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Phase 4 - GI, MSK, Infectious Diseases > GI > Flashcards

GI Flashcards

1
Q

Describe the pathophysiology of Primary Biliary Cholangitis

A

Autoimmune condition affecting interlobular bile ducts (in the liver), causing inflammation and damage = obstruction of bile flow (cholestasis)

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2
Q

Name 3 things released by the gallbladder and how these cause symptoms of Primary Biliary Cholangitis

A

1) Bile Acids (help with absorption/digestion of fats) = itching/pruritus, greasy stools, fat malabsorption

2) Bilirubin = pale stools and dark urine, jaundice

3) Cholesterol = xanthelasma (deposits in the skin) and xanthomas (larger nodules in skin/joints)

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3
Q

Symptoms of Primary Biliary Cholangitis

A

RUQ pain
Hepatomegaly
Itching/Pruritus
Pale/Greasy Stools
Dark Urine
Fatigue
Xanthelasma and Xanthomas
Jaundice
Hyperpigmentation

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4
Q

Management for Primary Biliary Cholangitis?

A

1st Line - Ursodeoxycholic Acid

Cholestyramine (for pruritus)

Fat Soluble Vitamin Supplements (A, D, E, K)

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5
Q

How do we test for Primary Biliary Cholangitis?

A

LFTs - raised ALP

Raised Serum AMA (Anti-Mitochondrial Antibodies) - most specific to PBC

Raised Serum ANA Anti-Nuclear Antibodies)

Raised Serum IgM

Imaging (excludes extrahepatic cause) - RUQ ultrasound or MRCP

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6
Q

Complications of Primary Biliary Cholangitis?

A

Cirrhosis = Portal Hypertension = Ascites, Variceal Haemorrhage

Osteomalacia and Osteoporosis (due to VitD deficiency)

Increased risk of HCC

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7
Q

What diseases are associated with Primary Biliary Cholangitis

A

Sjogren’s Syndrome (80%)
Rheumatoid Arthritis
Thyroid Disease

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8
Q

What is the pathophysiology of Primary Sclerosing Cholangitis?

A

Inflammation and sclerosis (fibrosing/thickening) of the intra and extra-hepatic bile ducts

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9
Q

What is the difference between Primary Biliary Cholangitis and Primary Sclerosing Cholangitis?

A

PBC affects only the intra-hepatic bile ducts while PSC affects both

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10
Q

What are the investigations for Primary Sclerosing Cholangitis

A

LFTs - raised ALP

MRCP - shows strictures in the bile ducts

ERCP

p-ANCA may be positive

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11
Q

What are the symptoms of Primary Sclerosing Cholangitis

A

RUQ pain
Itching/Pruritus
Fatigue
Jaundice
Hepatomegaly

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12
Q

What is the management of Primary Sclerosing Cholangitis

A

Dilation of strictures using stents guided by ERCP

Cholestyramine - pruritus

Fat Soluble Vitamin Supplements

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13
Q

What are the complications of Primary Sclerosing Cholangitis

A

Biliary Strictures
Cholangiocarcinoma
Cirrhosis
Osteoporosis
Acute Bacterial Cholangitis

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14
Q

What disease is Primary Sclerosing Cholangitis associated with?

A

Ulcerative Colitis - 70/80% of patients with PSC have UC

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15
Q

What is the pathophysiology of Acute Cholangitis

A

Infection and inflammation of the bile ducts

High mortality due to sepsis and septicaemia

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16
Q

What are the 2 main causes of Acute Cholangitis

A

Obstruction of bile flow (i.e. Gallstone)
Infection during ERCP

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17
Q

Most common organisms causing Acute Cholangitis

A

E.coli
Klebsiella species
Enterococcus species

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18
Q

Symptoms of Acute Cholangitis

A

RUQ pain
Fever
Jaundice

N+V
Pruritus
Pale stools
Dark Urine

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19
Q

What is Charcot’s triad

A

RUQ pain
Fever
Jaundice (raised bilirubin)

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20
Q

What is the management of Acute Cholangitis

A

Treat for sepsis:
Take blood cultures
Check lactate
Check urine output
Give Oxygen
Give IV fluids
Give IV antibiotics
Nil by mouth

ERCP to remove stone
Percutaneous transhepatic cholangiogram - drain through skin, liver and bile ducts relieves obstruction (for patients less suitable for ERCP or if it has failed)

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21
Q

What are the investigations for Acute Cholangitis

A

FBC - raised WBCs
LFTs - raised Bilirubin, ALP, GGT
Raised CRP
MRCP
ERCP
Abdominal Ultrasound

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22
Q

Pathophysiology of Acute Cholecytitis

A

Inflammation of the gallbladder

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23
Q

Causes of Acute Cholecystitis

A

Calculous AC - stone in the neck of gallbladder or cystic duct

Acalculous AC - patients on TPN or long periods of fasting where gallbladder is not being stimulated and leads to build-up pressure

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24
Q

Presentation of Acute Cholecystitis

A

RUQ pain (may radiate to right shoulder)
Fever
N+V
Murphy’s Sign
Tachycardic and tachypnoeic

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25
Q

Investigations for Acute Cholecystitis

A

FBC - raised WCC
Raised Inflammatory markers
Abdominal Ultrasound
MRCP - visualise stones

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26
Q

What is Murphy’s Sign

A

Place a hand in RUQ and apply pressure

Ask the patient to take a deep breath in

The gallbladder will move downwards during inspiration and come in contact with your hand

Stimulation of the inflamed gallbladder results in acute pain and sudden stopping of inspiration

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27
Q

What would an Abdominal Ultrasound show in Acute Cholecystitis

A

Thickening of gallbladder wall
Stones/Sludge in gallbladder
Fluid around gallbladder

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28
Q

Treatment of Acute Cholecystitis

A

Nil by mouth
IV Fluids
IV antibiotics
ERCP - to remove potential stones
Cholecystectomy

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29
Q

Complications of Acute Cholecystitis

A

Sepsis
Gallbladder perforation
Gallbladder empyema (infected tissue and pus collecting in the gallbladder) - IV antibiotics and cholecystectomy/cholecystostomy

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30
Q

Main risk factor for cholangiocarcinoma

A

Primary Sclerosing Cholangitis

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31
Q

Presentation of cholangiocarcinoma

A

Jaundice
Weight loss
Pale stools
Dark urine
Palpable Gallbladder
RUQ pain
Hepatomegaly

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32
Q

What is Courvoisier’s law

A

Palpable Gallbladder + Jaundice = cholangiocarcinoma

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33
Q

2 causes of painless jaundice

A

cholangiocarcinoma
pancreatic cancer

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34
Q

Tumour marker of cholangiocarcinoma and pancreatic cancer

A

CA19-9 (remembering tip: 9 looks like a pancreas and 9 is also a ‘g’ for gallbladder)

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35
Q

Investigations of cholangiocarcinoma

A

CT TAP for staging
CA19-9 (carbohydrate antigen)
MRCP - assess obstruction

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36
Q

Treatment of cholangiocarcinoma

A

None
ERCP - relieve obstruction and gain biopsy of tumour

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37
Q

Risk factors for biliary colic

A

4 F’s
Fat - enhanced cholesterol synthesis and secretion
Female
Fertile - pregnancy increases risk
Forty

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38
Q

Why does biliary colic occur

A

Gallbladder contracting against a stone in the cystic duct

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39
Q

Presentation of biliary colic

A

Severe colicky epigastric or RUQ pain often after meals
N+V

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40
Q

What triggers contraction of the gallbladder

A

Fatty meals = release of cholecystokinin (CKK) = contraction

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41
Q

Investigations for gallstones

A

LFTs - bilirubin may be raised if flow is blocked, raised ALP and less raised ALT/AST
Ultrasound - gallstones in gallbladder or ducts, duct dilatation
MRCP
ERCP

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42
Q

Treatment for gallstones

A

Cholecystectomy for symptomatic patients

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43
Q

What is a Kocher incision

A

a right subcostal “Kocher” incision is used in cholecystectomies

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44
Q

Complications of cholecystectomy

A

Bleeding
Infection
Perforation
Stones left over
Damage to nearby organs

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45
Q

What is Post-cholecystectomy syndrome

A

Non-specific symptoms that can occur after a cholecystectomy

They may be attributed to changes in the bile flow after removal of the gallbladder. Symptoms often improve with time. Symptoms include:

Diarrhoea
Indigestion
Epigastric or right upper quadrant pain and discomfort
Nausea
Intolerance of fatty foods
Flatulence

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46
Q

Causes of acute pancreatitis

A

IGETSMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion Venom
Hyperlipidaemia
ERCP
Drugs (furosemide, thiazide diuretics, and azathioprine)

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47
Q

What drugs can cause acute pancreatitis

A

Furosemide
Thiazide diuretics
Azathioprine

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48
Q

Presentation of acute pancreatitis

A

Severe epigastric pain radiating through to the back
Epigastric tenderness
Vomiting
Systemically unwell - low grade fever and tachycardia

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49
Q

What is Cullen’s and Grey-Turner’s sign

A

Sign of pancreatitis

Cullen’s - peri-umbilical discolouration (yellow/blue/purple bruising)

Grey-Turner’s - flank discolouration (yellow/blue/purple bruising)

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50
Q

What tool do we use for assessing severity of acute pancreatitis? What is measured in it? What is the scoring system?

A

Glasgow-Imrie scoring system:
P - Pao2 < 8KPa (hypoxic)
A - Age > 55
N - Neutrophils (WBC > 15)
C - Calcium < 2mmol/L
R - uRea > 16mmol/L
A - Albumin < 32g/L
S - Sugar (Glucose < 10mmol/L)

0 or 1 = mild
2 = moderate
3 or more = severe

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51
Q

Investigations for acute pancreatitis

A

Amylase - raised more than 3 times normal limit
Lipase - more sensitive and specific than amylase
CRP
Ultrasound - to assess for gallstones
CT abdomen - assess for complications

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52
Q

Management of acute pancreatitis

A

IV fluids - aim for > 0.5ml/kg/hr
IV Analgesia
Nil by mouth - parenteral or enteral nutrition (to stop activation of pancreas in response to food in duodenum)
Antibiotics - only if there is evidence of necrosis or abscess formation
Cholecystectomy - if gallstones
ERCP - if obstructed biliary tree
Surgical drainage if necrosis

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53
Q

Difference between total parenteral and enteral nutrition

A

Enteral nutrition - feeding though a tube inserted into the stomach, duodenum or jejunum

TPN - feeding through a vein

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54
Q

Complications of acute pancreatitis

A

Necrosis of pancreas
Infection of necrosed area
Abscess formation
Peripancreatic fluid collection
Pseudocysts in pancreas
Chronic pancreatitis

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55
Q

Presentation of chronic pancreatitis

A

Chronic epigastric pain
Loss of exocrine function - less lipase hence steatorrhea
Weight loss
Loss of endocrine function - diabetes develops
Formation of pseudocysts and abscess

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56
Q

Investigations for chronic pancreatitis

A

CT - shows atrophy and calcification of pancreas
Faecal elastase - assesses exocrine function

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57
Q

Management of chronic pancreatitis

A

Analgesia
Drinking and smoking abstinence
Creon - pancreatic enzyme replacement
Subcutaneous insulin regimes - to treat diabetes

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58
Q

What are the stages of Alcohol Related Liver Disease?

A

1) ALcoholic Fatty Liver (hepatic steatosis) - accumalation of fat droplets in the liver

2) Alcoholic hepatitis

3) Cirrhosis - functional liver tissue replaced with scar tissue

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59
Q

What is the reccomended alcohol consumption per wee?

A

14 units

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60
Q

Presentation of Alcohol Related Liver Disease

A

Jaundice
RUQ pain
Hepatomegaly
Peripheral oedema
Palmar erythema (abnormal oestrogen = raised NO synthase = dilation)
Clubbing
Dupuytren’s contracture
Xantomas
Spider angiomas

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61
Q

Investigations for Alcohol Related Liver Disease

A

ALT - raised
AST - raised
AST:ALT ratio > 2:1
GGT raised
ALP raised
Bilirubin raised
Serum Albumin raised
Prolongues prothrombin time
Liver ultrasound - can show farrt cganges and cirrhosis
Fibroscan - shows degree of fibrosis

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62
Q

Management for Alcohol Related Liver Disease

A

Alcohol abstinence
Glucocorticoids - prednisolone
Pentoxyphylline
Nutritional support - vitamin B1

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63
Q

How do you screen for harmful alcohol use?

A

CAGE questionnaire
C – CUT DOWN? Do you ever think you should cut down?
A – ANNOYED? Do you get annoyed at others commenting on your drinking?
G – GUILTY? Do you ever feel guilty about drinking?
E – EYE OPENER? Do you ever drink in the morning to help your hangover or nerves?

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64
Q

What withdrawals symptoms can occur 6-12hours after alcohol abstinence?

A

Tremor
Sweating
Headaces
Tachycardia
Anxiety

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65
Q

What can occur 12-24 hours after alcohol abstinence?

A

Hallucinations

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66
Q

What can occur 36 hours after alcohol abstinence?

A

Seizures

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67
Q

What can occur 3 days after alcohol abstinence?

A

Delirium Tremens (DT = day three)

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68
Q

Pathophysiology of alcohol withdrawal

A

alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)

chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors

extreme excitability of the brain and excessive adrenergic (adrenalin-related) activity.

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69
Q

Feature of delirium tremens

A

Confusion
Severe agitation
Auditory and visual hallucinations
Delusions
Tremor
Ataxia
Fever
Tachycardia

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70
Q

Treatment of delirium tremens

A

Lorazepam (benzodiazepine)

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71
Q

How to treat alcohol withdrawal

A

1st line = Chlordiazepoxide hydrochloride
Diazepam (Alternative)
Carbamazepine

Pabrinex (High dose vitamin B) given IM or IV
Followed by oral thiamine (if diet is deficient)

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72
Q

What drug reduces alcohol cravings?

A

Acamprosate (agonist of NMDA receptors = improved abstinence)

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73
Q

What drug promotes abstinence of alcohol?

A

Disulfiram (causes severe reaction after alcohol consumption)

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74
Q

What causes Wernicke’s encephalopathy

A

Thiamine deficiency due to alcohol excess
Thiamine poorly absorbed in presence of alcohol
Excess alcohol use = decreased absorption of Thiamine = Wernicke’s encepholopathy

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75
Q

Feature of Wernicke’s encephalopathy

A

ACON:
Ataxia
Confusion
Opthalmoplegia
Nystagmus

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76
Q

Treatment of Wernicke’s encephalopathy

A

Urgent replacement of Thiamine

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77
Q

If Wernicke’s encepholopahy goes untreated what may develop?

A

Korsakoff syndrome

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78
Q

What are the features of Korsakoff syndrome?

A

Anterograde and Retrograde amenesia
Confabulation
+ symptoms of Wernicke’s encephalopathy

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79
Q

What are the symptoms of anal fissures

A

Bright red rectal bleeding
Pain around the anus
Pruritus ani
Discharge
Constipation

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80
Q

What is the management of Acute (<1wks) and Chronic (>1wks) anal fissures

A

Acute:
Soften stool - through a high fiber and water diet OR bulk-forming laxatives (1st line)
Lubricants
Topical anesthetics
analgesia

Chronic :
Topical GTN
If Topical GTN not working then:
Sphincterotomy or Botulinum toxin

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81
Q

Symptoms of appendicitis

A

Peri-umbilical abdominal pain that migrates to the right iliac fossa
N+V
Anorexia
Fever
Guarding
Rigidity

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82
Q

What is Rosving’s sign?

A

Palpation of left iliac fossa results in pain in the right iliac fossa

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83
Q

What signs are present if the appendix has potentially been perforated?

A

Rebound and percussion tenderness

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84
Q

Investigations for appendicitis

A

Raised inflammatory markers
Nuetrophil dominant leucocystosis
Urinalysis - exclude pregnancy, UTI and renal colic
Ultrasound - exclude gynaecological/obstetric causes

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85
Q

Differential for appendicits

A

Ectopic pregnancy
Ovarian cyst torsion/rupture
Mesenteric adenitis
Meckel’s diverticulum

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86
Q

Treatment for appendicitis

A

Appendectomy
Prophylactic antibiotics

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87
Q

Potential complications of appendectomy

A

Bleeding
Removal of normal appenix
Perforation
Damage to nearby organs
VTE

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88
Q

How do we determine the cause of ascites

A

using serum-ascites albumin gradient
If > 11g/L then indicated portal hypertension

If < 11g/L then indicates other cause

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89
Q

What are the possible causes of ascites if the SAAG is > 11g/L

A

Liver disorders:
cirrhosis/alcoholic liver disease
acute liver failure
liver metastases

Cardiac:
righ heart failure
constrictive pericarditis

Other
Budd-Chiari syndrome
portal vein thrombosis
veno-occlusive crisis
myxodema

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90
Q

What are the possible causes of ascites if the SAAG is <11g/L

A

Hypoalbuminaemia:
nephrotic syndrome
severe malnutrition (e.g. kwashiorkor)

Malignancy:
peritoneal carcinomatosis

Infections:
tuberculous peritonitis

Other:
pancreatitis
bowel obstruction
biliary ascites
post-operative lymphatic leak
serositis in connective tissue disease

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91
Q

Management for ascites

A

Reduce dietary sodium
Aldosterone antagonist - spironolactone
Drainage - therapeutic abdominal paracentesis
Prophylactic antibitoics for SBP

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92
Q

How is cirrhosis diagnosed

A

Transient elastography (Fibroscan)
+ upper endoscopy to check for varices in patients with new diagnosis of cirrhosis

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93
Q

Individuals carrying which haplotypes are genetically predisposed to coeliac disease?

A

HLA-DQ2 or HLA-DQ8

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94
Q

What are the GI related symptoms of coeliac disease

A

Diarrhoea
Abdominal pain or bloating
Steatorrhoea
N+V

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95
Q

What are the extraintestinal symptoms of coeliac disease

A

Dermatitis herpatiformis
Mouth ulcers
Iron deficiency anaemia
Weight loss
Bone pain, fractures, osteoporosis or osteopenia - impaired vitamin D absorption
Peripheral neuropathy
Fatigue

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96
Q

Investigations for coeliac disease

A

Serum anti-tTG antibodies (highest sensitivity and specificity)
Serum anti-EMA antibodies
Total serum IgA antibodies - excludes selective IgA deficiency

Duodenal biopsy (gold standard)

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97
Q

What 3 things are seen on a duodenal biopsy in coeliac disease

A

Crypt hyperplasia
Villous atrophy
Increased intraepithelial lymphocytes

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98
Q

Management for coeliac disease

A

Gluten free diet
Supplements for any deficiencies
Pneumococal vaccine (for functional hyposplenism)

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99
Q

What other conditions is coeliac disease linked with

A

T1DM
Thyroid disease
(autoimmune)

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100
Q

Complications of coeliac disease

A

Nutritional deficiencies
Anaemia
Osteoporosis
Hyposplenism
Ulcerative jejunitis
Non-Hodgkin lymphoma
Small bowel adenocarcinoma

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101
Q

Risk factors for bowel cancer

A

Familial adenomatous polyposis
Hereditary non-polypsis colorectal cancer
IBD
Increased age
Diet (high in red/processed meat and low fibre)
Smoking
Obesity
Alcohol

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102
Q

Presentation of bowel cancer

A

Change in bowel habit
Rectal bleeding
Unexplained abdominal pain
Iron deficiency anaemia
Abdominal or rectal mass

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103
Q

What is the screening for bowel cancer

A

Faecal Immunochemical Test (FIT test) - detects amount of human heamoglobin in stools

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104
Q

From what age are you offered routine bowel cancer screening

A

FIT test every two years from 50-74

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105
Q

What is the tumour marker for bowel cancer

A

Carcinoembryonic antigen (CEA)

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106
Q

Investigations for bowel cancer

A

Colonoscopy
Sigmoidoscopy (if only rectal bleeding is present)
CT colonogrophy (for patients less fit for colonoscopy)
Staging TAP CT scan

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107
Q

What two classification systems are used for bowel cancer

A

Dukes’
TNM

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108
Q

Summarise Dukes’ classification for bowel cancer

A

Dukes A - confined to mucosa and part of the muscle of the bowel wall
Dukes B - extending through the muscle of the bowel wall
Dukes C - lymph node involvement
Dukes D - metastatic disease

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109
Q

Summarise TNM classification for bowel cancer

A

T for Tumour:

TX – unable to assess size
T1 – submucosa involvement
T2 – involvement of muscularis propria (muscle layer)
T3 – involvement of the subserosa and serosa (outer layer), but not through the serosa
T4 – spread through the serosa (4a) reaching other tissues or organs (4b)

N for Nodes:

NX – unable to assess nodes
N0 – no nodal spread
N1 – spread to 1-3 nodes
N2 – spread to more than 3 nodes

M for Metastasis:

M0 – no metastasis
M1 – metastasis

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110
Q

Management for bowel cancer

A

Surgical resection
Chemotherapy
Radiotherapy
Palliative care

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111
Q

Define the following:
Right hemicolectomy
Left hemicolectomy
High anterior resection
Low anterior resection
Abdomino-perineal resection (APR)
Hartmann’s procedure

A

Right hemicolectomy -removal of the caecum, ascending and proximal transverse colon.

Left hemicolectomy -removal of the distal transverse and descending colon.

High anterior resection -removing the sigmoid colon (may be called a sigmoid colectomy).

Low anterior resection -removing the sigmoid colon and upper rectum but sparing the lower rectum and anus.

Abdomino-perineal resection (APR) - removing the rectum and anus (plus or minus the sigmoid colon) and suturing over the anus. It leaves the patient with a permanent colostomy.

Hartmann’s procedure (usually an emergency procedure) - the removal of the rectosigmoid colon and creation of an colostomy.

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112
Q

What is and what are the features of low anterior resection syndrome

A

occur after resection of a portion of bowel from the rectum, with anastomosis between the colon and rectum

Urgency and frequency of bowel movements
Faecal incontinence
Difficulty controlling flatulence

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113
Q

What is meaured during follow up of curative bowel cancer surgery

A

CEA
CT TAP

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114
Q

What is diverticular disease

A

herniation of colonic mucosa through the muscular wall of the colon

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115
Q

Where does diverticular disease commonly occur

A

The site between the taenia coli where vessels pierce the muscle to supply the mucosa. For this reason, the rectum, which lacks taenia, is often spared.

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116
Q

Symptoms of diverticular disease

A

Altered bowel habit (constipation)
Rectal bleeding
Abdominal pain (left lower quadrant)

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117
Q

Investigations for diverticular disease

A

Colonoscopy
CT cologram
Barium enema

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118
Q

What is the name of the classification system of diverticular disease?

A

Hinchey Classification:
I - Para-colonic abscess
II - Pelvic abscess
III - Purulent abscess
IV - Faecal peritonitis

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119
Q

Treatment of diverticular disease

A

Increase dietary fibre intake

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120
Q

Define diverticulitis

A

The infection of a diverticulum

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121
Q

Difference between diverticulosis and diverticulitis

A

Diverticulosis = presenceof diverticula
Diverticulitis = infection of a diverticula

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122
Q

Risk factors for diverticulitis

A

Age
Lack of dietary fibre
Obesity
Sedentary lifestyle

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123
Q

Symptoms of diverticulitis

A

Severe abdominal pain (left iliac fossa although may be right in Asian people)
N+V
Fever
Change in bowel habit
Urinary frequency, urgency or dysuria (irritation of bladder by inflamed bowel)
PR bleeding
Guarding, rigidity and rebound tenderness

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124
Q

Investigations for diverticulitis

A

FBC - raised WCC
CRP - riased
ERECT CXR - pneumoperitoneum in case of perforation
AXR - dilated bowel loops, obstruction or abscess
CT - may show abscess
Colonoscopy - should be avoided initially due to perforation risk

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125
Q

Management of diverticulitis

A

Oral antibiotics - co-amoxiclav for at least 5 days
Analgesia - NSAIDs or opiates
Liquid diet

If symptoms dont settle within 72 hours = IV antibiotics (cephalosporin + metronidazole), IV fluids , Analgesia, Nil by mouth

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126
Q

Complications of diverticulitis

A

Perforation
Peritonitis
Pereidiverticular abscess
Large haemorrhage
Fistula between colon and bladder (= pneumaturia or faecaluria) or vagina (vaginal passage of flatus or faeces)
Ileus or obstruction

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127
Q

Most prevalant type of gastric cancer

A

Gastric adenocarcinoma (arises from glandular epithelium in stomach lining)

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128
Q

Risk factors for gastric cancer

A

Helicobacter Pylori - inflammation of lining = atrophy and intestinal metaplasia = dysplasia
Pernicious anaemia caused atrophic gastritis
Diet high in salt, nitrates and salt preserved foods
Smoking
Ethnicity - Japanese and Chinese

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129
Q

Feature of gastric cancer

A

Abdominal pain (vague epigastric pain)
Weight loss and anorexia
N+V
Dysphagia (if originated in proximal stomach)
Upper GI bleeding
Virchows node and Sister Mary Joseph’s node (if lymphatic spread)

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130
Q

Where are Virchow’s node and Sister Mary Joseph’s node

A

Virchow = left supraclavicular lymph node
Sister MJ node = Periumbilical node

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131
Q

Investigations for gastric cancer

A

OGD with biopsy (may see signet ring cells)
CT CAP for staging

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132
Q

Management of gastric cancer

A

Surgery:
- Endoscopic mucosal resection
- Partial gastrectomy
- Total gastrectomy
Chemotherapy

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133
Q

Define GORD

A

The flow of stomach acid from the stomach into the oesophagus through the lower oesophageal sphincter

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134
Q

What type of epithelium is in the stomach and oesophagus

A

Stomach = columnar
Oesophagus = squamous

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135
Q

Risk factors for GORD

A

Greasy and spicy foods
Smoking
Obesity
H.pylori
Hiatus hernia
Stress
NSAIDs
Alcohol
Coffee and tea

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136
Q

Presentation of GORD

A

Dyspepsia:
Heartburn
Retrosternal or epigastric pain
Reflux of stomach acid into oesophagus
Bloating
Nocturnal cough
Hoarse voice
Odynophagia (painful swallowing)

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137
Q

GORD red flags

A

Dysphagia
Age over 55
Weight loss
Upper abdominal pain and mass
Reflux
Treatment-resistant dyspepsia
N+V
Anaemia (from bleeding)
Raised platelet count

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138
Q

What can an OGD be used for?

A

Gastritis
Peptic ulcers
Upper gastrointestinal bleeding
Oesophageal varices (in liver cirrhosis)
Barretts oesophagus
Oesophageal stricture
Malignancy of the oesophagus or stomach

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139
Q

What is a hiatus hernia and what are the four types?

A

Herniation of the stomach up through the diaphragm

Type 1: Sliding
Type 2: Rolling (a separate portion of the stomach (i.e., the fundus), folds around and enters through the diaphragm opening)
Type 3: Combination of sliding and rolling
Type 4: Large opening with additional abdominal organs entering the thorax (pancreas, bowel etc)

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140
Q

Investigations for hiatus hernia

A

CXR
CT
Endoscopy
Barium swallow test

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141
Q

Investigations for GORD

A

Upper GI endoscopy (OGD) if:
age > 55 years
symptoms > 4 weeks or persistent symptoms despite treatment
dysphagia
relapsing symptoms
weight loss

If endoscopy is negative consider 24-hr oesophageal pH monitoring (the gold standard test for diagnosis)

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142
Q

Management of GORD

A

Lifestyle changes
Review meds (stop NSAIDs)
Antacids (gaviscon)
PPIs (omeprazole or lansaprozole) for 4 weeks
Histamine H2-receptor antagonists (famotidine) - if inadequate response to PPIs
Surgery

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143
Q

What is the surgery for GORD called and what does it involve

A

Laproscopic fundoplication (Nissen’s) - tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.

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144
Q

What type of bacteria is H.pylori

A

Gram negative aerobic bacteria

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145
Q

Mechanism of action of H.pylori

A

H. pylori produces ammonium hydroxide, which neutralises the acid surrounding the bacteria. It also produces several toxins. The ammonia and toxins lead to gastric mucosal damage.

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146
Q

Investigations for H.pylori

A

Stool antigen test
Urea breath test using radiolabelled carbon 13
H.pylori antibody test (blood)
Rapid urease test - biopsy of stomach from endoscopy added to medium containing urea, urease enzyme from H.pylori neutralises the acid = change in colour of pH indicator

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147
Q

What is the H.pylori eradication scheme

A

Triple therapy:
PPI + 2 antibiotics (amoxicillin and clarithromycin) for 7 days

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148
Q

What is Barret’s oesophagus

A

It refers to the metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium.

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149
Q

Risk factors for Barret’s oesophagus

A

GORD
Male
Smoking
Obesity (central)

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150
Q

Symptoms for Barret’s oesphagus

A

same as GORD

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151
Q

Management of Barret’s oesophagus

A

High dose PPI
Endoscopy every 3-5 years
If dysplasia present - Radiofequency ablation
or
Endoscopic mucosal resection

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152
Q

What is Zollinger-Ellison syndrome

A

Condition characterised by excessive levels of gastrin secondary to a gastrin-secreting tumour. The majority of these tumours are found in the first part of the duodenum, with the second most common location being the pancreas.

153
Q

Triad of features for Zollinger-Ellison syndrome

A

Multiple gastroduodenal ulcers
Diarrhoea
Malabsorption

154
Q

Investigations for Zollinger-Ellison syndrome

A

Fasting gastrin levels
Secretin stiumlation test:
Gastrin levels measured –> given an injection of secretin –> Gastrin levels will be measured again –> If Zollinger-Ellison present = gastrin levels will rise dramatically

155
Q

What is the typical location of haemorrhoids (mucosal vascular cushions) in the anal canal

A

Left lateral
Right posterior
Right anterior portions of the anal canal
(3 o’clock, 7’o’clock and 11 o’clock respectively)

156
Q

Features of haemorrhoids

A

Painless rectal bleeding
Pruritus
Pain (only significant if piles are thrombosed)
Soiling may occur with thrid or fourth degree piles

157
Q

What are the two different types of haemorrhoids

A

External:
- Originate below dentate line
- Prone to thrombosis

Internal:
- Originate above dentate line
- Do not generally cause pain

158
Q

Define haemorrhoids nased on grading them from Grade I to IV

A

I - do not proplapse out of anal canal
II - prolapse on defecation but reduce spontaneously
III - can be manually reduced
IV - cannot be reduced

159
Q

Investigations for haemorrhoids

A

Based on examination
External - visible on inspection
Internal - PR exam

Proctoscopy - required for proper visualise and insepction

160
Q

Management of haemorrhoids

A

Non-surgical:

Soften stool - high fibre diet and increase fluid intake
Topical local anaesthetics (Anusol) and sterois (Anusol HC)
Germaloids cream - contain lidocaine
Proctosedyl ointment (contains cinchocaine and hydrocortisone – short term only)

Rubber band ligation
Injection sclerotherapy

Surgical:
Haemorrhoid artery ligation
Haemorrhoidectomy
Staple haemorrhoidectomy

161
Q

Features of thrombosed haemorrhoid and management of them

A

Appear as:
Purplish, very tender, swollen lumps around the anus.

Resolve with time
If extremely painful - surgery

162
Q

What type of virus is Hepatitis A

A

RNA

163
Q

What is the four stages of liver infection?

A

Incubation phase (period between coming into contact with virus and developing symptoms)

Prodromal phase (period where symptoms develop before fully developed acute illness)

Icteric phase (period of established infection)

Convalescent phase (period of recovery after acute illness)

164
Q

What is the mode of transmission of Hepatitis A

A

Faecal-oral route

165
Q

What are the symptoms of Hepatitis A

A

Incubation phase: none

Prodromal phase:
Flu like prodromol symptoms
N+V
Diarrhoea
Fever
Abdominal pain (RUQ)

Icteric phase:
Tender hepatomegaly
Jaundice
Pruritus
Dark urine
Pale stools

Convalescent phase:
Muscle weakness
Malaise
Anorexia
Hepatic tenderness

166
Q

Investigations for Hepatitis A

A

PCR test for Hepatitis A RNA
Hepatitis A virus Immunoglobulin M (HAV-IgM = produced when person is first infeced) and HAV-IgG (past exposure/immunity)

Positive IgM and Positive IgG = acute Hep A infection

Positive IgM and Negative IgG = past infection or immunity

High IgG and Moderate IgM = recent infection

LFTs = raised ALT and AST
Raised ALP (but less than 2 time normal)

167
Q

Management of Hepatitis A

A

no specific treatment as usually self limiting
Pain relied
Anti-emetics etc.

168
Q

Is there a vaccine for Hepatitis A

A

Yes

169
Q

What type of virus is Hepatitis B

A

Double-stranded DNA

170
Q

What is the mode of transmission of Hepatitis B

A

Blood or bodily fluids
E.g. sexual intercourse, sharing needles, vertical transmission (from mother to to child during pregnancy)

171
Q

What do the following markers mean?
HBsAg (surface antigen)
HBeAg (E antigen)
HBcAb (Core antibodies)
HBsAb (Surface Antibodies)
HBV DNA (Hep B DNA)

A

HBsAg = active infection (is what is injected through vaccines)

HBeAg = marker of infectivity

HBcAb = distinguishes between acute, chronic or past infection
Has two versions: IgM and IgG versions
- IgM = active infection - high titre in acute and low titre in chronic
- IgG = past ingection

HBsAb = immune response to HBsAg

HBV DNA = direct count of viral load

172
Q

What are the symptoms of Hep B

A

Asymptomatic
None specific symptom:
Fever
Malaise
Anorexia
Fatigue

Symptoms of chronic liver disease:
Palmar erythema
Spider angiomata
Asterixis
Easy bruising

Symptoms of cirrhosis and portal hypertension:
Ascites
Hepatomegaly
Splenomegaly
Peripheral oedema
Caput medusae

Extra-hepatic manifestiations:
Polyarteritis nodosa

173
Q

Investigations for Hepatitis B

A

LFTs: raised ALT and AST
ALP and GGT raised but not much
Raised AST:ALT ratio (but not more than 2)

Previous vaccine: Positive HBsAb everything else negative
Previous Infection:
Positive HBsAb, Positive HBcAb
Acute HBV:
Positive HBsAg, Positive HBcAb (IgM), negative HBsAb
Chronic Infection:
Positive HBsAg, Positive HBcAb (IgG), Negative HBsAb

FBC: Hb and MCV (to check for bleeding)
U+Es: usually normal

Synthetic function:
Albumin: reduced
Prothrombin time and INR : prolonged

174
Q

Management of Hepatitis B (Acute and Chronic)

A

Acute:
Tenofovir or Entecavir (antivirals) until HBsAg is normal

Chronic:
Antiviral therapy - first-line treatments are entecavir, tenofovir or peginterferon alfa 2a (if no cirrhosis), and entecavir or tenofovir (if cirrhosis present)

175
Q

Complications of Hepatitis B

A

Cirrhosis
HCC
FLuminant hepatic failure

176
Q

What is the treatment of Hepatitis B in pregnancy

A

Babies born to mothers who are chronically infected with hepatitis B or to mothers who’ve had acute hepatitis B during pregnancy should receive a complete course of vaccination + hepatitis B immunoglobulin

177
Q

What type of virus is Hepatitis C

A

RNA

178
Q

What is the mode of transmission of Hepatitis C

A

Blood and bodily fluids
Vertical Transmission

179
Q

Symptoms of Hepatitis C

A

Transient rise in ALT & AST
Fatigue
Arthralgia

180
Q

Investigations for Hepatitis C

A

HCV RNA

181
Q

Management of Acute and Chronic Hepatitis C

A

Combination of protease inhibitors (e.g.
Daclatasvir + sofosbuvir
or
Sofosbuvir + simeprevir
with or without ribavirin are used

182
Q

Complications of Hepatitis C

A

Eyes: Sjogrens
Rheumatological: arthralgia, arthritis
Cirrhosis
HCC

183
Q

What type of virus is Hepatitis D

A

RNA

184
Q

What is the mode of transmission of Hepatitis D

A

Blood and bodily fluids

185
Q

What disease is Hepatitis D associated with

A

Hepatitis B

186
Q

Difference between co-infection and superinfection of Hepatitis D

A

Co-infection = Hep B and D infection at same time

Superinfection = Hep B positive patient develops Heb D (associated with high risk of fluminant hepatitis, cirrhosis, chronic hepatitis)

187
Q

Investigation of Hepatitis D

A

Reverse polymerase chain reaction of hepatitis D RNA

188
Q

Treatment of Hepatitis D

A

Pegylated interferon alpha

189
Q

What type of virus is Hepatitis E

A

RNA

190
Q

Mode of transmission of Hepatitis E

A

Faecal-oral

191
Q

How many types of autoimmune hepatitis are there

A

3

192
Q

What antibodies are present in all 3 autoimmune hepaitits

A

I:
ANA (anti-nuclear antibodies)
SMA (anti-smooth muscle antibodies)

II:
LKM1 (anti-liver/kidney microsomal tpe 1 antibodies)

III:
Soluble licer-kidney antigen

193
Q

Symptoms of autoimmune hepatitis

A

Signs of chronic liver disease
Fever
Jaundice
Amenorrhoea

194
Q

Investigations for autoimmune hepatitis

A

Serum ANA/SMA/LKM1antibodies
IgG levels: raised
Liver biopsy

195
Q

Management of autoimmune hepatitis

A

Steroids - prednisolone
Immunosuppresants - azathioprine
Liver transplant

196
Q

What gender are more likely to get inguinal hernias

A

Male

197
Q

Symptoms of inguinal hernia

A

Groin lump - superior and medial to pubic tubercle (disappears on pressure/when patient lies down)
Discomfort and ache - worse with activity
Strangulation- rare

198
Q

Management of inguinal hernias

A

Mesh repair - unilateral is open and bilateral is laprascopic

199
Q

Complications of inguinal hernia repair

A

Early - bruising and wound infection
Late - chronic pain and reoccurence

200
Q

Risk factors for abdominal wall hernias

A

obesity
ascites
increasing age
surgical wounds

201
Q

What is a femoral hernia

A

Section of bowel or any other part of the abdominal viscera pass into the femoral canal via the femoral ring

202
Q

Symptoms of a femoral hernia

A

Lump in groin
Typically non-reducible
Cough impule is absent

203
Q

What gender are more likely to get femoral hernias

A

Women - during pregnancy there is increased intra-abdominal pressure

204
Q

Differentials for femoral hernia

A

Lymphadenopthy
Abscess
Femoral artery aneurysm
Hydrocoele or varicocele in males
Lipoma
Inguinal hernia

205
Q

Complications of femoral hernia

A

Incarceration - where herniated tissue cannot be reduced
Strangulation - can follow on from incarceration and is a surgical emergency
Bowel obstruction
Bowel iscaemia and resection

206
Q

Management of femoral hernia

A

Surgery - via laparotomy or laproscopic

207
Q

Symptoms of strangulated inguinal hernia

A

Pain
Fever
Increase in hernia size
Erythema of overlying skin
Guarding and localised tenderness
Bowel obstruction - distension and N+V
Bowel iscaemia - bloody stools

208
Q

What does a strangulated inguinal hernia show on bloods

A

Leukocytosis
Raised lactate

209
Q

Causes of hyposplenism

A

Sickle cell disease
Coeliac disease
Dermatitis herpatiformis
Graves’ disease
SLE
Amyloid
Splenectomy

210
Q

Symptoms of hyposplenism

A

Fever
Headache
Myalgia

211
Q

Investigations for hyposplenism

A

Blood smears:
Howell-Jelly bodies
Siderocytes

212
Q

What is postoperative/paralytic ileus

A

Complication after surgery involving extesive handling of the bowel
Results in reduction in peristalsis = pseudo-obstruction

213
Q

Symptoms of paralytic ileus

A

Abdominal distension/bloating
Abdominal pain
N+V
Inability to pass flatus
Inability to tolerate oral diet

214
Q

Differential for paralytic ileus

A

Deranged electrolytes - check K+, Mg, Phosphate
Inflammation/infection to nearby bowel
Injury to bwel

215
Q

Treatment of paralytic ileus

A

Nil-by-mouth initiall - may progress to small sips of fluid
NG tube if vomiting
IV fluids to maintain normovolaemia
TPN - required for severe/prolonged cases

216
Q

What mnemonic can be used to remember the features of ulcerative colitis

A

CLOSE UP
Continuous inflammation
Limited to colon and rectum
Only superficial mucosa affected
Smoking is protective
Excrete blood and mucus
Use aminosalicylates
Primary sclerosing cholangitis is associated

217
Q

Symtpms of ulcerative colitis

A

Diarrhoea
Abdominal pain
Rectal bleeding
Weight loss
Fatigue
Blood or mucus in the stool

218
Q

Investigations for ulcerative colitis

A

FBC - may show anaemia, leukocytosis or thrombocytosis
CRP/ESR - raised
Faecal calprotectin - raised
Colonoscopy/sigmoidoscopy + biopsy - gold standard
Abdominal and pelvic CT - for complications (abscess, strictures or perforation)

219
Q

Why would a sigmoidoscopy be preferred rather than a colonoscopy for ulcerative colitis diagnosing

A

Performing colonoscopy in patients with severe UC may cause perforations

220
Q

What would a colonoscopy show in ulcerative colitis

A

Red, raw mucosa that bleeds easily
No inflammation beyond submucosa
Widespread ulceration

221
Q

What does a barium enema show in ulcerative colitis

A

Loss of haustrations
Superficial ulceration
Pseudopolyps
Drainpipe colon - colon is narrow and short

222
Q

How do you determine the severity of a patients ulcerative colitis

A

Mild: < 4 stools/day, only a small amount of blood

Moderate: 4-6 stools/day, varying amounts of blood, no systemic upset

Severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

223
Q

What is the treatment of ulcerative colitis (inducing and maintaining remission)

A

INDUCING REMISSION
Mild-moderate UC:

Proctitis - topical aminosalicylates (mesalazine)
- if remission not achieved within 4 weeks = add an oral ASA
- if remission still not achieved add oral corticosteroid

Proctosigmoiditis:
- topical ASA
- if remission not acheived in 4 weeks then add oral ASA
- If still no remission then use oral ASA and oral corticosteroid

Extensive:
- topical ASA + oral ASA
- if no remission in 4 weeks offer oral ASA + oral corticosteroid

Severe UC:
First line = IV steroids (hydrocortisone)
IV cyclosporins is second line
If not improved within 72 hours then add IV ciclosporins to IV hydrocortisone

MAINTAINING REMISSION
- oral ASA
- topical ASA
- topical ASA + oral ASA

Severe relapse or >= 2 exacerbatopns in past year = oral azathioprine or mercaptopurine

Surgery
- Panproctocolectomy with an ileostomy or ileo-anal anastomosis (J-pouch)

224
Q

Complications of IBD

A

Colorectal cancer

225
Q

What is the mnemonic for learning the features of crohn’s disease

A

crow’s NESTS
No blood or mucus
Entire GI tract affected
Skip lesions on endoscopy
Terminal ileum most affected and Transmural inflammation
Smoking is a risk factor

226
Q

Symptoms of crohn’s disease

A

Abdominal pain
Diarrhoea
Weight loss
Perianal disease - skin tags, ulcers, anal fissures, perianal abscess or fistulas

227
Q

Investigations for crohn’s disease

A

FBC - anaemia
Vitamin B12 and D - low
Faecal calprotectin - raised
ESR/CRP - raised
Colonoscopy - deep ulcer and skip lesions - cobblestone appearance
Histology of biopsy - inflammation in all layers, goblet cells and granulomas

228
Q

What will a small bowel enema show in crohn’s disease

A

strictures: ‘Kantor’s string sign’
proximal bowel dilation
‘rose thorn’ ulcers
fistulae

229
Q

What is the treatment of crohn’s disease (inducing and maintaining remission)

A

INDUCING REMISSION
Corticosteroids - prednisolone
+ azathioprine or mercaptopurine
or
+ methotrexate
or
+ infliximab or adalimumab
2nd line to corticosteroids = ASA
+ enteral nutrition

MAINTAINING REMISSION
First line = azathioprine or mercaptopurine
2nd line = methotrexate

Surgery
- Distal ileum resection
- Treating strictures
- Treating fistulas

230
Q

What do you assess before offering azathioprine or mercaptopurine

A

Thiopurine methyltransferase (TPMT) activity

231
Q

Complications of crohn’s disease

A

Colorectal cancer
Small bowel cancer
Osteoporosis

232
Q

How do you make a diagnosis of IBS

A

Abdominal pain or discomfort present for at least 6 months and:
- Is either relieved by defecation or associated with altered bowel frequency or stool form
Plus at least 2 of the following:
- Altered stool passage (straining, urgency, incomplete evacuation)
- Abdominal bloating, distension, hardness or tenison
- Made worse by eating
- Passage of mucus

233
Q

Extra-instestinal features of IBS

A

Lethargy
Nausea
Back pain
Headache

234
Q

Investigations for IBS

A

FBC - check for anaemia
ESR/CRP - check for IBD
Anti-TTG/EMA - for coeliacs

235
Q

Treatment for IBS

A

Diarrhoea - loperamide
Constipation - bulk-forming laxatives (isaghula husk) - LINACLOTIDE is alternative
Cramps - antispasmodics (mebeverine, hyoscine butylbromide) - TCAs (amitriptilyine) is second line then SSRIs (citalopram)
CBT

236
Q

What dietary advice can you give someone for IBS

A

Regular meals and take time
Avoid missing meals
Drink at least 8 cups of water
Restrict caffeine (tea and coffee) and alcohol
Consider high fibre diet

237
Q

What is mesenteric adenitis?

A

Inflamed lymph nodes within the mesentery
It can cause similar symptoms to appendicitis

238
Q

What is malnutrition defined as

A

BMI of less than 18.5 OR
unintentional weight loss greater than 10% within the last 3-6 months OR
a BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months

239
Q

What tool is used for screening for malnutrition and what is included in it

A

MUST (Malnutrition Universal Screening Tool)
Takes into account BMI, recent weight change and the presence of acute disease

240
Q

Managment of malnutiriton

A

Dietician support
Food first approach
Oral nutritional supplements

241
Q

Are gastric ulcers or duodenal ulcers more common

A

Duodenal

242
Q

What are the risk factors for peptic ulcers

A

H.pylori infection
NSAIDs
Stress
Alcohol
Caffeine
Smoking
Spicy foods

243
Q

What medications increase the risk of a peptic ulcer bleeding

A

NSAIDs
Aspirin
Anticoagulants (DOACs)
Steroids
SSRIs

244
Q

What are the symptoms of peptic ulcers

A

Epigastric pain
N+V
Duodenal ulcers - epigastric pain when hungry relieved by eating
Gastric ulcers - epigastric pain worsened by eating

245
Q

Investigations for peptic ulcers

A

H.pylori testing - urease breath test or stool antigen test
Endoscopy (OGD)

246
Q

Management of peptic ulcers

A

Stopping NSAIDs
PPIs (lansoprazole or omeprazole) - if H.pylori -ve
Treating H.pylore infections - triple therapy = PPI + 2 antibiotics (amoxicillin and clarithromycin) for 7 days

247
Q

Complications of peptic ulcer disease

A

Bleeding
Perforation

248
Q

What artery is the source of bleeding in peptic ulcer disease

A

Gastroduodenal artery

249
Q

Symptoms of a bleeding associated with peptic ulcer disease

A

Haematemesis
Coffee ground vomiting
Melaena
Hypotension
Tachycardic

250
Q

Treatment for a GI bleed associated with peptic ulcer disease

A

ABCDE approach
IV PPIs
1st line = endoscopic intervention
2nd line = urgent interventional angiograpy with transarterial embolisation
OR surgery

251
Q

Symptoms of a perforation associated with peptic ulcer disease

A

Epigastric pain which becomes more generalised
Syncope

252
Q

Investigation and treatment for a perforation associated with peptic ulcer disease

A

Erect CXR - free air under the diaphragm

Treatment - surgery

253
Q

What viruses commonly cause viral gastroenteritis

A

Rotavirus
Norovirus
Adenovirus (tends to cause respiratory symptoms)

254
Q

What bacterial organisms can cause gastroenteritis

A

E.coli
Campylobacter Jejuni
Shigella
Salmonella
Bacillus Cereus
Yersinia Enterocolitica
Staphylococcus Aureus

255
Q

What parasite can cause gastroenteritis

A

Giardiasis

256
Q

What are the symptoms of gastroenteritis

A

Abdominal pain/cramps
Diarrhoea (at least 3 times in 24 hours)
N+V
Fever
General malaise

257
Q

What gastroenteritis-causing bacteria produce the Shiga toxin

A

E.coli 0157
shigella

258
Q

What bacteria can cause bloody diarrhoea in the context of gastroenteritis

A

E.coli
Shigella
Amoebiasis

259
Q

What bacteria can cause Haemolytic Uraemic Syndrome in the context of gastroenteritis

A

Shiga toxin producing organisms:
E.coli 0157
Shigella

260
Q

Investigations for gastroenteritis

A

Clinical diagnosis but can consider:
Stool culture and sensitivity

261
Q

What is the treatment of gastroenteritis for the following causative organisms:
C.jejuni
Giardiasis
(Other organisms do not require antibiotics)

A

Oral rehydration salt (ORS) - diaoralyte
C.jejuni = clarithromycin (if severe symptoms i.e. high fever, bloody and/or high output diarrhoea)
Giardiasis = metronidazole 2000mg once daily for 3 days

262
Q

What are possible complications of gastroenteritis

A

Lactose intolerance
IBS
Reactive arthritis
Guillain–Barré syndrome
Haemolytic uraemic syndrome

263
Q

How is C.jejuni spread

A

Raw or improperly cooked poultry
Untreated water
Unpasteurised milk

264
Q

How is salmonella spread

A

Eating raw eggs or poultry

265
Q

How is Bacillus Cereus spread

A

It grows on food not immediately refrigerated after cooking (e.g., fried rice or cooked pasta left at room temperature)
Produces cerulide toxin

266
Q

What gastroenteritis causing organism can mimic appendicitis

A

Yersinia Enterocolitica
Can present with right sided abdominal pain (mesenteric lymphadenitis) and fever

267
Q

What is a volvulus

A

Torsion of the colon around it’s mesenteric axis resulting in compromised blood flow and closed loop obstruction.

268
Q

What are the 2 types of volvulus

A

Sigmoid volvulus - more common in older patients and caused by chronic constipation
Caecum volvulus - more common in younger patients

269
Q

What are the symptoms of a volvulus

A

Constipation
Abdominal bloating
Abdominal pain
N+V (green bilious vomiting)

270
Q

Investigations for volvulus

A

Abdominal film (X-ray) - coffee bean sign (dilated and twisted sigmoid colon looks like a giant coffee bean)
Large, dilated loop of colon, often with air-fluid levels
Contrast CT

271
Q

Management of volvulus

A

Nil by mouth, NG tube, IV fluids
Sigmoid volvulus: rigid sigmoidoscopy with rectal tube insertion
Caecal volvulus: management is usually operative. Right hemicolectomy is often needed

272
Q

What is the most common site of pancreatic cancers?

A

Head of pancreas

273
Q

What are the risk factors for pancreatic cancer

A

Increased age
Smoking
Diabetes
Chronic pancreatitis
BRCA2 gene
KRAS gene
Hereditary non-polyposis colorectal carcinoma
Multiple endocrine neoplasia

274
Q

Symptoms of pancreatic cancer

A

Painless jaundice - pale stools, dark urine, pruritus
Hepatomegaly, Gallbladder, Epigastric mass may be palpable
Steatorrhea - loss of exocrine function
Diabetes - loss of endocrine function
Atypical back pain
Migratory thrombophlebitis

275
Q

Investigation for pancreatic cancer

A

CT abdomen for diagnosis and staging (CT CAP)
CA19-9
MRCP - assess obstruction
ERCP - for stent insertion and obtain biopsies
Biopsy

276
Q

Management of pancreatic cancer

A

Surgery to remove tumour:
Total pancreatectomy
Distal pancreatectomy
Pylorus-preserving pancreaticoduodenectomy (PPPD) (modified Whipple procedure)
Radical pancreaticoduodenectomy (Whipple procedure) - Head of pancreas, pylorus, duodenum, gallbladder, bile duct, lymph nodes all removed

Also:
Stent insertion - for palliation
Chemotherapy
Radiotherapy

277
Q

What is the most common type of oesophageal cancer

A

Adenocarcinoma (near the gastroesophageal junction)

278
Q

What are the two types of oesophageal cancer

A

Adenocarcinoma - lower two thirds
Squamous cell carcinoma - upper two thirds

279
Q

What are the risk factors of oesophageal adenocarcinoma

A

GORD
Barret’s oesophagus
Smoking
Obesity

280
Q

What are the risk factors for oesophageal squamous cell carcinoma

A

Smoking
Alcohol
Achalasia
Plummer-Vinson syndrome
Diets rich in nitrosamines

281
Q

Symptoms of oesophageal cancer

A

Dysphagia
Anorexia
Weight loss
Vomiting
Odynophagia
Hoarse voice
Melaena
Cough

282
Q

Investigations for oesophageal cancer

A

Upper GI endoscopy
Endoscopic ultrasound - for locoregional staging
CT CAP - initial staging

283
Q

Treatment of oesophageal cancer?

A

Surgical resection - Ivor-Lewis esophagectomy
Adjuvant chemotherapy

284
Q

Causes of generalised abdominal pain

A

Peritonitis
Ruptured abdominal aortic aneurysm
Intestinal obstruction
Ischaemic colitis

285
Q

Causes of right upper quadrant pain

A

Biliary colic
Acute cholecystitis
Acute cholangitis

286
Q

Causes of epigastric pain

A

Gastritis
Peptic ulcer disease
Pancreatitis
Ruptured AAA

287
Q

Causes of central abdominal pain

A

Ruptured AAA
Intestinal obstruction
Ischaemic colitis
Early stages of appendicitis

288
Q

Causes of right iliac fossa pain

A

Acute appendicitis
Ectopic pregnancy
Ruptured ovarian cyst
Ovarian torsion
Meckel’s diverticulitis

289
Q

Causes of left iliac fossa pain

A

Diverticulitis
Ectopic pregnancy
Ruptured ovarian cyst
Ovarian torsion

290
Q

Causes of suprapubic pain

A

Lower urinary tract infection
Acute urinary retention
Pelvic inflammatory disease
Prostatitis

291
Q

Causes of loin to groin pain

A

Renal colic (kidney stones)
Ruptured AAA
Pyelonephritis

292
Q

Symptoms of spontaneous bacterial peritonitis

A

Ascites
Abdominal pain
Fever

293
Q

Investigations for spontaneous bacterial peritonitis

A

Paracentesis - neutrophil count over 250 cells/ul

294
Q

Most common organism causing spontaneous bacterial peritonitis

A

E.coli

295
Q

Management of spontaneous bacterial peritonitis

A

IV cefotaxime

296
Q

What is haemochromatosis

A

Autosomal recessive genetic condition resulting in iron overload. There is excessive total body iron and deposition of iron in tissues.

297
Q

Symptoms of haemochromatosis

A

Lethargy
Joints - arthralgia, arthritis
Gonads - erectile dysfunction, menstrual irregularities
Abdominal pain
Mood disturbances

298
Q

Complications of haemochromatosis

A

Skin - bronze pigmentation
Pancreas - diabetes mellitus
Liver - features of chronic liver disease: hepatomegaly, cirrhosis
Heart - cardiomyopathy
Joints - arthritis in the hand specifically - ‘iron fist’ sign
Gonads - hypogonadism

299
Q

Investigations for haemochromatosis

A

Serum ferritin - raised
Transferrin saturation - raised
Genetic testing - for HFE gene
LFTs
Liver biopsy
MRI - helps visualise iron concentration in liver

300
Q

Management of haemochromatosis

A

Venesection - aim for transferrin saturation below 50% and serum ferritin concentration below 50ug/l
Desferrioxamine - second line

301
Q

What is Wilson’s disease

A

Autosomal recessive genetic condition resulting in the excessive accumulation of copper

302
Q

Symptoms of Wilson’s disease

A

Liver: hepatitis and cirrhosis
Neurological:
- Tremor
- Dystonia
- Parkinsonism - tremor, bradykinesia, rigidity
Psychiatric:
- Abnormal behaviour
- Depression
- Psychosis
- Cognitive impairment
Kayser-Fleischer ring in cornea
Can also have Haemolytic anaemia and Renal tubular acidosis

303
Q

Investigations for Wilson’s disease

A

Slit lamp examination - for Kayser-Fleischer ring
Serum caeruloplasmin (carries copper in the blood)- reduced
Total serum copper - reduced (As all is bound to caeruloplasmin)
Free serum copper - raised
24hr urinary copper excretion - raised
Genetic analysis

304
Q

Management of Wilson’s disease

A

Penicillamine - chelates copper
Trientine hydrocholoride - second line chelating agent
Zinc salts (inhibit copper absorption in the gastrointestinal tract)

305
Q

How is diarrhoea defined

A

> 3 loose or watery stool per day

306
Q

What are the acute causes of diarrhoea

A

Gastroenteritis
Diverticulitis
Antibiotics
Constipation causing overflow

307
Q

Chronic causes of diarrhoea

A

IBS
IBD
Colorectal cancer
Coeliac disease

308
Q

Define constipation

A

Less than 3 stools a week
Hard stools that are difficult to pass
Rabbit dropping stools
Straining and painful passages of stools

309
Q

What is the management of constipation

A

Treat underlying cause
Increase dietary fibe
Ensure adequate fluid intake
Ensure adequate activity levels

1st Line = bulk-forming laxative - ispaghula
2nd Line = osmotic laxative - macrogol

310
Q

Complications of constipation

A

Overflow diarrhoea
Acute urinary retention
Haemorrhoids

311
Q

What is Gilbert’s Syndrome

A

Autosomal recessive condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase.

312
Q

Feature of Gilbert’s syndrome

A

Unconjugated hyperbilirubinemia (i.e. not in urine)
Jaundice may only be seen during an intercurrent illness, exercise or fasting

313
Q

What are the risk factors for developing hepatocellular carcinoma

A

Alcohol-related liver disease
Non-alcoholic fatty liver disease (NAFLD)
Hepatitis B
Hepatitis C
Rarer causes (e.g., primary sclerosing cholangitis)

314
Q

What is the tumour marker for HCC

A

AFP - alpha-fetoprotein

315
Q

How often are patients with liver cirrhosis screened for HCC? What tests does this include?

A

Every 6 months
Ultrasound
Alpha-fetoprotein (AFP)

316
Q

Symptoms of HCC

A

Tends to present late
Jaundice
RUQ pain
Ascites
Hepatomegaly
N+V
Pruritis
Weight loss

317
Q

Investigations for HCC

A

Ultrasound
AFP
CT and MRI for staging
Biopsy

318
Q

Management of HCC

A

Surgical resection - for early disease
Liver transplant
Radiofrequency ablation
Transarterial chemoembolisation (TACE)
Sorafenib: a multikinase inhibitor

319
Q

Causes of cirrhosis

A

Alcohol-related liver disease
Non-alcoholic fatty liver disease (NAFLD)
Hepatitis B
Hepatitis C
Autoimmune hepatitis
Primary biliary cirrhosis
Haemochromatosis
Wilsons disease
Alpha-1 antitrypsin deficiency
Cystic fibrosis

320
Q

What are the examination findings of liver cirrhosis

A

Cachexia (wasting of the body and muscles)
Jaundice caused by raised bilirubin
Hepatomegaly (enlargement of the liver)
Small nodular liver as it becomes more cirrhotic
Splenomegaly due to portal hypertension
Spider naevi (telangiectasia with a central arteriole and small vessels radiating away)
Palmar erythema caused by elevated oestrogen levels
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising due to abnormal clotting
Excoriations (scratches on the skin due to itching)
Ascites (fluid in the peritoneal cavity)
Caput medusae (distended paraumbilical veins due to portal hypertension)
Leukonychia (white fingernails) associated with hypoalbuminaemia
Asterixis (“flapping tremor”) in decompensated liver disease

321
Q

What does a non-invasive liver screen consist of

A

Ultrasound - to diagnose fatty liver
Hepatitis B and C serology
Autoantibodies - autoimmune hepatitis, PBC, PSC
Immunoglobulins
Caeruloplasmin
Alpha-1-antitrypsin levels
Ferritin and Transferrin saturation

322
Q

What will LFTs look like in decompensated cirrhosis

A

Raised Bilirubin, ALT, AST, ALP
Low albumin
Increased PT time
Thrombocytopenia
Hyponatraemia - occurs with fluid retention

323
Q

What does the enhanced liver fibrosis (ELF) blood test test for

A

Fibrosis in NAFLD

324
Q

What are the enhanced liver fibrosis blood test ranges

A

10.51 or above – advanced fibrosis
Under 10.51 – unlikely advanced fibrosis (NICE recommend rechecking every 3 years in NAFLD)

325
Q

What does an ultrasound show in liver cirrhosis

A

Nodularity on surface
‘corkscrew’ appearance to hepatic arteries
Enlarged portal vein with reduced flow
Ascites
Splenomegaly

326
Q

Who is a fibroscan recommended for

A

Patients at risk of cirrhosis:
Chronic Hepatitis B and C
ARLD
Heavy alcohol drinkers
NAFLD

327
Q

What does the Child-Pugh score assess?

A

Assesses the severity of cirrhosis and prognosis

328
Q

What is used in the Child-Pugh score

A

ABCDE mnemonic
Albumin
Bilirubin
Clotting - INR
Dilation - ascites
Encephalopathy

329
Q

What are the 6 complications of liver cirrhosis

A

Malnutrition
Portal hypertension
Varices (bleeding varices possible)
Ascites
SBP
Hepatorenal syndrome
Hepatic encephalopathy

330
Q

How does cirrhosis cause malnutrition and how to treat it

A

Reduced appetite
Deranged protein metabolism and production in the liver
Deranged glucose storage and glycogen storage
Regular meals
High protein and calorie intake
Avoid alcohol

331
Q

what is the most common site of varices due to liver cirrhosis

A

Distal oesophagus (oesophageal varices)
Anterior abdominal wall (caput medusae)

332
Q

How to treat oesophageal varices

A

Prophylactic beta blockers - propranolol
Variceal band ligation - if BB contraindicated

333
Q

How to treat bleeding oesophageal varices

A

Blood transfusion
Treat any coagulopathy (e.g., with fresh frozen plasma)
Vasopressin analogues (e.g., terlipressin or somatostatin)
Prophylactic broad-spectrum antibiotics (shown to reduce mortality)
Urgent endoscopy with variceal band ligation
Consider intubation and intensive care
TIPS

334
Q

How to manage ascites

A

Low sodium diet
Aldosterone antagonists (e.g., spironolactone)
Paracentesis (ascitic tap or ascitic drain)
Prophylactic antibiotics (ciprofloxacin or norfloxacin) when there is <15 g/litre of protein in the ascitic fluid
Transjugular intrahepatic portosystemic shunt (TIPS) is considered in refractory ascites
Liver transplantation is considered in refractory ascites

335
Q

How does hepatorenal syndrome develop in patients with cirrhosis

A

Portal hypertension causes the portal vessels to release vasodilators, which cause significant vasodilation in the splanchnic circulation (the vessels supplying the gastrointestinal organs). Vasodilation leads to reduced blood pressure. The kidneys respond to the reduced pressure by activating the renin-angiotensin-aldosterone system, which leads to vasoconstriction of the renal vessels. Renal vasoconstriction combined with low systemic pressure results in the kidneys being starved of blood and significantly reduced kidney function.

336
Q

How does cirrhosis cause hepatic encephalopathy

A

Build up of ammonia - produced by intestinal bacteria

337
Q

What factors can trigger or worsen hepatic encephalopathy

A

Constipation
Dehydration
Infection
High protein diet

338
Q

Management of hepatic encephalopathy

A

Lactulose - to prevent constipation
Rifaximin - reduced number of intestinal bacteria producing ammonia

339
Q

What is the MELD score used for and what is included in the scoring system?

A

The MELD score estimates a patient’s chances of surviving their disease during the next three months

Includes:
Bilirubin
Creatinine
INR

340
Q

What is the MELD score used for and what is included in the scoring system?

A

The MELD score estimates a patient’s chances of surviving their disease during the next three months

Includes:
Bilirubin
Creatinine
INR

341
Q

What is the difference between compensated and decompressed liver cirrhosis

A

Compensated: liver is still able to function relatively well, despite scarring from the disease
Decompensated: liver is no longer able to function properly, and patients experience serious symptoms and complications

342
Q

What is the difference between compensated and decompressed liver cirrhosis

A

Compensated: liver is still able to function relatively well, despite scarring from the disease
Decompensated: liver is no longer able to function properly, and patients experience serious symptoms and complications

343
Q

What are the three stages of non-alcoholic fatty liver disease

A

Steatosis
Steatohepatitis
Cirrhosis

344
Q

Risk factors for non-alcoholic fatty liver disease

A

Obesity
T2DM
Hyperlipidaemia
Sudden weight loss/starvation
Jejunoileal bypass

345
Q

What are the symptoms of NAFLD?

A

Hepatomegaly
ALT greater than AST
Increased echogenicity on liver ultrasound

346
Q

Management of NAFLD

A

Lifestyle changes (particularly weight loss) and monitoring

347
Q

What are the oesophageal causes of an upper GI bleed?

A

Oesophageal varices
Oesophagitis
Cancer
Mallory-Weiss tear

348
Q

What are the gastric causes of an upper GI bleed?

A

Gastritis
Gastric cancer

349
Q

What are the duodenal causes of an upper GI bleed?

A

Duodenal ulcer
Aorta-enteric fistula

350
Q

What scoring systems are used for upper GI bleeds and what is included in them?

A

Blatchford bleeding score - helps clinicians decide whether patients can be managed as outpatients or not
Includes:
Hb
Urea
Initial systolic BP
Sex
Heart rate > 100
Malaena present
Recent syncope
Hepatic disease history
Cardiac failure present

Rockfall scoring system - provides a percentage risk of rebleeding and mortality
Includes:
Age
Shock
Comorbidities
Diagnosis
Major stigmata of recent haemorrhage

351
Q

How to treat an upper GI bleed

A

ABCDE approach with wide bore cannula access
Platelet transfusion if actively bleeding
FFP for patients with reduced fibrinogen or prolonged PT time

Endoscopy after ABCDE

If non-variceal bleed then: give PPIs
If variceal bleed:
Terlipressin
Band ligation
TIPS - if not controlled with above

352
Q

What are the extra-intestinal manifestations of IBD?

A

Erythema nodosum
Pyoderma gangrenosum
Inflammatory arthritis
Scleritis
Uveitis
Primary sclerosing cholangitis (more so with UC)

353
Q

What is infectious colitis

A

Colonic infection by bacteria, viruses, or parasites

354
Q

What are the common causative organisms of infectious colitis

A

Bacterial:
C.jejuni
Salmonella
E.coli
Shigella

Viral:
Norovirus
Rotavirus
Adenovirus
CMV

Parasitic:
Entamoeba

STDs:
Neisseria gonorrhoeae
Chlamydia trachomatis
Herpes simplex 1 and 2

355
Q

Investigations for infectious colitis

A

Stool MCS
FBC
ESR/CRP

356
Q

Treatment for infectious colitis

A

Treat according to causative agent

357
Q

What organism causes rice water stools

A

Cholera

358
Q

Define bowel obstruction

A

When the passage of food, fluids and gas through the intestines becomes blocked

359
Q

What is third-spacing

A

Abnormal loss of fluid in bowel obstruction. GI tract releases fluids which are later reabsorbed in the colon. If there is a blockage, they cannot be reabsorbed meaning fluid is lost from the intravascular space into the GI tract. This leads to hypovolemia and potentially shock.

360
Q

What are the three main causes of bowel obstruction

A

Hernias
Malignancies (tumor)
Adhesions

361
Q

What is the most common cause of large bowel obstruction

A

Tumors - most common
Volvulus
Diverticular disease

362
Q

What is the most common cause of small bowel obstruction

A

Adhesions
followed by hernias

363
Q

What are the 4 main causes of intestinal adhesion

A

Abdominal or pelvic surgery
Peritonitis
Abdominal or pelvic infection (e.g. PID)
Endometriosis

364
Q

Define a closed loop obstruction

A

Where there are two points of obstruction along the bowel, meaning the middle section is sandwiched between the two obstructions

365
Q

What are the causes of a closed loop obstruction

A

Adhesions
Volvulus
Hernias
A single point of obstruction in the large bowel with a competent ileocaecal valve (the valve doesn’t allow contents to pass back through it)

366
Q

What are the symptoms of large bowel obstruction

A

Absence of passing stools or flatus
Abdominal pain
Abdominal distension
N+V
Peritonism - if bowel perforation is present

367
Q

What are the symptoms of small bowel obstruction

A

Diffuse central abdominal pain
N+V (typically bilious vomiting)
Constipation and lack of flatulence
Abdominal distension (more apparent in lower level obstructions)
Tinkling bowel sounds

368
Q

Investigations for bowel obstruction

A

Abdominal X-ray - 1st line
CT scan - gold standard
U&Es - assess electrolytes
VBG - metabolic acidosis due to vomiting stomach acid
Lactate - raised due to bowel ischaemia

369
Q

What is shown on an x-ray in small bowel obstruction

A

Distended small bowel loops with fluid levels
Consider dilated if the small bowel is >3cm in diameter

370
Q

What is shown on an x-ray in large bowel obstruction

A

Diameter greater than the normal diameter limits, which are:
Caecum: 10-12cm
Ascending colon: 8cm
Recto-sigmoid colon: 6.5cm

371
Q

What might indicate bowel perforation on an abdominal x-ray

A

The presence of free intra-peritoneal gas (air under the diaphragm) indicates colonic perforation

372
Q

What are the normal limits for the diameter of the small bowel, caecum, ascending colon and recto-sigmoid colon and why are these relevant

A

Small bowel: 3m
Caecum: 10-12cm
Ascending colon: 8cm
Recto-sigmoid colon: 6.5cm

They are relevant as anything over this might indicate bowel obstruction

373
Q

What is the initial management of bowel obstruction

A

‘Drip and suck’:
Nil by mouth
IV fluids
NG tube with free drainage

374
Q

What is the management of bowel obstruction if the initial management is not successful

A

Surgery, to either:
Find the cause with explorative surgery
To treat adhesions - adhesiolysis
Hernia repair
Emergency resection of the obstructing tumour (or stents to push tumour out of the way)

375
Q

What would the management of bowel obstruction be if there was a perforation as well

A

Emergency surgery
IV antibiotics

376
Q

What is achalasia

A

Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus i.e. LOS contracted, oesophagus above dilated

377
Q

Symptoms of achalasia

A

Dysphagia of both liquids and solids
Heartburn
Regurgitation of foods - may lead to cough or aspiration pneumonia

378
Q

Investigations for achalasia

A

Oesophageal manometry - excessive LOS tone which doesn’t relax on swallowing
Barium swallow - bird beak appearance
CXR - wide mediastinum and fluid level

379
Q

Treatment of achalasia

A

Pneumatic (balloon) dilation
Surgery - Heller cardiomyotomy
Intra-sphincteric injection of botulinum toxin

Phase 4 - GI, MSK, Infectious Diseases (3 decks)

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