Gastroenterology Flashcards
1
Q
What is the route of the oesophagus?
A
Fibromuscular tube transporting food from pharynx to stomach beginning at cricoid cartilage (C6) to cardiac sphincter/orifice (T11)
2
Q
What are the layers of the oesophagus?
A
Mucosa
Submucosa
Muscle layer
Adventitia
3
Q
What are the two oesophageal sphincters?
A
• Upper Oesophageal Sphincter (UOS @ T11): Anatomical sphincter consisting of striated muscle at pharyngoesophageal junction;
Resting tone contracted reduce air entry
• Lower Oesophageal Sphincter (LOS; cardiac sphincter @ L1): Physiological (functional) sphincter present at gastro-oesophageal junction with no muscle but 4 factors maintaining function (acute angle + compressed when positive IAP + Mucosal folds + R Crus of Diaphragm)
Resting tone constricted prevent reflux
3
Q
What are the two oesophageal sphincters?
A
• Upper Oesophageal Sphincter (UOS @ T11): Anatomical sphincter consisting of striated muscle at pharyngoesophageal junction;
Resting tone contracted reduce air entry
• Lower Oesophageal Sphincter (LOS; cardiac sphincter @ L1): Physiological (functional) sphincter present at gastro-oesophageal junction with no muscle but 4 factors maintaining function (acute angle + compressed when positive IAP + Mucosal folds + R Crus of Diaphragm)
Resting tone constricted prevent reflux
4
Q
State the 4 oesophageal constrictions.
A
Mnemonic: ABCD
- Arch of aorta
- Bronchus (L)
- Cricoid cartilage
- Diaphragmatic hiatus (T10)
5
Q
Which arteries supply the oesophagus?
A
- Oesophageal branch of Inferior Thyroid Artery (Fr. Thyrocervical Trunk)
- Oesohageal arteries (Fr. Thoracic aorta): 4-5x from anterior abdominal aorta + anastomose with oesophageal branches of inferior thyroid arteries + below with ascending branches of L phrenic + L gastric
- Left Gastric artery: Branches to anterior and posterior branch to supply intramural and submucosal plexuses
6
Q
Which veins drain the oesophagus?
A
- Oesophageal veins (From peri-oesophageal venous plexus): Drain submucosal plexus -> Inferior thyroid vein (cervical) OR Azygous Veins, Hemiazygos Veins, Intercostal and Bronchial veins (abdominal)
- Left gastric veins: Drain into portal vein
7
Q
Give 5 conditions where you may get mouth ulcers.
A
- Idiopathic
- Anaemia
- IBD
- Coeliac
- Behcet’s Disease
- Reiter’s Disease
- SLE
- Pemphigus
- Pemphigoid
- Drug Reactions
- SCC
- HSV 1
- Coxsackie A
- HZV
8
Q
Give 3 conditions in which you may get oral white patches?
A
- Candida
- SLE
- Trauma: Mechanical/Irritative
- Immunocompromised
- Leucoplakia (pre-malignant)
9
Q
Give 3 causes of glossitis.
A
Allergy
Burns
B12 deficiency
Folate deficiency
Infection
Kawasaki disease
Scarlett fever
10
Q
Give a cause of Filiform Papillae.
A
- Unknown
- Heavy smoking
- Antiseptic mouthwashes
11
Q
Describe Geographic Tongue.
A
Idiopathic condition presenting with erythematous areas surrounded by well-defined, irregular margins which are usually painless
12
Q
What are the two subtypes of GORD?
How are they determined?
A
- Erosive Reflux Disease (ERD): Erosions present on endoscopy
- Non-Erosive Reflux Disease (NERD): No erosions present on endoscopy
Determined on endoscopy
13
Q
What are the clinical features of GORD?
A
- Heartburn (or dyspepsia)
- Acid regurgitation
- Water-brash (sialorrhea + bad taste)
- Halitosis
- Odynophagia
- Cough
- Dental erosion
- Globus pharyngeus (FOSIT)
14
Q
How do you diagnose GORD?
A
- Clinical diagnosis
- PPI Trial: Sx improvement over 8-week trial
Consider
• H. pylori testing: Urea breath test (-> detection of Carbon dioxide)
• Serology: IgG Ab
15
Q
How do you manage GORD?
A
• Supportive: Diet/Weight reduction/Smoking cessation/ NSAID cessation
+
• PPI: Omeprazole (20mg PO OD)/ Lansoprazole (15-30mg PO OD)/ Esomeprazole (20-40mg PO OD)
(H. pylori infection)
+
• H. pylori eradication therapy: PPI + Metronidazole/Amoxicillin + Macrolide for 7/7
16
Q
A patient with GORD has a positive Urea breath test.
What is the management?
A
H. pylori eradication therapy: Amoxicillin + Erythromycin + PPI
+
Gaviscon
17
Q
What are the over the counter options for dyspepsia?
A
Gaviscon (Alginates)
Antacids (MgOH2)
Simeticone (antifoaming agents)
18
Q
Describe Barrett’s Oesophagus.
A
Change in the stratified squamous epithelium (SSE) of oesophagus to the simple columnar epithelium (SCE) in intestinal metaplasia thus displacement of the squamo-columnar junction of the oesophagus
19
Q
How is Barrett’s Oesophagus diagnosed?
A
- Upper GI Endoscopy + Biopsy: Abnormal epithelium (violaceous near to GO junction); Z-line (SC junction) migration cephalad (boundary at oesophageal and gastric epithelium junction); Ulceration; Strictures; Nodularity
- Biopsy: histologically ∆ from SSE -> SCE
20
Q
How do you manage Barrett’s Oesophagus?
A
Depending on if it there is evidence of Dysplasia.
Non-Dysplasia:
Annual surveillance
+ PPI
Dysplasia
• Intervention: Radiofrequency ablation ± Endoscopic mucosal resection
21
Q
Describe Achalasia.
A
Oesophageal motor disorder of unknown aetiology characterised by oesophageal aperistalsis and insufficient lower oesophageal (cardiac) sphincter relaxation following swallowing
22
Q
The co-occurrence of Achalasia, Alacrima and Adrenal insufficiency is termed?
A
Allgrove Syndrome (Triple A)
23
Q
Allgrove Syndrome describes…
A
Adrenal Insufficiency
Achalasia
Alacrima
24
What are the core clinical features of Achalasia?
* Dysphagia: Difficulty swallowing liquids and solids
* Retrosternal pressure/pain
* Regurgitation
* Gradual weight loss
* Recurrent chest infections (2º to regurgitation)
* Globus pharyngeus
* Coughing/Choking whilst recumbent
25
What type of food is difficult to swallow in Achalasia?
Solids and liquids
26
What investigations would you order to positively identify Achalasia?
* Upper GI Endoscope: Retained frothy saliva, oesophageal dilation, sigmoid oesophagus (tortuous)
* Barium swallow: Loss of peristalsis; delayed oesophageal emptying; dilated oesophagus tapering to narrowing (beak-like narrowing)
* Oesophageal manometry: Incomplete relaxation of lower oesophageal sphincter; oesophageal aperistalsis
27
What is the gold-standard investigation to accurately rule-in Achalasia?
Barium swallow - a loss of peristalsis, beak-like narrowing is observed
28
A patient who has been struggling to swallow both solids and liquids, with regurgitation and retrosternal pain undergoes a barium swallow.
A beak-like narrowing is shown with dilated oesophagus present and tapering at area of narrowing.
He is 34 years old and otherwise healthy with an ASA classification of 1.
How would you manage this patient?
• Pneumatic dilatation (balloon to mechanically stretch lower oesophageal sphincter)
OR
• Laparoscopic cardiomyotomy (Heller Procedure = opens tight cardiac sphincter
29
A patient who has been struggling to swallow both solids and liquids, with regurgitation and retrosternal pain undergoes a barium swallow.
A beak-like narrowing is shown with dilated oesophagus present and tapering at area of narrowing.
He is 34 years old and has Diabetes Mellitus, Cystic Fibrosis and recurrent chest infections with an ASA classification of 4.
How would you manage this patient?
Poor Surgical Candidate
• CCBs: Nifedipine/Verapamil
2nd Line
• Botulinum toxin type A (Paralysis of cardiac sphincter)
30
What is the second line treatment for Achalasia in a non-surgical candidate?
• Botulinum toxin type A (Paralysis of cardiac sphincter)
31
Describe Systemic Sclerosis.
Condition in which smooth muscle layer is replaced by fibrous tissue and LOS pressure is reduced which results in secondary GORD
32
Outline the clinical features of Systemic Sclerosis.
CREST symptoms
```
Calcinosis cutis
Raynaud's
(o)Oesophageal dysmotility - GORD
Sclerodactyly
Telangiectasia
```
33
What antibodies are present in Systemic Sclerosis?
Anti-Scl70
Anti-Centromere
34
How do you manage the GI symptoms of Systemic Sclerosis?
* Oral corticosteroid: Prednisolone
* PPI
If gastroparesis
• Prokinetic agent: Erythromycin/Azithromycin
35
How can you manage the Raynaud's Phenomenon in Systemic Sclerosis?
• Lifestyle: Cold exposure, hand exercises, smoking cessation
+
• CCB: Amlodipine
+ (Digital Ulceration)
• PDE-5 inhibitor: Sildenafil/Tadalafil
36
What is a Hiatus Hernia?
Protrusion of the IA contents through the oesophageal hiatus (T10) of the diaphragm characterised by heartburn, regurgitation, chest/abdominal pain and bowel sounds in chest.
37
How may Hiatus Hernias be classified?
Grade 1: GO junction into thorax
Grade 2: Fundus/ portion of stomach into thorax
Grade 3: Mixed (both)
Grade 4: IA contents into thorax
38
What are the clinical features of a Hiatus Hernia?
* Heartburn
* Regurgitation/Vomiting
* Chest pain
* SOB
* Cough
* Dysphagia
* Odynophagia
* Hematemesis
* Non-bilious vomiting
39
What would the gold-standard imaging be for a suspected Hiatus Hernia?
What would you expect to see?
• CXR: Retrocardiac air bubble
40
How do you manage a Hiatus Hernia?
• Surgical repair ± anti-reflux procedure: Laparoscopic transabdominal surgery OR Open transabdominal surgery
41
Following treatment of a hiatus hernia via laparoscopic transabdominal repair, Mr. Johnson, a 57 year old male, is vomiting blood. Additionally, he reports pain.
O/E he is hypotensive and tachycardic. AXR shows pneumoperitoneum.
What is your differential?
How would you manage this?
Iatrogenic Oesophagus Perforation
• Endoscopic Oesophageal stenting
±
• Confirmatory water-soluble contrast XR-A
42
Describe Boerhaave's Syndrome.
Transmural tears of distal oesophagus induced by sudden intra-oesophageal pressure rise characterised by retching, vomiting and severe epigastric/retrosternal pain
43
What is the pathological difference between Boerhaave's Syndrome and Mallory-Weiss Tears?
Boerhaave's = transmural
Mallory-Weiss = partial tears
44
What is the name of the crunching sound of the heart heard on auscultation due to air in the thorax?
Hamman's Sign
45
A 47 year old man presents with brisk haematemesis and severe abdominal pain following a large meal and a night on the beers. He is retching.
O/E his RR is 26, his HR is 130bpm, regular and S1+S2 appear to have a crunching sound.
What investigations would you order?
What is your differential?
What screening tool may you use to calculate the risk of a GI bleed?
How would you manage this patient?
* CXR: Mediastinal, peritoneal, prevertebral air; widened mediastinum
* Water-soluble contrast swallow: Localises lesion
* CT: Confirmatory findings = oesophageal wall oedema, peri-oesophageal fluid ± bubbles and widened mediastinum
Boerhaave's Syndrome
Blatchford Score
```
• IV Fluid Resuscitation
+
• Broad-spectrum ABX
±
• Surgery
```
46
Describe Mallory-Weiss Syndrome.
Non-transmural tear of tissue in lower oesophagus associated with violent coughing or vomiting
47
How would you manage a Mallory-Weiss Syndrome?
• Endoscopy (endoscopic hemostasis) ± Blood transfusion: Identify cause of bleeding, stop bleeding (adrenaline ± cautery/clips) ± Blood transfusion
48
Describe what Oesophageal Varices are.
Enlarged veins within the oesophagus due to obstructed blood flow in the portal system characterised by brisk haematemesis, melaena and pre-syncope/LOC.
49
Outline the pathophysiology of how Oesophageal varices may occur.
A hepatic pathology e.g. Cirrhosis occurs which results in increased intrahepatic resistance. The retrograde pressure of blood via the portal vein, results in distension of the L Gastric (coronary) vein. Blood is then shunted into the azygous veins and venous hypertension occurs in the peri-oesophageal plexus resulting in distension and varices.
50
What are the clinical features of oesophageal varices?
* Brisk hematemesis
* Melaena
* Pre-syncope/LOC
* Jaundice
* Ascites
* Hepatic encephalopathy
* Spider naevi
* Hair loss
* Leukonychia
* Anorexia
* Weight loss
* Hepatomegaly
51
Why does leukonychia occur in chronic liver disease?
Chronic hypoalbuminaemia
52
What is the eponymous term for Leukonychia striata?
Muerhcke's Nails
53
How do you manage a patient with bleeding Oesophageal varices?
• Endoscopy (endoscopic hemostasis) ± Blood transfusion: Identify cause of bleeding, stop bleeding (adrenaline ± cautery/clips) ± Blood transfusion
+
• NSBBs: Propanolol/Carteolol
54
What is the order of treatment in an Oesophageal variceal bleed?
A-E
Terlipressin + Band ligation
If controlled, calculate Child-Pugh Score
If uncontrolled, repeat and try cautery/clips.
If continuous bleeding, try TIPS
55
Give 5 RFs for Oesophageal Varices
Hepatitis
Cirrhosis
Portal hypertension
Budd-Chiari Syndrome
Alcoholism
Drug use
PMHx Varices
Parasitic infection
Thrombotic disorders
56
A 37 y/o M patient presents with dysphagia 3/12, heartburn and nausea and vomiting. He reports some abdominal pain. He has previously undergone a PPI trial which helped a bit but he is still getting symptoms.
His PMHx is asthma and rhinitis. Both of which are well controlled.
What investigations would you order?
H. Pylori breath test
OGD + Biopsy
57
A 37 y/o M patient presents with dysphagia 3/12, heartburn and nausea and vomiting. He reports some abdominal pain. He has previously undergone a PPI trial which helped a bit but he is still getting symptoms.
His PMHx is asthma and rhinitis. Both of which are well controlled.
The OGD shows focal oesophageal strictures, narrowing and crepe paper mucosa. A biopsy shows a Eosinophilic count of 30 per microscopy field.
What is the threshhold of eosinophilic count for this condition in an oesophageal biopsy?
What is your differential?
How would you manage this condition?
> 15 per microscopy field
Eosinophilic Oesophagitis
• Oral corticosteroid: Budesonide/Fluticasone
(inhaler)
±
• Endoscopic oesophageal dilatation
58
Describe what an Oesophageal cancer is.
Neoplasm in the mucosa originating from epithelial cells lining oesophagus, presenting with dysphagia and odynophagia
59
What is the most common type of Oesophageal cancer?
Adenocarcinoma
60
State 5 RFs for Oesophageal cancer.
```
GORD
Barrett's Oesophagus
High BMI
Smoking
Alcohol
HPV
```
61
What is the initial investigation for a patient with suspected Oesophageal cancer?
• Oesophagogastroduodenoscopy (OGD) + Biopsy: Mucosal lesion; Histology shows SCC or AC
62
Which tool can be used to assess the risk of an Upper GI bleed?
Blatchford Score
Rockall Score
63
Give the components of the Blatchford Score.
Active: syncope/melaena
Blood urea: >7mmol/L
Circulatory (mmHg): <100mmHg
Drop in Hb: 129; 119
Elevated pulse: >100bpm
Failure: heart or liver
64
What tool can be used to predict the risk of rebleeding and mortality following a GI endoscopy?
What are the components.
Rockall Score
```
Age
Blood pressure
Comorbidity
Diagnosis
Endoscopy findings
```
65
What assessment tool is used to assess the prognosis of chronic liver disease (e.g. cirrhosis) in patients?
Child-Pugh Score
66
What are the components of the Child-Pugh Score?
```
Albumin
Bilirubin
Coagulation (PT)
Disability (ascitic fluid)
Encephalopathy (hepatic)
```
67
What are your management options for Oesophageal cancer?
Stage 0 + 1A
• Endoscopic resection ± ablation (if <2cm, carcinoma in situ)
Surgical Candidate (Stages 1B-3)
• Oesophagectomy
± (Stage 2B-3)
• Chemoradiotherapy: Cisplatin + Fluorouracil + Radiotherapy (CFR)
Non-surgical candidate (Stages 1B-3)
• Chemoradiotherapy or radiotherapy alone: CFR or Radiotherapy
```
Stage 4
• Chemotherapy: Fluorouracil + Cisplatin
±
• Radiotherapy: Radiotherapy
±
• Endoscopic ablation ± Stenting
```
68
How do you manage Nausea in a patient?
Supportive: trigger avoidance; fizzy drinks
Medical: Hyoscine; Cyclizine; Metoclopramide; Ondansetron
69
What class of drug is Hyoscine?
Anti-M1
70
What class of drug is Cyclizine?
Anti-H1
71
What class of drug is Promethazine?
Anti-H1
72
What class of drug is Domperidone?
D2 antagonist
73
What class of drug is Metoclopramide?
D2 antagonist
74
What class of drug is Ondansetron?
5HT3 antagonist
75
Which anti-emetic is safe in Parkinson's disease?
Domperidone
76
What are the side effects of Metoclopramide?
Extrapyramidal side effects
Prolactin release
77
What are the side effects of Promethazine?
Anticholinergic syndrome
78
What are the side effects of Cyclizine?
Anticholinergic syndrome
Angle closure glaucoma
79
Describe Peptic Ulcer Disease.
Breach in mucosal lining of stomach or duodenum (> 5mm in diameter) with penetration to the submucosa.
```
Caused by:
• H. pylori
• NSAIDs
• Zollinger-Ellison Syndrome -> Passaro’s triangle (gallbladder-D2/D3-pancreas)
• Vascular insufficiency
• Sarcoidosis
• Crohn’s Disease
```
80
What is the term for the site where most gastronomas occur?
Passaro's Triangle
Gallbladder-D2/3-Pancreas
81
What test is suggestive of a H. pylori infection causing an ulcer?
* H. pylori urea breath test/stool antigen test: Positive if H. pylori present
* Upper GI endoscopy: Peptic ulcer
82
What hormone will be elevated in Zollinger-Ellison Syndrome?
• Serum gastrin level: Hypergastrinemia in Z-E Syndrome
83
What is the difference between an ulcer and an erosion?
Ulcer > 5mm (diameter)
Erosion < 5mm
84
How do you manage Peptic Ulcer disease?
Supportive: Take medication regularly; eat good meals; reduce spicy foods
Medical: PPI;
H. Pylori eradication: Amoxicillin + PPI + Clarithromycin
Surgical: Endoscopic haemostasis (adrenaline + clips/ banding)
--> If an active bleed
85
Describe Gastritis.
Gastric mucosal inflammation often caused by H. pylori/ NSAIDs/ alcohol use/bile reflux or infection which is characterised by nausea, vomiting, loss of appetite, severe emesis, acute abdominal pain and fever.
86
What are the causes of Gastritis?
* H. pylori
* NSAIDs
* Alcohol
* Bile reflux
* Stress-induced (critically-ill)
* Auto-immune (Abs to Parietal cells)
* Infection by S. aureus; Streptococci; E. coli; Enterobacter; C. welchii
87
How do you treat Gastritis?
PPI/H2A
88
Describe Atrophic Gastritis?
Condition of mucosal atrophy, gland loss and metaplastic changes caused by chronic inflammation either from autoimmune (AMAG) or environmental causes (EMAG) characterised by haematemesis, epigastric pain, abdominal paraesthesia, dyspepsia and anaemia.
89
What are the two types of Atrophic Gastritis?
* Autoimmune Metaplasic Atrophic Gastritis (AMAG)
| * Environmental Metaplasic Atrophic Gastritis (EMAG)
90
What is the main difference between Atrophic Gastritis and Gastritis?
Mucosal atrophy and gland loss occurs due to chronic gastritis (in Atrophic Gastritis)
91
Describe Menetrier's Disease.
Rare disease featuring mucosal cell (foveola) overgrowth in mucosal lining on a background of inflammation characterised by epigastric pain, nausea, vomiting, diarrhoea, weight loss or anorexia or may be asymptomatic
92
What is the gold standard investigation for diagnosing Menetrier's Disease?
• Endoscopy: Variable – gastric erosions ± atrophy + Foveolar cell proliferation
93
How do you manage gastric cancer?
• Surgery: Resection
± (T2 or higher and any N)
• Chemotherapy (Peri vs Post): Peri (ECF) Epirubicin + Cisplatin + Flurouracil; Post (Radiotherapy + Fluorouracil)
Localised Non-Surgical Candidate
• Chemoradiation: Radiotherapy + Fluorouracil
Advanced
• Chemoradiation: Radiotherapy + Fluorouracil
94
What is a GIST?
Common type of stromal/mesenchymal tumour in the GI tract present commonly in the stomach and proximal SI which have malignant potential and are asymptomatic.
95
How are Gastrointestinal Stromal Tumours found?
• Endoscopic
Often an incidental find
96
How may GISTs be managed?
Surgical Candidate
• Resection
Non-Surgical Candidate
• Imatinib (TKI)
97
What is the most common cause of a Gastric Lymphoma?
• H. pylori infection (90% cases)
98
Describe Zollinger-Ellison Syndrome.
Gastrin-secreting tumour resulting in gastric acid (HCl) hypersecretion with secondary ulceration characterised by symptoms of epigastric pain and diarrhoea.
99
How may ZES be diagnosed?
* Upper GI endoscopy: Prominent gastric folds ± Ulcer
* Endoscopic US (EUS): Identification of tumours
* Fasting Serum Gastrin: Elevated
* Basal Acid Output (BAO): Elevated
100
How do you measure a Basal Acid Output?
Continuous suction at subatmospheric pressure of 30-50mmHg via syringe in 15 minute periods
101
A patient with known Zollinger-Ellis Syndrome is shown to have elevated BAO and endoscopy shows multiple tumours. CT-CAP shows hepatic metastasis.
How would you manage this patient?
PPI
+
SS analogue
102
What is the role of Octreotide in ZES?
Octreotide is a SS analogue thus inhibits the secretion of Gastrin from G-cells
103
Describe Coeliac disease.
Systemic autoimmune disease triggered by dietary gluten peptide (a-gliadin) which triggers an immune reaction causing villous atrophy, hypertrophy of crypts and lymphocyte infiltration characterised by symptoms of bloating, diarrhoea, abdominal pain/discomfort
104
What is the offending agent in Coeliac disease?
alpha Gliadin
104
What anti
105
What dermatological manifestation of Coeliac disease exists?
Where is this most commonly found?
• Dermatitis herpetiformis: Pruritic papulovesicular lesions on extensor surfaces of arms, legs, buttocks, trunk, neck and scalp.
106
Outline the key clinical features of Coeliac disease.
* Bloating
* Weight loss
* Fatigue/Malaise
* Diarrhoea
* Abdominal pain/discomfort
* Anaemia: Microcytic (Iron-deficiency anaemia)/ Macrocytic (Folate/Vit B12 deficiency)
• Dermatitis herpetiformis: Pruritic papulovesicular lesions on extensor surfaces of arms, legs, buttocks, trunk, neck and scalp.
107
What is the gold-standard investigation in the diagnosis of Coeliac disease?
EMA Abs
IgA-tTG
108
Why is IgA used as the marker in Coeliac disease, not IgG?
IgA is the predominant antibody in the lining of the respiratory and gastrointestinal mucosa cf IgG being the predominant antibody in bodily fluids
IgG may be used in IgA deficiency - shown by blood test
109
What is the management for Coeliac disease?
Supportive: Annual Review; Vitamin D; Vitamin B12; Folate; Iron
± Coeliac Crisis
Corticosteroids
± Hyposplenism
Pneumococcal vaccine
110
What is the management for Coeliac disease?
Supportive: Annual Review; Vitamin D; Vitamin B12; Folate; Iron
± Coeliac Crisis
Corticosteroids
± Hyposplenism
Pneumococcal vaccine
111
What is a Coeliac crisis?
Initial presentation of Coeliac disease with severe diarrhoea, dehydration, weight loss, hypoproteinaemia and metabolic/electrolyte disturbances
112
What pathogen causes Whipple's Disease?
Tropheryma whipplei
113
What are the clinical features of Whipple's disease?
* Fever
* Night sweats
* Diarrhoea
* Weight loss
* Abdominal pain
* Arthralgia
* Skin hyperpigmentation to sun exposed areas
* Lymphadenopathy
* Neurological Sx: Seizures; Confusion; Nystagmus; Brisk reflexes; Hypertonia; Ataxia
114
How would you manage Whipple's disease?
• ABX: Ceftriaxone OR Benzylpenicillin sodium
115
Outline the clinical features of GI TB.
* Cough: 2-3 weeks; dry -> productive
* Fever (low-grade)*
* Anorexia*
* Weight loss*
* Malaise*
* Night sweats*
* Diarrhoea*
* Abdominal pain*
* Abdominal mass*
* Hepatomegaly*
* Ascites*
* Dyspnea
* Crackles
* Bronchial breathing
* Amphoric breath sounds (distant hollow breath sounds heard over cavities)
* Clubbing
* Erythema Nodosum
116
How do you test for TB using AFB smear?
3 specimens, 8 hours apart which must be positive
117
How do you treat TB?
RIPPE
```
Rifampicin
Isoniazid
Pyridoxine
Pyrazinamide
Ethambutol
```
118
How do you treat multi-drug resistant TB?
MKIPE
```
Moxifloxacin
Kanamycin
Isoniazid
Pyridoxine
Pyrazinamide
Ethambutol
```
119
What are the side effects of Rifampicin?
Red coloured urine
Rash
Purpura
Abdominal Pain/ Nausea
120
What are the side effects of Ethambutol?
Reduced visual acuity
Optic Neuritis
121
What are the side effects of Pyrazinamide?
Hyperuricaemia (gout)
122
What are the side effects of Isoniazid?
Peripheral neuropathy
Sideroblastic anaemia
Hepatitis
123
Describe what a protein-losing enteropathy is?
Umbrella term for conditions causing loss of serum protein via GI tract causing hypoproteinaemia characterised by peripheral oedema, ascites and other GI Sx dependent on cause.
124
What are the clinical features of a protein-losing enteropathy?
* Ascites
* Peripheral oedema
* Abdominal distension
• Other Sx + S relevant to cause e.g. CD/UC/Coeliac’s/Enteritis/Lymphangiectasis
125
Describe a Meckel's Diverticulum.
Congenital malformation of the bowel which forms a diverticulum (blind tube from a cavity) near the ileocaecal valve due to abnormal vitelline duct healing (5/40) in foetal development characterised by lack of symptoms (asymptomatic) or presentation with haematochezia, obstipation, abdominal pain and abdominal tenderness.
126
What is the foetal remnant that fails to heal in a Meckel's Diverticulum?
Abnormal vitelline duct healing
127
What age do Meckel's Diverticuli tend to present?
2 y/o
128
What proportion of the population have Meckel's Diverticulum?
2%
129
Where are Meckel's Diverticulum situated?
2 foot proximal to ileocaecal valve
130
How long are Meckel's Diverticuli?
2 inches
131
What rule can be used when remembering the properties of a Meckel's Diverticulum?
‘Rule of 2’ – Presents before 2 years age, 2% population, 2 feet of ileocaecal valve (proximal) and 2 inches in length.
132
Outline the clinical features of a Meckel's Diverticulum.
• Asymptomatic
* Hematochezia
* Obstipation (= cannot pass hard faeces)
* Nausea
* Vomiting
* Lower Abdominal pain
* Diffuse abdominal tenderness
133
What diagnostic tests may be used to diagnose a Meckel's Diverticulum?
* Meckel’s Scan (Technetium Pertechnetate Scan and y-camera): Ectopic focus/Hot spot; enhancing diverticulum
* CT-Abdomen: Blind-ending, fluid-filled/gas-filled structure
* Surgical Exploration of Abdomen: Meckel’s diverticulitis/diverticulum identified
134
How would you manage a Meckel's Diverticulum?
Asymptomatic
• Surveillance
Symptomatic
• Surgery: Excision of diverticulum and opposing region of ileum
135
What are the types of Ischaemic Bowel Disease?
* Acute Mesenteric Ischaemia: Sudden reduction in perfusion to SI resulting in necrosis and disruption of barrier + sepsis risk
* Chronic Mesenteric Ischaemia: Slow progressing stenosis of two or more thus postprandial mismatch and pain
* Colonic Ischaemia (Ischaemic Colitis): Disruption of SMA/IMA compromised with hypoxia and necrosis ± infarction and necrosis (gangrenous type) and potential sepsis
136
How may Ischaemic Bowel Disease present?
* Haematochezia
* Melaena
* Diarrhoea
* Abdominal tenderness
* Abdominal pain
* Tenesmus
* Weight loss
• Abdominal bruit
137
What is the management for an Acute Bowel Ischaemia?
• Supportive + Resuscitation: Fluids/ Inotropic support/ Oxygen/ NG tube for decompression/ Correct heart arrhythmias or metabolic abnormalities
-> Hemodynamically stabilize pt
+
• ABX: Ceftriaxone + Metronidazole
+
• Surgery: Exploratory laparotomy/laparoscopy
+ Bowel resection and Bypass surgery
138
How is Acute Bowel Ischaemia Diagnosed?
CT angiography
ABG
Lactate
139
What cell type does an Adenocarcinoma arise from?
Epithelial cells
140
How is Peutz-Jeghers Syndrome inherited?
Autosomal dominant
141
What gene is mutated in Peutz-Jeghers Syndrome?
STK11, a tumour suppressor gene
142
What are the clinical features of Peutz-Jeghers Syndrome?
* Diarrhoea/Constipation
* Hematochezia
* Multiple hamartomatous polyps in GI tract
* Pigmentation: Oral Mucosa and Lips
* Mucocutaneous lesions
* FHx of polyps
143
How do you manage Peutz-Jeghers Syndrome?
Polypectomy
144
In a Carcinoid syndrome, what hormone is secreted?
Serotonin (5-HT) and other vasoactive peptides - e.g. Vasoactive Intestinal Peptide
145
What are the clinical features of Carcinoid Syndrome from a GI NET?
* Diarrhoea
* Abdominal cramps/pain
* Telangiectasia
* Hepatomegaly
* Palpitations
* SOB
* Cardiac murmurs
* JVP Raised
* Peripheral oedema
* Wheeze
* Abdominal mass
146
What investigation will accurately rule-in a Carcinoid Syndrome from a NET of the GUT?
* ChromograninA (CgA): Positive
| * Urinary 5-hydroxyindoleacetic acid (5-HIAA): Positive/Elevated
147
How do you treat a GI NET causing Carcinoid Syndrome?
```
Surgical Candidate
• Surgery: Surgical resection
+
• Perioperative octreotide infusion
±
• Radiofrequency ablation
```
Non-Surgical Candidate
• Octreotide
148
What criteria are used in the diagnosis of IBS?
What does it outline?
Rome IV Criteria
Must have 1 episode per week for 3 months AND ≥2:
- Form
- Frequency
- Flatulence
- Defaecation
149
Describe Irritable Bowel Syndrome.
Chronic condition characterised by abdominal pain, relieved by defecation, + bowel dysfunction ± bloating.
150
Give 3 RFs for Irritable Bowel Syndrome.
* Abuse: Physical or Sexual
* PTSD
* Age < 50 years
* Female Sex
* FH
* PMHx enteric infection
151
What are the clinical features of Irritable Bowel Syndrome?
* Abdominal pain/discomfort
* ∆ bowel habits
* Bloating/Distension
* Passage of mucous with stool
* Tenesmus (urge of defecation)
152
What investigations are used to differential IBS from IBD?
Give examples and say which investigations is best for each disease.
Lactoferrin (IBS)
Calprotectin (IBD)
Occult Blood (IBD)
Coeliac (negative in both)
CRP (IBD)
Colonoscopy (IBD)
153
How may you manage IBS?
Supportive: Education/ Reduce stimulants/ Reduce lactose/ Reduce fructose/ Increase fibre/ Probiotics
If constipated:
- Lactulose
- Sodium Docusate
If bloating:
- Lactulose
- Hyoscyamine
If diarrhoea:
- Loperamide
154
When do you offer Psychiatric intervention in IBS?
If symptoms persist for 12 months then offer CBT
155
What are the pathological changes of Crohn's Disease?
* Any GI Region: Oral and perianal disease
* Discontinuous involvement (skip lesions)
* Deep ulcers and fissures = cobblestone appearance
* Transmural inflammation
* Granulomas
156
Outline the clinical features of Crohn's Disease.
* Fever: Low grade
* Fatigue
* Weight loss
* Abdominal pain/tenderness/mass: RLQ
* Diarrhoea: Non-bloody
* Malabsorption
* Perianal lesions: Skin tags, fistulae, abscesses, scarring
Extra-GI Sx
• Eyes: Uveitis/ Episcleritis/ Conjunctivitis
• MSK: Arthralgia/Arthritis/Monoarticular arthritis/Ankylosing Spondylitis/ Inflammatory back pain
• Skin: Erythema nodosum/ Pyoderma gangrenosum
• Hepatobiliary: Fatty liver/ Primary Sclerosing Cholangitis/ Hepatitis/ Cirrhosis/ Gallstones
• GU: Oxalate stones
• Vascular: VTE
157
Cobblestoning is a feature of CD or UC?
CD
158
Skip lesions are a feature of CD or UC?
CD
159
Transmural damage is a feature in UC or CD?
CD
160
What type of granulomas are present in IBD?
Which type of IBD are these a feature of?
Non-caseating granulomas are a feature of UC
161
If a patient has 1 episode of Crohn's Disease in a year, what is the management?
Monoepisode thus Monotherapy
Supportive: Smoking cessation; Diet
+
Corticosteroids: Prednisolone
162
Describe Ulcerative Colitis.
Type of Inflammatory Bowel Disease (IBD) that arises from dysregulation between gut barrier, immune host defense and environment, affecting the distal colon/rectum and characterised by bloody diarrhoea, rectal bleeding, tenesmus and abdominal pain.
163
What are the pathological features of Ulcerative Colitis?
```
Colon and rectum affected only
Continuous involvement
Erythema
Mucosal granularity
Friable mucosa
```
Mucosa change
No granulomas
Crypt abscess
164
How do you manage mild ulcerative colitis?
Depends on if it is limited to one region such as proctitis or distal colitis (sigmoid, left colon and rectum)
Topical ASA: Mesalazine
±
Oral ASA: Mesalazine
165
What are the main differences between CD and UC regarding macroscopic pathology?
CD:
- Any part of GI tract
- Oral and perianal disease
- Discontinuous (skip lesions)
- Deep ulcers and fissures (cobblestone mucosa)
UC:
- Affects only colon
- Begins in rectum and extends proximally
- Continuous involvement
- Red, friable mucosa
166
What are the main differences between CD and UC regarding microscopic pathology?
CD:
- Transmural inflammation
- Granulomas present
UC:
- Mucosal inflammation
- No granulomas
- Goblet cell depletion
- Crypt abscesses
167
Goblet cell depletion occurs in which from of IBD?
UC
168
Non-caseating granulomas occur in which form of IBD?
CD
169
Crypt abscesses occur in which type of IBD?
UC
170
How may you manage constipation?
```
Correct underlying cause
+
Supportive: Fluids; Fibre; Diet
+
Laxatives: Ispaghula husk; Senna; Lactulose/PEG/Docusate
```
171
What are the different types of diarrhoea?
- Osmotic: Hypertonic solutes draw water into intestine causing watery stools
- Secretory: Active intestinal secretion + reduced absorption
- Inflammatory: Damage to mucosal cells causes fluid loss and reduced absorption
- Motility: Hypermotility of GI tract
Mnemonic: MISO
Motility
Inflammatory
Secretory
Osmotic
172
How may you manage Diarrhoea?
```
• Underlying cause
+
• Supportive: Oral rehydration/ IV rehydration
+
• Antidiarrheal drugs: Loperamide
```
173
What are the clinical features of Appendicitis?
* Central umbilical pain moving to the right hand side
* RIF tenderness
* Nausea and vomiting
* Fever
* Anorexia
* Rovsings sign- pain in the RIF when the LIF is pressed
* Psoas sign-pain on extending hip if retrocaecal appendicitis
174
What is the term for the pain experienced in the RIF when the LIF is palpated?
Rosving's Sign
175
What is the term for pain extending the thigh at the hip in Apprendicitis?
Psoas Sign
176
What is the first-line investigation to diagnose Appendicitis?
US-Abdomen
177
How is Appendicitis managed?
* Appendicectomy
| * Antibiotics- start pre-op and continue post op
178
What is the difference between Diverticulitis and Diverticulosis?
Diverticulosis is a mucosal pouch formed by extrusions via colonic muscular wall
Diverticulitis is inflammation caused by faecal obstruction of the neck of the mucosal pouch (diverticulum)
179
Can diverticula form in the rectum?
Unlikely as the rectum has an outer longitudinal muscle layer completely surrounding the diameter of the rectum
180
What classification system may be used to describe the severity of an Acute Diverticulitis?
Outline the stages.
Hinchey Classification
Stage 0 = mild clinical diverticulitis
Stage 1a = pericolic inflammation/phlegmon
Stage 1b = pericolic/mesocolic abscess
Stage 2 = pelvic, IA or RP abscess
Stage 3 = generalised purulent peritonitis
Stage 4 = generalised faecal peritonitis
181
Outline the clinical features of an Acute Diverticulitis.
* Abdominal pain: LLQ
* Pelvic tenderness: Guarding + PR tenderness
* Bloating
* Constipation
* Fever
* Rectal bleeding: Abrupt + Painless
• Palpable abdominal mass
182
How do you manage an Acute Diverticulitis.
• Analgesia: Paracetamol
+
• ABX: Ciprofloxacin + Metronidazole
± Perforation/Bleed
Surgery: Hartmann's Procedure (resection of bowel and anastomoses)
183
Describe Hirschprung's Disease.
Congenital condition causing partial/complete functional colonic obstruction due to aganglionic colon segment(s) characterised by symptoms of vomiting, abdominal distension and explosive diarrhoea
184
What are the potential clinical complications of a Diverticulitis?
```
Obstruction/Ileus
Fistulating disease
Perforation
Peritonitis
Large haemorrhage
```
185
How is Hirschprung's Disease classified?
Outline the classifications.
Classified by length of segment involved
Total: Ileocaecal valve to rectum
Long: hepatic flexure to descending colon
Typical: rectosigmoid
Short
186
What investigations may be helpful in diagnosing Hirschprung's Disease?
AXR
CT-Abdomen
Rectal Biopsy
187
What investigation can confirm the diagnosis of Hirschprung's Disease?
Rectal biopsy
188
How is Hirschprung's disease managed?
```
Laxatives
+
Bowel irrigation
+
Surgery: Swenson procedure / Soave procedure; Ileorectal anastomosis + Ileostomy
```
189
What pathogen causes Chagas disease?
Trypanosoma cruzi
190
What are the clinical features of Chagas disease?
* Fever
* Fatigue
* Anorexia
* Headaches
* Myalgia
* Irritability
* Dizziness/Syncope/Pre-syncope
* Palpitations
* Abdominal pain
* Abdominal distension
* Jaundice
* Rash ± Pruritus
* Tachycardia
* Hypotension
* Cardiomegaly
* Hepatosplenomegaly
* VTE Sx: Pleuritic chest pain; SOB; Hot, swollen leg; Painful leg; Sensory deficit
191
Where is T. cruzii commonly found?
South America
192
What is the management for T. cruzii (Chagas Disease)?
• Antiparasitics: Benznidazole
193
Describe Toxic Megacolon.
Complication of acute colitis with non-obstructive, colonic distention (≥ 6cm) associated with systemic toxicity which is characterised by abdominal pain/discomfort, abdominal distension, fever/chills, tachycardia and mental status.
194
What are the key clinical features of Toxic Megacolon?
```
Abdominal pain
Abdominal bloating
Fever/chills
Diarrhoea
Tachycardia
Mental status change
```
195
What imaging would be the first line diagnostic investigation in Toxic Megacolon?
AXR or CT-CAP
196
How do you manage a patient with Toxic Megacolon?
```
• Resuscitation + Monitoring: IV fluids; Electrolyte monitoring; FBC monitoring; CRP monitoring; Obs
+
• ABX: Ciprofloxacin + Metronidazole
±
• Nasogastric decompression
```
+ (Refractory to Tx ≥ 72 hours)
• Colectomy
+ (Inflammatory colitis)
• IV Corticosteroids: Hydrocortisone
197
What is a colon polyp?
Polyp = mucosal projection into intestinal lumen due to abnormal tissue growth
198
What features increase the risk of a polyp becoming cancerous?
Size (>1cm)
Number
Sessile polyps (cf pedunculated)
Villous histology
Severe dysplasia
199
What are the Family Colon Cancer Syndromes?
Give examples
Group of syndromes which give rise to polyps within the colon with increased risk of progression to Colorectal Cancer.
FAP
HNPCC (Lynch)
MYH-Associated Polyposis
PJS
200
APC gene mutation leads to which of the Familial Polyposis Syndromes?
FAP
201
Describe FAP?
What subtypes are associated with FAP?
Mutation of the APC gene leading to >100 colorectal polyps and extracolonic features
Turcot's: CHRPE + Brain tumours
Gardner's Syndrome: CHRPEs + Desmoid tumours + Osteomas
202
What are the features of Turcot's Syndrome?
CHRPEs
Brain Tumours
203
What are the features of Gardner's Syndrome?
CHRPEs
Desmoid tumours
Skull osteomas
204
Describe HNPCC regarding gene, onset and penetrance.
Hereditary Non Polyposis Colorectal Cancer (Lynch Syndrome) is caused by a mutation in DNA mismatch repair gene (MSH2; MLH1; MSH6) resulting in a lower number of polyps with a high mutation rate (<10 polyps)
Onset is in the 4th decade
80% penetrance
Risk of Endometrial Cancer
205
Which extracolonic cancer is most associated with Lynch Syndrome?
Endometrial cancer
206
What gene causes MYH-associated polyposis?
What is the onset age?
MYH gene (base-excision repair gene)
Multiple polyps (>15) by under 50
Increased cancer risk onset in 4th decade
207
What gene mutation is responsible for Peutz-Jeghers Syndrome?
What are the clinical features of PJS?
STK11
Pigmented spots on buccal mucosa
Multiple hamartamous polyps
208
How is PJS treated?
Endoscopic polypectomy
209
How is FAP treated?
FAP < 20 polyps
• Surgery: Colectomy + Ileorectal anastomosis + completion proctectomy
FAP > 20 polyps
• Surgery: Restorative proctocolectomy and ileal pouch-anal anastomosis (RCP-IPAA) + surveillance
210
How frequently is bowel screening offered in Scotland?
What screening test is used?
Every 2 years from 50-74 y/o
FIT testing
211
If a patient has a first degree relative with CRC, how regularly is screening undertaken?
Colonoscopy every 5 years from 50-75 y/o
212
If a patient has a familial polyposis syndrome, how regularly is screening undertaken?
Colonoscopy every 2 years from the age of 25
213
What classification system can be used for Bowel Cancer?
TNM Classification
214
What does a right hemicolectomy involve?
Removal of caecum, ascending and proximal transverse colon
215
What does a left hemicolectomy involve?
Removal of the distal transverse and descending colon.
216
What does a high anterior resection involve?
Removal of sigmoid colon (sigmoid colectomy)
217
What does a low anterior resection involve?
Removal of sigmoid colon and upper rectum
218
What does an abdomino-perineal resection (APR) involve?
Removal of rectum and anus and suturing over the anus - permanent colostomy
219
What does a Hartmann's procedure involve?
Give an example of an indication for this operation.
Usually emergency procedure removing rectosigmoid colon (low anterior resection) and creation of a colostomy.
Colostomy may be permanent or reversed
Indications:
- Acute obstruction
- Significant Diverticular disease
220
What is Low Anterior Resection Syndrome? Give the clinical features.
Occurs after anterior resection with anastomosis between colon and rectum.
Tenesmus and frequency of bowel movements
Faecal incontinence
Difficulty controlling flatulence
221
What cancer tumour marker is used to detect Colon Cancer?
CEA
222
How may Colon Cancer be managed?
Colon Cancer Stages I-IV: Surgical Candidate
• Surgery: Colon resection (CRC); Radical excision (Rectal Ca)
+
• Post-Op Chemo: Oxaliplatin + Fluouracil + Folinic Acid
± (Stage IV)
• Pre-Op Chemo
+
EGFR-i: Cetuximab
Colon Cancer Stages I-IV: Non-Surgical Candidate
• Chemotherapy: Oxaliplatin + Fluouracil + Folinic Acid
+
• EGFR-i: Cetuximab
±
• Surgery: Stenting
223
Describe a Zenker Diverticulum.
What are the clinical features?
How is this different to a Killian's diverticulum?
Pharyngeal pouch formed by diverticulum of the pharynx superior to the cricopharyngeal muscle
Dysphagia
Regurgitation
Cough
Haliosis
Killian's diverticulum is located inferior to the cricopharynxgeus on both sides of the muscles insertion into the cricoid cartilage
224
How may direct Bilirubin be raised?
Direct bilirubin is conjugated.
Therefore may be raised via an intrahepatic process or an extrahepatic process
225
How may indirect Bilirubin be raised?
Indirect bilirubin is unconjugated.
May be raised in:
- Overproduction
- Impaired uptake
- Impaired conjugation
226
What type of virus causes Hepatitis A?
HAV, RNA virus
227
How is hepatitis A spread?
Faeco-oral contamination
228
A patient presents with nausea and vomiting for 3/7. They are off food and have a distaste for cigarettes.
O/E they have an enlarged liver. They have recently returned from a holiday to Turkey.
What investigations would you run?
- LFTs: raised ALT + raised sBr; raised PT (if severe)
- FBC: low leukocytes; raised ESR
- Serology: +ve anti-HAV IgG
229
A patient presents with nausea and vomiting for 3/7. They are off food and have a distaste for cigarettes.
O/E they have an enlarged liver. They have recently returned from a holiday to Turkey.
His ALT is raised as with his Bilirubin.
What is your differential diagnosis?
Hepatitis A
230
A patient presents with nausea and vomiting for 3/7. They are off food and have a distaste for cigarettes.
O/E they have an enlarged liver. They have recently returned from a holiday to Turkey.
His ALT is raised as with his Bilirubin.
How would you manage this condition?
- Supportive: Fluids; Analgesia; Reassess
231
What type of virus causes Hepatitis B?
HBV, a DNA virus
232
How is Hepatitis B spread?
Blood-borne
233
A 23 y/o M presents with fevers and arthralgia. He describes a recent yellowing of his skin.
O/E you can see scleral jaundice, palmar erythema. He is haemodynamically stable. An enlarged liver is felt.
His LFTs show raised ALT, raised AST, raised ALP and raised Bilirubin with a reduced Albumin.
Serology shows positive HBsAG and positive anti-HBc however negative for anti-HBs. Additionally, there is positive IgM anti-HBc.
What is your differential?
Acutely infected Hepatitis B
234
A 26 y/o M presents with fevers and arthralgia. He describes a recent yellowing of his skin.
O/E you can see scleral jaundice, palmar erythema. He is haemodynamically stable. An enlarged liver is felt.
His LFTs show raised ALT, raised AST, raised ALP and raised Bilirubin with a reduced Albumin.
Serology shows negative HBsAG and positive anti-HBc however positive for anti-HBs.
What is your differential?
Immune due to natural Hepatitis B infection
235
A 23 y/o M presents with fevers and arthralgia. He describes a recent yellowing of his skin.
O/E you can see scleral jaundice, palmar erythema. He is haemodynamically stable. An enlarged liver is felt.
His LFTs show raised ALT, raised AST, raised ALP and raised Bilirubin with a reduced Albumin.
Serology shows positive HBsAG and positive anti-HBc however negative for anti-HBs. Additionally, there is negative IgM anti-HBc.
What is your differential?
Hepatitis B, chronically infected
236
A 23 y/o M presents with fevers and arthralgia. He describes a recent yellowing of his skin.
O/E you can see scleral jaundice, palmar erythema. He is haemodynamically stable. An enlarged liver is felt.
His LFTs show raised ALT, raised AST, raised ALP and raised Bilirubin with a reduced Albumin.
Serology shows negative HBsAg, negative anti-HBc, positive anti-HBs and negative IgM anti-HBc.
What is your differential?
Immune to hepatitis B vaccination
237
How do you manage Hepatitis B?
Suportive:
- Supportive: Alcohol avoidance; avoid risky behaviour; education)
+
- Antivirals: Tenofovir
238
How is hepatitis C managed?
Peg-interferon and fibavirin
239
How is Hepatitis D managed?
- Supportive: fluids; analgesia
+
- Immunostimulator: Pegylated a-2a interferon
240
Which of the faeco-orally transmitted Hepatitis viruses are more common?
Hepatitis A
241
What are the potential clinical features of acute liver failure?
- Jaundice
- Abdominal pain
- N+V
- Malaise
- RUQ tenderness
- Depression/suicidal ideation
- Hepatomegaly
- Hepatic encephalopathy: consciousness; anxiety; lethargy; dyspraxia; asterixis; nystagmus; hyperreflexia; clonus; rigidity
242
How do you manage a patient with acute liver failure?
- Admission to HDU/ITU
+
- Supportive: elevate head to 30º (reduce ICP); fluids; continuous assessment and monitoring
```
± Alcohol toxicity
- Thiamine (B1)
+
- Pabrinex
+
- Chlordiazepoxide
```
and
- Antabuse (disulfiram)
or
- Acamprosate
± Paracetamol toxicity
- Acetylcysteine
± HSV Hepatitis
- Aciclovir
± Autoimmune hepatitis
- Methylprednisolone
± Hepatitis B
- Tenofovir
+
- Anti-HB Igs
± Wilson’s disease
- Plasmapheresis
± Budd-Chiari Syndrome
- Anticoagulant: Heparin
243
What are the clinical features of Wernicke's Encephalopathy?
confusion + ataxia + ophthalmoplegia
244
What clinical investigation may be suggestive of autoimmune hepatitis?
- Autoantibody screen: Positive – ANA; LKM; SMA
- LFTs: AST; ALT; GGT; ALP; Br
- PT: Prolonged
245
How would you manage Autoimmune Hepatitis?
- Steroids: Prednisolone
246
The following investigations are suggestive of what condition?
- FBCs: Anaemia; Thrombocytopaenia
- LFTs: raised ALT; raised AST; raised ALP; raised AST; raised sBr; low Albumin
- Metabolic panel: Deranged
- Alpha fetoprotein: Normal
NAFLD
247
The following investigations come back from a patient in AMU. They are haemodynamically stable.
- FBCs: Anaemia; Thrombocytopaenia
- LFTs: raised ALT; raised AST; raised ALP; raised AST; raised sBr; low Albumin
- Metabolic panel: Deranged
- Alpha fetoprotein: Normal
How would you manage them?
- Supportive: Diet; exercise; weight loss; vitamin E (alpha tocopherol)
+
- Statins: Simvastatin
+ Tx other comorbidities
248
How may Liver cirrhosis be classified?
- Compensated = no clinical findings
| - Decompensated = clinical findings
249
What scoring system can be used to predict mortality in Liver Cirrhosis patients?
Child-Pugh Score
```
Albumin
Bilirubin
Confusion (encephalopathy)
Distended abdomen (ascites)
INR
```
250
- FBC: Thrombocytopenia
- LFTs: Deranged
- U+E:
- Albumin + Coag. Screen: reduced albumin; raised PT
- Liver biopsy: Distortion of liver parenchyma with regenerative nodules
- AFP: Negative
What is your differential?
Liver cirrhosis
251
How do you manage Liver Cirrhosis?
```
- Tx/remove underlying cause
+
- Supportive: monitoring; vitamin B supplementation; vitamin K
+
Tx consequences
```
```
(Ascites)
- Salt restricted diet
+
- Diuretics: Spironolactone
±
- Paracentesis
```
(Varices)
- Compensated: carvedilol/ variceal ligation
- Decompensated: Terlipressin + Banding
252
What are the complications of cirrhosis?
Portal Hypertension
253
A patient presents with brisk haematemesis and abdominal pain.
O/E the patient is clinically dry. His HR is 110bpm with his BP being 96/76mmHg.
- FBC: Anaemia; Thrombocytopenia
- BUN: Raised
- U+E: raised urea
What is your differential?
What scoring system can you use to calculate subsequent management?
Bleeding oesophageal varices
```
Calculate Blatchford Score (ABCDEF):
Active bleeding
BUN
Circulatory
Drop in Hb
Elevated pulse
Failure
```
Management:
- Supportive: A-E; stabilise; fluids; Terlipressin
+
- Endoscopic banding
or
Balloon tamponade with Sengstaken-Blakemore tube (if failed banding or CI)
(Failed attempt and 2nd re-bleed)
- TIPS
254
If bleeding continues following OGD, terlipressin and banding, what do you do?
2nd line: Sengstaken-Blakemore (SB) tube
3rd line: TIPS
255
A patient comes in with RUQ pain and recent weight loss. He reports having a few sherries last night.
O/E he has palmar erythema, hepatic flap and some distended veins around the umbilicus.
He has previously been admitted for alcohol intoxication on several occasions.
- CAGE questionnaire (Cut down/ Annoyed/ Guilty/ Eye-opener): 2+ yes
- FAST (Fucked/ Antisocial/ Shit memory/ Thought to cut down)
- FBC: Anaemia; Leukocytosis; Thrombocytopenia
- LFTs: raised ALT; raised AST; raised ALP; raised GGT; raised sBr
- Coag. And albumin: low albumin; elevated PT
- US-Liver: abnormal
- AFP: Negative
What is your diagnosis?
Alcoholic Liver Disease
256
A patient comes in with RUQ pain and recent weight loss. He reports having a few sherries last night.
O/E he has palmar erythema, hepatic flap and some distended veins around the umbilicus.
He has previously been admitted for alcohol intoxication on several occasions.
- CAGE questionnaire (Cut down/ Annoyed/ Guilty/ Eye-opener): 2+ yes
- FAST (Fucked/ Antisocial/ Shit memory/ Thought to cut down)
- FBC: Anaemia; Leukocytosis; Thrombocytopenia
- LFTs: raised ALT; raised AST; raised ALP; raised GGT; raised sBr
- Coag. And albumin: low albumin; elevated PT
- US-Liver: abnormal
- AFP: Negative
What would you do to manage this?
- Supportive: AA/CBT; weight reduction; smoking cessation; vitamin supplementation
+
- Benzodiazepam: Chlordiazepoxide
+ Alcohol dependence
- Antabuse
or
- Acamprosate
257
How must IV glucose and Thiamine be administered in an encephalopathy?
Thiamine given before IV Glucose as glucose increases thiamine demand thus will worsen encephalopathy if given before
258
A patient presents with RUQ pain, an enlarged liver and ascites.
His LFTs show a global raise. US-Liver shows abnormal venous flow and thickening.
What is your diagnosis?
Budd-Chiari Syndrome
259
A patient presents with RUQ pain, an enlarged liver and ascites.
His LFTs show a global raise. US-Liver shows abnormal venous flow and thickening.
What is your management plan for this condition?
Condition is Budd-Chiari Syndrome.
Management should involve
- Anticoagulant: Heparin
± (Sx < 72 hours)
- Thrombolysis: Alteplase
± (Ascites)
- Paracentesis
+
- Diuretics: Spironolactone
260
A patient presents with headaches and haemoptysis. He has RUQ and feels nauseous.
An enzyme-linked immunoelectrotransfer Blot (EITB) shows T solium.
US-Liver shows cysts.
What is your differential diagnosis?
Tapeworm Infection
261
A patient presents with headaches and haemoptysis. He has RUQ and feels nauseous.
An enzyme-linked immunoelectrotransfer Blot (EITB) shows T solium.
US-Liver shows cysts.
What is your management of this condition?
Tapeworm Infection
- Antiparasitics: Praziquantel
+
CNS disease
- Steroids: Dexamethasone
+
- Anticonvulsant: Lamotragine
+ Cysts
- Aspiration
262
What blood test is used to screen for Hepatocellular Carcinoma?
AFP
263
What are the management options in a patient with Hepatocellular Carcinoma?
Stage 0-A
- Surgical resection
Stage B
- TACE
```
Stage C (Portal invasion)
- Sorafenib
```
± End-Stage
- Palliative care
264
What is the management for haemangiomas of the liver?
Suportive - watch and wait
265
What gene mutation causes Hereditary Haemochromatosis?
HFE gene
266
A 36 year-old woman presents with fatigue and poor relations with his wife. He reports impotence and loss of libido.
O/E he has a grossly distended, tympanic abdomen with a fluid shift. He also has an enlarged liver.
Investigations show raised ALT and raised AST. Transferrin saturation is elevated. Ferritin is raised also.
An ECG shows depressed QRS complex and T wave flattening.
What is your differential diagnosis?
Hereditary Haemochromatosis
267
A 36 year-old woman presents with fatigue and poor relations with his wife. He reports impotence and loss of libido.
O/E he has a grossly distended, tympanic abdomen with a fluid shift. He also has an enlarged liver.
Investigations show raised ALT and raised AST. Transferrin saturation is elevated. Ferritin is raised also.
An ECG shows depressed QRS complex and T wave flattening.
What 2 investigations may confirm your differential diagnosis?
HFE gene mutation
Liver biopsy
268
What are the management options for a patient with Hereditary Haemochromatosis that is symptomatic.
```
- Phlebotomy
+
- Desferrioxamine
+
- Lifestyle modification (low iron, Hep A/B vaccination)
```
269
In a patient with raised transferrin but no symptoms in the clinical context of Hereditary Haemochromatosis, what is your management?
Stage 1
| - Observation (1 year) + Lifestyle modification (low iron, Hep A/B vaccination)
270
What gene mutation results in Wilson's Disease?
ATP7B gene mutation
271
A 30 year old patient presents with low mood and a recent personality change. His wife is worried. She says he has been off balance recently too.
He has no relevant PMHx. He has NKDA.
O/E he has a fine tremor. His speech is slightly slurred. He has some dysdiadochokinesis.
It appears there is a dark circle around the iris upon slit-lamp examination.
What is your diagnosis?
Wilson's Disease
272
What investigations are diagnostic of Wilson's disease?
Ceruloplasmin: Reduced
Serum copper: Raised
Urinary Copper: Raised
Slit-Lamp: Kayser-Fleischer Rings
ATPB7 gene mutation
MRI-Brain
Liver-Biopsy
273
What is the gold-standard investigation to diagnose Wilson's Disease?
- Liver biopsy: raised copper
274
How do you manage Wilson's Disease?
- Supportive: Copper-restricted diet
+
- Copper chelator: Zinc + D-penicillamine
± Liver failure
- Transplantation
275
A patient presents with RUQ pain. The pain is episodic, radiating to the shoulder and worse following a meal. It is refractory to paracetamol.
What investigations would you order?
FBC, U+Es, LFTs, CRP
Serum lipase
Serum amylase
US-Abdomen
276
A 45 year old F patient presents with RUQ pain. The pain is episodic, radiating to the shoulder and worse following a meal. It is refractory to paracetamol.
- LFTs: raised ALP; raised GGT; raised sBr
- Serum lipase: negative
- > Exclude pancreatitis
- US-Abdomen: Stones in bile duct
- MRCP: Stone
What is your differential diagnosis?
Biliary colic secondary to Choledocholithiasis
277
A 45 year old F patient presents with RUQ pain. The pain is episodic, radiating to the shoulder and worse following a meal. It is refractory to paracetamol.
- LFTs: raised ALP; raised GGT; raised sBr
- Serum lipase: negative
- > Exclude pancreatitis
- US-Abdomen: Stones in bile duct
- MRCP: Stone
How would you manage this patient?
- Analgesia: Diclofenac
±
- ERCP
or
- Laparoscopic cholecystectomy
278
State the main risk factors for Cholecystitis.
```
Female
Forty
Fat
Fair
Fertile
```
279
A 47 year old female presents with RUQ pain which is constantly present and radiates to the top of the shoulder. She says she feels hot and nauseous.
O/E she is tachycardia but normotensive. She shows a positive Murphy's sign.
LFTs are raised globally and US-abdomen shows an acoustic shadow within the gallbladder.
What is your differential?
Acute Cholecystitis.
280
A 47 year old female presents with RUQ pain which is constantly present and radiates to the top of the shoulder. She says she feels hot and nauseous.
O/E she is tachycardia but normotensive. She shows a positive Murphy's sign.
LFTs are raised globally and US-abdomen shows an acoustic shadow within the gallbladder and mural thickening with hypoechoic signal within the gallbladder.
What is your management for this patient?
```
- Supportive: no food; IV fluids; Opiate analgesia
+
- ABX: Cefuroxime + Metronidazole
+
- Surgery: Laparoscopic cholecystectomy
```
Remove the gallbladder as there is a gallbladder empyema.
281
What are the causes of Ascending Cholangitis?
Cholelithiasis
Iatrogenic
Chronic Pancreatitis
Parasitic infection: A. lumbricoides; F. hepatica
282
What is Charcot's Triad?
Fever + RUQ Pain + Jaundice
283
What is Reynold's Pentad?
Charcot's Triad + Hypotension + Confusion
284
A patient presents with RUQ pain and pruritus. He reports fevers, yellowing of the skin and pale stools.
He recently travelled from rural Texas.
FBC shows leukocytosis. LFTs show raised ALT, ALT, ALP and GGT. His bilirubin is raised also.
US-Abdomen shows dilated bile ducts and inflammation.
What is your differential diagnosis?
What could be the cause of this?
Ascending Cholangitis
Potential bacterial infection or A lumbricoides parasitic infection endemic to Southern States in the USA
285
A patient presents with RUQ pain and pruritus. He reports fevers, yellowing of the skin and pale stools.
He recently travelled from rural Texas.
FBC shows leukocytosis. LFTs show raised ALT, ALT, ALP and GGT. His bilirubin is raised also.
US-Abdomen shows dilated bile ducts and inflammation.
What is your management for this patient?
- Supportive: NBM; IV Fluids; Opiate analgesia; IV ABX (Cefuroxime + Metronidazole)
+
- ERCP
±
- Surgery: Laparoscopic cholecystectomy
286
Describe Primary Sclerosing Cholangitis.
Cholestatic liver disease causing progressive fibrosis and obliteration of the intra and extrahepatic biliary ducts – linked to men with IBD
287
A 24 year old Male patient presents with RUQ pain, pruritus and fatigue.
He has a PMHx of Ulcerative Colitis.
O/E he has a marked fever and an enlarged liver.
FBC shows thrombocytopenia and anaemia. LFTs show raised ALP, raised ALP and raised GGT. GGT and ALP are markedly raised. Autoantibodies to ANA are present.
What is the gold-standard investigation to make a diagnosis?
MRCP
288
A 24 year old Male patient presents with RUQ pain, pruritus and fatigue.
He has a PMHx of Ulcerative Colitis.
O/E he has a marked fever and an enlarged liver.
FBC shows thrombocytopenia and anaemia. LFTs show raised ALP, raised ALP and raised GGT. GGT and ALP are markedly raised. Autoantibodies to ANA are present.
MRCP shows involvement of intrahepatic and extrahepatic bile ducts with fibrosis and dilation.
What is your differential diagnosis?
Primary Biliary Sclerosis
289
A 24 year old Male patient presents with RUQ pain, pruritus and fatigue.
He has a PMHx of Ulcerative Colitis.
O/E he has a marked fever and an enlarged liver.
FBC shows thrombocytopenia and anaemia. LFTs show raised ALP, raised ALP and raised GGT. GGT and ALP are markedly raised. Autoantibodies to ANA are present.
MRCP shows involvement of intrahepatic and extrahepatic bile ducts with fibrosis and dilation.
How would you manage this patient?
```
Supportive: Observation; reduce weight; reduce alcohol; Colestyramine (stop itch)
+
Medical: Colestyramine + Steroids
+
ERCP: Biliary decompression
```
290
What antibodies tend to be present in Primary Biliary Cirrhosis?
AMA Antibodies
291
A 37 year old woman presents with pruritus and fatigue. She says these symptoms have come on gradually.
She has a PMHx of asthma. FHx is that her mother had Sjogren's.
O/E you see xerostomia and xanthelasma; with an enlarged liver.
Investigations show a raised ALP and anti-AMA antibodies.
What is the gold-standard investigation to diagnose this condition?
US-Liver biopsy
292
A 37 year old woman presents with pruritus and fatigue. She says these symptoms have come on gradually.
She has a PMHx of asthma. FHx is that her mother had Sjogren's.
O/E you see xerostomia and xanthelasma; with an enlarged liver.
Investigations show a raised ALP and anti-AMA antibodies.
US-Liver biopsy shows anti-AMA.
What is your differential diagnosis and management?
Primary Biliary Cirrhosis
- Supportive: Urseodeoxycholic acid; Colestyramine
+
- Steroids: Prednisolone
293
What is gallstone ileus?
Gallstone eroding through the HPAV into the duodenum and causing bowel obstruction
294
What tumour markers are raised in a cholangiocarcinoma?
Raised:
Ca-19.9
Ca-125
CEA
On the b/g of a cholestatic picture
295
How do you manage a cholangiocarcinoma that is intrahepatic?
- Partial liver resection
296
How do you manage a cholangiocarcinoma that is extrahepatic?
- Surgical excision
297
What are the causes of Acute Pancreatitis?
Idiopathic
Gallstones
Ethanol
Trauma
```
Steroids
Mumps
Autoimmune
Scorpion stings
Hyperlipidaemia
ERCP
Drugs (Thiazide diuretics)
```
298
What is the gold-standard investigation to diagnose Acute Pancreatitis?
- Serum amylase
299
How do you manage Acute Pancreatitis?
- Supportive: IV fluids + analgesia; urinary catheter + NJ feeding ( pancreas stimulation)
± Infection
- ABX: Ciprofloxacin
± Gallstones
- ERCP
± Severe Acute Pancreatitis (3+ from Modified Glasgow Criteria)
- Admission to ITU/HDU
300
What criteria in Acute Pancreatitis can be used to decide if a patient requires admission to ITU?
Modified Glasgow Criteria
Mnemonic: PANCREAS
PaO2 >60mmHg
Age >55 y/o
Neutrophils >15x10^9/L
Calcium <2mmol/L
Raised urea >16
Enzyme (LDH) >600U/L
Albumin <32g/L
Sugar >10mmol/L
301
What is Trousseau's Syndrome?
Migratory thrombophlebitis associated with malignancy e.g. Pancreatic Cancer
302
What cancer marker is elevated in Pancreatic Cancer?
Ca19.9
303
How is Pancreatic Cancer managed?
Stage 1-2
- Surgical resection: Whipple’s Pancreatoduodenectomy
+
- Radiotherapy/Chemotherapy
Stage 3
- Non-curative surgery (stent insertion)
304
How is Splenic Rupture managed?
Supportive: Admission; A-E; Oxygen; Fluids; TXA
± Stable
- Supportive: Monitoring
± Unstable
Medical: Embolisation; Splenectomy
305
What conditions may a high serum-ascites albumin gradient indicate?
SAAG >1.1g/dL suggests portal hypertension:
- Cirrhosis
- Alcoholic hepatitis
- Portal vein thrombosis (Budd-Chairi Syndrome)
- Heart failure
- Massive hepatic metastases
306
What is the term for a gastric tumour which metastasises to the Ovaries?
Krukenberg tumour
307
What is the term for the radiographic find of bowel positioned between the right diaphragm and the liver?
Chiltaiditi's Sign
308
What is emphysematous cholecystitis?
How is it diagnosed?
an acute infection of the gallbladder wall caused by gas-forming organisms
CT-Abdomen
309
What are the risks of colonoscopy?
RR reduced - respiratory failure
Perforation
Infection
Missed lesions
310
What choices of analgesia are there for a colonoscopy?
Benzodiazepines
Fentanyl
Pethidine
Entonox
311
What classification system is used for Polyps?
Outline it.
Paris classification
Ip = pedunculate
Is = sessile
IIa = superficial, raised
IIb = superficial, flat
Iic = superficial, depressed
312
You observe a normal gross appearance on colonoscopy of the LI in a patient experiencing diarrhoea and abdominal pain.
On histology, lymphocytes are seen within the biopsied tissue.
What is your diagnosis?
Microscopic colitis
