV hydrocortisone is used for severe disease * Immunomodulators (indicated in patients with refractory disease Clinical role: maintenance agent (maintenance of remission) + steroid sparing check TPMT level if available. AZA (azathioprine) --> 6-MP --> 6TG and 6MMP 6TG levels predict bone marrow toxicity and therapeutic efficacy. 6MMP levels predicts hepatotoxicity. High TPMT activity: higher 6-MMP and increase risk of hepatotoxicity Low TPMT activity (homozygous mutation of TPMT): higher 6-TG and increase risk of myelosuppression Dsoage: azathioprine 1.5-2.5mg/kg/day 6-mercaptopurine = 0.75-1.5mg/kg/day AE of AZA: myelosuppression, hepatotoxicity, pancreatitis Methotrexate is NOT effective in UC unlike in Crohns * Biologic therapies Must screen for TB with CXR/quantiFERON TB Gold + HBV infection with HBsAg. Requires TB prophylaxis with isoniazid/rifampicin, requires HBV prophylaxis with entecavir Contraindications: latent untreated or active TB, lymphoma, heart failure of NYHA class III-IV Infliximab (1st line), adalimumab Infliximab induction IV 5mg/kg at 0,26 weeks. Maintenance = IV 5mg/kg Adalimumab induction = SC 160 mg at 0 week and 80 mg at 2 weeks; Maintenance = SC 40 mg Q2 weeks

Answer 47

* Pain and spasm resulting from contraction of a hollow organ against an obstruction o Biliary colic o Ureteric colic o Intestinal colic

Answer 48

* Kidney stones o Causes symptoms when stone passes from renal pelvis into ureter o Patients can have flank pain, back pain and abdominal pain * Pyelonephritis o May or may not have symptoms such as dysuria, frequency, urgency or hematuria o Presents with fever, chills, flank pain and costovertebral angle tenderness

Answer 49

* Gastroenteritis: viral gastroenteritis presents with diarrhea, nausea and vomiting * Diverticulosis * GI malignancy * Intestinal obstruction. Cardinal features: abd pain + distension + vomiting +absolute constipation * IBD: crohns disease, ulcerative colitis * Irritable bowel syndrome * Mesenteric ischemia * Spontaneous bacterial peritonitis: occurs in liver cirrhosis with advanced liver disease and ascites * Celiac disease: presents with diarrhea with bulky, foul smelling, floating stools due to steatorrhea and flatulence * Ketoacidosis * Lactose intolerance: abd pain, bloating, flatulence, diarrhea

Answer 50

* Defined as a persistent or intermittent non-painful sensation of a lump or foreign body in the throat with occurrence of sensation between meals * ABSENCE of dysphagia and odynophagia

Answer 51

 Subjective sensation of difficulty or abnormality of swallowing suggesting presence of organic abnormality in passage of solids or liquid from oral cavity to stomach  Chief complaint ranges from inability to initiate a swallow to the sensation of solid or liquid being hindered during the passage through esophagus into stomach

Answer 52

 Most likely diagnosis = Functional dyspepsia * Commonest cause of epigastric discomfort * Common presentation in the Chinese * Estimated population prevalence of 10 – 20 %  Functional dyspepsia has to be distinguished from uninvestigated dyspepsia * Uninvestigated dyspepsia refers to initial presentation to family doctors o GERD o Peptic ulcers o Esophageal and gastric cancer o Gallbladder and related biliary disorder o Pancreatitis o Pancreatic cancer  Diagnosed of exclusion by investigations * Blood tests * Upper endoscopy * Ultrasound (USG)

Answer 53

* Hematemesis * Hematochezia * Fresh PR bleeding * Fresh blood aspirated from NG tube * Tachycardia

Answer 54

* Age>60 * Coagulopathy * Hb < 8.0 g/dL on presentation * Shock on presentation * Require blood transfusion

Answer 55

HPI Nature, rate and duration of bleeding Severity of bleeding: anemic symptoms (pallor/palpitations/cold and clammy extremities), orthostatic hypotension Associated symptoms: * Epigastric, RUQ pain --> peptic uler disease * Dysphagia, odynophagia, GERD --> esophagitis/esophageal ulcer * Dysphagia, early satiety, weight loss and cachexia --> malignancy * Vomiting, coughing prior to haematemesis --> mallory-Weiss tear * Jaundice, abd distension, anorexia, fatigue --> varicess/portal hypertension gastropathy

Answer 56

Resuscitation and stabilize patient NPO Risk stratification applyingh Rockall score or Blatchford scare 2 large bore IV lines for fluid resuscitation NG tube if massive haematemesis Arrange OGD within 24 hours (emergency OGD if not responsive to initial resuscitation) Close monitoring of vitals Withhold anticoagulants and antiplatelts O2 supplementation Blood transfusion: Hb <7g/dL in low risk patients, Hb >9g/dL in high risk patients (elderly, CAD) Bleeding: FFP for coaguloapthy, platelets for thrombocytopenia PPI: pantaprazole Antibiotics: amoxicillin clavulanate (for all cirrhotic patients for spontaneous bacterial peritonitis prophylaxsi) Peptic ulcer disease: haemoclip, haemospray Esophageal varices: Endoscopic variceal banding: keep trying if repeated failure do SB tube

Answer 57

* Diverticular bleeding (15-55% most common): sac like protrusion of colonic wall --> penetrating vessels are draped over the dome of diverticulum as diverticulum forms and the vessels are separated from bowel lumen only by mucosa (weakness of the artery predispose to rupture into bowel lumen. * Angiodysplasia (most common in age >65): dilated tortuous submucosal vessels (bleeding is venous in origin and tends to be less massive than divertiulcar bleeding) * Hemorrhoids (most common in age <50) * Colitis: infectious/ischemic/radiation colitis * IBD: crohns disease and ulcerative colitis * CRC * Anorectal disorders (fresh PR blood): rectal ulcers, rectal varices, anal ulcers, anal fissures and dieulafoys lesion * Radiation telangiectasia and proctitis * Following biopsy or polypectomy (post polypectomy syndrome) * Massive bleeding from small bowel sources: meckels diverticulitis, crohns disease (ileitis), angiodysplasia, hemangioma

Answer 58

* Colonoscopy * Proctoscopy: exclusion of bleeding from anorectal disorders (part of PE) * OGD: indicated if bleeding source not identified in colonoscopy * CT angiography * Radionuclidie imaging: 99mTc RBC labeled scan : 0.1-0.5ml/min --> poor localization of bleeding * Angiography: requirs 0.5-1ml/min --> intrarterial vasopressin/transcatheter embolization

Answer 59

 Bilirubin is formed by breakdown of heme present in haemoglobin (Hb) (80 – 90%), myoglobin, cytochrome, catalase and peroxidase * HemeBiliverdin + CO by heme oxygenase o Heme oxygenase is an enzyme that is present in reticuloendothelial cells of spleenand Kupffer cells of liver o Measurement of CO production can be used as indices of bilirubin production * Biliverdin Bilirubin by biliverdin reductase

Answer 60

Binding of bilirubin to albumin: binding to albumin and high density lipoprotien keeps bilirubin in plasma. Prevention of bilirubin deposition into extrahepatic tissue including the brain. Uptake and storage of bilirubin by hepatocytes Conjugation of bilirubin: conjugated with glucuronic acid into bilirubin diglucuronide by UDP-glucuronosyl transferase in the endoplasmic reticulum of hepatocytes. Conjugated bilirubin is more water soluble than unconjugated bilirubin and hence is excretede in bile into the gut

Answer 61

LA classification

Answer 62

 Infective esophagitis  Pill esophagitis  Eosinophilic esophagitis  Esophageal motor disorders  Peptic ulcer disease  Non-ulcer dyspepsia  Coronary artery disease

Answer 63

* PPI testing: 1-4 weeks --> symptoms relieved * Esophageal manometry: not routine * Ambulatory 24 hour esophageal pH monitoring is gold standard (BRAVO system): radiotelometry pH sensitive prove 5cm above EGJ. pH <4 for more than 6-7% of study time is diagnostic of reflux diseases * OGD: evaluate for esophagitis, strictures and Barrets esophagus. Indications for OGD * Alarming features (dysphagia/odynophagia/ haematemesis/melena/anemia/vomiting/weight loss/family history of esophageal or gastric cancer/chronic NSAIDs usage) * History of esophageal stricture who have recurrent dysphagia * Suspected complication such as esophagitis and Barrets esophagus * Persistent symptoms despite PPIs * Severe esophagitis (LA grade C-D) after 8 weeks of PPI to asess healing * Evaluation after anti-reflux surgery

Answer 64

 Behavioral modifications * Weight loss * Smoking cessation * Avoidance of tight belts or corsets * Remains upright after meal for at least 1 hour * Elevation of bed head to improve nocturnal symptoms  Dietary modifications * Low-fat diet * Avoidance of alcoholism * Avoidance of chocolate, spicy food, coffee * Eat small frequent meals * Avoidance of late meals (eating later than 2 – 3 hours before bedtime)

Answer 65

 Esophagitis * Reflux esophagitis (Erosive esophagitis)  Esophageal ulcers  Esophageal stricture  Esophageal adenocarcinoma  Barrett’s esophagus

Answer 66

Essentially all acute cholecystitis patients shoulder under laparoscopic cholecystectomy due to improvement in surgical outcome regardless of late presentation (do drainage first).

Answer 67

Cholangitis is one of the 2 most common complications of CBD stones with the other being gallstone pancreatitis Clinical syndrome characterized by fever, jaundice and abd pain. Results from stasis then infection (biliary sepsis) in biliary tract)

Answer 68

 Gram +ve organisms * Enterococcus sp.  Gram -ve organisms * Escherichia coli * Klebsiella pneumoniae * Enterobacter sp. * Bacteroides fragilis

Answer 69

 Choledocholithiasis (most common)  Benign or malignant strictures (MBO) of bile ducts or at biliary-enteric anastomosis  Indwelling stents (stent occlusion) or instrumentation of ducts  Tumours  Parasitic infection

Answer 70

 Surgical drainage for acute cholangitis is reserved for patients in whom other methods of biliary drainage cannot be performed or have failed  Treatment according to underlying causes * Choledocholithiasis o Laparoscopic/ Open ECBD with removal of stones and placement of T-tube (OR) o Cholecystectomy in patients who are hemodynamically stable * Malignant biliary obstruction (MBO) o Resection (Whipple operation) o Bypass (Hepaticojejunostomy/Choledochojejunostomy)

Answer 71

* CBC with DC: thrombocytoepnia, anemia * Clotting profile for child pughs score: PT and INR * LFT: hyperbilirubinemia, increased AST>ALT (in most liver diseases except in alcoholic liver diseae, liver cirrhosis adn HCC). Increased ALP and GGT * HBV serology: HBsAg, anti HBc, HBV DNA * HCV serology: anti HCV antibodies, HCV RNA * Serum AFP: for monitoring treatment. (other causes of increased AFP: pregnancy, germ cell tumors, hepatitis, liver cirrhosis, gastric cancer)

Answer 72

* USG (screening patients with HCC): poorly defined margins, coarse irregular internal echoes, hypoechoic in smalll tumors * Triphasic CT scan with contrast of the abdomen. Non rim hyperenhancement during arterial phase, rapid venous washout in venous and delayed phase * MRI scan: high intensity pattern on T2Wi and low intensity on T1Wi. Enhanced in aterial phase because of hypervascularity and becomes hypointense in delayed phase due to contrast washout after gadolinium injection * Hepatic arteriography and post lipiodol CT scan * Dual tracer PET scan * Percutaneous liver biopsy * Imaging modalities to detect extrahepatic metastasis: CXR/CT thorax, bone scan

Answer 73

 Distant metastasis  Moderate or severe liver function impairment  AV shunting around the tumour  Portal vein thrombosis * Non-tumorous liver may be completely dependent on hepatic arterial blood supply  Diffuse HCC * Response is very unlikely

Answer 74

 Hepatic resection  Radiofrequency ablation for small tumours  Liver transplantation

Answer 75

 Transarterial chemoembolization (TACE)  Sorafenib

Answer 76

 Wilson’s disease is due to a genetic abnormality inherited in an autosomal recessive (AR) manner that leads to impairment of cellular copper (Cu2+) transport * Defective protein fails in copper incorporation into ceruloplasmin and biliary copper excretion leading to accumulation of copper in several organs most notably the liver, brain and cornea

Answer 77

 Depression  Irritability  Psychosis  Labile mood  Personality change  Inappropriate behavior  Declining school performance

Answer 78

* CBC with DC: coombs negative hemolytic anemiae (Decreaed fibrinogen, haptoglobin, increased reticulocyte count), thrombocytopenia (hypersplenism due to portal hypertension in patietn with liver cirrhosis) * Clotting profile: coagulopathy secondary to cirrhosis or acute liver failure * LFT: increased AST, ALT * HBV and HCV serology (HBsAg, anti HBc, HBV DNA, HCV antibodies, HCV RNA) * Serum copper level * Serum ceruloplasmin level (protein synthesized by hepatocytes --> decreased in WD) * 24 hour urinary copper excretion: WD associated with 24 hour urinary copper excretion >100mcg/day. Normal range should be <40mcg/day * Liver biopsy (cold standard for dx): for hepatic copper concentration and histology. Dx when hepatic copper concentration >250mcg/g of dry weight * Mutation analysis (not used for initial dx). Family screening of sibling should begin with mutation analysis for ATP7B mutation if identified patient has been treatead.

Answer 79

 Malnutrition  Intrabdominal malignancy  Ascites  Chronic liver disease  Chronic renal disease  Immunosuppression  Splenectomy

Answer 80

 Enveloped double-stranded DNA virus  Hepadnavirus in the family Hepadnaviridae