Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MBChB Year 3 > Week 13 - GI/Liver > Flashcards

Week 13 - GI/Liver Flashcards

1
Q

Describe the vasculature of the liver?

A
  • Incoming portal vein and hepatic artery

- Outgoing hepatic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is the normal liver structure arranged?

A

Portal tracts & parenchyma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

List the 7 broad causes of injury to the liver?

A
  1. Drugs or toxins incl. alcohol
  2. Abnormal nutrition/metabolism
  3. Infection
  4. Obstruction to bile or blood flow
  5. Autoimmune liver disease
  6. Genetic/deposition disease
  7. Neoplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is inflammation generally?

A

Body’s response to injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is acute inflammation?

A

Agent causes injury but is the removed (days to weeks)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is fulminant inflammation?

A

Severe acute, rapidly progressing towards liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is chronic inflammation?

A

Agent causes injury then persists (months to years)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is acute-on-chronic inflammation?

A

Chronic liver disease often presents with acute exacerbation plus evidence of underlying chronicity e.g. fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does the injurious agent cause?

A

Cell damage and sometimes death, often with inflammatory cell infiltrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the main location of liver injury?

A

Parenchyma (hepatocytes) or bile ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What 4 structures are interdependent in the liver?

A
  1. Parenchyma
  2. Bile ducts
  3. Blood vessels
  4. Connective tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is cirrhosis equal to?

A

End-stage liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the 3-fold definition of cirrhosis?

A

Diffuse process with Fibrosis + Nodule formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the main aim of diagnosing and treating chronic hepatitis?

A

Avoid progression to cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the 2 types of investigations for liver disease?

A
  1. Blood tests: LFTs, haematology, viral and autoimmune serology, metabolic tests
  2. Radiology: at least ultrasound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List the 7 brand patterns/types of liver disease?

A
  1. Acute hepatitis
  2. Acute cholestasis
  3. Fatty liver disease
  4. Chronic hepatitis
  5. Chronic biliary disease
  6. Hepatic vascular disease
  7. Deposition/genetic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What 2 patterns/types of liver disease may progress to cirrhosis?

A

Fatty & chronic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the histological appearance of acute hepatitis of autoimmune cause?

A
  • Diffuse hepatocyte injury seen as swelling
  • A few have died, described as “spotty necrosis”
  • There is an inflammatory cell infiltrate in all areas: portal tracts, interface and parenchyma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are dying hepatocytes called?

A

Acidophil body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the 2 causes of acute cholestasis/cholestatic hepatitis?

A
  1. Extrahepatic biliary obstruction

2. Drug injury e.g. antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the histological appearance of acute cholestasis/cholestatic hepatitis?

A

Brown bile (bilirubin) pigment +/- acute hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are 2 causes of chronic biliary/cholestatic disease?

A
  1. Primary biliary cirrhosis (PBC)

2. Primary sclerosing cholangitis (PSC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the histological appearance of chronic biliary/cholestatic disease?

A

Focal, portal-predominant inflammation and fibrosis with bile duct injury; granulomas (arrow) in PBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Give 3 examples of Genetic/deposition liver disease?

A
  1. Haemochromatosis (iron)
  2. Wilson’s disease (copper)
  3. Alpha-1-antitrypsin deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the 3 causes of acute hepatitis liver disease?

A
  1. Hepatitis viruses A-E
  2. Drug injury
  3. Autoimmune liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the 3 causes of acute cholestasis or cholestatic hepatitis liver disease?

A
  1. Hepatitis virus esp. A & E
  2. Drug injury
  3. Extrahepatic biliary obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the 3 causes of Fatty liver disease (steatosis and steatohepatitis)?

A
  1. Drug injury
  2. Alcohol
  3. Metabolic syndrome ie. obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the 3 causes of chronic hepatitis?

A
  1. Hepatitis viruses esp B & C (& D)
  2. Autoimmune liver disease
  3. Genetic/deposition e.g. haemochromatosis, Wilson’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the 3 causes of Chronic biliary/cholestatic disease?

A
  1. Extrahepatic biliary obstruction
  2. Chronic biliary disease e.g. PBC
  3. Genetic/deposition e.g. haemochromatosis, Wilson’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the 2 causes of hepatic vascular disease?

A
  1. Drug injury

2. Vascular disease e.g. venous obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the 4 aims of investigation of diffuse liver disease?

A
  1. Establish DIAGNOSIS in terms of pattern (morphology) of disease
  2. Establish CAUSE, if possible
  3. If appropriate, establish GRADE of disease (severity = activity of inflammation)
  4. If chronic liver disease, establish STAGE (severity of fibrosis i.e. how far towards cirrhosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the 2 types of treatment for diffuse liver disease?

A
  1. Specific treatment against cause: removal of alcohol or drug, weight loss, optimal diabetic control, specific antivirals or immunosuppression, AND/OR
  2. Supportive treatment for severe acute hepatitis or for cirrhosis in general
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is a common type of liver disease?

A

Drug induced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are most drug hepatotoxicities?

A

Idiosyncratic (rare but usually single clinical pattern) thus difficult to investigate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the 2 types of drug-induced liver disease causes?

A
  1. Predictable liver damage: paracetamol, methotrexate

2. Non-prescribed drugs: over internet or herbal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What may Augmentin (co-amoxiclav) cause?

A

Acute cholestatic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the main differential diagnoses for liver masses (space occupying lesions or focal lesions)?

A

Inflammatory and other benign lesions and cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is a focal liver disease equal to?

A

Space occupying lesions (SOLs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the 2 types of liver space occupying lesions (SOLs)?

A
  1. Non-neoplastic: Developmental/ degenerative (cysts), Inflammatory (abscess)
  2. Neoplastic: benign, malignant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the 2 usual origins of liver cysts?

A
  1. Developmental

2. Degenerative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the commonest liver cyst?

A

Von Meyenberg complex (= simple biliary hamartoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Why are Von Meyenberg complexes important?

A

Can resemble metastases by naked eye at operation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the treatment for Von Meyenberg complexes?

A

No treatment required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Give 3 examples of benign (5%) liver neoplasms?

A
  1. Hepatocellular adenoma
  2. Bile duct adenoma (rare)
  3. Haemangioma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Give 4 malignant liver neoplasms?

A
  1. Hepatocellular carcinoma (HCC)
  2. Cholangiocarcinoma
  3. Angiosarcoma
  4. Metastases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Why is haemangioma and hepatic adenoma’s important?

A

Differential diagnosis with metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Describe a Haemangioma?

A
  • Benign blood vessel tumour

- Biopsy avoided because of risk of bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Describe a hepatic adenoma?

A
  • Rare
  • Mainly young women, often associated with hormonal therapy
  • Risk of bleeding and rupture so excision if large
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the most common primary liver tumour?

A

Hepatocellular carcinoma (HCC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Describe how Hepatocellular carcinoma (HCC) usually arises?

A

In cirrhosis and associated with elevated serum AFP (alpha feto-protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the 6 normal functions of the liver?

A
  1. Protein, carbohydrate and fat metabolism
  2. Plasma protein and enzyme synthesis
  3. Production of bile
  4. Detoxification
  5. Storage of proteins, glycogen, vitamins and metals
  6. Immune functions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What makes at least 70% of liver disease in the West population?

A

Fatty liver due to alcohol or obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

List the 4 signs & symptoms of liver disease?

A
  1. From liver itself: hepatomegaly
  2. From portal hypertension: ascites
  3. From chronic liver dysfunction: pruritis, spider naevi
  4. Non-specific: nausea, falls, tremor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the 2 symptoms & signs of an abnormal biliary system?

A
  1. Accumulation of bilirubin (esp. acute cholestasis): jaundice
  2. Accumulation of bile acids (esp. chronic cholestasis): pruritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the 3 symptoms of abnormal parenchyma?

A
  1. RUQ pain
  2. In chronic disease: hormonal changes
  3. Liver failure only once <25% function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the sign of abnormal connective tissue matrix in the liver?

A

Portal hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

List 5 liver function tests (biochemistry)?

A
  1. Transaminases: AST, ALT
  2. Alkaline phosphatase (Alk P)
  3. Gamma glutamyl transferase (GGT)
  4. Bilirubin (Bil)
  5. Albumin (Alb)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is a liver-related haematology test?

A

Prothrombin time (PTT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Give 5 examples of liver investigations?

A
  1. Viral serology
  2. Autoimmune serology
  3. Tests for liver metabolic/genetic disease
  4. Radiology (imaging): especially masses
  5. Biopsy (in only few cases)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Give 3 examples of tests for liver metabolic/genetic disease?

A
  1. Iron
  2. Copper
  3. Alpha-1-antitrypsin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Give 3 examples of radiology tests for liver disease?

A
  1. Ultrasound of abdomen
  2. CT scan of abdomen
  3. ERCP/MRCP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Describe the presentation of acute hepatitis?

A
  • Short history of RUQ tenderness, malaise etc

- Elevated AST/ALT (and often Bil)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Describe the clinical presentation of fatty liver disease?

A
  • Acute OR chronic “hepatitis”, or

- Asymptomatic abnormal LFTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the 3 causes of fatty liver disease (steatosis and steatohepatitis)?

A
  1. Alcohol
  2. Non-alcoholic or so-called metabolic syndrome, including Type II diabetes, obesity and hyperlipidaemia
  3. Drugs: methotrexate, amiodarone, steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Describe hepatitis C pathology?

A

Mainly in portal tracts, as chronic inflammation with lymphoid aggregates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the clinical definition of chronic hepatitis?

A

Liver inflammation (abnormal LFTs) for at least 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Describe the clinical presentation of chronic biliary/cholestatic disease?

A
  • Chronic liver disease: itch (symptoms more of excess bile acids than excess bilirubin), OR
  • Abnormal LFTs: mainly AlkP and GGT, often relatively mild, persisting for >6 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Describe the histology of chronic biliary/cholestatic disease?

A

Focal, portal-predominant inflammation and fibrosis with bile duct injury; granulomas (arrow) in PBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Describe Primary biliary cirrhosis?

A
  • Auto-immune disease with serum anti-mitochondrial antibodies (AMA) and high IgM
  • NOT cirrhotic from outset, but progresses to fibrosis then cirrhosis
  • No cure but ursodeoxycholic acid eases symptoms and slows progression
  • Liver transplantation, if available, at end-stage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Describe Primary sclerosing cholangitis (PSC)?

A
  • Rare, associated with ulcerative colitis

- Risk of progression to cholangiocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Describe the relevance of primary hepatic vascular disease?

A

Rare (by comparison with cirrhosis) but serious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the main form of primary hepatic vascular disease?

A

Hepatic vein outflow obstruction (Budd-Chiari syndrome) which is often fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Describe symptomatic focal liver disease presentation?

A

Hepatomegaly, RUQ pain or jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What investigations would you perform for focal liver disease?

A

Imaging by ultrasound and/or CT scan +/- biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Where may a liver abscess arise from?

A
  • Ascending cholangitis

- Hydatid and other parasitic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is Cholangiocarcinoma?

A

Adenocarcinoma of bile ducts, either intra- or extra-hepatic i.e. also primary liver tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How do you diagnose a Cholangiocarcinoma?

A

Imaging & cytology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the prognosis & treatment for Cholangiocarcinoma?

A
  • Prognosis: poor

- Treatment: curative surgery or palliation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are liver metastases mainly?

A

Metastatic carcinoma esp adenocarcinoma from gastro-intestinal tract (portal blood supply)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Other than the liver, what may cause a raised ALP?

A

Bone pathologies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Other than the liver, what may cause a raised AST?

A

Muscle pathologies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Other than the liver, what may cause a raised isolated bilirubin?

A

Haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Advanced cirrhosis may have ________?

A

Normal blood tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What 3 tests is liver function indicated by?

A
  1. Albumin
  2. Bilirubin
  3. Prothrombin time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What 3 investigations would you do for chronic viral hepatitis (Chronic)?

A
  1. Ultrasound
    2, HBV
  2. HCV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What 4 investigations would you do for autoimmune liver disease (Chronic)

A
  1. ANA / SMA / LKM (AIH)
  2. AMA (PBC)
  3. Immunoglogulins
  4. Ultrasound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What 4 investigations would you do for metabolic liver disease (Chronic)?

A
  1. Ferritin (haemochromatosis)
  2. Caeruloplasmin (Wilson’s Disease)
  3. Alpha 1 anti-trypsin deficiency
  4. Ultrasound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What 6 investigations would you do for acute viral hepatitis?

A
  1. HAV
  2. HBV
  3. HCV
  4. HEV
  5. CMV
  6. Ultrasound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What level would you investigate for acute liver injury?

A

Paracetamol levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What are the 4 most common causes of abnormal liver blood tests?

A
  1. Fatty liver
  2. Chronic viral hepatitis (Chronic HCV)
  3. Autoimmune liver disease
  4. Haemochromatosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Describe the 3 steps in alcoholic fatty liver disease?

A

Alcoholic steatosis –> Alcoholic hepatitis –> Alcoholic cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Describe the 3 steps in non-alcoholic fatty liver disease?

A

Steatosis –> Nonalcoholic steatohepatitis (NASH) –> NAFLD cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Describe the histological appearance of the steatosis stage of fatty liver disease?

A

Macrovesicular steatosis with lipid vacuole filling the hepatocyte cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Describe the histological appearance of the steatohepatitis stage of fatty liver disease?

A

Neutrophils and lymphocytes surrounding hepatocytes with Mallory hyaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Describe the histological appearance of the cirrhotic stage of fatty liver disease?

A

Pericellular fibrosis as well as bands of fibrous tracts between portal tracts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are the 3 main associations of Non-alcoholic fatty liver disease (NAFLD)?

A
  1. Obesity
  2. Type 2 Diabetes
  3. Hyperlipidaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What 2 things increase the severity of Non-alcoholic Fatty Liver Disease (NAFLD)?

A
  1. Type 2 Diabetes

2. Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

List the blood result features of non-alcoholic fatty liver disease (NAFLD)?

A
  • Fasting plasma glucose or HbA1c: Often Elevated
  • ALT: Elevated or normal
  • AST: Normal
  • AST/ALT ratio: <0.8
  • GGT: Elevated or normal
  • Triglycerides: Elevated
  • HDL-cholesterol: Low
  • Mean corpuscular volume: Normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

List the blood result features of alcoholic fatty liver disease (ALD)?

A
  • Fasting plasma glucose or HbA1c: usually normal
  • ALT: Elevated or normal
  • AST: elevated
  • AST/ALT ratio: >1.5
  • GGT: Markedly Elevated
  • Triglycerides: Variable, may be elevated
  • HDL-cholesterol: Elevated
  • Mean corpuscular volume: Elevated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

List the 10 clinical features of alcoholic fatty liver disease (ALD) from mild to severe?

A
  1. Malaise
  2. Nausea
  3. Hepatomegaly
  4. Fever
  5. Jaundice
  6. Sepsis
  7. Encephalopathy
  8. Ascites
  9. Renal Failure
  10. Death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

List the 5 essential features of the newly jaundiced ALD patient (alcoholic hepatitis)?

A
  1. Excess alcohol within 2 months
  2. Bilirubin > 80mmol/l for less than 2 months
  3. Exclusion of other liver disease
  4. Treatment of Sepsis/ GI Bleeding
  5. AST < 500 (AST: ALT ratio >1.5)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What are the 4 characteristic features of the newly jaundiced ALD patient (alcoholic hepatitis)?

A

Hepatomegaly +/- fever +/- leucocytosis +/- hepatic bruit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is GAHS?

A

The Glasgow Alcoholic Hepatitis Score (GAHS)

- Ranges from 1-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What 3 features is the rate of Hepatitis C progression related to?

A
  1. Male sex
  2. Age >40 at time of acquisition
  3. Alcohol >50g/week
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

List the 5 risk factors for hepatitis C virus?

A
  1. Intravenous drug use (80% of users)
  2. Blood transfusions
  3. Sexual transmission
  4. Vertical transmission (~3%)
  5. Needle-stick transmission (~5-10%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What are the 5 stages of liver fibrosis?

A
  1. None
  2. Portal fibrosis
  3. Portal fibrosis with septa
  4. Bridging fibrosis
  5. Cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Machine is used as a non-invasive test of liver fibrosis?

A

FibroScan®

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What are 2 commercially available blood tests?

A
  1. Enhanced Liver Fibrosis Test (ELF)

2. FibroTest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

List 5 signs of chronic liver disease?

A
  1. Spiders
  2. Fœtor
  3. Encephalpathy
  4. Prolonged prothrombin time
  5. Hypoalbuminaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

List 3 signs of portal hypertension?

A
  1. Caput medusa
  2. Hypersplenism
  3. Thrombocytopenia (pancytopenia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What score assessed the severity of liver fibrosis?

A

Childs-Turcotte-Pugh Score

  • Grade A: 5-6 (mild)
  • Grade B: 7-9 (moderate)
  • Grade C: 10-15 (severe)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is the model for end-stage liver disease (MELD) used for now?

A

Allocate donor organs in USA for liver transplant

  • Mild: <10
  • Moderate: 10-15
  • Severe >15
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What causes hypersplenism (thrombocytopenia) in chronic liver disease?

A

Raised portal pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What causes oesophago-gastric varices in chronic liver disease?

A

Porto-systemic shunting from raised portal hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What causes encephalopathy in chronic liver disease?

A

Porto-systemic shunting from raised portal hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What causes hyperdynamic circulation in chronic liver disease?

A

Reduced effective circulating volume from vasodilation (nitric oxide) and splanchnic vasodilatation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What causes ascites in chronic liver disease?

A

Sodium retention from compensatory vasopressors (RAAS, catecholamines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What causes hepato-renal syndrome in chronic liver disease?

A

Renal vasoconstriction from compensatory vasopressors (RAAS, catecholamines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What are the 2 tests in the diagnostic tap for assessing ascites?

A
  1. Cell count

2. Albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What cell count suggests spontaneous bacterial peritonitis (SBP)?

A

> 500 WBC/ cm3 and/ or >250 neutrophils/cm3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What does lymphocytosis suggest?

A

TB or peritoneal carcinomatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What is the serum ascites albumin gradient (SAAG) equal to?

A

Serum albumin MINUS ascitic albumin g/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What SAAG = portal hypertension?

A

SAAG >11g/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What are the 5 ways to manage ascites?

A
  1. Low salt diet
  2. Diuretics
  3. Paracentesis
  4. Transjugular intrahepatic portosystemic shunt (TIPSS)
  5. Liver transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Give 2 examples of diuretics used for ascites?

A
  1. Spironolactone

2. Furosemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What should patients with ascites aim for?

A

Weight loss of 0.5-1 kg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What 2 things should be monitored when managing ascites?

A
  1. Renal function

2. Electrolytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

List the 4 side effects of Spironolactone diuretic?

A
  1. Gynaecomastia
  2. Hyperkalaemia
  3. Hyponatraemia
  4. Impotence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What is the main side effect of Frusemide (Furosemide) diuretic?

A

Hyponatraemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What are the 5 common precipitating factors for hepatic encephalopathy?

A
  1. Gastrointestinal bleeding
  2. Infections
  3. Constipation
  4. Electrolyte imbalance
  5. Excess dietary (esp. animal) protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What 3 things do the 5 precipitating factors for hepatic encephalopathy lead to?

A
  1. Reduction of hepatic or cerebral function
  2. Stimulation of an inflammatory response
  3. Increasing ammonia levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What are the 3 exacerbating factors to avoid with hepatic encephalopathy?

A
  1. Regular sedation
  2. Caution with opiates
  3. Avoid hyponatraemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What scoring system is used to grade mental state in hepatic encephalopathy?

A 
Conn Score (West Haven classification) 
- Grade 0-4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What should you aim for when prescribed a Non-absorbable Disaccharides (ie lactulose)?

A

2-3 soft stool/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What does gut ‘decontamination’ reduce?

A

Urease and protease activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

List the 5 non-specific symptoms for hepatitis?

A
  1. Malaise, fever, headaches
  2. Anorexia, nausea and vomiting
  3. Right upper quadrant abdominal pain
  4. Dark urine
  5. Jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Describe the 2 lab results for hepatitis?

A
  1. Raised ALT / AST / Bilirubin

2. Clotting Derangement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Describe chronic hepatitis?

A
  • Hepatitis virus present for more than 6 months

- Usually asymptomatic by this stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What are the 2 routes of transmission for hepatitis?

A
  1. Faecal oral

2. Blood Borne- contact with body fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

List the 7 causes of acute hepatitis?

A
  1. Infections
  2. Toxins
  3. Drugs
  4. Alcohol
  5. Autoimmune
  6. Wilsons
  7. Haemochromatosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

List 7 infections which can cause acute hepatitis?

A
  1. Hep A, B, C, D, E
  2. EBV, CMV, Toxo
  3. Leptospirosis
  4. Q Fever
  5. Syphilis
  6. Malaria
  7. Viral hemorrhagic fevers (VHFs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

What are the 2 ways to diagnose viral hepatitis via laboratory tests?

A
  1. Detection of specific immune response (IgM or IgG)

2. Viral nucleic acid detection (RNA or DNA), or Antigen detection (HBV and HCV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Describe the features of Hepatitis A?

A
  • RNA virus
  • Virus can survive for months in contaminated water
  • Virus shed via bilary tree into gut
  • Good Immunity after infection or vaccination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What is the unique feature of hepatitis A virus?

A

No Chronic Carriage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What are the 2 routes of transmission for hepatitis A?

A
  1. Faeco-oral

2. Human reservoir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

What determines the severity of Hepatitis A virus?

A

Age:

  • Mostly asymptomatic in children < 5 yrs
  • Mortality rate 1.5% if > 50 year
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Describe the management/prognosis of hepatitis A virus?

A
  • No specific treatments
  • Maintain hydration, avoid alcohol
  • Usually self-limiting illness
  • No role for Vaccine or IgG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

How do you diagnose acute hepatitis A?

A

IgM Positive or RNA in blood or stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

How do you diagnose previous hepatitis A or vaccinated?

A

IgG Positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Describe the hepatitis A vaccine?

A
  • Inactivated virus
  • 95% efficacy after 4 weeks
  • 2nd dose gives life protection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

In what 4 people would you give pre-exposure hepatitis A vaccine?

A
  1. Travellers
  2. Homosexual men
  3. IVDU
  4. Chronic liver disease patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

When would you give pre-exposure Hepatitis A Immune Globulin?

A
  • Vaccine allergic
  • <4 wks to travel
  • Confers 3-6 months immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Describe the features of hepatitis E virus?

A
  • RNA virus
  • More common than Hep A in the UK
  • 4 genotypes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What are the 3 modes of transmission for hepatitis E virus?

A
  1. Faeco-oral
  2. Pork products
  3. Minimal person-to-person transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Describe the clinical features of hepatitis E virus?

A
  • Similar to Hepatitis A plus rare reports of neurological effects
  • Case-fatality rate: 1 - 3%, higher in pregnant women for some genotypes (G1)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Describe the management of hepatitis E virus?

A
  • Treatment: Supportive

- No Vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

When would you see chronic hepatitis E virus & how would you treat them?

A
  • Very immunosuppressed patients: bone marrow transplants

- Treatment with ribavirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

List the 4 neurological manifestations which are associated with hepatitis E?

A
  1. Guillaine Barre syndrome
  2. Encephalitis
  3. Ataxia
  4. Myopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

Describe the features of hepatitis B virus?

A
  • DNA virus

- HBV vaccination included in immunisation schedule in most countries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

List the 6 routes of transmission for hepatitis B virus?

A
  1. Mother to baby- vertical transmission usually at birth
  2. Contaminated needles & syringes
  3. Child to child
  4. Organs and tissue transplantation
  5. Fluids (blood, semen)
  6. Transfusion (blood, blood products)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What is the most common worldwide route of transmission for hepatitis B virus?

A

Vertically at birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What 2 things does the age at the time of hepatits B infection determine?

A
  1. Severity of acute illness

2. Risk of Chronic HBV Infection (CHB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

Describe the difference between hepatitis B infection at birth & as an adult?

A
  • Infection at birth / young child is usually asymptomatic but leads to chronic infection
  • Infection as an adults is usually symptomatic but is cleared
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

List the 6 clinical signs of hepatitis B virus (vague so difficult to diagnose)?

A
  1. Weight loss
  2. Abdo pain
  3. Fever
  4. Cachexia
  5. Mass in abdomen
  6. Bloody ascites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What blood result suggests hepatitis B virus?

A

HBsAg +ve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

List the 5 problems with chronic hepatitis B virus?

A
  1. Development of chronic liver disease in 25%
  2. Cirrhosis
  3. Decompensation
  4. Hepatocellular Carcinoma (HCC)
  5. Death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

List the 6 hepatitis B lab tests that we measure?

A
  1. sAg: Surface antigen- marker of infection
  2. sAb: Surface antibody- marker of immunity
  3. cAb: Core antibody
  4. eAg: e antigen- suggests high infectivity
  5. eAb: e antibody- suggests low infectivity
  6. HBV DNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What test results give a diagnosis of hepatitis B virus?

A

sAg or DNA are detectable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

What is the definition of chronic hepatitis B virus?

A

sAg detectable for >6/12months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What are the 2 groups of chronic hepatitis B carriers?

A
  1. eAg +ve (early disease)- High viral load, high risk of CLD and HCC, highly infectious
  2. eAg –ve (late disease)- Low viral load, lower risk of CLD and HCC, less infectious
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What is the treatment for acute hepatitis B virus?

A

No treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What is the treatment for chronic hepatitis B virus?

A
  • Most do not require treatment
  • Immuno-modulatory: Inferferon
  • Suppress viral replication: Tenofovir or Entecavir
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

When would you treat chronic hepatitis B patients?

A

Only treat those with liver inflammation (LFT or Biopsy) or

fibrosis (on Fibroscan or Biopsy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

What are the 3 ways to prevent hepatitis B virus?

A
  1. Education (safe sex, injecting etc)
  2. Immunisation with HBV sAg Vaccine
  3. HBV vaccination to newborn- 6 doses in first year
  4. Tenofovir during the last trimester of pregnancy if high Viral Load
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

Describe the features of hepatitis D virus?

A
  • ss RNA virus
  • Requires HBV to replicate
  • Transmission same as Hep B
  • Vertical transmission is rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

In what 3 ways is hepatitis D acquired?

A
  1. Co-infection with HBV
  2. Super-infection of chronic HBV carriers
  3. Increases risk of chronic liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

How do you treat hepatitis D virus?

A

Peg IFN only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Describe the aims of hepatitis B treatment?

A

Not curative, but reduce risk of complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

Describe the features of hepatitis C virus?

A
  • RNA virus
  • No vaccine, no post exposure prophylaxis
  • No reliable immunity after infection
  • Multiple Genotypes of HCV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What are 3 ways to transmit hepatitis C virus?

A
  1. Injecting drugs
  2. Transfusion + Transplant
  3. Sexual / vertical rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

What are the 2 types of hepatitis C infections?

A
  1. Chronic infection (70%)- cirrhosis (25%) or HCC (1-5%)

2. Clear infection (30%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

Describe the clinical signs of hepatitis C virus?

A
  • Mostly asymptomatic

- Multitude of extra-hepatic manifestations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

How are most hepatitis C infections diagnosed?

A

By screening of high risk groups- drug users & immigrants to UK from high prevalence countries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

What blood test result indicates chronic hepatitis C infection or cleared infection?

A

Anti HCV IgG positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

What blood test result indicates current hepatitis C infection/viraemia?

A

PCR or Antigen positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

What is the aim of hepatitis C treatment?

A

Cure infection- cure rates of >95% within 8-12 weeks of oral treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

How do you treat hepatitis C virus?

A
  • Direct Acting Antiviral (DAAs) inhibit different stages of the replication cycle
  • The DAA regimen is decided according to Genotype and degree of fibrosis / cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

What 2 types of hepatitis viruses have an effective treatment?

A

HBV and HCV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

What 3 types of hepatitis viruses can lead to chronic hepatitis?

A
  1. HBV
  2. HCV
  3. HDV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

What 2 things can gallstones be made of?

A

Cholesterol or Bile pigment (most are mixed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

What do 10% of gallstones have?

A

Sufficient calcium to be seen on plain X-rays

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

How are most gallstones diagnosed?

A

By ultrasound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

How much bile does the liver secrete daily?

A

500mls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

Describe the cholesterol in bile?

A

Not water soluble and is kept in solution by micelles containing bile acids and phospholipid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

What causes the colour of bile?

A

Bile pigment, bilirubin which is a breakdown product of haemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

When does bile become lithogenic (stone forming) for cholesterol?

A

If there is excessive secretion of cholesterol or decreased secretion of bile salts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

What is the 1st indication of the presence of gallstones in a 1/3rd of patients?

A

Acute Cholecystitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

Describe the presentation of Acute Cholecystitis?

A

Severe right upper quadrant pain, tenderness and fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

Describe the blood results of Acute Cholecystitis?

A

Leucocytosis and normal serum amylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

Describe the prognosis of Acute Cholecystitis?

A

Usually resolves spontaneously but can progress to empyema, gangrene and rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

What initiates Acute Cholecystitis?

A

Stone obstruction of cystic duct causing supersaturation of bile and chemical irritation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

Describe the cause of chronic cholecystitis?

A
  • May be a sequel to repeated attacks of acute cholecystitis

- Inflammation secondary to chemical damage (supersaturated bile) rather than bacterial infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

What is virtually always present in chronic cholecystitis?

A

Gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

What are the 3 most common causes of acute pancreatitis?

A
  • 50% secondary to alcohol abuse
  • 30% secondary to gallstones
  • 20% other causes: “GET SMASHED”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

Describe the presentation of acute pancreatitis?

A

Presents with severe upper abdominal pain, fever, leucocytosis and raised serum amylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

What are 2 potential complications of acute pancreatitis?

A
  1. Pancreatic Abscess

2. Pseudocyst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

Describe a Pancreatic Abscess?

A
  • Infected pancreatic necrosis
  • Avascular haemorrhagic pancreas good culture medium
  • Drainage or necrosectomy plus antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

What is the cause of 85% of chronic pancreatitis?

A

Alcohol abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

Describe the features of chronic pancreatitis?

A
  • Stones and concretions in ducts
  • Can be hereditary
  • Usually painful
  • May present with exocrine or endocrine failure
210
Q

Describe a pancreatic pseudocyst?

A
  • No epithelial lining
  • Commonly in lesser sac
  • High concentration of pancreatic enzymes
  • May resolve spontaneously
  • May be drained into stomach
211
Q

Describe a pancreatic Intraductal papillary mucinous neoplasm?

A

In continuity with main pancreatic duct or side branch duct, dysplastic papillary lining secreting mucin

212
Q

Describe a pancreatic Mucinous cystic neoplasm?

A
  • Mucinous lining

- “Ovarian-type” stroma

213
Q

Describe a pancreatic Serous cystadenoma?

A
  • No mucin production

- Almost always benign

214
Q

Describe a carcinoma of the pancreas?

A
  • 5% of cancer deaths

- 66% in head of pancreas

215
Q

What are 3 types of carcinomas of the pancreas?

A
  1. Ductal adenocarcinoma- most common
  2. Perineural invasion
  3. Pre-malignant PanIN asymptomatic
216
Q

What are the 2 risk factors for carcinoma of the pancreas?

A
  1. Germline mutations (e.g. BRCA) account for small proportion of patients,
  2. SMOKING is by far biggest risk factor
217
Q

List the 3 signs and symptoms of a carcinoma of the pancreas?

A
  1. Painless obstructive jaundice
  2. New onset diabetes
  3. Abdominal pain due to pancreatic insufficiency or nerve invasion
218
Q

Describe the “double duct sign” on radiology of a carcinoma of the pancreas?

A

Tumours in head may obstruct pancreatic duct and bile duct

219
Q

When would you perform a Whipple’s resection?

A
  • Only for tumours of head of pancreas

- Only about 10% of these patients suitable for operation

220
Q

What is the average life expectancy following a Whipple’s resection?

A

20 months

221
Q

Describe the (Neo)adjuvant therapy for carcinoma of the pancreas?

A

Folfirinox chemotherapy associated with (limited) improvement in metastatic disease

222
Q

Describe Pancreatic Neuroendocrine Tumours?

A
  • Rare
  • May secret hormones (functional)
  • Commonest functional tumour is insulinoma which presents with hypoglycaemia
223
Q

What % of insulinomas are benign?

A

90%

224
Q

What type of pancreatic tumours have the better prognosis?

A

Malignant endocrine tumours have much better prognosis than pancreatic carcinoma

225
Q

Describe a carcinoma of the ampulla of vater?

A
  • Presents when smaller than carcinoma of pancreas

- May arise from pre-existing adenoma

226
Q

What is the 5 year survival rate of a carcinoma of the ampulla of vater?

A

25% 5 year survival following Whipples’ resection

227
Q

How is a Cholangiocarcinoma classified?

A

Intrahepatic / extrahepatic depending on origin

228
Q

What does a Intrahepatic cholangiocarcinoma need to be distinguished from?

A

From metastatic adenocarcinoma (which may have similar histology) and hepatocellular carcinoma

229
Q

Describe Extrahepatic cholangiocarcinoma?

A
  • Similar morphology and prognosis to pancreatic carcinoma

- Treatment is currently Whipple’s operation to remove common bile duct and involved pancreas/duodenum

230
Q

Describe carcinoma of the gallbladder?

A
  • Rare
  • Adenocarcinoma
  • Local infiltration may make gallbladder seem abnormally stuck down at theatre
231
Q

What is the prognosis of carcinoma of the gallbladder?

A

Dismal prognosis unless found incidentally in a gallbladder removed for chronic cholecystitis

232
Q

What are the 2 functions of the pancreas?

A
  1. Exocrine- Manufacture and secretion of enzymes to digest food
  2. Endocrine- Glucose control
233
Q

Describe the 3 parts to diagnosing acute pancreatitis?

A
  1. Pain in keeping with pancreatitis
  2. Amylase 3 times upper limit of normal
  3. Characteristic CT appearance
234
Q

Describe mild acute pancreatitis?

A

Absence of organ failure/ local/ systemic complications

235
Q

Describe moderately severe acute pancreatitis?

A

Presence of transient organ failure or presence of local/ systemic complications in absence of organ failure

236
Q

Describe severe acute pancreatitis?

A

Persistent organ failure

237
Q

List the 9 causes of acute pancreatitis?

A
  1. Gallstones
  2. Ethanol
  3. Trauma
  4. Steroids
  5. Mumps
  6. Autoimmune
  7. Scorpion sting
  8. ERCP
  9. Drugs
238
Q

Describe the initial treatment of acute pancreatitis?

A

ABC’s

  • Fluids
  • Oxygen
  • Organ support
  • Antibiotics
239
Q

What is the pro of giving antibioitcs for acute pancreatitis?

A

Several studies suggested meropenem for 1 week in pancreatitis with necrosis decreases mortality

240
Q

What is the con for giving antibiotics for acute pancreatitis?

A

Concern that giving broad spectrum antibiotics in sterile necrosis will select out MRSA or fungal infection with higher mortality

241
Q

Describe early feeding in acute pancreatitis?

A

Nasogastric or nasojujenal

242
Q

List the 3 investigations for acute pancreatitis?

A
  1. US to assess for gallstones
  2. MRCP to assess for CBD stones
  3. CT if diagnostic doubt or concern about complications
243
Q

What are 2 differential diagnosis for acute pancreatitis?

A
  1. Perforated duodenum

2. Ischaemic bowel

244
Q

Describe early phase acute pancreatitis?

A
  • Systemic disturbance from host response to local pancreatic injury (usually over by one week).
  • SIRS may progress to MODS
245
Q

Describe late phase acute pancreatitis?

A

Local and septic complications

246
Q

What is the % mortality for severe acute pancreatitis?

A

Up to 25% dependant on age and comorbidities

247
Q

List 4 further managements of acute pancreatitis to treat the cause?

A
  1. ERCP
  2. Lap Cholecystectomy
  3. Alcohol addictions advice
  4. Stop medication
248
Q

Describe the sequelae of pancreatitis?

A
  • Complete resolution with / without organ dysfunction
  • Necrosis with/ without infection
  • Fluid collection: peripancreatic fluid collection, pseudocyst, pancreatic fistula
249
Q

Describe pancreatic necrosis?

A

Predicts complicated disease but initial management not altered

250
Q

What is the purpose of serial CT for pancreatic necrosis?

A

For resolution, or repeat if deterioration in organ function/ increase in organ support

251
Q

Describe Infected pancreatic necrosis?

A
  • Ongoing sepsis and progression to MODS

- Requires intervention

252
Q

What are the 3 types of managements for infected pancreatic necrosis?

A
  1. Open necrosectomy
  2. Percutaneous necrosectomy
  3. Radiological drainage
253
Q

List the 2 complications of pancreatic necrosis?

A
  1. Bleeding- interventional radiology

2. Erosion to surrounding structures- surgery

254
Q

Describe the Interventional radiology for bleeding?

A
  • Access via groin
  • Selective cannulation of coeliac trunk
  • Commonly splenic artery aneurysm, may be gasproduodenal artery
  • Usually coils placed before and after bleed, can be stunted
255
Q

Describe the prognosis of a Pancreatic Pseudocyst?

A

May settle without intervention (almost always by 12 weeks)

256
Q

What may a pancreatic pseudocyst require if its symptomatic?

A

Drainage

257
Q

Describe the drainage of a Pancreatic Pseudocyst?

A
  • Can drain to stomach laparoscopically or endoscopically

- May drain transpapillary

258
Q

Describe the management of a pancreatic fistula?

A
  • May require period of parenteral nutrition
  • Would attempt endoscopic treatment in first instance
  • May require salvage distal pancreatectomy
259
Q

List the 5 after affects of pancreatitis?

A
  1. May be diabetic
  2. May require creon pancreatic enzyme supplements
  3. May require restorative surgery
  4. Significant impact on quality of life
  5. If gallstones- needs gallbladder removed
260
Q

Describe the spread of head and neck cancer?

A

May spread to lymph nodes in neck, usually on the same side

261
Q

What are the 2 risk factors of head & neck cancer?

A
  1. Smoking

2. Alcohol

262
Q

What is a classic presentation of head/neck cancer?

A

A persistent, non-healing ulcer without definite, identifiable cause

263
Q

List the 4 layers of the oesophagus?

A
  1. Mucosa (non-keratinising stratified squamous)
  2. Muscularis mucosae
  3. Submucosa
  4. Muscularis propria
  5. Advenitia
264
Q

Describe the normal oesophageal mucosa?

A

Lining of non-keratinising stratified squamous epithelium

265
Q

Describe the histological appearance of reflux oesophagitis (GORD)?

A
  • Acid and digestive enzymes injure squamous epithelium lining oesophagus
  • Increased numbers of inflammatory cells and the basal zone of the squamous epithelium is hyperplastic
266
Q

List 2 potential infections of the oesophagus?

A
  1. Candida albicans (fungus)

2. Herpes simplex virus

267
Q

List 3 chemicals causing inflammatory oesophageal pathology?

A
  1. Peptic oesophagitis / GORD: reflux of acid, bile
  2. Caustics: lye (NaOH, caustic soda)
  3. Pills: iron, bisphosphonates, tetracycline
268
Q

Describe the histological appearance of Candida oesophagitis?

A

Active chronic inflammation with many neutrophils especially near the luminal surface of the epithelium

269
Q

What stain confirms spores & hyphae of Candida albicans?

A

PAS stain

270
Q

Describe the histological appearance of oral herpes simplex infection?

A
  • Atypical squamous cells

- Inflammatory exudate and cells (‘slough’)

271
Q

What is Barrett’s oesophagus?

A

A metaplastic response to mucosal injury e.g. from long term GORD

272
Q

Describe the histological appearance of Barrett’s oesophagus?

A

Squamous epithelium becomes glandular, usually intestinal with goblet cells

273
Q

What is Barrett’s oesophagus associated with?

A

Development of benign strictures but also with adenocarcinoma

274
Q

What are the 3 types of dysplasia?

A
  1. ‘Indefinite for dysplasia‘
  2. Low grade dysplasia
  3. High grade dysplasia
275
Q

What is dysplastic epithelium?

A

Architecturally & cytologically abnormal

276
Q

Describe low grade dysplasia?

A
  • Cells polarised

- Nuclei stratified

277
Q

Describe high grade dysplasia?

A
  • Polarity lost.
  • Nuclei rounder, vesicular
  • Prominent nucleoli
  • Abnormal mitoses
  • Necrosis
278
Q

What is the risk of Barrett’s oesophagus?

A

Cancer risk ~0.4% per annum due to dysplastic cells

279
Q

Who is more likely to get Barrett’s oesophagus?

A

Males > Females (increasing)

280
Q

Describe the different risks of cancer between low and high grade dysplasia in Barrett’s?

A
  • Increased risk but progression to cancer still slow

- LGD has nearly the same cancer risk as HGD

281
Q

Describe the role of surveillance/screening in Barrett’s oesophagus?

A
  • 4 biopsies (Seattle Protocol) every 2cm effective at finding dysplasia, but laborious
  • Targeted biopsy may eventually replace it with improvements in endoscopy
282
Q

What endoscopic treatment may avoid the need for radical surgery in Barrett’s oesophagus?

A

Radiofrequency ablation- reduced cancer risk

283
Q

What are 2 types of oesophageal cancers?

A
  1. Squamous carcinoma

2. Adenocarcinoma

284
Q

What is oesophageal Squamous carcinoma associated with?

A
  1. Smoking

2. Drinking

285
Q

What is adenocarcinoma of the oesophagus associated with?

A
  1. Gastro-oesophageal reflex (GORD)

2. Obesity

286
Q

List 5 causes of acute gastritis?

A
  1. Alcohol
  2. Medication e.g. NSAIDs
  3. Severe trauma
  4. Burns (Curling’s ulcers)
  5. Surgery
287
Q

List 3 causes of chronic gastritis?

A
  1. Autoimmune
  2. Bacterial (H pylori)
  3. Chemical
288
Q

What is autoimmune gastritis?

A

Destruction of parietal cells due to auto-antibodies against intrinsic factor & parietal cell antibodies in blood

289
Q

List 4 things that autoimmune gastritis leads to?

A
  1. Complete loss of parietal cells with pyloric & intestinal metaplasia
  2. Achlorhydria -> bacterial overgrowth
  3. Hypergastrinaemia -> endocrine cell hyperplasia /carcinoids
  4. Persistent inflammation which can lead to epithelial dysplasia and may lead to cancer
290
Q

What effect does H. pylori have?

A

Colonises gastric mucosa causing active chronic inflammation

291
Q

What does IL-8 do?

A

From epithelial cells attracts neutrophils

292
Q

Describe the 2 patterns of gastritis occurring after exposure to H. pylori?

A
  1. Antral-predominant gastritis -> hypergastrinaemia and duodenal ulceration
  2. Pangastritis -> hypochlorhydria, multifocal atrophic gastritis, intestinal metaplasia, cancer
293
Q

What is thought to be the reason why two patterns of gastritis occur after exposure to H. pylori?

A

Microbe-host interface

294
Q

What type of gastritis do patients with higher IL-8 tend to get?

A

Pangastritis

295
Q

What type of gastritis do patients with lower IL-8 tend to get?

A

Antral gastritis

296
Q

List the 2 associations of the formation of peptic ulceration?

A
  1. Impaired mucosal defense (due to NSAID interfering with mucosal prostaglandin synthesis, bile reflux)
  2. Microbe factors (CagA + variants associated with more severe inflammation)
297
Q

List 3 signs of Helicobacter pylori infection?

A
  1. Haematemesis
  2. Melena
  3. Abdominal pain
298
Q

List 3 consequences of peptic ulceration?

A
  1. Haemorrhage
  2. Perforation
  3. Fibrosis (leading to stenosis)
299
Q

Describe the histological appearance of chemical gastritis?

A
  • Few inflammatory cells

- Surface congestion oedema, elongation of gastric pits, tortuosity, reactive hyperplasia / atypia, ulceration

300
Q

Where in the stomach is chemical gastritis commonly seen?

A

Antrum more than corpus

301
Q

List 4 causes of chemical gastritis?

A
  1. Bile reflux
  2. NSAIDs
  3. Ethanol
  4. Oral iron
302
Q

What is gastric cancer strongly associated with?

A

Chronic gastritis: H pylori or autoimmune

303
Q

Describe the histological appearance of gastric cancer?

A
  • Background atrophic mucosa
  • Chronic inflammation
  • Intestinal metaplasia
  • Dysplasia
304
Q

What is gastric cancer morphologically classified as via the Lauren Classification?

A

‘Intestinal’ or ‘ diffuse’ types

305
Q

What is diffuse gastric cancer?

A

Individual malignant cells with mucin vacuoles (‘signet ring’ cells)

306
Q

Why is diffuse gastric cancer called linitis plastica (‘leather bottle stomach’)?

A

May invade extensively without being endoscopically obvious

307
Q

Describe the 3 clinical signs of diffuse gastric cancer?

A
  1. Metastasis to ovaries (‘Krukenberg tumour’)
  2. Supraclavicular lymph node (‘Virchow’s node’)
  3. ‘Sister Joseph’s nodule’ (umbilical metastasis)
308
Q

List 3 presenting features of upper GI bleeding?

A
  1. Haematemesis
  2. “Coffee ground” vomiting
  3. Melaena
309
Q

What are the 3 sources of upper GI bleeding?

A
  1. Oesophagus
  2. Stomach
  3. Duodenum
310
Q

What is the % mortality & rebreeding of upper GI bleeding (in the UK)?

A
  • Mortality: 10%

- Rebleeding: 13%

311
Q

List 7 causes of upper GI bleeding & their % occurrence?

A
  1. Peptic ulcer- 36%
  2. Oesophagitis- 24%
  3. Gastritis- 22%
  4. Duodenitis- 13%
  5. Varices- 11%
  6. Malignancy- 4%
  7. Mallory-weiss tear- 4%
312
Q

What are 3 causes of peptic ulcers?

A
  1. Acid
  2. H. pylori
  3. NSAIDs
313
Q

Describe the management of upper GI bleeding?

A
  • Resuscitate if required
  • Risk assessment & timing of endoscopy
  • Drug therapy & transfusion
314
Q

Describe how to resuscitate in an upper GI bleed?

A
  • Pulse & BP - IV access for fluids/blood (check bloods, esp Hb & urea) - Lie flat & give oxygen
315
Q

Describe how the risk of an upper GI bleed affects the timing of endoscopy?

A
  • High risk:emergency endoscopy
  • Moderate risk: admit & next day endoscopy
  • Low risk:out-patient management
316
Q

What is the endoscopic risk score for upper GI bleeding?

A

Rockall (predicts mortality)

317
Q

What are the 3 endoscopic risk scores for upper GI bleeding?

A
  1. “Admission” Rockall
  2. Glasgow Blatchford (predicts need for intervention or death)
  3. AIMS 65
318
Q

What does a Glasgow Blatchford score (GBS) of <= 1 mean?

A

Identifies those at very low risk of poor outcome: can be discharged for out-patient endoscopy

319
Q

When do most upper GI bleed patients get their endoscopy?

A

Within 24 hrs (even at weekend)

320
Q

When do low risk upper GI bleed patients (GBS <= 1) get their endoscopy?

A

Can be discharged for out-patient endoscopy

321
Q

When do very high risk upper GI bleed patients (haemodynamic instability or severe ongoing bleeding) get their endoscopy?

A

Emergency endoscopy

322
Q

List the 4 things needed for endoscopic therapy?

A
  1. AdrenaIine injection
  2. Heater probe
  3. Endoscopic clips
  4. Thrombin, laser
323
Q

What is the benefit of IV proton pump inhibitors (PPIs) in upper GI bleeding?

A
  • Not beneficial prior to endoscopy

- Reduces rebleeding & mortality if given post-endoscopy to the higher risk patients who required endoscopic therapy

324
Q

What should you do for upper GI bleed patients on aspirin & NSAIDs?

A
  • Continue low dose aspirin after upper GI bleeding once haemostasis achieved (& add PPI)
  • Stop NSAIDs
325
Q

What should you do for upper GI bleed patents on Clopidogrel, Warfarin & DOACs?

A

Once haemostasis achieved, discuss risks & benefits with cardiologist/stroke team & patient, but generally try to restart these medications

326
Q

When would you transfuse blood in an upper GI bleed?

A

Once Hb <7-8g/dL

327
Q

When would you transfuse platelets in an upper GI bleed?

A

If actively bleeding & platelet count <50x109/L

328
Q

When would you give Fresh frozen plasma in an upper GI bleed?

A

If INR>1.5

329
Q

When would you give prothrombin complex concentrate in an upper GI bleed?

A

If on warfarin & active bleeding

330
Q

What are 3 ways to treat oesophageal varices?

A
  1. Endoscopic banding
  2. TIPS
  3. B-Blocker drugs
331
Q

What is the % mortality rate for variceal bleeding?

A

30-40%

332
Q

What is the reason for an increase in variceal bleeding?

A

Due to the rise in alcohol, hepatitis C & fatty liver disease

333
Q

How would you resuscitate an acute variceal bleed?

A
  • Restore circulating volume - Transfuse once Hb<7 g/dL - Consider airway protection
334
Q

How do you diagnose an acute variceal bleed?

A

Endoscopy

335
Q

What are the 3 therapies for an acute variceal bleed?

A
  1. Antibiotics early

2. Vasopressors (Terlipressin) early - 3. Endoscopic band ligation

336
Q

What does TIPS stand for?

A

Trans-jugular intrahepatic stent shunt

337
Q

What are 3 ways to manage uncontrolled variceal bleeding?

A
  1. Sengstaken tube
  2. TIPS useful “rescue” procedure for failed endoscopy & drug therapy (high mortality)
  3. Surgical shunt/transection (very rarely used)
338
Q

What are the 2 primary prophylaxis for Variceal Bleeding?

A

Beta-blockers or Banding

339
Q

What are 5 treatments for acute variceal bleeding?

A
  1. Antibiotics & Terlipressin (in A&E)
  2. Banding first line for oesophageal variceal bleeding
  3. Tissue glue injection for gastric variceal bleeding
  4. TIPS for uncontrolled variceal bleeding
  5. Balloon tamponade (as temporary salvage)
340
Q

What are the 2 treatments for prevention of variceal rebleeding?

A

Beta-blocker + repeated Banding

341
Q

What are the 4 key points to optimal management of an upper GI bleed?

A
  1. Resuscitate
  2. Risk assess
  3. Timing of endoscopy
  4. Drug therapy & transfusion
342
Q

List the 5 layers of the intestines?

A
  1. Mucosa
  2. Submucosa
  3. Muscular propria
  4. Subserosal fat
  5. Peritoneal surface
343
Q

What are the crypts called in the small intestine?

A

Crypts of Lieberkuhn

344
Q

List 9 causes of inflammation in the intestines?

A
  1. Coeliac Disease (small intestine)
  2. Idiopathic Chronic Inflammatory Bowel Disease
  3. Crohns Disease
  4. Ulcerative Colitis (large intestine)
  5. Infection
  6. Ischaemia
  7. Radiation colitis
  8. Diversion colitis
  9. Microscopic colitis
345
Q

What is the cause of Coeliac disease?

A

Immunological response to gliadin (gluten derived peptide)

346
Q

Describe how the immunological response to gliadin in coeliacs disease leads to malabsorption?

A

Gliadin presented by HLA molecules to helper T cells –> lymphocytic response –> epithelial damage –> flattening of villi –> less surface area for absorption of nutrients –> malabsorption

347
Q

Describe the inheritance/genetics of coeliacs disease?

A
  • Prevalence in 1st degree relatives is approx 10%

- Strong association between coeliac disease & HLA haplotypes DQ2 & DQ8

348
Q

What is elevated in classical coeliacs sprue?

A

Serum TTG elevated

349
Q

How is coeliacs disease managed?

A

Removal of gluten-containing foods from diet

350
Q

What happens to the small intestine structure in coeliacs disease?

A

Crypt hyperplasia

351
Q

What are the 3 types of Chronic Inflammatory bowel diseases?

A
  1. Crohn’s Disease
  2. Ulcerative Colitis
  3. “Indeterminate colitis”
352
Q

List the 5 intestinal chronic changes in IBD?

A
  1. Crypt distortion
  2. Loss of crypts
  3. Submucosal fibrosis
  4. Paneth cell metaplasia
  5. Neuronal Hyperplasia
353
Q

List the 4 acute changes seen during active disease of chronic IBD?

A
  1. Cryptitis
  2. Loss of goblet cells
  3. Crypt abscess formation
  4. Ulceration
354
Q

Describe the symptoms of ulcerative colitis?

A
  • Relapsing
  • Bloody mucoid diarrhoea (stringy mucus) with pain/cramps relieved by defecation
  • Lasts days/months, then remission for months/years
  • Initial attack may cause medical emergency for fluid & electrolyte imbalance
355
Q

What % of UC patients have 1 relapse per 10 year period?

A

97%

356
Q

List 9 extra intestinal manifestations of ulcerative colitis?

A
  1. Migratory polyarthritis
  2. Ankylosing spondylitis
  3. Erythema nodosum
  4. Clubbing of fingertips
  5. Primary sclerosing cholangitis
  6. Pericholangitis
  7. Cholangiocarcinoma (rare)
  8. Uveitis
  9. Sacroiliitis
357
Q

List the 5 complications of ulcerative colitis?

A
  1. Perforation
  2. Toxic megacolon
  3. Iliac vein thrombosis
  4. Carcinoma
  5. Lymphoma
358
Q

What % of ulcerative colitis patients require colectomy during first 3 years?

A

30%

359
Q

What is recommended in patients with long-standing extensive UC & why?

A

Regular colonoscopy with biopsy to detect precancerous dysplastic changes

360
Q

What is Crohn’s disease?

A

Transmural granulomatous disease affecting oesophagus to anus but discontinuous, usually involves small intestine & colon with rectal sparing, less severe in distal vs. proximal colon (i.e. preferential right-sided involvement)

361
Q

What is the prevalence of Crohn’s disease in primary western populations?

A

3 per 100,000, peaks in teens/twenties & ages 50-69

362
Q

List the 4 symptoms of Crohn’s disease?

A
  1. Episodic mild diarrhea
  2. Fever
  3. Pain
  4. May be precipitated by stress: if colon affected, may have anemia
363
Q

What do 20% of people with Crohn’s disease have?

A

Abrupt onset, resembling acute appendicitis or bowel perforation

364
Q

List the 5 complications of Crohn’s disease?

A
  1. Fibrosing strictures (common in terminal ileum)
  2. Fistula
  3. Malabsorption
  4. Toxic megacolon
  5. Carcinoma (but lower risk than in UC)
365
Q

List the 7 additional histological features of Crohn’s disease (different from UC features)?

A
  1. Skip lesions
  2. Fistulas / sinus tracts
  3. Malabsorption (if ileum involved)
  4. Granulomas
  5. Deep ulcerations
  6. Marked lymphocytic infiltration
  7. Serositis
366
Q

What are the long term risks of IBD?

A
  • Higher risk of colonic carcinoma than general population

- Colonic/rectal adenocarcinoma is the most common intestinal malignancy

367
Q

What is the lifetime risk of colorectal cancer in the UK?

A
  • 1 in 16 men

- 1 in 20 women

368
Q

Describe how genetic abnormalities occur?

A

At the cellular level secondary to damage to DNA of existing stem cells, allowing the cells to survive when they should normally undergo apoptosis

369
Q

What may abnormalities in response to proliferative stimuli result in?

A

Increased cell proliferation

370
Q

Why are numerous abnormalities required for a cancer to develop its malignant potential?

A

Because of the numerous checks on cells division

371
Q

What does it mean when a cell is dysplastic?

A

The abnormal cell morphology has survived as its stayed compatible with the development of some abnormalities

372
Q

Describe adenomas of the colon?

A
  • Also known as benign glandular neoplasms

- Dysplastic, and the majority are polyps

373
Q

What are 4 differentials of adenomas?

A
  1. Hyperplastic (metaplastic) polyps
  2. Hamartomatous polyps
  3. Inflammatory polyps
  4. Submucosal lesions (lipoma, leiomyoma)
374
Q

List 5 risk factors for colorectal cancer?

A
  1. Adenoma- size, number
  2. IBD
  3. Family History
  4. Other Carcinomas
  5. Polyposis syndromes- FAP, Lynch syndrome
375
Q

What size of polyps increase the risk of colorectal cancer?

A

> 2cm

376
Q

What histological type of polyp is more likely to turn malignant?

A

Flat polyps with a villous pattern have a much larger surface area & no stalk

377
Q

List 2 scoring systems for colorectal cancer?

A
  1. Dukes’ staging

2. TNM staging

378
Q

Describe Dukes’ A & B colorectal cancers?

A

Fat better prognosis so no need to expose to toxic side effects of chemotherapy

379
Q

What may individual colorectal tumours be targeted by?

A

Preoperative neoadjuvant therapy

380
Q

List 3 ways to detect colorectal cancer early?

A
  1. Screening colonoscopy of UC Patients
  2. Bowel Cancer Screening Programme faecal occult blood of >50 -75 year old (+ve –> colonoscopy)
  3. Patient education of symptoms
381
Q

List 3 other primary tumours arising in the small or large intestines?

A
  1. Neuroendocrine tumours
  2. GISTs
  3. Lymphomas
382
Q

What is proctitis?

A

Distal colitis limited to the rectum

383
Q

What is proctosigmoiditis?

A

Colitis limited to retum & sigmoid

384
Q

What is left sided colitis?

A

UC to the splenic flexure

385
Q

What is extensive colitis?

A

UC to the hepatic flexure

386
Q

What is pan colitis?

A

Colitis of the whole colon

387
Q

What is the definition of ulcerative colitis?

A

Diffuse mucosal inflammation limited to the colon

388
Q

What 2 factors define Crohn’s disease?

A
  1. Location- colonic, terminal ileal, perianal etc

2. Pattern of disease- inflammatory, fistulating, stricturing

389
Q

What is the definition of Crohn’s disease?

A

Patchy transmural inflammation affecting any part of GI tract

390
Q

Is ulcerative colitis or crohn’s more common?

A

Ulcerative colitis is more common

391
Q

Slight _____ preponderance in Crohn’s?

A

Female

392
Q

Slight ____ preponderance in UC?

A

Male

393
Q

Describe the epidemiology of IBD?

A
  • Diseases of young people
  • Peak incidence between 10-40 years
  • 15% present at 60+
  • Approx 240,000 people with IBD in the UK
394
Q

Describe the pathogenesis of IBD?

A
  • Aetiology unknown

- “Host response to environmental triggers in genetically susceptible individuals”

395
Q

Describe the relationship between smoking and IBD?

A
  • Increases risk of Crohn’s

- Reduces risk of UC

396
Q

List the 7 things to ask about when taking an IBD history?

A
  1. Stool frequency, consistency, urgency, blood
  2. Abdo pain, malaise, fever
  3. Weight loss
  4. Extraintestinal symptoms (joint, eyes, skin)
  5. Travel
  6. Family Hx
  7. Smoking
397
Q

List the 6 things to do when performing an examination to diagnose IBD?

A
  1. Weight
  2. Pulse
  3. Temperature
  4. Anaemia
  5. Abdominal tenderness
  6. Perineal examination
398
Q

List the 8 investigations to do when diagnosing IBD?

A
  1. FBC, ESR, U&E’s, LFTs, CRP
  2. Stool cultures + C. Difficile toxin
  3. Faecal Calprotectin
  4. AXR
  5. Rigid sigmoidoscopy
  6. Colonoscopy
  7. Small bowel radiology
  8. Labelled WCC scanning
399
Q

What investigation should you avoid in severe IBD disease?

A

Endoscopic examination

400
Q

List the 3 treatments common to UV & Crohn’s?

A
  1. Coricosteroids
  2. Thiopurines
  3. Biologics
401
Q

What is the treatment for UC alone?

A

5ASAs

402
Q

What are the 2 treatments for Crohn’s disease alone?

A
  1. Methotrexate

2. Immune modulating diets

403
Q

List the 4 glucocorticoids for IBD treatment?

A
  1. IV hydrocortisone, methylprednisolone
  2. Oral Prednisolone
  3. Budesonide
  4. Beclometasone
404
Q

What effect do steroids have on IBD?

A
  • Rapid induction of remission

- Poor evidence for maintaining remission

405
Q

Describe the slow reducing course of steroids?

A
  • Prednisolone 40mg daily/1 week

- Reduce by 5mg/ week

406
Q

List the 5 significant side effects of steroids?

A
  1. Immunosuppression
  2. Impaired glucose tolerance
  3. Osteoporosis
  4. Weight gain
  5. Cushingoid appearances
407
Q

What is the most widely used aminosalicylates?

A

Mesalazine

408
Q

List the 3 ways to give Mesalazine (aminosalicylates)?

A
  1. pH dependent release/resin coated (Asacol, Salofalk)
  2. Time controlled release (Pentasa)
  3. Delivery by carrier molecules (sulphasalazine, osalazine, balsalazide)
409
Q

What are Aminosalicylates also effective as?

A

Topical therapy- enemas/suppositries

410
Q

List 4 brand names for Mesalazine?

A
  1. Asacol
  2. Pentasa
  3. Octasa (cheapest)
  4. Ipocol
411
Q

List the 2 main roles of Aminosalicylates?

A
  1. Induction of remission in mild-moderate ulcerative colitis
  2. Maintenance of remission in UC
412
Q

What is Aminosalicylates reliant on?

A

Compliance rather than delivery system

413
Q

What does a higher dose (4-4.8g day) of Aminosalicylates do?

A
  • Higher remission rates

- Better mucosal healing

414
Q

What is the pro and con of Aminosalicylates?

A
  • PRO: Maintenance therapy may reduce cancer risk

- CON: Little evidence to support use in Crohn’s

415
Q

What % of people have adverse effects on Sulphasalazine?

A

10-45%

416
Q

What % of people have an intolerance to Mesalazine?

A

15%

417
Q

Describe the adverse effects of Aminosalicylates?

A

Renal impairment (interstial nephritis, nephrotic syndrome) is rare and idiosynchratic

418
Q

Give 2 examples of Thiopurines unlicensed for IBD therapy?

A

Azathioprine and mercaptopurine

419
Q

What are Thiopurines effective for?

A

Maintenance therapy for UC and Crohn’s

420
Q

Describe the steroid sparing agent aspect of Thiopurines?

A
  • Those requiring 2+ course steroids in a year
  • Relapse on <15mg prednisolone
  • Post-op prophylaxis in complicated Crohn’s
421
Q

Describe Thiopurines?

A
  • Purine anti-metabolites
  • Immune modulating drugs
  • Essentially prevent T cell clonal expansion in response to antigenic stimuli
  • Allow T cell apoptosis
422
Q

What is the dose of Azathioprine (Thiopurines)?

A

1.5–2.5mg/kg/day

423
Q

What is the dose of Mercaptopurine (Thiopurines)?

A

1–1.5mg/kg/day

424
Q

What may predict Leucopenia?

A

Thiopurine methyl transferase (TPMT)

425
Q

How do you monitor Thiopurines?

A

Weekly FBC + LFTs for 8/52 then at least every 3/12

426
Q

Describe how/why we measure thiopurines 6TGN (6-Thioguanine nucleotides) active metabolites?

A
  • Tailored dosing to ensure drug within therapeutic window

- Assessment of compliance

427
Q

Describe why we measure thiopurines 6MMP (6-methylmercaptopurine) metabolite?

A

Associated with risk of hepatotoxiciy

428
Q

List the 7 common side effects of Thiopurines?

A
  1. Leucopenia
  2. Nausea, vomiting
  3. Arthralgia
  4. Pancreatitis
  5. Hepatitis
  6. Squamous skin cancers
  7. Haematological malignancy
429
Q

What is methotrexate?

A
  • Anti-metabolite

- Folate scavenger so need folate supplements

430
Q

What is the dose for methotrexate?

A

15-25mg weekly SC

431
Q

What is methotrexate effective for treating?

A
  • Effective in Crohn’s
  • Little evidence in UC
  • Widely used in inflammatory disease
432
Q

List the 5 side effects of methotrexate?

A
  1. GI upset
  2. Hepatotoxicity
  3. Immunosuppression
  4. Sepsis
  5. Pulmonary fibrosis
433
Q

What is Infliximab?

A

Murine Anti-TNF alpha monoclonal antibody

434
Q

What is Infliximab effective for treating?

A
  • Severe or fistulating Crohn’s
  • Rescue acute severe UC
  • Moderate to severe UC refractory to other treatment
435
Q

What is Infliximab now available as?

A

A variety of “biosimilars”

436
Q

Describe the dose of Infliximab?

A
  • Loading regime at 0/2/6 weeks

- 2 monthly intravenous infusion

437
Q

What are 3 CONS of Infliximab?

A
  1. Loss of efficacy
  2. Allergic reactions
  3. Expensive
438
Q

What is Adalumimab?

A

Humanised Anti-TNF alpha monoclonal antibody

439
Q

What is the dose for Adalumimab?

A

Fortnightly SC injections

440
Q

What are the 2 CONS of Adalumimab?

A
  1. Less reactions

2. Less need for concomitant immunosuppression

441
Q

What is Golimumab?

A

Humanised anti-TNF alpha

442
Q

What is the dose of Golimumab?

A

2 weekly sc injections

443
Q

What is Golimumab licensed for?

A

Moderate to severe Ulcerative colitis (not Crohn’s)

444
Q

What are the 2 infection risks associated with Anti-TNF biologic drugs?

A
  1. Reactivation of TB

2. Reactivation of Hepatitis B

445
Q

What are the 2 neurological side effects associated with Anti-TNF biologic drugs?

A
  1. Incidence of MS

2. Progressive multifocal leucoencephalopathy

446
Q

What type of malignancy does biologics increase your risk of?

A

Lymphoma

447
Q

How does Vedoluzimab work?

A

Anti-adhesin- binds Integrin α4β7 (lymphocyte adhesion molecule)

448
Q

What is Vedoluzimab effective for treating?

A
  • Gut specific so few risks of neurotoxicity

- Appears better for UC than Crohn’s

449
Q

What type of IBD patient warrant hospital admission?

A

Patients who fail to respond to optimal treatment with 5ASA/prednisolone or with severe disease

450
Q

What is the management of acute severe colitis?

A
  • Intravenous steroid therapy required

- Liaison with colorectal surgeon

451
Q

What factors predicts colectomy in 85% of acute severe colitis patients?

A

Stool frequency >8/day / CRP >45 on day 3

452
Q

List the 4 investifations for acute severe colitis?

A
  1. Daily FBC, ESR, U+Es, CRP
  2. Stool cultures (including C.Difficile)
  3. Daily AXR
  4. Sigmoidoscopy
453
Q

What is the treatment for acute severe colitis?

A
  • Prophylatic LMW heparin

- IV hydrocortisone 100mg QDS or Methylprednisolone 30mg BD

454
Q

What are the 2 options for changing the treatment of acute severe colitis after 72 hrs?

A
  1. Improving- oral prednisolone 40mg

2. No improvement- rescue therapy

455
Q

What are the 3 types of rescue therapy for acute severe colitis?

A
  1. Ciclosporin 2mg/kg/day IV
  2. Infliximab 5mg/kg single dose
  3. Surgery
456
Q

Describe surgery for ulcerative colitis?

A
  • Surgery “curative”

- Ileo-anal pouch or ileostomy

457
Q

Describe surgery for Crohn’s disease?

A
  • Indicated for stricturing, perforation, fistulizing disease
  • Sparing as will come back
458
Q

What are the 6 aetiologies of the “acute abdomen”?

A
  1. Burst
  2. Blocked
  3. Inflamed
  4. Lost its blood supply
  5. Combination
  6. Nothing to do with the abdomen
459
Q

What 2 conditions, unrelated to the abdomen, can cause an acute abdomen?

A
  1. Myocardial infarction

2. Pneumonia

460
Q

What are 3 reasons why there is an increased use of imaging?

A
  1. Increased availability
  2. Increasing number elderly patients
  3. Increased accuracy
461
Q

How useful is lmaging?

A
  1. Depends on what’s wrong with the patient

2. Depends on quality of clinical assessment

462
Q

What are the 3 types of imaging available for the abdomen?

A
  1. Plain films (Xray)
  2. Ultrasound
  3. CT
463
Q

What are the 3 different densities of the plain abdominal film?

A
  1. Gas
  2. Soft tissue: fat, muscle, bowel wall, solid organ, blood vessel
  3. Bone
464
Q

What does the plain abdominal imagine reaching the X-ray detector depend on?

A

Densities encountered as X-ray travels through body

465
Q

Are gallstones usually visible on plain X-ray?

A

NO

466
Q

What are 3 normal gals shadows on a plain abdominal X-ray?

A
  1. Colon externally
  2. Small bowel centrally
  3. Stomach medial LUQ
467
Q

Describe the movement of different parts of the colon?

A
  • Ascending & descending colon- usually fixed

- Transverse & sigmoid- variable

468
Q

What is Chilaiditi syndrome?

A

Rare condition when pain occurs due to transposition of a loop of large intestine (usually transverse colon) in between the diaphragm & liver, visible on plain abdominal X-ray or chest X-ray

469
Q

What type of inflammatory conditions is an abdominal X-ray useful for?

A
  • Colitis

- Not specific in other inflammatory conditions

470
Q

What type of inflammatory condition is an abdominal ultrasound useful for?

A

Cholecystitis (and appendicitis if young and slim)

471
Q

What is the 1st choice of imaging for abdominal inflammation?

A

CT

472
Q

What is a chest X-ray sensitive for?

A

Free gas (good for perforation)- approx 80% sensitive

473
Q

What imagine is good/bag for an abdominal perforation?

A
  • GOOD: CT

- BAD: AXR as it’s very subtle

474
Q

What 2 types of imaging is useful for abdominal obstruction?

A
  • Abdominal X-ray

- CT for cause

475
Q

What 4 things should you look for when imaging for abdominal obstruction?

A
  1. Small &/or large bowel dilatation?
  2. How much gas in colon?
  3. Any gas in rectum?
  4. Any complications- ischaemia, perforation?
476
Q

What occurs in an incomplete small bowel obstruction?

A
  • Some gas is still seen in the colon

- Small bowel more distended than large

477
Q

What occur in a complete small bowel obstruction?

A
  • No gas is seen in the colon

- Small bowel more distended than large

478
Q

What are the 2 types of volvulus in the abdomen?

A
  1. Caecum

2. Sigmoid

479
Q

What abdominal imaging is non-specific for ischaemia?

A

Abdominal X-ray

480
Q

What do positive ischaemic signs on an abdominal X-ray suggest?

A

Advanced ischaemia

481
Q

WHat is the 1st choice of imaging for ischaemia?

A

CT but <60% sensitive

482
Q

What clinical sign can a plain abdominal X-ray show?

A

Pneumoperitoneum

483
Q

What is the radiation dose for CXR, AXR & Abdo/pelvis CT?

A
  • CXR: 0.02 mSv
  • AXR: 0.5 mSv
  • CT abdomen/pelvis: 6-10mSv
484
Q

What is 10mSv radiation dose equal to?

A

1:1000 life time risk of fatal cancer (for adult age 30-39)

485
Q

How common are coincidentalomas due to radiation?

A

Up to 25% in >70’s

486
Q

What 2 things are plain radiography’s especially good at detecting?

A
  1. CXR- perforation

2. AXR- obstruction

487
Q

List the 3 main examination findings indicating chronic liver disease?

A
  1. Clubbing
  2. Palmar erythema
  3. Spider naevi
488
Q

What are 4 special investigations for liver disease?

A
  1. Hepatitis serology
  2. Ferritin & transferrin sat
  3. Liver autoantibodies
  4. Alpha-fetoprotein
489
Q

What haematology results suggest cirrhosis?

A
  • Raised bilirubin & Prothrombin

- Low albumin & platelets

490
Q

What are 4 complications of cirrhosis?

A
  1. Ascites
  2. Variceal bleeding
  3. Encephalopathy
  4. Hepatocellular carcinoma
491
Q

What is Diagnostic paracentesis?

A

Removal of a small quantity of fluid for testing

492
Q

When would you undertake Diagnostic paracentesis?

A

All patients with new onset ascites, admission with worsening ascites or clinical condition

493
Q

What 3 things are tested in a Diagnostic paracentesis?

A
  1. PMN count and culture (plain container & blood culture bottles)
  2. Total ascitic protein & albumin
  3. Cytology
494
Q

What is the definition of Spontaneous Bacterial Peritonitis (SBP)?

A

> 250 neutophils/mm3 in ascites in absence of intra-abdominal source of infection or malignancy (often culture -ve)

495
Q

What is spontaneous Bacterial Peritonitis?

A

Frequent, life threatening infection in cirrhotic patients

496
Q

What is type of bacteria typically causes spontaneous Bacterial Peritonitis?

A

Usually gram-ve bacteria

497
Q

What is the % mortality rate of spontaneous bacterial peritonitis?

A

10-40%

498
Q

How would you treat spontaneous bacterial peritonitis?

A

IV antibiotics + IV albumin

499
Q

How would you manage ascites?

A

Salt restriction & Diuretics: Oral Spironolactone +/- Frusemide

500
Q

What 3 things is refractory ascites (fluid overload) unresponsive to in <10% of patients?

A
  1. Sodium restriction
  2. 400mg/day spironolactone
  3. 160mg/day frusemide
501
Q

What are the 3 treatments for refractory ascites?

A
  1. Large Volume paracentesis (LVP)
  2. Transjugular Intra-hepatic stent (TIPS)
  3. Liver transplant (if suitable)
502
Q

What does genetic haemochromatosis (C282Y mutation) lead to?

A

Excessive absorption of dietary iron which leads to iron overload in liver, heart, pancreas, joints, skin (“bronze diabetes”)

503
Q

What are 3 things diagnosing genetic haemochromatosis?

A
  1. Raised ferritin & transferrin saturation
  2. HFE gene
  3. Liver biopsy rarely needed
504
Q

How is genetic haemochromatosis treated?

A

Venesection

505
Q

What are 4 causes of hyperamylasaemia?

A
  1. Pancreatitis, disruption pancreatic duct
  2. Biliary conditions (gallbladder infection/ perforation, choledocolithiasis, cholangitis)
  3. Enteric contents to peritoneum/ circulatory system (perforated viscus/ ischaemia)
  4. Other source of amylase parotid gland (viral infection, stone parotid duct)
506
Q

What are raised transaminases a sign of?

A

Destruction of hepatocytes

507
Q

What is raised all phos a sign of?

A

Damage to bile ducts

508
Q

What is the initial management of pancreatitis?

A

IV fluids, catheter & nil by mouth

509
Q

List 3 haemostatic therapies?

A
  1. Endoscopic: Variceal band ligation
  2. Balloon Tamponade (temporary)
  3. Transjugular intrahepatic stent (TIPS)
510
Q

Describe the surveillance tests for Hepatocellular carcinoma (HCC) in cirrhosis?

A

6-monthly ultrasound +/- the level of alpha-fetoprotein

511
Q

List the 3 management techniques for small curable Hepatocellular carcinoma (HCC)?

A
  1. Liver transplant if suitable
  2. Resect tumour
  3. Radio-frequency ablation (RFA)
512
Q

List the 3 management techniques for larger incurable Hepatocellular carcinomas (HCC)?

A
  1. Trans-arterial Chemoembolisation (TACE)
  2. Oncology drug therapy (Sorafenib)
  3. Palliative care
513
Q

Describe the epithelial surface of a normal oesophagus?

A

Non-keratinising stratified squamous epithelium

514
Q

What is the 3 part cancer pathway of Barrett’s oesophagus?

A

Metaplasia –> Dysplasia –> Adenocarcinoma

515
Q

What is the prevalence & epidemiology of oesophageal cancer?

A
  • 1700 new patients/year
  • Median age 72yrs
  • Male > females
516
Q

When is oesophageal cancer often diagnosed?

A

Advanced stage

517
Q

What is the 5 year survival of oesophageal cancer for males & females?

A

Male: 10%
Female: 16%

518
Q

What are 5 investigations to stage oesophageal cancer?

A
  1. CT scan
  2. PET-CT scan
  3. Endoscopic Ultrasound (EUS)
  4. Laparoscopy
  5. MRI, bone scan
519
Q

What are the 3 curative options for oesophageal cancer?

A
  1. Surgery: no locally advanced disease, metastases, significant comorbidities
  2. Oncology: local disease & no metastases
  3. Endoscopic therapy: if very early disease
520
Q

What are the 3 Palliative options for oesophageal cancer?

A
  1. Oncology
  2. Endoscopic therapy
  3. Supportive care

MBChB Year 3 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions