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Phase 2a Medicine > Liver and GI > Flashcards

Liver and GI Flashcards

1
Q

What causes death when the liver fails?

A

Hypoglycaemia due to failed glucogenesis and glycogenolysis

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2
Q

What are the functions of the liver?

A
  • Protein synthesis (albumin, clotting factors)
  • Glucose and fat metabolism
  • Defence against infection
  • Detoxification and excretion (e.g. ammonia, drugs, hormones)
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3
Q

Where does the liver get its blood supply?

A

Dual supply from portal vein from the gut and hepatic artery

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4
Q

Which vessel carries blood away from the liver?

A

Hepatic vein

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5
Q

Which part of the liver lobule is most likely to be affected by toxins?

A

Zone 3 (i.e. the hepatocytes around the hepatic vein as these have the least access to oxygen and nutrients)

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6
Q

What does acute liver injury lead to?

A

Either liver failure or recovery

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7
Q

What does chronic liver injury lead to?

A

Either recovery or cirrhosis (which can lead on to acute on chronic liver failure, varices and hepatoma)

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8
Q

What is seen on histology in acute liver injury?

A
  • Apoptosis (seen as eosinophilic areas)
  • Fibrosis
  • Macrophages
  • Ballooned hepatocytes
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9
Q

How does acute liver injury present?

A

Malaise, nausea, anorexia, jaundice (rarely - confusion and liver pain)

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10
Q

How does chronic liver injury present?

A

Ascites, oedema, haematemesis, malaise, anorexia, wasting, easy bruising, itching, hepatomegaly, abnormal LFTs
(rarely - jaundice, confusion)

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11
Q

Which blood tests give some index of liver function?

A

Serum bilirubin, albumin and prothrombin time

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12
Q

Which blood ‘liver function tests’ actually give no index of liver function?

A

Serum liver enzymes, alkaline phosphatase, gamma-GT, transaminases (AST, ALT)

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13
Q

What is jaundice?

A

Yellow appearance of the skin caused by raised serum bilirubin

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14
Q

What is pre-hepatic jaundice and what causes it?

A

Pre-hepatic jaundice is caused by raised unconjugated serum bilirubin and is caused by Gilbert’s syndrome and haemolysis

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15
Q

Raised conjugated bilirubin is found in which types of jaundice?

A

Hepatic (liver disease), post-hepatic (due to bile duct obstruction)

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16
Q

What is Gilbert’s syndrome?

A

An inherited liver disorder that affects the body’s ability to process bilirubin - don’t produce enough liver enzymes to keep bilirubin at a normal level

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17
Q

What are the possible causes of hepatic jaundice?

A

Hepatitis (caused by drugs/autoimmune/alcohol), ischaemia, neoplasm and congestion

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18
Q

What are the possible causes of post-hepatic jaundice?

A

Gallstones, malignancy, ischaemia, inflammation

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19
Q

How can we differentiate between pre-hepatic and hepatic/post-hepatic jaundice?

A

Pre-hepatic: normal urine, normal stools, no itching, normal liver tests

Hepatic/post-hepatic: Dark urine, potentially pale stools, possible itching, abnormal liver tests

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20
Q

What does very high AST/ALT suggest?

A

Liver disease (although some exceptions), jaundice with high AST/ALT enzymes more likely to have hepatic cause.

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21
Q

Besides blood tests, what other investigations can be useful in assessing jaundice?

A

CT
MRCP (magnetic resonance cholangiogram)
ERCP (endoscopic retrograde cholangiogram)

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22
Q

What are gallstones made of?

A

Cholesterol, bile duct pigment +/- calcium

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23
Q

What are the three classifications of gallstones?

A
  1. Intrahepatic bile duct stones (hepatolithiasis)
  2. Extrahepatic bile duct stones (choledocholithiasis) in the common bile duct
  3. Gallbladder stones (cholecystolithiasis)
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24
Q

How do gallbladder stones (cholecystolithiasis) normally present?

A

Right upper quadrant pain, cholecystitis, possible obstructive jaundice, no evidence of cholangitis or pancreatitis

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25
Q

How do bile duct stones (choledocholithiasis) normally present?

A

No cholecystitis or ‘biliary’ pain. Obstructive jaundice, cholangitis and pancreatitis present.

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26
Q

How are gallbladder stones normally managed?

A

Via laparoscopic cholecystectomy (if symptomatic)

Can offer bile acid dissolution therapy instead if patient is not fit for surgery

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27
Q

How are bile duct stones usually managed?

A

ERCP with sphincterotomy with removal (via basket or balloon), crushing (mechanical/laser) and possible stent placement.
Large stones may need to be removed surgically.

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28
Q

Acute stone obstruction will normally show what on liver enzyme tests?

A

Alkaline phosphatase usually normal

Initial ALT often high >1000

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29
Q

Which antibiotic used to treat and prevent TB can be associated with elevated transaminases?

A

Isoniazid

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30
Q

Which drugs are most likely to cause liver injury?

A

Antibiotics, CNS drugs (e.g. valproate, carbamazepine), immunosuppressants (e.g. azathioprine), analgesics (e.g. diclofenac), GI drugs (e.g. PPIs), dietary supplements.

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31
Q

What drugs apparently don’t cause liver injury?

A 
Low dose aspirin
NSAIDs (except diclofenac)
Beta blockers
HRT
ACE inhibitors
Thiazides
Calcium channel blockers
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32
Q

What drug is given to treat paracetamol overdose?

A

N acetylcysteine (NAC)

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33
Q

When might a paracetamol overdose require an emergency liver transplant?

A
  • Late presentation (NAC less effective >24h)
  • Acidosis
  • Prothrombin time >70s
  • Serum creatinine >300umol/l
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34
Q

Why is ascites associated with chronic liver disease?

A

CLD causes systemic dilatation, which leads to the secretion of renin, noradrenaline and vasopressin, which causes fluid retention.
Low albumin also leads to ascites.

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35
Q

What are the management options for ascites?

A

Fluid and salt restriction, high caloric intake
Diuretics: spironolactone +/- furosemide
To drain fluid:
Large-volume paracentesis
Trans-jugular intrahepatic portosystemic shunt (TIPS)

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36
Q

What is normally seen in the early stages of alcoholic liver disease?

A

Fatty liver

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37
Q

What is cirrhosis of the liver?

A

Irreversible architectural change to the liver due to fibrosis

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38
Q

What is the main cause of liver death in the UK?

A

Alcoholic liver disease

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39
Q

Why might a patient with liver disease present with haematemesis?

A

Due to bleeding varices in the oesophagus

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40
Q

What drug can be used to treat alcoholic liver disease, although the response is variable?

A

Prednisolone

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41
Q

What are the main reversible causes of encephalopathy in liver disease patients?

A
  • Constipation
  • Drugs
  • GI bleed
  • Infection
  • Hypo- (natraemia, kalaemia, glycaemia..)
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42
Q

What infections are liver patients vulnerable to?

A

Spontaneous bacterial peritonitis, septicaemia, pneumonia, skin infections, UTIs

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43
Q

What is the most common serious infection seen in liver cirrhosis patients?

A

Spontaneous bacterial peritonitis

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44
Q

What might cause renal failure in liver disease patients?

A

Drugs (esp. diuretics, NSAIDs, ACE inhibitors)

Infection, GI bleeding, myoglobinuria, renal tract obstruction

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45
Q

What drugs must be avoided completely in patients with liver disease?

A

NSAIDs (due to renal failure)
ACE inhibitors (although these patients don’t tend to have high BP anyway)
Aminoglycosides (e.g. gentamicin)

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46
Q

What are the possible causes of chronic liver disease?

A
  • Alcohol
  • NASH (Non-alcoholic steatohepatitis)
  • Viral hepatitis
  • Immune disease (e.g. autoimmune hepatitis, primary biliary cholangitis, sclerosing cholangitis)
  • Metabolic disease: haemochromatosis, Wilson’s disease, alpha-1 antitrypsin deficiency
  • Vascular disease: Budd-Chiari
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47
Q

Which immunoglobulin is raised in autoimmune hepatitis?

A

IgG

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48
Q

Which immunoglobulin is raised in primary biliary cholangitis?

A

IgM

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49
Q

What are the three main autoimmune liver diseases?

A

Autoimmune hepatitis
Primary biliary cholangitis
Primary sclerosing cholangitis

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50
Q

Which autoimmune liver disease responds well to steroid treatment with prednisolone +/- azathioprine?

A

Autoimmune hepatitis

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51
Q

How can primary biliary cirrhosis/cholangitis present?

A

Asymptomatic abnormal LFTs (bilirubin, thrombin time, albumin), itching, fatigue, dry eyes, joint pain, variceal bleeding, liver failure.

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52
Q

What can be used to treat cholestatic itch?

A
  • Antihistamines don’t help much
  • Cholestyramine helps in 50% of cases
  • Opiate antagonists (e.g. naloxone)
  • UV light
  • Plasmapheresis
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53
Q

What can be used to treat fatigue in primary biliary cholangitis?

A

Modafinil

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54
Q

What abnormalities would show up on blood tests for primary sclerosing cholangitis?

A

Raised alkaline phosphatase and GGT

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55
Q

How does primary sclerosing cholangitis often present?

A

Itching, pain +/- rigors, jaundice

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56
Q

What are the clinical features of haemochromatosis?

A
  • Hepatomegaly
  • Cirrhosis
  • Hepatocellular carcinoma
  • Flat, white nails
  • Koilonychia (spoon nails)
  • Joint pain and osteoporosis
  • Chronic fatigue
  • Diabetes mellitus
  • Melanoderma, skin dryness
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57
Q

What would a liver biopsy of a patient with hepatocellular carcinoma show?

A

Hepatocytes growing in large clumps with large nuclei

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58
Q

What do 50% of hepatocellular carcinoma patients produce?

A

Alpha fetoprotein

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59
Q

What drug has recently been shown to extend the lives of patients with hepatocellular carcinoma?

A

Sorafenib

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60
Q

How might hepatic vein occlusion present?

A

Abnormal liver tests
Ascites
Acute liver failure

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61
Q

What are the treatment options for hepatic vein occlusion?

A

Anticoagulation
Transjugular intrahepatic portosystemic shunt
Liver transplantation

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62
Q

What is the definition of diarrhoea?

A

The passage of increased loose/watery stools, at least 3 times in 24 hours

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63
Q

How are acute, persistent and chronic diarrhoea defined?

A

Acute - 14 days or fewer
Persistent - 14-30 days
Chronic - >30 days

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64
Q

What is dysentery?

A

An infection of the GIT that leads to diarrhoea containing blood or mucus

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65
Q

What are the potential non-infective causes of diarrhoea?

A

Cancer and related treatments, chemical diarrhoea (poisoning, medication, sweeteners), IBD (Crohn’s, UC), IBS, malabsorption, endocrine causes (e.g. thyrotoxicosis)

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66
Q

Which common viruses cause watery diarrhoea?

A

Rotavirus, norovirus

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67
Q

Which parasites cause watery diarrhoea?

A

Giardia and cryptosporidium

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68
Q

What are the 6 pathogenic serotypes of E coli?

A
  1. ETEC (enterotoxigenic)
  2. EHEC (enterohaemorrhagic
  3. EIEC (enteroinvasive)
  4. EPEC (enteropathogenic)
  5. EAEC (enteroaggregative)
  6. DAEC (diffusely adherent)
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69
Q

What is the most common cause of traveller’s diarrhoea?

A

Enterotoxigenic E coli (ETEC)

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70
Q

What pathogen associated with canned meat can cause severe diarrhoea and vomiting?

A

Clostridium perfringens

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71
Q

What bacterium can cause a type of quick-onset self-limiting food poisoning as a result of food not being refrigerated?

A

Staph aureus

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72
Q

Persistent infective diarrhoea is more likely to be caused by which pathogens?

A

Parasites - Giardia, Cryptosporidium

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73
Q

Which invasive bacteria cause diarrhoea?

A 
CESSY
Campylobacter
E Coli (EIEC, STEC)
Salmonella enteritidis
Shigella dysenteriae
Yersinia (rare)
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74
Q

Which antibiotics have the biggest association with diarrhoea?

A

Cephalosporins (Cefuroxime, Cefalexin, Ceftriaxone)
Clindamycin
Co-amoxiclav
Ciprofloxacin

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75
Q

What pathogen causes significant diarrhoea in healthcare settings as a result of antibiotics killing off the natural protective bacteria in the gut?

A

Clostridioides (previously known as C diff)

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76
Q

What drug is used to treat clostridioides?

A

Vancomycin

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77
Q

What stool tests should be requested when investigating diarrhoea?

A 
Microscopy
Culture
Multi-pathogen molecular panels
Ova, cysts and parasites
Toxin detection
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78
Q

What blood tests should be requested when investigating diarrhoea?

A

Blood cultures
Inflammatory markers
Electrolytes and creatinine

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79
Q

What are the ‘red flags’ for diarrhoea patients?

A
  1. Dehydration
  2. Electrolyte imbalance
  3. Renal failure
  4. Immunocompromise
  5. Severe abdominal pain
  6. Cancer risk factors (over 50, chronic diarrhoea, weight loss, blood in stool, FH of cancer)
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80
Q

What are the two types of liver abscesses?

A
  1. Pyogenic (pus forming - bacterial)

2. Amoebic

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81
Q

How do liver abscesses present?

A

Fever, RUQ pain, nausea, vomiting, anorexia, weight loss, malaise

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82
Q

How are liver abscesses diagnosed?

A

Imaging - abdo CT/USS
Blood cultures
Aspirate and culture of abscess material

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83
Q

How are liver abscesses treated?

A

Drainage and antibiotics

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84
Q

Which pathogen increases the risk of gastritis and peptic ulcers?

A

Helicobacter pylori

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85
Q

What is the treatment for H pylori?

A

Omeprazole (or other PPI), clarithromycin and amoxicillin

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86
Q

How is H pylori diagnosed?

A

Stool antigen test
Breath test
Blood test for antibodies
Endoscopy for biopsy (biopsy urease test, histology)

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87
Q

Which pathogens cause enteric fever?

A 
Salmonella typhi (typhoid)
Salmonella paratyphi (paratyphoid)
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88
Q

How does enteric fever present?

A 
Generalised abdominal pain, fever and chills
Headache and myalgia
Relative bradycardia
Rose spots (rare)
Constipation/green diarrhoea
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89
Q

How is enteric fever diagnosed?

A

Blood/bone marrow cultures

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90
Q

What are the potential complications of enteric fever?

A

GI bleed, perforation/peritonitis, myocarditis, abscesses

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91
Q

What antibiotics can be used to treat enteric fever?

A

Azithromycin, ciprofloxacin, cephalosporins

Meropenem only as a last resort

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92
Q

What are the three types of GI obstruction?

A
  1. Intraluminal obstruction
  2. Intramural obstruction
  3. Extramural obstruction
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93
Q

Name three possible causes of intraluminal obstruction in the gut.

A
  1. Tumours - more common in the large bowel
  2. Diaphragm disease - a fibrous diaphragm forms in the gut lumen, leaving only a tiny hole for contents to move through
  3. Gallstone ileus - caused by massive gallstone forming a fistula so the gallstone ends up in the bowel (rare)
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94
Q

Name four possible causes of intramural obstruction in the gut.

A
  1. Crohn’s disease
  2. Diverticulitis
  3. Intramural tumours
  4. Hirschsprung’s disease
95
Q

What is diverticulitis?

A

Outpouchings of the bowel (diverticula) form - possibly due to pressure with low fibre diet pushing the mucosa through the holes in the muscle layers where the blood vessels are.

96
Q

What is a major possible complication of diverticulitis?

A

Rupture of diverticuli, which can result in faecal contents leaking into the peritoneal cavity, which leads to peritonitis.

97
Q

What is Hirschsprung’s disease?

A

A lack of ganglia in the wall of the bowel, leading to a lack of innervation, hence gut is unable to contract and the gut becomes dilated and distended.

98
Q

Name three possible causes of extramural obstruction in the gut

A
  1. Adhesions
  2. Volvulus
  3. Peritoneal deposits from tumours
99
Q

What causes adhesions in the gut?

A

Fibrous bands of tissue in the peritoneal cavity that draw loops of bowel together and cause obstruction. Often caused by abdominal surgery (inflammation).

100
Q

How are gut adhesions treated?

A

Adhesiolysis

101
Q

Why does volvulus only occur in the sigmoid colon?

A

Because it’s not fixed to the peritoneum by mesentery like the rest of the colon is

102
Q

What type of cancer can easily spread through the peritoneal cavity and why?

A

Ovarian carcinoma - the peritoneal cavity is a smooth, moist membrane with a blood supply, making a favourable environment for secondary cancers to grow.

103
Q

What condition that happens in the elderly and children results in ‘telescoping’ of a section of gut into another section of gut?

A

Intussusception

104
Q

Name four possible aetiologies of non-mechanical small bowel obstruction

A
  1. Paralytic ileus after abdominal surgery
  2. Localised intrabdominal abscess and generalised peritonitis
  3. Mesenteric thromboembolism
  4. Intestinal pseudo-obstruction
105
Q

Name two possible aetiologies of non-mechanical large bowel obstruction

A
  1. Retroperitoneal haematoma leading to chronic dilatation of the large bowel (Ogilvie’s syndrome)
  2. Idiopathic slow gut motility
106
Q

How can intestinal obstruction cause death?

A

Dilation caused by increased intraluminal pressure results in compression of blood vessels with oedema of the bowel wall, leading to bacterial colonisation, necrosis, perforation, peritonitis and haemodynamic compromise, resulting in death.

107
Q

What are the main features of bowel obstruction?

A

Abdominal pain
Nausea and vomiting
Constipation
Distension

108
Q

How does small bowel obstruction present?

A

Severe sudden onset with central, colicky pain, distension, constipation and vomiting straight away, which may contain bile.

109
Q

How does large bowel obstruction present?

A

Chronic lower abdominal colicky pain, vaguely localised. Possible delayed vomiting, absolute constipation (no gas or stool) followed by peripheral distension.

110
Q

What might you see on visual inspection of a patient with bowel obstruction?

A

Surgical scar
Distension (centrally in SBO, peripherally in LBO)
Visible peristalsis

111
Q

What might you feel on palpation of a patient with bowel obstruction?

A

An abdominal mass in the case of a tumour or strangulated bowel
Rigidity and rebound tenderness indicative of ischaemia and peritoneal irritation

112
Q

What might you notice on percussion of a patient with bowel obstruction?

A

Resonance

Tenderness on percussion indicative of peritonitis

113
Q

What might you notice on auscultation of a patient with bowel obstruction?

A

Metallic sounding clicks
Silence if the bowel is completely worn out
Borborygmi (very loud bowel sounds that don’t require a stethoscope)

114
Q

When performing a rectal examination, what might you notice in a patient with bowel obstruction?

A

Impacted faeces, rectal cancer, blood

115
Q

What might blood on rectal examination indicate in a patient with symptoms of bowel obstruction?

A

Mesenteric artery occlusion intussusception, volvulus

116
Q

What blood tests should be carried out on a patient admitted with bowel obstruction?

A
  • FBC
  • Serum electrolytes + U&Es
  • Arterial blood gas analysis
  • G&S in case patient needs to go to theatre
117
Q

What radiological examinations can be performed to help diagnose bowel obstruction?

A 
CT scan (preferred)
Abdominal x-ray
118
Q

What non-operative treatments can be given to manage dynamic bowel obstruction in stable patients with a partial obstruction only?

A
  1. GI decompression, NG tube insertion and aspiration
  2. IV fluids
  3. Antibiotics
  4. Gastrografin follow-through
119
Q

What types of invasive management can be used to treat bowel obstruction?

A
  1. Endoscopic decompression for volvulus

2. Surgery to treat the cause of bowel obstruction e.g. bowel resection/anastomosis/stoma formation

120
Q

How can paralytic ileus be managed?

A

IV fluids, NG decompression, electrolyte correction, endoscopic decompression, insertion of flatus tube, IV neostigmine, segmental resection and anastomosis/stoma, caecostomy/ileostomy

121
Q

What is Barrett’s oesophagus?

A

Metaplasia in the oesophagus causes some of the squamous epithelium to become glandular mucosa instead. Precursor to oesophageal cancer.

122
Q

Why would squamous epithelium in the oesophagus become glandular mucosa?

A

Acid reflux damages the squamous epithelium and it grows back as glandular epithelium with a mucin layer to protect the oesophagus from acid.

123
Q

What type of cancer can form in the oesophagus due to Barrett’s oesophagus?

A

Adenocarcinoma (carcinoma formed from glandular tissue)

124
Q

What is a late symptom of oesophageal cancer?

A

Dysphagia (caused by obstruction)

125
Q

What foods are potentially linked to gastric cancer?

A

Smoked foods and pickles

126
Q

What pathogen increases the risk of gastric cancer slightly?

A

Helicobacter pylori

127
Q

What is the natural history of gastric cancer?

A

Normal gastric mucosa undergoes intestinal metaplasia, then becomes dysplastic and can form an intramucosal carcinoma, which can then become invasive, particularly if growing out of the stomach.

128
Q

What are the greatest risk factors for colorectal cancer?

A
  • Adenomas
  • Age (1/3 of people over 60 have colorectal adenomas)
  • Hereditary conditions e.g. familial adenomatous polyposis (almost always causes colon cancer)
129
Q

What staging system is used for bowel cancer?

A

Duke’s staging - A/B/C/D - depending on invasion of bowel wall

130
Q

Why might aspirin help prevent colorectal cancer?

A

Because NSAIDs appear to reduce the frequency of adenomas

131
Q

Why does colorectal cancer have a higher survival rate than oesophageal and gastric cancer?

A

Detected earlier because:

  1. Symptoms of constipation, diarrhoea, rectal bleeding more likely to be reported and investigated than e.g. indigestion and heartburn
  2. Colorectal cancer screening for over 60s leads to more early cancers being detected.
132
Q

What is diarrhoea?

A

A change in frequency and consistency of stools

133
Q

Give 6 non-infective causes of diarrhoea

A
  1. Neoplasm
  2. Inflammatory
  3. Irritable bowel
  4. Hormonal
  5. Anatomical (e.g. abnormality that prevents bowel from being cleared properly)
  6. Chemical (e.g. toxins)
134
Q

What is a marker for inflammation of the bowel?

A

Faecal calprotectin

135
Q

Which organisms cause bloody diarrhoea?

A 
Campylobacter
Some strains of E coli
Shigella
Salmonella
Yersinia
136
Q

Which organisms cause non-bloody diarrhoea?

A

Clostridium, viruses (e.g. rotavirus, norovirus)

137
Q

How long does it take for bacterial-mediated infection to cause diarrhoea symptoms?

138
Q

Which gram negative organism produces a toxin that causes profuse watery diarrhoea and is common in places such as refugee camps?

A

Vibrio cholerae

139
Q

What parasite infects animals, causes diarrhoea and can’t be killed by chlorine?

A

Cryptosporidium

140
Q

Why is E coli UTI sometimes difficult to eradicate?

A

Because some E coli bacilli have tails and hooks for hooking onto mucosa

141
Q

Why does norovirus spread so quickly?

A

Aerosolised vomit has great infective power

142
Q

Why should you always wash your hands after coming into contact with a patient who has C diff diarrhoea?

A

C difficile produces spores that are highly resistant to chemicals and cannot be killed by hand gel.

143
Q

How would you manage a patient with symptomatic clostridium difficile?

A
  • Isolate patient
  • Test stool samples
  • Environmental cleaning
  • Treat with metronidazole or vancomycin
144
Q

Are HIV, bird flu and vCJD notifiable diseases?

145
Q

What sorts of diseases are notifiable?

A
  • Diseases that are normally vaccinated against as these tend to be highly transmissible
  • Diseases that need specific control measures e.g. acute infectious hepatitis, scarlet fever, TB
  • Scary stuff that isn’t endemic to UK e.g. anthrax, cholera, plague, rabies, SARS, smallpox, yellow fever
  • Some really serious diseases e.g. brucellosis, HUS (haemolytic uraemic syndrome), legionnaires disease
146
Q

What are the symptoms of acute hepatitis?

A

Non-specific symptoms e.g. malaise, lethargy, myalgia
GI upset, abdominal pain
Possibly jaundice, pale stools and dark urine

147
Q

What are the signs of acute hepatitis?

A

Tender hepatomegaly +/- jaundice

Signs of fulminant hepatitis (acute liver failure) e.g. bleeding, ascites, encephalopathy

148
Q

What would LFTs in a patient with acute hepatitis normally show?

A 
Raised transaminases (AST/ALT >> GGT/ALP)
\+/- raised bilirubin
149
Q

What are the possible viral causes of acute hepatitis?

A

Hepatitis A B+/-D C and E
Herpes, Varicella, Cytomegalovirus, Epstein-Barr
Covid-19

150
Q

What are the possible non-viral causes of acute hepatitis?

A

Spirochaetes, mycobacteria, bacteria, parasites

151
Q

What are the possible non-infective causes of acute hepatitis?

A

Drugs, alcohol, toxins/poisoning, pregnancy, non-alcoholic liver disease

152
Q

What are the signs and symptoms of chronic hepatitis?

A

May have no symptoms or only non-specific symptoms
May have signs of chronic liver disease e.g. spider naevi, palmar erythema, clubbing, Dupuytren’s contracture
If decompensated, may have jaundice, ascites, bacterial peritonitis, encephalopathy, varices…

153
Q

What would blood results in a patient with chronic hepatitis show?

A

Transaminases (ALT/AST) can be normal
If compensated, all LFTs can be normal
If decompensated, increased platelets and INR, increased bilirubin, low albumin.

154
Q

Which viruses cause chronic hepatitis?

A

Hepatitis B+/-D, C and E

155
Q

Which individuals are at risk of hepatitis A in developing countries?

A

Travellers, MSM, IVDU

156
Q

How is hepatitis A managed?

A

Supportive management - condition is self-limiting and rarely causes acute liver failure
Monitor liver function just in case (INR, albumin, bilirubin etc), management of close contacts

157
Q

Which of the 4 genotypes of hepatitis E is found in high income countries?

A

G3, which is found in undercooked pork products

158
Q

How is hepatitis E transmitted?

A

Faeco-oral transmission

159
Q

Which patients are at risk of chronic infection with hepatitis E?

A

Immunosuppressed patients e.g. transplant, HIV

160
Q

How is hepatitis E managed?

A

Supportive management only for most patients (usually self-limiting). Monitor for liver failure - transplant may be required in some cases.

161
Q

How can hepatitis E be prevented?

A

Avoid eating undercooked meats (especially if immunocompromised)
Screening of blood donors
Vaccines (in development)

162
Q

How is chronic hepatitis E infection managed?

A

If HEV RNA is present beyond 6 months, reverse immunosuppression if possible, treat with ribavirin as first line treatment, second line treatment PEGylated interferon-alpha

163
Q

Why are babies and at risk mothers vaccinated against hepatitis B?

A

Neonates and infants find it more difficult to clear hepatitis B as the immune system is not yet fully developed. Whilst chronic hep B is rare in immunocompetent adults, 90% of infected babies will develop it.

164
Q

What is the marker for current hepatitis B infection?

A

Hep B surface antigen

165
Q

How is acute hepatitis B managed?

A

Supportive management and monitor liver function - do not use interferon!
Most patients will clear the virus within 6 months

166
Q

What do the NICE guidelines recommend as first line treatment for chronic hepatitis B?

A

Pegasys (PEGylated interferon alpha 2a)

167
Q

What are the risks of Pegasys treatment?

A

Thyroid disease, type 1 diabetes, lowered white cell count

168
Q

How is hepatitis D transmitted?

A

Via blood and bodily fluids - mainly blood products, iatrogenic causes and IVDU

169
Q

How would you test for hepatitis D?

A

Check for hep D antibody first; if positive, test for HDV RNA

170
Q

How is hepatitis D treated?

A

Pegasys (PEGylated interferon alpha) for 48 weeks

171
Q

Which type of hepatitis virus will normally progress to chronic infection?

A

Hepatitis C

172
Q

What is the greatest risk factor for hepatitis C in the UK?

A

IV drug use

173
Q

Name some of the fancy new drugs that can be used to treat hepatitis C

A

NS3/4A inhibitors: glecaprevir/grazoprevir
NS5A inhibitors: pibrentasvir/elbasvir

Maviret contains glecaprevir and pibrentasvir
Zepatier contains elbasvir and grazoprevir

174
Q

What causes gastritis/stomach ulceration?

A

Destruction of the neutral mucin layer (e.g. due to ischaemia) in the stomach, which results in stomach epithelium being exposed to low pH and cells are killed by the stomach acid.

175
Q

Why is gastric mucosal ischaemia common in patients in cardiovascular shock?

A

The body sends the blood to more ‘important’ organs, rather than the stomach.

176
Q

How can NSAIDs cause gastritis?

A

NSAIDs are not dissolved by the time they get to the stomach and sit on the mucosa, exhibiting a locally corrosive effect due to inhibition of COX2.

177
Q

Name 5 causes of gastritis.

A
  1. H pylori infection
  2. NSAIDs
  3. Stress
  4. Strong alcohol
  5. Anatomical abnormalities that allow bile reflux into the stomach (corrosive)
178
Q

What can happen in cases of chronic H pylori infection?

A

Intestinal metaplasia occurs (intestinal epithelium is more resistant to the effects of H pylori)

179
Q

What is the treatment for H pylori?

A

Metronidazole for 1 week

180
Q

What can eventually happen in cases of severe gastric ulceration?

A

The ulcer grows, eventually hits a blood vessel and can cause torrential haemorrhage and subsequent haemodynamic shock.

181
Q

How does malabsorption present?

A

Change in bowel habits
Weight loss
Iron deficiency anaemia

182
Q

Why are there lymphocytes on top of the small bowel epithelium?

A

To protect the epithelium as food is foreign material

183
Q

Give 5 causes of malabsorption

A
  1. Insufficient intake
  2. Defective intraluminal digestion
  3. Insufficient absorptive area
  4. Lack of digestive enzymes
  5. Defective epithelial transport
184
Q

Give 4 possible causes of defect intraluminal digestion

A
  1. Pancreatic insufficiency (e.g. pancreatitis, CF)
  2. Biliary obstruction (resulting in defective bile secretion, fats can’t be emulsified, therefore can’t be absorbed)
  3. Ileal resection (decreased bile salt uptake)
  4. Bacterial overgrowth (can block intraluminal digestion)
185
Q

What antibodies are produced by coeliac patients?

A

Gliadin antibodies

186
Q

Which parasite (usually acquired by drinking contaminated water) blocks absorption of nutrients?

A

Giardia lamblia

187
Q

What procedure, sometimes carried out for morbid obesity, Crohn’s disease or infarcted small bowel, can result in malabsorption?

A

Small intestinal resection/bypass

188
Q

What are the two types of idiopathic inflammatory bowel disease?

A

Crohn’s disease

Ulcerative colitis

189
Q

What kind of appearance can sometimes be seen in severe cases of chronic Crohn’s disease?

A

Cobblestoning

190
Q

Describe the endoscopic appearances of Crohn’s disease

A

Patchy inflammation with little white ulcers appearing anywhere along the GI tract (from mouth to anus). Inflammation may contain granulomas.

191
Q

What complications can occur as a result of Crohn’s disease?

A

Malabsorption (due to inflammation or surgical resections)
Bowel obstruction due to fibrosis and scarring
Perforation and subsequent peritonitis
Fistula formation
Anal skin tags/fissures/fistulas

Amyloid protein (systemic complication)

192
Q

What part of the GI tract is affected by ulcerative colitis?

A

The colon mucosa only - extends continuously from the rectum but will not go any further than the caecum. Inflammation doesn’t go any deeper than mucosa - no perforation or granulomas.

193
Q

What organs besides the colon can be affected by ulcerative colitis?

A

Liver, joints, eyes and skin

194
Q

What are functional GI disorders?

A 
A group of disorders classified by GI symptoms related to any of the following:
Visceral hypersensitivity
Motility disturbances
Altered mucosal and immune function
Altered CNS processing
Altered gut microbiota
195
Q

Why do some patients with functional GI disorders have mood disorders too?

A

Because gut-brain interaction runs both ways

196
Q

Why are women more affected by functional GI disorders than men?

A

Because of hormonal influence - may also explain, at least partially, why functional GI disorders are more common in young adults

197
Q

What are the features of IBS?

A

Chronic frequent abdominal pain
Altered bowel habit (diarrhoea/constipation/both)
Bloating

198
Q

Why should abdominal bloating always be investigated in women >45?

A

It could be a sign of uterine/ovarian/endometrial cancer

199
Q

Name 3 organic conditions that mimic IBS

A
  1. Coeliac disease
  2. Colon cancer
  3. Inflammatory bowel disease
200
Q

Why should everyone with IBS have a test for coeliac disease?

A

Coeliac disease is more common in IBS patients

201
Q

Name two common functional GI disorders

A
  1. Functional dyspepsia

2. Irritable bowel syndrome

202
Q

What are the ‘alarm features’ that would prompt endoscopic investigation of a patient with GI symptoms?

A 
Age >45 years at onset
Short history of symptoms
Documented unintentional weight loss
Nocturnal symptoms
Family history of GI cancer
GI bleeding
Palpable abdominal mass/lymphadenopathy
Evidence of iron deficiency anaemia on blood testing
Evidence of inflammation on blood/stool testing
203
Q

What are the first line investigations for a patient with chronic lower GI symptoms?

A

FBC, CRP, coeliac serology, faecal calprotectin, stool MC&S

204
Q

What is stool faecal calprotectin?

A

A degradation product from neutrophils, which serves as a marker for inflammation.

205
Q

What do you do with faecal calprotectin results?

A

FC is normal in IBS but present in IBD
If <50, negligible chance of IBD
If 50-150, repeat in one month
If >150, refer to gastro

206
Q

What is post infectious IBS?

A

Lingering GI symptoms following a bout of gastroenteritis - occurs in about 1 in 10 patients and more common in those with adverse life events or history of depression/anxiety.

207
Q

What drug can sometimes be prescribed for functional GI disorders to help dampen brain-gut connection?

A

Amitriptyline

208
Q

What are the functions of the peritoneum in health?

A
  1. Visceral lubrication

2. Fluid and particulate absorption

209
Q

What are the functions of the peritoneum in disease?

A
  1. Pain perception
  2. Inflammatory and immune responses
  3. Fibrinolytic activity
210
Q

What is peritonitis?

A

Inflammation of the peritoneum

211
Q

How is peritonitis classified

A

By onset (acute/chronic) and source of origin (primary/secondary)

212
Q

What causes peritonitis?

A
  • Bacteria
  • Chemicals
  • Trauma
  • Ischaemia
  • Miscellaneous causes e.g. familial Mediterranean fever
213
Q

What conditions can cause peritonitis due to GI perforation?

A

Perforated ulcer/appendix/diverticulum

214
Q

What conditions can cause peritonitis via transmural translocation?

A

Pancreatitis, ischaemic bowel, primary bacterial peritonitis

215
Q

What other possible routes for peritoneal infection are there apart from perforation and transmural translocation?

A 
Exogenous contamination (e.g. drains, open surgery, trauma, peritoneal dialysis)
Female genital tract infection, e.g. pelvic inflammatory disease
Haematogenous spread (rare) e.g. septicaemia
216
Q

What GI microorganisms can cause peritonitis?

A
  • E coli
  • Streptococci
  • Enterococci
  • Bacterioides
  • Clostridium
  • Klebsiella pneumoniae
217
Q

What are the clinical features of localised peritonitis?

A
  • Signs and symptoms of underlying condition
  • Pain
  • Nausea and vomiting
  • Fever
  • Tachycardia
  • Localised guarding
  • Rebound tenderness
  • Shoulder tip pain
  • Tender rectal and/or vaginal examination
218
Q

What are the early clinical features of diffuse (generalised) peritonitis?

A
  • Abdominal pain made worse by breathing/moving
  • Generalised guarding
  • Infrequent bowel sounds, which may stop altogether (paralytic ileus)
  • Fever
  • Tachycardia
219
Q

What are the late clinical features of diffuse (generalised) peritonitis?

A
  • Generalised rigidity
  • Distension
  • Absent bowel sounds
  • Circulatory failure
  • Thready, irregular pulse
  • Hippocratic face
  • Loss of consciousness
220
Q

What investigations are carried out for peritonitis?

A
  • Urine dipstick to check for UTI
  • ECG if in doubt as to cause of abdominal pain
    Bloods: U&E, FBC, serum amylase, group and save
221
Q

How is peritonitis managed conservatively?

A
  • Correction of fluid loss and circulating volume
  • Urinary catheterisation +/- gastrointestinal decompression
  • Antibiotics
  • Analgesia
222
Q

How is peritonitis managed surgically?

A

Depending on cause
- Remove/divert cause e.g. repair perforated ulcer, excise perforated organ
+/- drainage
- Peritoneal lavage

223
Q

Name 5 special forms of peritonitis

A
  1. Bile peritonitis
  2. Spontaneous bacterial peritonitis
  3. Primary pneumococcal peritonitis
  4. Tuberculous peritonitis
  5. Familial Mediterranean fever (periodic peritonitis)
224
Q

What is ascites?

A

An accumulation of excess serous fluid within the peritoneal fluid

225
Q

How much fluid should a healthy adult have in the peritoneal cavity?

A

Men - no fluid

Women - up to 20ml

226
Q

How is ascites classified?

A

Classified into 4 stages:
Stage 1: Detectable only after careful examination/USS
Stage 2: Easily detectable but relatively small volume
Stage 3: Obvious, but not tense ascites
Stage 4. Tense ascites

227
Q

What is tense ascites?

A

When the abdomen becomes distended and painful

228
Q

How do we check whether ascites is transudative or exudative?

A

Measuring protein concentration. <25g/l = transudative, >25g/l = exudative

229
Q

What are the causes of transudative ascites?

A
  • Low plasma protein concentrations due to malnutrition, nephrotic syndrome, protein-loss enteropathy
  • High central venous pressure due to congestive cardiac failure
  • Portal hypertension due to portal vein thrombosis/cirrhosis
230
Q

What are the causes of exudative ascites?

A
  • Peritoneal malignancy
  • Tuberculous peritonitis
  • Budd-Chiari syndrome
  • Pancreatic ascites
231
Q

What accounts for 75% of ascites cases?

A

Liver cirrhosis

232
Q

How does ascites present?

A
  • Abdominal distension
  • Nausea, loss of appetite
  • Constipation
  • Cachexia (wasting syndrome)
  • Pain/discomfort in case of malignant causes
  • Other symptoms associated with underlying cause e.g. jaundice
233
Q

How is ascites investigated?

A
  • Investigate underlying cause (e.g. LFTs, cardiac function)
  • Imaging (x-ray if at least 500ml, USS if 200-500ml, CT abdomen if smaller amount)
  • Ascitic aspiration under imaging guidance
  • Fluid for microscopy, cytology, culture, analysis of protein content and amylase
234
Q

How is ascites treated?

A
  • Treatment of specific cause e.g. TIPS procedure
  • Sodium restriction
  • Diuretics
  • Paracentesis (up to 4-6l/day with colloid replacement)
  • Indwelling drain (for home paracentesis, useful for smaller volumes)

Phase 2a Medicine (13 decks)

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