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PHASE 2A (Mine) > GI/ LIVER > Flashcards

GI/ LIVER Flashcards

1
Q

What is GORD?

A

Gastro-oesophageal reflux disease–> Where acid from the stomach refluxes through the lower oesophageal sphincter, irritating the lining of the oesophagus.

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2
Q

What epithelium lines the oesophagus?

A

Squamous epithelium, making it more sensitive to the effects of stomach acid.

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3
Q

What epithelium does the stomach have?

A

Columnar epithelium, protecting it against stomach acid.

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4
Q

What is dyspepsia?

A

Indigestion–> Feeling of burning, pain or discomfort in the digestive tract

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5
Q

What are the symptoms of GORD?

A 
Dyspepsia:
Heart burn
Acid regurgitation
Retrosternal/ epigastric pain
Bloating
Nocturnal cough
Hoarse voice
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6
Q

What is endoscopy used for and when might it be used in GORD?

A

Patients with evidence of GI bleed or other concerning features would be reffered.
Assesses for peptic ulcers and oesophageal or gastric malignancies.

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7
Q

What are the key red flags that would make you suspicious of cancer and therefore need a 2 week endoscopy referral?

A 
Dysphagia
Over 55
Weight loss
Upper abdominal pain/ reflux
Treatment resistant dyspepsia
Nausea/ vomiting
Low haemoglobin/ raised platelets
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8
Q

What lifestyle advice would be given to patients with GORD?

A 
Reduce tea, coffee and alcohol
Weight loss
Avoid smoking
Smaller, lighter meals
Avoid heavy meals before bed
Stay upright after meals
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9
Q

What medication can be given to manage GORD?

A

Acid neutralising medicine-> Gaviscon/ Rennie
Proton pump inhibitors (reduce acid secretion)–> Omeprazole/ Lansoprazole
Ranitidine

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10
Q

What is Ranitidine and its action?

A

Medicine used as an alternative to PPIs to treat GORD. H2 receptor antagonist which reduces stomach acid.

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11
Q

What is the surgery that can be used to treat GORD called?

A

Laparoscopic fundoplication–> Ties the fundus of the stomach around the lower oesophagus to lower the sphincter.

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12
Q

What stomach bacteria test is offered to anyone with dyspepsia and what kind of bacteria is it?

A

Helicobacter pylori

Gram negative aerobic bacteria

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13
Q

How does H. pylori avoid the acidic environment in the stomach?

A

Forces its way into the gastric mucosa

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14
Q

How does H. pylori cause damage?

A

Causes breaks in the mucosa, exposing the epithelial cells underneath to acid and causing gastritis, ulcers and increased risk of stomach cancer.

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15
Q

What does H. pylori produce to neutralise stomach acid and how does this cause damage?

A

Ammonia which directly damages epithelial cells.

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16
Q

What tests can be used to look for H. pylori?

A

Urea breath test
Stool antigen test
Rapid urease test

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17
Q

What is a rapid urease test?

A

Small biopsy taken of the stomach mucosa during endoscopy. Urea is added to the sample and if H. pylori is present, they produce enzymes that convert the urea to ammonia.

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18
Q

How is H. pylori eradicated?

A

Triple therapy: Proton pump inhibitor + 2 antibiotics for 7 days

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19
Q

What is Barretts oesophagus?

A

When the oesophagus epithelium changes from squamous to columnar due to constant acid reflux. (metaplasia).

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20
Q

Why do patients with Barrets oesophagus have to be monitored with regular endoscopy?

A

It is premalignant and increases the risk of adenocarcinoma development.

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21
Q

How can Barretts oesophagus be treated?

A

Proton pump inhibitors, ablation treatment during endoscopy.

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22
Q

Where do peptic ulcers most commonly form?

A

Duodenum (and stomach)

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23
Q

Why do ulcers form?

A

When there is a breakdown in the protective layer of the stomach or duodenum and an increase in stomach acid.

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24
Q

What makes up the protective layer of the stomach and how can it be broken down?

A

Mucus and bicarbonate

Can be broken down by medications (Steroids or NSAIDs) or H. Pylori

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25
Q

What can cause an increase in stomach acid?

A 
Stress
Alcohol
Caffeine
Smoking
Spicy foods
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26
Q

What are the key presentations of a peptic ulcer?

A 
Epigastric discomfort or pain
Nausea and vomiting
Dyspepsia
Bleeding--> causes haematemesis, 'coffee gound' vomiting and melaena
Iron deficiency anaemia
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27
Q

How might you tell the difference between a gastric and duodenal ulcer in terms of their presentation?

A

Eating worsens pain of gastric ulcers and improves pain of duodenal ulcers.

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28
Q

What is haematemesis?

A

Vomiting blood

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29
Q

How are peptic ulcers diagnosed?

A

Endoscopy
(Rapid urease/ CLO test can be performed to check for H. Pylori)
*Biopsy should be considered to exclude malignancy.

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30
Q

How are peptic ulcers treated?

A

Same as GORD–> usually with high dose proton pump inhibitors.

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31
Q

What complications can peptic ulcers cause?

A
  • Bleeding from ulcer (common and potentially life threatening)
  • Perforation resulting in acute abdomen and peritonitis.
  • Scarring and strictures of the muscle and mucosa, leading to pyloric stenosis.
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32
Q

What is pyloric stenosis and how does it present?

A

Narrowing of the pylorus (stomach exit), leading to difficulty in emptying stomach contents. Presents with upper abdominal pain, distention, nausea and vomiting.

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33
Q

What are the causes of an upper GI bleed?

A
  • Oesophageal varices (enlarged veins)
  • Mallory-Weiss tear (tear of mucous membrane)
  • Peptic ulcers
  • Stomach/ duodenal cancers
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34
Q

How do upper GI bleeds present?

A
  • Haematemesis
  • ‘Coffee ground’ vomit
  • Melaena
  • Haemodynamic instability causes large blood loss, causing low blood pressure, tachycardia and other signs of shock
  • Symptoms of underlying pathology–> e.g. epigastric pain/ dyspepsia in peptic uclers
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35
Q

What causes ‘coffee ground’ vomit?

A

Vomiting digested blood that looks like coffee grounds

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36
Q

What is melaena?

A

Tar like, black greasy stool caused by digested blood.

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37
Q

What is the Glasgow-Blatchford score?

A

Scoring system in suspected upper GI bleed that scores patients based on their clinical presentation. >0 indicates high risk for upper GI bleed

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38
Q

What features are taken into account in the Glasgow-Blatchford score that indicate an upper GI bleed?

A
  • Drop in Hb
  • Rise in urea
  • Blood pressure
  • Heart rate
  • Melaena
  • Syncopy
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39
Q

Why do urea levels rise in upper GI bleeds?

A

Blood in the GI tract gets broken down by the acid and digestive enzymes, releasing urea which is then absorbed in the intestines.

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40
Q

What is the Rockall score?

A

Used for patients that have had an endoscopy to calculate their risk of rebleeding and overall mortality.

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41
Q

How is an upper GI bleed managed?

A 
ABATED:
ABCDE approach to immediate resuscitation
Bloods
Access (cannula)
Transfuse
Endoscopy
Drugs (stop anticoagulants and NSAIDs)
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42
Q

What is looked for in the bloods taken for a suspected GI bleed?

A 
Haemoglobin (FBC)
Urea (U&E's)
Coagulation (INR. FBC for platelets)
Liver diease (LFTs)
Crossmatch
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43
Q

What are the two main types of inflammatory bowel disease?

A

Ulcerative colitis and Crohn’s disease

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44
Q

What are common of both crohn’s and ulcerative colitis?

A

Both involve inflammation of the walls of the GI tract and have periods of remission and exacerbation

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45
Q

What makes Crohn’s different to Ulcerative colitis? (NESTS)

A

No blood or mucus
Entire GI tract
Skip lesions (patchy inflammation)
Terminal ileum most affected and Transmural (full thickness) inflammation
Smoking is a risk factor
Also associated with weight loss, strictures and fistulas

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46
Q

What makes Ulcerative Colitis different to Crohn’s?

A 
Continuous inflammation
Limited to colon and rectum
Only superficial mucosa affected
Smoking is protective
Excrete blood and mucus
Use aminosalicylates to treat
Primary sclerosing cholangitis
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47
Q

What are the main presentations of inflammatory bowel disease?

A

Diarrhoea
Abdominal pain
Passing blood
Weight loss

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48
Q

How is inflammatory bowel disease tested for?

A
  • Endsocopy with biopsy–> Diagnostic.
  • Routine bloods for anaemia, infection, thryoid, kidney and liver function
  • CRP indicates inflammation and active disease
  • Faecal calprotectin
  • Imaging to look to complications
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49
Q

What is Faecal calprotectin ?

A

Useful screening test for IBD—> Protein released by intestines when they are inflamed

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50
Q

What is the first line treatment for inducing remission in Crohn’s? What can be added if these don’t work alone

A

Steroids (e.g. oral prednisolone or IV hydrocortisone)

Can add immunosuppressant

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51
Q

What are the first line medications offered to Crohn’s patients to maintain remission?

A

Azathioprine

Mercaptopurine

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52
Q

When can surgery be offered to those with Crohn’s?

A

When the disease only affects the distal ileum, it is possible to surgically resect it and prevent further flares.
Can be used to treat secondary strictures and fistulas.

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53
Q

How is mild-moderate Ulcerative colitis treated to induce remission?

A

First line: Aminosalicylate

Second line: Corticosteroids

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54
Q

How is severe ulcerative colitis treated to induce remission?

A

First line: IV corticosteroids

Second line: IV ciclosporin

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55
Q

How can the disease be removed in ulcerative colitis?

A

Panproctocolectomy–> Removing colon and rectum will remove the disease.

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56
Q

What are the two outcomes of surgery used to treat ulcerative colitis?

A

Permanent ileostomy or ileo-anal anastomosis (J-pouch)

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57
Q

What is a J-pouch?

A

When the colon and rectum are removed and the ileum is folded back in itself and fashioned into a larger pouch that functions like a rectum. It is attached to the anus and collects stools.

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58
Q

What is Colostomy Surgery?

A

Part of the colon is removed, and a stoma is created- stoma is when part of the intestine is pulled through the abdominal wall to create an opening through which stool leaves the body.

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59
Q

What is IBS?

A

Functional bowel disorder- no identifiable organic disease underlying the gut symptoms.

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60
Q

How much of the population has IBS and who are more affectesd?

A

Up to 20% of population.

More common in women and young people.

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61
Q

What are the main symptoms of IBS?

A 
Diarrhoea
Constipation
Fluctuating bowel habits
Abdominal pain
Bloating 
(Worse after eating, improved by opening bowels)
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62
Q

What is the criteria for diagnosis of IBS?

A

Diagnosis of exclusion:

  • Normal FBC, EST, CRP blood tests
  • Negative faecal calprotectin
  • Negative coeliac disease serology
  • Cancer excluded/ not suspected
  • Symptoms that suggest IBS
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63
Q

What is the firstline management of IBS?

A

Lifestyle advice:

  • Adequate fluid intake
  • Regular small meals
  • Limit processed foods, caffeine and alcohol
  • Low FODMAP diet
  • Trial of probiotic
  • CBT
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64
Q

What is are the medication treatment options for IBS?

A 
First line: 
-Loperamide for diarrheoa
-Laxatives for constipation
-Antispasmodics for cramps
Second line:
- Tricyclic antidepressants
Third line:
-SSRIs antidepressants
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65
Q

What is coeliac disease?

A

Autoimmune condition where exposure to gluten causes an autoimmune reaction that causes inflammation in the small bowel.

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66
Q

When does coeliac disease usually develop?

A

In early childhood (but can at any age)

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67
Q

What are the two auto-antibodies involved in coeliac disease?

A
  • Anti-tissue transglutaminase (anti-TTG)

- Anti-endomysial (anti-EMA)

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68
Q

What happens on exposure to gluten in coeliac disease?

A

Auto-antibodies are created that target the epithelial cells of the intestine and lead to inflammation.

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69
Q

Where does inflammation caused by coeliac disease particularly affect and what does it cause?

A

Affects small bowel- especially jejunum

Causes atrophy of intestinal villi which causes malabsorption of nutrients and the symptoms of disease

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70
Q

How does coeliac disease present?

A

Often asymptomatic

  • Failure to thrive in children
  • Diarrhoea
  • Fatigue
  • Weight loss
  • Mouth ulcers
  • Anaemia (secondary to iron, B12 or folate deficiency)
  • Dermatitis herpetiformis (Skin rash)
  • Occasional neurological symptoms
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71
Q

What are the genetic associations with coeliac disease?

A

HLA-DQ2 (90%)

HLA-DQ8 gene

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72
Q

How is coeliac disease tested?

A
  • Investigations must be carried out whilst the patient is on a diet the contains gluten.
  • Check IgA levels to exclude IgA deficiency.
  • Antibody tests: Raised anti-TGG and anti endomysial antibodies
  • Endoscopy and intestinal biopsy–> Show crypt hypertrophy and villous atrophy.
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73
Q

What other conditions is coeliac disease associated with?

A 
Type 1 diabetes
Thyroid disease
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
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74
Q

What are the complications of untreated coeliac disease?

A 
Vitamin deficiency
Anaemia
Osteoporosis
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma of intestine
Non-Hodgkin lymphoma
Small bowel adenocarcinoma
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75
Q

What is the treatment of coeliac disease?

A

Lifelong gluten-free diet

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76
Q

What is a Mallory-Weiss tear and what usually causes it?

A

Linear mucosal tear at the oesophagastric junction that causes an upper GI bleed. Caused by a sudden increase in intra-abdominal pressure (e.g. coughing, retching, dry-heaves)

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77
Q

What cells does the mucose of the upper two thirds of the stomach contain?

A

Parietal cells
Chief cells
Enterochromaffin-like cells (ECL)

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78
Q

What do parietal cells secrete?

A

HCl

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79
Q

What do Chief cells secrete and what does this initiate?

A

Pepsinogen which initiates proteolysis

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80
Q

What do ECL cells release and what does this stimulate?

A

Histamine- stimulates acid release

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81
Q

What cells does the antral contain and what do they secrete?

A

Mucus secreting cells–> Release mucin and bicarbonate
G cells–> Secrete gastrin (stimulate acid release)
D cells–> Secrete somatostatin (suppresses acid secretion)

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82
Q

What is achalasia?

A

Failure of the LES to relax/ open during swallowing.

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83
Q

How does achalasia present?

A

Intermittent dysphagia (of both solids and liquids)
Regurgitation of food
Substernal cramps

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84
Q

What is scleroderma?

A

Systemic sclerosis–> a chronic autoimmune disease that causes hardening of connective tissue.

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85
Q

How does scleroderma affect the GI tract?

A

Diminished peristalsis and oesophageal clearance due to replacement of smooth muscle by fibrous tissue.
Causes GORD.

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86
Q

What is the definition of diarrhoea?

A

Loose/ liquid stools more than 3 times daily

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87
Q

What is acute diarrhoea?

A

Diarrhoea lasting < 14 days

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88
Q

What is persistent diarrhoea?

A

Diarrhoea lasting 14-30 days

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89
Q

What is chronic diarrhoea?

A

Diarrhoea lasting >14 days

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90
Q

What are the main non-infective causes of diarrhoea?

A 
Cancer
IBD
IBS
Hormonal
Radiation
Chemical (antibiotics)
Anatomical
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91
Q

What are the main infective causes of diarrhoea?

A

Viral
Bacteria
Parasites

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92
Q

What antibiotics can give rise to diarrhoea?

A

Climpamycin, Ciprofloxacin, Co-amoxiclav, Cephalosporins can all give rise to C.Diff

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93
Q

What are the main viral causes of diarrhoea?

A

Rotavirus, Norovirus

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94
Q

What are the main bacterial causes of diarrhoea?

A

Campylobacter, Shigellla, Salmonella, S.aureus, B.cereus, E.coli, C.Diff, Cholera

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95
Q

What are the main parasitic causes of diarrhoea?

A

Giardia, crypto.

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96
Q

What causes watery diarrhoea?

A

Non-inflammatory causes (enterotoxins or superficial adherence/ invasion)

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97
Q

What causes bloody/ mucoid diarrhoea?

A

Inflammatory causes (invasion/ cytotoxins)

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98
Q

What is gastroenteritis?

A

Inflammation all the way from the stomach to the intestines that presents with nausea, vomiting and diarrhoea

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99
Q

What is dysentery?

A

Infectious gastroenteritis with bloody diarrhoea

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100
Q

What is norovirus and how long does it last?

A

Single-stranded RNA virus. Lasts 24-72 hours.

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101
Q

What is rotavirus and how long does it last?

A

Double stranded RNA virus. Lasts 3-8 days.

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102
Q

What is E.coli and what does it produce that causes diarrhoea?

A

Gram -ve bacteria that produces Shiga toxin.

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103
Q

What does Shiga toxin do?

A

Causes abdominal cramps, bloody diarrhoea and vomiting. Also destroys blood cells which leads to haemolytic uraemic syndrome.

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104
Q

What is campylobacter and what causes it?

A

Gram negative bacteria- main cause of travellers diarrhoea. Caused by raw/ improperly cooked poultry, untreated water and unpasteurised milk.

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105
Q

What is shigella and how is it spread?

A

Bacteria spread by faeces contaminated water, pools and food.

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106
Q

What is salmonella and how is it spread?

A

Bacteria spread by raw eggs, poultry or food contaminated with infected faeces of small animals.

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107
Q

What is Bacillus Cereus and how is it spread?

A

Gram positive bacteria spread through inappropriately cooked foods. Common on food not refrigerated immediately (e.g. rice)

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108
Q

After how long does Bacillus Cereus cause symptoms and how long does it last?

A

Cramping and vomiting within 5 hours of ingestion.
Watery diarrhoea after 8 hours when it reaches the intestines.
Resolves within 24 hours.

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109
Q

What is Yersinia Enterocolitica and how is it spread?

A

Gram -ve bacillus spread by raw/ undercooked pork, and contamintation with the urine/ faeces of other mammals/

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110
Q

How long is Yersinia Enterocolitica incubation and how long does it last?

A

incubation is 4-7 days.

Can last 3 weeks or more.

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111
Q

How does Staph. Aureus cause infection?

A

Produces enterotoxins when growing on food. that cause enteritis.

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112
Q

What is giardia lamblia and how does it spread?

A

Microscopic parasite that lives in intestines of mammales and releases cysts in their stools. These can then contaminate food or water.

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113
Q

What does the pancreas consist of?

A

Exocrine (98%) and Endocrine cells

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114
Q

What is the function of the exocrine pancreas?

A

Secretion of digestive enzymes, ions and water into the duodenum.

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115
Q

What is the functional unit of the exocrine pancreas?

A

Acinus and its draining ductule

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116
Q

Where does the pancreatic duct enter the duodenum?

A

Joins to the common bile duct to enter at the ampulla of Vater.

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117
Q

What digestive enzymes do acinar cells produce?

A

Amylase, lipase, colipase, phospholipase, proteases

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118
Q

What is the action of the endocrine pancreas?

A

Release hormones into blood to control blood glucose levels

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119
Q

What cells does the endocrine pancreas contain and what do they secrete?

A 
Alpha cells- glucagon
Beta cells - insulin
Delta cells- somatostatin
Pancreatic polypeptide cells
Enterochrommaffin cells - serotonin.
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120
Q

What is acute pancreatitis?

A

Rapid onset of pancreatic inflammation and symptoms

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121
Q

What is chronic pancreatitis?

A

Longer-term inflammation and symptoms with progressive and permanent deterioration in pancreatic function.

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122
Q

What are the three main causes of pancreatitis?

A

Gallstones
Alcohol
Post-ERCP

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123
Q

What is ERCP?

A

Procedure that uses an endoscope and X-rays to look at your bile duct and your pancreatic duct.

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124
Q

What is gallstone pancreatitis?

A

When gallstones get trapped at the ampulla of Vater, blocking the flow of bile and pancreatic juice into the duodenum and resulting in inflammation of the pancreas.

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125
Q

Why does alcohol cause pancreatitis?

A

Alcohol is directly toxic to pancreatic cells, resulting in inflammation.

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126
Q

What are the causes of pancreatitis?

A 
I GET SMASHED:
Idiopathic
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Mumps
Autoimmune
Scorpion sting
Hyperlipidaemia
ERCP
Drugs
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127
Q

What are the main presentations of acute pancreatitis?

A 
Severe epigastric pain
Pain that radiates to the back
Vomiting
Abdominal tenderness
Systemically unwell (fever, tachycardia)
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128
Q

What are the initial investigations of pancreatitis?

A 
Glasgow score
Amylase--> Raised to >3X normal
C-reactive protein- monitors inflammation
Ultrasound (assesses for gallstones)
CT abdomen (assesses for complications)
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129
Q

What is the Glasgow score and what is the criteria needed to work it out?

A 
Used to assess severity of pancreatitis. 
(0-1= mild
2= moderate
3 or more= severe)
PANCREAS pneumonicL
Pa02<60
Age >55
Neutrophils (WBC>15)
Calcium <2
uRea >16
Enzymes 
Albumin 
Sugar (glucose>10)
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130
Q

How is acute pancreatitis managed?

A 
Resuscitation (ABCDE)
IV fluids
Nil by mouth
Analgesia
Careful monitoring
Treatment of gallstones if needed
Antibiotics if needed
Treatment of complications
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131
Q

What are the main complications of acute pancreatitis?

A 
Necrosis
Infection
Abscess formation
Acute peripancreatic fluid collections
Pseudocysts
Chronic pancreatitis
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132
Q

What does chronic pancreatitis cause?

A

Fibrosis and reduced pancreatic function

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133
Q

What is the most common cause of chronic pancreatitis?

A

Alcohol

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134
Q

What are the key complications of chronic pancreatitis?

A

Chronic epigastric pain
Exocrine function loss causing lack of pancreatic enzymes
Endocrine function loss leading to diabetes
Damafe and strictures to duct system causing obstruction in excretion of pancreatic juice and bie
Formation of pseudocysts and abscesses

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135
Q

How is chronic pancreatitis managed?

A

Abstain form alcohol/ smoking
Analgesia
Replacement of pancreatic enzymes
Subcutaneous insulin regimes if diabetes develops
ERCP with stenting to treat strictures and obstruction.
Surgery may be required.

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136
Q

What are the main functions of the liver?

A
  • Glucose and fat metabolism
  • Detoxification and excretion–> Bilirubin, ammonia, drugs, hormones
  • Protein synthesis–> Albumin, clotting factors
  • Defence against infection
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137
Q

What are the main causes of acute liver injury?

A 
Viral (A,B,EBV)
Drugs
Alcohol
Vascular
Obstruction
Congestion
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138
Q

What are the main causes of chronic liver injury?

A

Alcohol
Viral (B,C)
Autoimmune
Metabolic (iron, copper)

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139
Q

What is the alternative outcome to recovery in acute liver injury?

A

Liver failure

140
Q

What is the alternative to recovery in chronic liver injury?

A

Cirrhosis leading to liver failure (Varices of hepatoma)

141
Q

What are the common symptoms of acute liver injury?

A

Malaise, nausea, anorexia, occasionally jaundice

142
Q

What are the common symptoms of chronic liver injury?

A

Ascites (fluid in peritoneal cavity)

Oedema, Haematemesis, mailaise, anorexia, wasting, easy bruising, itching, hepatomegaly, abnormal LFTs

143
Q

What are LFTs and what do they look for?

A

Serum Liver function tests:

Serum albumin, bilirubin, prothrombin time

144
Q

What is serum albumin a good marker for?

A

Synthetic function (ability of liver to synthesise proteins)

145
Q

What serum measurements are good indications of synthetic function?

A

Prothrombin time (PT)/
International normalised ratio (INR)
Platelet count and albumin levels

146
Q

What is prothrombin time?

A

Blood test that measures how long it takes blood to clot- Results given as INR (International normalised ratio)

147
Q

What are aminotransferases and what happens to them during liver cell damage?

A 
Enzymes contained in hepatocytes that leak into the blood during liver cell damage. 
Aspartate aminotranferase (AST)
Alanine aminotransferase (ALT)
148
Q

What are bile pigments?

A

Substances formed from the haem portion of haemoglobin when erythrocyes are broken down in the spleen and liver.

149
Q

What is the predominant bile pigment and what colour is it?

A

Bilirubin- yellow.

150
Q

Where are erythrocytes broken down?

A

By macrophages in the spleen and bone marrow and by kupffer cells in the liver.

151
Q

What are erythrocytes broken down into?

A

Haem and globin

152
Q

What is globin broken down into and what happens to it?

A

Amino acids which are used to generate new erythrocytes in the bone marrow

153
Q

What is haem broken down into?

A

Biliverdin, Fe2+ and CO

154
Q

What happens to the Fe2+ from the breakdown of haem?

A

It is transported to bone marrow to be implemented into new erythrocytes.

155
Q

What happens to biliverdin?

A

It is reduced into unconjugated bilirubin which is toxic.

156
Q

Where does unconjugated bilirubin go?

A

It is toxic and must be secreted. It is lipid soluble so must be transported to the liver bound to albumin.

157
Q

What happens to unconjugated bilirubin in the liver?

A

It undergoes glucuronidation to make its soluble to be excreted and becomes conjugated bilirubin

158
Q

Where does conjugated bilirubin travel to once it leaves the liver and what happens to it there?

A

The small intestine until it reaches the ileum where it is reduced to form urobilinogen

159
Q

What happens to urobilinogen?

A

10% is reabsorbed into the blood bound to albumin and transported back to the liver where it is recycled into bile or transported to the kidneys and excreted in urine.
90% is oxidised into stercobilin which is excreted into the faeces

160
Q

What is jaundice and what causes it?

A

Yellow discolouration of the skin due to raised serum bilirubin

161
Q

What are the three steps in the progression of alcoholic liver disease?

A
  1. Alcohol related fatty liver
  2. Alcoholic hepatitis
  3. Cirrhosis
162
Q

What is alcohol related fatty liver?

A

When drinking leads to a build-up of fat in the liver. Process can be reversed in around 2 weeks

163
Q

What is alcoholic hepatitis?

A

When drinking alcohol over a long period or binge drinking causes inflammation of the liver

164
Q

What is liver cirrhosis?

A

When the liver is made up of scar tissue rather than healthy liver tissue. Irreversible

165
Q

What is the recommended drinking limit?

A

14 units per week. (over 3 or more days)

166
Q

What are the complications of excessive alcohol consumption?

A 
Alcoholic liver disease
Cirrhosis 
Alcohol dependance/ withdrawal
Wenicke-Korsakoff syndrome (WKS)
Pancreatitis
Alcoholic cardiomyopathy
167
Q

What are the main signs of liver disease?

A 
Jaundice
Hepatomegaly 
Spider naevi
Palmar erythema (red palms)
Gynaecomastia (males developing breast tissue)
Bruising (due to abnormal clotting)
Acites
Caput medusae (distended epigastric veins) 
Asterixis (hand tremor)
168
Q

What investigations are done to look for alcoholic liver disease?

A 
Bloods
Ultrasound
Endoscopy
CT/ MRI scans
Liver biopsy
169
Q

What bloods are done to look for alcoholic liver disease and what do they show?

A

FBC- Raised MCV
LFTs- Elevated ALT and AST (Transaminases). Raised gamma-GT and ALP. Low albumin. Raised bilirubin in cirrhosis
Clotting- Elevated prothrombin time
U&Es- may be deranged. in hepatorenal syndrome

170
Q

What can an ultrasound of the liver show?

A 
Fatty changes (increased echogenicity). 
Changes related to cirrhosis
171
Q

What is the general management of alcoholic liver disease?

A 
Stop drinking alcohol permanently. 
Detox regime 
Nutritional support (vitamins and high protein) 
Treat complications of cirrhosis
Steroids in severe cases
Referral for liver transplant.
172
Q

What are the different stages of alcohol withdrawal and their timings?

A

6-12 hours: tremor, sweating, headache, craving, anxiety
12-24 hours: Hallucinations
24-48 hours: seizures
24-72 hours: Delerium tremens

173
Q

What is delerium tremens?

A

Medical emergency associated with alcohol withdrawal that has a mortality of 35% if untreated.

174
Q

What causes delirium tremens?

A

Alcohol stimulates GABA receptors in the brain (which have a relaxing effect) and inhibits glutamate (NMDA) receptors, having a further inhibitory effect on the brains electrical activity.
Chronic alcohol use results in the GABA system becoming down-regulated and the glutamate system become up-regulated to balance the effects of alcohol. When alcohol is removed, GABA under-functions and glutamate over-functions causing extreme excitability with excess adrenergic activity.

175
Q

What are the presentations of delirium tremens?

A 
Acute confusion
Sever agitation
Delusions/ hallucinations
Tremor
Tachycardia
Hypertension
Hyperthermia
Ataxia
Arrhythmias
176
Q

How is alcohol withdrawal managed?

A

CIWA-Ar assessment tool used to score the patient.
Chlordiazepoxide is a type of sedative used to combat the effects.
IV high-dose B vitamins followed by low dose thiamine

177
Q

What is Wernicke-Korsakoff Syndrome (WKS)?

A

A disease that begins with Wernicke’s encephalopathy followed by Korsakoff’s syndrome. Caused by alcohol excess leading to thiamine (Vit B1) deficiency due to poor absorption in the presence of alcohol and poor diets of alcoholics.

178
Q

What are the key features of Wernicke’s encephalopathy?

A

Confusion
Oculomotor disturbances
Ataxia

179
Q

What is ataxia?

A

Difficulties with coordinated movements

180
Q

What are the key features of Korsakoff’s syndrome?

A

Memory impairment and behavioural changes

181
Q

What causes liver cirrhosis?

A

Chronic inflammation causes damaged liver cells to be replaces with scar tissue (fibrosis) and nodules of scar tissue form within the liver

182
Q

What are the most common causes of liver cirrhosis?

A

Alcoholic liver disease
Non alcoholic fatty liver disease
Hep B
Hep C

183
Q

What are less common causes of liver cirrhosis?

A 
Autoimmune hepatitis
Primary biliary cirrhosis
Haemochomatosis
Wilsons disease
Alpha-1 antitrypsin deficiency
Cystic fibrosis
Drugs
184
Q

What are the key signs of cirrhosis?

A 
Jaundice
Hepatomegaly
Splenomegaly (caused by portal hypertension)
Spider naevi
Palmar erythema 
Gynaecomastia and testicular atrophy
Bruising
Ascites
Caput medusae
Asterixis
185
Q

What are spider naevi?

A

When widened venules cause threadlike red lines or patterns on the skin

186
Q

What is palmar erythema and what causes?

A

Red palms caused by increased dilatation of surface capillaries in the hand due to hyperdynamic circulation.

187
Q

What is gynaecomastia and what causes it?

A

Condition by which males develop breast tissue due to an imbalanced ratio of oestrogen and androgen activity.

188
Q

What investigations can be done to check for liver fibrosis?

A 
Bloods (ELF)
Ultrasound
Fibroscan
Endoscopy
CT/ MRI scan
Liver biopsy
189
Q

What bloods indicate liver cirrhosis?

A
  • ALT, AST, ALP and Bilirubin become deranged in decompensated cirrhosis
  • Albumin and PT time indicate synthetic function
  • Hyponatraemia indicates fluid retention in severe cases
  • Urea and createnine become derganged in hepatorenal syndrome.
  • Enhanced liver fibrosis (ELF) blood test is first line in non-alcoholic fatty liver disease
190
Q

What may a cirrhosis ultrasound show?

A 
Nodules on liver surface
Corkscrew appearance to arteries with increased flow (to compensate for reduced portal flow) 
Enlarged portal vein
Ascites
Splenomegaly
191
Q

What is a FibroScan

A

Test used to check the elasticity of the liver by sending high frequency sound waves into it to assess the degree of fibrosis.

192
Q

What is the general management of cirrhosis?

A 
Ultrasound/alpha-fetoprotein every 6 months for hepatocellular carcinoma
Endoscopy every 3 years
High protein, low sodium diet
MELD score every 6 months
Possible liver transplant
Manage complications
193
Q

What is the 5 year survival once cirrhosis has developed?

A

50%

194
Q

What are the main complications of cirrhosis?

A

Malnutrition
Portal hypertension–>varices and variceal bleeding
Ascites and spontaneous bacterial peritonitis
Hepato-renal syndrome
Hepatic encephalopathy
Hepatocellular carcinoma

195
Q

Why does cirrhosis lead to malnutrition?

A

It leads to increased use of muscle tissue as fuel and reduces the protein available for muscle growth by affecting the metabolism of proteins in the liver. It also disrupts the livers ability to store glucose as glycogen and release it when required, resulting in the body using muscle tissue as fuel.

196
Q

How is malnutrition caused by cirrhosis managed?

A

Regular meals
Low sodium (to minimise fluid retention)
High protein and high calorie
Avoid alcohol

197
Q

What are the sources of the portal vein?

A

Superior mesenteric vein and splenic vein

198
Q

What is the action of the portal vein?

A

Brings venous blood from the spleen, pancreas, and small intestine so that the liver can process the nutrients and byproducts of food digestion

199
Q

Why does cirrhosis cause portal hypertension?

A

Increases the resistance of blood flow in the liver, causing increased back-pressure into the portal system.

200
Q

What does portal hypertension result in and where?

A

Varices at the sites where the portal system anastomoses with the systemic venous system:

  • Gastro oesophageal junction
  • Ileocaecal junction
  • Rectum
  • Anterior abdominal wall via the umbilical vein
201
Q

What the varices?

A

enlarged/ swollen veins.

202
Q

When do varices cause symptoms?

A

When the high blood flow causes bleeding.

203
Q

How are stable varices treated?

A

Propanolol (beta blocker) reduces portal hypertension
Elastic band litigation
Injection of sclerosant
Transjugular intra-hepatic portosystemic shunt (TIPS)

204
Q

How are bleeding oesophageal varices treated?

A

Vasopressin analogues–> cause vasoconstriction and slow bleeding.
Correct any coagulopathy with vit. K and fresh frozen plasma
Urgent endoscopy–> Injection os sclerosant or elastic band ligation.
Sengstaken-Blakemore tube-inflatable tube inserted to tamponade the bleeding varices

205
Q

What is ascites?

A

Fluid in the peritoneal cavity

206
Q

Why does cirrhosis cause ascites?

A

Increased pressure in the portal system causes fluid to leak out of the liver and bowel capillaries and into the peritoneal cavit.

207
Q

What is transudative ascites?

A

Low protein content ascites

208
Q

What does the fluid loss into the peritoneal space in ascites cause?

A

Drop in circulating volume, leading to reduction in blood pressure entering the kidneys. They sense this lower pressure and release renin, which leads to increased aldosterone secretion and reabsoprtion of fluid and sodium in the kidneys.

209
Q

How is ascites managed?

A

Low sodium diet
Anti-aldosterone diuretics
Paracentesis (ascitic drain)
Prophylactic antibiotics against SBP

210
Q

What is spontaneous bacterial peritonitis (SBP)?

A

When an infection develops in the ascitic fluid and peritoneal lining. (occurs in 10% of patients with ascites secondary to cirrhosis)

211
Q

What are the key presentations of spontaneous bacterial peritonitis?

A 
Asymptomatic
Fever
Abdominal pain
Deranged bloods
Ileus
Hypotension
212
Q

What is Hepatorenal syndrome?

A

When portal hypertension leads to loss of blood volume in other areas of the circulation, including the kidneys. This leads to hypotension in the kidney and therefore the activation of the RAAS system, causing renal vasoconstriction. This combined with low circulating volume leads to starvation of blood to the kidney, causing rapid deterioration of kidney function. Fatal within a week unless there is a liver transplant

213
Q

What is hepatic encephalopathy?

A

When a build of toxins (e.g. ammonia) affects the brain

214
Q

Why does ammonia build up in the blood in patients with cirrhosis?

A

Functional impairment of the liver cells prevents them from metabolising it.
Collateral vessels between the portal and systemic circulation mean that the ammonia bypasses the liver altogether and enters the systemic system directly.

215
Q

What is the acute presentation of hepatic encephalopathy?

A

Reduced consciousnnes and confusion.

216
Q

What are the precipitating factors of hepatic encephalopathy?

A 
Constipation
Electrolyte disturbance
Infection
GI bleed
High protein diet
Medications
217
Q

How is hepatic encephalopathy managed?

A

Laxatives–> Encourage excretion of ammonia
Antibiotics –> Reduce number of intestinal bacteria producing ammonia
Nutritional support

218
Q

What is alcoholic fatty liver disease and what percentage of adults have it?

A

When fat is deposited in liver cells, intefering with their function.
30 % of adults

219
Q

What are the 4 stages of NAFLD?

A
  1. NAFLD
  2. NASH (Non-alcoholic steatohepatitis)
  3. Fibrosis
  4. Cirrhosis
220
Q

Wha are the risk factors for NAFLD?

A 
Obesity
Poor diet
Sedentary lifestyle
T2 diabetes
High cholesterol
Advancing age
Smoking
High BP
221
Q

What are the common liver function tests?

A 
Alanine transaminase (ALT). 
Aspartate transaminase (AST). 
Alkaline phosphatase (ALP). 
Albumin and total protein. 
Bilirubin. 
Gamma-glutamyltransferase (GGT). 
L-lactate dehydrogenase (LD). 
Prothrombin time (PT).
222
Q

What is the next step when someone presents with abnormal liver function tests without clear cause and what does this include?

A

Non-invasive liver screen:

  • Liver ultrasound
  • Hep B/ C serology
  • Autoantibody tests
  • Immunglobulins
  • Ceruloplasmin
  • Alpha 1 Anti-trypsin levels
  • Ferritin and transferrin saturation
  • ELF (enhanced liver fibrosis) blood test
223
Q

What autoantibodies are tested for in a non-invasive liver screen?

A 
Antinuclear antibodies (ANA)
Smooth muscle antibodies (SMA)
Antimitochondiral antibodies (AMA)
Antibodies to liver kidney microsome type-1 (LKM-1)
224
Q

How is non-alcoholic fatty liver disease managed?

A 
Weight loss
Exercise
Stop smoking
Control of diabetes, BP and cholesterol
Avoid alcohol
225
Q

What are the causes of hepatitis?

A 
Alcoholic hepatitis
Non alcoholic liver disease
Viral
Autoimmune
Drug induced (paracetamol overdose)
226
Q

What are the symptoms of hepatitis?

A
  • Asymptomatic or non-specific
  • Abdominal pain
  • Fatigue
  • Pruritis (itching)
  • Muscle and joint aches
  • Nausea and comiting
  • Jaundice
  • Fever
227
Q

What are the typical biochemical findings in hepatitis (hepatic picture)?

A

Liver function tests become deranged with high transaminases (AST/ALT) and proportionally less rise of ALP.

228
Q

What are transaminases?

A

Liver enzymes released into the blood as a result of inflammation of the liver cells.

229
Q

What is the most common viral hepatitis worldwide?

A

Hep. A

230
Q

What is Hep. A and how is it transmitted?

A

An RNA virus transmitted via the faecal-oral route (usually contaminated water or food)

231
Q

How does Hep. A present?

A

Nausea, vomiting, anorexia and jaundice.

Can cause cholestasis.

232
Q

What is cholestasis and what does it cause?

A

Slowing of bile through the biliary system that presents with dark urine and pale stools.

233
Q

How quickly does Hep A resolve and what is its management?

A

Resolves in 1-3 months with no treatment.

Management is with basic analgesia

234
Q

What is Hep B and how is it transmitted?

A

DNA virus transmitted by direct contact with blood or bodily fluids (e.g. sex or IV drug users, sharing toothbrushes, contact between minor cuts)
Can also be passed from mother to child during birth (Vertical transmission)

235
Q

How quickly does Hep B resolve?

A

Within 2 months - however 10% become chronic Hep B carriers

236
Q

What are the different types of viral markers for Hep B?

A 
Surface antigens
E antigen
Core antibodies
Surface antibodies
Hep B virus DNA
237
Q

What is the abbreviation for surface antigens and what do they indicate?

A

HBsAg

If present, indicate active infection

238
Q

What is the abbreviation for E antigens and what do they indicate?

A

HBeAg

Marker of viral replication and implies high infectivity

239
Q

What is the abbreviation for core antibodies and what do they indicate?

A

HBcAb

Implies past or current infection

240
Q

What is the abbreviation for surface antibodies and what do they indicate?

A

HBsAb

Implies vaccination or past or current infection

241
Q

What is the abbreviation for Hep B virus DNA and what does its presence indicate?

A

HBV DNA

Direct count of viral load.

242
Q

What is tested for when screening for Hep B?

A

HBcAb (for previous infection)
HBsAg (for active infection)
If positive, test for HBeAg and viral load.

243
Q

How can you differentiate between acute, chronic and past Hep B infections?

A

Measure IgM and IgG versions of the HBcAb (core antibody). IgM implies active infection (high titre with acute infection, low titre with chronic infection), IgG indicates past infection.

244
Q

What does a high level of HBeAg indicate?

A

The patient is in the acute phase of infection when the virus is actively replicating, meaning they are highly infectious.

245
Q

How is Hep B managed?

A 
Low threshold for screening in those at risk. 
Refer for specialist management.
Notify public health
Stop smoking/ alcohol
Education about reducing transmission 
Test for complications
Antiviral medication
246
Q

What are symptoms of Hep B and when do they develop?

A

Most people do not get symptoms.
If symptoms do develop, they tend to happen 2 or 3 months after exposure to the hepatitis B virus:
Flu-like symptoms–> tiredness, fever, and general aches and pains
Loss of appetite
Nausea/ vomiting/ diarrhoea
Jaundice
These symptoms will usually pass within 1 to 3 months (acute hepatitis B), although occasionally the infection can last for 6 months or more (chronic hepatitis B).

247
Q

Who is hep B vaccine routinely offered to?

A

Vaccine is offered to all babies born in the UK (need 3 top ups)

Also those at high risk:
-Babies born to hepatitis B-infected mothers
-Close family and sexual partners of someone with hepatitis B
-People travelling to a part of the world where hepatitis B is widespread
-Families adopting or fostering children from high-risk countries
-People who inject drugs or have a sexual partner who injects drugs
-People who change their sexual partner frequently
men who have sex with men
male and female sex workers
-People who work somewhere that places them at risk of contact with blood or body fluids, such as nurses, prison staff, doctors, dentists and laboratory staff
-People with chronic liver or kidney disease

248
Q

What is Hep C and how is it transmitted?

A

RNA virus spread by blood and bodily fluids.

249
Q

What is the disease course of hep C?

A

1 in 4 makes full recovery

3 in 4 become chronic –> Complications include liver cirrhosis and hepatocellular carcinoma

250
Q

How is Hep C tested for?

A

Hep C antibody screening test

Hep C RNA testing used to confirm diagnosis, calculate viral load and assess for individual genotype

251
Q

How is Hep C managed?

A

Same as hep B but direct acting antivirals can also be used to cure infection in 90% of patients

252
Q

What is hep D and which patients can get it?

A

RNA virus that can only survive in patients who also have Hep B. Attaches to HBsAg and can’t survive without it so there are very low rates in the UK.

253
Q

Are all forms of viral hepatitis notifiable diseases?

A

Yes

254
Q

What is Hep E and how is it transmitted?

A

RNA virus transmitted by the faecal oral route. Very rare in UK

255
Q

What is autoimmune hepatitis (what are the two types)?

A

Rare cause of chronic hepatitis with unknown cause- linked to genetic predisposition and triggered by environmental factors.
Type 1: occurs in adults
Type 2: occurs in children

256
Q

How is autoimmune hepatitis treated?

A

With high dose steroids (prednisolone) that are tapered over time as other immunosuppressants are introduced.

257
Q

What is haemochromatosis?

A

Iron storage disorder that results in excessive total body iron and deposition of iron in tissues

258
Q

What causes haemochromatosis?

A

Autosomal recessive mutations in the HFE (human haemochromatosis protein) gene on chromosome 6.

259
Q

What are the symptoms of haemochromatosis?

A
  • Chronic tiredness
  • Joint pain
  • Pigmentation
  • Hair loss
  • Erectile dysfunction
  • Amenorrhoea
  • Cognitive symptoms
260
Q

How is haemochromatosis diagnosed?

A

Serum ferritin levels
Transferrin saturation–> Allows distinction between high ferritin levels caused by iron overload or by other causes (inflammation or NAFLD)
Genetic testing to confirm
Liver biopsy with Perl’s stain—> Establishes iron concentration in parenchymal cells
CT abdomen
MRI

261
Q

What are the complications of haemochromatosis?

A

T1 diabetes (Iron in pancreas)
Liver cirrhosis
Endocrine/ sexual problems –>hypogonadism, impotence, amenorrhea, infertility (caused by iron deposits in pituitary and gonads)
Cardiomyopathy (iron deposits in heart)
Hepatocellular carcinoma
Hypothyroidism (iron deposits in thyroid)
Chrondocalcinosis/ pseudogout (calcium deposits in joints causing arthritis)

262
Q

How is haemochromatosis managed?

A

Venesection (weekly to decrease total iron)
Monitor serum ferritin
Avoid alcohol
Monitor/ treat complications

263
Q

What are the most common metabolic liver diseases?

A

Haemochromatosis
Alpha-I antitrypsin deficiency (AATD)
Wilson Disease

264
Q

What is metabolic liver disease?

A

Disorders in which abnormal chemical reactions in the body disrupt the body’s metabolism.

265
Q

What is Wilson disease?

A

Excessive accumulation of copper in the body and tissues

266
Q

What causes Wilson disease?

A

Autosomal recessive mutation in the Wilson disease protein (ATP7B copper-binding protein) on chromosome 13.

267
Q

What is the function of the Wilson disease gene?

A

Responsible for various functions including the removal of excess copper in the liver.

268
Q

What are the key features of Wilson disease?

A

Copper deposition leading to :
Hepatic problems (40%)
Neurological problems (50%)
Psychiatric problems (10%)
Kayser-Fleischer rings in cornea (brownish circles around iris)
Haemolytic anaemia
Renal tubular acidosis (caused by renal tubular damage meaning acids aren’t excreted)
Osteopenia (loss of bone mineral density)

269
Q

What does excess copper to to the liver?

A

Copper deposition in the liver leads to chronic hepatitis and eventually liver cirrhosis.

270
Q

What neurological and psychiatric symptoms can Wilson disease cause?

A 
Concentration and coordination issues
Dysarthria (speech difficulties)
Dystonia (abnormal muscle tone)
Deposition in ganglia leads to Parkinsonism (tremor, bradykinesia and rigidity) 
Depression
Psychosis
271
Q

How is Wilson disease diagnosed?

A

Low serum caeruloplasmin (copper transport protein)
Liver biopsy for liver copper content.
Elevated 24 hour urine copper assay

272
Q

How is Wilson disease treated?

A

Copper chelation agents:
Penicillamine
Trientene

273
Q

What is alpha-1-antitrypsin and where is it mainly produced?

A

Protease (enzymes that catalyse proteolysis) inhibitor produced in the liver.

274
Q

What is elastase (action + where is is secreted from)?

A

An enzyme secreted by neutrophils that digests connective tissues.

275
Q

What is the action of A1AT?

A

Binds to neurophil elastase, protecting tissues against digestion.

276
Q

What is alpha-1-antitrypsin deficiency?

A

Autosomal recessive defect in the gene for A1AT on chromosome 14 causing a deficiency.

277
Q

What 2 organs are mainly affected by alpha-1-antitrypsin deficiency and what does it do to them?

A

Liver–> Liver cirrhosis

Lungs–> Bronchiectasis and emphysema

278
Q

How does alpha-1-antitrypsin deficiency cause liver damage?

A

The mutant version of the protein is produced in the liver and gets trapped. It builds up and causes liver damage which progresses to cirrhosis over time.

279
Q

How does alpha-1-antitrypsin deficiency cause lung damage?

A

The lack of functioning alpha-1-antitrypsin protein leads to an excess of protease enzymes that attack the connective tissue in the lungs, leading to bronchiectasis and emphysema over time.

280
Q

How is alpha-1-antitrypsin deficiency diagnosed?

A

Low serum alpha-1-antitrypsin.
Liver biopsy–> Cirrhosis and acid-Schiff-positive staining globules
Genetic testing for A1AT gene
CT thorax

281
Q

How is alpha-1-antitrypsin deficiency managed?

A

Stop smoking
Symptomatic management
Organ transplant if necessary

282
Q

Where is bile produced and where is it stored? Where does it go once released

A

Produced in the liver and stored in the gallbladder. Released into the duodenum when needed

283
Q

What does bile consist of?

A 
95% water with things dissolved: 
Bile salts
Bilirubin phospholipid
Cholesterol
Amino acids
Steroids
Enzymes
Porphyrins
Citamins
Heavy metals
Exogenous drugs
Xenobiotics 
Environmental toxins
284
Q

Where is bile initially secreted from and how does it get to the gallbladder?

A

Initially secreted from hepatocytes. Drains from both lobes of the liver via canaliculi, intralobular ducts and collecting ducts into the left and right hepatic ducts. These ducts amalgamate to form the common hepatic duct, which descends and joins the cystic duct- which allows bile to flow in and out of the gallbladder for storage and release. At this point, the common hepatic duct and cystic duct combine to form the common bile duct.

285
Q

What is primary biliary cirrhosis?

A

Condition where the immune system attacks the small bile ducts of the liver.

286
Q

What are the first areas to be affected in primary biliary cirrhosis and what does this cause?

A

Intralobar ducts (Canals of Hering) which causes obstruction of the outflow of bile (cholestasis)

287
Q

What is cholestasis?

A

Obstruction of the outflow of bile

288
Q

Why does primary biliary cirrhosis lead to liver failure?

A

The back-pressure of bile obstruction caused by autoimmune destruction of small bile ducts leads to fibrosis, cirrhosis and ultimately liver failure.

289
Q

What key chemicals are usually excreted through the bile ducts into the intestines and what happens when they are not?

A

Bile acids, bilirubin and cholesterol

Build up in the blood

290
Q

What does excess serum bile acids cause?

A

Itching

291
Q

What does excess serum bilirubin cause?

A

Jaundice

292
Q

What does raised serum cholesterol cause?

A

Xanthelasma (Cholesterol deposits in skin and blood vessles)–> Increases risk of heart disease.

293
Q

What are bile acids responsible for in the gut and what does a lack of them cause?

A

Help the gut digest fats. Therefore a lack causes GI disturbance, malabsorption of fats and greasy stools.

294
Q

What does a lack of bilirubin in the stools cause?

A

Pale stools (bilirubin responsible for the dark colour)

295
Q

What are the key presentations of primary biliary cirrhosis?

A

Fatigue
Pruritus (itching)
GI disturbance/ pain
Jaundice
Pale stools
Xanthoma/ Xanthelasma (cholesterol deposits in skin/ blood vessels)
Signs of cirrhosis and liver failure (ascites, splenomegaly, spider naevi)

296
Q

How is primary biliary cirrhosis diagnosed?

A 
Liver function tests
Autoantibodies
Raised ESR
Raised IgM
Liver biopsy
297
Q

What is the first liver enzyme to be raised in obstructive pathology?

A

Alkaline phosophatase (ALP)

298
Q

How is alkaline phosophatase treated?

A

Ursodeoxycholic acid–> Reduces intestinal absorption of cholesterol
Colestyramine–> Binds to bile acids to prevent absorption in the gut
Liver transplant for end stage liver disease
Immunosuppression

299
Q

What is steatorrhoea?

A

Greasy stools due to lack bile salts to digest fats

300
Q

What is primary sclerosing cholangitis?

A

Condition where the intra/extrahepatic ducts become strictured (abnormally narrowed) and fibrotic, causing obstruction of flow of bile out of the liver.

301
Q

What is cholangitis?

A

Inflammation of the bile duct system

302
Q

What are the associated causes of primary sclerosing cholangitis?

A

Causes unclear but linked to genetic, autoimmune, microbiome and environmental factors.
70% of cases linked to ULCERATIVE COLITIS

303
Q

What are the risk factors for primary sclerosing cholangitis?

A

Male
30-40 y/o
Ulcerative colitis
Family history

304
Q

What are the key presentations of primary sclerosing cholangitis?

A 
Jaundice
Chronic right upper quadrant pain
Pruritis
Fatigue
Hepatomegaly
305
Q

What do liver function tests show in primary sclerosing cholangitis?

A

Cholestatic picture: deranged ALP (alkaline phosphatase)

May be rise in bilirubin as strictures become more severe, preventing it from being excreted.

306
Q

How is primary sclerosing cholangitis diagnosed?

A

MCRP–> Magneic resonance cholangiopancreatography (MRI scan of the liver, bile ducts and pancreas which may show lesions or strictures)
LFTs
Autoantibodies

307
Q

What are the complications of primary sclerosing cholangitis?

A 
Cholangiocarcinoma (10-20% cases)
Colorectal cancer
Cirrhosis and liver failure
Biliary strictures
Fat soluble deficiencies
308
Q

How is primary sclerosing cholangitis managed?

A 
Liver transplant (Can be curative but can also bring other problems) 
ERCP to stent strictures
Ursodeoxycholic acid
Colestyramine
Monitor/ treat complications
309
Q

What is ERCP?

A

Endoscopic Retrogade Cholangio-Pancreatography–> Inserting a camera through GI tract to ampulla of Vater where it enters the bile duct. Uses X-rays and injecting contrast to identify any strictures which can then be dilated and stented.

310
Q

What is primary liver cancer and what are the two main types?

A

Cancer that originates in the liver:
Hepatocellular carcinoma (80%)
Cholangiocarcinoma (20%)

311
Q

What is secondary liver cancer?

A

Metastasis to the liver that can occur from almost any cancer.

312
Q

What is the first stage in treating secondary liver cancer?

A

Look for the primary cancer (full body CT, thorough history, skin and breast exam)

313
Q

What is the main risk factors for hepatocellular carcinoma (HCC)?

A

Liver cirrhosis due to:

  • Viral hepatitis (B/C)
  • Alcohol
  • NAFLD
  • Other chronic liver disease
314
Q

What condition is cholangiocarcinoma associated with?

A

Primary sclerosing cholangitis (10% cases)

315
Q

How does liver cancer present?

A 
Asymptomatic for long period and presents late.
Non specific:
-Weight loss
-Abdominal pain
-Anorexia
-Nausea/vomiting
-Jaundice
-Pruritis
316
Q

What investigations can be done for liver cancer?

A
  • Alpha-feoprotein= tumour marker for hepatocellular carcinoma
  • CA19-9= tumour marker for cholangiocarcinoma
  • Liver ultrasounds
  • CT/ MRI scans
  • ERCP to take biopsies
317
Q

What is the prognosis of primary liver cancer?

A

Very poor unless diagnosed early

318
Q

How is hepatocellular carcinoma treated?

A

-Resection of early disease
- Liver transplant if isolated to liver
- Kinase inhibitors (inhibit proliferation of cancer cells)
(resistant to chemo and radiotherapy)

319
Q

How is cholangiocarcinoma treated?

A
  • Surgical resection of early disease

- ERCP to place stent in bile duct where cancer is compressing duct.

320
Q

What are Haemangiomas?

A

Common benign tumours of the liver often found incidentally

321
Q

What is focal nodular hyperplasia?

A

Benign liver tumour made of fibrotic tissue often found incidentally and often related to oestrogen

322
Q

What is an orthotopic transplant?

A

When an entire liver is transplanted straight from a deceased patient to a recipient.

323
Q

What is a living donor transplant?

A

When a portion of liver is taken from a living donor and transplanted into a patient. The liver can then regenerate in both patients.

324
Q

What are the main indications for liver transplant?

A

Acute liver failure–> Most commonly acute viral hepatitis and paracetamol overdose
Chronic liver failure–> May take around 5 months for liver to become available

325
Q

When would a liver transplant be unsuitable?

A
  • Significant co-morbidities
  • Excessive weight loss and malnutritioin
  • Active infection
  • End-stage HIV
  • Active alcohol use (6 months abstinence required)
326
Q

What are the 3 types of jaundice?

A

Pre-hepatic
Hepatocellular
Post-hepatic

327
Q

What is pre-hepatic jaundice?

A

When excessive red cell breakdown overwhelms the body’s ability to conjugate bilirubin, causing excess unconjugated bilirubin in the blood.

328
Q

What causes pre-hepatic jaundice?

A

Gilberts syndrome

Haemolytic anaemia

329
Q

What is hepatocellular jaundice?

A

When dysfunction of hepatic cells means the liver loses its ability to conjugate bilirubin

330
Q

What causes hepatocellular jaundice?

A 
Hepatitis (Viral, autoimmune) 
Alcoholic liver disease
Haemochromatosis
Primary biliary cirrhosis/ sclerosing cholangitis
Hepatocellular carcinoma
Latrogenic (medication)
331
Q

What is post-hepatic jaundice?

A

Obstruction of biliary drainage, leading to lack of conjugated bilirubin excretion

332
Q

What causes post-hepatic jaundice?

A 
Intra-luminal causes (gallstones)
Mural causes (Cholangiocarcinoma, strictures)
Extra-mural causes (Pancreatic cancer, abdominal masses)
333
Q

What type of jaundice is it likely to be if there is no dark urine, stools are normal colour and there is no itching?

A

Pre-hepatic

334
Q

What is biliary colic?

A

The pain associated with the temporary obstruction of the cystic or common bile duct due to a stone migrating from the gallbladder

335
Q

What is cholecystitis?

A

Gallbladder inflammation

336
Q

What is a reducible hernia?

A

Hernia what can be pushed back into the abdominal cavity

337
Q

What is an irreducable hernia?

A

Hernia that cannot be pushed back into place

338
Q

What are the three main complications of hernias?

A

Incarceration
Obstruction
Strangulation

339
Q

What is incarceration?

A

When a hernia cannot be reduced back into its proper position and gets trapped in the herniated position

340
Q

What is hernia obstruction?

A

Where a hernia causes a blockage in the passage of faeces through the bowel .

341
Q

What is hernia strangulation?

A

Where a hernia is non-reducible and the base of the hernia becomes so tight it cuts off the blood supply.

342
Q

What does the inguinal canal run between?

A

Deep inguinal ring (connects to the peritoneal cavity) to the superficial inguinal ring (where it connects to the scrotum)

343
Q

What is the purpose of the inguinal canal in men?

A

Allows the spermatic cord and its contents to travel from the peritoneal cavity to the scrotum.

344
Q

What passes through the inguinal canal in women?

A

Round ligament (passes from uterus to labia majora)

345
Q

What is the processus vaginalis?

A

Pouch of peritoneum that extends from the abdominal cavity through the inguinal canal during fetal development, allowing the testes to descend through the inguinal canal into the scrotum.

346
Q

What is a direct inguinal hernia?

A

When the deep inguinal ring remains patent and the processus vaginalis remains intact, allowing the bowel to herniate through the inguinal canal.

347
Q

How do you differentiate a direct and indirect inguinal hernia?

A

When pressure is applied to the deep inguinal ring, an indirect inguinal hernia will remain reduced.

PHASE 2A (Mine) (15 decks)

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