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Pocket MSRA - Book 1 > Gastroenterology & Hepatology > Flashcards

Gastroenterology & Hepatology Flashcards

1
Q

What is Achalasia and what mechanism underlies it?

A

Motility disorder of the lower oesophagus
Degeneration of Auerbach’s plexus
-uncoordinated peristalsis
-lower sphincter fails to relax

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2
Q

How does achalasia present?

A

Dysphagia for both solids AND liquids
Halitosis
Increased risk of SCC

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3
Q

How can achalasia be investigated?

A

Manometry - high pressure
Barium swallow - Bird’s beak/dilated tapering of oesophagus

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4
Q

How is achalasia treated?

A

CCB/nitrates
Endoscopic dilation
Heller’s myotomy

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5
Q

What is the MoA of Cyclizine as an anti-emetic and in which circumstances is it effective?

A

H1 antagonist
GI causes
Emetogenic chemo
PONV
Vestibular causes

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6
Q

What D2 antagonists are commonly used as antiemetics?

A

Metoclopramide
Haloperidol
Domperidone
Prochlorperazine

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7
Q

In which circumstances are D2 antagonists effective as antiemetics?

A

GI causes
Emetogenic chemo
Vestibular causes
Opiates

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8
Q

What are the side effects of D2 antagonists?

A

Prokinetic (not used in BO)
Dystonias
Oculogyric crises

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9
Q

What is the MoA of Ondansetron as an anti-emetic and in which circumstances is it effective?

A

5-HT3 antagonist
Emetogenic chemo
Surgery

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10
Q

What scoring systems can be used for UGI bleeds?

A

Rockall
Glasgow-Blatchford

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11
Q

Describe the Rockall score

A

Risk stratification (mortality)
Done pre/post endoscopy

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12
Q

What criteria make up the Rockall score?

A

Age
Shock
Co-morbidity
POST-ENDOSCOPY DX
SIGNS OF HAEMORRHAGE ON ENDOSCOPY

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13
Q

Describe the Glasgow-Blatchford Score

A

Risk stratifies patients for inpatient vs outpatient endoscopy in UGI bleed

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14
Q

What is a Mallory-Weiss tear?

A

Mucosal tear caused by persistent vomiting or retching
-arterial bleed
-self limiting

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15
Q

What are the complications of a Mallory-Weiss tear?

A

Generally self limiting
Boerrhave syndrome

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16
Q

What is Boerrhave syndrome?

A

Oesophageal RUPTURE due to vomiting against closed glottis

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17
Q

How does Boerrhave syndrome present?

A

SEVERE retrosternal chest pain
Respiratory distress
SC emphysema
-Hamman sign

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18
Q

What is Hamman sign?

A

Crunching sound on ascultation due ot mediastinal emphysema

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19
Q

What are the common causes of UGI bleeds?

A

Mallory-Weiss tears
Peptic ulcers
Varices

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20
Q

How can gastric and duodenal ulcers be distinguished?

A

Gastric ulcers - pain WITH meals
Peptic ulcers (4x more common) - pain AFTER meals

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21
Q

What are the risk factors for gastric ulcers?

A

H. pylori infection
Smoking
NSAIDs/steroids
Reflux
Delayed gastric emptying
Burns (Curling’s ulcer)
Neurosurgery (Cushing’s ulcer)

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22
Q

What are the risk factors for peptic ulcers?

A

H. pylori infection
Smoking
NSAIDs/steroids
Increased gastric emptying
Blood group O

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23
Q

What is Zollinger-Ellison syndrome?

A

Gastrin secreting pancreatic adenoma
-associated w/ MEN 1

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24
Q

When should Zollinger-Ellison syndrome be suspected?

A

Multiple ulcers of stomach/duodenum
FHx
Associated w/ MEN 1
-parathyroid adenoma –> sx hypercalcameia

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25
Q

How should Zollinger-Ellison syndrome be ix?

A

Gastrin levels
Scintigraphy (octreoscan)
Check for hepatic mets (20%)

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26
Q

Why are post. duodenal ulcers high risk?

A

Near to gastroduodenal aa
-can erode into it

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27
Q

How should UGI bleeds be managed?

A

Airway, NBM
IVI + RBC + correct clotting abnormalities
Abx cover
Urgent endoscopy +/-
-endotherapy
-embolisation (IR) or surgery
-sengsataken-blakemore tube
72hrs PPI POST-ENDOSCOPY
If variceal
-Terlipressin
-TIPS

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28
Q

How does Terlipressin work?

A

Vasoconstriction
-reduces portal pressure
-renoprotective

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29
Q

What is the major s/e of Terlipressin?

A

Vasoconstriction of coronary vessels
-arrhythmias
-MI

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30
Q

What is the TIPS procedure?

A

Trans-jugular intrahepatic portal systemic stenting

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31
Q

What are the common s/e of PPIs?

A

Hyponatraemia/hypomagnesaemia
Diarrhoea (C. diff)
Tubular interstitial nephritis
Osteoporosis
Interacts w/ Clopidogrel

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32
Q

How does GORD present?

A

Dyspepsia post meals
Water-brash (salivation)
Nocturnal asthma
Chronic cough/sore throat
Sinusitis

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33
Q

What are the two types of hiatus hernia?

A

Sliding (most common)
Rolling (para-oesophageal)
-higher risk of strangulation

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34
Q

What lifestyle advice should be given for GORD?

A

Stop smoking
Small regular meals
Reduce hot drinks/EtoH/citrus/spicy food/caffeine
Avoid eating <3hr before bed
Sleep more upright

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35
Q

How can GORD be managed medically?

A

Antacids
PPI
H2RA if refractory

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36
Q

How can GORD be managed surgically?

A

Nissen fundoplication
Hiatal hernia repair

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37
Q

What are the common s/e of H2 receptor antagonists?

A

Diarrhoea/GI upset
Liver dysfunction
CYP450 inhibition - CIMETIDINE ONLY

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38
Q

What are the common causes of dyspepsia?

A

Ulcers
GORD
Oesophagitis/gastritis/duodenitis
Malignancy

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39
Q

What are the red-flag sx for gastric ca in dyspeptic patients?

A

ALARMS 55
Anaemia
Wt loss
Anorexia
Recent onset/progressive sx
Melaena/haematemesis
Swallowing difficulties
>55

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40
Q

How should dyspepsia be treated?

A

If ALARMS 55 +ve - 2ww gastroscopy
If ALARMS 55 -ve
-lifestyle changes and 4/52 review
-if no improvement test/treat H. pylori

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41
Q

How should H. pylori infection be ix?

A

C13 breath test

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42
Q

How is H. pylori infection treated?

A

Triple therapy 4/52
-PPI
-Amoxicillin
-Clarithromycin/Metronidazole

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43
Q

How can functional dyspepsia be managed?

A

PPIs
CBT
Low-dose amitriptylien ON

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44
Q

What is Barrett’s oesophagus?

A

Metaplasia of stratified squamous to columnar epithelium 2o GORD
-risk of progression to adenocarcinoma

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45
Q

How should Barrett’s oesophagus be managed?

A

If no dysplasia AND <3cm –> discharge
If no dysplasia AND >3cm –> surveillance every 2-3 years
If low-grade dysplasia –> repeat endoscopy 6/12 +/- RF ablation
If high-grade dysplasia or carcinoma-in situ –> endoscopic resection +/- RF ablation

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46
Q

What are the distinguishing features of Ulcerative Colitis?

A

Mucosal/submucosal (superficial)
Rectum to caecum (continuous)
LLQ pain w/ bloody diarrhoea
Crypt abscesses
Pseudo-polyps, haustral loss (lead-piping)
Smoking PROTECTS
Middle aged males

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47
Q

What are the distinguishing features of Chron’s?

A

Full-thickness w/ fissures/fistula
Mouth to anus (skip lesions)
RLQ pain w/ non-bloody darrhoea
Lymphoid aggregates w/ granulomas
Cobblestone appearance, strictures
Smoking INCREASES RISK
M=F

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48
Q

What are the extra-intestinal manifestations of UC?

A

Arthritis (ank spond)
Uveitis
Erythema nodosum
Pyoderma gangrenosum
PRIMARY SCLEROSING CHOLANGITIS
p-ANCA positive

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49
Q

What are the extra-intestinal manifestations of Chron’s?

A

Arthritis (ank spond)
Uveitis
Erythema nodosum
Pyoderma gangrenosum
OXALATE STONES (renal colic)

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50
Q

What are the complications of UC?

A

Toxic megacolon
Ca

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51
Q

What are the complications of Chron’s?

A

Malabsorption
Fistula
Ca

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52
Q

What is the Truelove-Witts score and what criteria are included in it?

A

Severity score for UC
-motions/day
-PR bleed
-fever
-resting HR
-Hb
-ESR

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53
Q

What maintenance therapy is used for UC?

A

Mild - 5-ASA (mesalazine)
Moderate
-steroids (remission) then 5-ASA
-monoclonal biologics

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54
Q

What is the management of severe/acute UC?

A

Admission
IV/PR steroids
Ciclosporin/Infliximab if poorly responding
Colectomy if not improving/toxic megacolon

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55
Q

What maintenance therapy is used for Chron’s?

A

Mild/Mod
-steroids PO/PR
-azathioprine/6-mercaptopurine –> methotrexate
-monoclonal biologics

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56
Q

What levels should be checked before starting Azathioprine/6-mercaptopurine in Chron’s?

A

Thiopurine methyltransferase/TPMT activity
-if low/absent use MTX instead

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57
Q

What surveillance is offered in IBD?

A

Colonoscopy
-if presenting w/ sx >10 yrs
High risk - every 1 yr
Intermediate risk - every 3 yrs
Low risk - every 5 yrs

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58
Q

How does infective colitis present?

A

Profuse watery diarrhoea - characteristic smell in C. diff
Raised inflammatory markers/low albumin
Pseuodemembrane on endoscopy

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59
Q

What are the complications of infective colitis?

A

Ileus –> toxic megacolon (>5.5cm) –> perforation
Complications of diarrhoea/volume loss e.g. AKI

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60
Q

What drugs should be avoided in infective colitis?

A

Antibiotics
PPIs
Anti-spasmodics

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61
Q

How should infective colitis be managed?

A

Metronidazole +/- Vancomycin
Colectomy if uncontrolled

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62
Q

How does infective gastroenteritis present?

A

Predominantly vomiting
More rapid onset
Can cause bloody diarrhoea

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63
Q

What are the common bacterial causes of food poisoning and which foods are they found in?

A

Campylobacter - poultry
Salmonella - poultry, uncooked eggs
S. aureus - sliced meat, creams
B. cereus - reheated rice/soup
Listeria - unpasteurised milk, refrigerated meat, raw veg
E. coli - unpasteurised milk, raw fruit/veg, undercooked ground beef
Norovirus - shellfish

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64
Q

What are the key characteristics of Norovirus?

A

1/7 incubation
2/7 D&V
V. infectious - spread by food/contact
Dx - stool antigen

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65
Q

What are the key characteristics of Rotavirus?

A

1-3/7 incubation
1/52 D&V
Dx - stool antigen
PPx - live vaccine 12/52 & 8y/o

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66
Q

What are the key characteristics of Campylobacter jejuni?

A

2-5/7 incubation
Dysentery + pain + headache
Tx - Clarithyromcyin/Ciprofloxacin
Cx - Sepsis, hepatitis, pancreatitis, reactive arthritis, GBS, miscarriage

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67
Q

What are the key characteristics of Salmonella?

A

6hr-3/7 incubation
Dysentery + cramps
Tx - Clarithromycin/Ciprofloxacin
Cx - Sepsis, meningitis, osteomyelitis + septic arthritis

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68
Q

What are the key characteristics of Staph aureus?

A

30min-6hr incubation
Sudden D&V + cramps

69
Q

What are the key characteristics of Bacillus cereus?

A

8-16hr incubation
D&V - self limiting

70
Q

What are the key characteristics of Listeria monocytogenes?

A

Variable incubation
Flu-like sx –> diarrhoea if immunocompromised
Tx - amoxicillin
Cx - abscess, endocarditis, mengoencephalitis, pregnancy loss, preterm delivery

71
Q

What are the key characteristics of E.coli ?

A

0157:H7 E.coli (shiga toxin producing) –> haemorrhagic colitis
Cx - 10% HUS, renal damage
DO NOT GIVE ABX - increases risk HUS

72
Q

What are the key characteristics of Shigella?

A

1-2/7 incubation
Dysentery, tenesmus
Cx - reactive arthritis, HUS, megacolon

73
Q

What are the key characteristics of Vibrio cholorae?

A

2-5/7 incubation
Watery diarrhoea
Tx - electrolyte replacement

74
Q

What are the key characteristics of Giardia?

A

1-3/52 incubation
Faecal-oral spread
Persistent diarrhoea, flatulence, bloating, malabsorption sx (weeks - months)
Dx - stool microscopy, need 3 samples
Tx - metronidazole

75
Q

What are the key characteristics of Cryptosporidium?

A

Self-limiting diarrhoea in immunocompetent
Severe/chronic in immunosuppressed

76
Q

What are the key characteristics of Enatamoeba histolytica?

A

Faecal-oral spread
Dx - microscopy
Tx - metronidazole
Cx - liver abscess, toxic megacolon, appendicits

77
Q

What are the presenting features of Coeliac disease?

A

Steatorrhoea
Wt loss
Anaemia (B12/folate) +/- B12 neuropathy

78
Q

What are the extraintestinal manifestations of Coeliac disease?

A

Dermatitis herpetiformis
Osteoporosis/osteopenia
Hyposplenism –> need flu/pneumococcal vaccines
GI T-cell lymphoma/ca

79
Q

How should suspected Coeliac disease be ix?

A

Anti-Ttg
-check IgA levels alongside
Duodenal bx
Trial gluten-free diet

80
Q

How is coeliac disease tx?

A

Gluten free diet lifelong
Dapsone - dermatitis herpetiformis

81
Q

What are the diagnostic criteria for IBS?

A

Rome criteria
Recurrent abdo pain >1/7 per week in last 3 /12 AND >2 of
-defecation related/relieved
-change in stool frequency
-change in stool form
-no red flags

82
Q

How should IBS be managed?

A

Constipation-predominant
-water/fibre intake
-bulk forming laxatives (macrogol)
-stimulant laxatives(senna)
Diarrhoea-predominant
-loperamide
Colic/bloating
-anti-spasmodics (mebeverine, hyoscine)
Visceral pain
-low dose Amitriptyline
FODMAP diet

83
Q

What are the consequences of B1 (thiamine) deficiency?

A

Wernicke encephalopathy
-confusion + opthalmoplegia + ataxia
Korsakoff syndrome
-psychosis + personality change + permanent memory loss
Dry beriberi
-polyneuritis w/ muscle wasting
Wet beriberi
-high output HF

84
Q

What are the consequences of B2 (riboflaviin) deficiency?

A

Cheilosis of lips

85
Q

What are the consequences of B3 (niacin) deficiency?

A

Pellagra
-dermatitis
-diarrheoa
-dementia
-death

86
Q

What are the consequences of B6 (pyridoxine) deficiency?

A

Neuropathy
Seizures
Sideroblastic anaemia

S/e of Isoniazid

87
Q

What are the consequences of B9 (folate) deficiency?

A

Megaloblastic anaemia

88
Q

What are the consequences of B12 (cobalamin) deficiency?

A

Megaloblastic anaemia
Subacute combined degeneration of cord

89
Q

How does Subacute combined degeneration of cord present?

A

Loss of proprioception/vibration sense (dorsal column)
Pyramidal/UMN signs + distal paraesthesia (lateral corticospinal)
Ataxia (spinocerebellar)

Mixed LMN/UMN

90
Q

What are the consequences of Vit A deficiency?

A

Night blidness
Keratomalacia
Sicca/xeropthalmia
Bitot spots
Immunosuppression
Dry skin

91
Q

What are the consequences of Vit D deficiency?

A

Decreased Ca/PO4
High PTH - 2o hyperparathyroidism
High ALP
Rickets (children) OR osteomalacia (adults)
-bony pain & weakness

92
Q

What are the consequences of Vit E deficiency?

A

Haemolytic anaemia
Blisters
Neurological presentation similar to SACDC

93
Q

What are the consequences of Vit K deficiency?

A

Clotting defects (protein C, S, factors 2/7/9/10)

94
Q

What are the consequences of Vit C (ascorbate) deficiency?

A

Scurvy
-swollen gums
-petechiae
-poor wound healing

95
Q

Which vitamins are fat-soluble?

A

ADEK

96
Q

What are the distinguishing features of pre-hepatic jaundice?

A

Increased UNCONJUGATED bilirubin
Increased urobilinogen
Normal urine/stools
Gallstones

97
Q

What are the distinguishing features of hepatic jaundice?

A

Increased UNCONGJUGATED/CONJUGATED bilirubin
Dark urine
Normal stools

98
Q

What are the distinguishing features of post-hepatic jaundice?

A

Increased CONJUGATED bilirubin
Decreased urobilinogen/sterocobilinogen
Dark urine
Pale stools + steatorrhoea
Pruritis

99
Q

What are the causes of pre-hepatic jaundice?

A

Haemolysis
Ineffective EPO (B12 deficiency)

100
Q

What are the causes of hepatic jaundice?

A

Hepatitis
Cirrhosis
Drugs
Gilbert’s

101
Q

What are the causes of post-hepatic jaundice?

A

Cholangitis
Pancreatitic ca
Cholangiocarcinoma
Parasites
Liver flukes
Strictures

102
Q

What is Gilbert’s syndrome?

A

Intermittent jaundice during times of stress
Due to lack of UGT-1A1 activity (conjugates bilirubin)
BENIGN

103
Q

What commonly prescribed drugs are hepatotoxic?

A

Paracetamol
TB drugs
Valproate
Statins
COC
MAO inhibitors
Halothane anaesthetics

104
Q

What are the LFT changes of alcoholic liver disease?

A

AST>ALT
High bilirubin
Normal ALP
High GGT
(Macrocytosis)

105
Q

What are the LFT changes of NAFLD?

A

Mildly raised ALT (ALT > AST)

106
Q

What are the LFT changes of ischaemic liver disease?

A

ALT ++++
High LDH

107
Q

What are the LFT changes of drug induced liver disease?

A

ALT ++++

108
Q

What are the LFT changes of acute viral hepatitis?

A

ALT +++
High bilirubin

109
Q

What are the LFT changes of chronic viral hepatitis?

A

ALT ++

110
Q

What are the LFT changes of autoimmune hepatitis?

A

ALT +++
(in young woman of child-bearing age)

111
Q

What are the LFT changes of a cholestatic problem?

A

High ALP & GGT (>AST/ALT)

112
Q

What are the potential causes of a massively raised ALT (1000s)?

A

Acute viral hepatitis
Drug-induced/toxic
Ischaemic liver disease (Budd-Chiari)
Autoimmune liver disease

113
Q

What are the complications of alcohol hepatitis?

A

Cirrhosis
Portal HTN –> ascites, splenomegaly, portosystemic shunts
HCC risk
Malnutrition –> peripheral neuropathy, macrocytic anaemia
Dilated cardiomyopathy

114
Q

What are the common complications of alcohol withdrawal?

A

Delirium tremens
-visual/tactile hallucinations + haemodynamic instability + confusion/tremors –> seizures
-10-72hrs
Wernicke/Korsakoff’s

115
Q

How should acute alcohol withdrawal be managed?

A

Thiamine (Pabrinex)
Chlordiazepoxide

116
Q

What are the consequences of liver failure?

A

Failure of synthetic function - clotting, low Alb, low oestrogen (UGI bleed)
Failure of metabolic function - hypoglycaemia, jaundice
Failure of toxin clearance - encephalopathy, sepsis
Abnormal haemodynamics
Hepatorenal syndrome

117
Q

How should liver failure be managed?

A

Diet - low salt/fluid restricted
Spironolactone high dose
Paracentesis (replace w/ HAS)
TIPS

118
Q

What is spontaneous bacterial peritonitis?

A

Infection of ascitic fluid
-WCC >300-500 million/L
-neutrophils >250 million/L

119
Q

What organisms commonly cause spontaneous bacterial peritonitis?

A

E. coli
Klebsiella
Streptococci

120
Q

What is the management of spontaneous bacterial peritonitis?

A

Tx - IV Ceftriaxone (empirical) + targeted abx
PPx - PO Ciprofloxacin

121
Q

How should hepatorenal syndrome be managed?

A

Stop diuretics
Salt-poor albumin infusion
Dialysis/TIPS/transplant
Avoid hypoK

122
Q

How does acute/decompensated liver failure present?

A

Triad of:
-jaundice
-upper GI bleed/coagulopathy
-encephalopathy

123
Q

What medications should be avoided in acute liver failure?

A

Constipating meds
Sedatives
PO hypoglycaemics
0.9% NaCl
CYP450 inhibitors
Hepatotoxics

124
Q

How should encephalopathy in acute liver failure be managed?

A

Reduce nitrogen load
-avoid constipation/UGI bleed/transfusion/AKI
Tx - Lactulose (traps Ammonia in gut)
PPx - Rifaximin (kills nitrogen forming gut flora)

125
Q

What scoring system can be used to assess Cirrhosis, and what criteria are included?

A

Child-Pugh
-encephalopathy
-ascites
-bilirubin
-PT
-ascites

126
Q

What are the risk factors for NAFLD?

A

Age
Obesity
Dyslipidaemia
Diabetic
HTN/vasculopathy

127
Q

How should suspected NAFLD be ix?

A

Elastrography USS (fibroscan)
Biopsy

128
Q

How should NAFLD be managed?

A

Address obesity/cardiovascular risk factors
Avoid EtoH

129
Q

What are the key features of Hepatitis A?

A

2-6/52 incubation
Constitutional sx + arthralgia
Spread by faecal-oral route

130
Q

What are the key features of Hepatitis E?

A

Constitutional sx + arthralgia
Present in pigs, seafood and contaminated water
High mortality in pregnancy –> fulminant hepatitis

131
Q

What are the key features of Hepatitis B?

A

DNA virus
1-6/12 incubation
Spread by blood/sex

132
Q

What is significant about the presence of HBeAG/HBV DNA?

A

Indicates infectivity

133
Q

What is significant about the presence of HBcAb (core)?

A

Not present in vaccinated groups
Implies acute/past infection

134
Q

What is the management of Hepatitis B?

A

PPx - vaccination
Tx - INF a, Tenofovir

135
Q

What are the non-hepatic complications of Hepatitis B?

A

Polyarteritis nodosa
Membranous nephropathy

136
Q

What are the key features of Hepatitis C?

A

RNA virus
Spread by blood
Chronic cirrhosis
HIV co-infection common

137
Q

What is the management of Hepatitis C?

A

Sofosbuvir/ledipasvir (inhibitors)
Ribavirin (nucleoside analogue)
HIV testing/treatment

138
Q

What do anti-HCV/HCV PCR indicate about Hepatitis C infection?

A

Anti-HCV = exposure
HCV PCR = ongoing/chronic

139
Q

What are the complications of Hepatitis C?

A

Cryo-globulinamaemia
Autoimmune disease (hepatitis, polymyositis, thyroiditis)
Porphyria

140
Q

What infective causes of hepatitis are there?

A

Hepatitis viruses
EBV
CMV
MALARIA
Yellow fever
Leptospirosis

141
Q

What is Fitz-High-Curtis syndrome?

A

Liver capsule inflammation due to transabdominal spread of chlamydia/gonorrhoea
RUQ pain +/- PID +/- ‘violin-string’ adhesions

142
Q

What are the two types of autoimmune hepatitis?

A

Type 1 (80%) - anti SM +ve, sometimes ANA +
Type 2 - LKM1 +ve, ANA negative

143
Q

What is the management of autoimmune hepatitis?

A

Steroids
AZA
Ciclosporin
Transplant

144
Q

What is Budd-Chiari syndrome?

A

Infarction of liver 2o hepatic vv obstruction

145
Q

How does Budd-Chiari syndrome present?

A

PAINFUL hepatomegaly
Ascites
Abdo pain
Cardiovascular shock

146
Q

What are the risk factors for Budd-Chiari syndrome?

A

HCC
Steroids

147
Q

What is the management of Budd-Chiari syndrome?

A

Surgery
-100% mortality if not treated

148
Q

What are the distinguishing features of primary biliary cholangitis?

A

Middle aged women
Obstructive jaundice
Malabsorption
Anti-mitochondrial Ab +ve
ALP/cholesterol +++
Cirrhosis/HCC

149
Q

What are the distinguishing features of primary sclerosing cholangitis?

A

Middle aged men w/ IBD
Malabsorption
Periductal fibrosis w/ onion-skin appearance
MRCP - beaded appearance
pANCA +ve
ALP +++
High risk for cholangiocarcinoma

150
Q

What is primary biliary cholangitis?

A

Autoimmune granulomatous destruction of INTRAHEPATIC bile duct

151
Q

What is primary sclerosing cholangitis?

A

Fibrotic (strictures) of intra AND extrahepatic bile ducts

152
Q

What are the common genetic causes of liver disease?

A

Wilson’s
Haemochromatosis
A1AT

153
Q

What is the underlying mechanism of Wilson’s disease?

A

ATP7B ATPase mutation
Lack of copper transport –> accumulation

154
Q

What is the inheritance pattern of Wilson’s disease?

A

Autosomal recessive

155
Q

How does Wilson’s disease present?

A

Haemolysis
Arthritis, grey skin, blue nails
Kayser-Fleischer rings
CNS –> movement disorders + cognitive decline + depression

156
Q

How should suspected Wilson’s disease be ix?

A

24hr urinary excretion
LFTs (mod raised)
Serum Ca/caeruloplasmin LOW
Biopsy
Gene testing

157
Q

What is the management of Wilson’s disease?

A

Lifelong Penicillamine
Liver transplant
Avoid high copper foods - liver, chocolate, nuts, mushroom, shellfish

158
Q

What are the s/e of Penicillamine?

A

Drug-induced lupus
Nephrotic syndorme
Pancytopenia

159
Q

What is the underlying mechanism of haemochromatosis?

A

HFE mutations –> increased intestinal Fe absorption –> Fe excess

160
Q

How does haemochromatosis present?

A

Arthritis + pseudogout of knee
Slate-grey pigmentation
Chronic liver disease –> HCC
Dilated cardiomyopathy
Insulin-dependent diabetes
Hypongadism

161
Q

How should suspected haemochromatosis be ix?

A

Ferritin/transferrin sats HIGH
LFTs (mod raised)
Biopsy (w/ Perl’s/Prussian blue stain)

162
Q

How is haemochromatosis managed?

A

Regular venesection
Chelators (Desferrioxamine)
Avoid Fe rich foods

163
Q

What is the underlying mechanism of A1AT deficiency?

A

Inability to transport serine protease inhibitor out of liver
Presents w/ liver/lung disease

164
Q

How should suspected A1AT deficiency be ix?

A

A1AT levels (low)
Spirometry (obstructive)
Liver biopsy
Genotyping

165
Q

How should A1AT deficiency by managed?

A

Smoking cessation
Vaccines
IV A1AT
Lung/liver transplant

166
Q

What 1o tumours commonly metastatize to the liver?

A

Breast
Bronchus
Bowl
Babies (uterus)

167
Q

What are the risk factors for HCC?

A

Hep B/C
Cirrhosis
NAFLD
Anabolic steroids
Aflatoxin (aspergillus)

168
Q

What benign masses are commonly found in the liver?

A

Haemangioma
Adenomas
-associated w/ COCP, anabolic steroids, pregnancy

Pocket MSRA - Book 1 (7 decks)

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