Year 2 – Diseases Processes 6 – Gastrointestinal

Front 1

Significance of raised conjugated/unconjugated bilirubin in the blood

Back 1

Pre-hepatic failure – Raised unconjugated

Haemolytic anaemia

Trauma

Gilbert’s

Hepatic – Raised unconjugated and conjugated

Hepatitis

Drugs

Alcohol

Post-Hepatic – Raised conjugated

Primary biliary cirrhosis

Cholestasis

Primary sclerosing cholangitis

Front 2

Differentiate the following presentations:

Biliary colic

Peptic ulcers

Crohn's disease

Ectopic pregnancy

Appendicitis

Referred pain from chest disease

Back 2

Biliary colic

Colicky pain, radiates to scapula, no fever, WCC normal

Peptic ulcers

Pain related to meals (either just before or just after)

Heartburn

Worse in the early morning

Possibly anaemia, haematemesis and melaena

Crohn's disease

Chronic diarrhoea

Extra-intestinal symptoms

Weight loss

Appendicitis

Pain moving

Constipation

Low grade fever

Ectopic pregnancy

Similar to appendicitis => Need for a pregnancy test

Referred pain from chest disease

Look for a chest disease

Front 3

Name 6 differential for abdominal pain

Back 3

Biliary colic

Peptic ulcers

Crohn's disease

Ectopic pregnancy

Appendicitis

Referred pain from chest disease

Front 4

Outline the timeline of biliary colic

Back 4

Front 5

What are the physical signs of biliary colic?

Back 5

Usually none (perhaps some non-specific ones related to pain itself)

Front 6

What is an ectopic appendix? How does it present?

Back 6

An appendix that is not in its expected orientation (e.g. rotated).

It may present with pain and can be inflamed

Front 7

What causes chronic cholecystitis?

Back 7

1. Repeated episodes of acute cholecystitis

2. Repeated episodes of infection

Both cause thickening andfibrosis of gallbladder.

Front 8

Besides gallstones, what may cause cholecystitis?

Back 8

Infection

Front 9

Relate non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH)

Back 9

NASH is an extreme form of NAFLD

Front 10

3 most common causes of cirrhosis (and another 3)

Back 10

Most common

Chronic alcohol abuse

Chronic viral hepatitis (Hep B and Hep C)

Non-alcoholic steatosis

Others

Non-alcoholic steatohepatitis

Autoimmune

Primary biliary cirrhosis (♀)

Primary sclerosing cholangitis (♂)

Autoimmune hepatitis

Genetic

Haemochromatosis (iron overload)

Alpha1-Antitrypsin deficiency

Wilson's disease

Front 11

Name one sign of cirrhosis elicited on palpation

Back 11

Early stage: hepatomegaly

Later: shrinkage

Front 12

Significance of IgG raised in acute Hep A

Back 12

Patient has been exposed to HAV before

(Remember "G-General", "M-Moment")

Front 13

Diagnosis of Hep A

Back 13

Hep A IgM

Front 14

Incubation period for HAV, HBV and HCV

Back 14

HAV 2-6 weeks

HBV 1-6 months

HCV 2-6 weeks

Front 15

Treatment for Hep A

Back 15

No chronic phase => supportive treatment (fluid, anti-emetics or nothing)

Front 16

What non-hep virus can cause acute hepatitis

Back 16

EBV, CMV

Front 17

Where is Hep B prevalent?

Back 17

Africa, North Canada, North part of South America, South-East Asia

Front 18

Structure of the Hep B virus

Back 18

Front 19

Diagnosis of Hep B infection

Back 19

Hep B surface antigen (HBsAg)

Hep B core antigen (HBcAg)

Virus count

Front 20

Significance of Anti-HBs raised

Back 20

Vaccination or cleared infection

Front 21

Significance of Anti-HBc raised

Back 21

Cleared infection (not vaccination)

Front 22

Transmission of HBV

Back 22

Body fluids (sex, blood, IV drug) and vertical (from mother)

Front 23

What biochemical test may differentiate acute from chronic Hep B infection?

Back 23

Anti-HBc

Front 24

Significance of raised HBsAg and raised HBeAg

Back 24

Acute on chronic hepatitis B infection

Front 25

Risk factor for acute Hep B infection

Back 25

IV drug, blood products, sexual, homosexual, infected mum

Front 26

What Hep viruses do we have vaccines for?

Back 26

A and B

Front 27

Treatment of HBV

Back 27

Supportive

Trace contacts (sexual, other drug users, children) and vaccinate them

IFN alpha

Oral antiviral therapy (entecavir, tenofovir)

Front 28

How likely is acute liver failure to develop in patients with viral acute hepatitis?

Back 28

Unlikely

Front 29

What are the phases of Hep B infection?

Back 29

Incubation (high virus, no damage)

Clearance (HBeAg positive, high ALT)

Low virus carrier (Anti-HBe positive, normal ALT)

Reactivation phase (Anti-HBe positive, high ALT)

Front 30

Patients with signs of hepatitis. Blood tests reveal Anti-HBe positive and high ALT. Likely explanation?

Back 30

Reactivation phase of HBV infection

Front 31

In what phase of HBV infection do we give treatements?

Back 31

Phase 2 (Clearance) and 4 (reactivation)

Front 32

Name two drugs that can be given for HBV? How long should patient take them?

Back 32

Entecavir, tenofovir -> Taken for up to 20 years (because of reactivation)

Front 33

Transmission of HCV

Back 33

Blood products (transfusion, IV drug, healthcare needles not sterilised), sexual transmission is very rare

Front 34

Diagnosis of Hep C

Back 34

IgG test

Virus load (only chronic so no acute presentation)

Front 35

When do patients with HCV infection presents?

Back 35

Usually when cirrhosis develops, possibly triggered by alcohol

Front 36

Advise given to patients with HCV

Back 36

Limit alcohol intake, do not share razors, normal lifestyle

Front 37

Complications of HCV

Back 37

Liver failure and death

Front 38

Treatment of HCV

Back 38

New revolutionary treatments with 90% cure rates, given orally for 8-12 weeks (£80,000)

Front 39

Patient with acute viral hepatitis but negative hep A IgM and negative HBsAg and hep B core IgM. Likely cause?

Back 39

EBV, CMV, Hep E

Front 40

Compare ALT, AST, ALP, γGT, Bilirubin and urine bilirubin in hepatitis and obstruction

Back 40

Front 41

Name 3 symptoms of ascending cholangitis

Back 41

Charcot's triad

Jaundice

RUQ pain

Fever and Rigor

Front 42

Outline the possible outcomes of Hep C infections

Back 42

Front 43

Outline the possible outcomes of Hep B infections

Back 43

Front 44

How do ALT, serology and symptoms evolve in acute Hep C which progresses to chronic Hep C?

Back 44

Front 45

How do ALT, serology and symptoms evolve in acute Hep C which resolve?

Back 45

Front 46

How would LFT, HBsAg, HBeAg, Anti-HBs, Anti-HBe, Anti-HBc IgM and Anti-HBc IgG in incubation?

Back 46

HBsAg +

HBeAg +

Not yet any immunology against it

Front 47

How would LFT, HBsAg, HBeAg, Anti-HBs, Anti-HBe, Anti-HBc IgM and Anti-HBc IgG in acute infection?

Back 47

LFT ➚➚➚

HBsAg +

HBeAg - (early) | + (late)

Anti-HBe - (early) | + (late)

Anti-HBc IgM +

Anti-HBc IgG -

Front 48

How would LFT, HBsAg, HBeAg, Anti-HBs, Anti-HBe, Anti-HBc IgM and Anti-HBc IgG in chronically infected?

Back 48

Note: the difference between chronically infected and carrier is that in chronically affected there is active replication so HBeAg + and Anti-HBe - while the converse is true for carriers)

LFT ➚

HBsAg + (there is an active infection)

HBeAg + (there is an active replication)

Anti-HBs - (otherwise there wouldn't be active infection)

Anti-HBe -

Anti-HBc IgM - (at this stage, the first immune response is over)

Anti-HBc IgG + (the long-term response is on)

Front 49

How would LFT, HBsAg, HBeAg, Anti-HBs, Anti-HBe, Anti-HBc IgM and Anti-HBc IgG in carriers?

Back 49

Note: the difference between chronically infected and carrier is that in chronically affected there is active replication so HBeAg + and Anti-HBe - while the converse is true for carriers)

LFT ➚

HBsAg + (there is an active infection)

HBeAg - (there is no active replication)

Anti-HBs - (otherwise there wouldn't be active infection)

Anti-HBe + (otherwise there would be active replication)

Anti-HBc IgM - (at this stage, the first immune response is over)

Anti-HBc IgG + (the long-term response is on)

Front 50

Significance of raised HBeAg

Back 50

Active viral replication.

If it remains high for long, it is a sign of conversion to chronic Hep B infection.

Front 51

Significance of raised Anti-HBe

Back 51

Acute infection has peaked and is on the wane

Front 52

How would LFT, HBsAg, HBeAg, Anti-HBs, Anti-HBe, Anti-HBc IgM and Anti-HBc IgG in vaccinated?

Back 52

Only Anti-HBs is positive

Front 53

How are Anti-HBc IgG and Anti-HBc IgM measured?

Back 53

Anti-HBc IgM is measured directly

Anti-HBc IgG is inferred from total Anti-HBc and Anti-HBc IgM

Front 54

Transmission of HAV, HBV and HCV

Back 54

HAV

Ingestion of contaminated water andfoods and is shed in the stool for 2 to 3 weeks before and1 week after the onset of jaundice.

HBV

Body fluids (sex, blood, IV drug) and vertical (from mother)

HCV

Blood products (transfusion, IV drug, healthcare needles not sterilised), sexual transmission is very rare

Front 55

Presentation of Hep A, Hep B and Hep C

Back 55

Hep A

Mild (jaundice, fever, malaise) or asymptomatic

Rarely fulminent (in adults)

Hep B

More severe than Hep A: arthralgia (pain in joint) and urticaria

Hep C

Mild or asymptomatic early infection

Chronic: Silent (most), cirrhosis (25%) of whom 4% develop hepatoma

Front 56

How long does Hep A take to resorb?

Back 56

5-20 weeks

Front 57

Type of virus of HAV, HBV and HCV

Back 57

HAV: ssRNA

HBV: dsDNA

HCV: ssRNA

Front 58

Frequency of chronic infection due to HAV, HBV and HCV

Back 58

HAV – Never

HBV – 10%

HCV – 80%

Front 59

How are we immunised against HAV, HBV and HCV?

Back 59

HAV – Inactivated protein

HBV – Deactivated HBsAg (active) or Anti-HBs (passive for post-exposure)

HCV – None

Front 60

LFT in Hep A

Back 60

AST and ALT rise

Front 61

What is the infectious agent in HBV?

Back 61

HBsAg (this explains why positive HBsAg implies ongoing symptoms)

Front 62

Name 2 complications of Hep B

Back 62

Chronic hepatitis and cirrhosis

Hepatocellular carcinoma

Front 63

What is an hepatoma?

Back 63

Synonymous of hepatocellular carcinoma

Front 64

Name one virulence factor of HCV

Back 64

Poor fidelity of RNA replication => Many variants in a single organism

Front 65

Most likely cause of death in pt with advanced cirrhosis?

Back 65

Rupture oesophageal varices

Front 66

Define alcoholic liver disease

Back 66

Combination of

Fatty liver disease

Alcoholic steatohepatitis

Cirrhosis

Front 67

Clinical presentation of alcoholic liver disease

Back 67

Steatosis ⇒ Hepatomegaly

Hepatitis signs and symptoms

Cirrhosis ⇒ Silent or signs of complications (see question of cirrhosis presentation)

Front 68

How does cirrhosis present clinically?

Back 68

Three possibilities

A) Silent

B) Features of portal hypertension (ascites, oesophageal varices, caput medusa, ...)

C) Features of liver failure (oedema, coagulopathy, encephalopathy)

Front 69

Among the 3 diseases of alcoholic liver disease, which one is the first to occur?

Back 69

Steatosis (fatty liver)

Front 70

What two conditions do patients with cirrhosis die of?

Back 70

Hepatic failure => oesophageal varices

Hepatocellular carcinoma

Front 71

What is non-alcoholic fatty liver disease associated with (3)?

Back 71

Obesity

Dyslipidaemia

Diabetes

Front 72

Outline the pathological features of cirrhosis

Back 72

Nodules of regenerating hepatocytes surrounded by broad bands of fibrous tissues.

Front 73

Autopsy of the liver reveals nodules of regenerating hepatocytes surrounded by broad bands of fibrous tissues. What is the process?

Back 73

Cirrhosis

Front 74

Name 3 blood test results that you expect in early stages of cirrhosis and 3 in later stages

Back 74

Early (hepatocyte damages)

AST raised

ALT raised

ALP raised

GGT raised

Late (synthetic function impaired)

Albumin decreased

PT raised

Late (spleen engorgement)

Platelet decreased

WCC decreased

Front 75

Name 3 lines of management that are general (i.e. not related to a specific aetiology or presentation) of cirhhosis

Back 75

Maintain good nutrition

Avoid alcohol

Avoid NSAIDs, sedatives and opiates

Front 76

How would you treat ascites

Back 76

Bed rest

Fluid restriction

Low salt

Spironolactone

Therapeutic paracentesis may be tried

Front 77

Name 2 indications for liver transplant and 2 contraindications.

Back 77

Indications

- Advanced cirrhosis (only some aetiologies including the most common ones, the genetic and autoimmune ones but not NASH)

- Hepatocellular cancer

Contraindications

Non-compliance with drug therapy

Systemic sepsis

Extrahepatic malignancy

Front 78

Distinguish two types of liver failure based on timing.

Back 78

Acute (affecting a previously healthy individual)

Acute-on-chronic (affecting an individual with an underlying liver disease)

Front 79

What are the causes of liver failure?

Back 79

Acute-on-chronic

The same as those of cirrhosis

Acute

Paracetamol overdose

Amanita phalloides (mushroom) toxins

Front 80

Relate cirrhosis and liver failure

Back 80

Cirrhosis is a pathology (Nodules of regenerating hepatocytes surrounded by broad bands of fibrous tissues) that usually accompanies acute-on-chronic liver failure.

If acute, liver failure may exist in the absence of cirrhosis.

Front 81

Name 6 common signs of liver failure and explain their pathogenesis. Outline which are general to liver failure and which are specific to a specific aetiology.

Back 81

General

Jaundice – Bilirubin is no more excreted and is present in the blood

Encephalopathy – Ammonia is no more cleared and passes into the brain where it is taken up by astrocytes causing oedema

Asterixis – Due to encephalopathy

Signs of chronic liver disease

Oedema – Low albumin

Bruises – Low clotting factors

Bleeding gums and nose – Spleen engorged leading to low platelets and WCC

Leuconychia – Low albumin

Spider naevi – Raised oestrogens

Gynaecomastia – Raised oestrogens

Loss of body hair – Raised oestrogens

Ascites – Portal hypertension

Splenomegaly – Portal hypertension

Oesophageal varices – Portal hypertension

Caput medusae – Portal hypertension

Hepatomegaly or small liver – Damage to the liver parenchyma

Palmar erythema – Pathogenesis unknown

Clubbing – Pathogenesis unknown

Fetor hepaticus – Portal hypertension allows some chemicals to reach the lungs directly

Front 82

Which clotting factors may be affected by liver failure?

Back 82

II, VII, IX, X

Front 83

How is the diagnosis of cirrhosis confirmed?

Back 83

Liver biopsy confirming the presence of nodules of regenerating hepatocytes surrounded by broad bands of fibrous tissues.

Front 84

A man with a known history of alcohol excess presents to the hospital with a one day history of confusion and agitation. On further questioning, he explains that he has decided to quit drinking 4 days ago. What is the likely diagnosis and what is the mechanism?

Back 84

Delirium tremens

Alcohol excess (usually) ⟹ GABA receptors are potentiated ⟹ GABA receptor down-regulationAlcohol stopped abruptly ⟹ GABA activity ➘➘ ⟹ “Overactivity”

Front 85

Name 3 symptoms of delirium tremens

Back 85

Agitation

Aggression

Confusion

Hallucinations

Palpitations (arrhythmias)

Front 86

Name one context in which delirium tremens is particularly prevalent

Back 86

Alcoholic admitted to hospital as it may not receive his dose of alcohol

Front 87

Name 3 physical signs of delirium tremens

Back 87

Irregular HR

Shaking

Shivering

Sweating

Front 88

What two things may you prescribe to a patient in alcohol withdrawal?

Back 88

Benzodiazepines

Thiamine (B1), B6 and B12