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MBBS VI Medicine > Gastrointestinal system > Flashcards

Gastrointestinal system Flashcards

1
Q

What are the general features of hep A
Mode of transmission
Incubation period

A

Self limited disease and does not become chronic: no carrier state and no chronicity

Mode of transmission
* Fecal oral route: person to person contact, consumption of contaminated food
* Bloodborne transmission can occur but uncommon: blood transfusion, acupuncture, tattoing

Incubation period: 15-50 days –> infected individuals are ccontagious during incubation period and remain for about a week after jaundice occurs. HAV replicates in the liver and is shed in the stool in high concentrations from 2-3 weeks before to 1 week after onset of critical illness

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2
Q

What are the RF for HAV infection?

A
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3
Q

What is the pathogenesis of hepatitis in HAV?

A

 Hepatic injury occurs as a result of host immune response to HAV
* Viral replication in hepatocyte cytoplasm
* Hepatocellular damage and destruction of infected hepatocytes is mediated by human
leukocyte antigen, HAV-specific CD8+ T-cells and NK cells
* IFN-γ facilitates clearance of infected hepatocytes

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4
Q

What SS for acute HAV?

A
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5
Q

What is the ddx for HAV?

A
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6
Q

What biochemical tests done for HAV?

A
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7
Q

What are recommendations for HAV?

A

 NO alcohol for 6 months in acute hepatitis
* Especially for hepatitis C infection
 NO known drugs that can hasten recovery or modify acute or exacerbation of hepatitis

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8
Q

What are the complications of acute hep A

A
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9
Q

What can done for prevention of acute HAV?

A
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10
Q

What are the possibilities of a +ve IgM anti-HAV antibodies with absence of clinical symptoms of hepatitis?

A

 Previous HAV infection with persistent IgM
 False positive (FP) result
 Asymptomatic infection
* Common in children < 6 years of age than older children and adults

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11
Q

What are the chances of acute infection in HBV
Presence of chronicity depends on age
Risk of cirrhosis and HCC
Mode of transmission

A
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12
Q

What is the terminology for different clinical states of hep B?

A
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13
Q

What is the micbio of HBV?

A

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

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13
Q

What is the pathogenesis of HBV?

A
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14
Q

What is the clinical course of HBV?

A
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15
Q

What are the SS of HBV?

A
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16
Q

What is the ddx for HBV?

A

 Hepatitic episodes in chronic hepatitis
* Superinfection with other hepatitis virus
* Drug-induced hepatitis
* Wilson’s disease

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17
Q

What PE and Ix for HBV?

A

PE
General exam: fever, jaundice
Abd exam: stigmata of chronic liver disease, hepatomegaly, splenomegaly, abd tenderness, ascites, peripheral edema

Biochemical tests
* CBC with DC: leukopenia and thrombocytopenia: due to hypersplenism in liver cirrhosis
* LFT: increased AST and ALT: ALT is typically higher than AST in the acute phase. ALT can be as high as 50x ULN in acute exacerbation of chronic hep B infection. Persistent elevation of serum ALT >6 months indicates a progression into chronic hepatitis. Safe ALT level is defined as 0.5 ULN (male: 30IU/L, female:19IU/L)
* Clotting profile: increased PT

HBV serology
* HBsAg: serological hallmark for HBV infection
* Anti-HBs: confers long term immunity
* Anti-HBc
* HBeAg
* Anti-HBe: associated with high levels of HBV DNA, higher rates of transmission of HBV infection and active liver disease
* HBV DNA: assess HBV DNA replication, assess suitability for antiviral therapy (high pretreatment HBV DNA levels are unlikely to respond to IFN). Assess response to antiviral treatment: suppression of HBV DNA to undetectable levels by PCR is the goal

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18
Q

What is the HBV serology for different phases of acute and chronic hep B infeciton?

A
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19
Q

What is the interpretation of hep B serological panel?

A
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20
Q

How do you differentiate acute HBV infection from acute exacerbation of chronic HBV infection?

A
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21
Q

When to start and end treatment in HBV?

A
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22
Q

What are the indications for management of acute HBV?

A
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23
Q

What are the antiviral treatments for HBV?

A

TAF is 1st line, TDF 1st line in pregnancy (not done in clinical trial for safety)

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24
Q

What are the complications from hep B infection?

A
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25
Q

What are the factors predictive of disease progression in HBV?

A
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26
Q

What are the possible coinfections of HBV with other hep viruses?

A
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27
Q

What is done for prevention of infants born to mothers who are HBsAg +ve
transplant recipients

A
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28
Q

What is done for prevention for prexposure HBV vaccination?

A
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29
Q

What is done for prevention of HBV reactivation by steroids?

A
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30
Q

What is done for prevention for reactivation of HBV by anti CD20 and anti CD52?

A
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31
Q

What is done for prevention for reactivation of HBV after liver transplantation?

A
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32
Q

How do you differentiate acute hepatitis B and exacerbation (flare) of chronic hepatitis B when IgM anti-HBc are both +ve?

A

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

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33
Q

What are the possible reasons for HBV chronicity in neonates?

A

 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

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34
Q

Why do we have to give hepatitis B cover (e.g. Entecavir) when prescribing corticosteroids?

A

 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

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35
Q

What are the precaution of prescribing anti-CD20 (e.g. Rituximab) and anti-CD52 medication in chronic hepatitis B?

A

 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

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36
Q

What are the general features of hep C infection?
Presence of chronicity
Mode of transmission?

A
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37
Q

What are the characteristics of HCV?

A
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38
Q

What are the extrahepatic manifestation of HCV?

A
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39
Q

What biochemical tests for HCV infection?

A
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40
Q

What is medical treatment of HCV infection?

A

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

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41
Q

What are the complications of chronic HCV infection?

A
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42
Q

What is done for prevention of HCV infection?

A
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43
Q

Is HEV a self limiting disease
Mode of tansmission?
Incubation period

A
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44
Q

What is the micbio of HEV
genotypes

A
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45
Q

What is the general epidemiology of HEV?

A
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46
Q

RF for HEV infection?

A

 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

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47
Q

SS of HEV?

A
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48
Q

ddx for acute HEV?

A
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49
Q

What is treatment for acute and chronic (immunocompromised) hep E?

A
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50
Q

What are the complications of HEV infection?

A
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50
Q

What is the Ranson criteria: scoring system for severity of acute pancreatitis?

A
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51
Q

What scoring system to allow continual assessment of acute pancreatitis?

A
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52
Q

What are the causes of acute pancreatitis?

A
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53
Q

What is the characteristics of pancreas (location), arterial supply and venous drainage

A
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54
Q

What is the pathophysiology of acute pancreatitis?

A
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55
Q

What is the ddx of acute pancreatitis?

A

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

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56
Q

What is diagnostic criteria of acute pancreatitis?

A

 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)

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57
Q

What PE for acute pancreatitis?

A
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58
Q

What Ix for suspected acute pancreatitis?

A
  • 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)
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59
Q

What radiological Ix for acute pancreatitis
What grading according to Ix?

A
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60
Q

What is the general management of acute pancreatitis?

A
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61
Q

What is medical and surgical management of acute pancreatitis?

A
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62
Q

What are the local complications of acute pancreatitis?

A
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63
Q

What are the peripancreatic vascular complications of acute pancreatitis?

A
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64
Q

What are the systemic complications and organ failure in acute pancreatitis?

A
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65
Q

What is the management of peripancreatic fluid collection post acute pancreatitis?

A

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

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66
Q

What is the management of pancreatic pseudocyst and walled off necrosis (WON) post acute pancreatitis and indications for intervention?

A
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67
Q

What is the management of infected necrosis (acute necrotic collection or walled off necrosis) post acute pancreatitis?

A
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68
Q

What is the management of pseudoaneurysm post acute pancreatitis?

A

 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

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69
Q

How to prevent acute pancreatitis?

A
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70
Q

What are the types of liver abscess
Route of spread

A
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71
Q

What is the micbio of liver abscess?

A
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72
Q

What PE of liver abscess
What Ix

A

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

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73
Q

What is the medical and surgical management of liver abscess?

A
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74
Q

What are the complications of liver abscess
What association with underlying condition

A
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75
Q

What are the alcohol limits set by medicine?
What is alcohol unit?

A
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76
Q

What are the 3 major lesions for pathology of alcoholic liver diseases?

A
  • Alcoholic fatty liver disease
  • Alcoholic hepatitis
  • Alcoholic cirrhosis
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77
Q

How is alcohol metabolized in the body”

A
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78
Q

What is the pathological course for alcoholic liver disease?

A
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79
Q

How does the clinical manifestation differ in alcoholic fatty liver disease (AFLD) vs alcoholic hepatitis vs alcoholic cirrhosis

A
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80
Q

What are the stigmata of chronic liver disease?

A
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81
Q

What history taking for alcoholic liver disease and PE?

A
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82
Q

What biochemical Ix done for alcoholic liver disease?

A
  • 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
  • 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)
  • Liver biopsy: may be necessary in patients with suspected alcoholic liver disease when dx if unclear due to atypical features of possible concomitant disease
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83
Q

What liver diseases reversed ALT/AST ratio?

A

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

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84
Q

What radiological Ix for alcoholic liver disease?

A
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85
Q

What is the treatment for alcoholic liver disease?

A
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86
Q

A patient present with jaundice, liver palms and distended epigastrium. The liver is firm, enlarged with an irregular surface. There is ascites and there is no spleen.
Q1: What are the causes for cirrhosis with a large liver?

A

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

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87
Q
A
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88
Q

What typical abnormalities may laboratory investigations reveal?

A
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89
Q

Besides liver cirrhosis, what other liver disease entities may result from abusing alcohol?

A
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90
Q

What is management for variceal bleeding?

A
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91
Q

What is long term strategy needed to manage patient with decompensated alcoholic liver disease?

A

 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

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92
Q

What are the RF for decompensation of cirrhosis?

A

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

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93
Q

What are the causes of liver cirrhosis?

A
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94
Q

What are SS of chronic liver disease
Cirrhosis complications

A
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95
Q

What is the pathophyiology of portal hypertension?
What is normal value and clinically significant pressure?

A

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

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96
Q

What biochemical ix for liver cirrhosis and expected results?

A
  • 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
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97
Q

What radiological ix for cirrhosis?

A
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98
Q

What are the complications of liver cirrhosis (decompensated cirrhosis)?

A
  • 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
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99
Q

What is the management for ascites and edema in liver cirrhosis?

A

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

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100
Q

What are the different types of bacterial peritonitis complicating liver cirrhosis?

A
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101
Q

What is pathogenesis and treatment for portal hypertensive gastropathy (complication of liver cirrhosis)?

A
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102
Q

What is pathogenesis and treatment for variceal hemorrhage (complication of liver cirrhosis)?

A

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

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103
Q

How to grade hepatic encephalopathy and pathogenesis (complication of liver cirrhosis)

A
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104
Q

What are the precipitating factors for hepatic encephalopathy?

A
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105
Q

What are the clinical features of hepatic encephalopathy?

A
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106
Q

How to dx hepatic encephalopathy
Management
medical treatment

A
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107
Q

What is pathophysiology of hepatorenal syndrome?
What clinical presentation?

A
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108
Q

What is the diagnostic criteria for hepatorenal syndrome?

A
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109
Q

What is the management of hepatorenal syndrome?

A
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110
Q

What is hepatic hydrothorax, management and precautions?

A
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111
Q

What is the physiology of hepatopulmonary syndrome
what treatment

A
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112
Q

What is the physiology of portoopulmonary syndrome
clinical features
what treatment

A
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113
Q

How to assess prognosis of liver cirrhosis?

A
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114
Q

What components in MELD for liver disease?

A
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115
Q
A

 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

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116
Q

How did the patent acquire the hepatitis B infection?

A

 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

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117
Q

What evidence is there that his abdominal distension is not due to obesity and why are cirrhotic
patients more prone to develop ascites at an early stage of disease?

A

 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

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118
Q

What relevant Ix done?

A
  • 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
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119
Q

How would you treat this patient?

A
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120
Q

How to classify autoimmune hepatitis?

A
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121
Q

What are the associated conditions of autoimmune hepatitis?

A
  • Autoimmine thyroiditis
  • Graves disease
  • Ulcerative colitis
  • Immune thrombocytopenia
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122
Q

What is the ddx of autoimmune hepatitis?

A

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

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123
Q

What biochemical Ix for suspected autoimmune hepatitis?

A

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

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124
Q

What is treatment indications regimen for autoimmune hepatitis?

A
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125
Q

What is the pathophysiology of recurrent pyogenic cholangiits?

A
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126
Q

What is the etiology of recurrent pyogenic cholangitis?

A
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127
Q

What is the components for pathogenesis of RPC?

A

 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

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128
Q

What SS of RPC
What radiological tests

A
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129
Q

What is treatment of RPC?

A
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130
Q

What are hepatobiliary and specific complications of RPC?

A
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131
Q

What is the general features of primary sclerosing cholangitis
What associated medical conditions?

A
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132
Q

What is the ddx for primary sclerosing cholangitis (PSC)?

A

 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

133
Q

What PE and biochemical Ix for primary sclerosing cholangiits?

A
134
Q

What radiological ix and results for primary sclerosing cholangitis?

A
135
Q

What is medical and surgical management of primary sclerosing cholangitis?

A
136
Q

What are the complications of primary sclerosing cholangitis?

A
137
Q

What are the general features of primary biliary cholangitis
What are the associated medical conditions?

A
138
Q

What are the SS of primary biliary cholangitis?

A
  • Pruritis
  • Fatigue
  • Steatorrhea: decreased bile acid production
  • RUQ discomfort
139
Q

What is the diagnostic criteria for PBC and PE results?

A
140
Q

What biochemical Ix done for primary biliary cirrhosis?

A

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

141
Q

What is treatment (conservative, medical and surgical) of primary biliary cirrhosis?

A
142
Q

What is the management of complications of PBC (primary biliary cirrhosis)?

A
143
Q

What are the complications of PBC?

A
144
Q

What are the prognostic factors of PBC?

A

 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)

145
Q

What is the basis for diagnosing primary biliary cirrhosis (PBC)?

A
146
Q

Is there any specific drug treatment for PBC and how effective is it?

A

 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

147
Q

How would you manage hepatic encephalopathy?

A

 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

148
Q

What is moa and AE of lactulose for hepatic encephalopathy?

A

 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

149
Q

What issues need consideration when contemplating liver transplantation?

A
150
Q

In what way is the MELD score superior to the Childs-Pugh score?

A

 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

151
Q

What are the clinical subtypes of Crohns disease?

A
152
Q

How to assess the disease activity of crohns disease?

A
153
Q

What phenotypical classification used for crohns disease?

A
154
Q

Compare between crohns disease and ulcerative colitis in clinical presentation, biochemical features, histological features and endoscopic features?

A
155
Q

What is the epidemiology in for crohns disease?

A

 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

156
Q

What are the SS of crohns disease?

A
157
Q

What are the SS of complications for crohns disease?

A
158
Q

What are the extraintestinal manifestation of crohns disease?

A
159
Q

What is the ddx of crohns disease?

A
160
Q

What biochemical tests done for Crohns disease?

A
161
Q

What imaging done for crohns disease and what to observe?

A
162
Q

What are not 1st line imaging for crohns disease?

A
163
Q

What are the principles of management of crohns disease?

A
164
Q

What is the medical treatment for crohns disease?

A
  • 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
165
Q

What is surgical treatment for crohns disease?

A

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

166
Q

What is the screening of colorectal cancer in crohns disease?

A
167
Q

What are the areas affected in ulcerativ colitis?

A
168
Q

What is the criteria used for assessing severity of ulcerative colitis and whether or not admission is needed?

A
169
Q

What is the phenotyping classification of ulcerative colitis?

A

Montreal classification

170
Q

What are the RF and protective factors of ulcerative colitis?

A
171
Q

What are the SS of ulcerative colitis?

A
172
Q

What are the extraintestinal manifestations of ulcerative colitis?

A
173
Q

What biochemical tests for ulcerative colitis?

A
174
Q

What imaging done for ulcerative colitis?
What histological and endoscopic findings?

A
175
Q

What are not 1st line imagings for ulcerative colitis that may be considered?

A
176
Q

What is the treatment principle for ulcerative colitis?

A
177
Q

What is the medical treatment of ulcerative colitis?

A
  • 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
178
Q

What are the indications for surgical treatment for ulcerative colitis and its complications?

A
179
Q

What are the complications of ulcerative colitis?
What are the prognostic indicators?

A
180
Q

What are the different types of pain in terms of varying location?

A
181
Q

What is colicky pain?

A
  • Pain and spasm resulting from contraction of a hollow organ against an obstruction
    o Biliary colic
    o Ureteric colic
    o Intestinal colic
182
Q

What is the ddx of abd pain according to 9 quadrants

A
183
Q

What is the ddx for RUQ pain?

A
184
Q

What is the ddx for epigastric pain?

A
185
Q

What is the ddx for LUQ pain?

A
186
Q

What is the ddx for umbilical region pain?

A
187
Q

What is the ddx for left and right flank pain?

A
  • 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
188
Q

What is the ddx for RLQ pain?

A
189
Q

What is the ddx for suprapubic pain?

A
190
Q

What is the ddx for LLQ pain?

A
191
Q

What is the ddx for diffuse abd pain?

A
  • 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
192
Q

Define globus sensation

A
  • 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
193
Q

Define dysphagia

A

 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

194
Q

How to classify dysphagia?

A
195
Q

What is the ddx for oropharyngeal and esophageal dysphagia?

A
196
Q

What history taking for dysphagia?

A
197
Q

What is imaging done for dysphagia?

A
198
Q

What is the definition of dyspepsia?
What are alarming features of dyspepsia?

A
199
Q

What are the causes of dyspepsia?

A
200
Q

What is the pathophysiology of functional dyspepsia?

A
201
Q

What history taking for dyspepsia
What PE?

A
202
Q

What Ix done for dyspepsia?

A
203
Q

What treatment for dyspepsia?

A
204
Q

Most likely dx?
How is functional dyspepsia diagnosed?

A

 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)

205
Q

How common is H. pylori infection and how should it be diagnosed?

A
206
Q

What are features of ongoing upper GIB?

A
  • Hematemesis
  • Hematochezia
  • Fresh PR bleeding
  • Fresh blood aspirated from NG tube
  • Tachycardia
207
Q

What are RF of recurrent UGIB?

A
  • Age>60
  • Coagulopathy
  • Hb < 8.0 g/dL on presentation
  • Shock on presentation
  • Require blood transfusion
208
Q

What is the presentation of UGIB?

A
209
Q

What are common causes of UGIB?

A
210
Q

What are less common causes of UGIB?

A
211
Q

What is important history for UGIB?

A

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

212
Q

What is done for PE of UGIB?

A
213
Q

What biochemical tests for UGIB?

A
214
Q

What 1st line imaging Ix for UGIB?

A
215
Q

In UGIB if OGD and colonoscopy are negative what alternative imaging Ix are available?

A
216
Q

What is general management, medication and surgical treatment for UGIB?

A

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

217
Q

What is the rockall score for risk stratification of UGIB?

A
218
Q

What is the Glasgow-Blatchford score for risk stratification of UGIB?

A
219
Q

What are the common causes of lower GI bleeding?

A
  • 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
220
Q

What history taking for LGIB?

A
221
Q

What PE done for LGIB?

A
222
Q

What is biochemical tests for LGIB?

A
223
Q

What is the imaging for LGIB?

A
  • 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
224
Q

What is treatment of LGIB (diverticular bleeding)?

A
225
Q

What is treatment of LGIB (angiodysplasia)?

A
226
Q

How to classify diarrhea?

A
227
Q

Differentiate between small and large bowel diarrhea

A
228
Q

What are the infectious causes of diarrhea?

A
229
Q

What are the non infectious causes of diarrhea?

A
230
Q

What is history taking for diarrhea?

A
231
Q

What is done for PE of diarrhea

A
232
Q

What are the biochemical tests for diarrhea?
Differentiate between IBD and IBS with test

A
233
Q

What is general management and medical treatment for diarrhea?

A
234
Q

How is bilirubin formed?

A

 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

235
Q

How is bilirubin metabolized?

A

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

236
Q

How is bilirubin excreted?
What is the pathophysiology of dark urine and pale stools?

A
237
Q

What is general feature sof physiological jaundice in children
Pathophysiology
Risk factors for NMJ (neonatal jaundice)

A
238
Q

What are the causes of pathological jaundice in children (increased bilirubin production, decreased bilirubin clearance)?

A
239
Q

Cause of jaundice in children due to increased enterohepatic circulation

A
240
Q

What are the hepatic and post hepatic causes of conjugated hyperbilirubinemia in children?

A
241
Q

What are the causes of jaundice in adults (unconjugated bilirubin and conjugated bilirubin)?

A
242
Q

What is history taking for jaundice in children?

A
243
Q

What biochemical test and results in unconjugated vs conjugated hyperbilirubinemia?

A
244
Q

What is medical treatment for jaundice in children?

A
245
Q

What is surgical treatmetn for jaundice in children (if indicated)?

A
246
Q

What are are the complications of hyperbilirubinemia?

A
247
Q

How to classify GERD?

A
248
Q

What is the grading of esophagitis?

A

LA classification

249
Q

What is the pathophysio of GERD?

A
250
Q

What SS of GERD
Extra esophageal symptoms
Characteristics of symptoms

A
251
Q

What ddx for GERD?

A

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

252
Q

How to make dx of GERD?

A
  • 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
253
Q

What is treatment regiment for GERD?

A
254
Q

What is non pharmacological treatment for GERD?

A

 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)

255
Q

What is medical treatment of GERD?

A
256
Q

What is surgical treatment of GERD?

A
257
Q

What are complications of GERD?

A

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

258
Q

What is acute vs chronic cholecystitis?

A
259
Q

What are the general features of acalculous cholecystitis?
Who is affected by this condition?

A
260
Q

What is the pathogenesis of cholecystitis
What is histological appearance

A
261
Q

What is the ddx of cholecystitis?

A
262
Q

What is the SS of acute cholecystitis?

A
263
Q

What is the diagnostic criteria for acute cholecystitis?

A
264
Q

What is PE of acute cholecystitis?

A
265
Q

What Ix (biochemical and imaging) done for cholecystitis?

A
266
Q

What is guideline used to assess and guide treatment for acute cholecystitis?

A

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

267
Q

What are the indications for gallbladder drainge in acute cholecystitis
What options are there for drainage?

A
268
Q

What are the complications of acute cholecystitis?

A
269
Q

What is the general feature of acute cholangitis?
What is pathophysiology
What is the pathogenesis?

A

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)

270
Q

What is the pathogens causing biliary sesis?

A

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

271
Q

Causes of acute cholangitis?

A

 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

272
Q

SS of acute cholangitis
ddx?

A
273
Q

What is the diagnostic criteria for acute cholangitis?

A
274
Q

What Ix (biochemical and imaging) done for acute cholangitis?

A
275
Q

What is the treatment of acute cholangitis?

A
276
Q

How can ERCP be utilized to manage the most common cause of acute cholangitis?

A
277
Q

When is surgical drainage indicated in acute cholangitis?

A

 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)

278
Q

What is spread of HCC?

A
279
Q

What are the RF of HCC?

A
280
Q

What is ddx of HCC?

A
281
Q

What is gross and histological appearance of HCC?

A
282
Q

What is TNM staging of HCC?

A
283
Q

What are SS of HCC?
What are constitutional symptoms
symptoms of distant metastasis
Paraneoplastic syndromes

A
284
Q

What is diagnostic guideliens for HCC
What PE?

A
285
Q

What is the ddx of hepatomegaly?

A
286
Q

What are teh stigmata of chronic liver disease?

A
287
Q

What basic blood tests for HCC?

A
  • 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)
288
Q

What imaging done for suspected HCC?

A
  • 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
289
Q

What is the hong kong liver cancer prognostic classicification scheme?

A
290
Q

What is the child pugh classification?

A
291
Q

What are factors affecting rescectability of liver cancer?
What is preop assessment of feasibility of resection?

A
292
Q

When may be liver augmentation done for liver cancer
What are the complications?

A
293
Q

What are the indications for ablative therapy in liver cancer?
What are ablative options?

A
294
Q

What scoring system used for liver transplantation?

A
295
Q

What is the UCSF and milan criteria for liver transplantation in liver cancer?
Contraindications for liver transplantation?

A
296
Q

What are indications and contraindciatiosn for TACE in HCC?

A
297
Q

What are the complications of TACE in HCC?

A
298
Q

What medical drugs may be used in HCC?

A
299
Q

Prognosis of HCC
Complications of HCC

A
300
Q

What is surveillance time for HCC?

A
301
Q
A
302
Q

Why is the prognosis so often very poor in HCC and what clinical or biochemical parameters can indicate the likely prognosis?

A
303
Q

What are the contraindications to transcatheter arterial chemoembolization (TACE) in HCC?

A

 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

304
Q

What are the 3 curative treatment options for HCC?

A

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

305
Q

What are the treatment options for HCC if curative treatment is not available?

A

 Transarterial chemoembolization (TACE)  Sorafenib

306
Q

What is wilsons disease?

A

 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

307
Q

What is the genetics of wilsons disease?

A
308
Q

What is hepatic manifestation of wilsons disease?

A
309
Q

What is neurological manifestation of wilsons disease?

A
310
Q

What are the psychiatric manifestations of wilsons disease?

A

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

311
Q

What is ocular manifestation of wilsons disease?

A
312
Q

What is the diagnostic criteria for Wilsons disease?

A
313
Q

What to do for PE of wilsons disease?

A
314
Q

What are the basic Ix done for Wilsons disease?

A
  • 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.
315
Q

What is FP of low ceruloplasmin and FN results (normal or high ceruloplasmin) in Wilsons disease?

A
316
Q

What imaging doen for wilson disease?

A
317
Q

What is general appraoch to treating Wilsons disease?

A
318
Q

What is medical treatment for Wilsons disease?

A
319
Q

What are the variants of familial adenomatous polyposis
What is colonic and extracolonic manifestation?

A
320
Q

Hopw to make dx and surveillance of FAP
Treatment of FAP and its indications

A
321
Q

What mutations involved in HNPCC
What is clinical manifestation?

A
322
Q

What is the diagnostic criteria for HNPCC?

A
323
Q

What is the surveillance and treatment for HNPCC?

A
324
Q

What is PMH, FH and social history for colorectal cancer?

A
325
Q

What is the classification of peritontiits?

A
326
Q

What is the RF for peritonitis?

A

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

327
Q

What are the causes of peritonitis?

A
328
Q

What is the micbio of peritonitis?

A
329
Q

What is diagnostic criteria for
spontaneous bacterial peritontiis
CAPD peritonitis
Secondary bacteria peritonitis

A
330
Q

What is ascitic fluid analysis by paracentesis for peritonitis?

A
331
Q

What are imaging for peritonitis?

A
332
Q

What is treatmetn for primary and secondary peritonitis?

A

MBBS VI Medicine (98 decks)

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