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Phase 2a Medicine - Hannah's version > GI and Liver > Flashcards

GI and Liver Flashcards

1
Q

How long does hepatitis persist for to be deemed chronic?

A

6 months.

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2
Q

Give 3 infective causes of acute hepatitis.

A
  1. Hepatitis A to E infection - VIRAL
  2. Herpes viruses (e.g. EBV, CMV, VZV) - VIRAL
  3. Coxiella (Q fever) - NON-VIRAL
  4. Toxoplasmosis - NON-VIRAL
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3
Q

Give 4/5 non-infective causes of acute and chronic hepatitis.

A
  1. Alcohol.
  2. Drugs.
  3. Toxins.
  4. Autoimmune.
  5. Hereditary metabolic.
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4
Q

Give 3 infective causes of chronic hepatitis.

A
  1. Hepatitis B (+/-D).
  2. Hepatits C.
  3. Hepatitis E.
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5
Q

What is the presentation of symptomatic acute hepatitis?

A
  1. General malaise
  2. Myalgia
  3. GI upset
  4. Abdominal pain (upper right quadrant)
  5. ± cholestatic jaundice
  6. Tender hepatomegaly
  7. Raised AST, ALP ± bilirubin
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6
Q

What are the signs of chronic liver disease?

A
  1. Clubbing
  2. Palmar erythema
  3. Dupuytren’s contracture
  4. Spider naevi
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7
Q

What are the potential complications of chronic hepatitis?

A

Uncontrolled inflammation -> fibrosis -> cirrhosis -> HCC.

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8
Q

Is HAV an RNA or DNA virus?

A

RNA virus

HAV = ACUTE HEPATITIS only

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9
Q

How is HAV transmitted?

A
  1. Faeco-oral transmission
  2. Contaminated food and water
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10
Q

Who could be at risk of HAV infection?

A
  1. Travellers
  2. Food handlers
  3. Children / young adults
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11
Q

Is HAV acute or chronic?

A

Acute! There is 100% immunity after infection.

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12
Q

Describe the pathophysiology of Hep A virus

A
  • Picornavirus
  • Replicates in liver, excreted in bile, then excreted in faeces for 2 weeks before clinical presentation, and 1 week after
  • Maximally infectious just before onset of jaundice
  • Incubation period = 2-6 weeks
  • Self-limiting - rarely causes fulminant hepatitis
  • 100% immunity after infection
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13
Q

Describe the clinical presentation of HAV

A
  • Viraemic symptoms (non-specific symptoms, e.g. nausea, fever)
  • Jaundice (after 1-2 weeks, goes away within 3-6 weeks)
  • Dark urine and pale stools - intrahepatic cholestasis
  • Hepatosplenamegaly
  • IgM production
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14
Q

How might you diagnose someone with HAV infection?

A

LFT;

  • Prodromal stage (between initial symptoms and jaundice)
  • Bilirubinuria and raised urinary urobilinogen
  • Raised serum AST / ALT
  • Icteric stage (once jaundice is apparant)
  • Serum bilirubin reflects level of jaundice

Viral serology: initially anti-HAV IgM and then anti-HAV IgG.

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15
Q

Describe the management of HAV infection.

A
  1. Supportive.
  2. Monitor liver function to ensure no fulminant hepatic failure.
  3. Manage close contacts - give HNIG for Hep A to contacts
  4. NO ALCOHOL
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16
Q

Describe the primary prevention of HAV.

A
  1. Good hygiene
  2. Chlorinated water
  3. Active immunisation - vaccination
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17
Q

Is HEV a RNA or DNA virus?

A

Small RNA virus.

Only causes ACUTE hepatitis

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18
Q

How is HEV transmitted?

A

Faeco-oral transmission

  • Usually spread by contaminated water, rodents, dogs, and pigs
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19
Q

Is HEV acute or chronic?

A

Usually acute but there is a risk of chronic disease in the immunocompromised.

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20
Q

How might you diagnose someone with HEV infection?

A

Viral serology

  • Initially anti-HEV IgM and then anti-HEV IgG.
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21
Q

Describe the primary prevention of HEV.

A
  1. Good food hygiene.
  2. Vaccination.
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22
Q

Is HBV a RNA or DNA virus?

A

DNA virus! It replicates in hepatocytes.

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23
Q

How is HBV transmitted?

A
  • Blood-borne transmission - IVDU, needle-stick, sexual
  • Vertical transmission - MTCT
  • Horizontal transmission - minor abrasions, survives on household items

HBV is highly infectious!

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24
Q

Describe the pathophysiology of HBV infection

A
  • Virus = inner core / nucleocapsid + outer envelope of surface protein (HBsAg - Hepatitis B surface antigen)
  • HBsAg is produced in excess by infected hepatocytes
  • HBsAg can exist independently in the serum and body fluid
  • Following acute HBV infection, 1-5% will not clear the virus and will develop chronic Hep B
  • Chronic Hep B can lead to cirrhosis or hepatocellular carcinoma (VERY BAD)
  • Cirrhosis can lead to either HCC or decompensated cirrhosis
  • Chronic Hep B results in ongoing hepatocellular damage
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25
Q

What HBV protein triggers the initial immune response?

A

The core proteins.

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26
Q

Describe the clinical presentation of a Hepatitis B infection

A
  • Similar to Hep A
  • Likely to be subclinical
  • Incubation period = 1-6 months
  • Viraemia
  • Rashes (e.g urticaria)
  • Polyarthritis
  • Jaundice (after 1-2 weeks, rare in children)
  • Intrahepatic cholestasis
  • Hepatosplenomegaly
  • Serology: HBsAg present
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27
Q

How might you diagnose someone with HBV?

A

Viral serology:

  • HBsAg present 1-6 months after exposure
  • HBsAg present 6m+ after exposure suggests Hepatitis carrier status
  • Anti-HBV core IgM after 3 months
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28
Q

Describe the management of an acute HBV infection.

A
  1. Supportive.
  2. Monitor liver function.
  3. Manage contacts - give HBIG
  4. Follow up at 6 months to see if HBV surface Ag has cleared. If present -> chronic hepatitis.
  5. Avoid alcohol.
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29
Q

Describe the management for chronic Hepatitis B infection

A
  1. Give SC pegylated interferon-alpha 2A.
    - Immunomodulatory (stimulated an immune response
    - Weekly SC injections
    - Best long term treatment, but not always effective
    - SFX; general malaise, lethargy, autoimmune disease, leukopenia, thrombocytopenia, anxiety, mental issues
  2. Nucleos(t)ide analogues
    - Inhibit viral replication
    - One tablet a day
    - High barrier to resistance
    - Minimal side effects
    - May be required life-long since no immune response stimulated
    - e.g. oral tenofovir, oral entecavir
    - Tenofovir requires renal monitoring
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30
Q

Is HDV a RNA or DNA virus?

A

It is a defective / incomplete RNA virus.

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31
Q

What does HDV rely on for successful host invasion?

A

HBV infection!

HDV can’t exist without HBV as it needs HBsAg to protect it.

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32
Q

How is HDV transmitted?

A

Blood-borne transmission, particularly IVDU.

  • All the same ways as HBV
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33
Q

What is HDV co-infection?

A
  • Infection of HBV and HDV simultaneously
  • Clinically indistinguishable from acute icteric HBV infection
  • Distinguish by serum presence of IgM anti-HDV and IgM anti-HBV
  • Co-infection increases severity of infection
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34
Q

What is HDV superinfection?

A
  • When a person with chronic HBV gets HDV
  • Chronic HBV is usually dormant (i.e. HBV DNA is low)
  • Results in secondary acute infection
  • Increases rate of liver fibrosis progression
  • Rise in serum AST or ALT
  • Can result in hepatocellular carcinoma
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35
Q

Is HCV a RNA or DNA virus?

A

HCV is a RNA virus.

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36
Q

Describe the epidemiology of HCV infection

A
  • Very high incidence in Egypt due to failed public health initiative resulting in spread
  • Blood borne transmission
  • Common in haemophiliacs treated before blood products were screened
  • Limited sexual transmission
  • Vertical transmission is rare
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37
Q

What is the issue with a hepatitis C vaccination?

A

HCV mutates rapidly, so envelope proteins change all the time so a vaccine is difficult to develop

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38
Q

Describe the clinical presentation of HCV infection

A
  • Most acute infections are asymptomatic
  • 10% have mild flu-like illness with jaundice and rise in serum ALT / AST
  • Most patients present years later with abnormal ALT / AST values or chronic liver disease
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39
Q

How might you diagnose someone with HCV infection?

A

HCV antibody

  • Present within 4-6 weeks
  • False negative in immunosuppresssed patients (no antibodies produced) and in acute infection (i.e. before 4 weeks)

HCV RNA

  • Indicates current / acute infection
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40
Q

You want to find out if someone has previously been infected with HCV. How could you do this?

A

Viral serology - anti-HCV IgM/IgG indicates that someone has either a current infection or a previous infection.

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41
Q

Describe the treatment for HCV.

A

SC pegylated interferon-alpha 2A + Oral ribavirin

  • Ribavarin causes haemolytic anaemia and anxiety
  • Interferons cause lots of mental side effects so DAAs are better

Triple therapy with direct acting antivirals (DAAs)

  • NS5A (initiates viral replication) inhibitor ending in ‘asvir’ (e.g. ledipasvir)
  • NS5B (needed for viral replication) inhibitors ending in ‘buvir’ (.e.g sofosbuvir)
  • Oral ribavirin
  • EXTREMELY EXPENSIVE THERAPY

Lots of new drugs have been developed recently for HCV infection. Direct acting antivirals (DAA) are currently in use e.g. NS5A and NS5B.

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42
Q

What percentage of people with acute HCV infection will progress onto chronic infection?

A

Approximately 70%.

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43
Q

What percentage of people with acute HBV infection will progress onto chronic infection?

A

Approximately 5%.

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44
Q

How can HCV infection be prevented.

A
  1. Screen blood products.
  2. Lifestyle modification.
  3. Needle exchange.

There is currently no vaccination and previous infection does not confer immunity.

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45
Q

What types of viral hepatitis are capable of causing chronic infection?

A
  • B (+/-D)
  • C
  • E in the immunosuppressed.
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46
Q

What are the rhymes for summarising hepatitis?

A

A is Acquired by mouth from Anus, is Always cleared Acutely, and only Appears once

E is Even in England and can be Eaten (pigs), if not always beaten

B is Blood-Borne and if not Beaten can be Bad

B and D is a BastarD

C is usually Chronic but Can be Cured at a Cost

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47
Q

What is acute pancreatitis?

A

Process that occurs on the background of a previously normal pancreas, and can return to normal after resolution of the episode

It is caused by the destructive effect of premature activation of pancreatic enzymes, which causes self-perpetuating pancreatic inflammation by enzyme-mediated auto-digestion

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48
Q

What is the mortality rate of acute pancreatitis?

A

In the most severe form of acute pancreatitis, mortality rate is 40-80%

Due to either necrosis or haemorrhage

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49
Q

List 11 causes of acute pancreatitis

A

I GET SMASHED

I - idiopathic

G - gallstones

E - ethanol

T - trauma

S - steroids

M - mumps

A - autoimmune

S - scorpion venom

H - hyperlipidaemia

E - ERCP (endoscopic retrograde cholangiopancreatography)

D - drugs (e.g. NSAIDs, ACE inhibitors)

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50
Q

Describe the pathophysiology of gallstone pancreatitis

A
  1. Accumulation of enzyme-rich fluid within pancreas due to pancreatic duct obstruction
  2. Intracellular Ca2+ increases -> early activation of trypsinogen
  3. Trypsinogen is cleaved to trypsin
  4. Trypsin degradation is impaired, thus leading to overwhelming build-up of trypsin
  5. Increased enzymatic digstion of pancreas
  6. Extensive acinar damage
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51
Q

Describe the pathophysiology of alcohol-induced pancreatitis

A
  1. Contraction of ampulla of Vater -> increased stimulation of enzyme secretion and obstruction of duct
  2. Alcohol then interferes with Ca2+ homeostasis, causing trypsinogen cleavage
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52
Q

What are the consequences of prematurely activated pancreatic enzymes on the body?

A
  1. Enzymes digest vessel walls in pancreas -> leakage of fluid into tissues -> oedema, inflammation, and hypovolaemia (as fluid is trapped in gut, peritoneum, and retroperitoneum)
  2. Digested blood vessels -> haemorrhage
  3. Destruction of adjacent islets of Langerhans -> destroyed beta cells -> less insulin -> hyperglycaemia
  4. Lipolytic enzymes -> fat necrosis -> skin discolouration (Grey Turner’s sign) (if associated with anterior abdominal wall
  5. Released fatty acids bind to Ca2+ -> form white precipitates in necrotic fat -> hypocalcaemia (if extensive) presenting with tetany
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53
Q

Describe the clinical presentation of acute pancreatitis

A
  1. Gradual / sudden severe epigastric / umbilical pain which radiates to back (relieved by sitting forward)
  2. Anorexia, nausea, vomiting
  3. Tachycardia
  4. Fever
  5. Jaundice
  6. Dehydration
  7. Hypotension
  8. Abdominal guarding / tenderness
  9. Periumbilical ecchymosis - Cullen’s sign (skin discolouration due to blood under skin)
  10. Left flank bruising - Grey Turner’s sign
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54
Q

How can acute pancreatitis be diagnosed?

A

Blood tests

  • Raised serum amylase - 3-fold the normal upper limit - levels fall 3-5 days after acute event, and may be triggered by other things
  • Raised urinary amylase - DIAGNOSTIC as remains raised for a long time
  • Raised serum lipase - most sensitive / specific for pancreatitis
  • CRP level for monitoring severity & prognosis

Erect CXR - essential for gastroduodenal perforation exclusion (which also raise serum amylase) and identifying gallstones / calcification

Abdominal ultrasound - gallstone pancreatitis diagnosis

Contrast enhanced CT - identify extent of necrosis

MRI - identify degree of damage, and can differentiate fluid and solid inflammatory masses

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55
Q

Name 2 pancreatic scoring systems and briefly describe them

A

Glasgow & Ranson scoring system

  • Use various factors (e.g. age, neutrophils, calcium, etc.) to predict a severe attack (80% sensitive)
  • Can only predict attack 48hrs after presentation

APACHE II score

  • Used to assess severity
  • Based on common physiological and laboratory values, age, and chronic conditions (e.g. obesity)
  • High sensitivity
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56
Q

What 8 points make up the glasgow scoring system?

A

PaO2 < 8kPa.

Age > 55 years.

Neutrophils > 15x10^9.

Calcium < 2mmol/L.

Raised urea > 15mmol/L.

Elevated enzymes.

Albumin < 32g/L.

Sugar - serum glucose > 15mmol/L.

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57
Q

Describe the treatment for acute pancreatitis.

A
  1. ANALGESIA! - IV morphine
  2. Catheterise and ABC approach for shock patients.
  3. Drainage of oedematous fluid collections.
  4. Prophylactic antibiotics (e.g. beta-lactams) - reduce risk of infected pancreatic necrosis
  5. Nil by mouth, nasogastric tube for dietary supplements (support patients nutritionally to decrease pancreatic stimulation)
  6. Bowel rest.
  7. Severity assessment
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58
Q

Give 2 potential complications of acute pancreatitis.

A
  1. Systemic inflammatory response syndrome.
    - Any two of;
  2. Tachycardia >90bpm
  3. Tachypnoea >20 breaths/pm
  4. Pyrexia > 38 degrees
  5. High white cell count
  6. Multiple organ dysfunction.
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59
Q

What is chronic pancreatitis?

A

Debilitating contuining inflammatory process resulting in progressive loss of exocrine pancreatic tissue, which is replaced by fibrosis

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60
Q

What are the main causes of chronic pancreatitis?

A
  1. Long-term alcohol excess (~65%)
  2. CKD
  3. Inherited defects in trypsinogen gene
  4. Cystic fibrosis
  5. Autoimmune pancreatitis - raised IgG4 (seen in many autoimmune disorders) triggers pancreatitis
  6. Trauma
  7. Idiopathic
  8. Recurrent acute pancreatitis
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61
Q

Describe the pathogenesis of chronic pancreatitis.

A
  1. Obstruction / reduction in bicarbonate secretion (alkaline pH stabilises trypsinogen) -> activation of trypsinogen
  2. Trypsin causes pancreatic tissue necrosis -> eventual fibrosis
  3. Increased intrapancreatic enzyme activity causes precipitation of proteins within duct lumen -> forms plug in duct
  4. Plugs are calcified -> further damage
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62
Q

Describe how alcohol can cause chronic pancreatitis.

A

Alcohol -> proteins precipitate in the ductal structure of the pancreas (obstruction) -> pancreatic fibrosis.

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63
Q

What immunoglobulin might be elevated in someone with autoimmune chronic pancreatitis?

A

IgG4.

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64
Q

How do you diagnose chronic pancreatitis?

A

Serum amylase and lipase

  • May be elevated
  • In advanced disease, there may not be sufficient residual acinar cells to produce elevation

Abnormal feacal elastase - in patients with moderate-severe disease

Abdominal ultrasound / contrast enhanced CT - detects pancreatic calcification and dilated pancreatic duct to CONFIRM DIAGNOSIS

MRI with MRCP to identify subtle abnormalities

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65
Q

Describe the clinical presentation of chronic pancreatitis

A
  1. Epigastric pain which radiates to back
    - Episodic or unremitting
    - Relieved by sitting forward
  2. Nausea, vomiting, anorexia
  3. Exocrine dysfunction - malabsorption
    - Weight loss
    - Diarrhoea
    - Steatorrhoea
    - Protein deficiency
  4. Endocrine dysfunction - diabetes mellitus
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66
Q

What is the treatment for chronic pancreatitis?

A
  1. Alcohol cessation
  2. Opiates (e.g. tramadol) for abdominal pain
  3. Duct drainage
  4. Shock wave lithotripsy to fragment gall stones in head of pancreas
  5. Pancreatic enzyme supplements for steatorrhoea
    - PPIs to help supplement pass stomach
  6. Insulin if diabetic
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67
Q

How is autoimmune chronic pancreatitis treated?

A

It is very steroid responsive

Give oral prednisolone for 4-6 weeks

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68
Q

Give 4 functions of the liver.

A
  1. Glucose and fat metabolism.
  2. Detoxification and excretion.
  3. Protein synthesis e.g. albumin, clotting factors.
  4. Defence against infection.
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69
Q

Name 3 things that liver function tests measure.

A
  1. Serum bilirubin.
  2. Serum albumin - marker of synthetic function
  3. Pro-thrombin time - marker of synthetic function
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70
Q

LFTs: What is useful about serum albumin levels?

A
  • Marker of synthetic function
  • Useful for gauging severity of chronic liver disease
  • Falling serum albumin is a bad prognostic sign
  • In acute disease, initial albumin levels may be normal
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71
Q

What information do you get from a liver biochemistry test?

A
  1. Aminotransferases - enzymes within hepatocytes which leak into blood with liver cell damage
    - Aspartate aminotransferase (AST)
  • Present in heart, muscle, kidney, and brain
  • High levels seen in hepatic necrosis, MI, muscle injury, and CCF
  • Alanine aminotransferases (ALT)
  • Specific to liver
  • Only rises in liver disease
  1. Alkaline phosphatase
    - Raised in intrahepatic and extrahepatic cholestatic disease of any cause, due to increased synthesis
    - Raised in hepatic infiltrations (e.g. metastasis) and cirrhosis
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72
Q

What enzymes increase in the serum in hepatocellular liver disease?

A

Transaminases e.g. AST and ALT.

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73
Q

Name a cholestatic enzyme.

A

Alkaline phosphatase.

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74
Q

Give 2 possible outcomes of acute liver disease.

A
  1. Recovery.
  2. Liver failure.
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75
Q

Give 5 causes of acute liver disease.

A
  1. Viral hepatitis.
  2. Drug induced hepatitis.
  3. Alcohol induced hepatitis.
  4. Vascular.
  5. Obstruction.
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76
Q

Give 3 symptoms of acute liver disease.

A
  1. Malaise.
  2. Lethargy.
  3. Nausea and anorexia.
  4. Jaundice may develop later on.
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77
Q

Give 3 possible outcomes of chronic liver disease.

A
  1. Cirrhosis.
  2. Liver failure.
  3. Recovery.
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78
Q

Give 5 causes of chronic liver disease.

A
  1. Alcohol.
  2. NAFLD.
  3. Viral hepatitis (B, C, E).
  4. Autoimmune diseases.
  5. Metabolic e.g. haemochromatosis.
  6. Vascular e.g. Budd-Chiari.
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79
Q

What is Budd-Chiari syndrome?

A

A vascular disease associated with occlusion of hepatic veins that drain the liver.

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80
Q

Give 10 signs of chronic liver disease.

A
  1. Ascites.
  2. Oedema.
  3. Malaise.
  4. Anorexia.
  5. Bruising.
  6. Itching.
  7. Clubbing.
  8. Palmar erythema.
  9. Spider naevi.
  10. Hepatomegaly
  11. Abnormal LFTs
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81
Q

Drug induced liver injury is common. What question should you remember to ask in a patient history?

A

Have you started taking any new medication recently?

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82
Q

Name a drug that can cause drug induced liver injury.

A
  1. Co-amoxiclav.
  2. Flucloxacillin.
  3. Erythromyocin.
  4. TB drugs.
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83
Q

Name 3 drugs that are not known to cause drug induced liver injury.

A
  1. Low dose aspirin.
  2. NSAIDS.
  3. Beta blockers.
  4. HRT.
  5. CCB.
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84
Q

What enzyme is responsible for ‘mopping up’ reactive intermediates of paracetamol and so prevents toxicity and liver failure?

A

Glutathione transferase.

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85
Q

What are the potential consequences of hepatocyte regeneration in someone with liver cirrhosis?

A

Neoplasia and therefore HCC.

Hepatocyte regeneration is liable to errors.

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86
Q

What is haemochromatosis?

A

Inherited disorder of iron metabolism, in which there is increased intestinal iron absorption, leading to deposition in joints, liver, heart, pancreas, pituitary, adrenals, and skin

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87
Q

Give 3 causes of iron overload.

A
  1. Genetic disorders e.g. haemochromatosis.
  2. Multiple blood transfusions.
  3. Haemolysis.
  4. Alcoholic liver disease.
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88
Q

What are the main causes of haemachromatosis?

A
  1. HFE gene mutation - 90% of cases caused by this mutation
  2. High intake of iron and chelating agents (e.g. ascorbic acid)
  3. Alcoholism
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89
Q

Haemochromatosis is a genetic disorder. How is it inherited?

A

Autosomal recessive inheritance.

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90
Q

Describe the pathophysiology of haemochromatosis.

A
  1. HFE gene protein interacts with transferrin receptor 1, which mediates intestinal iron absorption
  2. Hepcidin (protein made in liver) increases when iron deficient, and decreases with iron overload
  3. Mutated HFE genes mean hepcidin is underproduced -> iron overload
  4. Inappropriately high levels of iron are absorbed by mucosal cells in SI -> exceeds binding capacity of transferrin
  5. Excess iron precipitates fibrosis and deposition

Normal person’s iron = 3-4mg

Symptomatic patient’s iron = 20-40mg

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91
Q

What is the clinical presentation for haemochromatosis?

A
  1. Male (women protected by menstruation / dietary intake)
  2. Patient in 50s
  3. Tiredness
  4. Arthralgia
  5. Hypogonadism - secondary to pituitary dysfunction
  6. Slate-grey skin pigmentation
  7. Signs of chronic liver disease (ascites, oedema, bruising)
  8. Hepatomegaly, cirrhosis, dilated cardiomyopathy, osteoporosis, heart failure, arryhthmias
  9. Bronze skin, hepatomegaly, DM - in GROSS iron overload
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92
Q

How might you diagnose someone with haemochromatosis?

A
  1. Raised ferritin - non-specific
  2. Raised iron - 20-40mg
  3. HFE genotyping.
  4. Liver biopsy - assess extent of damage / disease severity
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93
Q

How do you treat haemochromatosis?

A
  1. Venesection
    - Regular removal of blood allows body to use excess iron to make new RBCs
    - Prolongs life and may reverse tissue damage
  2. Chelation therapy, e.g. desferrioxamine
    - For patients who can’t tolerate venesection
    - Chelating agent = substance whose molecules can form several bonds to a signle metal ion, thus preventing absorption
  3. Treat diabetes
  4. Treat hypogonadism
  5. Low-iron diet
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94
Q

Name 3 metabolic disorders that can cause liver disease.

A
  1. Haemochromatosis - iron overload.
  2. Alpha 1 anti-trypsin deficiency.
  3. Wilson’s disease - disorder of copper metabolism.
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95
Q

Describe the pathophysiology of alpha-1-antitrypsin deficiency?

A

Alpha-1-antitrypsin inhibits the proteolytic enzyme (neutrophil elastase), and protects the lungs against tissue damage

Defiency results in emphysema, cirrhosis, and HCC

Protein retention in liver -> cirrhosis

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96
Q

Describe the clinical presentation of alpha-1-antitrypsin deficiency

A

Presents as liver disease in children, and respiratory problems in adults

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97
Q

What is Wilson’s disease?

A

An autosomal recessive disorder of copper metabolism; there is excessive deposition of copper in the liver. This can lead to fulminant hepatic failure and cirrhosis.

Defect within the gene coding for copper-transporting ATPase

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98
Q

What is the clinical presentation of Wilson’s disease?

A
  • Children present with hepatic problems (e.g. hepatitis, cirrhosis, fulminant liver failure)
  • Adults present with CNS problems (e.g. tremor, dysarthria, dysphagia)
  • Reduced memory
  • Liver disease varies from acute hepatitis, to chronic hepatitis, to cirrhosis
  • Kayser-Fleischer ring - copper deposition in cornea resulting in brownish pigment at corneoscleral junction
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99
Q

Describe the pathophysiology of Wilson’s disease

A
  • Dietary copper is absorbed in stomach / upper SI, and loosely bound to albumin for tranpsort to the liver
  • In the liver, it is incorporated into glycoprotein caeruloplasmin
  • The excess copper is excreted in the bile, and then in the faeces
  • Wilson’s disease results in copper deposition in the liver, basal ganglia, and cornea
  • Basal ganglia shows cavitation, kidneys show tubular degeneration, and bones are eroded
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100
Q

How do you diagnose Wilson’s disease?

A
  • Reduced serum copper and caeruloplasmin (sometimes)
  • High 24hr urinary copper excretion
  • Liver biopsy - high hepatic copper, hepatitis, and cirrhosis
  • MRI showing basal ganglia degeneration
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101
Q

How do you treat Wilson’s disease?

A
  1. Avoid high copper foods (e.g. liver, chocolate, etc.)
  2. Lifelong chelating agents, e.g. penicillamine
  3. Liver transplant if severe
  4. Screen siblings as asymptomatic homozygotes need treating
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102
Q

What can cause raised unconjugated bilirubin?

A

PRE-HEPATIC JAUNDICE

  • Haemolysis due to sickle cell disease, spherocytosis, hypersplenism etc.
  • Gilbert’s
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103
Q

Describe the presentation of pre-hepatic jaundice

A

Pre-hepatic jaundice = raised unconjugated bilirubin

Urine = normal

Stools = normal

Itching = No

LFTs = Normal

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104
Q

What can cause raised conjugated bilirubin?

A

Raised conjugated bilirubin = hepatic / post-hepatic jaundice (aka. cholestatic jaundice)

  • Liver disease (hepatic)
  • Bile-duct obstruction (post-hepatic)
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105
Q

Describe the presentation of cholestatic jaundice

Cholestatic jaundice = hepatic or post-hepatic

A

Urine = dark

Stools = pale (maybe)

Itching = maybe

LFTs = abnormal

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106
Q

Give 3 causes of duct obstruction.

A
  1. Gallstones.
  2. Stricture (narrowing) e.g. malignant, inflammatory.
  3. Carcinoma.
  4. Blocked stent.
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107
Q

Give 4 causes of hepatic jaundice.

A
  1. Viral hepatitis / alcholic hepatitis
  2. Congestive cardiac failure
  3. Ischaemia.
  4. Neoplasm.
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108
Q

Give 3 symptoms of jaundice.

A
  1. Biliary pain - RUQ pain that radiates to shoulder
  2. Rigors - indicate an obstructive cause.
  3. Abdomen swelling.
  4. Weight loss.
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109
Q

What is ascites?

A

An accumulation of free fluid in the peritoneal cavity that leads to abdominal distension.

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110
Q

Give 4 pathophysiological causes of ascites and an example for each.

A
  1. Local inflammation e.g. peritonitis.
  2. Leaky vessels e.g. imbalance between hydrostatic and oncotic pressures.
  3. Low flow e.g. cirrhosis, thrombosis, cardiac failure.
  4. Low protein e.g. hypoalbuminaemia.
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111
Q

Describe the pathogenesis of ascites.

A

Inflammation

  • Local inflammation -> fluid accumulation

Low protein

  • Inability to pull fluid back into intravascular space

Low flow

  • Fluid cannot move forwards through a system (e.g. due to a clot) -> raises pressure in vessel -> fluid leaks out
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112
Q

Describe the clinical presentation for ascites

A
  • HISTORY!
  • Length of swelling, drugs, weight loss, medical history
  • Distended abdomen
  • Fullness in flanks and SHIFTING DULLNESS!
  • Mild abdominal pain
  • Severe pain = query bacterial peritonitis?
  • Respiratory distress
  • Difficulty eating
  • Peripheral oedema
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113
Q

How do you diagnose ascites?

A
  • SHIFTING DULLNESS!
  • Diagnostic aspiration of 10-20ml of fluid using ascitic tap
  • Raised white cell count = bacterial peritonitis
  • Gram stain and culture
  • Cytology to identify malignancy
  • Amylase to exclude pancreatic ascites
  • Protein measurement of ascitic fluid
  • Transudate = low protein (<30g/L) - less bad
  • portal hypertension, constrictive pericarditis, etc
  • Exudate = high protein (>30gL) - EXTREMELY BAD
  • malignancy, peritoneal TB, peritonitis
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114
Q

How do you treat ascites?

A
  1. Treat underlying cause
  2. Reduce sodium to help liver and reduce fluid retention
  3. Increase renal sodium excretion
    - Aldosterone antagonist (e.g. oral spirolactone) since it spares K+
  4. Drain fluid (paracentesis) - drain 5L at a time
  5. Shunts - transjugular intrahepatic portosystemic shunt (TIPS)
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115
Q

What are the 3 phases of alcoholic liver disease.

A
  1. Fatty change - hepatocytes contain triglycerides.
  2. Alcoholic hepatitis.
  3. Alcoholic cirrhosis - destruction of liver architecture and fibrosis.
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116
Q

What might be seen histologically that indicates a diagnosis of alcoholic liver disease?

A

Neutrophils and fat accumulation within hepatocytes.

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117
Q

What is non-alcoholic steato-hepatitis (NASH)?

A

An advanced form of non-alcoholic fatty liver disease.

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118
Q

Give 3 causes of non-alcoholic fatty liver disease.

A
  1. Type 2 diabetes mellitus.
  2. Hypertension.
  3. Obesity.
  4. Hyperlipidaemia.
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119
Q

Describe the physiology of alcohol consumption

A
  1. Ethanol is metabolised in liver, increasing NADH:NAD ratio
  2. Altered redox potential causes increased hepatic fatty acid synthesis with decreased FA oxidation
  3. Results in hepatic accumulation of FAs which are esterified into glycerides
  4. Redox changes also impair carbohydrate & protein metabolism, are cause centrilobular necrosis of the hepatic acinus (typical of alcohol damage)
  5. TNF-alpha released from Kupffer cells causes release of ROS -> tissue damage and necrosis
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120
Q

Describe the pathophysiology of fatty liver

A
  1. Alcohol metabolism produces fat in liver
    - Minimal with small amounts of alcohol
    - Larger amounts -> swollen cells (steatosis)
  2. Fat disappears when alcohol is removed
  3. In some cases, collagen is laid down around central hepatic veins, sometimes progressing to cirrhosis without preceding hepatitis
  4. Alcohol directly affects stellate cells, turning them into collagen-producing myofibroblast cells
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121
Q

Describe the pathophysiology of alcoholic hepatitis

A
  1. In addition to fatty change, there is infiltration by polymorphonuclear leucocytes and hepatocyte necrosis
  2. Dence cytoplasmic inclusions (Mallory bodies) are sometimes seen in hepatocytes
  3. Giant mitochondria are also a feature of alcoholic hepatitis
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122
Q

Describe the pathophysiology of alcoholic cirrhosis

A

As well as fatty change, micronodular cirrhosis is seen

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123
Q

What is the clinical presentation of the various stages of alcoholic liver disease?

A

Fatty liver

    • Often asymptomatic*
    • Sometimes vague abdominal symptoms (e.g. nausea, vomiting)*
    • Hepatomegaly (maybe)*
    • Chronic liver disease symptoms (maybe)*

Alcoholic hepatitis

    • Possibly asymptomatic*
  • Hepatitis only apparent on liver biopsy
  • Mild-moderate symptoms of ill-health (e.g. mild jaundice)
    • Chronic liver disease (maybe)*
  • Biochemistry & histology is deranged and diagnostic

Alcoholic cirrhosis

  • Can be well with few symptoms
  • Chronic licer disease (e.g. ascites, bruising, clubbing, Dupuytren’s contracture)
  • Alcohol dependency
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124
Q

How do you diagnose alcoholic liver disease?

A

Fatty liver

  • Raised MCV (indicates heavy drinking)
  • Raised ALT and AST
  • Ultrasound / CT / histology will reveal fatty infiltration

Alcoholic hepatitis / cirrhosis

  • Leucocytosis
  • Raised serum bilirubin
  • Raised AST / ALT
  • Raised alkaline phosphate
  • Decreased prothrombin time
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125
Q

How do you treat alcoholic liver disease?

A

STOP DRINKING ALCOHOL!!!

- Diazepam for delirium tremens

  • IV thiamine to prevent Wernicke-Korsakoff encephalopathy (occurs from alcohol withdrawal 6-24hrs after last drink)

Fatty liver - stop alcohol

Alcoholic hepatitis

  • Vitamins and protein diet
  • Steroids for short-term benefit
  • Prophylactic anti-fungals

Alcoholic cirrhosis

  • Reduce salt intake
  • Avoid NSAIDs and aspirin
  • Liver transplant
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126
Q

What is cirrhosis?

A

A chronic disease of the liver resulting from necrosis of liver cells followed by fibrosis. The end result is irreversible impairment of hepatocyte function and distortion of liver architecture.

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127
Q

Give 3 causes of cirrhosis.

A
  1. Alcohol!
  2. Hepatitis B (±D) and C.
  3. Any chronic liver disease e.g. autoimmune, metabolic, vascular etc.
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128
Q

What is the treatment of liver cirrhosis?

A
  1. Deal with the underlying cause e.g. stop drinking alcohol.
  2. Screening for HCC.
  3. Consider transplant.
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129
Q

Approximately what percentage of blood flow to the liver is provided by the portal vein?

A

75%.

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130
Q

Portal hypertension can lead to varices. Explain why.

A

Obstruction to portal blood flow e.g. cirrhosis leads to portal hypertension. Blood is diverted into collaterals e.g. the gastro-oesophageal junction and so causes varices.

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131
Q

Give 3 causes of portal hypertension.

A
  1. Cirrhosis and fibrosis (intra-hepatic causes). 2. Portal vein thrombosis (pre-hepatic). 3. Budd-Chiari (post-hepatic cause).
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132
Q

What are the potential consequences of varices?

A

If they rupture -> haemorrhage.

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133
Q

What is the primary treatment for varices?

A

Endoscopic therapy - banding.

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134
Q

What is peritonitis?

A

Inflammation of the peritoneum often due to infection.

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135
Q

What can cause peritonitis?

A
  1. Bacterial infection due to a perforated organ; spontaneous bacterial peritonitis; infection secondary to peritoneal dialysis. 2. Non-infective causes e.g. bile leak; blood from ruptured ecotopic pregnancy.
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136
Q

What is the commonest serious infection in those with cirrhosis?

A

Spontaneous bacterial peritonitis. It can also affect immunocompromised people and those undergoing peritoneal dialysis.

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137
Q

Name a bacteria that can cause spontaneous bacterial peritonitis.

A
  1. E.coli. 2. S.pneumoniae.
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138
Q

How can spontaneous bacterial peritonitis be diagnosed?

A

By looking for the presence of neutrophils in ascitic fluid.

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139
Q

Give 3 symptoms of peritonitis.

A
  1. Pain. 2. Tenderness. 3. Systemic symptoms e.g. nausea, chills, rigor.
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140
Q

Name a cause of pelvic inflammatory disease.

A

A complication of chlamydial infection.

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141
Q

Give 4 reasons why liver patients are vulnerable to infection.

A
  1. They have impaired reticulo-endothelial function. 2. Reduced opsonic activity. 3. Leukocyte function is reduced. 4. Permeable gut wall.
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142
Q

What is primary biliary cirrhosis?

A

An autoimmune disease where there is progressive lymphocyte mediated destruction of intra-hepatic bile ducts -> cholestasis -> cirrhosis.

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143
Q

Describe 2 features of the epidemiology of primary biliary cirrhosis.

A
  1. Females affected more than men. 2. Familial - 10 fold risk increase.
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144
Q

Describe the pathophysiology of primary biliary cirrhosis.

A

Lymphocyte mediated attack on bile duct epithelia -> destruction of bile ducts -> cholestasis -> cirrhosis.

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145
Q

Give 3 diseases associated with primary biliary cirrhosis.

A
  1. Thyroiditis. 2. RA. 3. Coeliac disease. 4. Lung disease. (Other autoimmune diseases).
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146
Q

Give 5 symptoms of primary biliary cirrhosis.

A
  1. Itching. 2. Fatigue. 3. Dry eyes, 4. Joint pains. 5. Variceal bleeding.
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147
Q

What is the treatment for primary biliary cirrhosis?

A

Ursodeoxycholic acid; improves liver enzymes; reduces inflammation and portal pressure and therefore the rate of variceal development.

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148
Q

Give 3 risk factors for gallstone development.

A
  1. Female. 2. Obese (fat). 3. Fertile.
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149
Q

How can gallstones be removed from the gall bladder?

A

Laproscopic cholecystectomy.

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150
Q

Give 4 potential complications of gallstones in the bile duct.

A
  1. Biliary pain. 2. Obstructive jaundice. 3. Cholangitis (infection of the biliary tract). 4. Pancreatitis.
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151
Q

What is ascending cholangitis?

A

Obstruction of biliary tract causing bacterial infection. Regarded as a medical emergency.

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152
Q

Name the triad that describes 3 common symptoms of ascending cholangitis.

A

Charcot’s triad: 1. Fever. 2. RUQ pain. 3. JAUNDICE (cholestatic)!

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153
Q

What is charcot’s triad?

A

It describes 3 common symptoms of ascending cholangitis: 1. Fever. 2. RUQ pain. 3. Jaundice (cholestatic)!

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154
Q

What investigations might you do in someone who you suspect might have ascending cholangitis?

A
  1. Ultrasound. 2. Blood tests - LFT’s. 3. ERCP - definitive investigation.
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155
Q

Describe the management of ascending cholangitis.

A
  • IV fluid. - IV antibiotics e.g. cefotaxime and metronidazole. - ERCP to remove stone. - Stenting.
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156
Q

What is the difference between ascending cholangitis and acute cholecystitis?

A

A patient with acute cholecystitis would not have signs of jaundice!

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157
Q

What is acute cholecystitis?

A

Inflammation of the gall bladder caused by blockage of the bile duct -> obstruction to bile emptying.

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158
Q

Give 3 symptoms of acute cholecystitis.

A
  1. RUQ pain. 2. Fever. 3. Raised inflammatory markers. - NO JAUNDICE!
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159
Q

Give 2 risk factors for acute cholecystitis.

A
  1. Obesity. 2. Diabetes.
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160
Q

Describe the pathophysiology of primary sclerosing cholangitis.

A

Inflammation of the bile duct -> strictures and hardening -> progressive obliterating fibrosis of bile duct branches -> cirrhosis -> liver failure.

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161
Q

Give 3 symptoms of primary sclerorsing cholangitis.

A
  1. Itching. 2. Rigor. 3. Pain. 4. Jaundice. 75% also have IBD.
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162
Q

What is biliary colic?

A

Gallbladder attack - RUQ pain due to a gall stone blocking the bile duct.

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163
Q

What can trigger biliary colic?

A

Eating a heavy meal especially one that is high in fat.

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164
Q

Give 5 causes of diarrhoeal infection.

A
  1. Traveller’s diarrhoea. 2. Viral e.g. rotavirus, norovirus. 3. Bacterial e.g. E.coli. 4. Parasites e.g. helminths. 5. Nosocomial e.g. c.diff.
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165
Q

Give 5 causes of non-diarrhoeal infection.

A
  1. Gastritis/peptic ulcer disease e.g. h.pylori. 2. Acute cholecystitis. 3. Peritonitis. 4. Typhoid/paratyphoid. 5. Amoebic liver disease.
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166
Q

Give 3 ways in which diarrhoea can be prevented.

A
  1. Access to clean water. 2. Good sanitation. 3. Hand hygiene.
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167
Q

What is the diagnostic criteria for traveller’s diarrhoea?

A

>3 unformed stools per day and at least one of: - Abdominal pain. - Cramps. - Nausea. - Vomiting. It occurs within 3 days of arrival in a new country.

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168
Q

Give 3 causes of traveller’s diarrhoea.

A
  1. Enterotoxigenic e.coli (ETEC). 2. Campylobacter. 3. Norovirus.
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169
Q

Describe the pathophysiology of traveller’s diarrhoea.

A

Heat labile ETEC modifies Gs and it is in a permanent ‘locked on’ state. Adenylate cyclase is activated and there is increased production of cAMP. This leads to increased secretion of Cl- into the intestinal lumen, H2O follows down as osmotic gradient -> diarrhoea.

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170
Q

Which type of e.coli can cause bloody diarrhoea and has a shiga like toxin?

A

Enterohaemorrhagic e.coli (EHEC) aka e.coli 0157.

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171
Q

What does EIEC stand for?

A

Enteroinvasive e.coli.

172
Q

Which type of e.coli is responsible for causing large volumes of watery diarrhoea?

A

Enteropathogenic e.coli (EPEC).

173
Q

What does EAEC stand for?

A

Enteroaggregative e.coli.

174
Q

What does DAEC stand for?

A

Diffusely adherent e.coli.

175
Q

What is the leading cause of diarrhoeal illness in young children?

A

Rotavirus. There is a vaccine - rotarix.

176
Q

Name a helminth responsible for causing diarrhoeal infection.

A

Schistosomiasis.

177
Q

Give 5 symptoms of helminth infection.

A
  1. Fever. 2. Eosinophilia. 3. Diarrhoea. 4. Cough. 5. Wheeze.
178
Q

Briefly describe the reproductive cycle of schistosomiasis.

A
  1. Fluke matures in blood vessels and reproduces sexually in human host. 2. Eggs expelled in faeces and enter water source. 3. Asexual reproduction in an intermediate host. 4. Larvae expelled and penetrate back into human host.
179
Q

Why is c.diff highly infectious?

A

It is a spore forming bacteria. (Gram positive).

180
Q

Give 5 risk factors for c.diff infection.

A
  1. Increasing age. 2. Co-morbidities. 3. Antibiotic use. 4. PPI. 5. Long hospital stays.
181
Q

Describe the treatment for c.diff infection.

A

Metronidazole and vancomyocin (PO).

182
Q

Name 5 antibiotics prone to causing c.diff infection.

A
  1. Ciprofloxacin. 2. Co-amoxiclav. 3. Clindamycin. 4. Cephlasporins. 5. Carbapenems. RULE OF C’s!
183
Q

What can helicobacter pylori infection cause?

A

H.pylori produces urease -> ammonia -> damage to gastric mucosa -> neutrophil recruitment and inflammation. This can cause gastritis; peptic ulcer disease and gastric cancer.

184
Q

Describe h.pylori.

A

A gram negative bacilli with a flagellum.

185
Q

Describe the treatment for H.pylori infection.

A

Triple therapy: 2 antibiotics and 1 PPI e.g. omeprazole, clarithromyocin and amoxicillin.

186
Q

Who is most likely to be affected by diverticular disease?

A

Older patients and those with low fibre diets.

187
Q

Describe the pathophysiology of diverticulitis.

A

Out-pouching of bowel mucosa -> faeces can get trapped here and obstruct the diverticula -> abscess and inflammation -> diverticulitis.

188
Q

What part of the bowel is most likely to be affected by diverticulitis?

A

The descending colon.

189
Q

What is acute diverticulitis?

A

A sudden attack of swelling in the diverticula. Can be due to surgical causes.

190
Q

Describe the signs of acute diverticulitis.

A

Similar to the signs of appendicitis but on the left side e.g. pain in the left iliac fossa region, fever, tachycardia.

191
Q

Name the 3 broad categories that describe the causes of intestinal obstruction.

A
  1. Blockage. 2. Contraction. 3. Pressure.
192
Q

Intestinal obstruction: give 3 causes of blockage.

A
  1. Tumour. 2. Diaphragm disease. 3. Gallstones in ileum (rare).
193
Q

Intestinal obstruction: what is thought to cause diaphragm disease?

A

NSAIDS.

194
Q

Intestinal obstruction: give 3 causes of contraction.

A
  1. Inflammation. 2. Intramural tumours. 3. Hirschprung’s disease.
195
Q

Describe how Crohn’s disease can cause intestinal obstruction.

A

Crohn’s disease -> fibrosis -> contraction -> obstruction.

196
Q

Describe how Diverticular disease can cause intestinal obstruction.

A

Out-pouching of mucosa -> faeces trapped -> inflammation in bowel wall -> contraction -> obstruction.

197
Q

What is Hirschprung’s disease?

A

A congenital condition where there is a lack of nerves in the bowel and so motility is affected. This leads to obstruction and gross dilatation of the bowel.

198
Q

Intestinal obstruction: give 3 causes of pressure.

A
  1. Adhesions. 2. Volvulus. 3. Peritoneal tumour.
199
Q

Intestinal obstruction: what are adhesions?

A

Adhesions often form secondary to abdominal surgery. Loops of bowel stick together and the bowel is pulled and distorted. 40% of intestinal obstructions are due to adhesions.

200
Q

Intestinal obstruction: what causes adhesions?

A

Adhesions often form secondary to abdominal surgery.

201
Q

Intestinal obstruction: what is volvulus?

A

Volvulus is a twist/rotation in the bowel; closed loop obstruction. There is a risk of necrosis.

202
Q

Intestinal obstruction: which areas of the bowel are most likely to be affected by volvulus?

A

Volvulus occurs in free floating areas of the bowel e.g. bowel with mesentery. The sigmoid colon has a long mesentery and so can twist on itself.

203
Q

Give 4 common causes of small bowel obstruction in adults.

A
  1. Adhesions. 2. Hernias. 3. Crohn’s disease. 4. Malignancy.
204
Q

Which is more common: small bowel obstruction or large bowel obstruction?

A

Small bowel obstruction is more common; it makes up 75% of intestinal obstruction.

205
Q

Give 3 common causes of small bowel obstruction in children.

A
  1. Appendicitis. 2. Volvulus. 3. Intussusception.
206
Q

Intestinal obstruction: what is intussusception?

A

Intussusception is when part of the intestine invaginates into another section of the intestine -> telescoping. It is caused by force in-balances.

207
Q

Define hernia.

A

The abnormal protrusion of an organ into a body cavity it doesn’t normally belong.

208
Q

What are the risks of hernia’s if left untreated?

A

They can become strangulated and you may not be able to return them into their correct body cavity - irreducible.

209
Q

Give 2 symptoms of hernia.

A
  1. Pain. 2. Palpable lump.
210
Q

Give 5 symptoms of small bowel obstruction.

A
  1. Vomiting. 2. Pain. 3. Constipation. 4. Distension. 5. Tenderness.
211
Q

Would dilatation, distension and increased secretions be seen proximal or distal to an intestinal obstruction?

A

Proximal.

212
Q

Give 4 signs of small bowel obstruction.

A
  1. Vital signs e.g. increased HR, hypotension, raised temperature. 2. Tenderness and swelling. 3. Resonance. 4. Bowel sounds.
213
Q

What investigations might you do in someone who you suspect to have a small bowel obstruction?

A
  1. Take a good history - ask about previous surgery (adhesions)! 2. FBC, U+E, lactate. 3. X-ray. 4. CT, ultrasound, MRI.
214
Q

What is the management/treatment for small bowel obstruction?

A
  1. Fluid resuscitation. 2. Bowel decompression. 3. Analgesia and anti-emetics. 4. Antibiotics. 5. Surgery e.g. laparotomy, bypass segment, resection.
215
Q

Give 2 common causes of large bowel obstruction.

A
  1. Colorectal malignancy. 2. Volvulus (especially in the developing world).
216
Q

Give 5 symptoms of large bowel obstruction.

A
  1. Tenesmus. 2. Constipation. 3. Abdominal discomfort. 4. Bloating. 5. Vomiting. 6. Weight loss.
217
Q

What investigations might you do in someone who you suspect to have a large bowel obstruction?

A
  1. Digital rectal examination. 2. Sigmoidoscopy. 3. Plain X-ray. 4. CT scan.
218
Q

Describe the management for a large bowel obstruction.

A
  1. Fast the patient. 2. Supplement O2. 3. IV fluids to replace losses and correct electrolyte imbalance. 4. Urinary catheterisation to monitor urine output.
219
Q

Give 3 consequences of untreated intestinal obstructions.

A
  1. Ischaemia. 2. Necrosis. 3. Perforation.
220
Q

Describe the progression from normal epithelium to colorectal cancer.

A
  1. Normal epithelium. 2. Adenoma. 3. Colorectal adenocarcinoma. 4. Metastatic colorectal adenocarcinoma.
221
Q

Define adenocarcinoma.

A

A malignant tumour of glandular epithelium.

222
Q

What is familial adenomatous polyposis?

A

Familial adenomatous polyposis is a genetic condition where you develop thousands of polyps in your teens.

223
Q

Describe the pathophysiology of familial adenomatous polyposis.

A

There is a mutation in apc protein and so the apc/GSK complex isn’t formed -> beta catenin levels increase -> up-regulation of adenomatous gene transcription.

224
Q

Describe the pathophysiology of HNPCC.

A

There are no DNA repair proteins meaning there is a risk of colon cancer and endometrial cancers.

225
Q

How can adenoma formation be prevented?

A

NSAIDS are believed to prevent adenoma formation.

226
Q

What is the treatment for adenoma?

A

Endoscopic resection.

227
Q

What is the treatment for colorectal adenocarcinoma?

A

Surgical resection can be done when there is no spread. Remember to balance risks v benefits. The patient has a pre-op assessment.

228
Q

What is the treatment for metastatic colorectal adenocarcinoma?

A

Chemotherapy and palliative care.

229
Q

Give 3 reasons why bowel cancer survival has increased over recent years.

A
  1. Introduction of the bowel cancer screening programme. 2. Colonoscopic techniques. 3. Improvements in treatment options.
230
Q

Give 5 risk factors for colorectal cancer.

A
  1. Low fibre diet. 2. Diet high in red meat. 3. Alcohol. 4. Smoking. 5. A PMH of adenoma or ulcerative colitis. 6. A family history of colorectal cancer; FAP or HNPCC.
231
Q

What can affect the clinical presentation of a colorectal cancer?

A

How close the cancer is to the rectum affects its clinical presentation.

232
Q

Give 3 signs of rectal cancer.

A
  1. PR bleeding. 2. Mucus. 3. Thin stools. 4. Tenesmus.
233
Q

Give 2 signs of a left sided/sigmoid cancer.

A
  1. Change of bowel habit e.g. diarrhoea, constipation. 2. PR bleeding.
234
Q

Give 3 signs of a right sided cancer.

A
  1. Anaemia. 2. Mass. 3. Diarrhoea that doesn’t settle.
235
Q

Describe the emergency presentation of a left sided colon cancer.

A

The LHS of the colon is narrow and so the patient is likely to present with signs of obstruction e.g. constipation; colicky abdominal pain; abdominal distension; vomiting.

236
Q

Describe the emergency presentation of a right sided colon cancer.

A

The RHS of the colon is wide and so the patient is likely to present with signs of perforation.

237
Q

What investigations might you do in someone who you suspect might have colorectal cancer?

A

Colonoscopy = gold standard! It permits biopsy and removal of small polyps. - Tumour markers are good for monitoring progress. - Faecal occult blood is used in screening but not diagnosis.

238
Q

Give 5 non-infective causes of diarrhoea.

A
  1. Neoplasm. 2. Inflammatory. 3. Irritable bowel. 4. Anatomical. 5. Chemical. 6. Hormonal. 7. Radiation.
239
Q

Give 3 infective causes of dysentery.

A
  1. Shigella. 2. Salmonella. 3. Campylobacter. 4. E.coli 0157.
240
Q

Give 2 infective causes of non-bloody diarrhoea.

A
  1. Rotavirus. 2. Norovirus.
241
Q

Describe the chain of infection.

A

Reservoir -> agent -> transmission -> host -> person to person spread.

242
Q

Give 3 ways in which infection can be transmitted.

A
  1. Direct e.g. faeco-oral. 2. Indirect e.g. vectorborne (malaria). 3. Airborne e.g. respiratory route.
243
Q

What is the treatment for vibrio cholerae infection?

A

HYDRATE e.g. ORS. What goes out must be replaced.

244
Q

Describe the management of c.diff infection.

A
  1. Control antibiotic use. 2. Infection control measures. 3. Isolate the case. 4. Case finding. 5. Test stool samples for toxin.
245
Q

Give 4 groups at risk of diarrhoeal infection.

A
  1. Food handlers. 2. Health care workers. 3. Children who attend nursery. 4. Persons of doubtful personal hygiene.
246
Q

Give 3 causes of peptic ulcers.

A
  1. Prolonged NSAID use -> decreased mucin production. 2. H.pylori infection. 3. Hyper-acidity. 4. Delayed gastric emptying. 5. Blood group O
247
Q

Give 3 symptoms of peptic ulcers.

A
  1. Burning epigastric pain - VERY SPECIFIC, worse at night and when hungry 2. Nausea 3. Anorexia / weight loss
248
Q

What investigations might you do in someone who you suspect to have peptic ulcers?

A
  1. H.pylori test e.g. urease breath test and faecal antigen test. 2. Gastroscopy. 3. Barium meal.
249
Q

Give 5 treatments for peptic ulcers.

A
  1. Stop NSAIDs. 2. PPIs e.g. omeprazole. 3. H2 antagonists 4. Lifestyle changes 5. H.pylori eradication - IF POSITIVE
250
Q

Give 2 potential complications of oesophago-gastroduodenoscopy (OGD).

A
  1. Cardiopulmonary. 2. Small risk of bleeding or perforation.
251
Q

Give 3 indications for OGD.

A
  1. Dyspepsia. 2. Dysphagia. 3. Anaemia. 4. Suspected coeliac disease.
252
Q

Give 3 indications for colonoscopy.

A
  1. Altered bowel habit. 2. Diarrhoea +/- dysentery. 3. Anaemia.
253
Q

Give 8/9 symptoms of GORD.

A

OESOPHAGEAL 1. Heart burn. 2. Acid reflux. 3. Odynophagia. 4. Belching 5. Water brash. EXTRA-OESOPHAGEAL 6. Nocturnal asthma 7. Chronic cough 8. Laryngitis 9. Sinusitis

254
Q

Describe the pathophysiology of coeliac disease.

A

> Gliadin is resistant to digestion by pepsin and chymotrypsin, thus remains in intestinal lumen > Gliadin peptides pass through epithelium and are deaminated by TG2 -> INCREASES IMMUNOGENICITY > Peptides bind to APC which interact with CD4+ T cells in lamina proprietary via HLA class II DQ2 or DQ8 > HLA class II molecules activate gluten-sensitive T cells > T cells produce pro-inflammatory cytokines and initiate inflammatory response > Response produces metaloproteinases which cause villous atrophy, crypt hyperplasia, and intraepithelial lymphocytes > Proximal small bowel mucosa is most affected > Mucosal damage means B12, folate, and iron cannot be absorbed -> ANAEMIA

255
Q

Describe the clinical presentation of Coeliac disease

A
  1. Diarrhoea / steatorrhoea 2. Weight loss. 3. Irritable bowel. 4. Iron deficiency ANAEMIA. 5. Mouth ulcers. 6. Abnormal liver function. 7. Abdominal pain 8. Bloating 9. Nausea and vomiting 10. Angular stomatitis 11. Fatigue 12. Osteomalacia
256
Q

What investigations might you do in someone who you suspect to have coeliac disease?

A
  1. Serology - look for auto-antibodies - TTG and EMA. 2. Gastroscopy - duodenal biopsies.
257
Q

What part of the bowel is commonly affected by Crohn’s disease?

A

Can affect anywhere from the mouth to anus.

258
Q

What part of the bowel is commonly affected by ulcerative colitis?

A

It only affects the rectum. It spreads proximally but only affects the colon.

259
Q

Give 5 complications of Crohn’s disease.

A
  1. Malabsorption. 2. Fistula. 3. Obstruction. 4. Perforation. 5. Anal fissures. 6. Neoplasia. 7. Amyloidosis (rare).
260
Q

Give 5 complications of ulcerative colitis.

A
  1. Colon: blood loss and colorectal cancer. 2. Arthritis. 3. Iritis and episcleritis. 4. Fatty liver and primary sclerosing cholangitis. 5. Erythema nodosum.
261
Q

Give an example of a functional bowel disorder.

A

IBS.

262
Q

Describe the multi-factorial pathophysiology of IBS.

A

The following factors can all contribute to IBS: - Psychological morbidity e.g. trauma in early life. - Abnormal gut motility. - Genetics. - Altered gut signalling (visceral hypersensitivity).

263
Q

Give 3 symptoms of IBS.

A
  1. ABDOMINAL PAIN! 2. Pain is relieved on defecation. 3. Bloating. 4. Change in bowel habit. 5. Mucus. 6. Fatigue.
264
Q

Give an example of a differential diagnosis for IBS.

A
  1. Coeliac disease. 2. Lactose intolerance. 3. Bile acid malabsorption. 4. IBD. 5. Colorectal cancer.
265
Q

What investigations might you do in someone who you suspect has IBS?

A
  1. Bloods - FBC, U+E, LFT. 2. CRP. 3. Coeliac serology.
266
Q

Describe the treatment for mild IBS.

A

Education, reassurance, dietary modification e.g. FODMAP.

267
Q

Describe the treatment for moderate IBS.

A

Pharmacotherapy and psychological treatments: - Antispasmodics for pain. - Laxatives for constipation. - Anti-motility agents for diarrhoea. - CBT and hypnotherapy.

268
Q

Describe the treatment for severe IBS.

A

MDT approach, referral to specialist pain treatment centres. - Tri-cyclic anti-depressants.

269
Q

Why are all gastric ulcers re-scoped 6-8 weeks after treatment?

A

All peptic ulcers are re-scoped to ensure they’ve healed. If they haven’t healed it could be a sign of malignancy.

270
Q

What is the criteria for dyspepsia?

A

>1 of the following: - Postprandial fullness. - Early satiation. - Epigastric pain/burning.

271
Q

Give 5 causes of dyspepsia.

A
  1. Excess acid. 2. Prolonged NSAIDS. 3. Large volume meals. 4. Obesity. 5. Smoking/alcohol. 6. Pregnancy.
272
Q

Give 5 red flag symptoms that you might detect when taking a history from someone with dyspepsia.

A
  1. Unexplained weight loss. 2. Anaemia. 3. Dysphagia. 4. Upper abdominal mass. 5. Persistent vomiting.
273
Q

What investigations might you do in someone with dyspepsia?

A
  1. Endoscopy. 2. Gastroscopy. 3. Barium swallow. 4. Capsule endoscopy.
274
Q

What is the management for dyspepsia if the red flag criteria has been met?

A
  1. Suspend NSAID use and review medication. 2. Endoscopy. 3. Refer malignancy to specialist.
275
Q

What is the management for dyspepsia without red flag symptoms?

A
  1. Review medication. 2. Lifestyle advice. 3. Full dose PPI for 1 month. 4. Test and treat h.pylori infection.
276
Q

What kind of lifestyle advice might you give to someone with dyspepsia?

A
  1. Lose weight. 2. Stop smoking. 3. Cut down alcohol. 4. Dietary modification.
277
Q

Describe the treatment for GORD.

A
  1. PPI. 2. Lifestyle modification. 3. Anti-reflux surgery.
278
Q

Give a potential consequence of anterior ulcer haemorrhage.

A

Acute peritonitis.

279
Q

Give a potential consequence of posterior ulcer haemorrhage.

A

Pancreatitis.

280
Q

Name 5 things that can break down the mucin layer in the stomach and cause gastritis.

A
  1. Not enough blood - mucosal ischaemia. 2. H.pylori. 3. Aspirin, NSAIDS. 4. Increased acid - stress. 5. Bile reflux - direct irritant. 6. Alcohol.
281
Q

Describe the treatment for gastritis.

A
  1. Reduced mucosal ischaemia. 2. PPI. 3. H2RA. 4. Enteric coated aspirin.
282
Q

Give 5 broad causes of malabsorption.

A
  1. Defective intra-luminal digestion. 2. Insufficient absorptive area. 3. Lack of digestive enzymes. 4. Defective epithelial transport. 5. Lymphatic obstruction.
283
Q

Malabsorption: what can cause defective intra-luminal digestion?

A
  1. Pancreatic insufficiency due to pancreatitis, CF. There is a lack of digestive enzymes. 2. Defective bile secretion due to biliary obstruction or ileal resection. 3. Bacterial overgrowth.
284
Q

Why can pancreatitis cause malabsorption?

A

Pancreatitis results in pancreatic insufficiency and so a lack of pancreatic digestive enzymes. There is defective intra-luminal digestion which leads to malabsorption.

285
Q

Malabsorption: what can cause insufficient absorptive area?

A
  1. Coeliac disease. 2. Crohn’s disease. 3. Extensive parasitisation. 4. Small intestine resection.
286
Q

Malabsorption: give an example of when there is a lack of digestive enzymes.

A

Lactose intolerance - disaccharide enzyme deficiency.

287
Q

Malabsorption: what can cause lymphatic obstruction?

A
  1. Lymphoma. 2. TB.
288
Q

Describe the distribution of inflammation seen in Crohn’s disease.

A

Patchy, granulomatous, transmural inflammation (can affect just the mucosa or go through the bowel wall).

289
Q

Describe the distribution of inflammation seen in ulcerative colitis.

A

Continuous inflammation affecting only the mucosa.

290
Q

Histologically, what part of the bowel wall is affected in ulcerative colitis?

A

Just the mucosa.

291
Q

Histologically, what part of the bowel wall is affected in crohn’s disease?

A

Can affect just the mucosa or can go all the way through to the bowel wall -> transmural inflammation.

292
Q

What is the treatment for crohn’s disease and ulcerative colitis?

A

Anti-inflammatories.

293
Q

Name the break down product of gluten that can trigger coeliac disease.

A

Gliadin.

294
Q

What part of the small intestine is mainly affected by coeliac disease?

A

Duodenum.

295
Q

What disorders might be associated with coeliac disease?

A

Other autoimmune disorders: 1. T1 diabetes. 2. Thyroxoicosis. 3. Hypothyroidism. 4. Addisons disease. Osteoporosis is also commonly seen in people with coeliac disease.

296
Q

What is the prevalence of coeliac disease?

A

1%.

297
Q

What cells normally line the oesophagus?

A

Stratified squamous non-keratinising cells.

298
Q

What is Barrett’s oesophagus?

A

When squamous cells undergo metaplastic changes and become columnar cells.

299
Q

What can cause Barrett’s oesophagus?

A
  1. GORD. 2. Obesity.
300
Q

Give a potential consequence of Barrett’s oesophagus.

A

Adenocarcinoma.

301
Q

Describe how Barrett’s oesophagus can lead to oesophageal adenocarcinoma.

A
  1. GORD damages normal oesophageal squamous cells. 2. Glandular columnar epithelial cells replace squamous cells (metaplasia). 3. Continuing reflux leads to dysplastic oesophageal glandular epithelium. 4. Continuing reflux leads to neoplastic oesophageal glandular epithelium - adenocarcinoma.
302
Q

Give 5 symptoms of oesophageal carcinoma.

A
  1. Dysphagia. 2. Odynophagia (painful swallowing). People often present very late. 3. Vomiting. 4. Weight loss. 5. Anaemia. 6. GI bleed. 7. Reflux.
303
Q

Give 3 causes of squamous cell carcinoma.

A
  1. Smoking. 2. Alcohol. 3. Poor diet.
304
Q

What can cause oesophageal adenocarcinoma?

A

Barrett’s oesophagus.

305
Q

Give 3 causes of gastric cancer.

A
  1. Smoked foods. 2. Pickles. 3. H.pylori infection. 4. Pernicious anaemia.
306
Q

Describe how gastric cancer can develop from normal gastric mucosa.

A

Smoked/pickled food diet leads to intestinal metaplasia of the normal gastric mucosa. Several genetic changes lead to dysplasia and then eventually intra-mucosal and invasive carcinoma.

307
Q

Give 3 causes of oesophageal carcinoma.

A
  1. GORD -> Barrett’s. 2. Smoking. 3. Alcohol.
308
Q

What investigations might you do in someone who you suspect to have oesophageal carcinoma?

A
  1. Barium swallow. 2. Endoscopy.
309
Q

Describe the 2 treatment options for oesophageal cancer.

A
  1. Medically fit and no metastases = operate. The oesophagus is replaced with stomach or sometimes the colon. The patient often has 2/3 rounds of chemo before surgery. 2. Medically unfit and metastases = palliative care. Stents can help with dysphagia.
310
Q

Give 3 signs of gastric cancer.

A
  1. Weight loss. 2. Anaemia. 3. Vomiting blood. 4. Melaena. 5. Dyspepsia.
311
Q

A mutation in what gene can cause familial diffuse gastric cancer?

A

CDH1 - 80% chance of gastric cancer. Prophylactic gastrectomy is done in these patients.

312
Q

What investigations might you do in someone who you suspect has gastric cancer?

A
  1. Endoscopy. 2. CT. 3. Laparoscopy.
313
Q

What is the advantage of doing a laparoscopy in someone with gastric cancer?

A

It can detect metastatic disease that may not be detected on ultrasound/endoscopy.

314
Q

What is the treatment for proximal gastric cancers that have no spread?

A

3 cycles of chemo and then a full gastrectomy. Lymph node removal too.

315
Q

What is the treatment for distal gastric cancers that have no spread?

A

3 cycles of chemo and then a partial gastrectomy if the tumour is causing stenosis or bleeding. Lymph node removal too.

316
Q

What vitamin supplement will a patient need following gastrectomy?

A

They will be deficient in intrinsic factor and so will need vitamin B12 supplements to prevent pernicious anaemia.

317
Q

Give 3 symptoms of spontaneous bacterial peritonitis.

A
  1. Dull to percussion. 2. Temperature. 3. Abdominal pain.
318
Q

What investigations might you do in someone who you suspect could have peritonitis?

A
  1. Blood tests: raised WCC, platelets, CRP, amylase. Reduced blood count. 2. CXR: look for air under the diaphragm. 3. Abdominal x-ray: look for bowel obstruction. 4. CT: can show inflammation, ischaemia or cancer. 5. ECG: epigastric pain could be related to the heart. 6. B-HCG: a hormone secreted by pregnant ladies.
319
Q

Give 5 potential complications of peritonitis.

A
  1. Hypovolaemia. 2. Kidney failure. 3. Systemic sepsis. 4. Paralytic ileus. 5. Pulmonary atelectasis (lung collapse). 6. Portal pyaemia (pus in the portal vein).
320
Q

Explain how paralytic ileus can lead to respiratory problems.

A

Peristaltic waves stop -> dilation of bowel -> distended abdomen therefore increased pressure -> pushes on diaphragm -> respiration affected.

321
Q

What is the management for peritonitis?

A
  1. ABC. 2. Treat the underlying cause! 3. Call a surgeon. 4. Set up post-management support.
322
Q

What can cause exudative ascites?

A

Increased vascular permeability secondary to infection; inflammation (peritonitis) or malignancy.

323
Q

What can cause transudative ascites?

A

Increased venous pressure due to cirrhosis, cardiac failure or hypoalbuminaemia.

324
Q

Give 2 signs of ascites.

A
  1. Flank swelling. 2. Dull to percuss and shifting dullness.
325
Q

What investigations might you do in someone who you suspect has ascites?

A
  1. Ultrasound. 2. Ascitic tap.
326
Q

Describe the treatment for ascites.

A
  1. Restrict sodium. 2. Diuretics. 3. Drainage.
327
Q

Where in the colon do the majority of colon cancers occur?

A

In the descending/sigmoid colon and rectum.

328
Q

Why do proximal colon cancers have a worse prognosis?

A

They have fewer signs and so people often present with them at a very advanced and late stage.

329
Q

What 3 histological features are needed in order to make a diagnosis of coeliac disease?

A
  1. Raised intraepithelial lymphocytes. 2. Crypt hyperplasia. 3. Villous atrophy.
330
Q

What investigation is it important to do in someone with chronic liver disease and ascites? Explain why it is important.

A

It is important to do an ascitic tap so you can rule out spontaneous bacterial peritonitis as soon as possible.

331
Q

What would be raised in the blood tests taken from someone with primary biliary cirrhosis?

A
  1. Raised IgM. 2. Raised ALP. 3. Positive AMA.
332
Q

What 4 features would you expect to see in the blood test results taken from someone who has overdosed on paracetamol.

A
  1. Metabolic acidosis. 2. Prolonged pro-thrombin time (due to coagulability). 3. Raised creatinine (renal failure). 4. Raised ALT.
333
Q

What 3 symptoms make up the triad of Wernicke’s encephalopathy?

A
  1. Ataxia. 2. Opthalmoplegia. 3. Confusion.
334
Q

How can Wernicke’s encephalopathy be reversed?

A

Give IV thiamine.

335
Q

What histological stain can be used for haemochromatosis?

A

Perl’s stain.

336
Q

Name 4 fat soluble vitamins.

A

A, D, E and K.

337
Q

What is the main difference between biliary colic and acute cholecystitis?

A

Acute cholecystitis has an inflammatory component!

338
Q

What is the treatment for acute cholecystitis?

A

Laparoscopic cholecystectomy.

339
Q

Why might someone with primary biliary cirrhosis experience itching as a symptom?

A

Because there is a build up of bilirubin.

340
Q

Give 3 components of gallstones.

A
  1. Cholesterol. 2. Bile pigment. 3. Phospholipid.
341
Q

What investigations might you do in someone who you suspect has gallstones?

A

Ultrasound! ERCP.

342
Q

Are most liver cancers primary or secondary?

A

Secondary - they have metastasised to the liver from the GI tract, breast and bronchus.

343
Q

Where have most secondary liver cancers arisen from?

A
  1. The Gi tract. 2. Breast. 3. Bronchus.
344
Q

Describe the aetiology of HCC.

A

Most HCC is in patients with cirrhosis. This is often due to HBV/HCV and alcohol.

345
Q

Give 5 symptoms of HCC.

A
  1. Weight loss. 2. Anorexia. 3. Fever. 4. Malaise. 5. Ascites.
346
Q

What investigations might you do on someone who you suspect has HCC?

A
  1. Bloods: serum AFP may be raised. 2. US or CT to identify lesions. 3. MRI. 4. Biopsy if diagnostic doubt.
347
Q

Describe the treatment for HCC.

A
  1. Surgical resection of solitary tumours. 2. Liver transplant. 3. Percutaneous ablation.
348
Q

How long after infection with hepatitis B virus is HBsAg present in the serum for?

A

HBsAg will be present in the serum from 6 weeks - 3 months after infection.

349
Q

How long after infection with hepatitis B virus is anti-HBV core (IgM) present in the serum for?

A

Anti-HBV core (IgM) slowly rises from 6 weeks after infection and its serum level peaks at about 4 months.

350
Q

Give 3 symptoms of haemochromatosis.

A
  1. Hepatomegaly. 2. Cardiomegaly. 3. Diabetes mellitus. 4. Hyperpigmentation of skin. 5. Lethargy.
351
Q

Name 3 diseases that lead to heamolytic anaemia and so a raised unconjugated bilirubin and pre-hepatic jaundice.

A

Causes of haemolytic anaemia: 1. Sickle cell disease. 2. Hereditary spherocytosis/elliptocytosis. 3. GP6D deficiency. 4. Hypersplenism.

352
Q

Give 3 causes of liver failure.

A
  1. Infection e.g. viral hepatitis B, C. 2. Induced e.g. alcohol, drug toxicity. 3. Inherited e.g. autoimmune.
353
Q

Hepatic encephalopathy is a complication of liver failure. Describe the pathophysiological mechanism behind this.

A

The liver can’t get rid of ammonia and so ammonia crosses the BBB -> cerebral oedema.

354
Q

Give 4 complications of liver failure.

A
  1. Hepatic encephalopathy. 2. Abnormal bleeding. 3. Jaundice. 4. Ascites.
355
Q

Describe the treatment for liver failure.

A
  1. Nutrition. 2. Supplements. 3. Treat complications. 4. Liver transplant.
356
Q

You do an ascitic in someone with ascites. The neutrophil count comes back as - Neutrophils > 250/mm3. What is the likely cause of the raised neutrophils?

A

Spontaneous bacterial peritonitis.

357
Q

Describe the treatment for spontaneous bacterial peritonitis.

A

Cefotaxime and metronidazole.

358
Q

Give 5 symptoms of ruptured varices.

A
  1. Haematemesis. 2. Melaena. 3. Abdominal pain. 4. Dysphagia. 5. Anaemia.
359
Q

How would you know if an individual had been vaccinated against hepatitis B?

A

They would have anti-HBVs IgG in their serum.

360
Q

What type of anaemia do you associate with alcoholic liver disease?

A

Macrocytic anaemia.

361
Q

Name a protozoa that can cause amoebic liver abscess?

A

Entemoeba histolytica.

362
Q

What are the symptoms of entemoeba histolytica?

A
  • RUQ pain. - Bloody diarrhoea. - Fever and malaise. Often the patient has a history of foreign/rural travel.
363
Q

What is the treatment for entemoeba histolytica?

A

Metronidazole.

364
Q

What is the treatment for mild/moderate UC?

A

Mesalazine.

365
Q

A 4-year-old girl presents with diarrhoea and is hypotensive. What is the physiological reason that fluid moves from the interstitium to the vascular compartment in this case?

A

Reduced hydrostatic pressure. Fluid will move from the interstitium into the plasma if there is an increase in osmotic pressure or a decrease in hydrostatic pressure. As this patient is hypotensive it is more likely to be the latter.

366
Q

What drug would you give to someone that has overdosed on paracetamol?

A

IV N-Acetyl-Cysteine.

367
Q

With which disease would you associate Reynold’s pentad?

A

Ascending cholangitis.

368
Q

Describe Reynold’s pentad.

A
  • Charcot’s triad (fever, RUQ pain and jaundice). - + hypotension. - + altered mental state.
369
Q

What is a potential consequence of h.pylori infection in a person with decreased gastric acid?

A

Gastric cancer.

370
Q

What is a potential consequence of h.pylori infection in a person with increased gastric acid?

A

Duodenal ulcer.

371
Q

What might pain radiating to the back be a sign of?

A

Pancreatitis or AAA.

372
Q

What blood test might show that someone has alcoholic liver disease?

A

Serum GGT (gamma-glutamyl transferase) will be elevated.

373
Q

What distinctive feature is often seen on biopsy in people suffering from alcoholic liver disease?

A

Mallory bodies.

374
Q

What feature seen on liver biopsy is diagnostic of cirrhosis?

A

Nodular regeneration.

375
Q

A man has his ascites drained and is advised to restrict his diet. Which non-hormonal substance will promote re-accumulation of the ascites?

A

Salt.

376
Q

What is the treatment for Wilson’s disease.

A

Lifetime treatment with penicillamine.

377
Q

Name the 2 main pathophysiological factors that contribute to the formation of ascites.

A
  1. High portal venous pressure. 2. Low serum albumin.
378
Q

Give 2 indications for the need of immediate surgical intervention in someone with a small bowel obstruction.

A
  1. Signs of perforation (peritonitis). 2. Signs of strangulation.
379
Q

Why is morphine contraindicated in acute pancreatitis?

A

Morphine increases sphincter of Oddi pressure and so aggravates pancreatitis.

380
Q

What two enzymes, if raised, suggest pancreatitis?

A

LDH and AST.

381
Q

Where is folate absorbed?

A

In the jejunum.

382
Q

Where is vitamin B12 absorbed?

A

In the terminal ileum.

383
Q

Where is iron absorbed?

A

In the duodenum.

384
Q

In someone with coeliac disease, what are they most likely to be deficient in - iron, folate, or B12?

A

Iron. Coeliac disease mainly affects the duodenum and iron is absorbed in the duodenum. Folate is absorbed in the jejunum and B12 in the terminal ileum.

385
Q

Give 5 histological features of a malignant neoplasm.

A
  1. High mitotic activity. 2. Rapid growth. 3. Border irregularity. 4. Necrosis. 5. Poor resemblance to normal tissues.
386
Q

What lymph nodes can oesophageal carcinoma commonly metastasise to?

A

Para-oesophageal lymph nodes.

387
Q

What hormone is responsible for the production of gastric acid?

A

Gastrin.

388
Q

State two pathological changes that occur in the liver with continued consumption of excessive amounts of alcohol.

A
  1. Fatty liver. 2. Alcoholic hepatitis. 3. Cirrhosis.
389
Q

A patient’s oedema is caused solely by their liver disease. State one possible pathophysiological mechanism for their oedema.

A

Hypoalbuminaemia.

390
Q

List 5 important questions a GP should ask when taking a history to establish a cause of diarrhoea.

A
  1. Blood or mucus in the stools. 2. Family history of bowel problems? 3. Abdominal pain. 4. Recent foreign travel history. 5. Bloating. 6. Weight loss.
391
Q

List two blood tests a GP might perform to help differentiate between the different causes of diarrhoea.

A
  1. FBC. 2. ESR/CRP.
392
Q

List two stool tests a GP might request to help differentiate between the different causes of diarrhoea.

A
  1. Stool culture. 2. Faecal calprotectin.
393
Q

State one histological feature that will be seen in ulcerative colitis.

A
  1. Crypt abscess. 2. Increase in plasma cells in the lamina propria.
394
Q

What investigations might you do in someone with inflammatory bowel disease?

A
  1. Bloods - FBC, ESR, CRP. 2. Faecal calprotectin - shows inflammation but is not specific for IBD. 3. Flexible sigmoidoscopy. 4. Colonoscopy.
395
Q

Name 3 drugs or classes of drugs that can cause acute pancreatitis.

A
  1. NSAIDs. 2. Diuretics. 3. Steroids.
396
Q

What 2 products does haem break down in to?

A

Haem -> Fe2+ and biliverdin.

397
Q

What enzyme converts biliverdin to unconjugated bilirubin?

A

Biliverdin reductase.

398
Q

What is the function of glucuronosyltransferase?

A

It transfers glucuronic acid to unconjugated bilirubin to form conjugated bilirubin.

399
Q

What protein does unconjugated bilirubin bind to and why?

A

Albumin. It isn’t H2O soluble therefore it binds to albumin so it can travel in the blood to the liver.

400
Q

What does conjugated bilirubin form?

A

Urobilinogen.

401
Q

What is responsible for the conversion of conjugated bilirubin into urobilinogen?

A

Intestinal bacteria.

402
Q

What can urobilinogen form?

A
  1. It can go back to the liver via the enterohepatic system. 2. It can go to the kidneys forming urinary urobilin. 3. It can form stercobilin which is excreted in the faeces.
403
Q

What disease could be caused by a non-functioning mutation in NOD2?

A

Crohn’s.

404
Q

What are the differential diagnoses for GORD?

A
  • CAD - Biliary colic - Peptic ulcer disease - Malignancy
405
Q

What are the causes of GORD?

A
  • Lower oesophageal sphincter hypotension - Hiatus hernia - Loss of oesophageal peristaltic function - Abdominal obesity - Gastric acid hypersecretion - Slow gastric emptying - Overating - Smoking - Alcohol - Pregnancy - Indigestion (fat, chocolate, coffee, alcohol) - Drugs (antimuscarinic, calcium channel blockers, nitrates) - Systemic sclerosis
406
Q

What is the pathophysiology for GORD?

A

There is much more transient lower oesophageal sphincter relaxations than usual, due to reduced muscle tone of LOS which allows gastric acid to flow back into oesophagus

407
Q

When do clinical features of GORD appear?

A

When the anti-reflux mechanisms fail, allowing prolonged contact between acid and lower oesophageal mucosa Hiatus hernias can impair anti-reflux mechanisms

408
Q

What exacerbates and relieves heartburn pain caused by GORD?

A

Exacerbated by hot drinks, alcohol, bending, stooping, and lying down Relieved by antacids

409
Q

What alarm bell signs result in a patient with symptoms of GORD requiring further investigations?

A
  • Weight loss - Haematemesis - Dysphagia
410
Q

If a patient with symptoms of GORD also has alarm bell signs, what investigations must be done?

A

Endoscopy - assess oesophagitis and hiatal hernia Barium swallow

411
Q

Why do you do an endoscopy in a patient with GORD symptoms?

A
  • Symptoms >4w - Alarm bell signs - Persistent vomiting - GI bleeding - Palpable mass - 55+ - Symptoms despite treatment
412
Q

What will a barium swallow reveal in a patient with symptoms of GORD?

A

Whether the GORD is due to a hiatal hernia

413
Q

What is confirmation of reflux which is identified on an endoscopy?

A
  • Oesophagitis - Barrett’s oesophagus
414
Q

If an endoscopy doesn’t reveal anything abnormal, how else can you investigate reflux?

A

Intraluminal pH monitoring over 24hrs

415
Q

What are the 4 lifestyle changes necessary to treating GORD?

A
  1. Weight loss 2. Smoking cessation 3. Small, regular meals 4. Avoid hot drinks, alcohol, citrus fruit, and eating <3hrs before bed
416
Q

What are the 4 pharmacological treatments for GORD?

A
  1. Antacids (e.g. magnesium trisilicate mixture) 2. Alginates (e.g. gaviscon) 3. Proton pump inhibitor (e.g. lansoprazole) 4. H2 receptor antagonists (e.g. cimetidine)
417
Q

What is the surgical treatment for GORD?

A

Nissen fundoplication - laparoscopically increases the resting LOS pressure Only use when unresponsive to therapy

418
Q

How do NSAIDs cause peptic ulcers?

A

> Cyclo-oxygenase-1 is needed for prostaglandin synthesis > Prostaglandins triggers inflammation and stimulates mucous secretion > NSAIDs inhibit cycle-oxygenase-1 > Less mucous production > Decreased mucosal defence

419
Q

How does H.pylori lead to peptic ulcers?

A

> H.pylori exclusively inhabits mucous layer of gastric epithelium > Causes major destruction to mucin layer that protects mucosa > Decrease in duodenal HCO3-, thus increasing acidity of stomach as there is less alkali to buffer acid > H.pylori also secretes urease, splitting urea into CO2 and ammonia > Ammonia + H+ = ammonium > Ammonium is toxic to gastric mucosa, resulting in less mucous production > Secreted proteases, phosphlipases, and vacuolating cytotoxin A can also attack gastric epithelium > Also increases gastrin release from G cells, increasing acid released from parietal cells

420
Q

How does ischaemia of gastric cells lead to peptic ulcers?

A

> Produces less mucin > Less protection from acid > Acid damages mucosa

421
Q

How can stress lead to peptic ulceration?

A

Stress can result in increased gastric acid production, damaging mucosal surface

422
Q

What is a complication of a duodenal ulcer?

A
  • Ulcer can get deeper and deeper until it hits the gastroduodenal artery > MASSIVE HAEMORRHAGE - Peritonitis as acid enters peritoneum - air under diaphragm on erect X-ray - Acute pancreatitis if ulcer reaches pancreas
423
Q

Describe non-invasive H.pylori testing

A

C-urea breath test - quick and reliable test for H.pylori - measure CO2 in breath after ingestion of C-urea - used to monitor infection after eradication - highly sensitive and specific Stool antigen test - immunoassay using monoclonal antibodies for detection of H.pylori - monitors efficacy of eradication

424
Q

Describe invasive H.pylori testing

A

Endoscopy - histology for direct visualisation - biopsy urease test

425
Q

What are the lifestyle changes advised for treating peptic ulcer disease?

A
  • Reduce stress - Avoid irritating food - Smoking cessation - Stop NSAIDS
426
Q

How do you eradicate H.pylori?

A

Triple therapy - PPI for acid suppression (e.g. lansoprazole) - Plus two of; > metronidazole > clarithromycin (high resistance) > amoxicillin (low resistance) > tetracycline (low resistance) > bismuth

Phase 2a Medicine - Hannah's version (9 decks)

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