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
Causes of chronic pancreatitis?
``` o Alcohol (70-80%) o Familial o CF o Haemochromatosis o Pancreatic duct obstruction (stones/tumour) o Hyperparathyroidism o Pancreas divisum ```
26
Symptoms of chronic pancreatitis?
``` 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 ```
27
Signs of chronic pancreatitis?
o Chronic liver disease o Epigastric tenderness o Jaundice Distention
28
When to refer in primary care of chronic pancreatitis?
- 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
29
Tests performed in chronic pancreatitis in secondary care
``` o Bloods – LFTs, glucose (raised) o Abdminal USS o CT  Pancreatic calcifications confirm diagnosis o MRCP + ERCP o AXR  Speckled calcification ```
30
Referral of suspected chronic pancreatitis from primary care?
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
31
Management of chronic pancreatitis - general advice?
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
32
Management of chronic pancreatitis -Surgery?
o Pancreatic duct obstructed – surgery open or minimally invasive o Pseudocysts drained using EUS-guided drainage o Pancreatojejunostomy
33
Management of chronic pancreatitis -follow up?
o Annual – HbA1c, DEXA scan, test for malnutrition or vitamin deficiencies
34
Complications of chronic pancreatitis?
- Malabsorption - Pseudocyst - Diabetes - Biliary obstruction - Local arterial aneurysm - Pancreatic carcinoma
35
Definition of chronic hepatitis?
o Inflammation of liver for >6 months
36
Causes of chronic hepatitis?
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
37
Symptoms of chronic hepatitis?
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
38
Signs of chronic hepatitis?
``` o Spider Naevi o Palmar erythema o Jaundice o Clubbing o Dupuytren’s contracture o Xanthomas o Splenomegaly o Hirsutism ```
39
Bloods to performed in chronic hepatitis?
``` 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 ```
40
Imaging to performed in chronic hepatitis?
o US | o CT/MRI
41
Diagnostic tests to performed in chronic hepatitis?
- Transient elastography | - Liver biopsy
42
Definition of subphrenic abscess?
- Localised collection of pus, underneath left/right hemidiaphragm
43
Causes of subphrenic abscess?
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
44
Epidemiology of subphrenic abscess?
- Commonest cause of intra-abdominal abscess
45
Symptoms of subphrenic abscess?
o Chest/shoulder tip pain o Abdominal pain o Swinging fever o Diarrhoea, nausea, malaise
46
Signs of subphrenic abscess?
o Swinging/Spikey temperature o Systemically unwell patient o Often few physical signs – subcostal abdominal tenderness o Leucocytosis
47
Investigations of subphrenic abscess?
``` - Bloods o FBC (High WCC) o Cultures - Urgent US – localises collection of pus - Ct detects abscess and estimate volume ```
48
Management of subphrenic abscess?
- IV Antibiotics – broad spectrum - US/CT-guided drainage - May need percutaneous drainage, laparoscopy or open surgery
49
Definition of liver abscess?
- Caused by organisms invading liver parenchyma
50
Epidemiology of liver abscess?
- UK – pyogenic most common | - Worldwide – amoebic most common
51
Aetiology of pyogenic liver abscess?
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)
52
Aetiology of amoebic liver abscess?
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
53
Symptoms of liver abscess?
``` o RUQ pain  Referred shoulder tip pain o Fever (swinging) o Night sweats o Nausea and vomiting o Anorexia and weight loss o Cough ```
54
Signs of liver abscess?
o Swinging fever o Tender RUQ o Hepatomegaly, palpable mass o Jaundice
55
Investigations of liver abscess?
``` 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
56
Management of pyogenic liver abscess?
Fluids/PRN analgesics Antibiotics  Cephalosporin + metronidazole 1st line US/CT-guided aspiration
57
Management of amoebic liver abscess?
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
58
Description of hepatocellular carcinoma?
o Primary hepatocyte neoplasia | o Spread – lung, portal vein, periportal nodes, bone and brain
59
Description of benign liver tumours?
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
60
Epidemiology of hepatocellular carcinoma?
- 90% of all primary liver tumours - Common in China and Africa - Men more common - 90% of liver tumours are secondary metastatic tumours
61
Types of malignant primary liver tumours?
```  HCC  Cholangiocarcinoma  Angiosarcoma  Hepatoblastoma  Hepatic GIST ```
62
Types of benign primary liver tumours?
```  Cysts  Haemangioma  Adenoma  Focal nodular hyperplasia  Fibroma ```
63
Origins of secondary liver tumours in liver?
o Men – Stomach, lung, colon o Women – breast, stomach, colon, uterus o Either Sex – Pancreas, leukaemia, lymphoma, carcinoid tumours
64
Causes of hepatocellular carcinoma?
``` 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 ```
65
Symptoms of hepatocellular carcinoma?
``` o Fatigue o Anorexia o RUQ pain o Weight loss o Pruritus o Abdominal distention ```
66
Signs of hepatocellular carcinoma?
``` o Hepatomegaly o Jaundice (late) o Ascites o Bruit over liver o Spider Naevi o Anaemia ```
67
Investigations of hepatocellular carcinoma - referral?
o Urgent direct access US (within 2 weeks) if upper abdominal mass consistent with enlarged liver
68
Investigations of hepatocellular carcinoma - secondary care?
o USS o AFP o CT o Fine-needle aspiration or biopsy
69
Investigations of hepatocellular carcinoma - other tests?
Blood  FBC, clotting, LFT, hepatitis serology, AFP Imaging  US  CT  ERCP if cholangiocarcinoma If suspected secondary:  CXR, mammogram, endoscopy, colonoscopy, CT, marrow biopsy
70
Investigations of hepatocellular carcinoma - Staging?
o Child-Pugh Stage | o Cancer of Liver Italian Program (CLIP) – prognostic marker
71
Management of hepatocellular carcinoma - surgical?
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
Management of hepatocellular carcinoma - non-resectable disease - Stage A/B?
o Stage A/B ineligible for surgery:  Radiofrequency/Microwave ablation  Chemo-embolisation into hepatic artery
73
Management of hepatocellular carcinoma - non-resectable disease - Stage C/D?
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
Surveillance in people at high risk of HCC?
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
Prognosis of HCC?
- Median survival from diagnosis is 6 months
76
Description, symptoms, Ix and management of hepatoblastoma?
- 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
Definition of cholangiocarcinoma?
- Carcinoma arising from any part of biliary tree – from small intrahepatic bile ducts to ampulla of Vater
78
Epidemiology of cholangiocarcinoma?
- Most commonly, perihilar region near bifurcation of hepatic ducts (Klatskin’s tumour) - 90% are ductal adenocarcinomas - 10% SCC - Common in South Asia
79
Causes of cholangiocarcinoma?
``` 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
Symptoms of cholangiocarcinoma?
``` o Jaundice early - painless o RUQ pain o Fatigue o Anorexia o Weight loss o Pruritus o Abdominal distention ```
81
Signs of cholangiocarcinoma?
``` o Hepatomegaly o Jaundice (early) o Ascites o Bruit over liver o Spider Naevi o Anaemia ```
82
Investigations of cholangiocarcinoma - primary care referral?
o Urgent direct access US if upper abdominal mass consistent with enlarged gall bladder
83
Investigations of cholangiocarcinoma - secondary care?
o CT o Biopsy - Fine-needle aspiration or biliary brush cytology o ERCP
84
Investigations of cholangiocarcinoma - other tests?
``` o LFTs (elevated conjugated bilirubin, raised alkaline phosphatase, raised GGT, raised aminotransferase) o Clotting o Tumour markers – Ca19-9, CEA, AFP (not raised) ```
85
Investigations of cholangiocarcinoma - staging?
o Bismuth-Corlette classification
86
Management of cholangiocarcinoma - surgical?
o Liver Resection (30%)  Major hepatectomy + extrahepatic bile duct excision + caudate lobe resection o Stenting of bile duct o Liver Transplant (rare)
87
Management of cholangiocarcinoma - non-resectable?
``` o Chemotherapy and radiotherapy  Photodynamic therapy  Internal radiation  Endoscopic bipolar radiofrequency  Hepatic artery chemosaturation ```
88
Types of hepatic failure?
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
Causes of hepatic failure - infection?
 Viral hepatitis (B, C, CMV, EBV)  Yellow Fever  Leptospirosis
90
Causes of hepatic failure - drugs, toxins & vascular?
Drugs  Paracetamol  Halothane  Isoniazid Toxins  Amanita phalloides Vascular  Budd-Chiari syndrome
91
Causes of hepatic failure - others?
```  Alcohol  PBC  Haemochromatosis  Autoimmune hepatitis  Alpha-1 antitrypsin deficiency  Wilson’s disease  HELLP syndrome  Malignancy ```
92
Signs of hepatic failure?
``` 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
Stages of hepatic encephalopathy of hepatic failure?
 1 = altered mood/behaviour, sleep disturbance, dyspraxia  2= drowsiness, confusion, slurred speech +/- flap  3= incoherent, restless, liver flap  4 = coma
94
Bloods to perform of hepatic failure?
``` o FBC (infection, GI bleed, thrombocytopenia) o U&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
Microbiology Ix of hepatic failure?
o Blood culture o Urine culture o Ascitic tap (M, C & S)
96
Imaging of hepatic failure?
o CXR | o Abdominal US and Doppler flow
97
Initial management of hepatic failure?
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
Monitoring in initial management of hepatic failure?
o Monitor  Temp, RR, HR, BP, pupils, urine output hourly  Blood glucose 4-hourly  Daily weight o Daily  FBC, U&E, LFT, INR
99
Drugs to avoid in hepatic failure?
 Opiates, hypoglycaemics, paracetamol, methotrexate, azathioprine, isoniazid, salicylates, tetracycline, mitomycin
100
When to liase with transplant team of hepatic failure?
• 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
Managing complication of hepatic failure?
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
Definition of epigastric hernia?
- Pass through linea alba above umbilicus
103
Epidemiology of epigastric hernia?
- Prevalence up to 10%, mostly middle-aged men
104
Aetiology of epigastric hernia?
o Typically secondary to raised chronic intra-abdominal pressure (obesity, pregnancy, ascites, straining, coughing)
105
Symptoms of epigastric hernia?
- Typical asymptomatic - Midline mass – disappears when lying on the back - Epigastric pain - N &V, often after meals
106
Investigations of epigastric hernia?
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
Management of epigastric hernia?
- Surgical repair essential – risk of strangulation or incarceration o Mesh and suture repair possible
108
Description of familial adenomatous polyposis?
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
Description of Peutz-Jeghers syndrome?
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
Description of Hereditary Non-Polyposis Colorectal cancer (Lynch syndrome)?
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
Description of juvenile polyposis?
o Multiple juvenile polyps in GI tract – benign hamartoma
112
Symptoms of Familial adenomatous polyposis?
```  Adenomas develop during 20s  Colorectal cancer by 50  Rectal bleeding  Diarrhoea  Abdominal pain  Mucous discharge  Obstruction – constipation, vomiting ```
113
Signs of Familial adenomatous polyposis?
```  Rectal polyps or masses  Congenital hypertrophy of retinal pigment epithelium  Supernumery teeth  Epidermoid cysts  Thyroid masses ```
114
Symptoms of Peutz-Jeghers syndrome?
``` o FHx o Deeply pigmented lesions on lips and buccal mucosa o Bouts of abdominal pain o GI bleeding o Iron-deficiency anaemia ```
115
Investigations in colonic polyposis?
- Bloods – FBCs, LFTs, TFTs - Faecal occult blood - Colonoscopy with biopsies diagnostic - Upper GI endoscopy - Genetic testing – APC gene - CT scan
116
Management of FAP - genetic analysis?
 If 2 1st-degree relative aged <70, one 1st degree relative aged <45, 3 close relatives <60 on average, FAP, HNPCC Endoscopic surveillance
117
Management of FAP - surgical?
 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
Management of FAP - surveillance?
 Upper GI endoscopy three-yearly
119
Management of Peutz-Jeghers syndrome - genetic analysis?
 If 2 1st-degree relative aged <70, one 1st degree relative aged <45, 3 close relatives <60 on average, FAP, HNPCC
120
Management of Peutz-Jeghers syndrome - Surgery?
 Endoscopic polypectomy |  Polypectomy
121
Management of Peutz-Jeghers syndrome - surveillance?
 2-yearly from 25 years old – colonoscopy & upper GI endoscopy
122
Management of HNPCC - genetic analysis?
 If 2 1st-degree relative aged <70, one 1st degree relative aged <45, 3 close relatives <60 on average, FAP, HNPCC
123
Management of HNPCC -surveillance?
 Annual or biannual colonoscopies from 25 years old |  Upper GI endoscopy every 2 years from 50
124
Management of Juvenile Polyposis - surgery?
 Colectomy
125
Management of Juvenile polyposis - surveillance?
 Colonoscopy every 18-24 months from 18 |  Upper GI endoscopy every 1-2 years from 25
126
Anatomy of anal canal?
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
Behaviour of anal cancer?
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
Spread of anal cancer?
o Above dentate line – spread to pelvic lymph nodes | o Below dentate line – spread to inguinal lymph nodes
129
Risk factors of anal cancer?
``` o Syphilis o Anal warts in HPV (SCC) o Anal intercourse o High number of sexual partners o MSM o HIV o Smoking ```
130
Types of anal cancer?
o Squamous Cell Carcinoma (80%) o Adenocarcinoma o Melanoma o Lymphoma
131
Symptoms of anal cancer?
- Bleeding - Pain - Change in bowel habit - Pruritus ani - Mass in or around anus - Anal ulceration
132
Referral for 2-week appointment of anal cancer?
- Refer for 2-week wait appointment if: | o Unexplained anal mass or anal ulceration
133
Assessment of anal cancer?
o DRE o Palpation of inguinal lymph nodes o Examination under anaesthetic (EUS) with biopsy o CT/MRI/US/PET
134
Management of AIN?
o Topical imiquimod, 5-FU | o Ablative electrocautery, laser
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Management of anal carcinoma?
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
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Definition of perianal haematoma?
- Blue or dark coloured swelling at anal verge | - Caused by rupture of small vein near anal margin then blood clots
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Risk factors of perianal haematoma?
- Caused by straining, constipation, anal sex, heavy lifting, coughing
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Symptoms of perianal haematoma?
- Acutely painful – usually after straining | - 2-4mm dark blueberry under skin at anal margin
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Referral of perianal haematoma?
- Refer for non-urgent assessment and management if <24 hours old
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Management of perianal haematoma?
o Spontaneous resolve over a few days to week o PRN analgesia o If pain intolerable:  Evacuated and drained under LA
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Definition of fistula-in-ano?
- Abnormal connection between skin and anal canal/rectum
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Classification of fistula-in-ano?
o Intersphincteric o Trans-sphincteric o Suprasphincteric o Extrasphincteric
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Pathology of fistula-in-ano? What is Goodsall's rule?
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
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Causes of fistula-in-ano?
``` o Perianal sepsis o Abscesses (90%) o Crohn’s o TB o Diverticular disease o Rectal carcinoma ```
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Symptoms of fistula-in-ano?
- Pain | - Leak blood or pus
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Investigations of fistula-in-ano?
- Proctoscopy to visualise anal canal and opening of tract - MRI - Endoanal US scan
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Park's classification of fistula-in-ano?
``` Extrasphincteric Suprasphincteric Transsphincteric Intersphincteric Submucosal ```
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Management of fistula-in-ano - if no symptoms?
- If no symptoms – conservative management (PRN analgesia)
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Management of fistula-in-ano - if symptoms?
- Fistulotomy & Excision o High fistula (involving continence muscles of anus) – need seton suture tightening over time to maintain continence o Low fistulas laid open
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Definition of re-feeding syndrome?
- Life-threatening complication of refeeding via any route after prolonged period of starvation
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Pathology of re-feeding syndrome?
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
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Symptoms of re-feeding syndrome?
- Rhabdomyolysis - Red and white cell dysfunction - Respiratory insufficiency - Arrhythmias - Cardiogenic shock - Seizures - Death
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Bloods to perform in re-feeding syndrome?
``` o Glucose o FBC o Albumin o U&Es o Urine and stool culture o Iron, B12, folate, TFTs, coeliac, Ca, PO4, Zn, Vitamin, selenium ```
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Prevention of re-feeding syndrome?
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
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Screening for malnutrition in people at risk of refeeding syndrome?
When  All hospital inpatients and done weekly How  BMI, % unintentional weight loss, Mid upper arm diameter  Malnutrition Universal Screening Test (MUST)
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Indications for nutritional support of re-feeding syndrome?
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
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Oral nutritional support - indications?
 People with safe swallow and malnorished or at risk of malnutrition
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Oral nutritional support - amount?
 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
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Oral nutritional support - people at risk of refeeding syndrome?
 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
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Oral nutritional support -monitoring?
 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
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Enteral feeding tube - indications?
 Malnourished or risk of and inadequate or unsafe oral intake & functional GI tract  People with unsafe swallow diagnosed by SALT team
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Enteral feeding tube - amount?
 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
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Enteral feeding tube - people at risk of re-feeding syndrome?
 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
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Enteral feeding tube - route and method of delivery?
 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
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Enteral feeding tube - monitoring?
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
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Parenteral nutrition - indications?
 Inadequate or unsafe oral and/or enteral nutritional intake and non-functional, inaccessible or perforated GI tract
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Parenteral nutrition -Amount?
 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
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Parenteral nutrition - people at risk of refeeding syndrome?
 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
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Parenteral nutrition - route and method of delivery?
 Peripherally inserted central catheter (PICC line) – if <14 days  Tunnelling subclavian line if >30 days  Continuous administration is preferred method
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Parenteral nutrition - monitoring?
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