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Medicine > Gastrointestinal system > Flashcards

Gastrointestinal system Flashcards

1
Q

What is the stepwise progression of alcoholic liver disease?

A
  • Alcohol related fatty liver (build up of fat in liver - reversible in 2 weeks)
  • Alcoholic hepatitis (inflammation of liver - mild is reversible)
  • Cirrhosis (scar tissue formation - irreversible)
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2
Q

What is the recommended daily alcohol consumption?

A

14 units per week / 3 days (pregnant avoid completely)

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3
Q

What are the CAGE questions to assess harmful alcohol use?

A

CUT DOWN ? Ever thought you should

ANNOYED? Annoyed at others comments?

GUILTY?

EYE OPENER?

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4
Q

What is the AUDIT questionnaire?

A

Developed by the WHO to screen for people with harmful alcohol use - 10 questions (8 indicates harmful)

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5
Q

What are some complications of alcohol dependency?

A

Alcoholic liver disease

Cirrosis (and hepatocellular carcinoma)

Alcohol dependence and withdrawal

Wernicke-Korsakoff Syndrome

Pancreatitis

Alcoholic cardiomyopathy

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6
Q

What are some signs of liver disease?

A

Jaundice

Hepatomegaly

Spider Naevi

Palmar Erythema

Bruising due to abnormal clotting

Ascites

Capus medusae (engorged superficial epigastric veins)

Asterixis - “flapping tremor” in decompensated liver disease

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7
Q

What blood tests can be used to assess alcoholic liver disease?

A

FBC - raised MCV

LFTs - elevated ALT and AST and gamma-GT low albumin due to reduced synthetic function of liver (ALP raised later in disease)

Low albumin (reduced synthetic function)

Clotting - elevated PT

U&Es may be deranged in hepatorenal syndrome

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8
Q

What imaging can be used for alcoholic liver disease?

A

Ultrasound - showing fatty changes

Fibroscan - assessing degree of cirrhosis

Endoscopy - for oesophageal varices

CT/MRI - carcinoma, hepatosplenomegaly, ascites

Liver biopsy

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9
Q

What is the general management of alcoholic liver disease?

A

Stop drinking (detox regime)

Nutritional support with vitamins (particularily thiamine)

Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy)

Referral for liver transplant (must abstain from alcohol for 3 months)

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10
Q

What are some symptoms of alcohol withdrawal?

A

6-12 hrs: Tremor, sweating, headache, anxiety

12-24 hrs: Hallucinations

24-48 hrs: Seizures

24-72 hrs: Delerium Tremens

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11
Q

What is delerium tremens, what happens?

A

Due to alcohol withdrawal (mortality 35% if untreated)

Alcohol stimulates GABA receptors in brain - relaxing it along with inhibiting glutamate

When alcohol is removed, to compensate long term alcohol use GABA underfunctions and glutamate overfunctions - causing extreme excitability in the brain

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12
Q

How does delerium tremens present?

A
  • Acute confusion
  • Severe agitation
  • Delusions and hallucinations
  • Tremor
  • Tachycardia
  • HTN
  • Hypertension
  • Hyperthermia
  • Ataxia (difficulty with coordination)
  • Arrhythmias
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13
Q

What should be given to manage alcohol withdrawal?

A

Chlordiazepoxide (benzo)

IV pabrinex (vit Bs) followed by low dose oral thiamine

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14
Q

What vitamin deficiency do alcoholics typically have ?

A

B1 (thiamine)

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15
Q

What can happen as a result of thiamine deficiency?

A

Wernicke-Korsakoff syndrome (Wernicke’s first)

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16
Q

How does Wernicke’s encephalopathy present?

A
  • Confusion
  • Oculomotor disturbances
  • Ataxia (no coordinated movements)
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17
Q

What are some features of Korsakoff’s syndrome?

A
  • Memory impairment
  • Behavioural changes
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18
Q

Is Korsakoff’s syndrome reversible?

A

No (require full time institutional care after)

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19
Q

What are the 4 most common causes of cirrhosis?

A

Alcoholic liver disease

Non-alcoholic liver disease

Hep B

Hep C

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20
Q

What are some rarer causes of cirrhosis?

A
  • Autoimmune hepatits
  • Primary biliary cirrhosis
  • Haemochromatosis
  • Wilsons disease
  • Alpha-1 antitrypsin deficiency
  • CF
  • Drugs (e.g. amiodarone, methotrexate, sodium valporate)
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21
Q

What are some signs of cirrhosis?

A
  • Jaundice
  • Hepatomegaly (liver then shrinks)
  • Splenomegaly (due to portal hypertensio)
  • Spider Naevi
  • Palmar erythema
  • Gynecomastia and testicular atrophy due to endocrine dysfunction
  • Bruising (abnormal clotting)
  • Ascites
  • Caput medusae
  • Asterixis - ‘flapping tremor’
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22
Q

What are the blood results for cirrhosis?

A
  • LFTs often normal (unless decompensated cirrhosis then ALT, AST, ALP and bilirubin becomes deranged - all the markers)
  • Albumin drops and PT time increases for synthetic function
  • Hyponatraemia indicates fluid retention
  • Urea and creatinin become deranged in hepatorenal syndrome
  • AFP for hepatocellular carcinoma
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23
Q

What is the first line investigation for patients with potential non-alcoholic fatty liver disease?

A

Enhanced liver fibrosis (can’t be used for cirrhosis of other causes)

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24
Q

What is the imaging for cirrhosis? What are you looking for?

A

Ultrasound (nodularity of the surface, corkscrew arteries, enlarged portal vein, ascites, splenomegaly)

Fibroscan (look at elasticity of liver)

Endoscopy (look for and treat oesophageal varices)

CT and MRI (hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessels)

Liver biopsy (to confirm diagnosis of cirrhosis)

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25
Q

What is used as a screening tool for hepatocellular carcinoma in patients with cirrhosis?

A

Ultrasound every 6 months

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26
Q

Who is at risk of cirrhosis and thus needs a fibroscan every 2 years?

A
  • Hep B/C
  • Heavy drinkers
  • Diagnosed ALD
  • Non-alcoholic fatty liver disease
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27
Q

What scoring system is used for cirrhosis?

A

Child-Pugh score

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28
Q

What does the MELD score tell you? When is it used?

A

Estimated 3 month mortality, helping guide referral for liver transplant

Used every 6 month in patients with compensated cirrhosis

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29
Q

What is the general management for cirrhosis?

A

Ultrasound and AFP every 6 months for HC carcinoma

Endoscopy every 3 years for varices

High protein, low sodium diet

MELD score every 6 months

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30
Q

What are some complications of cirrhosis?

A
  • Malnutrition
  • Portal hypertension, varices
  • Ascites
  • Hepato-renal syndrome
  • Hepatic Encephalopathy
  • Hepatocellular carcinoma
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31
Q

How can malnutrition caused by alcoholism be treated?

A

Regular meals (every 2-3 hours)

Low sodium (minimise fluid retention)

High protein and high calorie diet

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32
Q

What combines to form the portal vein?

A

Superior mesenteric vein and splenic vein

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33
Q

Where does the portal system anastamose with the systemic venous system (where varices occur)?

A

Gastro-oesophageal junction

Ileocaecal junction

Rectum

Anterior abdo wall (caput medusae)

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34
Q

What does exsanguinate mean? When can it happen?

A

Bleed out

Bleeding oesophageal varices

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35
Q

How are stable varices treated?

A

Propanolol

Elastic band ligation of varices

Injection of sclerosant

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36
Q

What is TIPS used for? How does it work?

A

Transjugular intra-hepatic portosystemic shunt (wire into jugular vein, vena cava and into liver via hepatic vein)

If other treatment of stable varices fails

Connection made between hepatic vein and portal vein

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37
Q

What does TIPS stand for?

A

Transjugular intra-hepatic porto-systemic shunt

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38
Q

What is used for treatment of bleeding oesophageal varices?

A

- Terlipressin (vasopressin anologue) cause vasoconstriction

  • Vit K and FFP
  • Broad spectrum Abx
  • Intubation and intensive care
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39
Q

What intervention can be used for bleeding varices?

A

Injecting sclerosant into varices (during endoscopy)

Elastic band ligation

Sengstaken-Blakemore Tube is an inflatable tube inserted into oesophagus to tamponade bleeding (after endoscopy fails)

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40
Q

What causes ascites?

A

Increased pressure in porto-systemic system

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41
Q

Why is ascites aggrevated?

A

Kidneys sense a lower circulating volume and so secrete renin

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42
Q

What type of ascites is caused by cirrhosis? How is ascites managed?

A

Transudate (low protein)

  • Low sodium diet
  • Anti-aldosterone diuretic (spironolactone)
  • Paracentesis (ascites tap/drain)
  • TIPS in refractory ascites
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43
Q

When can spontaneous bacterial peritonitis occur?

A

Spontaneous infection in ascitic fluid (10% of patients with ascites)

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44
Q

How does spontaneous bacterial peritonitis present?

A
  • Fever
  • Abdo pain
  • Deranged bloods (raised WBC, CRP, creatinine)
  • Ileus
  • Hypotension

Can be asymptomatic

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45
Q

What are the most common organisms for SBP?

A

E. Coli

Klebsiella

Gram positive cocci (staph/enterococcus)

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46
Q

How is SBP managed?

A

Ascitic culture

  • IV cefotaxime (cephalosporin)
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47
Q

What causes hepatorenal syndrome? Is it fatal?

A

In liver cirrhosis blood pools in the portal venous system (due to dilatation), causing hypotension in the kidney and activation of RAAS and vasoconstiction in kidney and then failure

Fatal within a week without liver transplant

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48
Q

What toxin builds up in liver cirrhosis causing hepatic encephalopathy?

A

Ammonia

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49
Q

Why does ammonia build up in cirrhosis?

A

Functional impairment of the liver cells prevent metabolism of ammonia

Also shunting of blood to the systemic circulation means that blood isnt filtered

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50
Q

What can precipitate hepatic encephalopathy?

A

Constipation

Electrolyte disturbance

Infection

GI bleed

High protein diet

Medications (particularly sedative)

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51
Q

How is hepatic encephalopathy managed?

A

Laxatives e.g. lactulose promotes excretion of ammonia

Antibiotics (i.e. rifaximin - poorly absorbed, stays in GI tract) reducing number of intestinal bacteria producing ammonia

Nutritional support

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52
Q

What are the stages of non-alcoholic fatty liver disease?

A
  • Non-alcoholic fatty liver disease
  • Non-alcoholic steatohepatits

- Fibrosis

- Cirrhosis

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53
Q

What are the risk factors for NAFLD?

A
  • Obesity
  • Poor diet / low activity levels
  • Type 2 diabetes
  • High cholesterol
  • Middle age onwards
  • Smoking
  • High blood pressure
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54
Q

When a patient presents with abnormal LFTs without a clear underlying cause what can be used?

A

Non-invasive liver screen

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55
Q

What forms the non-invasive liver screen?

A

Ultrasound Liver

Hepatitis B and C serology

Autoantibodies (autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis)

Immunoglobulins (autoimmune hepatitis and primary biliary cirrhosis)

Caeruloplasmin (Wilsons disease)

Alpha 1 Anti-trypsin levels (alpha 1 anti-trypsin deficiency)

Ferritin and Transferrin Saturation (hereditary haemochromatosis)

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56
Q

What are some liver autoantibodies?

A

Antinuclear antibody (ANA)

Smooth muscle antibody (SMA)

Antimitochondrial antibody (AMA)

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57
Q

What can be used to diagnose fatty liver?

A

Liver ultrasound (doesnt indicate severity/if fibrosis)

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58
Q

What can be used to assess fibrosis?

A

Enhanced liver fibrosis blood test

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59
Q

What is the second line assessment for liver fibrosis?

A

NAFLD fibrosis score (algorithm of age, liver enzymes, platelets, albumin)

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60
Q

What is the third line investigation for fibrosis?

A

Fibroscan (type of ultrasound)

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61
Q

What is the management of NAFLD?

A
  • Weight loss
  • Exercise
  • Stop smoking
  • Control diabetes, blood pressure, cholesterol
  • Avoid alcohol

Refer patients with liver fibrosis to a liver specialist where they may treat with vitamin E or pioglitazone

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62
Q

What is hepatitis?

A

Inflammation of the liver

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63
Q

What are some causes of hepatitis?

A
  • Alcoholic hepatitis
  • NAFLD
  • Viral hepatitis
  • Autoimmune hepatitis
  • Drug induced hepatitis (e.g. paracetamol overdose)
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64
Q

How does hepatitis present?

A

- Abdo pain

- Fatigue

- Pruritis (itching)

  • Muscle and joint aches
  • Nausea and vomiting

- Jaundice

- Fever (viral hepatitis)

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65
Q

How are the LFTs in hepatitis?

A

High AST/ALT proportionally less of a rise of ALP = “hepatic picture”

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66
Q

Is hep A common in the UK?

A

No ~1000 cases in 2017 (most common viral hepatitis worldwide)

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67
Q

How is Hep A transmitted?

A

Faecal-oral route

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68
Q

How does Hep A present?

A

Nausea

Vomiting

Anorexia

Jaundice

Cholestasis (dark urine / pale stools)

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69
Q

Does Hep A resolve?

A

Yes, without treatment in 1-3 months

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70
Q

How is hep A managed?

A

Basic analgesia

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71
Q

Is there a vaccination for Hep A?

A

Yes

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72
Q

Is Hep A a notifiable disease?

A

Yes

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73
Q

What kind of virus is Hep A?

A

RNA virus

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74
Q

What kind of virus is Hep B?

A

DNA virus

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75
Q

How is hep B transmitted?

A

Blood / bodily fluids

Sex, IVDU, mother to child

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76
Q

What percentage of people go on to get chronic hepatitis after Hep B infection?

A

10%

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77
Q

What do the following markers mean:

Surface antigen (HBsAg)

E antigen (HBeAg)

Core antibodies (HBcAb)

Surface antibody (HBsAb)

Hepatitis B virus DNA (HBV DNA)

A

Surface antigen (HBsAg) – active infection

E antigen (HBeAg) – marker of viral replication and implies high infectivity

Core antibodies (HBcAb) – implies past or current infection

Surface antibody (HBsAb) – implies vaccination or past or current infection

Hepatitis B virus DNA (HBV DNA) – this is a direct count of the viral load

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78
Q

For HBcAb how is past or current infection distinguished?

A

IgM and IgG is measured

IgM implies active infection

IgG indicates a past infection when HBsAg is negative

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79
Q

Is vaccination available for hep B?

A

Yes - injecting the hep B surface antigen

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80
Q

How is Hep B managed?

A
  • Screen for other BBV and STIs (hep A, B and HIV)
  • Refer to gastro, hepatology / infectious diseases
  • Notify Public Health
  • Educate about transmission
  • Test for complications: fibroscan for cirrhosis and ultrasound for hepatocellular carcinoma
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81
Q

What kind of virus is Hep C?

A

RNA

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82
Q

Is there a cure for Hep C?

A

Yes (no vaccine)

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83
Q

What percentage of patients with Hep C become chronic?

What are the complications?

A

3 in 4

Liver cirrhosis and hepatocellular carcinoma

84
Q

What is the screening test for Hep C?

What can confirm diagnosis?

A

Hep C antibody is the screening test

Hep C RNA testing

85
Q

What is the management of Hep C?

A
  • Screen for other BBV and STIs
  • Refer to gastro
  • Notify Public health
  • Stop smoking and alcohol
  • Educate about reducing transmission
  • Fibroscan and ultrasound
  • Antiviral treatment with direct acting antivirals
86
Q

What is hepatitis D?

A

RNA virus - can only survive in patients who have Hep B

Increases complications and disease severity of hep B

No specific treatment

87
Q

What type of virus is hepatits A-E

A

A = RNA

B = DNA

C = RNA

D = RNA

E = RNA

88
Q

How is hepatitis E spread?

A

Faecal-oral

89
Q

How does Hep E present?

A

Mild illness, clears in a month.

No vaccination.

Notifiable disease

Rarely progresses to chronic hepatitis and liver failure (more in immunocompromised)

90
Q

What causes autoimmune hepatitis? What are the two types?

A

We are not sure (could be genetic predisposition and triggered by environmental factors e.g. viral infection causing T-cell mediated response against liver cells)

Type 1 = adults (women in late 40s / 50s)

Type 2 = Children

91
Q

What will LFTs and immune screening show for auto-immune hepatitis?

A

Raised ALT and AST

Raised IgG

92
Q

What autoantibodies are raised in type 1 hepatitis?

A

Anti-nuclear antibodies (ANA)

Anti-smooth muscle antibodies (anti-actin)

93
Q

How is autoimmune hepatitis diagnosed?

A

Liver biopsy

94
Q

What is the treatment of auto-immune hepatitis?

A

High dose steroids e.g. prednisolone initially then tapered as:

Then immunosuppressants e.g. azathioprine

95
Q

Can autoimmune hepatitis reoccur in transplanted patients?

96
Q

What is haemochromatosis?

A

Iron storage disease leading to excessive iron and deposition of iron in tissues

97
Q

What is the mode of inheritance of haemochromatosis?

A

Autosomal recessive

98
Q

How does haemochromatosis present?

A

> 40 years old due to accumulation of iron (later in females as menstruation helps)

  • Chronic tiredness
  • Joint pain
  • Pigmentation (bronze)
  • Hair loss
  • Erectile dysfunction / amenorrhea
  • Memory and mood disturbance
99
Q

How is haemochromatosis diagnosed?

A

Serum ferritin levels (main diagnostic method)

Transferrin saturation can be used to distinguish if this has gone up because ferritin is an acute phase reactant (e.g. inflammation NAFLD)

Genetic testing confirms diagnosis

100
Q

What are some complications of haemochromatosis?

A
  • Type 1 diabetes (liver affects functioning of the pancreas)
  • Liver cirrhosis
  • Cardiomyopathy
  • Hepatocellular carcinoma
  • Hypothyroidism (iron deposits in the thyroid)
  • Hypogonadism/ impotence/ amenorrhea (deposits in the pituitary gland)
  • Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis
101
Q

What is the management of haemochromatosis?

A

Venesection

Monitoring serum ferritin

Avoid alcohol

Genetic counselling

Monitoring and treating complications

102
Q

What is Wilson’s disease?

A

Accumulation of copper in the body and tissues

Mutation on chromosome 13

103
Q

What is the genetic inheritance of Wilson’s disease?

A

Autosomal recessive

104
Q

How do patients with Wilson’s disease present?

A

Hepatic problems (chronic hepatitis then cirrhosis)

Neurological problems (concentration difficulties and dysarthria - speech difficulty, dystonia - abnormal muscle tone, copper in basal ganglia causes parkinsonism)

Asymmetrical motor symptoms

105
Q

What are the psychiatric problems in Wilson’s disease?

A

Mild depression to full psychosis

106
Q

What can be seen in the eyes of patients with Wilson’s disease?

A

Kayser-Fleischer rings in cornea - brown circles surrounding the iris

107
Q

What are some ‘other features’ of Wilson’s ?

A

Haemolytic anaemia

Renal tubular damage leading to renal tubular acidosis

Osteopenia (loss of bone mineral density)

108
Q

How is Wilson’s disease diagnosed?

A

Serum Caeruloplasmin (low is suggestive of Wilsons)

It is the protein that carries copper in the blood

109
Q

What is the gold standard test for Wilson’s disease?

A

Liver biopsy for copper contents (diagnosis can also be established if 24-hour urine copper assay is sufficiently elevated)

110
Q

How is haemochromatosis managed?

A

Copper Chelation (penicillamine /trientene)

111
Q

What is alpha 1 antitrypsin deficiency?

A

Inherited deficiency of a protease inhibitor (leading to an excess of protease enzymes)

112
Q

What enzyme is inhibited by alpha 1-antitrypsin?

A

Neutrophil elastase

113
Q

What is the mode of inheritance of A1AT?

A

Autosomal recessive

114
Q

What is the result of A1AT deficiency?

A

Liver cirrhosis

Pulmonary emphysema and bronchiectasis

115
Q

What is the screening for A1AT deficiency?

A

Levels of serum alpha 1 antitrypsin (would be low)

Liver biopsy for cirrhosis and acid-Schiff-positive staining globules

Genetic testing for A1AT gene

High resolultion CT thorax diagnoses bronchiectasis and emphysema

116
Q

What is the treatment of A1AT deficiency?

A
  • Stop smoking
  • Symptomatic management
  • Organ transplant for end stage liver / lung disease
  • Monitor for complications e.g. hepatocellular carcinoma

(NICE recommend against replacement of alpha-1-antitrypsin - debate ongoing)

117
Q

What is primary biliary cirrhosis?

A

Autoimmune condition targetting the

118
Q

What is the result of the inflammation from primary bilary cirrhosis?

A

Cholestasis and back pressure leading to fibrosis, cirrhosis and liver failure

119
Q

What is normally excreted through the bile ducts and into the liver?

A

Bile acids, bilirubin and cholesterol

120
Q

What is a result of the increase in bile acids in blood?

121
Q

What is the result of increased cholesterol in the blood?

A

Xanthelasma (or xanthoma if they are larger, nodular deposits)

122
Q

How do stools appear in Primary Biliary Cirhosis?

A

Greasy (lack of bile) and pale (lack of bilirubin)

123
Q

What are the presentations of primary biliary cirrhosis?

A
  • Fatigue
  • Pruritus
  • GI disturbances
  • Jaundice
  • Pale stool
  • Xanthoma / xanthelasma
  • Signs of cirrhosis and failure (e.g. ascites, splenomegaly, spider naevi)
124
Q

What are some associations of primary biliary cirrhosis?

A

Middle aged women

Other autoimmune conditions

Rheumatoid conditiosn (systemic sclerosis, Sjogrens, RA)

125
Q

How is primary bilary cirrhosis diagnosed?

A

LFTs = ALP first to rise

Autoantibodies = Anti-mitochondrial antibodies, Antinuclear antibodies

ESR raised, IgM raised

Liver biopsy for diagnosing

126
Q

What is used in the management of primary biliary cirrhosis?

A

Ursodeoxycholic acid - reduces intestinal absorption of cholesterol

Colestyamine - bile acid sequestrate

Liver transplant

Immunosuppression e.g. with steroids considered in some patients

127
Q

What are the end results of Primary Biliary Cirrhosis?

A

- Advanced liver cirrhosis

- Portal hypertension

  • Systemic pruritus, fatigue, steatorrhoea, distal renal tubular acidosis, hypothyroidism, osteoporosis, hepatocellular carcinoma
128
Q

What is primary sclerosing cholangitis?

A

Condition where intra/extrahepatic ducts become strictured and fibrotic

129
Q

What is the cause of Primary Sclerosing Cholangitis?

A

Mostly unclear although established link between UC and PSC (70% alongside)

130
Q

What are some risk factors for primary sclerosing cholangitis?

A
  • Male
  • Aged 30-40
  • UC
  • FH
131
Q

How does primary sclerosing cholangitis present?

A
  • Jaundice
  • Chronic right upper quadrant pain
  • Pruritis
  • Fatigue
  • Hepatomegaly
132
Q

What would the LFTs show for primary sclerosing cholangitis?

A

“Cholestatic” picture meaning ALP is the most deranged LFT

133
Q

Are there any specific antibodies for PSC?

A

Not really (maybe pANCA, ANA)

Helpful in indicating an autoimmune element to disease that may respond to immunosuppression

134
Q

What is the gold standard for diagnosis of PSC?

A

MRCP

magnetic resonance cholangiopancreatography (bile duct lesions/strictures)

135
Q

What are some associations and complications of PSC?

A
  • Acute bacterial cholangitis
  • Cholangiocarcinoma
  • Colorectal cancer
  • Cirrhosis and liver failure
  • Biliary strictures
  • Fat soluble vitamin deficiencies
136
Q

What is the management for primary sclerosing cholangitis?

A

- Liver transplant

  • ERCP to dilate and stent any strictures

- Ursodeoxycholic acid

- Colestryamine - bile acid sequestrate (prevents absorption in gut)

  • Monitor for complications (cholangiocarcinoma, cirrhosis, oesophageal varices)
137
Q

How can strictures from PSC be treated?

A

ERCP (endoscopic retrograde cholangio pancreatography) using a camera through throat, oesophagus, stomach and duodenum, through sphincter of Oddi and into ampulla of vater into bile ducts

Stenting the strictures

138
Q

What are the two main types of primary liver cancer?

A

Hepatocellular(80%) and cholangiocarcinoma

139
Q

What is the main risk factor for hepatocellular carcinoma?

A

Liver cirrhosis due to:

  • Viral Hep B/C
  • Alcohol
  • NAFLD
  • Other chronic liver disease
140
Q

What is cholangiocarcinoma typically associated with?

A

Primary Sclerosing Cholangitis

141
Q

How does liver cancer present?

A

(often asymptomatic for long time)

  • Weight loss
  • Abdo pain
  • Anorexia
  • N&V
  • Jaundice
  • Pruritus
142
Q

What are some investigations for liver cancer?

A

AFP for HCC

CA19-9 for cholangiocarcinoma (tumour markers)

Liver ultrasound for tumours

CT and MRI for diagnosis

ERCP - take biopsies / brushings to diagnose cholangiocarcinoma

143
Q

What is the mainstay of treatment for hepatocellular carcinoma?

A
  • Liver resection and / liver transplant
  • Kinase inhibitors (inhibit proliferation of cancer cells) e.g. sorafenib, regorafenib and lenvatinib to extend life by months
  • Generally considered resistant to chemo / RT
144
Q

What is the treatment of cholangiocarcinoma?

A

Very poor prognosis unless diagnosed early (potentially cured with surgical resection)

ERCP for stenting and improving symptoms

Resistant to chemo / RT

145
Q

What is a haemangioma? What is the treatment?

A

Common benign tumour of the liver, found incidentally, no symptoms / potential to become cancerous

No treatment / monitoring required

146
Q

What is focal nodular hyperplasia?

A

Benign liver tumour made of fibrotic tissue found incidentally (usually asymptomatic and no malignant potential)

Often related to oestrogen and so more common in women / COCP

No treatment / monitoring required

147
Q

What is the term for an entire liver transplanted from a desceased patient?

What is a living donor transplant?

A

Orthotopic transplant (if you split into two = split donation)

Living donor transplant = take a portion of organ from a living donor - both regenerate

148
Q

What causes acute liver failure? (requires immediate transplant - chronic liver failure can wait for 5 months)

A

Acute viral hepatitis

Paracetamol overdose

149
Q

What factors suggest unsuitability for a liver transplant?

A
  • Significant co-morbidities e.g. severe kidney / heart disease
  • Excessive weight loss and malnutrition
  • Active hep B, hep C or other infection
  • End stage HIV
  • Active alcohol use (6 months abstinence required)
150
Q

What incision is used in a liver transplant?

A

“rooftop” or “Mercedes Benz”

151
Q

What medications are involved in post-transplant care?

A

Lifelong immunosuppression

Steroids

Azathioprine

Tacrolimus

152
Q

What is the lifestyle advise for transplant patients?

A
  • Avoid alcohol and smoking
  • Treat oppurtunistic infections
  • Monitor for disease reccurence (i.e. of hepatitis / primary biliary cirrhosis)
  • Monitor for cancer higher risk in immunosuppression
153
Q

What may suggest liver transplant rejection?

A

Abnormal LFTs

Fatigue

Fever

Jaundice

154
Q

What is the lining of the oesophagus / stomach?

A

Oesophagus = squamous epithelial lining (more sensitive to stomach acid)

Stomach = columnar epithelial lining

155
Q

How does GORD present?

A

Dyspepsia (indigestion)

  • Heartburn
  • Acid regurg
  • Retrosternal pain
  • Bloating
  • Nocturnal cough
  • Hoarse voice
156
Q

When is an endoscopy used in clinical practise?

A

Assess:

  • Peptic ulcers
  • Oesophageal/gastric malignancy/maleana
157
Q

What are the key red flag symptoms for endoscopy referral?

A
  • Dysphagia (difficulty swallowing)
  • Weight loss
  • Upper abdo pain / reflux
  • Treatment resistant dyspepsia
  • N&V
  • Low Hb
  • Raised platelet count

EVIDENCE OF GI BLEED (meleana / coffee ground vomit) need admission / urgent endoscopy

158
Q

What is the management of GORD?

A

Lifestyle: Reduce tea, coffee, alcohol, weight loss, avoid smoking, smaller meals, avoid heavy meals before bed, stay upright after meals rather than flat

Acid neutralising medication: Gaviscon, rennie

PPI: Omeprazole, lansoprazole

Ranitidine: H2 receptor antagonist (alt to PPI), H2 receptor antagonist (antihistamine)

Surgery - laparoscopic fundoplication

159
Q

What is Helicobacter Pylori?

A

Gram negative aerobic bacteria which lives in stomach and damages it causing gastritis, ulcers and increasing risk of stomach cancer

160
Q

What does a H/ Pylori infection result in?

A
  • Gastritis
  • Ulcers
  • Increasing risk of stomach cancer
161
Q

What does H. Pylori produce?

A

Ammonia - neutralises stomach acid

162
Q

What are the different tests for H. Pylori?

A

Urea breath test

Stool antigen test

Rapid Urease test (CLO- campylobacter like organism - test stomach biopsy from endoscopy taken and added to urea - if H. Pylori is present it will produce urease to convert urea to ammonia - giving the solution an alkali pH)

MUST BE OFF PPI FOR 2 WEEKS BEFORE ANY TESTING

163
Q

What is the triple therapy for H. Pylori? How long is it usually taken for?

A

PPI

Amoxicillin

Clarithromycin

7 days

164
Q

What happens during Barrett’s oesophagus?

A

Metaplasia from squamous to columnar epithelium in lower oesophagus

165
Q

What happens to to GORD symptoms after Barett’s oesophagus?

A

Inprovement in reflux symptoms

166
Q

What is the risk factor with Barrett’s ?

A

Adenocarcinoma

167
Q

What is the treatment of Barrett’s oesophagus?

168
Q

What can the protective layer in the stomach be broken down by?

A

Steroids/ NSAIDs

Helicobacter pylori

169
Q

What can increased stomach acid result from?

A
  • Stress
  • Alcohol
  • Caffeine
  • Smoking
  • Spicy foods
170
Q

How do peptic ulcers present?

A

Epigastric discomfort / pain

N&V

Dyspepsia

Coffee ground vomit

Iron deficiency anaemia (due to constant bleeding)

171
Q

Which ulcers does eating improve/worsen symptoms?

A

Worsens gastric ulcers

Improves duodenal ulcers

172
Q

How are peptic ulcers diagnosed?

A

Endoscopy (CLO test also performed for H. pylori, biopsies for cancer)

173
Q

What is the treatment of Peptic Ulcers?

A

PPIs (endoscopy to monitor ulcer and ensure healing)

174
Q

What are the complications of peptic ulcers?

A

Bleeding

Perforation resulting in peritonitis and acute abdomen

Scarring and strictures of muscle and mucosa

Pyloric stenosis

175
Q

What are some causes of upper GI bleeds?

A
  • Oesophageal varices
  • Mallory-Weiss tear
  • Stomach ulcers
  • Cancers of stomach
176
Q

How do upper GI bleeds present?

A
  • Haematemesis
  • “Coffee ground” vomit (digested blood)
  • Melaena, tar like, black, greasy and offensive stool
  • Haemodynamic instability (causes low blood pressure, tachycardia and other signs of shock)
177
Q

What is used as a scoring system for risk of upper GI bleeds?

A

Glasgow-Blatchford Score (>0 indicates high risk)

178
Q

Why does urea raise in upper GI bleeds?

A

Digested product of blood in GI tract (then absorbed in intestines)

179
Q

What is the Rockall score used for?

A

Risk of rebleeding/mortality in patients who have had an endoscope

180
Q

What is the management of an upper GI bleed?

A

ABATED

A-E

Bloods

Access (2 large bore cannulas)

Transfuse

Endoscopy (within 24 hrs)

Drugs (stop anticoagulants / NSAIDs)

181
Q

What should be checked in upper GI bloods?

A

Haemoglobin (FBC)

Urea (U&Es)

Coagulation (INR, FBC for platelets)

Liver disease (LFTs)

Cross match 2 units of blood

182
Q

What are the additional steps of treatment for oesophageal varices?

A

Terlipressin

Prophylactic broad spectrum abx

183
Q

What is the definitive treatment of upper GI bleeds?

A

OGD - for interventions e.g. banding of varices / cauterisation

(NICE recommend against PPI prior to endoscopy - some senior doctors do this)

184
Q

What are the features of Crohn’s?

A

NESTS

No blood or mucus

Entire GI tract with skip lesions

Skip lesions on endoscopy

Terminal ileum usually affect with transmural inflammation

Smoking is a risk factor

Associated with weight loss, strictures and fistulas

185
Q

What are the features of UC?

A

U-C-CLOSE UP

Continuous inflammation from the colon/rectum

Limited to colon and rectum

Only superficial mucosa affected

Smoking is protective

Excrete blood and musus

Use amiosalicylates

PSC associated

186
Q

How does IBD present?

A

Diarrhoea

Abdo pain

Passing blood

Weight loss

187
Q

How is IBD diagnosed?

A

Bloods: anaemia, infection, thyroid, kidney and liver function

CRP for inflammation and active disease

Faecal calprotectin

Endoscopy with biopsy is diagnostic (OGD and colonoscopy)

Imaging to look for fistulas, abscesses and strictures

188
Q

What medications are used to induce remission / maintain Crohn’s?

A

Induce = Steroids (oral pred / IV hydrocortisone)

May add immunosuppressants:

Azathioprine/mercaptopurine/methotrexate/infliximab/adalimumab

Remission (reasonable to not take anything) OR:

First line: azathioprine, mercaptopurine

Second line: methotrexate, infliximab, adalimumab

189
Q

What is used to induce remission in UC?

A

Aminosalicylates (mesalazine)

Second line e.g. corticosteroids - prednisolone

In severe disease IV corticosteroids e.g. hydrocortisone or IV ciclosporin may be used

190
Q

What is used 2nd line to induce remission in UC?

What is used to maintain?

A

2nd line in acute = cortocosteroids

Maintaining = Aminosalicylates (mesalazine) or azathioprine or mercaptopurine

191
Q

What surgery can patients with UC have?

A

Panproctocolectomy (removing colon and rectum - typically only affects here)

Left with ileostomy or ileo-anal anastomosis (J pouch)

192
Q

What are some symptoms of IBS?

A
  • Diarrhoea
  • Constipation
  • Fluctuating bowel habit
  • Abdo pain
  • Bloating
  • Worse after eating and improved by opening bowels
193
Q

What is the NICE criteria for diagnosis of IBS?

A

Other pathology should be excluded:

  • Normal FBC, ESR and CRP blood tests
  • Faecal calprotectin negative
  • Negative coeliac disease serology (anti-TTG antibodies)
  • Cancer not suspected / excluded

Symptoms should suggest:

  • Abdo pain / discomfort: relieved by opening bowels / associated with change in bowel habit AND
  • 2 of: abnormal stool passage, bloating, worse symptoms after eating, PR mucus
194
Q

What are some general treatments for IBS?

A
  • Ensure adequate fluid intake
  • Regular small meals
  • Reduce processed food
  • Limit caffeine and alcohol
195
Q

What is the first line medication for diarrhoea in IBS?

Second line

Third line?

A

First line

Loperamide

Laxatives for constipation (avoid lactulose as it can cause bloating, linaclotide is a specialist laxative for patients with IBS not responding to first-line laxatives)

Antispasmodics for cramps e.g. hyoscine butylbromide (buscopan)

Second line

TCA e.g. amitriptyline 5-10mg at night

Third line

SSRI antidepressant

CBT is another option of help patients manage condition

196
Q

What happens in coeliacs?

A

Auto-antibodies in response to exposure to gluten targetting epithelial cells of intestine and lead to inflammation

197
Q

What are the antibodies in Coeliacs?

A

Anti tissue transflutaminase (Anti-TTG)

Anti-endomysial (anti-EMA)

Rise with disease activity

198
Q

Where is inflammation in Coeliacs typically?

A

Small intestine - Jejunum

199
Q

What happens to the bowel wall in Coeliacs?

A

Atrophy of intestinal villi

200
Q

What is the presentation of Coeliacs?

A
  • Failure to thrive in young children
  • Diarrhoea
  • Fatigue
  • Weight loss
  • Mouth ulcers
  • Anaemia second to iron, B12 or folate deficiency
  • Dermatitis herpetiformis (itchy blistering rash typically on abdomen)
  • Neuro symptoms: peripheral neuropathy, cerebellar ataxia, epilepsy
201
Q

How is Coeliacs diagnosed?

A

Diagnosed when patient is on a diet containing gluten

  • Exlude IgA deficiency before testing for:

Anti-TTG antibodies

Anti-endomyseal antibodies

202
Q

What will intestinal biopsy show for coeliacs?

A

Crypt hypertrophy

Villous atrophy

203
Q

What are some associations of Coeliacs?

A
  • Type 1 diabetes
  • Thyroid disease
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis
204
Q

What are some complications of untreated Coeliacs diease?

A
  • Vitamin deficiency
  • Anaemia
  • Osteoporosis
  • Ulcerative jejunitis
  • Enteropathy-associated T-cell lymphoma (EATL) of intestine
  • Non-hodgkin lymphoma (NHL)
  • Small bowel adenocarcinoma (rare)
205
Q

What is the treatment of Coeliacs?

A

Gluten free diet (lifelong)

Medicine (12 decks)

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