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Phase 2a Sheffield Medicine > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Define peritonitis?

A

Inflammation of the peritoneum

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2
Q

What are the causes of primary peritonitis?

A
  • Primary peritonitis - inflammation caused by spontaneous bacterial peritonitis. This is the most common type of peritonitis
    • e.g. E. coli, klebsiella, staphylococcus aureus
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3
Q

What are the causes of secondary peritonitis?

A
  • Secondary peritonitis - caused by something else e.g. chemical such as, bile
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4
Q

What are the clinical manifestations of peritonitis?

A
  • Perforation
  • Poorly localised
  • Rigid abdomen
  • Tenderness and guarding abdomen
  • Pain relieved by resting hands on abdomen
  • Lying still
  • Prostration
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5
Q

What are the investigations for peritonitis?

A
  • FBC
  • Abdominal X-ray
  • CT of the abdomen
  • PT and INR
  • Ascitic tap
  • Blood cultures
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6
Q

What is the management for peritonitis?

A
  • ABC
  • Nasogastric tube
  • IV antibiotics - First line IV cephalosporin e.g. Cefotaxime
  • IV fluids
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7
Q

What are the complications of peritonitis?

A
  • Toxaemia and Septicaemia
  • Local abscess formation
  • Kidney failure
  • Paralytic ileus
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8
Q

What is an ascites?

A

Ascites is the accumulation of free fluid within the peritoneal cavity.

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9
Q

What are the causes of ascites?

A
  • Malignancy
  • Infections especially TB
  • Low albumin
  • Pancreatitis
  • Bowel obstruction
  • Myxoedema
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10
Q

What are the causes of ascites when coupled with portal hypertension?

A
  • Cirrhosis
  • Congestive cardiac failure
  • Budd-Chari syndrome
  • IVC or PV thrombus
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11
Q

What are the risk factors for ascites?

A
  • High sodium diet
  • Hepatocellular carcinoma
  • Splanchnic vein thrombosis resulting in portal hypertension
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12
Q

What are the clinical manifestations of ascites?

A
  • Abdominal swelling
  • Distended abdomen
  • Mid abdominal pain and discomfort
  • Respiratory distress
  • Difficulty eating
  • Peripheral oedema
  • Weight loss
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13
Q

What is the management for ascites?

A
  • History (swelling, drugs, weight loss)
  • Percussion
  • Ascitic fluid tap
  • Ultrasound
  • The serum ascites-albumin gradient (SAAG)
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14
Q

What are some complications of ascites?

A
  • Severe hypovolemia due to reaccumulation of ascites post-drainage
    • Intravascular replenishment needed prior to drainage to avoid this complication.
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15
Q

What is Barrett’s Oesophagus?

A
  • Barrett’s oesophagus describes metaplasia (transformation of one differentiated cell type to another differentiated cell type) of the lower oesophageal lining from stratified squamous epithelium to mucous secreting columnar epithelium with goblet cells.
  • Barrett’s is classified as short segment (< 3 cm) and long segment (> 3 cm).
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16
Q

What are some risk factors for Barrett’s Oesophagus?

A
  • Gastro-oesophageal reflux disease:the single greatest risk factor for developing Barrett’s oesophagus
  • Age
  • Gender → Male > Female
  • Caucasian
  • Smoking
  • Obesity
  • Family history
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17
Q

What are the clinical manifestations of Barrett’s Oesophagus?

A

There are no specific symptoms or signs associated with Barrett’s oesophagus. It is typically diagnosed on endoscopy for upper gastrointestinal (GI) symptoms.

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18
Q

What are the investigations for Barrett’s Oesophagus?

A

Upper GI endoscopy (OGD) and biopsy

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19
Q

What is the Prague criteria?

A
  • The Prague criteria refers to the endoscopic description of BO, which is divided into two components:
    • Circumferential (C) extent: maximal circumferential height of BO
    • Maximal (M) length: refers to the longest segment of BO
  • and length:
    • Short segment Barrett’s(< 3cm)
    • Long segmentBarrett’s(> 3cm)
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20
Q

What is the management for underlying reflux for Barrett’s Oesophagus?

A
  • Lifestyle changes:weight loss, smoking cessation, alcohol abstinence
  • Proton pump inhibitor:omeprazole or lansoprazole; usually high dose
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21
Q

What is the management for non-dysplastic Barrett’s Oesophagus?

A

Repeat surveillance endoscopy: at least every 5 years or sooner depending on the length of oesophagus affected (usually every 3-5 years)

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22
Q

What is the management for low-grade dysplasia in Barrett’s Oesophagus?

A
  • Repeat endoscopy: every 6 months
  • Endoscopic therapy:radiofrequency ablation or mucosal resection
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23
Q

What is the management for high-grade dysplasia in Barrett’s Oesophagus?

A
  • Radiofrequency ablation:typically for flat lesions
  • Endoscopic mucosal resection:typically for raised lesions
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24
Q

What is the management for adenocarcinoma in Barrett’s Oesophagus?

A

Oesophagectomy: surgical intervention is indicated in non-metastatic disease

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25
Q

What are some complications of Barrett’s Oesophagus?

A
  • Associated with a50-100 foldincreased risk of oesophageal adenocarcinoma.
  • Endoscopic complications: oesophageal rupture, or stricture development
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26
Q

What is GORD?

A

Gastro-oesophageal reflux disease is where there is reflux of stomach content into oesophagus.

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27
Q

What are some causes of GORD?

A
  • Lower oesophageal hypotension
  • Oesophageal dysmotility
  • Gastric acid hypersecretion
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28
Q

What are some risk factors for GORD?

A
  • High BMI
  • Genetics
  • Pregnancy
  • Smoking
  • NSAIDs, Caffeine, Alcohol
  • Hiatus hernia
  • Scleroderma
  • Zollinger-Ellison syndrome
  • Medications that lower LOS pressure
    • Antihistamines
    • CCBs
    • Antidepressants
    • Benzodiazepines
    • Glucocorticoids
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29
Q

What are the clinical manifestations of GORD?

A
  • Heartburn (worse when lying down after eating)
  • Regurgitation
  • Dyspepsia
  • Chest pain
  • Bloating
  • Dysphagia
  • Odynophagia
  • Nausea
  • Water brash
  • Cough
  • Hoarse voice
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30
Q

What are the investigations for GORD?

A
  • Can be diagnosed based on clinical presentation and based on whether PPI trial would resolve the symptoms.
  • if patient displays red flags then do the following:
    • 24-hour pH monitoring
    • Endoscopy
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31
Q

What is the Los Angeles classification?

A

Used for the classification of GORD;
- Grade A: ≥1 mucosal break, each ≤ 5mm
- Grade B: ≥1 mucosal break > 5mm. Not continuous between top of mucosal folds.
- Grade C: ≥1 mucosal break, continuous between top of mucosal folds, not circumferential
- Grade D: mucosal breaks involving more thanthree quartersof luminal circumference.

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32
Q

What are the reflux phenotypes for GORD?

A

From worse to best:
- Erosive oesophagitis
- Non-erosive oesophagitis
- Acid hypertensive oesophagitis
- Functional heartburn

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33
Q

What are some differential diagnoses of GORD?

A
  • Functional heartburn
  • Achalasia(failed relaxation of LOS)
  • Eosinophilic oesophagitis
  • Peptic ulcer disease
  • Non-ulcer dyspepsia
  • Malignancy
  • Pericarditis
  • Ischaemic heart disease
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34
Q

What are some oesophageal complications of GORD?

A
  • Typical reflux syndrome
  • Reflux chest-pain syndrome
  • Reflux oesophagitis
  • Reflux stricture
  • Barrett’s oesophagus
  • Oesophageal adenocarcinoma
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35
Q

What are some extra-oesophageal complications of GORD?

A
  • Reflux cough syndrome
  • Reflux laryngitis syndrome
  • Reflux asthma syndrome
  • Reflux dental erosion syndrome
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36
Q

What are the medical and surgical management options for GORD?

A
  • PPI: prevent acid production within the stomach through inhibition of H+/K+ ATPases in parietal cells.
  • H2 receptor antagonist e.g. ranitidine: reduces stomach acid
  • Antacids e.g. Gaviscon: neutralise stomach acid
  • Nissen fundoplication: wrapping the fundus of the stomach around the lower oesophagus to tighten the sphincter
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37
Q

What are some lifestyle changes for patients with GORD?

A
  • Weight loss
  • Smoking cessation
  • Dietary modification: Smaller meals. Reduce tea, coffee, alcohol, spicy foods, fizzy drinks, chocolate
  • Patients should avoid eating within two hours of sleep
  • Patients should elevate the head of the bed
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38
Q

What are the 5 types of benign oesophageal cancer?

A
  • Leiomyomas are most common
  • Papillomas
  • Fibrovascular polyps
  • Haemangiomas
  • Lipomas
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39
Q

What are the clinical manifestations of benign oesophageal cancer?

A
  • Usually asymptomatic, found incidentally on barium swallow
  • Dysphagia
  • Retrosternal pain
  • Food regurgitation
  • Recurrent chest infections
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40
Q

What are the investigations for suspected benign oesophageal cancer?

A
  • Endoscopy and biopsy: to rule out malignancy
  • Barium swallow
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41
Q

What is the management for benign oesophageal cancer?

A
  • Endoscopic removal
  • Surgical removal of larger tumours
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42
Q

What is malignant oesophageal cancer?

A

Oesophageal cancer is when malignant or cancerous cells arise in the oesophagus. It is divided into adenocarcinoma and squamous cell carcinoma.

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43
Q

What are the two types of malignant oesophageal cancer?

A
  • Small cell carcinoma
  • Adenocarcinoma
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44
Q

What are the risk factors for oesophageal adenocarcinoma?

A
  • Age >60
  • Barrett’s Oesophagus
  • Obesity
  • Male
  • Smoking
  • Rarer -> Coeliac disease and scleroderma
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45
Q

What are the risk factors for oesophageal small cell carcinoma?

A
  • Age >60
  • Smoking
  • Alcohol
  • Achalasia
  • Plummer-Vinson syndrome
  • Palmoplantar keratoderma
  • Hot beverages
  • Nitrosamines(dietary)
  • Caustic strictures
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46
Q

What are the signs of malignant oesophageal cancer?

A
  • Lymphadenopathy
  • Vocal cord paralysis
  • Melaena on digital rectal examination: due to bleeding oesophageal cancer
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47
Q

What are the symptoms of malignant oesophageal cancer?

A
  • Progressive dysphagia (solids then liquids): most common feature
  • Regurgitation
  • Pyrosis (heartburn)
  • Pain in chest or back
  • Odynophagia
  • Weight loss and anorexia
  • Hoarseness: with recurrent laryngeal nerve involvement
  • Vomiting
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48
Q

What is the first line investigation for malignant oesophageal cancer?

A

Upper GI endoscopy (OGD) and biopsy: first-line investigation and allows for visualisation of masses and biopsy

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49
Q

What are staging investigations for malignant oesophageal cancer?

A
  • Barium swallow
  • CT of the chest
  • Endoscopic ultrasound
  • Staging laparoscopy
  • PET CT
  • HER2 testing
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50
Q

What staging system does malignant oesophageal cancer use?

A

TNM

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51
Q

What is the management for localised malignant oesophageal cancer?

A
  • Endoscopic mucosal resection
  • Ivor Lewis oesophagectomy
  • McKeown oesophagectomy
  • Transhiatal oesophagectomy
  • Chemotherapy
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52
Q

What is the management for localised small cell carcinoma of the oesophagus?

A

Radical chemoradiotherapy: localised SCC can be treated with curative chemoradiotherapy, although surgical resection may be offered

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53
Q

What is the management for advanced or metastatic oesophageal cancer?

A
  • Palliation: stenting for dysphagia
  • Chemotherapy or chemoradiotherapy: platinum-based agents
  • Trastuzumab (Herceptin): for HER2 positive metastatic oesophageal cancer, in combination with chemotherapy
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54
Q

What are some complications of malignant oesophageal cancer?

A
  • Tracheo-oesophageal or broncho-oesophageal fistula
  • Aspiration pneumonia
  • Metastasis
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55
Q

Define Mallory-Weiss syndrome?

A

Mallory-Weiss tear (MWT) refers to longitudinal lacerations limited to the mucosa and submucosa, at the border of the gastro-oesophageal junction.

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56
Q

What are some risk factors of Mallory-Weiss syndrome?

A
  • Age → 30-50 years
  • Any condition that predisposes to retching or vomiting: such as gastroenteritis, bulimia, hyperemesis gravidarum
  • Alcoholism
  • Chronic cough
  • Hiatus hernia
  • Gastro-oesophageal reflux disease
  • Trauma to chest or abdomen
  • Transoesophageal echocardiography
  • Heavy lifting or straining
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57
Q

What is the classic presentation of a patient with Mallory-Weiss syndrome?

A

The classic history of a Mallory Weiss tear is a patient with a background of alcohol excess presenting with episodes of violent retching or vomiting, followed by vomiting a small or moderate amount of fresh blood.

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58
Q

What are the signs of Mallory-Weiss syndrome?

A
  • Melaena on rectal examination: an uncommon feature
  • Features of shock: an uncommon feature
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59
Q

What are the symptoms of Mallory-Weiss syndrome?

A
  • Preceding retching and vomiting
  • Vomiting blood: usually a small to moderate volume of bright red blood, which is self-limiting
  • Melaena: rare
  • Epigastric pain
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60
Q

What are the investigations of Mallory-Weiss syndrome?

A
  • Upper GI endoscopy: gold-standard
  • FBC
  • U&Es
  • Coagulation profile
  • LFTs
  • Erect CXR
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61
Q

What is the Glasgow Blatchford Score?

A

Risk stratify patients with an upper GI bleed. Those with a score of 0 can be discharged and return for an outpatient endoscopy. If the score is more than 0, patients require admission for inpatient endoscopy.

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62
Q

What factors are taken into account for the Glasgow Blatchford Score?

A
  • Haemoglobin
  • Urea
  • Initial systolic blood pressure
  • Gender
  • Heart rate (tachycardia)
  • Melaena
  • History of syncope
  • Hepatic disease history
  • Cardiac failure present
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63
Q

What is the Rockall score?

A

Calculated after endoscopy, with the score including age, blood pressure, comorbidities, and endoscopic findings. It is used to identify patients at risk of adverse outcomes following endoscopic treatment of an upper GI bleed.

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64
Q

What are the differential diagnoses of Mallory-Weiss syndrome?

A
  • Boerhaave’s syndrome
  • Gastroenteritis
  • Peptic ulcer
  • Varices
  • Cancer
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65
Q

What is the primary management for Mallory-Weiss syndrome?

A
  • Upper GI endoscopy
    • Clipping
    • Thermal coagulation with adrenaline
    • Sclerotherapy with adrenaline
    • Variceal band ligation
  • High dose IV proton pump inhibitor
  • Manage contributing factors
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66
Q

What is secondary management for Mallory-Weiss syndrome?

A

Surgical repair or interventional radiology: only performed if endoscopic haemostasis has failed or transmural oesophageal perforation is present; this is very rarely needed for MWT

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67
Q

What are some complications of Mallory-Weiss syndrome?

A
  • Re-bleeding
  • Hypovolaemic shock
  • Oesophageal perforation
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68
Q

Define oesophageal varices?

A

Oesophageal varices are abnormal, dilated veins that occur at the lower end of the oesophagus; they account for 10-20% of upper GI bleeds. They develop as a consequence of portal hypertension.

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69
Q

What are the risk factors for oesophageal varices?

A
  • Portal hypertension
  • Cirrhosis
  • Alcoholism
  • Schistosomiasis infection

Risk factors for bleeding:
- Large varices
- Decompensated liver cirrhosis

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70
Q

What are some signs of oesophageal varices?

A
  • Features of chronic liver disease
  • Features of decompensated liver disease
  • Splenomegaly due to portal hypertension
  • Hypotension
  • Tachycardia
  • Pallor
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71
Q

What are some symptoms of oesophageal varices?

A

Patients can present as asymptomatic if varices aren’t bleeding.
- Haematemesis and melaena (dark sticky faeces)
- Abdominal pain
- Symptoms of blood loss (shock)
- Light-headedness
- Dyspnoea
- Chest pain
- Syncope

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72
Q

What are the investigations for oesophageal varices?

A
  • Upper GI endoscopy: gold standard
  • FBC
  • LFTs
  • Coagulation profile
  • Venous blood gas
  • Crossmatch/group and save
  • Erect CXR
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73
Q

What are the differential diagnoses for oesophageal varices?

A
  • Gastric varices
  • Mallory-Weiss tear
  • Peptic ulcer disease
  • Hiatal hernia
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74
Q

What is the management for non-bleeding oesophageal varices?

A

It is recommended patients undergo endoscopic surveillance and are commenced on a beta-blocker

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75
Q

What is the management for bleeding oesophageal varices?

A
  • ABDCE
  • IV fluids
  • Blood products
  • Terlipressin
  • Prophylatic antibiotics
  • Balloon tamponade
  • Oesophageal varices:endoscopic varicealband ligationis first line and is superior to sclerotherapy
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76
Q

What are some complications of oesophageal varices?

A
  • Re-bleed
  • Encephalopathy
  • Infection
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77
Q

What is achalasia?

A

Achalasia is an oesophageal motor disorder characterised by a loss of oesophageal peristalsis and failure of the lower oesophageal sphincter to relax in response to swallowing.

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78
Q

What are the clinical manifestations of achalasia?

A
  • Dysphagia.
  • Heart burn.
  • Weight loss (eating less).
  • Coughing while lying horizontally.
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79
Q

What are the investigations for achalasia?

A
  • Barium swallow X-ray
  • Oesophageal endoscopy with or without ultrasound
  • Endoscopic biopsy
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80
Q

What is the management for achalasia?

A
  • Calcium channel blockers for mild to moderate disease.
  • Nitrates effective before dilation occurs.
  • PPIs (after surgery to prevent reflux damage)
  • Surgery
    • Laparoscopic Heller myotomy.
    • Endoscopic myotomy.
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81
Q

Define gastritis?

A

Gastritis refers to inflammation of the lining of the stomach associated with mucosal injury.

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82
Q

Define gastropathy?

A

Gastropathy refers to epithelial cell damage and regeneration WITHOUT inflammation - commonest cause is mucosal damage associated with Aspirin/NSAIDs

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83
Q

What are the causes of gastritis?

A
  • Helicobacter pylori infection
  • Autoimmune gastritis
  • Duodenogastric reflux
  • Crohn’s disease
  • Mucosal ischemia
  • Increased acid
  • Aspirin and NSAIDs
  • Alcohol, smoking, caffeine
  • Viruses e.g. cytomegalovirus and herpes simplex
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84
Q

What are the risk factors for gastritis?

A
  • Alcohol
  • NSAIDs
  • H.pylori
  • CMV and herpes
  • Infectious: crowding and poor sanitation
  • Autoimmune: HLA-DR3 and B8
  • Reflux/hiatus hernia
  • Granulomas e.g. in Crohn’s
  • Zollinger-Ellison syndrome
  • Menetrier’s disease
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85
Q

What are the clinical manifestations of gastritis?

A
  • Nausea or recurrent upset stomach
  • Vomiting
  • Abdominal bloating
  • Epigastric pain
  • Indigestion
  • Haematemesis/ malaena
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86
Q

What are the investigations for gastritis?

A
  • Endoscopy - will be able to see it
  • Biopsy
  • Test for H. pylori
    • Clo test
    • H.pylori urea breath test
    • H.pylori stool antigen test
  • Autoimmune gastritis
    • Anti-IF antibody
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87
Q

What are the differential diagnoses of gastritis?

A
  • Peptic ulcer disease (PUD)
  • GORD
  • Non-ulcer dyspepsia
  • Gastric lymphoma
  • Gastric carcinoma
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88
Q

What is the management for gastritis (H.pylori negative)?

A
  • Remove causative agentssuch as alcohol/NSAIDs
  • Reduce stress
  • H2 antagonistse.g. ranitidine or cimetidine - to reduce acid release
  • PPIse.g. lansoprazole or omeprazole
  • Antacids
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89
Q

What is the management for gastritis (H.pylori positive)?

A

Same as before but also: Triple therapy
- PPIfor acid suppression e.g. lansoprazole or omeprazole
- Plus two of:metranidazole, clarithromycin, amoxicillin, tetracycline, bismuth
- Quinolones e.g. ciprofloxacin, furozolidone and rifabutinare used when standard regimens have failed as ‘rescue therapy’

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90
Q

What are the complications of gastritis?

A
  • Gastric cancers
  • Achlorydria: lack of HCl in stomach
  • Vitamin B12 deficiency
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91
Q

What are peptic ulcers?

A

A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter. Duodenal ulcers are more common than gastric ulcers.

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92
Q

What are the risk factors for a peptic ulcer?

A
  • Gender → Male > Female
  • More common with increasing age
  • More common in developing countries due to H. pylori infection
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93
Q

What are the signs of a peptic ulcer?

A
  • Evidence of bleeding
    • Hypotension and tachycardia (shock)
    • Melaena on rectal examination
  • Epigastric tenderness
  • Pallor, if anaemic
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94
Q

What are the symptoms of a peptic ulcer?

A
  • ‘Burning’ epigastric pain
    • Pain relieved by eating and worse when hungry:duodenal ulcer
    • Pain worsened by eating:gastric ulcer
  • Nausea and vomiting
  • Haematemesis or melaena
  • Dyspepsia (indigestion)
  • Reduced appetite and weight loss
  • Anaemia: due to bleeding
  • Fatigue
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95
Q

What are the symptoms of a peptic ulcer?

A
  • ‘Burning’ epigastric pain
    • Pain relieved by eating and worse when hungry:duodenal ulcer
    • Pain worsened by eating:gastric ulcer
  • Nausea and vomiting
  • Haematemesis or melaena
  • Dyspepsia (indigestion)
  • Reduced appetite and weight loss
  • Anaemia: due to bleeding
  • Fatigue
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96
Q

What are the investigations for non-bleeding peptic ulcers?

A

H. pyloribreath test and/or stool antigen with an upper GI endoscopy and biopsy is gold standard and used for diagnosis.

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97
Q

What are the investigations for bleeding peptic ulcers?

A

Same as non-bleeding but also:
- FBC
- U&Es
- LFTs
- Venous blood gas
- Erect CXR

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98
Q

What are the differential diagnoses for peptic ulcers?

A
  • Gastric malignancy
  • GORD
  • Non-ulcer dyspepsia
  • Gastritis
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99
Q

What is the management for non-bleeding peptic ulcers?

A

First line:
- Conservative:treat risk factors
- H. pylorinegative:proton pump inhibitor (PPI) - omeprazole
- H. pyloripositive:triple eradication therapy

Second line:
- Switch to alternative strategy

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100
Q

What is the management for bleeding peptic ulcers?

A

First line:
- IV crystalloid
- Blood transfusion
- Upper GI endoscopy
- Mechanical therapy
- Thermal coagulation with adrenaline
- Sclerotherapy with adrenaline
- High dose IC PPI

Second line:
- Surgery or embolisation by intravenous radiology

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101
Q

What are some complications of peptic ulcers?

A
  • Perforation
  • Gastric outlet obstruction / pyloric stenosis
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102
Q

Define gastroenteritis?

A

Gastroenteritis is inflammation all the way from the stomach to the intestines and presents with nausea, vomiting and diarrhoea.

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103
Q

Name some viral causes of gastroenteritis?

A
  • Rotavirus
  • Norovirus
  • Adenovirus
  • Astrovirus
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104
Q

Name some bacterial causes of gastroenteritis?

A
  • Campylobacter jejuni (most common)
  • E. coli (children)
  • Salmonella (children)
  • Shigella spp. (children)
  • Bacillus cereus
  • Yersinia enterocolitica
  • Vibrio cholerae
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105
Q

Name some parasitic causes of gastroenteritis?

A
  • Giardia lamblia - most common
  • Entamoeba histolytica
  • Cryptosporidium
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106
Q

What are the risk factors for gastroenteritis?

A
  • Foreign travel
  • PPI or H2 antagonist use
  • Crowded area
  • Poor hygiene
  • Risk factors for pseudomembranous colitis?
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107
Q

What are the clinical manifestations for gastroenteritis?

A
  • Bloody diarrhoea - associated with bacterial infection (salmonella, shigella, e.coli)
  • Vomiting
  • Abdominal cramping
  • Some causes (especially viral) present with:
    • Fever, fatigue, headache, muscle pain
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108
Q

What are the investigations for gastroenteritis?

A
  • FBC
  • ESR/CRP
  • U&Es
  • Stoll MCS
  • Abdominal X-ray
  • Sigmoidoscopy
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109
Q

What are the differential diagnoses for gastroenteritis?

A
  • Appendicitis
  • Volvulus
  • IBD
  • UTI
  • Diabetes mellitus
  • Pancreatic insufficiency
  • Short bowel syndrome
  • Coeliac disease
  • Laxative abuse
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110
Q

What is the management for gastroenteritis?

A
  • Isolate patient
  • Good hygiene
  • Treat causes
  • IV fluids if severely dehydrated
  • Oral rehydration and avoid high-sugar drinks in children (increases diarrhoea)
  • Antibiotics, where appropriate
  • Anti-motility agents e.g Loperamide
  • Anti-emetics - treat vomiting e.g. Metoclopramide
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111
Q

What is the management for C.diff gastroenteritis?

A
  • Metronidazole
  • Oral vancomycin
  • Rifampicin/Rifaximin
  • Stop C antibiotic
  • Stool transplant - for recurrent disease
  • Urgent colectomy if toxic megacolon
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112
Q

What is haematemesis?

A

Haematemesis is simply defined as “vomiting blood”. It is caused by bleeding from part of the upper portion of the gastrointestinal tract. It may be bright red or look like coffee grounds.

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113
Q

What is the management for haematemesis?

A
  • Rapid ABCDE assessment
  • High flow O2
  • Insert 2 large bore IV cannulae and take blood for FBC, LFT, U&E, clotting and crossmatch.
  • Startfluid resuscitationif needed
  • Insert urinary catheter to monitor and guide fluid replacement. Consider CVP line for monitoring fluid replacement
  • Transfuse if significant Hb drop
  • Correct clotting abnormalities - Vit K, fresh frozen plasma, platelets
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114
Q

What are the investigations for haematemesis?

A
  • FBC
  • LFTs
  • U&Es
  • Group and save
  • Oesophagogastroduodenoscopy (OGD)
  • Erect CXR
  • Ct abdomen
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115
Q

What are the four types of gastric cancer?

A
  • Gastric adenocarcinoma
  • Lymphoma
  • Carcinoid tumour
  • Leiomyosarcoma
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116
Q

What are the modifiable risk factors for gastric cancer?

A
  • H. pylori infection: commonest cause,
  • Smoking
  • Alcohol
  • Diet: smoked and preserved foods, nitrosamines; salty and spicy foods
  • Obesity
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117
Q

What are the non-modifiable risk factors for gastric cancer?

A
  • Male gender
  • Increasing age
  • Family history
  • Pernicious anaemia
  • Blood type A
  • Gastric adenomatous polyps
  • Lynch syndrome II
  • Autoimmune gastritis
  • Achlorhydria
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118
Q

What are the signs of gastric cancer?

A
  • Iron deficiency anaemia
  • Palpable mass
  • Melena
  • Acanthosis nigricans
  • Troisier’s sign
  • Leser-Trelat sign
  • Polyarteritis nodosa
  • Trousseau syndrome
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119
Q

What are the symptoms of gastric cancer?

A
  • Malaise
  • Loss of appetite
  • Anorexia and weight loss
  • Dyspepsia
  • Abdominal pain
  • Difficulty swallowing
  • Early satiety
  • Nausea and vomiting
  • May be malaena and haematamesis
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120
Q

What is the primary investigation for gastric cancer?

A

Upper GI endoscopy and biopsy: ulcer with heaped-up edges is a common presentation

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121
Q

What are the staging investigations for gastric cancer?

A
  • CT of the chest
  • PET
  • Staging laparoscopy
  • Endoscopic ultrasound
  • HER2 testing
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122
Q

What staging is used for gastric cancer?

A

TNM

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123
Q

What is Siewert’s classification?

A

Siewert’s classification is for gastro-oesophageal tumours.

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124
Q

What are the differential diagnoses for gastric cancer?

A
  • Peptic ulcer disease
  • Oesophageal cancer
  • Achalasia
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125
Q

What is the management for localised gastric cancer?

A
  • Oesophagogastrectomy
  • Total gastrectomy
  • Sub-total gastrectomy
  • Endoscopic submucosal resection
  • D2 lymph node dissection
  • Chemotherapy
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126
Q

What is the management for advanced or metastatic gastric cancer?

A
  • Chemotherapy or chemoradiotherapy: usually a combination of a platinum compound and fluorouracil
  • Palliative gastrectomy
  • Trastuzumab (Herceptin): for HER2 positive metastatic gastric cancer, in combination with chemotherapy
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127
Q

What is coeliac disease?

A

Coeliac disease is a systemic autoimmune disorder that affects the small intestine and is triggered by the ingestion of gluten peptides found in wheat, barley, rye and other related grains. Malabsorption is the hallmark of coeliac disease.

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128
Q

What are the risk factors for coeliac disease?

A
  • Family historyof coeliac disease
  • HLA-DQ2andHLA-DQ8:95% of patients have HLA-DQ2, and 80% have HLA-DQ8
  • Autoimmunity:type 1 diabetes, autoimmune thyroid disease and autoimmune hepatitis
  • IgA deficiency:allows increased gluten peptides to circulate in the submucosa
  • Down’s syndrome
  • Turner’s syndrome
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129
Q

What are the clinical manifestations of coeliac disease?

A
  • Persistent abdominal symptoms:
    • Indigestion
    • Diarrhoea (watery) or steatorrhoea (pale, floating stools)
    • Abdominal bloating or discomfort
    • Constipation
  • Prolonged fatigue
  • Unexpected weight loss
  • Failure to thrive in children
  • Severe or persistent mouth ulcers
  • Dermatitis herpetiformis: itchy vesicular skin eruption caused by IgA antibodies attacking tTG in the epidermis.
  • Anaemia secondary to iron, B12 or folate deficiency
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130
Q

What are the investigations for coeliac disease?

A
  • FIRST LINE - Tissue transglutaminase antibodies (tTG)
  • SECOND LINE - Anti-tTG, endomysial, or gliadin (IgG) antibodies
  • Anti-casein can also be measured
  • GOLD STANDARD - Small bowel biopsy.
  • FBC
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131
Q

What is the management for coeliac disease?

A
  • Gluten free diet
  • Dietary supplements - folate, B12, vitamin D, iron, calcium.
  • Vaccinations
  • Referral to specialist
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132
Q

What are the complications of coeliac disease?

A
  • Dermatitis herpetiformis
  • Malignancy - small bowel adenocarcinoma
  • Malabsorption related
    • Osteoporosis
    • Calcium / Vitamin D deficiency
    • Anaemia
    • Peripheral neuropathy
  • Infection
  • Lactose intolerance
  • Ulcerative jejunitis
  • Coeliac crisis
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133
Q

What is Chron’s Disease?

A

Crohn’s disease is a form of inflammatory bowel disease characterised by transmural inflammation of the gastrointestinal tract (anywhere from mouth to anus), with the terminal ileum and colon most commonly affected.

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134
Q

What are the risk factors of Chron’s disease?

A
  • Gender → Female > Male
  • Family History
  • Smoking
  • NSAIDs may exacerbate
  • Stress and depression
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135
Q

What are the signs of Chron’s disease?

A
  • Abdominal tenderness
  • Fever
  • Rectal examination: blood, skin tags, erythema, fissures, fistulas, ulceration
  • Aphthous mouth ulcers
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136
Q

What are some extra-intestinal manifestations of Chron’s disease?

A
  • Cutaenous
    • Erythema nodosum - inflammatory disorder affecting subcutaneous fat.
    • Pyoderma gangrenosum - rapidly enlarging, very painful ulcer.
  • Musculoskeletal
    • Pauci-articular arthritis: asymmetrical
    • Osteoporosis
    • Axial arthritis
    • Polyarticular arthritis: symmetrical
    • Clubbing
    • Sacroiliitis
    • Ankylosing spondylitis
  • Eyes
    • Episcleritis - inflammation of your episclera
    • Uveitis - eye inflammation
    • Conjunctivitis
  • Hepatobiliary
    • Primary sclerosing cholangitis
    • Autoimmune hepatitis
    • Gallstones
  • Other
    • Calcium oxalaterenal stones
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137
Q

What are the symptoms of Chron’s disease?

A
  • Diarrhoea
  • Abdominal pain (most commonly in RLQ where the ileum is)
  • Bloody stools: more common in ulcerative colitis
  • Delayed puberty and failure to thrive: in children
  • Weight loss
  • Systemic symptoms:
    • Anorexia
    • Fever
    • Malaise
    • Lethargy
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138
Q

What are the investigations for Chron’s disease?

A
  • Diagnostic - Colonoscopy
  • Faecal calprotectin
  • FBC
  • CRP and ESR
  • LFTs
  • U&Es
  • Assess for anaemia
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139
Q

What are the differential diagnosis for Chron’s disease?

A
  • Ulcerative colitis
  • Alternative causes of diarrhoea should be excluded e.g. Salmonella spp, Giardia intestinalis and rotavirus
  • Chronic diarrhoea
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140
Q

What is the management for inducing remission in Chron’s disease?

A
  • FIRST LINE - Glucocorticoids
    • Mild attacks - budesonide
    • Moderate/Severe attacks - Prednisolone
    • Severe - IV hydrocortisone
  • Add immunosuppressants if no remission induced
    • Azathioprine
    • Mercaptopurine
    • Methotrexate
  • Add biologics for refractory period
    • Infliximab
    • Adalimumab
  • Antibiotics can also be used in peri-anal disease
    • Metronidazole
    • Ciprofloxacin
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141
Q

What is the management for maintaining remission in Chron’s disease?

A
  • 1st line:Azathioprine or Mercaptopurine
  • 2nd line:Methotrexate, Infliximab, Adalimumab
  • Post-surgery: consider azathioprine, with or without methotrexate

Patients can either have no treatment, or pharmacological therapy depending on their risk of relapse. Glucocorticoids should not be offered

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142
Q

What surgical management can be used for Chron’s disease?

A
  • Ileocecal resection
  • Partial right hemicolectomy
  • Colectomy with ileostomy
  • Colectomy with ileo-rectal anastomosis
  • Panproctocolectomy
  • Stricturoplasy
  • Abscess drainage
  • Resection of bowel where fistulae have formed
  • Perianal fistula drainage
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143
Q

What is Ulcerative colitis?

A
  • Ulcerative colitis (UC) is a type of inflammatory bowel disease that characteristically involves the rectum and extends proximally to affect a variable length of the colon.
  • It never spreads proximally beyond the ileocecal valve and is, therefore, confined to the large bowel. It does not affect the anus.
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144
Q

What are the risk factors for ulcerative colitis?

A
  • Family history
  • HLA-B27
  • Caucasian
  • Non-smoker → 3x more common
  • NSAIDs → associated with flares
  • Chronic stress and depression → associated with flares
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145
Q

What are the signs of ulcerative colitis?

A
  • Abdominal tenderness
  • Fever - in acute UC
  • Tachycardia - in acute severe UC
  • Fresh blood on rectal examination
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146
Q

What are the symptoms of ulcerative colitis?

A
  • Diarrhoea
  • Blood and mucus in stool
  • Urgency and tenesmus (cramping rectal pain)
  • Abdominal pain: particularly in left lower quadrant
  • Weight loss and malnutrition
  • Fever and malaise during attacks
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147
Q

What is fulminant disease in ulcerative colitis?

A
  • Fulminant refers to an abrupt and severe onset of a UC flare
  • Suggested byoneof the following:
    • > 10 bowel movements per day
    • Continuous bleeding
    • Abdominal tenderness and distention
    • Toxicity
    • Colonic dilation
    • The need for blood transfusion
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148
Q

What are some extra-intestinal manifestations of ulcerative colitis?

A
  • Cutaenous
    • Erythema nodosum - inflammatory disorder affecting subcutaneous fat.
    • Pyoderma gangrenosum - rapidly enlarging, very painful ulcer.
  • Musculoskeletal
    • Pauci-articular arthritis: asymmetrical
    • Osteoporosis
    • Axial arthritis
    • Polyarticular arthritis: symmetrical
    • Clubbing
    • Sacroiliitis
    • Ankylosing spondylitis
  • Eyes
    • Episcleritis - inflammation of your episclera
    • Uveitis - eye inflammation
    • Conjunctivitis
  • Hepatobiliary
    • Primary sclerosing cholangitis
    • Autoimmune hepatitis
  • Other
    • Cholangiocarcinoma
    • Aphthous oral ulcer
    • Nutritional deficits
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149
Q

What does NESTS mean for Chron’s disease?

A

N - No blood of mucus.
E - Entire GI tract
S - Skip lesions on endoscopy
T - Terminal ilium most affected and Transmural inflammation
S - Smoking is a risk factor

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150
Q

What does CLOSEUP mean for Ulcerative colitis?

A

C - Continuous inflammation
L - Limited to the colon and rectum
O - Only superficial mucosa affected
S - Smoking is protective
E - Excrete blood and mucus
U - Use aminosalicylates
P - Primary sclerosing cholangitis

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151
Q

What are the investigations for ulcerative colitis?

A
  • GOLD STANDARD - Colonoscopy / Biopsy
  • Faecal calprotectin
  • FBC
  • LFTs
  • CRP and ESR
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152
Q

What are the differential diagnosis for ulcerative colitis?

A
  • Chron’s disease
  • Other causes of diarrhoea
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153
Q

What is the management for ulcerative colitis?

A
  • Mild = 1st line aminosalicylate and 2nd line corticosteroids
  • Severe = 1st line IV corticosteroid and 2nd line IV ciclosporin
  • Colectomy may be required: leaves patient with J-pouch (can be reversed) or ileostomy.
    • J- pouch: ileoanal anastomosis, colon removed and rectum fused to ileum
    • Ileostomy: colon and rectum are removed and the ileum brought out on
      to the abdominal wall as a stoma
  • Maintenance with aminosalicylate, azathioprine, mercaptopurine.
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154
Q

What are the complications of ulcerative colitis?

A
  • Toxic megacolon.
  • Perforation
  • Colonic adenocarcinoma
  • Strictures and obstruction
  • Extra-intestinal manifestations
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155
Q

What is pseudomembranous colitis?

A
  • An inflammatory condition of the colon characterized by elevated yellow-white plaques that come together to form pseudomembranes on the mucosa.
  • C. diff can replace the normal gut flora resulting in dangerous diarrhoea.
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156
Q

What are the clinical manifestations of pseudomembranous colitis?

A
  • Diarrhoea
  • Abdominal pain
  • Leucocytosis
  • History of recent antibiotic use
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157
Q

What are the investigations for pseudomembranous colitis?

A
  • FBC - Leucocytosis
  • Faecal occult blood test
  • Stool PCR
  • Abdominal X-Ray
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158
Q

What is the management for pseudomembranous colitis?

A
  • Oral fidaxomicin
  • OR vancomycin
  • OR metronidazole
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159
Q

What is irritable bowel syndrome?

A
  • Irritable bowel syndrome (IBS) is a chronic condition characterised by abdominal pain associated with bowel dysfunction. It is a functional bowel disorder (there is no identifiable organic disease underlying the symptoms).
    • IBS-C → with constipation.
    • IBS-D → with diarrhoea.
    • IBS-M → with constipation and diarrhoea.
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160
Q

What are the risk factors for IBS?

A
  • Gender -> Women > Men
  • Worsens symptoms:
    • Stress
    • Menstruation
    • Acute gastroenteritis
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161
Q

What are the clinical manifestations of IBS?

A
  • General abdominal tenderness may be felt.
  • Fluctuating bowel habit
  • Diarrhoea
  • Constipation
  • Incomplete evacuation
  • Urgency
  • Mucus PR
  • Abdominal pain
    • Pain worse after eating
    • Improved by opening bowels
  • Bloating

If for more than 6 months -> Chronic

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162
Q

What are the differential diagnoses for IBS?

A
  • Crohn’s disease
  • Ulcerative colitis
  • Coeliac disease
  • Malignancies
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163
Q

What is the diagnostic criteria for IBS?

A
  • Abdominal pain / discomfort:
    • Relieved on opening bowels, or
    • Associated with a change in bowel habit
  • AND 2 of:
    • Abnormal stool passage
    • Bloating
    • Worse symptoms after eating
    • PR mucus
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164
Q

What are the investigations for IBS?

A
  • Normal FBC, ESR and CRP blood tests
  • Faecal calprotectin - raised in IBD not IBS.
  • Negative coeliac disease serology
  • Colonoscopy to rule out cancer
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165
Q

What is the first line management for IBS?

A
  • Loperamidefor diarrhoea
  • Laxatives for constipation.
    • Avoidlactuloseas it can cause bloating.
    • Linaclotideis a specialist laxative for patients with IBS not responding to first-line laxatives
  • Antispasmodics for cramps e.g.hyoscine butylbromide(Buscopan)
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166
Q

What is the second and third line management for IBS?

A
  • SECOND LINE - Tricyclic antidepressants (i.e. amitriptyline 5-10mg at night)
  • THIRD - SSRIs antidepressants
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167
Q

What is appendicitis?

A

Acute appendicitis is an acute inflammation of the vermiform appendix, most likely due to obstruction of the lumen of the appendix.

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168
Q

What are the risk factors for appendicitis?

A
  • Young age:the highest incidence is between 10-20 years of age
  • Gender → Male > Female
  • Frequent antibiotic use:causes an imbalance in gut flora and a modified response to subsequent infection which may trigger appendicitis
  • Smoking
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169
Q

What is the key presentation of appendicitis?

A

Central abdominal pain which migrates to the right iliac fossa, low-grade pyrexia and anorexia. 50% of patients present with this characteristic history.

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170
Q

What are the signs of appendicitis?

A
  • Right iliac fossa tenderness
  • Guarding
  • Tachycardia
  • Rovsing’s sign
  • Psoas sign
  • Obturator sign
  • Digital rectal examination
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171
Q

What are the symptoms of appendicitis?

A
  • Periumbilical pain
  • Low-grade fever
  • Reduced appetite
  • Nausea and vomiting
  • Diarrhoea
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172
Q

What is the Alvarado score?

A

The Alvarado score is used to predict the likelihood of appendicitis. A score of ≥7 is predictive of acute appendicitis. A score of 5 or 6 may warrant an ultrasound or CT but this should be considered on a case-by-case basis.

  • Migratory right iliac fossa pain (1)
  • Anorexia (1)
  • Nausea and Vomiting (1)
  • Right iliac fossa tenderness (2)
  • Fever (1)
  • High white blood cell count (2)
  • Leukocyte left shit - 75% neutrophils (1)
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173
Q

What are the investigations for appendicitis?

A
  • FBC
  • CRP and ESR
  • U&Es
  • Urinalysis
  • Abdominal ultrasound
  • CT of abdomen with contrast
  • Diagnostic laparoscopy -> done to confirm diagnosis and then proceed to appendectomy in the same procedure.
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174
Q

What are the differential diagnosis of appendicitis?

A
  • Ectopic Pregnancy
  • Ovarian cyst
  • Meckel’s diverticulum
  • Mesenteric adenitis
  • UTI
  • Diverticulitis
  • Perforated ulcer
  • Food poisoning
  • Acute terminal ileitis
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175
Q

What is the management for appendicitis?

A
  • Initial management
    • Fluids
    • Analgesia
    • Antiemetics
    • Preoperative IV antibiotics
  • Appendectomy
  • Postoperative antibiotics
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176
Q

What are the complications for appendicitis?

A
  • Perforation
  • Appendix mass
  • Abscess
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177
Q

What is diverticulitis?

A

Diverticulitis:where diverticula become inflamed and infected, typically causing severe lower abdominal pain, fever, general malaise, and occasionally rectal bleeding

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178
Q

What is diverticulosis?

A
  • Diverticulosis:the presence of diverticula (out-pouching) in an asymptomatic patient
  • Diverticular disease: where diverticula cause symptoms, such as intermittent lower abdominal pain, without inflammation and infection
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179
Q

What are the risk factors for diverticular disease?

A
  • Increasing age:> 50 years; peak age is 50-70 years old
  • Low dietary fibre
  • Obesity: particularly in younger people
  • Sedentary lifestyle
  • Smoking increase risk
  • NSAIDs increase risk
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180
Q

What are the signs of diverticular disease?

A
  • Pyrexia
  • Left lower quadrant or iliac fossa tenderness and guarding
  • Left iliac fossa tender mass
  • Rigidity, guarding, rebound or percussion tenderness
  • Tachycardia and hypotension
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181
Q

What are the symptoms of diverticular disease?

A
  • Left lower quadrant pain
  • Fresh rectal bleeding and mucus
  • Constipation
  • Urinary symptoms
  • Nausea and vomiting
  • Flatulence
  • Erratic bowel habits
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182
Q

What are the investigations for diverticular disease?

A
  • FBC
  • U&Es
  • CRP and ESR
  • Venous Blood Gas
  • Blood cultures
  • CT of the abdomen with contrast
  • Group and Save crossmatch
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183
Q

What is the management for diverticular disease?

A
  • FIRST LINE - dietary and lifestyle changes
  • Analgesics
  • Antispasmodic
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184
Q

What is the management for diverticulosis?

A
  • Conservative management
  • Could give bulk forming laxatives
  • Tell patient to increase fibre
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185
Q

What is the management for mild diverticulitis?

A
  • Oral antibiotics
  • Analgesia
  • Antispasmodic
  • Low residue or liquid diet
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186
Q

What is the management for severe diverticulitis?

A
  • Supportive management - IV fluids, analgesia
  • IV antibiotics - Co-amoxiclav
  • Surgery if bleeding is not controlled
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187
Q

What is the management for a diverticular abscess?

A
  • Radiological drainage.
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188
Q

What is the management for recurrent diverticulitis?

A
  • Elective colonic resection
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189
Q

What are the complications of diverticular disease?

A
  • Fistulae
  • Abscess
  • Perforation
  • Structures
  • Haemorrhage
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190
Q

What is Meckel’s diverticulum?

A
  • Most common congenital abnormality of the small bowel.
  • Diverticulum projects from the wall of the ileum.
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191
Q

What are the investigations for Meckel’s diverticulum?

A
  • FBC
  • Meckel’s scan - technetium-99m pertechnetate scan.
  • CT of abdomen and pelvis
  • Ultrasound
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192
Q

What is the management for Meckel’s diverticulum?

A

Laparoscopic surgery to straighten the twisted bowel and removal of the diverticula.

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193
Q

What is a small bowel obstruction?

A
  • Small bowel obstruction (SBO) is a mechanical or functional obstruction of the small intestine that prevents the normal passage of digestive contents.
  • It can be partial or complete.
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194
Q

What are the signs of a small bowel obstruction?

A
  • Abdominal tenderness and distension
  • Tinkling bowel soundsin mechanical obstruction
  • Absent bowel soundsmay be present in functional obstruction
  • Empty rectal passage
  • Tachycardia and hypotension
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195
Q

What are the symptoms of a small bowel obstruction?

A
  • Colicky, central or generalised abdominal pain.
  • Nausea and vomiting
  • Abdominal bloating
  • Constipation
  • Anorexia
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196
Q

What are the investigations for small bowel obstruction?

A
  • GOLD STANDARD - CT abdomen and pelvis with contrast.
  • FIRST LINE - Abdominal X-ray
  • Bloods
    • FBC
    • U&Es
    • CRP and ESR
    • Group and save crossmatch
    • VBG
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197
Q

What is the initial management for a small bowel obstruction?

A
  • IV resuscitation
  • Nasogastric tube
  • IV antibiotics
  • Analgesia and anti-emetics
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198
Q

What is the surgical management for small bowel obstruction?

A
  • Emergency laparotomy
  • Adhesiolysis
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199
Q

What is a large bowel obstruction?

A

Large bowel obstruction (LBO) occurs due to mechanical or functional obstruction of the large intestine that prevents the normal passage of contents.

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200
Q

What are the risk factors of a large bowel obstruction?

A
  • Increasing age - >65 years old.
  • Volvulus
  • Colorectal cancer
  • Stricture
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201
Q

What are the signs of large bowel obstruction?

A
  • Abdominal tenderness and distention
  • Tinkling bowel sounds early on, absent later
  • Rectal examination:empty rectum, hard stools and blood
  • Tachycardia and hypotension
    • Third-spacing of fluid
    • Significant hypotension may indicate ischaemia, perforation or sepsis
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202
Q

What are the symptoms of large bowel obstruction?

A
  • Colicky, generalised abdominal pain
    • Pain is constant in LBO compared to SBO
  • Bloating
  • Constipation (may be absolute in distal obstruction): no passing of faeces or flatus
    • Occursearlierin LBO than in small bowel obstruction
  • Vomiting:
    • May be faeculent in nature
    • Alatesymptom in LBO, occurs earlier in small bowel obstruction

Symptoms of LBO present later and slower than that of SBO due to the LB being able to distant much greater → has a larger lumen as well as circular and longitudinal muscles.

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203
Q

What are the investigations for a large bowel obstruction?

A
  • GOLD STANDARD - CT abdomen and pelvis with contrast.
  • FIRST LINE - Abdominal X-ray
  • Bloods
    • FBC
    • U&Es
    • CRP and ESR
    • Group and save crossmatch
    • VBG
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204
Q

What is the initial and further management for a large bowel obstruction?

A
  • IV resuscitation
  • Nasogastric tube
  • IV antibiotics
  • Analgesia and anti-emetics
  • Further -> surgery for underlying cause.
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205
Q

What are the complications of small bowel obstruction?

A
  • Bowel ischemia
  • Sepsis
  • Aspiration pneumonia
  • Dehydration
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206
Q

What are the complications of large bowel obstruction?

A
  • Bowel ischemia
  • Sepsis
  • Aspiration pneumonia
  • Dehydration
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207
Q

What is a pseudo-obstruction?

A
  • Clinical picture mimicking colonic obstruction but with no mechanical cause.
  • Also known asOgilvie syndrome.
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208
Q

What are the clinical manifestations of a pseudo-obstruction?

A
  • Patients present with rapid and progressive abdominal distension and pain
  • Similar presentation to mechanical obstruction
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209
Q

What is the investigation for Pseudo-obstruction?

A

X-ray shows gas filled large bowel

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210
Q

What is the management for a pseudo-obstruction?

A
  • Treat underlying probleme.g. withdrawal of opiate analgesia
  • Correct U&E
  • IV Neostigmine- a cholinesterase inhibitor, may be given to encourage motility.
  • Endoscopic colonic decompressioncan be used in those failing to respond.
  • Those at increasing risk of or who have developed complications (e.g. necrosis, perforation) will typically needsurgical management, if appropriate.
211
Q

What is colorectal cancer?

A

Colorectal carcinoma is a neoplastic growth in the colon or rectum. The majority are adenocarcinomas.

212
Q

What staging system does colorectal cancer use?

A

TNM and Dukes’ staging used.

213
Q

What are the risk factors for colorectal cancer?

A
  • Gender → Male > Female
  • Increasing age
  • Smoking
  • Obesity
  • Red or processed meats
  • Diet low in fibre
  • Inflammatory bowel disease
  • Polyps
  • Hereditary conditions:FAP, HNPCC, Peutz-Jeghers syndrome
214
Q

Describe how the location of colorectal cancer can influence clinical manifestation?

A

Right-sided tumours are often asymptomatic, with the majority of patients presenting with incidental iron-deficiency anaemia. In contrast, left-sided tumours are particularly associated with a change in bowel habit and have higher rates of rectal bleeding and large bowel obstruction.

215
Q

What are the signs of right-sided colorectal cancer?

A
  • Iron deficiency anaemia: koilonychia, pallor, angular cheilitis
  • May be very largewithoutevident symptoms or signs
216
Q

What are the symptoms of right-sided colorectal cancer?

A
  • Progressive change in bowel habit: diarrhoea or constipation; more prominent in left-sided tumours
  • Abdominal discomfort
  • Symptoms of large bowel obstruction: more common in left-sided tumours
  • Constitutional symptoms e.g. weight loss
  • Dyspnoea and fatigue
217
Q

What are the signs of left-sided colorectal cancer?

A
  • Rectal mass
  • Anaemia is rare
218
Q

What are the symptoms of left-sided colorectal cancer?

A
  • Progressive change in bowel habit: diarrhoea or constipation; more prominent in left-sided tumours
  • Abdominal discomfort
  • Symptoms of large bowel obstruction: more common in left-sided tumours
    • Obstruction causes colicky abdominal pain, constipation, blood-streaked stools if stool is passed, abdominal distension, vomiting (faeculent)
  • Constitutional symptoms e.g. weight loss
  • Rectal bleeding and tenesmus
219
Q

What are the investigations for colorectal cacner?

A
  • GOLD STANDARD - Colonoscopy with biopsy
  • CT colonography - SECOND LINE alternative
  • FBC
  • LFTs
  • U&Es
  • CT chest, abdomen and pelvis if biopsy is diagnostic of malignancy
220
Q

What are the differential diagnosis for colorectal cancer?

A
  • IBS
  • Ulcerative colitis
  • Crohn’s disease
  • Haemorrhoids
  • Anal fissure
  • Diverticular disease
221
Q

What are the NHS screening tests for CRC?

A
  • NHS home screening test to detect traces of blood in stool
    • The two types of test are the Faecal Occult Blood (FOB) test and Faecal Immunochemical Test (FIT)
  • Screening sigmoidoscopy
    • Colonoscopy may be offered based on findings
222
Q

What is the management for colorectal cancer?

A
  • Initial - Iron replacement
  • Elective
    - Colon cancer - chemotherapy
    - Rectal cancer - radiotherapy or chemoradiotherapy
    - For all stages -> surgical resection including mets (FIRST LINE)
223
Q

What are the complications of colorectal cancer?

A
  • Cancer related
    • Metastasis
    • Large bowel obstruction
  • Treatment related
    • Surgical complications
224
Q

What are colorectal polyps?

A
  • A colonic polyp is an abnormal growth of tissue projecting from the colonic mucosa.
  • Polyps range from a few millimetres to several centimetres and are single or multiple
225
Q

What are the clinical manifestations of colorectal polyps?

A
  • Most polyps are asymptomatic and found by chance
  • Polyps in the rectum or sigmoid colon often present with bleeding
226
Q

What is the management for colorectal polyps?

A

Polyps are removed at colonoscopy to reduce development into cancer risk

227
Q

What is FAP?

A
  • Familial Adenomatous Polyposis
  • Autosomal dominant condition due to APC gene mutation.
  • Adenomas develop at 16 y/o and the cancer develops at 39 y/o.
228
Q

What is Lynch syndrome?

A
  • Hereditary Non-Polyposis Colon Cancer - HNPCC
  • Polyps formed in the colon and can rapidly develop to colon cancer.
  • Autosomal dominant condition in DNA mismatch repair genes → hMSH2 or hMSH1.
    • These genes maintain DNA stability in replication a defect causes micro satellites (just short repeated DNA sequences).
  • The gene mutation causes more DNA damage and thus colorectal carcinoma can develop.
  • Thus the cancer can develop much quicker.
229
Q

What is ischemia colitis?

A
  • Bowel ischaemia which affects the large bowel. This is mainly due to pathology in the inferior mesenteric artery territory and can range from mild ischaemia to gangrenous colitis.
  • Also known as chronic colonic ischaemia.
230
Q

What are the risk factors for ischemic colitis?

A
  • Older age
  • Peripheral vascular disease
  • Infective endocarditis
  • Atrial fibrillation
  • Atherosclerosis
  • Previous MI
  • Coagulation disorders
  • Cocaine use
  • Vasculitis
  • Hydroperfusion
231
Q

What are the signs of ischemic colitis?

A
  • Abdominal tenderness
  • Peritonism
  • Haemodynamic instability
  • Pyrexia - shock
  • Tachycardia - shock
232
Q

What are the symptoms of ischemic colitis?

A
  • Lower left sideabdominal pain(may be crampy in nature)
  • Diarrhoea+/- blood
  • Haematochezia- passage of fresh blood through the anus
  • Fever
  • There is a spectrum of disease from mild self-limiting insults to necrosis and bowel perforation.
233
Q

What are the investigations for ischemic colitis?

A
  • GI endoscopy - GOLD STANDARD
  • Abdominal X-ray
  • CT of abdomen with contrast
  • Bloods
    • FBC
    • U&Es
    • VBG
    • Coagulation screen
234
Q

What are the differential diagnosis for ischemic colitis?

A
  • Other causes of acute colitis e.g. IBD.
235
Q

What is the supportive management for ischemic colitis?

A
  • IV fluid resuscitation
  • Broad spectrum antibiotics
  • IV unfractionated heparin / LMW heparin
236
Q

What are the surgical management options for ischemic colitis?

A
  • Embolectomy
  • Thrombolysis
  • Mesenteric angioplasty and stenting
  • Laparotomy and resection of ischaemic/ necrotic segments
  • Stoma formation
237
Q

What are the complications of ischemic colitis?

A
  • Bowel infarction and perforation
  • Systemic inflammatory response syndrome (SIRS)
  • Strictures
238
Q

What is mesenteric ischemia?

A

Bowel ischemia which affects thesmall bowel. It refers to pathology affecting the superior mesenteric artery.

239
Q

What are the risk factors for mesenteric ischemia?

A
  • Age -> typically over 40
  • Gender → Female > Male
  • Atrial fibrillation
  • Atherosclerosis
  • Previous MI
  • Hypercoagulable state
  • Infective endocarditis
  • Vasculitis
  • Hypoperfusion
240
Q

What are the signs of mesenteric ischemia?

A
  • Oftenno abdominal signsandpain is out of proportion to clinical findings
  • Absence of bowel soundsas motility decreases: late sign
  • Epigastric bruiton auscultation: in chronic ischaemia
  • Rectal exam:bleeding
  • Hypotensive and tachycardic- shock due to hypovolaemia
241
Q

What are the symptoms of mesenteric ischemia?

A
  • Abdominal pain
    • Acute ischaemia: severe, out of proportion to abdominal signs
    • Chronic ischaemia: colicky, intermittent, post-prandial and described as ‘intestinal angina’
  • Nausea and vomiting
  • Diarrhoea
  • Fever
  • Weight loss: may be present with chronic ischaemia
242
Q

What are the investigations for mesenteric ischemia?

A
  • ECG
  • CT angiography - diagnostic test
  • CXR
  • Bloods
    • FBC
    • U&Es
    • VBG
    • Coagulation screen
243
Q

What is the initial management for mesenteric ischemia?

A
  • Bowel rest: nil-by-mouth and NG tube
  • IV fluids
  • IV broad antibiotics
  • IV heparin: anti-coagulation
  • Prompt laparotomy
244
Q

What is the definitive management for mesenteric ischemia?

A
  • Endovascular revascularisation
    • Embolisation
    • Angioplasty
  • Laparotomy
    • Embolectomy
    • Arterial bypass
    • Resection of necrotic bowel
245
Q

What are the complications of mesenteric ischemia?

A
  • Bowel infarction
  • Systemic inflammatory response syndrome (SIRS)
  • Short bowel syndrome
  • Strictures
246
Q

What is a hernia?

A

The protrusion of a viscus/ part of a viscus through a defect of the wall of its containing cavity into an abnormal position.

247
Q

How are hernias classified?

A
  • Irreducible - contents cannot be pushed back into place.
  • Obstructed - bowel contents cannot pass as the intestine is obstructed.
  • Strangulated - ischaemia occurs as blood supply of the sac is cut off - this requires urgent surgery.
  • Incarceration - contents of the hernial sac are stuck inside by adhesions.
248
Q

What is an inguinal hernia?

A
  • The protrusion of abdominal contents through the inguinal canal.
  • Commonest type of hernia in both men and women. Account for 70% of all abdominal hernias.
249
Q

What are the risk factors for an inguinal hernia?

A
  • Gender → Male > Female
  • Chronic cough
  • Constipation
  • Urinary obstruction
  • Heavy lifting
  • Ascites
  • Past abdominal surgery
250
Q

What are the clinical manifestations of an inguinal hernia?

A
  • Bulging associated with coughing or straining (bowel movement, heavy lifting)
  • Appearance of lump
  • Rarely painful
    • If painful then indicates strangulation
  • Patient can usually reduce the hernia themselves
251
Q

What are the investigations for an inguinal hernia?

A
  • Look for lump and previous scars, check for cough impulse (swelling expands when coughing) - compare to the other side.
  • Examine external genitalia
252
Q

What are the differentia diagnosis for an inguinal hernia?

A
  • Femoral hernia
  • Epididymitis
  • Testicular torsion
  • Groin abscess
  • Aneurysm
  • Hydrocele
  • Undescended testes
253
Q

What is the management for an inguinal hernia?

A
  • Use truss to contain and prevent further progression of hernia.
  • Pre-op - diet and stop smoking
  • Herniotomy, Herniorrhaphy, or Hernioplasty.
254
Q

What is a femoral hernia?

A
  • Bowel enters the femoral canal (presenting as a mass in upper medial thigh) or above the inguinal ligament (points down the leg).
  • Likely to be irreducible and to strangulate due to the rigidity of the canal’s borders.
255
Q

What are the risk factors for a femoral hernia?

A
  • Gender → Female > Male.
  • More common in middle-age and elderly.
256
Q

What are the investigations for a femoral hernia?

A

The neck of the hernia is felt inferior and lateral to the pubic tubercle.

257
Q

What is the differential diagnoses for a femoral hernia?

A
  • Inguinal hernia
  • Saphena varix (dilation of saphenous vein at junction of femoral vein in groin)
  • Enlarged cloquet’s node
  • Lipoma
  • Femoral artery aneurysm
  • Psoas abscess
258
Q

What is the management for a femoral hernia?

A
  • Surgical repair
    • Herniotomy - ligation and excision of the sac
    • Herniorrhaphy - repair of the hernial defect
259
Q

What is an umbilical hernia?

A

A type of paediatric hernia affecting 3% of life births.

260
Q

What are the risk factors for an umbilical hernia?

A
  • Low birth weight (<1500g).
  • African ancestry.
261
Q

What is the management for an umbilical hernia?

A

Rarely needed, most resolve by the age of 3.

262
Q

What are the complications of an umbilical hernia?

A

All are uncommon
- Post-operative → Infection and bleeding.
- Incarceration.
- Strangulation.
- Rupture.

263
Q

What is an incisional hernia?

A
  • Occurs when tissue protrudes through a surgical scar that is weak
  • They are a complication of abdominal surgery but can occur anywhere where there is an incision and follows a breakdown of muscle closure after surgery
264
Q

What are the risk factors for an incisional hernia?

A
  • Emergency surgery.
  • Wound infection post operation.
  • Persistent coughing and heavy lifting.
  • Poor nutrition.
265
Q

What is the management for an incisional hernia?

A
  • Repair is more difficult in those that are obese
  • Mesh repair - reduced recurrence but associated with high levels of infection
266
Q

What is an epigastric hernia?

A

Pass through the linea alba above the umbilicus

267
Q

What are the clinical manifestations of an epigastric hernia?

A
  • Pain
  • Tenderness
  • Redness
  • Impulse on cough
268
Q

What are the investigations and management for an epigastric hernia?

A
  • Investigations
    - Ultrasound
    - CT
  • Management
    - Surgery
269
Q

What is a hiatal hernia?

A
  • Protrusion of intra-abdominal contents into the thoracic cavity though an enlarged oesophageal hiatus of the diaphragm.
  • 2 subtypes:
    • Sliding hiatus hernia (80%).
    • Paraesophageal hernia (rolling hiatus hernia) (20%).
270
Q

What are the clinical manifestations of a hiatal hernia?

A
  • Small hernias - asymptomatic
  • Large hernias - GORD (50%)
271
Q

What are the investigations of a hiatal hernia?

A
  • Upper GI endoscopy - to visualise the mucosa, but cannot exclude hiatus hernia.
  • Barium swallow to confirm diagnosis.
272
Q

What is the management for a hiatal hernia?

A
  • Weight loss
  • Treatment of GORD
  • Surgical treatment, if:
    • High risk of strangulation
    • Intractable symptoms despite medical therapy
    • Complications
273
Q

What is diarrhoea?

A

The abnormal passage of loose or liquid stool more than 3 times daily

274
Q

What is acute diarrhoea?

A

Acute diarrhoea is defined as that lasting less than 2 weeks

275
Q

What are the investigations for acute diarrhoea?

A
  • Stool MCS- establish the causative organism and antibiotic sensitivities.
  • Flexible sigmoidoscopy with colonic biopsyis performed if symptoms persist and no diagnosis has been made
276
Q

What is the management for acute diarrhoea?

A

Treatment is symptomatic to maintain hydration with anti-diarrhoeal agents (Loperamide) for short-term relief and antibiotics for specific indications.

277
Q

What is chronic diarrhoea?

A

Chronic diarrhoea is defined as lasting more than 2 weeks.

278
Q

What are the investigations for chronic diarrhoea?

A
  • Faecal markers
  • U&Es
  • Stool MCS
  • Sigmoidoscopy with biopsy
  • CRP and ESR
  • Other bloods
279
Q

What is the management for chronic diarrhoea?

A
  • Treat cause
  • Oral rehydration
  • Anti-diarrhoeal e.g. loperamide or codeine phosphate
280
Q

What is an anal fissure?

A
  • Painful tear in squamous lining of lower anal canal, distal to the dentate line resulting in pain on defecation.
  • Can be acute: <4-6 weeks
  • Or chronic: >6 weeks
281
Q

What are the clinical manifestations of an anal fissure?

A
  • Extreme pain - especially on defecation
  • Bleeding
  • Faecal impaction and constipation due to avoidance of toileting
  • If chronic, there may be skin tags:
    • At distal end of the fissure, the tag is called a sentinel pile
    • At the proximal end of the fissure, the tag is called a hypertrophied anal papillae.
282
Q

What are the investigations of an anal fissure?

A
  • Can usually be made on history alone
  • Confirmed on perianal inspection
  • Rectal examination (sometimes not possible due to pain and sphincter spasm)
  • Individuals with rectal bleeding or an atypical location of the fissure should get further evaluation, including anoscopy, colonoscopy, or sigmoidoscopy to exclude secondary causes of an anal fissure or an alternative diagnosis like haemorrhoids.
283
Q

What is the management for an anal fissure?

A
  • Increase dietary fibre and fluids
  • Use of stool softeners
  • Hygiene advice
  • FIRST LINE - Lidocaine ointment + GTN ointment or topical diltiazem
  • SECOND LINE - Botulinum toxin injection (botox) and topical diltiazem
  • Surgery if medication fails: lateral partial internal sphincterotomy (the internal sphincter is divided to lower its resting pressure, which helps improve blood supply to the fissure and allows faster healing).
284
Q

What is an anal fistula?

A

An abnormal connection between the epithelial surface of the anal canal and skin - it is essentially a track that communicates between the skin and anal canal/rectum.

285
Q

What are the clinical manifestations of an anal fistula?

A
  • Pain
    • Usually intermittent and during defecation, during sitting or activity.
  • Malodorous discharge (bloody or mucus)
  • Pruritus ani (itchy bottom)
  • Perianal skin may be excoriated and inflamed
  • Systemic abscess if it becomes infected
286
Q

What are the investigations of an anal fistula?

A
  • In some cases, the internal opening can be palpated on digital rectal exam.
  • MRI:
    • To exclude sepsis
    • To detect associated conditions e.g. Crohn’s or TB
    • Imaging will show air or contrast material in the fistula
  • Endoanal ultrasound:
    • To determine tracks location and underlying causes
287
Q

What is the management for an anal fistula?

A
  • Surgical - Fistulotomy and excision
  • Treat with antibiotics if infected
288
Q

What is a haemorrhoid?

A
  • Haemorrhoids are normal spongy vascular structures in the anal canal that act as cushions for the stool as it passes through.
  • Hemorrhoidal disease (simply know as haemorrhoids) is when haemorrhoids get disrupted, swollen and inflamed.
289
Q

What is the grading system for internal haemorrhoids?

A
  • Grade I: no protrusion outside the anal canal.
  • Grade II: protrusion outside the anus during bowel movement, but they retract spontaneously.
  • Grade III: prolapsed haemorrhoids that don’t retract spontaneously, but they can be pushed back in manually.
  • Grade IV: prolapsed haemorrhoids that cannot be manually pushed back in.
290
Q

What is the difference between an internal and external haemorrhoid?

A

Internal haemorrhoids are ones above the dentate line, and external haemorrhoids are ones below the dentate line.

291
Q

What are the risk factors of haemorrhoids?

A
  • Obesity
  • Old age
292
Q

What are the clinical manifestations of external haemorrhoids?

A
  • Usually asymptomatic but can:
    • Get inflamed
    • Cause itching, burning, vague discomfort
    • Cause painless passage of bright red blood with a bowel movement
293
Q

What are the clinical manifestations of internal haemorrhoids?

A
  • Painful, especially when associated with thrombosed haemorrhoids
  • Thrombosed external haemorrhoids are tender and have a purplish hue
  • Swelling in the affected area
  • Mucus discharge
  • Itching
294
Q

What are the investigations of haemorrhoids?

A
  • Abdominal examination to rule out other diseases
  • Rectal exam
  • Proctoscopy for internal haemorrhoids.
  • Further testing with flexible sigmoidoscopy or colonoscopy to exclude proximal pathology if >50 years old
295
Q

What are the differential diagnoses for haemorrhoids?

A
  • Perianal haematoma
  • Anal fissure
  • Abscess
  • Tumour
  • Proctalgia fugax: anal pain that doesn’t have a specific cause
296
Q

What is the first degree management for haemorrhoids?

A
  • Increase fibre and fluid intake
  • Stool softeners
  • Topical analgesia
  • Topical steroids for short periods
297
Q

What is the second and third degree management for haemorrhoids?

A
  • Rubber band ligation
  • Sclerotherapy: injection of drugs causes coagulation
  • Infrared coagulation
  • Bipolar diathermy and direct current electrotherapy: local heat causes coagulation
298
Q

What are the surgical options for haemorrhoids?

A
  • Excisional haemorrhoidectomy
  • Stapled haemorrhoidopexy
299
Q

What is the management for prolapsed thrombosed piles?

A
  • Analgesia
  • Ice packs
  • Stool softeners
300
Q

What is a pilonidal abscess?

A

Hair follicles get stuck under the skin in the natal cleft (butt crack) ~6cm above the anus, resulting in irritation and inflammation leading to small tracks which can become infected (abscess)

301
Q

What are the risk factors for pilonidal abscess?

A
  • Gender → Male > Female
  • Commonly present between 20-30 years old.
  • Obese Caucasians and those from Asia, Middle East and Mediterranean are at increased risk
  • Large amount of body hair
  • Having deep gluteal clefts
  • Sedentary job
  • Family history
302
Q

What are the clinical manifestations of an acute pilonidal abscess?

A
  • Painful swelling over days
  • Pus filled with foul smell from abscess
  • Systemic signs of infection
303
Q

What are the clinical manifestations of chronic pilonidal sinus inflammation?

A
  • Associated mucoid, purulent, or bloody drainage.
  • 4 in 10 have repeated recurrent pilonidal sinus
  • Infection never clears completely
304
Q

What is the investigation for a pilonidal abscess?

A
  • Clinical examination detection.
305
Q

What is the management for a pilonidal abscess?

A
  • Acute pilonidal abscess requires incision and drainage
  • Chronic pilonidal disease and recurrent abscesses require:
    • Surgical excision and pus drainage
    • Pre-op antibiotics
    • Complex tracks can be laid open and packed individually
    • Skin flaps can be used to cover defect
  • Hygiene and hair removal advice (near sinus)
306
Q

What is Gilbert’s syndrome?

A
  • A genetic syndrome of mild unconjugated hyperbilirubinaemia.
  • Defined by concentration of <102 micromol/L.
  • The liver is otherwise functionally normal.
307
Q

What are the risk factors of Gilbert’s syndrome?

A
  • Family History
  • Post-pubertal age.
  • Mutation in the UGT1A1 gene.
308
Q

What are the clinical manifestations of Gilbert’s syndrome?

A
  • Asymptomatic
  • Mild jaundice (icterus) seen in times of fasting or physiological stress
309
Q

What are the investigations of Gilbert’s syndrome?

A
  • LFTs - normal
  • FBC - normal
  • Unconjugated bilirubin - Elevated
  • Liver biopsy is not needed but may be done to exclude other diagnosis
310
Q

What is the management for Gilbert’s syndrome?

A
  • Doesn’t need treating as there isn’t any liver damage
  • Patient education
  • Avoidance or reversal of inciting agents
311
Q

What is acute pancreatitis?

A
  • Acute pancreatitis refers to an acute inflammatory process involving the pancreas.
  • The 2 main causes of acute pancreatitis are gallstones and alcohol.
  • In the UK, around 50% of cases are caused by gallstones, 25% by alcohol, and 25% by other factors.
312
Q

What are the risk factors for acute pancreatitis?

A
  • Incidence increases with age.
313
Q

What are the key presentations of acute pancreatitis?

A
  • Acute pancreatitisshould be suspected in any person with:
    • Acute upper or generalised abdominal pain, particularly if they have a history or clinical features of gallstonesoralcohol misuse.
314
Q

What are the signs of acute pancreatitis?

A
  • Abdominal tenderness and guarding
  • Abdominal distention
  • Tachycardic and/or hypotensive - pt may be in shock
  • Jaundice
  • Cullen’s sign
  • Grey Turner’s syndrome
  • Fox’s sign
315
Q

What are the symptoms of acute pancreatitis?

A
  • Severe upper abdominal pain: epigastric, RUQ or LUQ pain which may radiate to the back
  • Nausea, vomiting and anorexia
  • Steatorrhoea: excess fat in faeces in acute-on-chronic pancreatitis
  • Poor urinary output
316
Q

What are the investigations for acute pancreatitis?

A
  • FBC
  • U&Es
  • LFTs
  • ABG
  • Serum glucose
  • Serum LDH
  • Serum calcium
  • CRP
317
Q

What is the modified Glasgow scoring used for?

A

Patients with a score of 3 points or more within the first 48 hours should be considered for referral to high-dependency care for acute pancreatitis.

P - pO2 (<8kPa)
A - Age (>55 years)
N - Neutrophils (WCC>15x10^9/L)
C - Calcium (<2mmol/L)
R - Renal function (Urea >16mmol/L)
E - Enzymes (AST >200U?L OR LDH >600U/L)
A - Albumin (<32g/L)
S - Sugar (Blood glucose >10mmol/L)

318
Q

What is the primary management for acute pancreatitis?

A

FIRST LINE management is supportive
- IV fluid resuscitation
- Catheterisation
- Oxygen supplementation
- Opiate analgesia
- Early nutritional support
- Antibiotics

319
Q

What is the specific management for acute pancreatitis?

A
  • Endoscopic Retrograde Cholangiopancreatography (ERCP)
  • Cholecystectomy
  • Alcohol cessation and withdrawal management (alcohol)
320
Q

What is chronic pancreatitis?

A

Chronic pancreatitis refers to inflammation of the pancreas. Unlike acute pancreatitis, chronic pancreatitis is irreversible. It is characterised by structural changes e.g. fibrosis, calcification and atrophy which leads to a decline in function of the pancreas.

321
Q

What are the risk factors for chronic pancreatitis?

A
  • Gender → Male > Female
  • Alcohol excess
  • Smoking
  • Family history
  • Ductal obstruction e.g. gallstones, tumours, structural abnormalities
  • Genetic - cystic fibrosis and haemochromatosis
322
Q

What are the signs of chronic pancreatitis?

A
  • Epigastric tenderness
  • Signs of liver disease due to alcohol excess e.g. jaundice and ascites
  • Skin nodules (rare) - pancreatic lipase leaks into circulation and causes fat necrosis in soft tissue
323
Q

What are the symptoms of chronic pancreatitis?

A
  • Diarrhoea
    • Foul-smelling stools which are hard to flush. Stool contains fat as pancreatic function declines and food isn’t digested properly
  • Nausea and vomiting
  • Weight loss and fatigue
  • Features ofdiabetes e.g. polyuria and polydipsia
324
Q

What are the key presentations of chronic pancreatitis?

A
  • Epigastric pain radiating to the back
  • Steatorrhea
  • Malnutrition
  • Diabetes mellitus
325
Q

What are the primary investigations for chronic pancreatitis?

A
  • FIRST LINE - CT or MRI
  • NICE FIRST LINE - Transabdominal ultrasound
326
Q

What are some other investigations for chronic pancreatitis?

A
  • MRCP
  • Faecal elastase
  • LFTs
  • HbA1c
  • IgG4
  • ERCP
  • Amylase and Lipase serum levels
327
Q

What is the primary management for chronic pancreatitis?

A
  • FIRST LINE - Lifestyle modification - smoking and alcohol cessation
  • Diet modification
  • Analgesia
  • Pancreatic enzyme replacement
328
Q

What is the secondary management for chronic pancreatitis?

A
  • Intervention procedures
    • Endoscopic stenting
    • Coeliac plexus nerve blocks
    • Drainage
    • Pancreatectomy
329
Q

What are the complications of chronic pancreatitis?

A
  • Malabsorption
  • Duct obstruction
  • Pseudocyst
  • Diabetes
  • Pancreatic cancer
  • Local vascular complications
  • Gastric varices
  • Metabolic bone disease
330
Q

What is pancreatic cancer?

A

‘Pancreatic cancer’ refers to primary pancreatic ductal adenocarcinoma, which accounts for >85% of all pancreatic neoplasms. These adenocarcinomas usually affect the head of the pancreas, but sometimes the body and tail. Some are multifocal.

331
Q

What are the risk factors of pancreatic cancer?

A
  • Male
  • Family history
  • Smoking
  • Alcohol
  • Obesity
  • Diet high in red meat
  • Diabetes: a risk factor and a potential consequence of pancreatic cancer
  • Chronic pancreatitis
  • Genetic: hereditary non-polyposis colorectal carcinoma, BRCA1 and BRCA2 mutations, Peutz-Jeghers syndrome
  • Multiple endocrine neoplasia
332
Q

What are the signs of pancreatic cancer?

A
  • Positive Courvoisier’s sign: In the presence of painless obstructive jaundice, a palpable gallbladder isunlikelyto be due to gallstones
  • Trousseau sign of malignancy: migratory thrombophlebitis (blood clots felt as small lumps under skin)
333
Q

What are the symptoms of pancreatic cancer?

A
  • Non-specific symptoms:
    • Epigastric or atypical back pain, anorexia, weight loss; these features are common
  • New-onset diabetes:
    • Thirst, polyuria, nocturia, weight loss
    • Due to the loss of endocrine function
  • Nausea and vomiting
  • Steatorrhoea: due to loss of exocrine function fats are not digested
  • Dark urine and pale stools: due to obstructive jaundice
  • Cancer related anorexia
  • Acute pancreatitis
334
Q

What are the key presentations of pancreatic cancer?

A
  • Painless obstructive jaundice.
335
Q

What are the investigations of pancreatic cancer?

A
  • Abdominal ultrasound - FIRST LINE
  • LFTs
  • Coagulation profile
  • CA 19-9
  • CT chest of abdomen and pelvis
  • PET CT if CT is inconclusive (NICE)
336
Q

What is the management for localised pancreatic cancer?

A
  • Surgical resection (Whipple’s resection or laparoscopic excision)
  • Adjuvant chemotherapy after surgery
  • Neoadjuvant therapy before surgery may be offered
337
Q

What is the management for locally advanced or metastatic pancreatic cancer?

A
  • Palliative management:
    • ERCP with stenting: for symptomatic relief of obstructive jaundice in patients with unresectable and metastatic tumours
    • Chemotherapy/chemoradiotherapy: offered if patients are able to tolerate it
    • Management of pain: opiates or radiotherapy
338
Q

What are the complications of pancreatic cancer?

A
  • Cancer related
    • VTE
    • New-onset diabetes mellitus
    • Cholangitis
  • Surgery related
    • Early dumping syndrome
    • Late dumping syndrome
339
Q

What is cholelithiasis?

A

Cholelithiasis (gallstones) refers to the development of a solid deposit or ‘stone’ within the gallbladder.

340
Q

What are the four F’s for gallstones and biliary colic?

A
  • Risk factors
  • Female - 2-3 x higher
  • Fat
  • Forties
  • Fertile - pregnancy
341
Q

Aside from the four F’s what are the risk factors for gallstones and biliary colic?

A
  • Genetic predisposition
  • Diabetes
  • Rapid weight loss / fasting
  • Medications
  • Chron’s disease
  • Haemolytic conditions
  • Diet high in fat and refined carbohydrates
342
Q

What are the clinical manifestations for gallstones?

A
  • Gallstones are normally asymptomatic
  • Biliary colic
  • Acute cholecystitis
  • Acute cholangitis
  • Acute pancreatitis
  • Mucocele/Empyema
  • Mirizzi’s syndrome
  • Obstructive jaundice
  • Gallstone ileus
  • Gallbladder cancer
343
Q

What is biliary colic?

A
  • Biliary colic refers to a pain in the RUQ/epigastrium caused by gallstones.
  • Though termed a ‘colic’ the pain is normally constant lasting from 30 minutes to 6 hours.
344
Q

What are the clinical manifestations of biliary colic?

A
  • Nausea and vomiting
  • Right upper quadrant pain
  • Epigastric pain
  • Pain may radiate to right shoulder or interscapular region
  • Episodes typically last 30 minutes - 6 hours. Often worse after ingestion of fatty foods.
  • Note: there are no signs on abdominal examination. Murphy’s sign negative.
345
Q

What are the investigations for biliary colic?

A
  • FIRST LINE - abdominal ultrasound
  • LFTs
  • FBC
  • CRP and ESR
  • Amylase level
346
Q

What are the differential diagnosis for biliary colic?

A
  • Cholecystitis
  • Ascending cholangitis
  • Common bile duct stone
  • Gastritis
  • Peptic ulcer disease
  • IBS
  • Carcinoma on right side of colon
  • Renal colic
  • Pancreatitis
347
Q

What is the management for biliary colic?

A
  • Symptomatic management
    • Analgesia - Paracetamol and NSAIDS
    • Diet modification - low fat
  • Surgical management
    • MRCP +/- ERCP for confirmation
    • On table cholangiogram
    • Elective laparoscopic cholecystectomy
348
Q

What are the complications of biliary colic?

A
  • Obstructive jaundice
  • Cholecystitis
  • Ascending cholangitis
  • Acute pancreatitis
  • Gallbladder empyema
  • Gallstone ileus
  • Gallbladder cancer
349
Q

What is acute cholecystitis?

A
  • Acute cholecystitis refers to inflammation of the gallbladder most commonly occurring due to impacted gallstones (calculous cholecystitis)
  • Relatively rarely acute cholecystitis occurs in the absence of gallstones (acalculous cholecystitis).
350
Q

What is acute cholecystitis?

A
  • Acute cholecystitis refers to inflammation of the gallbladder most commonly occurring due to impacted gallstones (calculous cholecystitis)
  • Relatively rarely acute cholecystitis occurs in the absence of gallstones (acalculous cholecystitis).
351
Q

What are the risk factors for acute cholecystitis?

A
  • Female - 2-3 x higher
  • Fat
  • Forties
  • Fertile - pregnancy
  • Genetic predisposition
  • Diabetes
  • Rapid weight loss / fasting
  • Medications
  • Chron’s disease
  • Haemolytic conditions
  • Diet high in fat and refined carbohydrates
352
Q

What are the signs of acute cholecystitis?

A
  • RUQ abdominal tenderness
    • Murphy’s sign positive:palpating the RUQ whilst the patient breathes in deeply causes pain
  • Abdominal mass
    • Due to distended gallbladder (present in 30-40%)
  • Pyrexia
  • Tachycardia
  • Hypotension (in severe cases)
353
Q

What are the symptoms of acute cholecystitis?

A
  • Nausea and vomiting
  • Fever
  • Right upper quadrant abdominal pain
    • Severe and lasting >30 minutes
    • Preceding history of biliary colic
  • Referred right shoulder tip pain
  • Note: jaundice should not be present. If jaundiced, this may suggest Mirizzi syndrome, CBD stone or ascending cholangitis.
354
Q

What are the investigations for acute cholecystitis?

A
  • FIRST LINE - Transabdominal ultrasound
  • GOLD STANDARD - Abdominal ultrasound
  • FBC
  • LFTs
  • U&Es
  • Coagulation profile
  • VBG
  • Inflammatory markers
355
Q

What are the differential diagnoses for acute cholecystitis?

A
  • Pancreatitis
  • Peptic ulcer disease
  • Cholangitis
  • Appendicitis
  • Basal pneumonia
356
Q

What is the first line management for acute cholecystitis?

A
  • ABC and sepsis 6
  • IV antibiotics - cefuroxime and metronidazole
  • IV fluids and analgesia
  • Nil by mouth
  • Note: before cholecystectomy, CBD stones should be checked for: MRCP or on-table cholangiogram.
    • Early laparoscopic cholecystectomy
357
Q

What is the second line management for acute cholecystitis?

A
  • Urgent cholecystostomy
358
Q

What are the complications of acute cholecystitis?

A
  • Gallbladder empyema
  • Gallstone ileus
  • Acute cholangitis
  • Obstructive jaundice
  • Procedure-related - bile duct injury
359
Q

What is chronic cholecystitis?

A

Chronic inflammation of the gallbladder +/- colic.

360
Q

What are the clinical manifestations of chronic cholecystitis?

A
  • Flatulent dyspepsia
  • Abdominal discomfort - RUQ pain (esp after meal)
  • Distension
  • Nausea
  • Fat intolerance (fat stimulates cholecystokinin release and gallbladder contraction)
361
Q

What are the investigations of chronic colecytitis?

A
  • Ultrasound - to image stone and assess CBD diameter
  • MRCP - used to find CBD stones
  • X-ray - may show porcelain gallbladder
362
Q

What are the differential diagnoses for chronic cholecystitis?

A
  • If symptoms persist post-treatment, consider:
    • Hiatus hernia
    • IBS
    • Peptic ulcer
    • Chronic pancreatitis
    • Tumour
363
Q

What is the management for cholesytitis?

A
  • Cholecystectomy
    • ERCP + sphincterotomy prior to surgery
364
Q

What is ascending cholangitis?

A

Acute cholangitis refers to infection of the biliary tree characteristically resulting in pain, jaundice and fevers.

365
Q

What are the risk factors for ascending cholangitis?

A
  • Gallstones:the most common predisposing factor
  • Stricture of the biliary tree:benign or malignant
  • Post-procedure injuryof the bile ducts e.g. post-ERCP
  • Age → > 50 years old.
366
Q

What are the key presentations for ascending cholangitis?

A
  • Right upper quadrant (RUQ) abdominal pain, jaundice, and fever is known as Charcot’s triad and suggests a diagnosis of ascending cholangitis. It is seen in 20-50% of patients.
  • The addition of hypotension and change in mental state/ confusion (shock) is known as Reynolds’ pentad and is associated with biliary sepsis.
367
Q

What are the signs of ascending cholangitis?

A
  • RUQ tenderness
  • Scleral icterus
  • Pyrexia
  • Hypotension: part of Reynold’s pentad
368
Q

What are the symptoms of ascending cholangitis?

A
  • RUQ abdominal pain
  • Jaundice
  • Fever: the most common feature
  • Nausea and vomiting
  • Malaise
  • Pruritis
  • Dark urine and pale stool (cholestasis)
  • Confusion: part of Reynold’s pentad
369
Q

What are the investigations for ascending cholangitis?

A
  • FIRST LINE - Transabdominal ultrasound
  • MRCP - GOLD STANDARD for diagnosis
  • FBC
  • LFTs
  • U&Es
  • CRP and ESR
  • VBG
  • Blood cultures
  • Inflammatory markers
370
Q

What are the differential diagnoses for ascending cholangitis?

A
  • Acute cholecystitis
  • Peptic ulcer disease
  • Pancreatitis
  • Hepatic abscess
  • Appendicitis
  • Biliary colic
371
Q

What is the medical management for ascending cholangitis?

A
  • ABC with sepsis 6
  • IV antibiotics e.g. cefotaxime and metronidazole for 4-7 days
  • IV fluids
  • Analgesia
372
Q

What is the surgical and non-medical management for ascending cholangitis?

A
  • Biliary decompression
    • ERCP
    • Percutaneous trans-hepatic cholangiography
    • Surgical drainage
  • Elective cholecystectomy
373
Q

What are the complications of ascending cholangitis?

A
  • Biliary sepsis
  • Acute pancreatitis
  • Hepatic abscess
  • Risk of ERCP
374
Q

What is cholangiocarcinoma?

A

Biliary tree cancer. Makes up 10% of the primary liver cancers.

375
Q

What are the risk factors for choalgiocarcinoma?

A
  • Inflammatory bowel disease
  • HBV
  • HCV
  • Infection with parasitic worms (flukes)
376
Q

What are the signs of choalgiocarcinoma?

A
  • Palpation - enlarged, irregular, tender liver may be felt
  • Signs of chronic liver disease
  • Signs of decompensation - jaundice, ascites
  • Listen for bruit - murmur over the liver
377
Q

What are the symptoms of cholangiocarcinoma?

A
  • Fever
  • Weight loss
  • Abdominal pain +/- ascites
  • Malaise
378
Q

What are the investigations for cholangiocarcinoma?

A
  • CT and ultrasound
  • MRI - staging
  • Biopsy
  • FBC
  • Clotting profile
  • Hepatitis serology
  • LFT
  • Serum alpha-fetoprotein
  • Bilirubin levels
  • ALP levels
379
Q

What is the management for cholangiocarcinoma?

A
  • Surgery (not possible in 70% of patients at presentation)
    • Intrahepatic then FIRST LINE is partial liver resection
    • Extrahepatic then surgical excision
  • Liver transplantation
  • Chemotherapy, Radiotherapy, Immunotherapy - high resistance
380
Q

What is portal hypertension?

A
  • Normal portal vein pressures range from 5–10 mm Hg. The term portal hypertension refers to elevated pressures in the portal venous system. Venous pressure more than 5 mm Hg greater than the inferior vena cava pressure is defined as portal hypertension.
  • Portal vein is formed by the union of the superior mesenteric and splenic veins
381
Q

What are the risk factors of portal hypertension?

A
  • Cirrhosis
  • Alcohol
  • Congestive heart failure
  • Hyper-coagulable state
382
Q

What are the clinical manifestations of portal hypertension?

A
  • Features of chronic liver disease
    • Leukonychia (white discolouration on nails)
    • Palmar erythema
    • Spider telangiectasia
    • Gynecomastia
  • Features of decompensated liver disease
    • Encephalopathy
    • Jaundice
    • Ascites
  • Splenomegaly due to portal hypertension
  • Variceal bleeding
383
Q

What are the investigations for portal hypertension?

A
  • Abdominal ultrasound - dilated portal vein
  • Doppler ultrasound - slow velocity and dilated portal vein
  • Endoscopy - for presence of oesophageal varices
384
Q

What is the management for portal hypertension?

A
  • Treat underlying cause
  • Salt reduction and diuretics
  • Beta-blockers and nitrate to reduce blood pressure
385
Q

What are the complications of portal hypertension?

A
  • Varices and variceal haemorrhage
  • Ascites
  • Hepatopulmonary syndrome
  • Liver failure
  • Hepatic encephalopathy
  • Cirrhotic cardiomyopathy
386
Q

What is chronic liver failure?

A
  • Chronic liver disease is caused by repeated insults to the liver, which can result in inflammation, fibrosis and ultimately cirrhosis.
  • CLD is generally defined as progressive liver dysfunction for six months or longer. The end result of chronic liver disease is cirrhosis, which describes irreversible liver remodelling.
387
Q

What are the early manifestations of chronic liver failure?

A
  • Non-specific signs:
  • Anorexia, lethargy
  • Weight loss
  • Hepatomegaly
  • Nausea
  • Disturbed sleep pattern.
388
Q

What are the signs of chronic liver disease?

A
  • Caput medusa
  • Splenomegaly
  • Palmar erythema
  • Dupuytren’s contracture
  • Leukonychia
  • Gynecomastia
  • Spider naevi
389
Q

What are the signs of decompensated liver disease?

A
  • Encephalopathy
  • Ascites
  • Jaundice
  • GI bleeding
  • Coagulopathy
390
Q

What are the investigations for chronic liver disease?

A
  • GOLD STANDARD - Liver biopsy
  • LFTs
  • FBC
  • Hyperbilirubinemia
  • Transient elastography
  • USS
  • CT or MRI
  • Non-invasive liver screen
391
Q

What is the management for chronic liver disease?

A
  • Treat underlying pathology
  • Transplantation - based upon UKELD score
  • Hepatic encephalopathy - FIRST LINE - laxatives
  • Ascites - aldosterone agonist e.g. spironolactone
  • GI bleeding - beta blockers and variceal band ligation
  • Spontaneous bacterial peritonitis - antibiotics
392
Q

What are the complications of chronic liver disease?

A
  • Hepatic encephalopathy
  • Ascites
  • Gastrointestinal bleeding(i.e. variceal bleed)
  • Bacterial infections(i.e. SBP)
  • Acute kidney injury
  • Hepatorenal syndrome
  • Hepatopulmonary syndrome
  • Hepatocellular carcinoma
  • Acute-on-chronic liver failure
393
Q

What is the monitoring for chronic liver disease?

A
  • HCC - 6-monthly surveillance
394
Q

What is alcohol-induced liver disease?

A

Alcoholic liver disease (ALD) has 3 stages of liver damage: fatty liver (steatosis), alcoholic hepatitis (inflammation and necrosis), and alcoholic liver cirrhosis. All are caused by chronic heavy alcohol ingestion.

395
Q

What are the risk factors for alcoholic liver disease?

A
  • Prolonged and heavy alcohol consumption
  • Hepatitis C - increased risk of cirrhosis
  • Female sex - ALD develops more rapidly and occurs at lower drinking levels in women than in men. However, most patients with ALD are male.
  • Genetic predisposition
  • Increasing age >65
  • Obesity
396
Q

What are the clinical manifestations of a fatty liver?

A
  • Often, no symptoms or signs
  • Vague abdominal symptoms of nausea, vomiting, diarrhoea are due to the more general effects of alcohol on the GI tract
  • Hepatomegaly, sometimes huge, can occur together with other features of chronic liver disease
397
Q

What are the clinical manifestations of hepatitis?

A
  • Mild jaundice may occur
  • Signs of chronic liver disease (ascites, bruising, clubbing, Dupuytren’s contracture)
  • Anorexia
  • Asterixis
  • Diarrhoea and vomiting
  • High temperature, pulse and respiration
  • Abdominal pain in severe cases
  • Deep jaundice, hepatomegaly and ascites in severe cases
398
Q

What are the clinical manifestations of cirrhosis?

A
  • Patients can be very well with few symptoms
  • On examination there are usually signs of chronic liver disease - ascites, bruising, clubbing and Dupuytren’s contracture
  • There are features of alcohol dependency
399
Q

What are the general signs of alcoholic liver disease?

A
  • Hepatomegaly
  • Abdominal pain
  • Haematemesis
  • Venous collaterals - engorged para-umbilical veins (caput medusae), present in advanced alcoholic liver disease.
  • Splenomegaly
  • Jaundice
  • Palmar erythema
  • Asterixis
  • Ascites
  • Weight loss
  • Fatigue
  • Confusion
  • Pruritis
  • Fever
  • Nausea and vomiting
  • Finger clubbing
  • Dupuytren’s contracture
  • Bruising - coagulopathy
  • Withdrawal symptoms - high pulse, low BP, tremor, confusion, fits, hallucinations
400
Q

What is the diagnostic criteria for alcohol induced liver disease?

A

A combination of clinical features and laboratory findings are used to make a diagnosis. A liver biopsy is usually reserved for severe case. It helps to assess severity, look for underlying cirrhosis and exclude alternative causes of liver disease.

401
Q

What are the investigations for alcohol induced liver disease?

A
  • FBC
  • U&Es
  • LFTs
  • Bone profile
  • CRP
  • Magnesium levels
  • INR
  • Non-invasive liver screen
  • Liver ultrasound
  • Liver biopsy
402
Q

What are the investigations for alcohol induced liver disease?

A
  • FBC
  • U&Es
  • LFTs
  • Bone profile
  • CRP
  • Magnesium levels
  • INR
  • Non-invasive liver screen
  • Liver ultrasound
  • Liver biopsy
403
Q

What is ‘CAGE’, in relation to alcoholic liver disease?

A
  • C – CUT DOWN? Ever thought you should?
  • A – ANNOYED? Do you get annoyed at others commenting on your drinking?
  • G – GUILTY? Ever feel guilty about drinking?
  • E – EYE OPENER? Ever drink in the morning to help your hangover/nerves?
404
Q

What are the different severity scoring systems for alcohol induced liver disease?

A
  • Maddrey discriminant function (DF) - used to assess the severity of alcoholic hepatitis. It is based on serum bilirubin and prothrombin time.
  • Model for End-stage liver disease (MELD) - assesses severity
  • Glasgow alcoholic hepatitis score (GAH) - predicts mortality among patients with alcoholic hepatitis. It is a slightly more complex score based on age, white blood cell count, urea, bilirubin and prothrombin time.
405
Q

What is the general management for alcoholism?

A
  • Alcohol cessation - Diazepam and/or IV thiamine to prevent Wernicke-Korsakoff encephalopathy.
  • Hydration
  • Nutrition
406
Q

What is the management for alcoholic hepatitis?

A
  • Nutrition must be maintained with enteral feeding (high protein diet) and if necessary vitamin supplementation e.g. Vit K
  • Steroids show short-term benefit e.g. prednisolone. Given to patients who score high on Maddrey Discriminant Factor scoring system.
  • Screen for infections (ascitic fluid tap) and treat spontaneous bacterial peritonitis
407
Q

What is the management for alcoholic cirrhosis?

A
  • Reduce salt intake
  • Avoid aspirin and NSAIDs
  • Liver transplantation
408
Q

What are the complications of alcohol induced liver failure?

A
  • Liver failure, hepatocellular carcinoma
  • CNS complications etc
  • Obesity, diarrhoea, vomiting etc
  • Arrhythmias, hypertension, cardiomyopathy, sudden death
  • Coagulopathy, thrombocytopaenia, anaemia, folate deficiency, haemolysis
409
Q

What is NAFLD?

A
  • Non-Alcoholic Fatty Liver Disease
  • NAFLD refers to a fatty liver that cannot be attributed to alcohol or viral causes
  • Spectrum of disease - steatosis, steatohepatitis, fibrosis, cirrhosis (least to most severe)
410
Q

What are the risk factors for NAFLD?

A
  • Older age
  • Obesity
  • Hypertension
  • Diabetes
  • Hypertriglyceridemia
  • Hyperlipidemia
411
Q

What are the clinical manifestations of NAFLD?

A

May be asymptomatic even at advanced stages

  • Sometimes symptoms may be vague
    • Fatigue
    • Malaise
  • Sufficient damage present with:
    • Hepatomegaly
    • Pain in RUQ
    • Jaundice
    • Ascites
    • Bruising
    • Pruritis
412
Q

What are the investigations for NAFLD?

A
  • Enhanced liver fibrosis scan - FIRST LINE
  • NAFLD fibrosis score - SECOND LINE
  • Fibroscan - THIRD LINE
  • Serum AST and ALT
  • LFTs
  • FBC
  • Imaging - US, CT, MRI
  • Liver biopsy - GOLD STANDARD
413
Q

What are the differential diagnosis for NAFLD?

A
  • Alcoholic liver disease
  • Autoimmune hepatitis
  • Hepatitis B and C
  • Hemochromatosis
  • DILI
  • Primary biliary cholangitis
  • Primary sclerosing cholangitis
  • Wilson’s disease
  • Alpha-1 antitrypsin deficiency
414
Q

What is the management for NAFLD?

A
  • Steatosis and steatohepatitis is reversible if underlying cause is addressed. Cirrhosis is not reversible.
  • Avoid alcohol consumption
  • Reverse factors that contribute to insulin resistance
    • Healthy diet
    • Active lifestyle
    • Medication to control blood glucose
  • Control risk factors e.g. bariatric surgery for obesity
  • Address cardiovascular risk (commonest cause of death)
  • Vitamin E may improve histology of fibrosis
415
Q

What are the complications of NAFLD?

A
  • Ascites
  • Varices and variceal haemorrhage
  • Encephalopathy
  • Hepatocellular carcinoma
  • Hepatorenal syndrome - renal disease secondary to liver failure
  • Hepatopulmonary syndrome - shortness of breath and hypoxemia caused by vasodilation in the lungs of patients with liver disease.
416
Q

What is cirrhosis?

A
  • Cirrhosis is a diffuse pathological process, characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules known as regenerative nodules, surrounded by fibrotic tissue.
  • It can arise from a variety of causes (chronic alcohol use or viral attack) and is the final stage of any chronic liver disease. It can lead to portal hypertension, liver failure, and hepatocellular carcinoma. In general, it is considered to be irreversible in its advanced stages, although there can be significant recovery if the underlying cause is treated.
417
Q

What are the risk factors for liver cirrhosis?

A
  • Alcohol misuse
  • IV drug use
  • Obesity
418
Q

What are the clinical manifestations of liver cirrhosis?

A
  • Leukonychia - white discolouration’s on nails due to hypoalbuminaemia
  • Clubbing
  • Palmar erythema
  • Dupuytren’s contracture
  • Spider naevi
  • Xanthelasma - yellow fat deposits under skin usually around eyelids
  • Gynaecomastia
  • Loss of body hair
  • Hepatomegaly
  • Splenomegaly
  • Bruising
  • Ankle swelling and oedema
  • Abdominal pain due to ascites
419
Q

What are the investigations for liver cirrohsis?

A
  • Liver biopsy - GOLD STANDARD
  • LFTs
  • FBC
  • Ascitic tap
  • Imaging - MRI or Ultrasound
420
Q

What are the differential diagnosis for liver cirrohsis?

A
  • Constrictive pericarditis
  • Budd-Chiari syndrome
  • Portal vein thrombosis
  • Splenic vein thrombosis
  • Schistosomiasis
  • Sarcoidosis
  • Inferior vena cava obstruction
421
Q

What is the management for liver cirrhosis?

A
  • Treatment of underlying condition - FIRST LINE
  • Promote change in diet and lifestyle
  • Liver transplant - SECOND LINE
  • Trans-jugular intrahepatic portosystemic shunt - SECOND LINE
422
Q

What are the complications of liver cirrhosis?

A
  • Coagulopathy
  • Encephalopathy
  • Hypoalbuminaemia
  • Hepatocellular carcinoma
  • Spontaneous bacterial peritonitis
  • Acute kidney injury
  • Portal hypertension
423
Q

What is the Child-Pugh score?

A
  • The severity of cirrhosis can be graded using the Child-Pugh score.
  • The different classes reflect theseverity of cirrhosis and providean estimated one year survival.
    • Class A:mild disease,one year survival 100%
    • Class B:moderate disease, one year survival80%
    • Class C:severe disease, one year survival 45%
424
Q

What is jaundice?

A
  • Yellow discolouration of the skin due to raised serum bilirubin.
  • Occurs at bilirubin levels greater than 51µmol/L or 3mg/dL.
425
Q

What are the three types of jaundice?

A
  • Pre-hepatic
  • Intra-hepatic or Hepatocellular
  • Post-hepatic
426
Q

Give 3 examples of pre-hepatic jaundice?

A
  • Haemolytic anaemia
  • Gilbert’s syndrome
  • Criggler-Najjar syndrome
427
Q

Give 3 examples of intra-hepatic jaundice?

A
  • Alcoholic Liver Disease
  • Viral hepatitis
  • Iatrogenic Hereditary Haemochromatosis
  • Autoimmune Hepatitis
  • Primary Sclerosing Cholangitis
  • Primary Biliary Cirrhosis
  • Hepatocellular Carcinoma
428
Q

Give 3 examples of post-hepatic jaundice?

A
  • Intra-luminal cause → Gallstones
  • Mural: cholangiocarcinoma, strictures, drug-induced cholestasis
  • Extra-mural: pancreatic cancer, abdominal masses
429
Q

What are the investigations for Jaundice?

A
  • Usually based on history and clinical observation of yellow discolouration.
  • LFTs
  • Coagulation tests
  • FBC
  • Ultrasound - looking for biliary obstruction
430
Q

What is the management for jaundice?

A
  • Based on the underlying cause.
431
Q

What is primary biliary cholangitis?

A

Primary biliary cholangitis (PBC), previously known as primary biliary cirrhosis, is an autoimmune condition characterised by granulomatous destruction of the intrahepatic biliary ducts, leading to cholestasis and subsequent leakage of bile into the circulation.

432
Q

What are the risk factors for primary biliary cholangitis?

A
  • Gender → Female > Male (x10 more)
  • Autoimmune conditions
  • Family history
  • Past pregnancy
  • Smoking
  • Excessive use of nail polish and hair dye
  • Chronic urinary tract infection
433
Q

What are the key presentations for primary biliary cholangitis?

A

The classic presentation of PBC is with significant itching in a middle-aged female. Some patients may be asymptomatic and be simply diagnosed on a routine blood test demonstrating abnormal LFTs (e.g. raised ALP).

434
Q

What are the signs of primary biliary cholangitis?

A
  • Skin hyperpigmentation: due to increased melanin
  • Clubbing
  • Mild hepatosplenomegaly
  • Xanthelasma and xanthomata (late sign) - due to leakage of cholesterol
  • Scleral icterus (late sign)
435
Q

What are the symptoms of primary biliary cholangitis?

A
  • Pruritis (itchy skin) - leakage of bile salts
  • Fatigue and weight loss
  • Dry eyes and dry mouth - Sjögren’s syndrome
  • Obstructive jaundice (late sign) - due to leakage of bile and conjugated bilirubin
    • Icteric
    • Pale stool and dark urine
436
Q

What are the investigations for primary biliary cholangitis?

A
  • Antimitochondrial antibodies (AMA) - DIAGNOSTIC
  • Antinuclear antibodies (ANA)
  • Smooth muscle antibodies
  • Raised serum cholesterol
  • LFTs
  • Coagulation profile
  • Serum immunoglobulin - IgM
  • Transabdominal ultrasound
437
Q

What are the differential diagnoses for primary biliary cholangitis?

A
  • Primary sclerosing cholangitis - AMA would not be found
  • Obstructive bile duct lesion
  • Drug induced cholestasis - can do liver biopsy
438
Q

What is the management for primary biliary cholangitis?

A
  • Bile acid analogue e.g. ursodeoxycholic acid - FIRST LINE
  • Fat soluble vitamin supplementation (A, D, E, and K)
  • Cholestyramine
  • Codeine phosphate
  • Bisphosphonates
  • Liver transplant - ONLY FOR END-STANG LIVER DISEASE
439
Q

What are the complications of primary biliary cholangitis?

A
  • Malabsorption of fat soluble vitamins (A, D, E, and K)
  • Hypercholesterolaemia
  • Liver cirrhosis
  • Hepatocellular carcinoma
  • Metabolic bone disease
440
Q

What is primary sclerosing cholangitis?

A

Primary sclerosing cholangitis (PSC) is an immune-mediated chronic liver disease that is characterised by inflammation, fibrosis and destruction of intrahepatic and/or extrahepatic bile ducts.

441
Q

What are the risk factors of primary sclerosing cholangitis?

A
  • Male
  • History of inflammatory bowel disease:usually ulcerative colitis(UC); 4% of patients with UChave PSC, 80% of patients with PSC have UC
  • Family history
  • Some association with HLA-A1, B8 and DR3
442
Q

What are the signs of primary sclerosing cholangitis?

A
  • Jaundice
  • Signs of complications:
    • Ascending Cholangitis: Charcot’s triad
    • Chronic liver disease:rare at first presentation, e.g. ascites or encephalopathy
443
Q

What are the symptoms of primary sclerosing cholangitis?

A
  • Pruritis
  • Fatigue
  • RUQ/ epigastric abdominal pain
  • Symptoms of underlying bowel disease: bloody stools, tenesmus, diarrhoea, steatorrhea
444
Q

What is Charcot’s triad?

A

Charcot’s triad, a classic presentation seen in 50% of patients with acute cholangitis, is characterized by fever, jaundice, and right upper quadrant pain.

445
Q

What are the investigations for primary sclerosing cholangitis?

A
  • MRCP - Magnetic resonance cholangiopancreatography - GOLD STANDARD
  • LFTs (ALP, bilirubin, GGT, ALT, albumin, AST)
  • Viral hepatitis screen
  • Antibodies screen
    • pANCA (anti-neutrophil cytoplasmic antibodies)
    • Antimitochondrial antibodies - not present
    • ANA
    • Anticardiolipin antibodies
  • Abdominal ultrasound
446
Q

What is the management for primary sclerosing cholangitis?

A
  • Observation and lifestyle change - FIRST LINE
  • Cholestyramine - pruritus relief
  • Fat soluble vitamin supplementation (A, D, E, and K)
  • Ursodeoxycholic acid - may improve LFTs
  • Antibiotics - for bacterial cholangitis
  • Liver transplant - FOR END STANGE LIVER DISEASE ONLY
447
Q

What are the complications of primary sclerosing cholangitis?

A
  • Cholangitis
  • Biliary strictures
  • Choledocholithiasis
  • Metabolic bone disease
  • End-stage liver disease
  • Cholangiocarcinoma
  • Hepatocellular carcinoma
  • Colorectal carcinoma
448
Q

What are the differences between PSC and PBC in terms of epidemiology?

A
  • PBC - more common in middle-aged women
  • PSC - More common in middle-aged men
449
Q

What are the differences between PSC and PBC in terms of pathophysiology?

A
  • PBC - Progressive destruction of only intrahepatic small and medium sized bile ducts.
  • PSC - Progressive chronic inflammation of intra-hepatic and/or extra-hepatic bile ducts.
450
Q

What are the differences between PSC and PBC in terms of associated conditions?

A
  • PBC - Sjorgen syndrome (25%), Raynauds syndrome (25%), Autoimmune thyroid disease(25%).
  • PSC - Inflammatory bowel disease (75%) - particularly ulcerative cholangitis.
451
Q

What are the differences between PSC and PBC in terms of presentation?

A
  • PBC - Often asymptomatic, fatigue and pruritis, Jaundice, Hepatomegaly
  • PSC - Similar to PBC, Symptoms of IBD, Charcot’s triad
452
Q

What are the differences between PSC and PBC in terms of serum tests?

A
  • PBC - Increased ALP, GGT and conjugated bilirubin. Anti-mitochondrial antibodies.
  • PSC - Increased ALP, GGT, pANCA
453
Q

What are the differences between PSC and PBC in terms of diagnosis?

A
  • PBC - Cholestatic LFTs, History, Examination, abdominal ultrasound
  • PSC - Cholestatic LFTs, History, MRCP
454
Q

What are the differences between PSC and PBC in terms of management?

A
  • PBC - Ursodeoxycholic acid, Cholestyramine, Fat soluble vitamins (ADEK)
  • PSC - Observation and lifestyle, Cholestyramine, Fat soluble vitamins (ADEK)
  • Liver transplant for both - AT END STAGE ONLY
455
Q

What is autoimmine hepatitis?

A

Autoimmune hepatitis (AIH) is a chronic inflammatory disease of the liver of unknown aetiology. It is characterised by the presence of circulating auto-antibodies with a high serum globulin concentration, inflammatory changes on liver histology, and a favourable response to immunosuppressive treatment.

456
Q

What are the risk factors for autoimmune hepatitis?

A
  • Gender → Female > Male (4:1)
  • Age → Type 1 = Adults, Type 2 = Children
  • Associated with other autoimmune conditions such as, Hashimoto’s thyroiditis and primary biliary cholangitis
  • HLA-DR3 and HLA-DR4 association
457
Q

What are the signs of autoimmune hepatitis?

A
  • Evidence of chronic liver disease:
    • Jaundice
    • Spider telangiectasia
    • Gynaecomastia
    • Splenomegaly
  • Evidence of acute liver failure (less common):
    • Jaundice
    • Ascites
    • Variceal bleed
    • Encephalopathy
458
Q

What are the symptoms of autoimmune hepatitis?

A
  • Fatigue
  • Fever
  • Malaise
  • Urticarial rash
  • Arthralgia
  • Weight loss
  • Nausea
  • Amenorrhoea
  • 25% of cases are asymptomatic and patients may be asymptomatic even if their disease has progressed to cirrhosis. If symptoms are present, most cases present with non-specific symptoms.
459
Q

What are the investigations for autoimmune hepatitis?

A
  • LFTs (ALT and AST elevated, bilirubin may be raised)
  • FBCs
  • Immunoglobulins
  • Liver biopsy
  • Viral screen
  • Autoimmune screen (ANA, anti-SMA, anti-SLA/LP, anti-LKM1, anti-LC1)
  • Hereditary screen
460
Q

What is the management for acute autoimmune hepatitis?

A
  • High dose corticosteroids - FIRST LINE e.g. methylprednisolone or prednisolone
  • Liver transplant
  • Hepatitis A and B vaccines
461
Q

What is the management for active autoimmune hepatitis?

A
  • Immunosuppression e.g. prednisoloneandazathioprine - FIRST LINE
  • High dose corticosteroids e.g. methylprednisolone or prednisolone
  • Hepatitis A and B vaccines
  • Liver transplant in severe cases
462
Q

What are the complications of autoimmune hepatitis?

A
  • Cirrhosis
  • Hepatocellular carcinoma
  • Iatrogenic - osteoporosis, Cushing’s syndrome (long term steroid use)
463
Q

What is Wilson disease?

A

Wilson’s disease is an autosomal-recessive disease of copper accumulation and copper toxicity caused by mutations in the ATP7B gene, which is part of the biliary excretion of copper pathway.

464
Q

What are the risk factors for Wilson disease?

A

Family history: suggests inherited mutations in the ATP7B gene

465
Q

What are the key presentations of Wilson disease?

A
  • Hepatic issues
  • Neurological issues
  • Psychiatric issues
466
Q

What are the clinical manifestations of Wilson disease?

A
  • Behavioural and psychiatric issues: such as depression and delusions, often the first presentation. Also, loss of libido and bad memory.
  • Parkinsonism: half of patients present with a tremor
  • Asterixis
  • Chorea
  • Dysarthria
  • Dystonia
  • Dementia
  • Hepatosplenomegaly
  • Hepatitis and cirrhosis
  • Jaundice
  • Ascites
  • Asterixis and encephalopathy
  • Renal tubular acidosis
  • Fanconi syndrome
  • Kayser-Fleischer rings: copper ring in iris.
  • Haemolytic anaemia
  • Blue nails
  • Arthritis
  • Grey skin
  • Hypermobile joints
467
Q

What are the investigations for Wilson disease?

A
  • Copper studies - serum ceruloplasmin
  • LFTs - increase in AST and ALT
  • Genetic testing: ATP7B mutation
  • Liver biopsy - GOLD STANDARD
  • MRI of the brain
468
Q

What is the management for Wilson’s disease?

A
  • Copper chelation e.g. Penicillamine or Trientene
  • Lifestyle advice
  • Liver transplantation
469
Q

What are the complications of Wilson disease?

A
  • Liver failure
  • Renal stones
  • Renal failure
  • Side effects of medication
470
Q

What is hemochromatosis?

A
  • Haemochromatosis is a multisystem disorder of dysregulated dietary iron absorption and increased iron release from macrophages.
  • Type 1 (HFE-related) hereditary haemochromatosis most commonly occurs in individuals of northern European descent (1 in 10 people carry a mutation).
471
Q

What are the risk factors of hemochromatosis?

A
  • Family history
  • Alcoholism
  • History of chronic transfusion: only relevant inacquiredhaemochromatosis, for example in patients with thalassaemia
472
Q

What are the signs of hemochromatosis?

A
  • Skin hyperpigmentation (bronze skin)
  • Arthritic joints
  • Testicular atrophy
  • Features of chronic liver disease e.g. hepatomegaly
  • Features of congestive cardiac failure e.g. peripheral oedema due to dilated cardiomyopathy
  • Signs of osteoporosis
473
Q

What are the symptoms of hemochromatosis?

A
  • Patients are usually asymptomatic, especially in early stages.
  • Early symptoms: lethargy, arthralgia (often in hands) and erectile dysfunction
  • Loss of libido: hypogonadism due to cirrhosis and pituitary dysfunction
  • Polyuria and polydipsia due to T1DM
474
Q

What are the investigations of hemochromatosis?

A
  • Serum ferratin levels - FIRST LINE
  • Serum transferrin saturation
  • LFTs
  • Genetic testing
  • Liver biopsy
  • CT or MRI
475
Q

What is the management for hemochromatosis?

A
  • Venesection - FIRST LINE
  • Iron chelation - SECOND LINE
  • Avoid alcohol
  • Low iron diet
  • Genetic counselling
476
Q

What are the complications of hemochromatosis?

A
  • Cirrhosis
  • Hepatocellular carcinoma
  • Diabetes Mellitus
  • Hypogonadism
  • Dilated cardiomyopathy
  • Congestive HF
  • Pseudogout
  • Osteoporosis
  • Skin hyperpigmentation
477
Q

What is alpha-1-antitrypsin deficiency?

A
  • Alpha-1 antitrypsin deficiency is a rare autosomal recessive disorder that causes liver and pulmonary disease.
  • A1AT is a type of serine protease inhibitor. Deficiency is called serinopathy.
478
Q

What are the risk factors for alpha-1-antitrypsin deficiency?

A

Family history: there may be a family history of early-onset COPD and/or AAT deficiency

479
Q

What are the key presentations of alpha-1-antitrypsin deficiency?

A

Early onset of COPD

480
Q

What are the symptoms of alpha-1-antitrypsin deficiency?

A
  • Jaundice
  • Hepatomegaly
  • Ascites
  • Inability to make coagulation factors
  • Build-up of toxins leading to hepatic encephalopathy
  • Portal hypertension and consequent complications
  • Dyspnoea and productive cough
  • Prolonged expiratory phase and wheeze with pursed-lip breathing
  • Weight loss
  • Barrel chested due to hyperexpanded lungs
481
Q

What are the investigations for alpha-1-antitrypsin deficiency?

A
  • Plasma AAT level - FIRST LINE
  • High resolution chest CT
  • Lung function test
  • Liver biopsy
  • Genetic tests:allows identification of the mutated allele and the patient’s genotype, e.g. PiZZ
482
Q

What are the differential diagnoses for alpha-1-antitrypsin deficiency?

A
  • Asthma
  • COPD
  • Bronchiectasis
  • Viral hepatitis
  • Alcoholic liver disease
483
Q

What is the management for alpha-1-antitrypsin deficiency?

A
  • Smoking cessation and pollution avoidance - FIRST LINE
  • Alcohol avoidance - FIRST LINE
  • COPD treatment
  • A1AT augmentation
  • Hepatitis A and B vaccinations
  • Organ transplant - END STAGE management
484
Q

What are the complications of alpha-1-antitrypsin deficiency?

A
  • Respiratory failure
  • Cirrhosis and hepatocellular carcinoma
  • Cholestasis
485
Q

What is hepatic encephalopathy?

A
  • Sometimes called portosystemic encephalopathy.
  • Hepatic encephalopathy is a neuropsychiatric syndrome caused by acute or chronic advanced hepatic insufficiency.
  • Characterised by confusion and drowsiness as well as other more worse symptoms.
486
Q

What are the risk factors for hepatic encephalopathy?

A
  • Cirrhosis
  • Acute hepatic failure
  • Portocaval shunt
487
Q

What are the clinical manifestations of hepatic encephalopathy?

A
  • Symptoms vary in severity from mildly altered mental state to coma but is often reversible with treatment.
  • Mood disturbances - euphoria or depression.
  • Sleep disturbances - insomnia or hypersomnia.
  • Motor disturbances - muscle rigidity, bradykinesia, hypokinesia, slow monotonous speech, tremor.
  • Advanced neurological deficits - hyper-reflexia, nystagmus, clonus.
  • Acutely it presents with reduced consciousness and confusion, but chronically is more changes to personality, memory and mood.
488
Q

What are the precipitating factors for hepatic encephalopathy?

A
  • Constipation
  • Electrolyte disturbance
  • Infection
  • GI bleed
  • High protein diet
  • Mediations such as sedatives
489
Q

What is the grading for hepatic encephalopathy?

A
  • I - Altered mood/behaviour, sleep disturbance, dyspraxia
  • II - Increasing drowsiness, confusion, slurred speech +/- liver
    flap, inappropriate behaviour/personality change
  • III - Incoherent, restless, liver flap, stupor
  • IV - Coma
490
Q

What is the management for hepatic encephalopathy?

A
  • Laxatives e.g. lactulose
    • Aim for 2-3 soft motions daily
  • Antibiotics e.g. Rifaximin
    • Reduce number of intestinal bacteria making ammonia
  • Nutritional support → NG tube maybe
491
Q

What are the 3 benign liver tumours?

A
  • Cavernous haemangioma
  • Nodal Nodular Hyperplasia
  • Hepatic adenoma
492
Q

What is hepatocellular carcinoma?

A

Primary hepatocyte neoplasia. Accounts for 90% of primary liver cancers.

493
Q

What are the risk factors for hepatocellular carcinoma?

A
  • Gender → Male > Female
  • HBV
  • HCV
  • Cirrhosis
494
Q

What are the signs of hepatocellular carcinoma?

A
  • Palpation - enlarged, irregular, tender liver may be felt
  • Signs of chronic liver disease
  • Signs of decompensation - jaundice (will appear late), ascites
  • Listen for bruit - murmur over the liver
495
Q

What are the symptoms of hepatocellular carcinoma?

A
  • Fever
  • Malaise
  • Fatigue
  • Loss of appetite
  • Weight loss
  • RUQ pain
  • Jaundice
  • Ascites
  • Haemobilia - bleeding into biliary tree
496
Q

What are the investigations of hepatocellular carcinoma?

A
  • Alpha-fetoprotein - tumour marker for HCC
  • Live ultrasound
  • CT and MRI scans
  • Biopsy
  • LFTs
497
Q

What is the management for hepatocellular carcinoma?

A
  • Resect solidary tumours - FIRST LINE
  • Liver transplant
  • Percutaneous ablation
  • Kinase inhibitors in advanced disease
  • HCC is considered resistant to chemotherapy and radiotherapy
498
Q

What is paracetamol overdose?

A
  • A toxic overdose is defined as ingestion of paracetamol >75mg/kg.
  • 12g/ 24 tablets or 150mg/kg in adults may be fatal
499
Q

What are the signs of paracetamol overdose?

A
  • Jaundice
  • Encephalopathy - reduced GCS - consciousness
  • Tachycardia/ hypotension
  • Evidence of self-harm
500
Q

What are the symptoms of paracetamol overdose?

A
  • Abdominal pain
  • Right upper quadrant pain
  • Nausea or vomiting
  • Confusion or coma
501
Q

What are the investigations for paracetamol overdose?

A
  • Serum paracetamol
  • LFTs
  • Clotting screen
  • U&Es
  • Arterial blood gas
502
Q

What is the management for paracetamol overdose?

A
  • Supportive care - FIRST LINE
  • Active charcoal
  • IV N-acetylcysteine (NAC)
  • Anti-emetics
  • Liver transplantation
  • Psychiatric output
503
Q

What are the complications of paracetamol overdose?

A
  • Acute liver failure
  • Acute kidney injury
  • Anaphylactoid reaction
504
Q

What is hepatitis A?

A

The Hepatitis A virus is a non-enveloped single-stranded RNA virus.

505
Q

What is hepatitis B?

A

Hepatitis B is caused by the hepatitis B virus (HBV). It is an enveloped DNA virus that belongs to the Hepadnaviridae family and can cause acute or chronic hepatitis:

506
Q

What is acute hepatitis B?

A

Acute: can occur at any age. Majority of patients have a subclinical or anicteric (no evidence of jaundice) illness. In adults and older children, usually a self-limiting illness. In young children, more likely to develop chronic infection.

507
Q

What is chronic hepatitis B?

A

Chronic: failure to clear the virus after acute infection. Defined as persistence of hepatitis B surface antigen (HBsAg) for >6 months. HBsAg is a viral protein that can be measured in the blood. Chronic hepatitis B (CHB) can lead to cirrhosis and hepatocellular carcinoma (HCC).

508
Q

What is hepatitis C?

A
  • Hepatitis C virus (HCV) is an infectious, hepatotropic virus belonging to the Flavivirus family. Infection may be acute and chronic.
  • Spread by blood transfusions, IV drug abuse, and sexual contact. Vertical transmission is rare.
509
Q

What is hepatitis D?

A
  • Hepatitis D virus (HDV) is a unique RNA virus that can only establish infection in the human liver with the help of Hepatitis Bvirus (HBV). HDV has an outer envelope that contains the HBV surface antigen (HBsAg). Therefore, it can only establish infection in HBsAg-positive patients.
510
Q

What is hepatitis E?

A
  • Hepatitis E is a small, non-enveloped RNA virus that can lead to acute and chronic hepatitis.
  • Now recognised as themost common cause of acute viral hepatitisin many countries.
  • HEV is spread via thefaeco-oral route.
511
Q

What are the common signs of hepatitis?

A
  • Fever
  • Malaise
  • Nausea
  • Hepatomegaly
  • RUQ pain
512
Q

What are the common symptoms of hepatitis?

A
  • Raised ALT and AST on LFTs
  • Atypical lymphocytosis
  • Jaundice
  • Increased urobilinogen in urine
513
Q

Give a summary for viral hepatitis?

A

A is Acquired by mouth from Anus, is Always cleared Acutely and only ever Appears once
E is Even in England and can be Eaten (found in pigs), if not always beaten
B is Blood-Borne and if not Beaten can be Bad
B and D is DastarDly
C is usually Chronic but Can be Cured - at a Cost

514
Q

What is acute liver failure?

A
  • Acute liver failure is a syndrome of acute liver dysfunction without underlying chronic liver disease.
  • ALF is characterised by coagulopathy (derangement in clotting) of hepatic origin and altered levels of consciousness due to hepatic encephalopathy (HE).
515
Q

What can acute liver failure be divided into?

A
  • Hyperacute: HE within 7 days of noticing jaundice. Best prognosis as much better chance of survival and spontaneous recovery.
  • Acute: HE within 8-28 days of noticing jaundice
  • Subacute: HE within 5-12 weeks of noticing jaundice (ALF may be defined up to 28 weeks). Worst prognosis as usually associated with shrunken liver and limited chance of recovery.
516
Q

What are the key presentations of acute liver failure?

A

Jaundice and hepatic encephalopathy

517
Q

What are the clinical manifestations of acute liver failure?

A
  • Hepatic encephalopathy
  • Raised intracranial pressure
  • Fetor hepaticus
  • Jaundice
  • RUQ pain
  • Hepatomegaly
  • Ascites
  • Bruising
  • GI bleeding
  • Hypotension
  • Signs of chronic liver disease
518
Q

What is the West Haven criteria?

A

The severity of HE can be graded using theWest Haven criteria:

  • Grade I: change in behaviour with minimal change in level of consciousness. May have mild asterixis or tremor.
  • Grade II: gross disorientation, drowsiness, asterixis and inappropriate behaviour
  • Grade III: marked confusion, incoherent speech, sleeping most of the time but rousable to verbal stimuli. Asterixis less noticeable, elements of rigidity.
  • Grade IV: coma that is unresponsive to verbal or painful stimuli. Evidence of decorticate or decerebrate posturing.
519
Q

What bloods should be done to investigate acute liver failure

A
  • FBC
  • U&Es
  • LFTs
  • Blood glucose
  • Arterial ammonia
  • ABG
  • Coagulation
  • Lactate dehydrogenase
  • Lipase/amylase
  • Blood cultures
520
Q

What are the non-invasive liver screen investigations in acute liver failure?

A
  • Paracetamol serum level
  • Alpha-1 antitrypsin levels
  • Caeruloplasmin levels
  • Ferritin levels
  • Autoimmune markers: ANA, autoantibodies, immunoglobulins, ANCA
  • Toxicology screen: serum/urine
  • Ascitic tap
  • Viral screen: blood and urine culture
521
Q

What are the imaging investigations for acute liver failure?

A
  • Ultrasound
  • Doppler ultrasound
  • Chest X-ray
  • CT abdomen and pelvis
522
Q

What is the management for acute liver failure?

A
  • Treat underlying cause
  • Intensive care management
    • Fluid resuscitation
    • Intubation and ventilation
    • NG feeding
  • Metabolic → blood glucose levels, acisosis, electrolyte balance
  • Renal → AKI common, renal replacement therapy or haemodialysis
  • Coagulopathy → blood products (FFP)
  • Liver transplant
523
Q

What are the complications of acute liver failure?

A
  • Acute kidney injury/ hepatorenal syndrome
  • Metabolic disturbance
  • Hypoglycaemia
  • Haemorrhage (e.g. GI Bleeding)
  • Cerebral dysfunction (e.g. seizures, irreversible brain injury).
  • Patients are at risk of high output cardiac failure due to low vascular resistance from the widespread inflammatory response.
  • Sepsis

Phase 2a Sheffield Medicine (10 decks)

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