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Year 5 Core Conditions > Gastrointestinal - Level 3 > Flashcards

Gastrointestinal - Level 3 Flashcards

1
Q

Definition of achalasia?

A
  • Oesophageal motor disorder characterised by loss of oesophageal peristalsis and failure of lower oesophageal sphincter relaxation in response to swallowing
  • Results from denervation of oesophageal myenteric plexus
  • Causes functional stenosis or stricture
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2
Q

Definition of pseudoachalasia?

A

o Achalasia-pattern dilatation of oesophagus due to narrowing of distal oesophagus from cause other than primary denervation
o E.g. Malignancy

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3
Q

Epidemiology of achalasia?

A
  • Incidence peaks at 60
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4
Q

Triggers of achalasia?

A

o Infection – Chagas, herpes, measles
o Autoimmunity – HLA Class 2
Genetic

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5
Q

Symptoms of achalasia?

A 
-	Dysphagia
o	Solids more than soft foods and liquids
o	Posturing to aid swallowing
-	Food bolus impaction
-	Regurgitation
-	Chest pain
o	After eating, retrosternal
-	Heartburn
-	Loss of weight – think malignancy
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6
Q

Investigations in suspected achalasia?

A
  • Endoscopy
  • Barium Swallow
  • Manometry of Oesophagus
  • CXR
  • Lower oesophageal pH monitoring
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7
Q

Endoscopy findings of achalasia?

A

o Essential first-line investigation to exclude malignancy

o Biopsies from cardia performed to exclude pseudoachalasia

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8
Q

Barium swallow findings of achalasia?

A

o Oesophagus dilated, contrast material passes slowly into stomach as sphincter opens intermittently
o Birds beak appearance of distal oesophagus

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9
Q

Manometry findings of achalasia?

A

o Gold standard – high resting pressure in cardiac sphincter, incomplete relaxation on swallowing and absent peristalsis

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10
Q

CXR findings of achalasia?

A

o Classical - vastly dilated oesophagus behind heart

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11
Q

Management of achalasia - medical - when and what?

A

Medical (waiting for definitive treatment OR if unable to tolerate other forms of treatment)
o Calcium channel blockers (Nifedipine OR Verapamil)
o Nitrates

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12
Q

Management of achalasia - surgical?

A

Laparoscopic Heller myotomy (cardio-myotomy)
 Muscle fibres of lower oesophagus divided in a longitudinal direction above stomach

Pneumatic Dilatation
 If unfit for myotomy, balloon inserted and inflated to rupture muscle of oesophagus
 Risk of perforation which requires emergency surgery
 Can have multiple times with increasing dilatation

Endoscopic injection of botulinum toxin
 If cannot tolerate any surgery

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13
Q

Complications of achalasia?

A
  • Nocturnal inhalation of material
  • Aspiration pneumonia
  • Perforation
  • GORD
  • Oesophageal cancer
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14
Q

Definition of gastritis?

A
  • Gastric mucosal inflammation
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15
Q

Causes of gastritis?

A 
o	Alcohol, NSAIDs
o	H.pylori
o	GORD, Hiatus Hernia, Atrophic Gastritis
o	Crohn’s, sarcoidosis
o	CMV
o	Zollinger-Ellison
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16
Q

Symptoms and signs of gastritis?

A
  • Epigastric pain
  • Nausea & Vomiting
  • Loss of Appetite
  • Haematemesis
  • Bloating
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17
Q

Investigations of gastritis - when to offer upper GI endoscopy?

A
  • Offer urgent access upper GI endoscopy if:
    o Dysphagia OR
    o >55 with weight loss and:
     Upper abdominal pain, reflux or dyspepsia
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18
Q

Investigations of gastritis if no alarm symptoms?

A 
o	H.pylori urea breath test
o	FBC (anaemia)
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19
Q

Management of gastritis - prevention?

A 
o	Eat smaller and frequent meals
o	Avoid spicy, acidic, fried or fatty foods
o	No alcohol
o	Stop smoking
o	Give PPI gastroprotection with NSAIDs
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20
Q

Management of gastritis - general measures?

A

 Reduce alcohol and NSAIDs if possible
 Lifestyle measures
 OTC antacids

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21
Q

Management of gastritis - if no improvement?

A

H.pylori Urea breath test or stool antigen test

If negative:
o PPIs/H2 blockers for 4 weeks
o Consider non-urgent endoscopy if no improvement

If positive:
o Eradicate H.pylori as needed
 PPI + Amoxicillin + Clarithromycin OR Metronidazole
o H.pylori breath test to test cure
o Consider non-urgent endoscopy if not improving

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22
Q

Complications of gastritis?

A
  • Peptic ulcer disease
  • Gastric Carcinoma
  • Gastric Lymphoma
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23
Q

Definition of chronic pancreatitis?

A
  • Chronic, irreversible, inflammation and fibrosis of pancreas
  • Inappropriate activation of enzymes leads to protein plugs in lumen and calcification
  • Ductal hypertension and damage leads to impaired function
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24
Q

Risk factors of chronic pancreatitis?

A

o Smoking, Sjogren’s, IBD
o Drugs – thiazide diuretics, azathioprine
o Gallstones

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25
Q

Causes of chronic pancreatitis?

A 
o	Alcohol (70-80%)
o	Familial
o	CF
o	Haemochromatosis
o	Pancreatic duct obstruction (stones/tumour)
o	Hyperparathyroidism
o	Pancreas divisum
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26
Q

Symptoms of chronic pancreatitis?

A 
o	Epigastric pain
	Deep, severe, dull pain into back
	Worsened with eating
	Relieved by sitting up or hot water bottles
o	Nausea and vomiting
o	Bloating
o	Steatorrhoea
o	Anorexia/Weight loss
o	Diabetes
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27
Q

Signs of chronic pancreatitis?

A

o Chronic liver disease
o Epigastric tenderness
o Jaundice
Distention

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28
Q

When to refer in primary care of chronic pancreatitis?

A
  • In primary care, if suspected – refer to gastroenterology or regional pancreatic specialist centre
    o Urgent if acute pancreatitis
    o Routine if chronic
     Perform LFTs, Abdominal USS
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29
Q

Tests performed in chronic pancreatitis in secondary care

A 
o	Bloods – LFTs, glucose (raised)
o	Abdminal USS
o	CT
	Pancreatic calcifications confirm diagnosis
o	MRCP + ERCP
o	AXR
	Speckled calcification
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30
Q

Referral of suspected chronic pancreatitis from primary care?

A

Urgent if acute pancreatitis or complications of chronic (malabsorption, DM, chronic pain, opioid dependency, low-trauma fracture)

Routine – all other suspected people

Investigations if no urgent admission/referral need
 Bloods
• LFTs
 Abdominal USS

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31
Q

Management of chronic pancreatitis - general advice?

A

Abstain from alcohol and smoking

Analgesia – NSAIDs, paracetamol, weak opioids
 If uncontrolled – ERCP to remove stones, adjuvant drugs or coeliac plexus block

Dietician referral
 Low fat diet, avoid legumes and high-fibre foods
 Pancreatin enzymes – contain lipase, amylase and protease (Creon)
 Fat soluble vitamins

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32
Q

Management of chronic pancreatitis -Surgery?

A

o Pancreatic duct obstructed – surgery open or minimally invasive
o Pseudocysts drained using EUS-guided drainage
o Pancreatojejunostomy

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33
Q

Management of chronic pancreatitis -follow up?

A

o Annual – HbA1c, DEXA scan, test for malnutrition or vitamin deficiencies

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34
Q

Complications of chronic pancreatitis?

A
  • Malabsorption
  • Pseudocyst
  • Diabetes
  • Biliary obstruction
  • Local arterial aneurysm
  • Pancreatic carcinoma
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35
Q

Definition of chronic hepatitis?

A

o Inflammation of liver for >6 months

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36
Q

Causes of chronic hepatitis?

A

o Viral – HepB, HepC, CMV, EBV
o Metabolic – NAFLD, haemochromatosis, Wilson’s disease, alpha-1-antitrypsin disease
o Toxins – alcoholic liver disease, amiodarone, isoniazid, methyldopa, methotrexate, nitrofurantoin
o Autoimmune – hepatitis, PBC, PSC
o Sarcoidosis

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37
Q

Symptoms of chronic hepatitis?

A

o Fatigue, anorexia, arthralgia, myalgia, weight loss
o RUQ pain
o Abdominal pain
o Ankle swelling
o Pruritus
o Gynaecomastia, testicular atrophy, loss of libido, amenorrhoea
o Confusion and drowsiness

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38
Q

Signs of chronic hepatitis?

A 
o	Spider Naevi
o	Palmar erythema
o	Jaundice
o	Clubbing
o	Dupuytren’s contracture
o	Xanthomas
o	Splenomegaly
o	Hirsutism
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39
Q

Bloods to performed in chronic hepatitis?

A 
o	FBC (anaemia)
o	Clotting
o	U&E
o	LFTs
o	Albumin
o	Immunoglobulins
o	Autoantibodies
o	Hepatitis B and C serology
o	Iron
o	AFP
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40
Q

Imaging to performed in chronic hepatitis?

A

o US

o CT/MRI

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41
Q

Diagnostic tests to performed in chronic hepatitis?

A
  • Transient elastography

- Liver biopsy

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42
Q

Definition of subphrenic abscess?

A
  • Localised collection of pus, underneath left/right hemidiaphragm
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43
Q

Causes of subphrenic abscess?

A

o Upper GI – malignancy, trauma, peptic ulcer perforation, endoscopy
o Lower GI – ischaemic bowel, diverticulitis, obstruction, hernia, IBD, appendicitis, trauma
o Biliary Tract/Pancreas – cholecystitis, malignancy, pancreatitis, endocarditis
o GU – PID, malignancy
o Bowel surgery

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44
Q

Epidemiology of subphrenic abscess?

A
  • Commonest cause of intra-abdominal abscess
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45
Q

Symptoms of subphrenic abscess?

A

o Chest/shoulder tip pain
o Abdominal pain
o Swinging fever
o Diarrhoea, nausea, malaise

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46
Q

Signs of subphrenic abscess?

A

o Swinging/Spikey temperature
o Systemically unwell patient
o Often few physical signs – subcostal abdominal tenderness
o Leucocytosis

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47
Q

Investigations of subphrenic abscess?

A 
-	Bloods
o	FBC (High WCC)
o	Cultures
-	Urgent US – localises collection of pus
-	Ct detects abscess and estimate volume
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48
Q

Management of subphrenic abscess?

A
  • IV Antibiotics – broad spectrum
  • US/CT-guided drainage
  • May need percutaneous drainage, laparoscopy or open surgery
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49
Q

Definition of liver abscess?

A
  • Caused by organisms invading liver parenchyma
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50
Q

Epidemiology of liver abscess?

A
  • UK – pyogenic most common

- Worldwide – amoebic most common

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51
Q

Aetiology of pyogenic liver abscess?

A

o Right lobe predominantly, can be single or multiple
o Secondary to abdominal infections (cholecystitis, cholangitis, stones, malignancy, diverticulitis, IBD, appendicitis, perforate peptic ulcer, iatrogenic, bacterial endocarditis)
o Organisms – Klebsiella pneumoniae, E.coli, Bacteroides, enterococci, staph/strep (endocarditis), Candida (immunocompromised)

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52
Q

Aetiology of amoebic liver abscess?

A

o Entamoeba histolytica – occurs in tropical/subtropical areas due to poor sanitation and overcrowding
o Faecal-oral transmission
o Invade intestinal mucosa and access portal venous system
o Symptoms – colitis, dysentery and liver abscess
o Right lobe 80%
o Endemic in South America, Indian subcontinent and Africa

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53
Q

Symptoms of liver abscess?

A 
o	RUQ pain
	Referred shoulder tip pain
o	Fever (swinging)
o	Night sweats
o	Nausea and vomiting
o	Anorexia and weight loss
o	Cough
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54
Q

Signs of liver abscess?

A

o Swinging fever
o Tender RUQ
o Hepatomegaly, palpable mass
o Jaundice

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55
Q

Investigations of liver abscess?

A 
Bloods
o	FBC (High WCC, normo, normo anaemia)
o	Raised ESR
o	LFTs (raised ALP, AST/ALT, bilirubin, low albumin)
o	Blood Cultures

Stool sample – cysts of E.histiolytica

USS
o Aspiration fluid sent for culture and sensitivity

CT definitive

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56
Q

Management of pyogenic liver abscess?

A

Fluids/PRN analgesics

Antibiotics
 Cephalosporin + metronidazole 1st line

US/CT-guided aspiration

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57
Q

Management of amoebic liver abscess?

A

Antibiotics
 Metronidazole 800mg TDS for 5 days (or tinidazole)
 Then, Diloxanide Furoate 500mg TDS for 10 days

US/CT-guided aspiration if large or no response to antibiotics after 72 hours

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58
Q

Description of hepatocellular carcinoma?

A

o Primary hepatocyte neoplasia

o Spread – lung, portal vein, periportal nodes, bone and brain

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59
Q

Description of benign liver tumours?

A

o Haemangiomas – commonest benign liver tumours, often incidental finding on US or CT and don’t require treatment
o Adenomas – common, caused: anabolic steroids, OCP, pregnancy. Treat if symptomatic or >5cm

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60
Q

Epidemiology of hepatocellular carcinoma?

A
  • 90% of all primary liver tumours
  • Common in China and Africa
  • Men more common
  • 90% of liver tumours are secondary metastatic tumours
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61
Q

Types of malignant primary liver tumours?

A 
	HCC
	Cholangiocarcinoma
	Angiosarcoma
	Hepatoblastoma
	Hepatic GIST
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62
Q

Types of benign primary liver tumours?

A 
	Cysts
	Haemangioma
	Adenoma
	Focal nodular hyperplasia
	Fibroma
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63
Q

Origins of secondary liver tumours in liver?

A

o Men – Stomach, lung, colon
o Women – breast, stomach, colon, uterus
o Either Sex – Pancreas, leukaemia, lymphoma, carcinoid tumours

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64
Q

Causes of hepatocellular carcinoma?

A 
o	Hepatitis B
o	Hepatitis C
o	Autoimmune hepatitis
o	Cirrhosis (alcohol, haemachromatosis, PBC)
o	NAFLD
o	Anabolic stenosis
o	Aflatoxins
o	DM and smoking
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65
Q

Symptoms of hepatocellular carcinoma?

A 
o	Fatigue
o	Anorexia
o	RUQ pain
o	Weight loss
o	Pruritus
o	Abdominal distention
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66
Q

Signs of hepatocellular carcinoma?

A 
o	Hepatomegaly
o	Jaundice (late)
o	Ascites
o	Bruit over liver
o	Spider Naevi
o	Anaemia
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67
Q

Investigations of hepatocellular carcinoma - referral?

A

o Urgent direct access US (within 2 weeks) if upper abdominal mass consistent with enlarged liver

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68
Q

Investigations of hepatocellular carcinoma - secondary care?

A

o USS
o AFP
o CT
o Fine-needle aspiration or biopsy

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69
Q

Investigations of hepatocellular carcinoma - other tests?

A

Blood
 FBC, clotting, LFT, hepatitis serology, AFP

Imaging
 US
 CT
 ERCP if cholangiocarcinoma

If suspected secondary:
 CXR, mammogram, endoscopy, colonoscopy, CT, marrow biopsy

70
Q

Investigations of hepatocellular carcinoma - Staging?

A

o Child-Pugh Stage

o Cancer of Liver Italian Program (CLIP) – prognostic marker

71
Q

Management of hepatocellular carcinoma - surgical?

A

o If platelets <50000 and planned invasive procedure, give Lusutrombopag
o Liver Resection (Child-Pugh A-B and ECOG 0-2)
 Radiofrequency Assisted Resection
 Laparoscopic Liver Resection
o Liver Transplant

72
Q

Management of hepatocellular carcinoma - non-resectable disease - Stage A/B?

A

o Stage A/B ineligible for surgery:
 Radiofrequency/Microwave ablation
 Chemo-embolisation into hepatic artery

73
Q

Management of hepatocellular carcinoma - non-resectable disease - Stage C/D?

A

o Chemotherapy (Stage C, D)
 Lenvatinib if:
• Child-Pugh grade A liver impairment and ECOG of 0/1
 Sorafenib & Regorafenib alternative

o Internal radiation therapy

74
Q

Surveillance in people at high risk of HCC?

A

o 6-monthly AFP and US

 If high risk for HCC – cirrhotic HBV carriers, non-cirrhotic HBV with high DNA, HCV-related or alcoholic cirrhosis

75
Q

Prognosis of HCC?

A
  • Median survival from diagnosis is 6 months
76
Q

Description, symptoms, Ix and management of hepatoblastoma?

A
  • Affects children <3
  • Associated with Beckwith-Wiedemann syndrome and FAP syndrome, fetal alcohol syndrome
  • Usually unifocal and affect right lobe
  • Symptoms – abdominal mass and distention, vomiting, anaemia and failure to thrive
  • Ix – AFP raised, normocytic normochromic anaemia, AXR, US and CT
  • Management – Surgical resection and chemotherapy
77
Q

Definition of cholangiocarcinoma?

A
  • Carcinoma arising from any part of biliary tree – from small intrahepatic bile ducts to ampulla of Vater
78
Q

Epidemiology of cholangiocarcinoma?

A
  • Most commonly, perihilar region near bifurcation of hepatic ducts (Klatskin’s tumour)
  • 90% are ductal adenocarcinomas
  • 10% SCC
  • Common in South Asia
79
Q

Causes of cholangiocarcinoma?

A 
o	Flukes (Clonorchis)
o	PSC
o	Biliary cysts
o	Caroli’s disease (congenital disorder of intrahepatic bile duct and polycystic kidney disease)
o	HBV
o	HCV
o	DM
o	N-nitroso toxins (chemicals in aircraft, rubber, wood-finishing)
80
Q

Symptoms of cholangiocarcinoma?

A 
o	Jaundice early - painless
o	RUQ pain
o	Fatigue
o	Anorexia
o	Weight loss
o	Pruritus
o	Abdominal distention
81
Q

Signs of cholangiocarcinoma?

A 
o	Hepatomegaly
o	Jaundice (early)
o	Ascites
o	Bruit over liver
o	Spider Naevi
o	Anaemia
82
Q

Investigations of cholangiocarcinoma - primary care referral?

A

o Urgent direct access US if upper abdominal mass consistent with enlarged gall bladder

83
Q

Investigations of cholangiocarcinoma - secondary care?

A

o CT
o Biopsy - Fine-needle aspiration or biliary brush cytology
o ERCP

84
Q

Investigations of cholangiocarcinoma - other tests?

A 
o	LFTs (elevated conjugated bilirubin, raised alkaline phosphatase, raised GGT, raised aminotransferase)
o	Clotting
o	Tumour markers – Ca19-9, CEA, AFP (not raised)
85
Q

Investigations of cholangiocarcinoma - staging?

A

o Bismuth-Corlette classification

86
Q

Management of cholangiocarcinoma - surgical?

A

o Liver Resection (30%)
 Major hepatectomy + extrahepatic bile duct excision + caudate lobe resection
o Stenting of bile duct
o Liver Transplant (rare)

87
Q

Management of cholangiocarcinoma - non-resectable?

A 
o	Chemotherapy and radiotherapy
	Photodynamic therapy
	Internal radiation
	Endoscopic bipolar radiofrequency
	Hepatic artery chemosaturation
88
Q

Types of hepatic failure?

A

Acute – suddenly in previous healthy liver

Acute-on-chronic – Decompensation of chronic liver disease

Fulminant – massive necrosis of liver cells
 Hyperacute = encephalopathy within 7 days of jaundice
 Acute = 8-28 days
 Subacute = within 5-26 weeks

89
Q

Causes of hepatic failure - infection?

A

 Viral hepatitis (B, C, CMV, EBV)
 Yellow Fever
 Leptospirosis

90
Q

Causes of hepatic failure - drugs, toxins & vascular?

A

Drugs
 Paracetamol
 Halothane
 Isoniazid

Toxins
 Amanita phalloides

Vascular
 Budd-Chiari syndrome

91
Q

Causes of hepatic failure - others?

A 
	Alcohol
	PBC
	Haemochromatosis
	Autoimmune hepatitis
	Alpha-1 antitrypsin deficiency
	Wilson’s disease
	HELLP syndrome
	Malignancy
92
Q

Signs of hepatic failure?

A 
o	Nausea, vomiting
o	Abdominal pain
o	Malaise
o	Jaundice
o	Hepatic Encephalopathy
o	Fetor Hepaticus (smells like pear drops)
o	Asterixis/Flap
o	Bleeding
o	Chronic liver disease suggest acute-on-chronic
93
Q

Stages of hepatic encephalopathy of hepatic failure?

A

 1 = altered mood/behaviour, sleep disturbance, dyspraxia
 2= drowsiness, confusion, slurred speech +/- flap
 3= incoherent, restless, liver flap
 4 = coma

94
Q

Bloods to perform of hepatic failure?

A 
o	FBC (infection, GI bleed, thrombocytopenia)
o	U&amp;E
o	LFT (raised AST/ALT, bilirubin)
o	Clotting (raised PT/INR)
o	Glucose (low)
o	Paracetamol levels
o	Hepatitis, CMV and EBV serology
o	Ferritin
o	Alpha-1 antitrypsin
o	Caeruloplasmin autoantibodies
95
Q

Microbiology Ix of hepatic failure?

A

o Blood culture
o Urine culture
o Ascitic tap (M, C & S)

96
Q

Imaging of hepatic failure?

A

o CXR

o Abdominal US and Doppler flow

97
Q

Initial management of hepatic failure?

A

o Nurse with bed 20o head-up tilt in ITU
o NG tube
o Insert urine and central venous catheter
o IV glucose
o If malnourished – thiamine and folate
o Seizures – lorazepam
o Renal failure – haemodialysis or haemofiltration

98
Q

Monitoring in initial management of hepatic failure?

A

o Monitor
 Temp, RR, HR, BP, pupils, urine output hourly
 Blood glucose 4-hourly
 Daily weight

o Daily
 FBC, U&E, LFT, INR

99
Q

Drugs to avoid in hepatic failure?

A

 Opiates, hypoglycaemics, paracetamol, methotrexate, azathioprine, isoniazid, salicylates, tetracycline, mitomycin

100
Q

When to liase with transplant team of hepatic failure?

A

• Paracetamol-Induced
o Arterial pH <7.3 24h after ingestion OR
o PT>100s, Creatinine >300umol/L, Grade ¾ encephalopathy

•	Non paracetamol liver failure
o	PT >100s OR
o	3 of the following:
	Drug-induced
	Age <10 or >40
	>1 week from jaundice to encephalopathy
	PT>50s
	Bilirubin >300umol/L
101
Q

Managing complication of hepatic failure?

A

o Cerebral oedema – ITU, mannitol IV, hyperventilate
o Ascites – restrict fluid, diuretics, low salt diet, daily weight
o Bleeding – Vitamin K IV
o Prophylactic Abx – Ceftriaxone IV
o Encephalopathy – Lactulose and regular enemas

102
Q

Definition of epigastric hernia?

A
  • Pass through linea alba above umbilicus
103
Q

Epidemiology of epigastric hernia?

A
  • Prevalence up to 10%, mostly middle-aged men
104
Q

Aetiology of epigastric hernia?

A

o Typically secondary to raised chronic intra-abdominal pressure (obesity, pregnancy, ascites, straining, coughing)

105
Q

Symptoms of epigastric hernia?

A
  • Typical asymptomatic
  • Midline mass – disappears when lying on the back
  • Epigastric pain
  • N &V, often after meals
106
Q

Investigations of epigastric hernia?

A

Clinical Examination

US and CT to confirm diagnosis if needed
o	Must be differentiated from diastasis recti (widening of linea alba without a defect in fascia)
	Usually resolves by age of 10
	US can help confirm not a hernia
	Treatments – strengthen core training
107
Q

Management of epigastric hernia?

A
  • Surgical repair essential – risk of strangulation or incarceration
    o Mesh and suture repair possible
108
Q

Description of familial adenomatous polyposis?

A

o Autosomal dominant condition with >100 tubular adenomas which carpet colon
o Germline mutation of APC gene (5q)
o Offspring 50% risk of being carrier and gene penetrance ~100% for colorectal cancer by 50 years old
o Associated with papillary thyroid cancer, carcinoid tumours of ileum, medullloblastomas and glioblastomas

109
Q

Description of Peutz-Jeghers syndrome?

A

o Autosomal dominant disorder characterised by mucosal pigmentation of lips and gums with multiple intestinal hamartomatous polyps
o Due to germline mutation in STK11
o Increased risk of GI, pancreatic, breast, thyroid, lung, uterine, testicular and ovarian tumours

110
Q

Description of Hereditary Non-Polyposis Colorectal cancer (Lynch syndrome)?

A

o Autosomal dominant aggregation of colorectal cancer (60%) +/- endometrium (40%)/ovarian/stomach/renal pelvis/small bowel/pancreas
o Mutation in DNA mismatch repair genes (1 of 5)

111
Q

Description of juvenile polyposis?

A

o Multiple juvenile polyps in GI tract – benign hamartoma

112
Q

Symptoms of Familial adenomatous polyposis?

A 
	Adenomas develop during 20s
	Colorectal cancer by 50
	Rectal bleeding
	Diarrhoea
	Abdominal pain
	Mucous discharge
	Obstruction – constipation, vomiting
113
Q

Signs of Familial adenomatous polyposis?

A 
	Rectal polyps or masses
	Congenital hypertrophy of retinal pigment epithelium
	Supernumery teeth
	Epidermoid cysts
	Thyroid masses
114
Q

Symptoms of Peutz-Jeghers syndrome?

A 
o	FHx
o	Deeply pigmented lesions on lips and buccal mucosa
o	Bouts of abdominal pain
o	GI bleeding
o	Iron-deficiency anaemia
115
Q

Investigations in colonic polyposis?

A
  • Bloods – FBCs, LFTs, TFTs
  • Faecal occult blood
  • Colonoscopy with biopsies diagnostic
  • Upper GI endoscopy
  • Genetic testing – APC gene
  • CT scan
116
Q

Management of FAP - genetic analysis?

A

 If 2 1st-degree relative aged <70, one 1st degree relative aged <45, 3 close relatives <60 on average, FAP, HNPCC Endoscopic surveillance

117
Q

Management of FAP - surgical?

A

 Proctocolectomy and ileostomy – abolishes risk of large bowel cancer but stoma required

 Colectomy and ileorectal anastomosis – does not abolish risk of large bowel cancer and need lifelong 6-monthly surveillance

118
Q

Management of FAP - surveillance?

A

 Upper GI endoscopy three-yearly

119
Q

Management of Peutz-Jeghers syndrome - genetic analysis?

A

 If 2 1st-degree relative aged <70, one 1st degree relative aged <45, 3 close relatives <60 on average, FAP, HNPCC

120
Q

Management of Peutz-Jeghers syndrome - Surgery?

A

 Endoscopic polypectomy

 Polypectomy

121
Q

Management of Peutz-Jeghers syndrome - surveillance?

A

 2-yearly from 25 years old – colonoscopy & upper GI endoscopy

122
Q

Management of HNPCC - genetic analysis?

A

 If 2 1st-degree relative aged <70, one 1st degree relative aged <45, 3 close relatives <60 on average, FAP, HNPCC

123
Q

Management of HNPCC -surveillance?

A

 Annual or biannual colonoscopies from 25 years old

 Upper GI endoscopy every 2 years from 50

124
Q

Management of Juvenile Polyposis - surgery?

A

 Colectomy

125
Q

Management of Juvenile polyposis - surveillance?

A

 Colonoscopy every 18-24 months from 18

 Upper GI endoscopy every 1-2 years from 25

126
Q

Anatomy of anal canal?

A

o Anal canal extends from anorectal junction to anal margin
o Dentate line marks junction between squamous and mucosal epithelium in anal canal
o Anal margin is pigmented skin surrounding anal orifice

127
Q

Behaviour of anal cancer?

A

o Anal margin – well differentiated, more common in men and good prognosis
o Anal canal – poorly differentiated, more common in women and poor prognosis

128
Q

Spread of anal cancer?

A

o Above dentate line – spread to pelvic lymph nodes

o Below dentate line – spread to inguinal lymph nodes

129
Q

Risk factors of anal cancer?

A 
o	Syphilis
o	Anal warts in HPV (SCC)
o	Anal intercourse
o	High number of sexual partners
o	MSM
o	HIV
o	Smoking
130
Q

Types of anal cancer?

A

o Squamous Cell Carcinoma (80%)
o Adenocarcinoma
o Melanoma
o Lymphoma

131
Q

Symptoms of anal cancer?

A
  • Bleeding
  • Pain
  • Change in bowel habit
  • Pruritus ani
  • Mass in or around anus
  • Anal ulceration
132
Q

Referral for 2-week appointment of anal cancer?

A
  • Refer for 2-week wait appointment if:

o Unexplained anal mass or anal ulceration

133
Q

Assessment of anal cancer?

A

o DRE
o Palpation of inguinal lymph nodes
o Examination under anaesthetic (EUS) with biopsy
o CT/MRI/US/PET

134
Q

Management of AIN?

A

o Topical imiquimod, 5-FU

o Ablative electrocautery, laser

135
Q

Management of anal carcinoma?

A

o Small well-differentiated carcinoma – local excision
o All other – chemo-radiotherapy (5-FU and mitomycin)
 Surgery if fail to respond, causing GI obstruction
• Anorectal excision & colostomy

136
Q

Definition of perianal haematoma?

A
  • Blue or dark coloured swelling at anal verge

- Caused by rupture of small vein near anal margin then blood clots

137
Q

Risk factors of perianal haematoma?

A
  • Caused by straining, constipation, anal sex, heavy lifting, coughing
138
Q

Symptoms of perianal haematoma?

A
  • Acutely painful – usually after straining

- 2-4mm dark blueberry under skin at anal margin

139
Q

Referral of perianal haematoma?

A
  • Refer for non-urgent assessment and management if <24 hours old
140
Q

Management of perianal haematoma?

A

o Spontaneous resolve over a few days to week
o PRN analgesia
o If pain intolerable:
 Evacuated and drained under LA

141
Q

Definition of fistula-in-ano?

A
  • Abnormal connection between skin and anal canal/rectum
142
Q

Classification of fistula-in-ano?

A

o Intersphincteric
o Trans-sphincteric
o Suprasphincteric
o Extrasphincteric

143
Q

Pathology of fistula-in-ano? What is Goodsall’s rule?

A

o Blockage of deep intramuscular gland ducts predisposes to abscesses, which discharge to form fistulas
o Goodsall’s rule
 If anterior – track is straight line (radial)
 If posterior – internal opening is always at 6 o’clock position

144
Q

Causes of fistula-in-ano?

A 
o	Perianal sepsis
o	Abscesses (90%)
o	Crohn’s
o	TB
o	Diverticular disease
o	Rectal carcinoma
145
Q

Symptoms of fistula-in-ano?

A
  • Pain

- Leak blood or pus

146
Q

Investigations of fistula-in-ano?

A
  • Proctoscopy to visualise anal canal and opening of tract
  • MRI
  • Endoanal US scan
147
Q

Park’s classification of fistula-in-ano?

A 
Extrasphincteric
Suprasphincteric
Transsphincteric
Intersphincteric
Submucosal
148
Q

Management of fistula-in-ano - if no symptoms?

A
  • If no symptoms – conservative management (PRN analgesia)
149
Q

Management of fistula-in-ano - if symptoms?

A
  • Fistulotomy & Excision
    o High fistula (involving continence muscles of anus) – need seton suture tightening over time to maintain continence
    o Low fistulas laid open
150
Q

Definition of re-feeding syndrome?

A
  • Life-threatening complication of refeeding via any route after prolonged period of starvation
151
Q

Pathology of re-feeding syndrome?

A

o As body turns to fat and protein metabolism in starved state, there is drop in circulating insulin, depletes intracellular phosphate
o When refeeding begins, insulin rises and causes increased cellular uptake of phosphate, potassium, magnesium, glucose, thiamine
o Hypophosphataemic state (<0.50) develops within 4d and is responsible for features of refeeding syndrome

152
Q

Symptoms of re-feeding syndrome?

A
  • Rhabdomyolysis
  • Red and white cell dysfunction
  • Respiratory insufficiency
  • Arrhythmias
  • Cardiogenic shock
  • Seizures
  • Death
153
Q

Bloods to perform in re-feeding syndrome?

A 
o	Glucose
o	FBC
o	Albumin
o	U&amp;Es
o	Urine and stool culture
o	Iron, B12, folate, TFTs, coeliac, Ca, PO4, Zn, Vitamin, selenium
154
Q

Prevention of re-feeding syndrome?

A

Identify at risk patients and monitor daily for 1 week and then 3x a week (glucose, lipids, sodium, potassium, phosphate, calcium, magnesium, zinc)

Group includes – anorexia, chronic alcoholic, cancer, elderly, uncontrolled diabetes, marasmus, prolonged fasting

Start refeeding at 50% energy requirement and increase to meet full needs over a week
 5-10cal/kg depending on level of risk in patient

155
Q

Screening for malnutrition in people at risk of refeeding syndrome?

A

When
 All hospital inpatients and done weekly

How
 BMI, % unintentional weight loss, Mid upper arm diameter
 Malnutrition Universal Screening Test (MUST)

156
Q

Indications for nutritional support of re-feeding syndrome?

A

o BMI <18.5
o Unintentional weight loss >10% within last 3-6 months
o BMI <20 and unintentional weight loss >5% within last 3-6 months
o Consider in people who have eaten nothing >5 days

157
Q

Oral nutritional support - indications?

A

 People with safe swallow and malnorished or at risk of malnutrition

158
Q

Oral nutritional support - amount?

A

 25-35kcal/kg/day total energy
 0.8-1.5g protein/kg/day
 30-35ml fluid/kg
 If not eaten for last 5 days – 50% requirements for 2 days to reduce risk of refeeding syndrome

159
Q

Oral nutritional support - people at risk of refeeding syndrome?

A

 1 or more of:
• BMI<16, WL >15%, little/no intake in 10 days, low K, PO4, Mg

 2 or more:
• BMI<18.5, WL>10%, little/no intake 5 days, Hx of alcohol, drug, insulin, diuretic abuse

 Starting nutrition at 10kcal/kg/day and increase slowly for needs to be met within 7 days (5kcal/kg/day in extreme cases)

 Oral thiamine 200-300mg daily, Vitamin B co strong and multivitamin daily

 May need IV/oral K, PO4, Mg

160
Q

Oral nutritional support -monitoring?

A

 Measurements
• Daily nutrient intake and fluid balance charts
• Weight and BMI daily if concerned but up to weekly

 Bloods
• FBC, U&E, LFT, glucose, Mg, PO4, Ca, CRP, Iron, Folate, B12, Zn, Cu, zelenium

161
Q

Enteral feeding tube - indications?

A

 Malnourished or risk of and inadequate or unsafe oral intake & functional GI tract
 People with unsafe swallow diagnosed by SALT team

162
Q

Enteral feeding tube - amount?

A

 25-35kcal/kg/day total energy
 0.8-1.5g protein/kg/day
 30-35ml fluid/kg
 If not eaten for last 5 days – 50% requirements for 2 days to reduce risk of refeeding syndrome

163
Q

Enteral feeding tube - people at risk of re-feeding syndrome?

A

 1 or more of:
• BMI<16, WL >15%, little/no intake in 10 days, low K, PO4, Mg

 2 or more:
• BMI<18.5, WL>10%, little/no intake 5 days, Hx of alcohol, drug, insulin, diuretic abuse

 Starting nutrition at 10kcal/kg/day and increase slowly for needs to be met within 7 days (5kcal/kg/day in extreme cases)

 Oral thiamine 200-300mg daily, Vitamin B co strong and multivitamin daily

 May need IV/oral K, PO4, Mg

164
Q

Enteral feeding tube - route and method of delivery?

A

 NG tube unless upper GI dysfunction

 If upper GI dysfunction – duodenal or jejunal feeding

 Gastrostomy (PEG) – likely need long-term (>4 weeks) enteral feeding
• PEG tubes – used for enteral feeding 4 hours after insertion

165
Q

Enteral feeding tube - monitoring?

A

Measurements
• Daily nutrient intake and fluid balance charts
• Weight and BMI daily if concerned but up to weekly
• N&V, Diarrhoea, constipation

Bloods
• FBC, U&E, LFT, glucose, Mg, PO4, Ca, CRP, Iron, Folate, B12, Zn, Cu, zelenium

166
Q

Parenteral nutrition - indications?

A

 Inadequate or unsafe oral and/or enteral nutritional intake and non-functional, inaccessible or perforated GI tract

167
Q

Parenteral nutrition -Amount?

A

 25-35kcal/kg/day total energy

 0.8-1.5g protein/kg/day

 30-35ml fluid/kg

 If not eaten for last 5 days – 50% requirements for 2 days to reduce risk of refeeding syndrome

168
Q

Parenteral nutrition - people at risk of refeeding syndrome?

A

 1 or more of: BMI<16, WL >15%, little/no intake in 10 days, low K, PO4, Mg

 2 or more: BMI<18.5, WL>10%, little/no intake 5 days, Hx of alcohol, drug, insulin, diuretic abuse

 Starting nutrition at 10kcal/kg/day and increase slowly for needs to be met within 7 days

 Oral thiamine 200-300mg daily, Vitamin B co strong and multivitamin daily

 May need IV/oral K, PO4, Mg

169
Q

Parenteral nutrition - route and method of delivery?

A

 Peripherally inserted central catheter (PICC line) – if <14 days
 Tunnelling subclavian line if >30 days
 Continuous administration is preferred method

170
Q

Parenteral nutrition - monitoring?

A

Measurements
• Daily nutrient intake and fluid balance charts
• Weight and BMI daily if concerned but up to weekly
• N&V, Diarrhoea, constipation

Bloods
• FBC, U&E, LFT, glucose, Mg, PO4, Ca, CRP, Iron, Folate, B12, Zn, Cu, zelenium

Year 5 Core Conditions (55 decks)

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