Gastrointestinal Flashcards

(449 cards)

1
Q

Define achalasia.

A
  • Oesophageal motility disorder
  • Loss of co-ordinated peristalsis
  • Failure of relaxation of the lower oesophageal sphincter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Explain the aetiology / risk factors of achalasia.

A
  • Degeneration of ganglion cells of myenteric plexus
  • In oesophagus
  • Cause = unknown

Risk factors

  • Herpes
  • Measles
  • Autoimmune disease
  • HLA Class I antigens
  • Consanguineous parents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Summarise the epidemiology of achalasia.

A
  • 1 in 100,000 (annual)
  • 25-60 years

Oesophageal infection “Trypanosoma cruzi” in Central/South America produces similar disorder = Chages’ disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Recognise the presenting symptoms of achalasia.

A
  • Intermittent dysphagia (solids & liquids)
  • Difficulty belching
  • Regurgitation
  • Heartburn
  • Chest pain (atypical, cramping, retrosternal)
  • Weight loss

Insidious onset & gradual progression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Recognise the signs of achalasia on physical examination.

A
  1. CXR
  2. Barium swallow
  3. Endoscopy
  4. Manometry

CXR

  • widened mediastinum, double right heart border –> dilated oesophagus
  • Air-fluid level in upper chest
  • Absence of gastric air bubble

Barium swallow

  • Dilated oesophagus
  • Tapers down to the sphincter –> beak shaped

Endoscopy
- Done to exclude malignancy, does mimic

Manometry

  • Elevated resting lower oesophageal sphincter pressure (>45mmHg)
  • Incomplete relaxation of lower oesophageal sphincter
  • Absence of peristalsis in distal (smooth muscle) oesophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Identify appropriate investigations for achalasia and interpret the results.

A
  1. CXR
  2. Barium swallow
  3. Endoscopy
  4. Manometry

CXR

  • widened mediastinum, double right heart border –> dilated oesophagus
  • Air-fluid level in upper chest
  • Absence of gastric air bubble

Barium swallow

  • Dilated oesophagus
  • Tapers down to the sphincter –> beak shaped

Endoscopy
- Done to exclude malignancy, does mimic

Manometry

  • Elevated resting lower oesophageal sphincter pressure (>45mmHg)
  • Incomplete relaxation of lower oesophageal sphincter
  • Absence of peristalsis in distal (smooth muscle) oesophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define acute cholangitis.

A
  • Inflammation of the common bile duct
  • Leads to obstruction
  • Leads to conjugated bilirubin buildup –> jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Explain the aetiology / risk factors of acute cholangitis.

A
  • Due to infected stone in common bile duct
  • Due to spread from infected gallbladder (cholecystitis)

Risk factors

  • Age >50 yrs
  • Cholelithiasis -
  • Benign or Malignant stricture
  • Post-procedure injury of bile ducts
  • Primary or Secondary sclerosing cholangitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Summarise the epidemiology of acute cholangitis.

A

1% of patients with cholelithiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Identify appropriate investigations for acute cholangitis and interpret the results.

A

Blood cultures - to establish the identity and antibiotic sensitivities of infective bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Generate a management plan for acute cholangitis.

A
  1. Blood cultures
  2. Antibiotics
  3. Endoscopic Retrograde Cholangiopancreatography (ERCP) drainage
  4. Monitoring

Blood cultures
- Establish the identity and antibiotic sensitivities of the infective bacteria

Antibiotics
- Broad-spectrum until exact sensitivities identified

ERCP Drainage

  • Physical drainage
  • Endoscope passed via oesophagus into duodenum
  • Catheter passed via sphincter of Oddi and into common bile duct
  • Pus is drained and sent for culturing
  • Small basket trawled through common bile duct to remove obstructing calculi/sludge
  • Sphincterotomy to aid further calculi/sludge passage
  • If ERCP fails - percutaneous transhepatic cholangiography (PTC)

Monitoring

  • Post-drainage keep in hospital
  • Antibiotics
  • Nil-by mouth
  • IV fluids
  • Analgesia
  • Monitor vital signs for sepsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Summarise the prognosis for patients with acute cholangitis.

A
  • Infection is not confined to gallbladder
  • Infection can spread up the common bile duct to the liver and systemic circulation

= ascending cholangitis

Untreated high mortality (10-30%)

ERCP only temporary fix - need elective cholecystectomy to prevent reoccurance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define alcohol withdrawal.

A
  • Withdrawal on cessation of alcohol
  • Tolerance
  • Compulsion to drink, difficulty controlling termination or levels of use
  • Persistent desire to cute down or control use
  • Time spent obtaining, using or recovering from alcohol
  • Neglect of other interests (social, occupational, recreational)
  • Continued use despite physical and psychological problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Explain the aetiology / risk factors of alcohol withdrawal.

A
  • Genetic factors (twin & family history - 1 in 3 with parent)
  • Cultural
  • Parental
  • Peer group influences
  • Availability of alcohol
  • Occupation - increased risk in publicans, doctors, lawyers
  • Depression
  • Anxiety
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Summarise the epidemiology of alcohol withdrawal.

A

2-9% of US (2004)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Recognise the presenting symptoms of alcohol withdrawal.

A

CAGE

  • Cut-down?
  • Annoyed by criticism?
  • Guilt?
  • Eye-opener (wake up)?

Withdrawal

  • Nausea
  • Sweating
  • Tremor
  • Restlessness
  • Agitation
  • Visual hallucination
  • Confusion
  • Seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Recognise the signs of alcohol withdrawal.

A
  • Duputreyn’s contracture
  • Palmar erythema
  • Bruising
  • Spider naevi
  • Tel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Recognise the signs of alcohol withdrawal.

A
  • Dupuytren’s contracture
  • Palmar erythema
  • Bruising
  • Spider naevi - spider veins with central red spot
  • Telangiectasia - spider veins
  • Facial mooning
  • Bilateral parotid enlargement
  • Gynaecomastia
  • Smell of alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Identify appropriate investigations for alcohol withdrawal and interpret the results.

A
  1. Bloods
  2. Acute Overdose

Blood

  • Raised MCV
  • Raised GGT
  • Raised transaminases
  • Raised uric acid, triglycerides, bilirubin, albumin, PT in liver

Acute Overdose

  • Blood alcohol
  • Glucose
  • ABG - risk of ketoacidosis or lactic acidosis
  • VBG
  • U&E
  • Toxic screen - e.g. barbiturates, paracetamol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Generate a management plan for alcohol withdrawal.

A
  • I.V. Vitamin B complex (Pabrinex)
  • Reducing doses of chlordiazepoxide
  • Watch dehydration, electrolyte imbalances, infections
  • Nutritional support (malnourishment)
  • Lactulose & phosphate enemas - help encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Identify the possible complications of alcohol withdrawal and its management.

A
  • Fits
  • Delirium tremors - coarse tremor, agitation, fever, tachycardia, confusion, delusions, hallucinations
  • Cerebral atrophy
  • Dementia
  • Cerebellar degeneration
  • Optic atrophy
  • Peripheral neuropathy
  • Myopathy
  • Hepatic encephalopathy
  • Thiamine deficiency
  • Wernicke’s Encephalopathy
  • Korsakoff’s Psychosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Summarise the prognosis for patients with alcohol withdrawal.

A

Depends on complications.
Alcoholic fatty liver - reversible with abstinence.

5 year rate of alcoholic cirrhosis is 60-70% if stop drinking, <40% if continue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Define Wernicke’s Encephalopathy.

A
  • Nystagmus
  • Ophthalmoplegia
  • Ataxia
  • Apathy
  • Disorientation
  • Disturbed memory

Treatment: Thiamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Define Korsakoff’s Psychosis.

A

Profound impairment of retrograde and anterograde memory with confabulation, due to damage to mammillary bodies and hippocampus.

Irreversible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Define alcoholic hepatitis.
Inflammatory liver injury caused by chronic heavy intake of alcohol.
26
Explain the aetiology / risk factors of alcoholic hepatitis.
- Due to excessive intake of alcohol - Centrilobular balooning degeneration and necrosis of hepatocytes - Steatosis - Neutrophilic inflammation - Cholestasis - Mallory hyaline inclusions - eosinophilic intracytoplasmic aggregates of cytokeratin intermediate filaments - Giant mitochrondria Risk factors: - Heavy alcohol intake (15-20 years) - Female - more florid illness than men - Trigger event (e.g. aspiration pneumonia, injury)
27
Summarise the epidemiology of alcoholic hepatitis.
10-35% of heavy drinkers.
28
Recognise the presenting symptoms of alcoholic hepatitis.
1. Asymptomatic 2. Mild Illness - Nausea - Malaise - Epigastric or right hypochondrial pain - Low grade fever 3. Severe Illness - Jaundice - Abdominal discomfort or swelling - Swollen ankles - GI bleeding
29
Recognise the signs of alcoholic hepatitis on physical examination.
- Febrile - Tachycardia - Jaundice - Bruising - Encephalopathy - e.g. hepatic foetor, liver flap, drowsiness, unable to copy 5 pointed star, disorientated - Ascites - Hepatomegaly - Splenomegaly
30
Identify appropriate investigations for alcoholic hepatitis and interpret results.
1. Blood 2. Ultrasound Scan - for other causes - e.g. malignancy 3. Upper GI Endoscopy - for varices 4. Liver biopsy - percutaneous, transjugular to distinguish cause 5. Electroencephalogram - for slow-wave activity (indicates encephalopathy) Blood - FBC - low Hb, high MCV, high WCC, low platelets - LFT - high transaminases, high bilirubin, low albumin, high AlkPhos, high GGT - U&E - low Urea & K+ - Prolonged PT
31
Generate a management plan for alcoholic hepatitis.
1. Thiamine, Vit C, multivitamins (parenterally) 2. Monitor and correct K+, Mg2+, glucose 3. Ensure adequate urine output Encephalopathy - treat with oral lactulose and phosphate enemas. Ascites - diuretics (spironolactone, furosemide), therapeutic paracentesis (body fluid sampling using needle) Hepatorenal Syndrome - glypressin, N-acetylcysteine 4. Nutrition - Oral or NG feeding - Increased calories - Avoid protein restriction (unless encephalopathic) - Consider total enteral nutrition = decreased mortality 5. Steroid Therapy (severe hepatitis)
32
Identify the possible complications of alcoholic hepatitis and its management.
- Acute liver decompensation - Hepatorenal syndrome - Cirrhosis
33
Summarise prognosis for patients with alcoholic hepatitis.
1st month mortality - 10% 1st year mortality - 40% Continue alcohol intake - 1-3 years before cirrhosis
34
Define amyloidosis.
Heterogenous group of diseases characterised by extracellular deposition of amyloid fibrils. Systemic or Localised.
35
Explain the aetiology / risk factors of amyloidosis.
Amyloid fibrils - polymers of low-molecular-weight subunit proteins. - Derived from proteins that undergo conformational changes to adopt an anti-parallel B-pleated sheet configuration - Associated with GAGs and serum amyloid P-component (SAP) - Deposition disrupts structure & function of normal tissue Risk factors: Type AA Amyloid (Serum Amyloid A protein) - Chronic inflammatory diseases - e.g. RA, seronegative arthritides, Crohn's - Chronic infections - e.g. TB, bronchiectasis, osteomyelitis - Malignancy - e.g. Hodgkin's, renal cancer Type AL Amyloid (Monoclonal Immunoglobulin Light Chains) - Subtle monoclonal plasma cell dyscrasoas - Multiple myeloma - Waldenstrom's macroglobulinaemia - B-cell lymphoma Type ATTR - familia, genetic-variant transthyretin - Autosomal dominantly transmitted mutations in gene for transthyretin (TTR)
36
Summarise the epidemiology of amyloidosis.
AA - 1-5% incidence among chronic inflammatory disease patients AL - 3000 U.S & 300-600 UK annually Hereditary - 5% of patients with systemic amyloidosis
37
Recognise the presenting symptoms of amyloidosis.
Depends on the tissues and organs affected, and presence of risk factors. Kidney Failure: - Swelling (oedema) - Tiredness - Weakness - Loss of appetite Heart failure: - Shortness of breath - Oedema - Arrhthmia Others: - Lightheaded - Fainting - Peripheral neuropathy (numbness & tingling) - Nausea, diarrhoea, constipation - Carpal tunnel syndrome - numbness, tingling, pain in wrist - Enlarged tongue (AL)
38
Recognise the signs of amyloidosis on physical examination.
Renal - proteinuria, nephrotic syndrome, renal failure Cardiac - restrictive cardiomyopathy, heart failure, arrhythmia, angina GI - macroglossia (AL) , hepatomegaly, splenomegaly, gut dysmotility, malabsorption, bleeding Neuro - sensory and motor neuropathy, autonomic neuropathy, carpal tunnel syndrome Skin - waxy skin, easy bruising, purpura around eyes (AL), plaques, nodules Joints - painful asymmetrical large joints, shoulder pad sign Haem - bleeding diathesis (Factor X binds to amyloid, decreased synthesis of coagulation factors)
39
Identify appropriate investigations for amyloidosis and interpret the results.
1. Tissue Biopsy - to diagnose, identify amyloid fibril protein (good for AA, poor for AL) 2. Urine 3. Blood 4. 123I-SAP Scan 5. Bone marrow 6. ECG 7. DNA analysis Urine - Proteinuria - Free Ig light chains in AL Blood - CRP - ESR - Rheumatoid factor - Ig levels - Serum protein electrophoresis - LFTs - U&E - SAA (monitoring in AA) 123-I-SAP Scan - Radiolabelled SAP localizes to deposits - Enables quantitative imaging of organs
40
Define anal fissure.
A tear in the squamous lining of the distal canal canal characterised by pain on defecation and rectal bleeding. 90% are posterior. Anterior - follow parturition.
41
Explain the aetiology / risk factors of anal fissure.
Risk Factors/Causes - Hard stool - Pregnancy - Opiate analgesia Rare Causes - Herpes - Syphilis - Trauma - Crohn's - Anal cancer - Psoriasis
42
Summarise the epidemiology of anal fissure.
Young to middle aged adults. | 1 in 350 people.
43
Recognise the presenting symptoms of anal fissure.
- Pain on defecation - Tearing sensation on passing stool - Fresh blood on stool or on paper
44
Recognise the signs of anal fissure on physical examination.
- Sentinel pile - Mucosal tag - ?Groin nodes - suggest complicating factor (HIV, immunosuppression)
45
Identify appropriate investigations for anal fissure and interpret the results.
Anal manometry - if resistant fissures | Anal ultrasound - with suspected anal sphincter deficits
46
Generate a management plan for anal fissure.
5% lidocaine ointment + 0.2-0.4% GTN ointment or 2% topical diltiazem Dietary fibre Fluids Stool softener Hygiene advice 2nd line - Botulinum toxin injection and 2% topical diltiazem = fever side effects
47
Identify the possible complications of anal fissure and its management.
Spasm may constrict the inferior rectal artery causing ischaemia and prolonged healing
48
Summarise the prognosis for patients with anal fissure.
If conservative methods fail, a lateral partial internal sphincterotomy is needed.
49
Define appendicectomy.
Surgical removal of the vermiform appendix.
50
Summarise the indications for an appendicectomy.
- Acute appendicitis = persistent abdominal pain, fever, peritonitis, leukocytosis present
51
Identify the possible complications of an appendicectomy.
- Perforation - <1% mortality - Elderly - 5% mortality - Infection - high temperature, discharge from wound, hot to touch, vomiting, pain and swelling - Shoulder pain - due to gas pumped into abdomen - Constipation - Haematoma - Scarring - Abscess - Hernia
52
Define appendicitis.
Acute inflammation of the vermiform appendix.
53
Explain the aetiology / risk factors of appendicitis.
Gut organisms invade the appendix wall after lumen obstruction by lymphoid hyperplasia, faecolith or filiarial worms. Leads to oedema ,ischaemia, necrosis and perforation. Risk factors: - <6 months of breastfeeding - Low dietary fibre - Improved personal hygiene - Smoking
54
Summarise the epidemiology of appendicitis.
Most common surgical emergency. Lifetime incidence 6%. Highest incidence 10-20yrs. Rare before 2 years old - cone shaped, wider lumen
55
Recognise the presenting symptoms of appendicitis.
- Periumbilical pain that moves to the right inferior flank - Anorexia - Nausea - Vomiting - Constipation
56
Recognise the signs of appendicitis on physical examination.
- Tachycardia - Fever - Peritonism - Guarding and rebound - Percussion tenderness in right inferior flank - Pain during PR examination - suggests inflamed, low-lying pelvic appendix - Rovsing's sign - pain greater in right inferior flank than left inferior flank, if left inferior flank is pressed - Psoas's sign - pain on extending hip if retrocaecal appendix - Cope sign - pain on flexion and internal rotation of right hip if appendix in close relation to obturator internus
57
Identify appropriate investigations for appendicitis and interpret the results.
- Blood tests - FBC, reveal neutrophil leukocytosis, elevated CRP - Abdominal CT - reduces -ve appendicectomy rate - Abdominal ultrasound - Urinalysis - Pregnancy test - Group and save - Abdominal MRI
58
Generate a management plan for appendicitis.
- Appendicectomy | - Antibiotics - piperacilin / tazobactam 4.5g/8h, 1 to 3 doses IV starting 1h pre-op
59
Identify the possible complications of appendicitis and its management.
- Perforation - more common if faecolith present, young children - Appendix mass - inflamed appendix covered in omentum - Appendix abscess - if mass fails to resolve, enlarges further
60
Summarise the prognosis for patients with appendicitis.
Perforation - <1% mortality | - Elderly - 5% mortality
61
Define autoimmune hepatitis.
Chronic hepatitis characterised by autoimmune features, hyperglobulinaemia and presence of circulating autoantibodies.
62
Explain the aetiology / risk factors of autoimmune hepatitis.
- Genetic predisposition - Virus' or drugs trigger hepatocyte expression of HLA antigens - T-cell mediated autoimmune attack - Raised ANA, ASM, anti-liver/kidney microsomes do not injure liver directly - Chronic inflammatory changes similar to chronic viral hepatitis --> lymphoid infiltration of portal tracts and hepatocyte necrosis - Leads to fibrosis and cirrhosis Type 1 - ANA, anti-smooth muscle antibodies (anti-SMA), anti-actin antibodies (AAA), anti-soluble liver antigen (anti-SLA) Type 2 - antibodies to liver/kidney microsomes (ALKM-1 directed at CYP2D6 epitope), antibodies to liver cytosol antigen (ALC-1) Risk factors: - Female gender - Genetic pre-disposition - Immune dysregulation - Measles virus
63
Summarise the epidemiology of autoimmune hepatitis.
Type 1 - all age groups (mainly women) Type 2 - disease of girls and young women
64
Recognise the presenting symptoms of autoimmune hepatitis.
Insidious onset: - Malaise - Fatigue - Anorexia - Nausea - Amenorrhoea - Epistaxis - nose bleeds Acute hepatitis (25%): - Fever - Anorexia - Nausea - Vomiting - Diarrhoea - RUQ pain - Serum sickness
65
Recognise the signs of autoimmune hepatitis on physical examination.
Insidious onset: - Weight loss - Jaundice ``` Acute hepatitis (25%): - Jaundice ``` Others: - Stigmata of chronic liver disease - e.g. spider naevi - Ascites - Oedema - Encephalopathy - Cushingoid features
66
Identify appropriate investigations for autoimmune hepatitis and interpret the results.
1. Blood 2. Liver biopsy - shows interface hepatitis or cirrhosis 3. Ultrasound, CT, MRI of liver or abdomen - visualise structural lesions 4. ERCP - rule out PSC 5. Others Blood - LFT - high AST, ALT, GGT, AlkPhos, bilirubin, low albumin - Clotting - high PT - FBC - low Hb, platelets, WCC - from hypersplenism if portal hypertension is present Others - Rule out other causes of liver disease - e.g. viral serology - Hep B & C - e.g. caeruloplasmin and urinary copper - Wilson's - e.g. ferritin and transferrin saturation - haemochromatosis - e.g. alpha-1-antitrypsin - deficiency - e.g. antimitochondrial antibodies - PBC
67
Define Barrett's oesophagus.
Metaplasia of oesophageal squamous epithelium and replacement with columnar epithelium. Pre-malignant condition - increased risk of dysplasia and adenocarcinoma.
68
Explain the aetiology / risk factors of Barrett's oesophagus.
- Chronic gastro-oesophageal reflux disease (GORD) - Increased age - Male sex - White ethnicity - Tobacco use - Obesity - Family history
69
Summarise the epidemiology of Barrett's oesophagus.
Middle-aged older adults Male White ethnicity 8% prevalence - varies massively
70
Recognise the presenting symptoms of Barrett's oesophagus.
- Heartburn - Regurgitation - Dysphagia - Chest pain - Laryngitis - Cough - Dyspnoea / wheeze
71
Recognise the signs of Barrett's oesophagus on physical examination.
- Heartburn - Regurgitation - Dysphagia - Chest pain - Laryngitis - Cough - Dyspnoea / wheeze
72
Identify appropriate investigations for Barrett's oesophagus and interpret the results.
- Biopsy - endoscopically visible columnarisation, record length using Prague classification - Barium oespehagogram
73
Generate a management plan for Barrett's oesophagus.
Detecting and preventing oesophageal adenocarcinoma. Endoscopic surveillance ever 2-3 years (if more extensive disease). If high-grade dysplasia, intramural carcinoma - endoscopic resection or mucosal radio-frequency ablation. Low-grade dysplasia - confirm by repeat examination after 6 months.
74
Identify the possible complications of Barrett's oesophagus and its management.
- Oesophageal adenocarcinoma - increase age, large length of oesophagus involved, dysplasia
75
Define cholangiocarcinoma.
Cancer arising from the bile duct epithelium. Intrahepatic or extrahepatic. [Perihilar or distal] Perihilar - involves bifurcation of the left and right hepatic ducts = Klatskin's tumours.
76
Define cholangiocarcinoma.
Cancer arising from the bile duct epithelium. Intrahepatic or extrahepatic. [Perihilar or distal] Perihilar - involves bifurcation of the ducts = Klatskin's tumours. Slow growing.
77
Explain the aetiology / risk factors of cholangiocarcinoma.
Causes: - Flukes - Caroli's disease - Biliary cysts Risk factors: - 50 years + - Cholangitis - Choledocholithiasis - Cholecytolithiasis
78
Summarise the epidemiology of cholangiocarcinoma.
95%+ are adenocarcinomas.
79
Recognise the presenting symptoms of cholangiocarcinoma.
- Abdominal pain - right upper quadrant - Fever - Pruritus - itchy skin - Malaise
80
Recognise the signs of cholangiocarcinoma on physical examination.
- Painless jaundice - Weight loss - Palpable gallbladder - Hepatomegaly
81
Identify appropriate investigations for cholangiocarcinoma and interpret the results.
- Bloods - bilirubin, AlkPhos, gamma-GT, aminotransferase, PT time - Abdominal ultrasound - Abdominal CT, MRI - MR angiography - ERCP
82
Define cholecystectomy.
Surgical removal of the gall bladder.
83
Identify the possible complications of a cholecystectomy.
Early: - Bleeding - Bile leak - Bile duct injury - Infection - Visceral injury Late: - Post-cholecystectomy syndrome - Biliary stricture - Port-site or incisional hernias
84
Identify the possible complications of a cholecystectomy.
Early: - Bleeding - Bile leak - Bile duct injury - Infection - Visceral injury Late: - Post-cholecystectomy syndrome - persistant dyspeptic symptoms - Biliary stricture - Port-site or incisional hernias
85
Explain the aetiology / risk factors of cholecystitis.
Develops as a complication of cholethiasis/ gallstones. - Complete cystic duct obstruction due to impacted gallstone in neck or cystic duct - Bile thickening due to dehydration (inspissation) - Bile stasis due to trauma or severe systemic illness Risk Factors: - Gallstones - Physical inactivity - Low fibre intake - Severe illness
86
Summarise the epidemiology of cholecystitis.
10% of patients with symptomatic gallstones progress to acute cholecystitis.
87
Recognise the presenting symptoms of cholecystitis.
- Pain in the right upper quadrant - Tenderness in the right upper quadrant - Right shoulder pain - Fever / chills - Nausea - Anorexia
88
Recognise the presenting symptoms of cholecystitis.
- Pain in the right upper quadrant - Tenderness in the right upper quadrant - Right shoulder pain - Fever / chills - Nausea - Anorexia Chronic: "Flatulent dyspepsia" - vague abdominal discomfort, distension, nausea, flatulence, fat intolerance
89
Recognise the signs of cholecystitis on physical examination.
- Tachycardia - Pyrexia - Right upper quadrant or epigastric tenderness - Possible guarding and rebound - Palpable mass - Murphy's sign - lay 2 fingers over the right upper quadrant, ask the patient to breath in - pain & arrest of inspiration as inflamed gallstone impinges on your fingers (only a +ve if the same does NOT happen over the left upper quadrant) - A Phlegmon - right upper quadrant mass of inflamed adherent omentum and bowel
90
Identify appropriate investigations for cholecystitis and interpret the results.
Bloods - High WCC Ultrasound - Thick-walled, shrunken gallbladder - Pericholecystic fluid - Stones - Common bile duct dilated (if >6mm) Abdominal X-Ray - Only shows 10% gallstones - Porcelain gallbladder - increased risk of cancer MRCP - To find stones ERCP + sphincterotomy before surgery
91
Generate a management plan for cholecystitis.
``` Nil by mouth. Avoidance of fat in diet. Pain relief. IV fluids. Antiemetics. Antibiotics. Laparoscopic cholecystectomy. Open if gallbladder perforates. Elderly/high risk - percutaneous cholecystostomy Obstruction - urgent biliary drainage by ERCP or percutaneous transhepatic cholangiogram (PTC) ```
92
Identify the possible complications of cholecystitis and its management.
- Cholangitis & obstructive jaundice as stone moves to common bile duct - Fail to improve - localized abcess or empyema - Predisposition to gallbladder cancer - Porcelain gallbladder
93
Summarise the prognosis for patients with cholecystitis.
2% with gallstones develop symptoms annually - surgery is an effective treatment
94
Define cirrhosis.
End-stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes. Decompensated - ascites, jaundice, encephalopathy, GI bleeding
95
Identify the possible complications of cholecystitis and its management.
- Cholangitis & obstructive jaundice as stone moves to common bile duct -
96
Explain the aetiology / risk factors of cirrhosis.
- Chronic alcohol misuse - Chronic viral hepatitis - Autoimmune hepatitis - Drugs - e.g. methotrexate, hepatotoxic drugs - Inherited - e.g. alpha-1-anti-trypsin deficiency, haemochromatosis, Wilson's, galactosaemia, cystic fibrosis - Vascular - Budd-Chiari syndrome or hepatic venous congestion - Chronic biliary diseases - primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), biliary atresia - Cryptogenic - Non-alcoholic steatohepatitis (NASH) - associated with obesity, diabetes, total parenteral nutrition, short bowel syndromes, hyperlipidaemia, drugs (e.g. amiodarone, tamoxifen) Decompensation: - Infection - GI bleeding - Constipation - High-protein meal - Electrolyte imbalances - Alcohol and drugs - Tumour development - Portal vein thrombosis Risk factors: - Alcohol misuse - IV drug use - Unprotected sex - Obesity
97
Recognise the presenting symptoms of cirrhosis.
Early: - Anorexia - Nausea - Fatigue - Weakness - Weight loss Reduced liver function: - Easy bruising - Abdominal swelling - Ankle oedema Reduced detoxification function: - Jaundice - Personality change - Altered sleep pattern - Amenorrhoea Portal hypertension: - Abdominal swelling - Haematemesis (blood in vomit) - PR bleeding - Melanea (black stool)
98
Recognise the signs of cirrhosis on physical examination.
Chronic liver disease ABCDE: ``` A = Asterixis (liver flap) B = Briuses C = Clubbing D = Dupuytren's contracture E = Erythema (palmar) ``` - Jaundice - Gynaecomastia - Leukonychia - Parotid enlargement - Spider naevi - Scratch marks - Ascites - shifting dullness, fluid thrill - Enlarged liver - shrunken in later stage - Testicular atrophy - Caput medusae - dilated superficial abdominal veins - Splenomegaly - indicates portal hypertension
99
Identify appropriate investigations for cirrhosis and interpret the results.
1. Bloods 2. Ascitic tap 3. Liver biopsy 4. Others 5. Imaging 6. Endoscopy 7. Child-Pugh Grading Bloods - FBC - low Hb, platelets - LFT - normal or high transaminases, AlkPhos, GGT, bilirubin, low albumin - Clotting - prolonged PT time, low synthesis of clotting factors - Serum AFP - high in chronic disease, may suggest hepatocellular carcinoma Ascitic Tap - Microscopy, culture, sensitivity, biochemistry, cytology - Neutrophils >250/mm^3 = spontaneous bacterial peritonitis (SBP) Liver Biopsy - Percutaneous or transjugular if clotting issues and ascites - Periportal fibrosis - Loss of normal liver architecture - Nodular appearance - Grade = degree of inflammation - Stage = degree of architectural distortion Others - determine cause - Viral serology - Alpha-1-antitrypsin - Caeruloplasmin (Wilson's) - Iron studies - haemochromatosis - Antimitochondrial antibodies - PBC - Antinuclear antibodies - ANA - SMA - autoimmune hepatitis Imaging - US, CT, MRI - detect complications of cirrhosis - MRCP - if PSC suspected Endoscopy - Check for varices, portal hypertensive gastropathy Child-Pugh Grading - Class A, B or C - Assess albumin, bilirubin, PT, ascites, encephalopathy
100
Generate a management plan for cirrhosis.
- Treat the cause - Avoid alcohol, sedatives, opiates, NSAIDs, drugs affecting liver - Nutrition - dietitian review, enteral supplements, NG feeding Complications: - Encephalopathy - treat infections, exclude GI bleed, lactulose, phosphate enemas, avoid sedation - Ascites - diuretics, dietary sodium restriction, therapeutic paracentesis, monitor weight daily, fluid restriction if sodium >120mmol/L, avoid NSAIDs and alcohol - SBP - antibiotics, prophylaxis against recurrent SBP with ciprofloxacin - Surgical - insertion of TIPS (Transjugular intrahepatic portosystemic shunt) to relieve portal hypertension (if recurrent variceal bleeds or diuretic-resistant ascites), liver transplant
101
Identify the possible complications of cirrhosis and its management.
- Ascites - Hepatocellular carcinoma - Hepatic or portal vein thrombosis - Portal hypertension - Encephalopathy - Variceal haemorrhage - SBP - Renal failure - hepatorenal syndrome - Pulmonary hypertension - hepatopulmonary syndrome
102
Summarise the prognosis for patients with cirrhosis.
Depends on aetiology and complications. Generally poor - 50% 5 year survival With ascites, 50% 2 year survival.
103
Define coeliac disease.
Inflammatory disease caused by intolerance to gluten, causing chronic intestinal malabsorption.
104
Explain the aetiology / risk factors of coeliac disease.
- Sensitivity to gliadin component in cereal = gluten - Triggers immunological reaction in SMALL intestine - Mucosal damage - Loss of villi Risk factors: - Family history - 10% of 1st degree relatives affected - Genetic - HLA-B8, DR3, DQW2 - IgA deficiency - Type 1 diabetes - Autoimmune thyroid disease
105
Summarise the epidemiology of coeliac disease.
European population - 1%
106
Recognise the presenting symptoms of coeliac disease.
- Abdominal discomfort - Abdominal pain - Abdominal distention - Steatorrhoea - pale bulky stool, offensive smell, difficult to flush - Diarrhoea - Tiredness - Malaise - Weight loss - Failure to thrive in children - Amenorrhoea in young adults
107
Recognise the signs of coeliac disease on physical examination.
- Anaemia - pallor - Malnutrition - short stature, abdominal distension, wasted buttocks, triceps skinfold thickness assessment (fat stores) - Vitamin deficiencies - osteopenia, osteomalacia, easy bruising - Itchy blisters on elbows, knees, buttocks = dermatitis herpetiformis
108
Identify appropriate investigations for coeliac disease and interpret the results.
1. Bloods 2. Serology 3. Stool 4. D-xylose test 5. Endoscopy Bloods - FBC (low Hb), iron, folate, U&E, albumin, Ca2+, phosphate Serology - IgG anti-gliadin (AGA) - IgA and IgG anti-endomysial transglutaminase - IgA deficiency common so measure Ig levels Stool - Culture to exclude infection - Faecal fat tests for steatorrhoea D-xylose test - Reduced urinary excretion after oral xylose load indicates small bowel malabsorption Endoscopy - Villous atrophy in small intestine (jejunum ,ileum) - Smooth, flat mucosa - Crypt hyperplasia of duodenum - Cuboidal epithelium - Inflammatory infiltrate of lymphocytes and plasma cells in lamina propria
109
Generate a management plan for coeliac disease.
Advice - Withdrawal of gluten from diet - Avoidance of wheat, rye, barley Medical - Vitamin and mineral supplements - Oral corticosteroids (if gluten withdrawal doesn't improve symptoms)
110
Identify the possible complications of coeliac disease and its management.
- Iron, folate and VitB12 deficiency - Osteomalacia - Ulcerative jejunoileitis - GI lymphoma (T-cell) - Bacterial overgrowth - Cerebellar ataxia
111
Summarise the prognosis for patients with coeliac disease.
Full recovery if adhere to gluten-free diet for life Symptoms - recover in weeks Histological changes - longer
112
Define colonoscopy.
Enables visual inspection of the entire large bowel from distal rectum to cecum.
113
Summarise the indications for a colonoscopy.
Diagnostic: - Rectal bleeding - Iron-deficiency anaemia - Persistent diahorrea - Positive faecal occult blood test - Assessment of suspicion of IBD - Colon cancer surveillance Therapeutic: - Haemostasis - by clipping vessel - Bleeding angiodysplasia lesion - argon beamer photocoagulation - Colonic stent deployment (cancer) - Volvulus decompression (flexi sig) - Psuedo-obstruction
114
Identify the possible complications of a colonoscopy.
- Abdominal discomfort - Incomplete examinatioon - Haemorrhage after biopsy or polypectomy - Perforation (<0.1%)
115
Define colorectal carcinoma.
Malignant adenocarcinoma of the large bowel.
116
Explain the aetiology / risk factors of colorectal carcinoma.
Sequence from epithelial dysplasia to adenoma and carcinoma - involves oncogenes (APC, K-ras) and tumour suppressor genes (p53, DCC). Risk factors: - Increasing age - Adenomatous polyposis coli (APC) mutation - Lynch syndrome - hereditary non-polyposis colorectal cancer - MYH-associated polyposis - Chronic bowel inflammation - e.g. IBD
117
Summarise the epidemiology of colorectal carcinoma.
60% in rectum and sigmoid colon. 20% in ascending colon 20% in transverse and descending colon 3rd most common cancer in western world. 4th leading cause of cancer deaths in the US. Rare below 40yrs.
118
Recognise the presenting symptoms of colorectal carcinoma.
Depends on locations. Left-sided colon and rectum: - Change in bowel habit - Rectal bleeding - Blood / mucous in stool - Tenesmus - sensation of incomplete emptying after defecation Right-sided colon: - Later presentation - Symptoms of anaemia, weight loss and non-specific malaise or lower abdominal pain
119
Recognise the signs of colorectal carcinoma on physical examination.
- Anaemia only sign in right-sided lesions - Abdominal mass - Low-lying tumours palpable on rectal examination Metastatic disease: - Hepatomegaly - Shifting dullness of ascites
120
Identify appropriate investigations for colorectal carcinoma and interpret the results.
1. Blood 2. Stool 3. Endoscopy 4. Barium contrast studies 5. Abdominal ultrasound scan Blood - FBC - for anaemia - LFT - Tumour markers - CEA and CA-19-9 to monitor treatment and reoccurance Stool - Occult or frank blood in stool - Screening Endoscopy - Sigmoidoscopy - Colonoscopy - Visualisation & biopsy - If small isolated carcinoma, perform polypectomy Barium Contrast Studies - Apple core stricture on barium enema Abdominal Ultrasound Scan - For hepatic metastases - CXR, CT, MRI, endorectal ultrasound
121
Define Crohn's disease.
Chronic granulomatous inflammatory disease that can affect any part of the gastrointestinal tract. Grouped with UC - together IBD.
122
Explain the aetiology / risk factors of Crohn's disease.
Unknown cause - genetic and environmental factors. Inflammation anywhere along the GI tract - 40% involving terminal ileum. Skip lesions with inflamed segments of bowel interspersed with normal segments. Risk factors: - White ancestry - Age 15-40 or 60-80 - Family history of Crohn's - Cigarette smoking
123
Summarise the epidemiology of Crohn's disease.
UK Incidence annually is 5-8 in 100,000. UK Prevalance is 50-80 in 100,000.
124
Recognise the presenting symptoms of Crohn's disease.
- Cramping abdominal pain - Diarrhoea - bloody or steatorrhoea - Fever - Malaise - Weight loss - Symptoms of complications
125
Recognise the signs of Crohn's disease on physical examination.
- Weight loss - Clubbing - Signs of anaemia - Aphthous ulceration of the mouth - Perianal skin tags - Fistulae - Abscesses - Signs of complications - e.g. eye disease, joint disease, skin diseases
126
Identify appropriate investigations for Crohn's disease and interpret the results.
1. Bloods 2. Stool microscopy and culture - to exclude infective colitis 3. Abdominal X-Ray - for evidence toxic megacolon 4. Erect Chest X-Ray - if risk of perforation 5. Small bowel barium follow-through 6. Endoscopy (OGD, colonoscopy) and biopsy 7. Radionuclide-labelled neutrophil scan - localisation of inflammation Blood - FBC - low Hb, high platelets, WCC - U&E - LFTs - low albumin - High CRP - high or normal - High ESR - Haematinics - look for deficiency states in ferritin, VitB12, red cell folate Small Bowel Barium Follow-Through - May reveal fibrosis or strictures - e.g. string sign of Kantor - Deep ulceration - rose thorn - Cobblestone mucosa Endoscopy & Biopsy - Differentiate between UC and Crohn's - Monitoring malignancy and disease progression - Mucosal oedema and ulceration with rose thorn fissures (cobblestone mucosa) - Fistulae - Abcesses - Transmural chronic inflammation with infiltration of macrophages - Lymphocytes and plasma cells - Granulomas with epithelioid giant cells may be seen in blood vessels or lymphatics
127
Generate a management plan for Crohn's disease.
Acute exacerbation: - Fluid resuscitation - Corticosteroids (oral or IV) - 5-ASA analogues - e.g. mesalazine, sulfasalazine - Analgesia - Elemental diet - Parental nutrition - Monitor markers of activity - e.g. fluid balance, ESR, CRP, platelets, stool frequency, Hb, albumin - Assess for complications Long Term: - Corticosteroids - 5-ASA analogues - Immunosuppression using steroid sparing agents - e.g. azathioprine - Anti-TNF agents - e.g. infliximab Advice: - Stop smoking - Dietitian referral - Education & advice - e.g. from IBD nurse specialist Surgery: - Failure of medical treatment - Failure to thrive in children - Presence of complications - Resection of affected bowel and stoma formation
128
Identify the possible complications of Crohn's disease and its management.
GI - Haemorrhage - Bowel strictures - Bowel perforation - Fistulae - between bowel, bladder, vagina - Perianal fistulae and abscess - GI carcinoma - Malabsorption Extra-intestinal Features: - Uveitis - Episcleritis - Gallstones - Kidney stones - Arthropathy - Sacroilitis - Ankylosing spondylitis - Erythema nodosum - Pyoderma gangrenosum - Amyloidosis
129
Summarise the prognosis for patients with Crohn's disease.
Chronic relapsing condition | 2/3rd need surgery, of those 2/3 >1 procedure.
130
Define diverticular disease.
The presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel, associated with complications - e.g. haemorrhage, infection, fistulae
131
Explain the aetiology / risk factors of diverticular disease.
- Low-fibre diet --> loss of stool bulk - High colonic intraluminal pressures generated to propel stool - Leads to herniation of mucosa and submucosa through muscularis - Sigmoid and descending colon - Sites of nutrient artery penetration Proposed Diverticular Obstruction: - By inspissated faeces - Bacterial overgrowth - Toxin production - Mucosal injury & diverticulitis - Perforation - Pericolic phlegmon - Abscess - Ulceration - Fistulation - Stricture
132
Summarise the epidemiology of diverticular disease.
60% of people living in industrialised countries develop colonic diverticula, rare <40yrs Right-sided diverticula more common in Asia.
133
Recognise the presenting symptoms of diverticular disease.
80-90% asymptomatic - PR bleeding - Diverticulitis - Left iliac fossa or lower abdominal pain - Fever Fistulation into bladder: - Pneumaturia - air bubbles passing in the urine - Faecaluria - Recurrent UTI
134
Recognise the signs of diverticular disease on physical examination.
- Tender abdomen | - Signs of local or generalised peritonitis if perforation has occurred
135
Identify appropriate investigations for diverticular disease and interpret the results.
1. Bloods 2. Barium enema 3. Flexible sigmoidoscopy and colonoscopy Bloods - FBC - high WCC, CRP - Check clotting and cross-match if bleeding Barium enema - Saw-tooth appearance of lumen - Reflects psuedohypertrophy of circular muscle Flexible Sigmoidoscopy and Colonoscopy - Exclude polyps and tumours - See diverticulae Acute setting: - Don't perform barium enema - CT scan to check for disease and complications
136
Generate a management plan for diverticular disease.
1 . Asymptomatic 2. GI bleeding 3. Diverticulitis 4. Surgery Asymptomatic - Soluble high fibre diet - 20-30g/day - Probiotics - Anti-inflammatories - e.g. mesalazine GI Bleed - IV rehydration - Antibiotics - Blood transfusion - Angiography, embolization or surgery if severe Diverticulitis - IV antibiotics - IV fluid rehydration - Bowel rest - Radiologically sited drains if there are localised collections or abscesses Surgery - With recurrent attacks or complications - Open or laparoscopic - Hartmann's procedure - resection and stoma - One-stage resection and anastomosis and defunctioning stoma - Drain placement - Periotoneal lavage
137
Identify the possible complications of diverticular disease and its management.
- Diverticulitis - Pericolic abscess - Perforation - Faecal peritonitis - Colonic obstruction - Fistula formation - bladder, small intestine, vagina - Haemorrhage
138
Summarise the prognosis for patients with diverticular disease.
- 10-25% of patients have 1+ episodes over diverticulitis | - 30% of those will have a second episode
139
Define endoscopic retrograde cholangiopancreatography (ERCP).
A technique that uses a combination of luminal endoscopy and fluoroscopy imaging to treat conditions associated with the pancreatobiliary system. The endoscopic portion of the examination uses a side-viewing duodenoscope that is passed through the oesophagus and stomach and into the second portion of the duodenum.
140
Identify the possible complications of endoscopic retrograde cholangiopancreatography (ERCP).
- Pancreatitis - Bleeding - Cholangitis - Perforation - Mortality <0.2% overall, 0.4% if performing stone removal
141
Summarise the indications for an endoscopy.
Diagnostic Indications: - Haematemesis/ melaena - Dysphagia - Dyspepsia - >55yr, alarm symptoms, treatment refractory - Duodenal biopsy - Persistent vomiting - Iron deficiency (
142
Define endoscopy.
A procedure that uses an endoscope to examine the interior of a hollow organ or cavity of the body.
143
Define feeding (enteral & parenteral).
Enteral feeding - a mode of feeding that uses the GI tract, such as oral or tube feeding. Parenteral feeding - a mode of feeding that delivers specialist nutritional products to a person intravenously, bypassing the usual process of eating and digestion.
144
Summarise the indications for feeding (enteral and parenteral).
Enteral Nutrition: - Functioning GI tract - Stroke - impairs ability to swallow - Cancer - may cause fatigue, nausea, vomiting - Critical illness or injury - reduces energy or ability to eat - Failure to thrive or inability to eat in young children - Serious illness - places body in state of stress - Neurological or movement disorders that increase caloric requirements while making it more difficult to eat - GI dysfunction or disease although this may required parenteral instead Parenteral Nutrition: -
145
Identify the possible complications of feeding (enteral & parenteral).
Enteral Nutrition: - Aspiration - food into the lungs - Refeeding syndrome - dangerous electrolyte imbalances - Infection of tube or insertion site - N&V results from too large and too fast feeds - Skin irritation at tube insertion site - Diarrhea due to liquid diet or medications - Tube dislodgement - Tube blockage if not flushed properly Parenteral Nutrition: - Sepsis - e.g. staphylococcus epidermidis, staphylococcus aureus, candida pseudomonas , infective endocarditis - Thrombosis - Metabolic imbalance - e.g. electrolyte abnormalities, deranged plasma glucose, hyperlipidaemia, deficiency syndromes, acid-base disturbance - Mechanical - e.g. pneumothorax, embolism of IV line tip
146
Define functional dyspepsia & irritable bowel syndrome (IBS)
Functional dyspepsia - when your upper digestive tract shows symptoms of upset, pain or early or prolonged fullness for a month or longer IBS - A functional bowel disorder defined as recurrent episodes of abdominal pain/discomfort for >6 months of the previous year associated with 2 of the following: - Altered stool passage - Abdominal bloating - Symptoms made worse by eating - Passage of mucous
147
Explain the aetiology / risk factors of functional dyspepsia & irritable bowel syndrome (IBS)
Absence of detectable organic pathology - unknown cause. - Visceral sensory abnormalities - Gut motility abnormalities - Psychosocial factors (stress) - Food intolerance (e.g. lactose)
148
Summarise the epidemiology of functional dyspepsia & irritable bowel syndrome (IBS)
Common - 10-20% of adults M:F 2:1
149
Recognise the presenting symptoms of functional dyspepsia & irritable bowel syndrome (IBS)
- >6 months abdominal pain (colicky in lower abdomen and relieved by defecation or flatus) - Altered bowel frequency with >3 bowel movements daily or <3 motions weekly - Abdominal bloating - Change in stool consistency - Passage with urgency or straining - Tenesmus - feeling of incomplete defecation NB: Screen for red flag: - Weight loss - Anaemia - PR bleeding - Late onset (>60 yrs)
150
Recognise the signs of functional dyspepsia & irritable bowel syndrome (IBS) on physical examination.
Nothing normally on examination Distended abdomen and mildly tender to palpate in one or both iliac fossa.
151
Recognise the presenting symptoms of functional dyspepsia & irritable bowel syndrome (IBS)
- >6 months abdominal pain (colicky in lower abdomen and relieved by defecation or flatus) - Altered bowel frequency with >3 bowel movements daily or <3 motions weekly - Abdominal bloating - Change in stool consistency - Passage with urgency or straining - Tenesmus - feeling of incomplete defecation NB: Screen for red flag: - Weight loss - Anaemia - PR bleeding - Late onset (>60 yrs) Risk factors: - Physical and sexual abuse - PTSD - Age <50yrs - Female sex
152
Generate a management plan for functional dyspepsia & irritable bowel syndrome (IBS)
Advice: - Explain and support with establishment of doctor-patient relationship - Dietary modification - reducing insoluble fibre - Exclusion diets - Probiotics Medical: - Antispasmodics - e.g. mebeverin, buscopan - Prokinetic agents - e.g. domperidone, metocloparamide - Antidiarrhoeals - e.g. loperamide - Laxatives - e.g. lactulose - Low dose tricyclic antidepressants - reduces visceral awareness Psychological
153
Identify the possible complications of functional dyspepsia & irritable bowel syndrome (IBS)
- Physical and psychological morbidity | - Increased incidence of clonic diverticulosis
154
Generate a management plan for functional dyspepsia & irritable bowel syndrome (IBS)
Advice: - Explain and support with establishment of doctor-patient relationship - Dietary modification - reducing insoluble fibre - Exclusion diets - Probiotics Medical: - Antispasmodics - e.g. mebeverin, buscopan - Prokinetic agents - e.g. domperidone, metocloparamide - Antidiarrhoeals - e.g. loperamide - Laxatives - e.g. lactulose - Low dose tricyclic antidepressants - reduces visceral awareness Psychological therapies: - CBT, relaxation, psychotherapy
155
Define gallstones and biliary colic.
Gallstones - stone formation in the gallbladder Biliary colic - sudden onset, severe right upper quadrant or epigrastric pain, constant in nature associated with the formation of stones in the gallbladder
156
Explain the aetiology / risk factors of gallstones and biliary colic.
3 types of stone: Mixed stones, Pure cholesterol stones, Pigment stones Mixed stones: - Contain cholesterol, calcium bilirubinate, phosphate and protein - Risk factors: older age, female, obesity, parenteral nutrition, drugs (OCP, ocreotide), family history, ethnicity (Pima Indians), interruption of the enterohepatic recirculation or bile salts (e.g. Crohn's), terminal ileal resection Pure Cholesterol Stones: - Risk factors: older age, female, obesity, parenteral nutrition, drugs (OCP, ocreotide), family history, ethnicity (Pima Indians), interruption of the enterohepatic recirculation or bile salts (e.g. Crohn's), terminal ileal resection Pigment Stones: - Black stones of calcium bilirubinate - high bilirubin secondary to haemolytic disorders, cirrhosis - Brown stones - bile duct infestation by liver fluke Clonorchis sinesis - Risk factors: Haemolytic disorders - e.g. sickle cell, thalassaemia, hereditary spherocytosis
157
Summarise the epidemiology of gallstones and biliary colic.
Very common UK prevalence = 10% Older age 3x more females in younger population Equal sex ratio after 65yrs
158
Recognise the presenting symptoms of gallstones and biliary colic.
90% Asymptomatic. Biliary colic: -
159
Recognise the presenting symptoms of gallstones and biliary colic.
90% Asymptomatic. Biliary colic: - Sudden onset, right upper quadrant or epigastric pain - Constant - Right scapula radiation - Precipitated by fatty meal - Nausea & Vomiting Acute Cholecystitis: - Patient systemically unwell - Fever - Prolonged upper abdominal pain - Referred to right shoulder due to diaphragmatic irritation Ascending Cholangitis - Right upper quadrant pain - Jaundice - Rigors - Hypotension - Confusion (1st 3 = Charcot's triad, +last 2 = Reynold's pentad)
160
Recognise the signs of gallstones and biliary colic on physical examination.
Biliary colic: - Right upper quadrant pain - Epigastric tenderness Acute Cholecystitis: - Tachycardia - Pyrexia - Right upper quadrant or epigastric tenderness - Guarding +/- rebound - Murphy's sign - upon placing a hand at the costal margin in the right upper quadrant and asking the patient to breath in deeply Ascending Cholangitis: - Pyrexia - Right upper quadrant pain - Jaundice
161
Identify appropriate investigations for gallstones and biliary colic and interpret the results.
1. Bloods 2. US Scan 3. Abdominal X-ray 4. Others Bloods - FBC - high WBC in cholecystitis and cholangitis - LFT - high AlkPhos, bilirubin in cholangitis, transaminases - Blood cultures - Amylase - risk of pancreatitis USS - Gallstones - acoustic shadow within gallbladder - Increased thickness of gallbladder wall - Dilatation of biliary tree = obstruction Others - Erect CXR - perforation - CT, MRCP, ERCP
162
Generate a management plan for gallstones and biliary colic.
Mild Symptoms: - Conservative - Avoid fat in diet Severe Biliary Colic: - Admission - IV fluids - Analgesia - Antiemetics - Antibiotics - If do not improve, check for abscess or empyema - drain by cholecystostomy and pigtail catheter - If obstructed, urgent biliary drainage by ERCP or percutaneous transhepatic cholangiogram Surgery: - Laparoscopic cholecystectomy +/- on table cholangiogram - Acute - within 72hrs or after weeks to let inflammation settle \
163
Generate a management plan for gallstones and biliary colic.
Mild Symptoms: - Conservative - Avoid fat in diet Severe Biliary Colic: - Admission - IV fluids - Analgesia - Antiemetics - Antibiotics - If do not improve, check for abscess or empyema - drain by cholecystostomy and pigtail catheter - If obstructed, urgent biliary drainage by ERCP or percutaneous transhepatic cholangiogram Surgery: - Laparoscopic cholecystectomy +/- on table cholangiogram - Acute - within 72hrs or after weeks to let inflammation settle
164
Identify the possible complications of gallstones and biliary colic and its management.
Stones within the gallbladder: - Biliary colic - Cholecystitis - Mucocoele - Gallbladder empyema - Porcelain gallbladder - Predisposition to gallbladder cancer Stones outside the gallbladder: - Obstructive jaundice - Pancreatitis - Ascending cholangitis - Perforation - Pericholecystic abscess - Bile peritonitis - Cholecystenteric fistula - Gallstone ileus - Mirizzi Syndrome - common hepatic duct obstruction by an extrinsic compression from an impacted stone in the cystic ducts - Bouveret's Syndrome - gallstones causing gastric outlet obstruction Of cholecystectomy: - Bleeding - Infection - Bile leak - Bile duct injury (0.3% lap, 0.2% open) - Post-cholecystectomy syndrome - persistent dyspeptic symptoms - Port-site hernias
165
Define gastric cancer.
Gastric malignancy, most commonly adenocarcinoma, more rarely lymphoma, leiomyosarcoma.
166
Explain the aetiology / risk factors of gastric cancer.
Environmental insult in genetically predisposed individuals --> mutation, unregulated cell growth Risk factors: - H.pylori infection - Atrophic gastritis - Diet high in smoked, processed foods, nitrosamines - Smoking - Alcohol
167
Summarise the epidemiology of gastric cancer.
Common cause of death worldwide Highest incidence - Asia, Japan 6th most common cancer in UK UK annual 15/100,000. M:F 2:1 Age >50 yrs Reducing incidence of cancer of antrum/body Cardia and GI/Oesophageal increasing.
168
Recognise the presenting symptoms of gastric cancer.
Early - asymptomatic - Early satiety - Epigastric discomfort - Weight loss - Anorexia - N&V - Haematemesis - Melaena - Symptoms of anaemia - Dysphagia - tumours of the cardia - Symptoms of metastases - e.g. abdominal swelling, jaundice
169
Recognise the signs of gastric cancer on physical examination.
- May be normal - Epigastric mass - Abdominal tenderness - Ascites - Signs of anaemia - Virchow's node/Troisier's sign - lymphadenopathy in left supraclavicular fossa - Sister Mary Joseph node - metastatic nodule on umbilicus - Krukenber's tumour - ovarian metastases
170
Identify appropriate investigations for gastric cancer and interpret the results.
1. Upper GI endoscopy - multiquadrant biopsy of gastric ulcers 2. Blood - FBC (anaemia), LFT 3. CT/MRI - staging of tumour, surgery 4. US of Liver - staging of tumour 5. Bone scan - staging of tumour 6. Endoscopic Ultrasound - assess depth of invasion, lymph node spread 7. Laparoscopy - determine if resectable
171
Define gastro-oesophageal reflux disease.
Inflammation of the oesophagus caused by the reflux of gastric acid and/or bile.
172
Explain the aetiology / risk factors of gastro-oesophageal reflux disease.
Disruption of mechanisms that prevent reflux - e.g. physiological lower oesophageal sphincter, mucosal rosette, acute angle of junction, intra-abdominal portion of oesophagus, prolonged oesophageal clearance
173
Explain the aetiology / risk factors of gastro-oesophageal reflux disease.
Disruption of mechanisms that prevent reflux - e.g. physiological lower oesophageal sphincter, mucosal rosette, acute angle of junction, intra-abdominal portion of oesophagus, prolonged oesophageal clearance Risk factors: - Family history of heartburn or GORD - Older age - Hiatus hernia - Obesity
174
Recognise the presenting symptoms of gastro-oesophageal reflux disease.
- Substernal burning discomfort or 'heartburn' - Aggrevated by lying supine, bending, large meals, alcohol - Pain relieved by antacids - Waterbrash - Regurgitation of gastric contents - Aspiration --> voice hoarseness, laryngitis, nocturnal cough, wheeze, pneumonia (rare) - Dysphagia - due to peptic stricture after long-standing reflux
175
Recognise the signs of gastro-oesophageal reflux disease on physical examination.
- Epigastric tenderness - Wheeze on chest auscultation - Dysphonia
176
Identify appropriate investigations for gastro-oesophageal reflux disease and interpret the results.
- Upper GI endoscopy, biopsy, cytological brushings - confirm oesophagitis, exclude malignancy (>45yrs) - Barium swallow - e.g. hiatus hernia, peptic stricture, extrinsic compression of oesophagus -
177
Identify appropriate investigations for gastro-oesophageal reflux disease and interpret the results.
- Upper GI endoscopy, biopsy, cytological brushings - confirm oesophagitis, exclude malignancy (>45yrs) - Barium swallow - e.g. hiatus hernia, peptic stricture, extrinsic compression of oesophagus - CXR - hiatus hernia (gastric bubble behind cardiac shadow) - 24hr oesophageal pH monitoring - pH probe in lower oesophagus to determine temporal relationship between symptoms and oesophagus pH
178
Generate a management plan for gastro-oesophageal reflux disease.
Advice - Lifestyle changes - Weight loss - Elevating head of bed - Avoid provoking factors - Stopping smoking - Lower fat meals - Avoiding large meals late in the evening Medical - Antacids - Alginates - H2 Receptor Antagonists - e.g. ranitidine - PPI - e.g. lansoprazole Endoscopy - Annual surveillance for Barrett's oesophagus - Stricture dilating - Stenting Surgery - Anti-reflux surgery for those with symptoms despite optimal medical management Nissen fundoplication - Fundus of stomach wrapped around lower oesophagus and held with seromuscular sutures to reduce hiatus hernia and reflux
179
Identify the possible complications of gastro-oesophageal reflux disease and its management.
- Oesophageal ulceration - Peptic stricture - Anaemia - Barrett's oesophagus - Oesophageal adenocarcinoma - Asthma - Chronic laryngitis
180
Summarise the prognosis for patients with gastro-oesophageal reflux disease.
50% respond to lifestyle measures. Drug therapy withdrawal associated with relapse. 20% patients undergoing endoscopy for GORD have Barrett's oesophagus.
181
Define gastroenteritis and infectious colitis.
Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort.
182
Explain the aetiology / risk factors of gastroenteritis and infectious colitis.
Caused by viruses, bacteria, protozoa or toxins in contaminated food or water. Virus - e.g. rotavirus, adenovirus, astrovirus, calcivirus, Norwalk virus, small round structured viruses Bacteria - e.g. Campylobacter jejuni, E.coli 0157, Salmonella, Shigella, Vibrio cholerae, Listeria, Yersinia enterocolitica Protozoal - e.g. Entamoeba histolytica, Cryptosporidium parvum, Giardia lamblia Toxins - e.g. from Staphylococcus aureus, Cryptosporidium parvum, Giardia lamblia ``` Commonly contaminated foods - Improperly cooked meat - e.g. S.aureus, C.perfringens - Old rice - e.g. B.cereus, S.aureus - Eggs & poultry - e.g. Salmonella - Milk and cheeses - e.g. Listeria, Campylobacter - Canned food - e.g. botulism ``` Non-inflammatory mechanisms - e.g. V. cholerae, enterotoxigenic E.coli (enterotoxins causing enterocytes to release water and electrolytes) Inflammatory mechanisms - e.g. Shigella, enteroinvasive E.coli (release cytokines, invade, damage epithelium), Salmonella typhi (greater invasion and bacteraemia)
183
Summarise the epidemiology of gastroenteritis and infectious colitis.
Common Under-reported Morbidity & mortality in developing world
184
Recognise the presenting symptoms of gastroenteritis and infectious colitis.
- Sudden onset nausea - Vomiting - Anorexia - Diarrhoea - bloody or watery - Abdominal pain / discomfort - Fever - Malaise NB: Enquire about recent travel, antibiotic use and recent food intake - how cooked, source, anyone else ill. Time of onset: - Toxins - early, 1-24h - Bacterial/Viral/Protozoal - 12h or later Effect of toxin: - Botulinum - paralysis - Mushrooms - fits, renal or liver failure
185
Recognise the signs of gastroenteritis and infectious colitis on physical examination.
- Diffuse abdominal tenderness - Abdominal distension - Increased bowel sounds Severe: - Pyrexia - Dehydration - Hypotension - Peripheral shutdown
186
Identify appropriate investigations for gastroenteritis and infectious colitis and interpret the results.
1. Blood 2. Stool 3. AXR or US 4. Sigmoidoscopy Blood - FBC, blood culture (bacteraemia), U&Es (dehydration) Stool - Faecal microscopy for polymorphs, parasites, oocytes, culture, EM (viraL) - Analyse for toxins, pseudomembranous colitis - e.g. Clostridium difficile toxin AXR or US - Exclude other causes of abdominal pain Sigmoidoscopy - IBD exclusion
187
Generate a management plan for gastroenteritis and infectious colitis.
- Bed rest - Fluids - Electrolyte replacement - Oral rehydration solution - glucose, salt - IV rehydration if severe vomiting - Antibiotic treatment if severe or infective agent identified - e.g. ciprofloxacin against Salmonella, Shigella, Campylobacter - Educate on basic hygiene and cooking NB: Botulism - Botulinum anti-toxin IM and manage in ITU
188
Identify the possible complications of gastroenteritis and infectious colitis and its management.
- Dehydration - Electrolyte imbalance - Pre-renal failure - Secondary lactose intolerance (infants) - Sepsis & shock (Salmonella, Shigella) - Haemolytic uraemic syndrome (E.coli 0157) - Guillian-Barré syndrome in weeks after Campylobacter gastroenteritis Botulism - respiratory muscle weakness, paralysis
189
Summarise the prognosis for patients with gastroenteritis and infectious colitis.
Majority of cases self-limiting
190
Define haemorrhoidectomy.
Surgical procedure for tying haemorrhoids and excising them.
191
Summarise the indications for haemorrhoidectomy.
Symptomatic 3rd and 4th degree haemorrhoids. 1st degree - haemorrhoids that do not prolapse 2nd degree - prolapse with defection, but reduce spontaneously. 3rd degree - prolapse and require manual reduction 4th degree - prolapsed and not reducible.
192
Identify the possible complications of haemorrhoidectomy.
- Pain - Bleeding - Recurrence - Incontinence (rare) due to sphincter injury - Anal stricture
193
Define gastrointestinal perforation.
A hole in the wall of part of the gastrointestinal tract - e.g. oesophagus, stomach, small intestine, large intestine.
194
Explain the aetiology / risk factors of gastrointestinal perforation.
GI contents spill into abdomen --> peritonitis (infection). May result in sepsis. Causes: - Trauma - e.g. surgical damage, knife/gunshot wound, severe blow to abdomen, damage by swallowed object or corrosive substance - Diverticulitis - Ulcerative colitis - Crohn's disease - Toxic megacolon - Strangulated hernia - Peptic ulcer disease - Forceful vomiting - Blood loss / poor blood flow to intestine due to artery blockage - Appendicitis - Colon cancer Risk factors: - Recent or prior abdominal surgery - Recent or prior pelvic surgery - >75 yrs - History of multiple medical problems - Trauma to abdomen or pelvis
195
Summarise the epidemiology of gastrointestinal perforation.
Incidence is 1-7% in paediatric trauma patients. | 10-15% of patients with acute diverticulitis develop free perforation.
196
Recognise the presenting symptoms of gastrointestinal perforation.
- Severe stomach pain - Abdominal distention - Chills - Fever - Nausea - Vomiting - Obstipation - severe or complete constipation
197
Recognise the signs of gastrointestinal perforation on physical examination.
- Abdominal distention - Severe abdominal pain - Tachycardia - Tachypnea - Hypotension - Decreased / absent bowel sounds - Loss of liver dullness on right upper quadrant percussion
198
Identify appropriate investigations for gastrointestinal perforation and interpret the results.
- Blood tests - for signs of infection & blood loss | - CT scan/Abdo X Ray
199
Generate a management plan for gastrointestinal perforation.
- Surgery - to repair perforation - Antibiotics - to treat infection - Fluids - Colostomy / Ileostomy - allows contents to empty into a bag through a stoma in abdomen, so that intestines can heal NB: Colostomy = left iliac fossa. Ileostomy / urostomy = right iliac fossa.
200
Identify the possible complications of gastrointestinal perforation and its management.
- Sepsis - Multi-organ failure - Bleeding - Abscess - Bowel infarction - death of part of the bowel - Permanent ileostomy or colostomy
201
Summarise the prognosis for patients with gastrointestinal perforation.
Medical emergency - recognise signs, symptoms and sepsis. Overall mortality = 20-40% due to septic shock and multi-organ failure TIME T = temperature (higher or lower than normal) I = infection (signs & symptoms) M = mental decline (confused, sleepy, difficult to rouse) E = extremely ill (severe pain, discomfort, shortness of breath)
202
Define haemochromatosis.
An inherited disorder of iron metabolism in which high intestinal iron absorption leads to iron deposition in joints, liver, heart, pancreas, pituitary, adrenals and skin. It is a multi-system disorder of dysregulated dietary iron absorption and increased iron release from macrophages.
203
Explain the aetiology / risk factors of haemochromatosis.
HFR gene - responsible for most of HH (homozygous) 2 mutations: - C282Y - 60-90% - variable penetrance - H63D - 1-3% - Compound heterozygotes - 4-7% Risk factors: - Middle age - Male gender - White ancestry - Family history NB: Women present 10 years later as menstrual blood loss is protective.
204
Summarise the epidemiology of haemochromatosis.
- Northern Europeans - 1 in 10 carrier rate - 1 in 200-400 homozygosity
205
Recognise the presenting symptoms of haemochromatosis.
Early: - Tiredness - Arthralgia - 2nd, 3rd MCP joints and knee pseudogout May present very advanced: - Cirrhosis - Hepatocellular cancer - Bronze diabetes - from iron deposition in pancreas - Heart disease - Slate-grey skin pigmentation - Chronic liver disease signs - Hypogonadism - decreased pituitary function
206
Recognise the signs of haemochromatosis on physical examination.
Early: - Tiredness - Arthralgia - 2nd, 3rd MCP joints and knee pseudogout May present very advanced: - Cirrhosis - Hepatocellular cancer - Bronze diabetes - from iron deposition in pancreas - Heart disease - Slate-grey skin pigmentation - Chronic liver disease signs - Hypogonadism - decreased pituitary function
207
Identify appropriate investigations for haemochromatosis and interpret the results.
- Serum transferrin saturation - high - Serum ferritin - high - HFE mutation analysis - MRI liver and heart - chondrocalcinosis (cartilage calcification) - LFTs - high LFT - Liver biopsy - Perl's stain quantifies iron loading
208
Define haemorrhoids.
Vascular-rich connective tissue cushions located within the anal canal. Internal - proximal to dentate line External - distal to dentate line Classes: 1st degree - haemorrhoids that do not prolapse 2nd degree - prolapse with defection, but reduce spontaneously. 3rd degree - prolapse and require manual reduction 4th degree - prolapsed and not reducible NB: Differential diagnosis - perianal haematoma, anal fissure, abscess, tumour, proctalgia fugax
209
Explain the aetiology / risk factors of haemorrhoids.
3 anal cushions - at 3,7, and 11 o'clock --> where the three major arteries that feed the vascular plexuses enter the anal canal Cushions attached by smooth muscle and elastic tissue --> become bulky and loose due to gravity, increased anal tone (stress) and effects of straining Protrude to form piles Vulnerable to trauma (from hard stools) and bleed readily from the underlying lamina propria capillaries May also be caused by congestion from pelvic tumour, pregnancy, CCF or portal hypertension. NO SENSORY FIBRES ABOVE DENTATE LINE --> not painful unless they thrombose when they protrude and are gripped by the anal sphincter blocking venous return Risk factors: - 45-65 years - Constipation - Pregnancy - Space-occupying pelvic lesion - Hepatic insufficiency
210
Summarise the epidemiology of haemorrhoids.
4.4% in general population worldwide.
211
Recognise the presenting symptoms of haemorrhoids.
- Bright red rectal bleeding (coating stools, on tissue, dripping into the pan after defecation) - Mucous discharge - Pruritus ani - Anaemia ``` Watch out for: - Weight loss - Tenesmus - Change in bowel habit (may be other pathology) ```
212
Recognise the signs of haemorrhoids on physical examination.
- Bright red rectal bleeding (coating stools, on tissue, dripping into the pan after defecation) - Mucous discharge - Pruritus ani - Anaemia
213
Identify appropriate investigations for haemorrhoids and interpret the results.
- Abdominal examination - PR exam - internal haemorrhoids are not palpable, but piles are very obvious - Colonoscopy / flexible sigmoidoscopy - exclude proximal pathology if >50 years old - Bloods - FBC - Stool - occult haem
214
Generate a management plan for haemorrhoids.
Medical: - Increase fluid - Increase fibre - Topical analgesia - Stool softener - Topical steroids Non-operative: - Rubber band ligation = produces an ulcer to anchor the mucosa (SE: bleeding, infection, pain) - Sclerosants - 2ml of 5% phenol in oil injected into pile above dentate line (SE: impotence, prostatitis) - Infra-red coagulation - coagulates vessels and tethers mucosa to subcutaneous tissue - Bipolar diathermy and direct current electrotherapy - coagulation and fibrosis after local application of heat Surgical: - Excisional haemorrhoidectomy - excision of piles and ligation of vascular pedicles - Stapled haemorrhoidopexy - used when large internal component
215
Identify the possible complications of haemorrhoids and its management.
- Recurrence or worsening of symptoms - Excessive bleeding - Non-reducible prolapse - Pelvic sepsis - Side effects (depends on treatment) - Surgical complications - e.g. constipation, infection, stricture, bleeding
216
Summarise the prognosis for patients with haemorrhoids.
Left untreated, they can protrude out of the anus to cause irritation, bleeding etc.
217
Define hepatocellular carcinoma.
Primary malignancy of hepatocytes, usually occurring in a cirrhotic liver.
218
Explain the aetiology / risk factors of hepatocellular carcinoma.
- Chronic liver disease - e.g. alcoholic liver disease, Hep B/C, autoimmune disease - Metabolic disease - e.g. haemochromatosis - Aflatoxins - e.g. Aspergillus flavus fungal toxin on stored grains or biological weapons Risk factors: - Cirrhosis - Chronic Hep B/Hep C - Chronic heavy alcohol use
219
Summarise the epidemiology of hepatocellular carcinoma.
1-2% of malignancies - common Less common than secondary liver malignancies Rare in the west - 1-2 per 100,000/year Common in HepB/C endemic countries - e.g. Asia and sub-Saharan Africa - 500 per 100,000/year
220
Recognise the presenting symptoms of hepatocellular carcinoma.
Symptoms of malignancy: - Malaise - Weight loss - Loss of appetite Symptoms of chronic liver disease: - Abdominal distension - Jaundice History of Carcinogen Exposure: - High alcohol intake - Hep B/C - Aflatoxins
221
Recognise the signs of hepatocellular carcinoma on physical examination.
Signs of malignancy: - Cachexia - Lymphadenopathy Hepatomegaly: - Nodular - Deep palpation elicits tenderness - Bruit heard over the liver Signs of chronic liver disease: - Jaundice - Ascites
222
Identify appropriate investigations for hepatocellular carcinoma and interpret the results.
1. Bloods - high AFP, VitB12-binding protein, LFT may show biliary obstruction (poor sensitivity and specificity) 2. Abdominal US - not sensitive if <1cm 3. Duplex scan of liver - demonstrate large vessel invasion 4. CT (thorax, abdomen, pelvis) - define structural lesion and spread 5. Hepatic angiography - using lipiodol 6. Liver biopsy - confirms histology (small risk of tumour seeding along biopsy tract) 7. Staging - CXR, CT (throax, abdomen, pelvis), radionuclide bone scan 8. Screening - AFP, abdominal ultrasound in at-risk individuals
223
# Define hernias (femoral, inguinal, miscellaneous). E.g. Paraumbilical, epigastric, incisional, spigelian, lumbar, Richter's, Maydl's, Littre's, obturator, sciatic, sliding, paediatric
The protrusion of a viscus or part of a viscus through a defect of the walls of its containing cavity into an abnormal position. Irreducible - contents cannot be pushes back into place Obstructed - bowel contents cannot pass (intestinal obstruction) Strangulated - ischaemia occurs Incarceration - contents of the hernial sac are stuck inside by adhesions. Types of Hernia: Indirect inguinal hernia - through the internal inguinal ring and out through the external ring Direct inguinal hernia - push directly forward through posterior wall of inguinal canal Femoral hernia - bowel enters the femoral canal Paraumbilical hernia - above or just below the umbilicus, omentum or bowel herniates through defect Epigastric hernia - pass through linea alba above the umbilicus Incisional hernia - follow breakdown of muscle closure after surgery Spigelian hernia - through linea semilunaris at lateral adge of the rectus sheath, below and lateral to the umbilicus Lumar hernia - through inferior or superior lumbar triangles in the posterior abdominal wall Richter's hernia - involve bowel wall only (not lumen) Maydl's hernia - double loop of bowel herniation, where the strangulated portion may reside as a single loop inside the abdominal cavity Littre's hernia - hernial sacs containing strangulated Meckel's diverticulum Obturator hernia - through obturator canal Sciatic hernia - through lesser sciatic foramen Sliding hernia - contain a partially extraperitoneal structure (e.g caecum on right, sigmoid colon on left), sac does not completely surround the contents Paediatrics - e.g. umbilic hernias, indirect inguinal hernias, gastroschisis, exomphalos
224
Explain the aetiology / risk factors of hernias (femoral, inguinal, miscellaneous).
Risk factors: - Male (8:1) - Old age - Smoking - Family history - Chronic cough - Constipation - Urinary obstruction - Heavy lifting - Ascites - Past abdominal surgery - e.g. damage to the iliohypogastric nerve during appendicectomy - Obesity & ascites (paraumbilical hernia) NB: Landmarks - Deep internal ring - the mid-point of the inguinal ligament, 1cm above femoral pulse (mid-inguinal point) - Superficial external ring - a split in the external oblique aponeurosis just superior and medial to the pubic tubercle - Pubic tubercle - bony prominence forming the medial attachment of the inguinal ligament
225
Summarise the prognosis for patients with hernias (femoral, inguinal, miscellaneous).
Indirect hernias: - Common (80%) - Can strangulate Direct hernias: - Less common (20%) - Reduce easily - Rarely strangulate Femoral hernias:
226
Recognise the presenting symptoms of hernias (femoral, inguinal, miscellaneous).
Inguinal hernia: - Bulge in the area around the pubic bone - Becomes more obvious if upright, coughing or straining - Burning / aching sensation at the bulge - Pain or discomfort in groin when bending, coughing or lifting Femoral hernia: - Bulge in the upper thigh next to the groin - Groin discomfort upon standing, coughing, lifting, straining - Severe - abdominal pain, nausea, vomiting
227
Recognise the signs of hernias (femoral, inguinal, miscellaneous) on physical examination.
Hernia Examination: - Look for previous scars - Feel the other side - more common on the right - Examine the external genitalia - Is the lump visible? - Ask the patient to reduce the lump - if he cannot, make sure it is not a scrotal lump - Ask him to cough - will appear superior and medical to the pubic tubercle - Repeat the examination with the patient standing To determine if inguinal or direct: - Reduce the hernia - Occlude the deep internal ring with 2 fingers - Ask the patient to cough or stand - If the hernia is restrained = indirect - If the hernia is not restrained = direct In surgery, to determine if inguinal or direct: - Direct - medial to inferior epigastric vessels - Indirect - lateral to inferior epigastric vessels
228
Identify appropriate investigations for hernias (femoral, inguinal, miscellaneous) and interpret the results.
- Hernia examination - Abdominal examination - Testicular examination - Inguinal lymph node assessment - Further imaging - e.g.ultrasound / CT Hernia Examination: - Look for previous scars - Feel the other side - more common on the right - Examine the external genitalia - Is the lump visible? - Ask the patient to reduce the lump - if he cannot, make sure it is not a scrotal lump - Ask him to cough - will appear superior and medical to the pubic tubercle - Repeat the examination with the patient standing To determine if inguinal or direct: - Reduce the hernia - Occlude the deep internal ring with 2 fingers - Ask the patient to cough or stand - If the hernia is restrained = indirect - If the hernia is not restrained = direct In surgery, to determine if inguinal or direct: - Direct - medial to inferior epigastric vessels - Indirect - lateral to inferior epigastric vessels
229
Generate a management plan for hernias (femoral, inguinal, miscellaneous).
Repair: - Weight loss - Stop smoking pre-op - Warn about chronic pain and re-ocurrance - Polypropylene mesh technique - reinforce the posterior wall - Local anaesthetics and ambulatory surgery - reduce cost - Laparoscopic repair - Rest for 4 weeks - Convalescence over 8 weeks - Laparoscopic repair allows return to manual work and driving after <2 weeks
230
Identify the possible complications of hernias (femoral, inguinal, miscellaneous) and its management.
- Incarceration - Bowel obstruction - Strangulation Surgery: - Infection - Bleeding - Incisional hernia How to reduce an irreducible hernia: - Use the flat of the hand - Direct the hernia from below, up towards the contralateral shoulder - As the hernia obstructs, reduction requires perseverance
231
Define hiatus hernias.
The protrusion of intra-abdominal contents through an enlarged oesophageal hiatus of the diaphragm. Commonly contains stomach, less commonly transverse colon, omentum, small bowel, spleen. Contents contained in sac of peritoneum.
232
Explain the aetiology / risk factors of hiatus hernias.
Sliding hiatus hernia = where the gastro-oesophageal junction slides up into the chest --> acid reflux commonly happens as LOS becomes less competent Paraoesophageal hiatus hernia (rolling hiatus hernia) = gastro-oesophageal junction ramins in the abdomen but a bulge of stomach herniates up into the chest alongside the oesophagus --> GORD less common as LOS remains intact Risk factors: - Obesity - Previous gastro-oesophageal procedure - Elevated intra-abdominal pressure - Male sex
233
Recognise the presenting symptoms of hiatus hernias.
- Heartburn - Regurgitation - Chest pain
234
Summarise the epidemiology of hiatus hernias.
80% sliding hiatus hernia | 30% rolling hiatus hernia
235
Recognise the presenting symptoms of hiatus hernias.
- Heartburn - Regurgitation - Chest pain - Dysphagia - Odynophagia - painful swallowing - Hoarseness - Asthma - Shortness of breath - Chest pain - Anaemia - Haematemesis - vomiting blood
236
Identify appropriate investigations for hiatus hernias and interpret results.
- Upper GI endoscopy - visualise the mucosa (?oesophagitis) | - Barium oesophagram
237
Generate a management plan for hiatus hernias.
- Lose weight - Treat GORD - weight loss, drugs - Surgery indications - intractable symptoms despite aggressive medical therapy, complications (e.g. Barrett's oesophagus)
238
Identify the possible complications of hiatus hernias and its management.
- Complications associated with GORD = e.g. Barrett's oesophagus, oesophagitis, ulcers, benign stricture, iron-deficienc - Strangulation (rolling hiatus hernia) - Mortality (operative) - 1-2% - Obstruction - Bleeding - Necrosis - Volvulus - when a loop of the intestine twists around itself and the supporting mesentery
239
Summarise the prognosis for patients with hiatus hernias.
- Some are asymptomatic | - Self-care can go a long way to reduce and prevent return
240
Define intestinal ischaemia.
Encompassess a heterogeneous group of disorders caused by acute or chornic processes, arising from occlusive or non-occlusive aetiologies, which result in decreased blood flow to the gastrointestinal tract. Obstruction of a mesenteric vessel results in bowel ischaemia and necrosis.
241
Summarise the epidemiology of intestinal ischaemia.
Uncommon. | Higher risk in elderly.
242
Explain the aetiology / risk factors of intestinal ischaemia.
3 types: - Acute mesenteric ischaemia - Chronic mesenteric ischaemia - Colonic ischaemia Acute: - Embolic mesenteric ischaemia - Thrombotic mesenteric ischaemia - Venous mesenteric ischaemia - may lead to acute or subacute intestinal ischaemia - Non-occlusive, low flow state, low O2. Chronic Mesenteric Ischameia: - Intestinal angina - Low flow + atheroma Diffuse atherosclerosis in 3 mesenteric arteries Chronic Colonic Ischaemia: - Ischaemic colitis - Low flow in IMA - Mild to gangrenous Can be a consequence of: - Volvulus - Intussusception - Bowel strangulation - Failed surgical resection Risk factors: - Old age - History of smoking - Hyper-coagulable states - arterial thrombosis (HCL, HTN, DM, smoking), venous thrombosis (portal HTN, splenectomy, septic thrombophlebitis, OCP, thrombophilia) - Atrial fibrillation - Endocarditis
243
Recognise the presenting symptoms of intestinal ischaemia.
- Abdominal pain - Diarrhoea - Weight loss - Haematochezia - passage of fresh blood through the anus, usually in stool - Melaena ACUTE: - Triad - acute severe abdominal pain + no 1 min abdomen signs + rapid hypovolaemia - SHOCK - Pain constant, central or RIF pain - Tender palpable mass - Low bowel sounds CHRONIC: - Triad - severe colicky post-prandial abdominal pain (gut claudication) + low height + upper abdominal bruit - With or without PR bleeding, malabsorption, N&V CHRONIC COLONIC - Low left-sided abdominal pain - With or without bloody diarrhoea
244
Recognise the signs of intestinal ischaemia on physical examination.
- Haematochezia - passage of fresh blood through the anus, usually in stool - Melaena - Abdominal tenderness
245
Identify investigations for intestinal ischaemia and interpret the results.
Dx after clinical suspicion / laparotomy. ACUTE - Bloods - high Hb (plasma loss), high WCC, high amylase, persistent metabolic acidosis (high lactate) - AXR - gas-less abdomen - CT/MRI - ischaemia + angiogenesis if doubt CHRONIC MESENTERIC - CT angiography - if stable CHRONIC COLONIC - CT - Colonoscopy (gold standard) NB: Watershed zone - area supplied by SMA and IMA near splenic flexure - most vulnerable to intestinal ischaemia.
246
Define intestinal obstruction.
A blockage that keeps food or liquid from passing through the small or large intestine.
247
Explain the aetiology / risk factors of intestinal obstruction.
Causes: - Small bowel - adhesions, hernias - Large bowel - colon cancer, constipation, diverticular structure, volvulus (loop of intestine twists around itself and supporting mesentery), sigmoid volvulus, caecal - Rarer - Crohn's stricture, gallstone ileus, intussusception, TB, foreign body Risk factors: - Older age - Female gender - Institutionalisation - Mental illness - Previous abdominal surgery - Malrotation - Crohn's disease - Hernia
248
Summarise the epidemiology of intestinal obstruction.
1. 47 per 100,000 in the US | 0. 15-0.29 per 100,000 in patients with colorectal cancer
249
Identify appropriate investigations for intestinal obstruction and interpret the results.
- Abdominal examination - Abdominal X-Ray - Bloods - WCC - Small or large bowel? If small = vomiting early, distension less, pain higher in abdomen If large = constant pain --> AXR - Ileus or mechanical obstruction? Ileus = functional obstruction from reduced bowel motility, with absent bowel sounds and less pain - Is it simple /closed loop / strangulated? Simple = 1 obstructing point, no vascular compromise Closed loop = 2 obstructing points, grossly distended bowel at risk of perforation Strangulated = vascular compromise, iller patient than expected, sharper & constant & localised pain, peritonism (inflammation of peritoneum), fever, high WCC
250
Recognise the signs of intestinal obstruction on physical examination.
- Abdominal Distention - Tinkling bowel sounds - Fever - Tachycardia
251
Identify appropriate investigations for intestinal obstruction and interpret the results.
- Abdominal examination - Abdominal X-Ray - Bloods - WCC, amylase, FBC, U&E - Small or large bowel? If small = vomiting early, distension less, pain higher in abdomen If large = constant pain --> AXR - Ileus or mechanical obstruction? Ileus = functional obstruction from reduced bowel motility, with absent bowel sounds and less pain - Is it simple /closed loop / strangulated? Simple = 1 obstructing point, no vascular compromise Closed loop = 2 obstructing points, grossly distended bowel at risk of perforation Strangulated = vascular compromise, iller patient than expected, sharper & constant & localised pain, peritonism (inflammation of peritoneum), fever, high WCC
252
Generate a management plan for intestinal obstruction.
General principles: - Cause, site,speed of onset, completeness of obstruction defines therapy - Strangulation and large bowel = surgery - Ileus and incomplete small bowel = initially conservative Immediate action: - Drip and suck - NG tube, IV fluids to rehydrate and correct electrolyte imbalance - Analgesia - Blood tests - amylase, FBC, U&E - AXR - Erect CXR - Catheterise to monitor fluid status Further imaging: - CT - establish cause - Oral Gastrografin prior to CT - determine level of obstruction and mild therapeutic action against mechanical obstruction - Colonoscopy - beware of perforation risk Surgery: - Strangulation - immediate - Closed loop obstruction - surgery or endoscopic decompression - Large bowel malignancies - endoscopic stenting for palliation or as bridge to surgery in acute obstruction - Small bowel obstruction due to adhesions - rarely lead to surgery
253
Identify the possible complications of intestinal obstruction and its management.
- Tissue death - intestinal wall - Infection (peritonitis) - Fluid and dyselectrolytaemia - Hypovolaemic / endotoxic shock - Adhesion / Garres' obstruction - benign fibrous stricture of the bowel due to a complicated strangulated hernia - Acute renal failure - Multiple organ failure Surgery complications: - Infection - Bleeding - Incisional hernia
254
Summarise the prognosis for patients with intestinal obstruction.
Without treatment, blocked parts of intestine can die leading to serious problems. Usually successfully treated.
255
Define laparoscopic abdominal surgery.
A surgical procedure that allows a surgeon to access the inside of the abdomen and pelvis without having to make large incisions to the skin. = keyhole surgery, minimally invasive surgery - Shorter stay - Faster recovery time - Less pain and bleeding after operation - Reduced scarring
256
Summarise the indications for laparoscopic abdominal surgery.
Most commonly used in: - Gynaecology - Gastroenterology - Urology Examples: - Pelvic inflammatory disease diagnosis - Endometriosis diagnosis - Ectopic pregnancy diagnosis - Ovarian cyst diagnosis - Fibroids diagnosis - Female infertility diagnosis - Undescended testicles diagnosis - Appendicitis diagnosis - Unexplained pelvic or abdominal pain diagnosis and investigation - Liver cancer diagnosis - Pancreatic cancer diagnosis - Ovarian cancer diagnosis - Bile duct cancer diagnosis - Gallbladder cancer diagnosis - Removing an inflamed appendix in appendicitis - Gallbladder removal - Intestinal removal - e.g. Crohn's disease, diverticulitis that doesnt respond to medicine - Hernia repair - Stomach ulcer repair - Weight loss surgery - Removing parts of organs affected by cancer - Treating ectopic pregnancy - Fibroid removal - Hysterectomy (womb removal) - e.g. used to treat pelvic inflammatory disease, endometriosis, heavy periods, painful periods
257
Identify the possible complications of laparoscopic abdominal surgery.
- Nausea and vomiting from general anaesthetic - Bloating, cramps and shoulder pain - due to gaseous inflation of the abdomen - Infection & Sepsis - e.g. fever, chills, severe vomiting, increasing abdominal pain, redness /discharge around wounds, abnormal vaginal discharge / bleeding, pain and swelling in one of legs, burning / stinging sensation on urination - Bleeding and bruising - Damage to an organ - e.g. bowel, bladder - Damage to a major artery - Complications due to use of carbon dioxide - e.g. gas entering veins or arteries - Allergic reaction to general anaesthetic - DVT & PE
258
Define liver abscesses.
Liver infection resulting in a walled off collection of pus.
259
Explain the aetiology / risk factors of liver abscesses.
Pyogenic: - E.coli - Klebsiella - Enterococcus - Bacteroides - Streptococci - Staphylococci - 60% caused by biliary tract disease - gallstones, strictures, congenital cysts - 15% are cryptogenic Amoebic: - Entamoeba histolytica Hydatid Cyst: - Tapeworm Echinococcus granulosis Others: - TB Risk factors: - Biliary tract disease - Age >50 years - Underlying malignancy - DM
260
Summarise the epidemiology of liver abscesses.
Pyogenic - 0.8 in 100,000, 60 yrs mean age, most common in industrialised world Amoebic - most common type worldwide (10% of world population) Hydatid disease - common in sheep-rearing countries
261
Recognise the presenting symptoms of liver abscesses.
- Fever - Malaise - Nausea - Anorexia - Night sweats - Weight loss - Right upper quadrant or epigastric pain - Referred shoulder pain due to diaphragmatic irritation - Jaundice - Diarrhoea - Pyrexia
262
Recognise the signs of liver abscesses on physical examination.
- Fever - continuous or spiking - Jaundice - Tender hepatomegaly, right lobe affected more commonly than left - Dullness to percussion at right base of lung - Reduced breath sounds at right base of lung (due to reactive pleural effusion)
263
Identify appropriate investigations for liver abscesses and interpret the results.
1. Bloods 2. Stool microscopy - for E. histolytica or tapeworm eggs 3. Liver US or CT/MRI - localise structure of mass 4. CXR - right pleural effusion or atelectasis, raised hemi-diaphragm 5. Aspiration and culture of the abscess material - most are polymicrobial, contain 'anchovy sauce' fluid of necrotic hepatocytes and trophozoits (amoebic abscesses) Bloods - FBC - mild anaemia, leukocytosis, high eosinophils in hydatid disease - LFTs - high AlkPhos, high bilirubin - High ESR - High CRP - Blood cultures - Amoebic and hydatid serology
264
Define liver cysts.
Liver infection resulting in a walled off collection of cyst fluid.
265
Explain the aetiology / risk factors of liver cysts.
Pyogenic: - E.coli - Klebsiella - Enterococcus - Bacteroides - Streptococci - Staphylococci - 60% caused by biliary tract disease - gallstones, strictures, congenital cysts - 15% are cryptogenic Amoebic: - Entamoeba histolytica Hydatid Cyst: - Tapeworm Echinococcus granulosis Others: - TB
266
Summarise the epidemiology of liver cysts.
Pyogenic - 0.8 in 100,000, 60 yrs mean age, most common in industrialised world Amoebic - most common type worldwide (10% of world population) Hydatid disease - common in sheep-rearing countries
267
Recognise the presenting symptoms of liver cysts.
- Fever - Malaise - Nausea - Anorexia - Night sweats - Weight loss - Right upper quadrant or epigastric pain - Referred shoulder pain due to diaphragmatic irritation - Jaundice - Diarrhoea - Pyrexia
268
Recognise the signs of liver cysts on physical examination.
- Fever - continuous or spiking - Jaundice - Tender hepatomegaly, right lobe affected more commonly than left - Dullness to percussion at right base of lung - Reduced breath sounds at right base of lung (due to reactive pleural effusion)
269
Identify appropriate investigations for liver cysts and interpret the results.
1. Bloods 2. Stool microscopy - for E. histolytica or tapeworm eggs 3. Liver US or CT/MRI - localise structure of mass 4. CXR - right pleural effusion or atelectasis, raised hemi-diaphragm 5. Aspiration and culture of the abscess material - most are polymicrobial, contain 'anchovy sauce' fluid of necrotic hepatocytes and trophozoits (amoebic abscesses) Bloods - FBC - mild anaemia, leukocytosis, high eosinophils in hydatid disease - LFTs - high AlkPhos, high bilirubin - High ESR - High CRP - Blood cultures - Amoebic and hydatid serology
270
# Define liver failure. Hyperacute, acute, subacute, acute-on-chronic.
Severe liver dysfunction leading to jaundice, encephalopathy and coagulopathy. Hyperacute - jaundice with encephalopathy occurring in < 7 days Acute - jaundice with encephalopathy occurring from 1 to 4 weeks of onset. Subacute - jaundice with encephalopathy occurring within 4-12 weeks of onset Acute-on-chronic - acute deterioration (decompensation) in patients with chronic liver disease
271
Explain the aetiology / risk factors of liver failure.
Viral - Hep A, B, D, E, non A-E hepatitis Drugs - paracetamol overdose, idiosyncratic drug reactions (e.g. anti-TB therapy) Less commonly - autoimmune hepatitis, Budd-Chiari syndrome, pregnancy-related, malignancy, haemachromatosis, mushroom poisoning (Amanita phalloides), Wilson's disease Pathogenesis of manifestations: - Jaundice --> decreased secretion of conjugated bilirubin - Encephalopathy --> increased delivery of gut-derived products into the systemic circulation and brain from decreased extraction of nitrogenous products by liver and portal systemic shunting , ammonia build up - Coagulopathy --> decreased synthesis of clotting factors, decreased platelets, hypersplenism (if chronic portal hypertension), platelet functional abnormalities associated with renal failure and jaundice.
272
Summarise the epidemiology of liver failure.
50% of acute liver failure = paracetamol overdose.
273
Recognise the presenting symptoms of liver failure.
- Fever - Nausea - Jaundice
274
Recognise the signs of liver failure on physical examination.
- Jaundice - Encephalopathy - Liver asterixis - negative myoclonus, liver flap - Fetor hepaticus - smell of pear drops - Ascites - Splenomegaly - Bruising - Bleeding from puncture sites or GI tract - Look for secondary causes - bronze skin colour, Kayser-Fleischer rings (Wilson's) - Pyrexia (infection or necrosis)
275
Identify appropriate investigations for liver failure and interpret the results.
1. Identify the cause 2. Bloods 3. US Liver, CT - image liver 4. Ascitic fluid 5. Doppler screening of hepatic or portal veins - exclude Budd-Chairi syndrome 6. Electroencephalogram - monitor encephalopathy Identification: - Viral serology - Paracetamol levels - Autoantibodies - e.g. ASM, LKM antibody, Ig - Ferritin - Caeruloplasmin - Urinary copper - Wilson's Bloods: - FBC - low Hb if GI bleed, high WCC if infection - U&E - renal failure (hepatorenal failure) - Glucose - LFT - high bilirubin, transaminases, AlkPhos, GGT, low albumin - ESR/CRP - Coagulation screen - high PT, INR - ABG - to determine pH - Group and save - for future transfusions Ascitic fluid: - Tap ascites and send for microscopy - Culture - Biochemistry (glucose, protein) - Cytology - >250 neutrophil/mm^3 = SBP NB: Budd-Chiari - hepatic venous outflow tract obstruction
276
Generate a management plan for liver failure.
- Resuscitation - according to airway, breathing, circulation --> ITU care, specialist unit support essential due to invasive ventilatory and CV support needed - Treat cause - N-acetylcysteine for paracetamol overdose Prevention of complications: - Monitor vital signs, PT, pH, creatinine, urine output, encephalopathy - Manage encephalopathy by lactulose and phosphate enemas - Antibiotic and antifungal prophylaxis - Hypoglycaemia treatment - Coagulopathy treatment - IV VitK, FFP, platelet infusion - Gastric mucosa protection - PPI, sulcralfate - Avoid sedatives or drugs metabolised by liver - Cerebral oedema - nurse patient at 30 degrees, reduced intracranial pressure by IV mannitol, hyperventilate Renal failure: - Haemofiltration - Nutritional support - King's College Hospital for liver transplant Surgical Treatment: If due to paracetamol overdose: - Arterial pH <7.3 - PT > 100s, creatinine >300 and severe encephalopathy For other causes (3 out of 5): - Age <10 or >40 years - Bilirubin >300 uM - Caused by non-A, non-E viral hepatitis or drugs - Interval from jaundice onset to encephalopathy >7days - PT >100s
277
Identify the possible complications of liver failure and its management.
- Infection - Coagulopathy - Hypoglycaemia - Disturbances of electrolyte - Acid-base and CV system failure - Hepatorenal syndrome - Cerebral oedema - Increased intracranial pressure - Respiratory failure
278
Summarise the prognosis for patients with liver failure.
Depends on severity and aetiology of liver failure. Poor prognostic indicators shown under surgical management. Use Childs-Pugh score.
279
Define Mallory-Weiss tear.
Persistent vomiting / retching causes haematemesis via an oesophageal mucosal tear. A tear of laceration often along the right border, or near, the gastro-oesophageal junction.
280
Explain the aetiology / risk factors of a Mallory-Weiss tear.
Risk factors: - Condition predisposing to retching, vomiting, straining - Chronic cough - Hiatal hernia - Retching during endoscopy or other instrumentation
281
Summarise the epidemiology of a Mallory-Weiss tear.
Accounts for 3-15% of patients' gastrointestinal bleed.
282
Recognise the presenting symptoms of a Mallory-Weiss tear.
- Haematemesis - vomiting blood - Light-headedness (dizziness) - Dysphagia - Odynophagia - painful swalling - Stools with blood in them (or black) - Weakness - Shortness of breath - Diarrhea - Abdominal pain
283
Recognise the signs of a Mallory-Weiss tear on physical examination.
- Haematemesis - vomiting blood - Postural / orthostatic hypotension - Stools with blood in them (or black) - Pallor - Abdominal pain
284
Identify appropriate investigations for a Mallory-Weiss tear and interpret the results.
Definitive diagnosis by oesophagogastroduodenoscopy. - Bloods - FBC, urea, LFT, PT/INR, CK, CK-MB, troponin - ECG
285
Generate a management plan for a Mallory-Weiss tear.
Actively bleeding patient --> therapeutic endoscopy to diagnose MWT and rule out other causes of upper GI bleeding. Rarely - angiography with embolisation of arteries supplying region, or surgical repair to control bleeding 1st line: Urgent evaluation + monitoring Plus: Endoscopy with/without intervention Plus: Anti-gastric acid therapy pre-endoscopy Adjunct: Anti-emetic pre-endoscopy Adjunct: Somatostatin analogue pre-endoscopy Adjunct: Erythromycin pre-endoscopy 2nd line: Surgical intervention or Sengstaken-Blakemore tube
286
Identify the possible complications of a Mallory-Weiss tear and its management.
- Severe internal bleeding - Rapid pulse, drop in blood pressure, trouble producing urine, shock - Anaemia with fatigue - Shortness of breath - Complications from endoscopy or surgery - e.g. bleeding, infection, organ damage
287
Define nasogastric tube insertion.
Gaining access to the stomach via the nose, to enable the drainage of gastric contents, decompression of the stomach, obtainment of a speciment of gastric contents, and introduction of a passage into the GI tract (e.g. enteral feeding, medication).
288
Summarise the indications for a nasogastric tube insertion.
- Malnutrition - Dysphagia - e.g. motor neurone disease, post CVA - Upper GI obstruction (stricture, tumour) - Sedation (in ICU) Need for: - Decompressing the stomach or GI tract - e.g. gastric outflow obstruction, ileus, intestinal obstruction - Gastric lavage - Administration of food and drugs
289
Identify the possible complications of a nasogastric tube insertion.
- Pain - Loss of electrolytes - Oesophagitis - Tracheal or duodenal intubation - Necrosis (retro- or nasopharyngeal) - Stomach perforation
290
Define non-alcoholic steatohepatitis (NASH) or non-alcoholic fatty liver disease (NAFLD).
A clinico-histopathological entity that includes a spectrum of conditions characterised histologically by macrovesicular hepatic steatosis in thsoe who do not consume alcohol in amounts generally considered harmful to the liver.
291
Define non-alcoholic steatohepatitis (NASH) or non-alcoholic fatty liver disease (NAFLD).
A clinico-histopathological entity that includes a spectrum of conditions characterised histologically by macrovesicular hepatic steatosis in thsoe who do not consume alcohol in amounts generally considered harmful to the liver.
292
Explain the aetiology / risk factors of non-alcoholic steatohepatitis (NASH) or non-alcoholic fatty liver disease (NAFLD).
High fat in hepatocytes = steatosis Cannot be attributed to other causes - consider if men < 18units a week, women <9 units a week Inflammation present - high LFT, high ALT Risk factors: - Obesity - Insulin resistance or diabetes - Dyslipidaemia - Hypertension - Older age
293
Summarise the epidemiology of non-alcoholic steatohepatitis (NASH) or non-alcoholic fatty liver disease (NAFLD).
Most common cause of chronic liver disease in the Western world. Leading indication for liver transplant soon - superseding HepC.
294
Recognise the presenting symptoms of non-alcoholic steatohepatitis (NASH) or non-alcoholic fatty liver disease (NAFLD).
- Fatigue - Malaise - Right upper quadrant abdominal discomfort - Pruritus
295
Recognise the signs of non-alcoholic steatohepatitis (NASH) or non-alcoholic fatty liver disease (NAFLD) on physical examination.
- Absence of significant alcohol use - Hepatomegaly - Splenomegaly - Right upper quadrant abdominal discomfort - Excoriations due to pruritus relief - Spider angioma
296
Identify appropriate investigations for non-alcoholic steatohepatitis (NASH) or non-alcoholic fatty liver disease (NAFLD) and interpret the results.
- Bloods - e.g. aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, AlkPhos, gamma glutamyl transferase, ammonia - Fasting insulin - Homeostatic model assessment (HOMA) calculation - Alpha fetoprotein
297
Identify the possible complications of non-alcoholic steatohepatitis (NASH) or non-alcoholic fatty liver disease (NAFLD) and its management.
- NASH - non-alcoholic steatohepatitis - Cirrhosis --> screen for HCC with ultrasound + AFP twice-yearly - Diabetes Mellitus
298
Summarise the prognosis for patients with non-alcoholic steatohepatitis (NASH) or non-alcoholic fatty liver disease (NAFLD).
Progression to cirrhosis may occur - need a biopsy or elastography.
299
Define oesophageal cancer.
Malignant tumour arising in the oesophageal mucosa. 2 major histological types - squamous cell carcinoma and adenocarcinoma.
300
Explain the aetiology / risk factors of oesophageal cancer.
Barrett's oesophagus (intestinal metaplasia) can progress to low-grade, high-grade and invasive carcinoma. Spread is typically initially direct (no serosa on oesophagus) and longitudinal --> via submucosal lymphatics to tracheobronchial, mediastinal, coeliac, gastric or cervical nodes. Rare oesophageal tumours = lymphoma, melanoma, leiomyosarcoma. Squamous Cell Carcinoma: - More common in mid-upper oesophagus - Alcohol - Tobacco - Nutritional deficiency - e.g. vitamines, trace elements - HPV infection - Achalasia - Paterson-Kelly (Plummer-Vinson) Syndrome - Tylosis (Howel-Evans Syndrome) - Scleroderma - Coeliac disease - Lye stricture - History of previous thoracic radiotherapy or upper aerodigestive squamous cancer - Dietary nitrosamines Adenocarcinoma: - More common in lower oesophagus or gastro-oesophageal junction - GORD - Barrett's oesophagus - intestinal metaplasia of distal oesophageal mucosa
301
Summarise the epidemiology of oesophageal cancer.
8th most common malignancy - UK 7000-8000 per year M:F 3-4:1 High incidence in northern China, Iran, southern Russia Adenocarcinoma more common in Westernized countries - 65% cases in UK, increasing by 5-10% per year Peak incidence 60-70 years
302
Recognise the presenting symptoms of oesophageal cancer.
Early: - Symptomatic of reflux Late: - Dysphagia - Regurgitation - Cough - Choking after food - Odynophagia - Weight loss - Fatigue - Voice hoarseness (recurrent laryngeal nerve palsy?)
303
Recognise the signs of oesophageal cancer on physical examination.
No physical signs evident - Weight loss - Supraclavicular lymphadenopathy - Hepatomegaly - Aspiration or direct tracheobronchial involvement --> respiratory signs
304
Identify appropriate investigations for oesophageal cancer and interpret the results.
1. Endoscopy 2. Imaging 3. Other Endoscopy - tumour location and biopsy, using narrow band imaging or magnification to grade and detect Imaging - e.g. Barium swallow, CT (chest, abdo, pelvis), PET (metastasis) Other - Bronchoscopy (if risk of tracheobronchial invasion), bone scan, laparscopy, peritoneal washings, thoracoscopy
305
Define open abdominal surgery (including laparotomy).
A surgical incision into the abdominal cavity, for diagnosis or in preparation for major surgery.
306
Summarise the indications for open abdominal surgery (including laparotomy).
- Rupture of an organ - e.g. spleen, aorta, ectopic pregnancy Signs: Blood loss & shock & abdominal swelling Think about: Trauma - blunt to spleen (can be very delayed), penetrating to liver? - Peritonitis - e.g. perforation of peptic ulcer, duodenal ulcer, diverticulum, appendix, bowel, gallbladder Signs: Prostration, shock, lying still ,+ve cough test, tenderness, board-like abdominal rigidity, guarding, no bowel sounds, gas under diaphragm. NB: Acute pancreatitis - similar signs, but does not require laparotomoy, always check serum amylase.
307
Define pancreatic cancer.
Malignancy arising from the exocrine or endocrine tissues of the pancreas.
308
Define pancreatic cancer.
Malignancy arising from the exocrine or endocrine tissues of the pancreas. [primary pancreatic ductal adenocarcinoma - 85%+ of pancreatic neoplasms]
309
Explain the aetiology / risk factors of pancreatic cancer.
Unknown cause. 5-10% familial component - Hereditary syndrome - BRCA2 mutation - Familial atypical multiple mole melanoma (CDKN2A) - Peutz-Jeghers (STK11/LKB1) - Hereditary pancreatitis (PRSS1) - MEN - HNPCC - FAP - Gardner - von Hippel-Lindau Syndromes Precursor lesions - e.g. pancreatic intraductal neoplasia, intraductal pancreatic mucinous neoplasm, mucinous cystic neoplasm Linear progression from pre-invasive pancreatic intraductal neoplastic lesions to invasive ductal adenocarcinoma. Risk factors: - Smoking - Family history of pancreatic cancer - Other hereditary cancer syndromes - Chronic sporadic pancreatitis
310
Summarise the epidemiology of pancreatic cancer.
8-12/100,000 8th cause of cancer deaths worldwide x2 males 60-80 years (peak age)
311
Recognise the presenting symptoms of pancreatic cancer.
Very non-specific: - Anorexia - Nausea - Malaise - Weight loss Later: - Jaundice - Epigrastric pain
312
Recognise the signs of pancreatic cancer on physical examination.
- Weight loss - Epigastric tenderness - Epigastric mass - Jaundice - Palpable gallbladder - Hepatomegaly (metastasis) - Trousseau's sign (due to superficial thrombophlebitis) - carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure for 3 minutes [Courvoisier's law - palpable gallbladder + painless jaundice isn't gallstones]
313
Identify appropriate investigations for pancreatic cancer and interpret the results.
1. Bloods 2. Imaging 3. Other Bloods - Tumour markers CA19-9, CEA elevated - If jaundiced, high bilirubin, high ALP, deranged clotting Imaging - US - Endoscopic ultrasound - FNA - CT - MRI - PET - Laparoscopy - ERCPY - biopsy, bile cytology, stenting Other - Staging laparoscopy - Intraoperative ultrasound
314
Define pancreatitis (acute and chronic).
Acute: An acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems. Chronic: Chronic inflammatory disease of the pancreas characterised by irreversible parenchymal atrophy and fibrosis leading to impaired endocrine and exocrine function and recurrent abdominal pain.
315
Explain the aetiology / risk factors of pancreatitis (acute and chronic).
Acute: - Insult results in activation of pancreatic proenzymes within the duct / acini resulting in tissue damage and inflammation - Most common: gallstones, alcohol - Others: drugs (steroids, azathioprine, thiazides, valproate), trauma, ERCP, abdominal surgery, infective (mumps, EBV, CMV, coxsackie B, mycoplasma), hyperlipidaemia, hyperparathyroidism, anatomical (pancreas divisum, annular pancreas), idiopathic Chronic: - Alcohol (70%), Idiopathic (20%) - Rare causes: recurrent acute pancreatitis, ductal obstruction, pancreas divisum, hereditary pancreatitis, tropical pancreatitis, autoimmune pancreatitis, hyperparathyroidism, hypertriglyceridemia.
316
Summarise the epidemiology of pancreatitis (acute and chronic).
Acute: - 10/10,000 - Peak age 60 years - Male - alcohol-induced - Female - gallstones Chronic: - 1/100,000 UK annual incidence - 3/100,000 UK annual prevalence - Mean age 40-50 years in alcohol-associated disease
317
Recognise the presenting symptoms of pancreatitis (acute and chronic).
Acute: - Severe epigastric or abdominal pain - Radiation of pain to back - Relieved by sitting forward - Aggravated by movement - Anorexia - Nausea - Vomiting - History of gallstones, alcohol intake Chronic: - Recurrent severe epigastric pain - Radiation of pain to back - Relieved by sitting forward - Exacerbated by eating or drinking alcohol - Weight loss - Bloating - Pale offensive stools = steatorrhoea Disruption of normal pancreatic glandular architecture due to chronic inflammation and fibrosis, calcification, parenchymal atrophy, ductal dilatation, cyst and stone formation. Pancreatic stellate cells are thought to play a role, converting fromquiescent fat stroing cells to myofibroblast-like cells forming extracellular matrix, cytokines and growth factors in response to injury Pain is associated with raised intraductal pressure and inflammation.
318
Recognise the signs of pancreatitis (acute and chronic) on physical examination.
Acute: - Epigastric tenderness - Fever - Shock - Tachycardia - Tachypnoea - Reduced bowel sounds - due to ileus - Turner's sign = flank bruising - Cullen's sign = periumbilical bruising Chronic: - Epigastric tenderness - Signs of complications - e.g. weight loss, malnutrition
319
Identify appropriate investigations for pancreatitis (acute and chronic) and interpret the results.
Acute: 1. Bloods - high amylase (3x normal), high WCC, high glucose, high CRP, low Ca2+, LFT deranged if gallstone/alcohol pancreatitis, ABG & U&Es 2. USS - for gallstones or biliary dilatation 3. CXR - pleural effusion? 4. AXR - other causes? psoas shadow may be lost 5. CT Scan - signs of sepsis, deterioration, Balthazar score, grade and degree of necrosis Chronic: 1. Bloods- glucose (high = endocrine dysfunction), glucose tolerance test, amylase, lipase, high Ig, high IgG4 in autoimmune pancreatitis 2. USS - percutaneous or endoscopic, show hyperechoic foci with post-acoustic shadowing 3. ERCP or MRCP - early (main duct dilatation, stumping of branches), late (duct strictures, alternating dilatation - chain of lakes) 4. AXR - pancreatic calcification may be visible 5. CT Scan - pancreatic cysts, calcification 6. Test of Pancreatic Exocrine Function - faecal elastase
320
Generate a management plan for pancreatitis (acute and chronic).
Acute: - Assessment by Modified Glascow combined with CRP (>210mg/L) - APACHE-II score - Ranson's criteria - only for alcoholic pancreatitis - Medical treatment - fluids, electrolytes, urinary catheter, NG tube, analgesia, blood sugar control, early HDU/ICU - Enteral nutrition shows reduced infective complications and mortality - Prophylactic antibiotics do NOT reduce mortality unless infective pancreatic necrosis develops - ERCP & Sphincterotomy - for gallstone pancreatitis, cholangitis, jaundice, dilated common bile duct within 72h, management of gallstones in 2 weeks - Early detection - if persistent symptoms, >30% pancreatic necrosis, signs of sepsis --> image guided fine needle aspiration for culture - Surgical - e.g. necrotising pancreatitis = necresectomy Chronic: - General - dietary advice, abstinence from alcohol and smoking, diabetes treatment, oral pancreatic enzyme replacements, analgesia - Chronic pain - sensory nerves to pancreas transverse the coeliac ganglia and splanchnic nerves = coeliac plexus block (CT or EUS-guided neurolysis) and transthoracic splanchnicetomy for pain relief - Endoscopic therapy - e.g. sphincterotomy, strone extraction, dilatation, stenting or strictures, extracorpeal shock-wave lithotripsy (fragmentation of stones) - Surgery - if medical management failed - e.g. lateral pancreaticojejunal drainage, resection, limited resection of pancreatic head, opening of pancreatic duct and excavation of pancreatic head (see book for names of procedures)
321
Identify the possible complications of pancreatitis (acute and chronic) and its management.
Acute: - Local - pancreatic necrosis, psuedocyst (persists >4 weeks), abscess, ascites, pseudoaneurysm, venous thrombosis - Systemic - multiorgan dysfunction, sepsis, renal failure, ARDS, DIC, hypocalcaemia, diabetes - Long term - chronic pancreatitis (with diabetes and malabsorption) Chronic: - Local - pseudocysts, biliary duct stricture, duodenal obstruction, pancreatic ascites, pancreatic carcinoma - Systemic - diabetes, steatorrhoea, reduced quality of life, chronic pain syndromes, dependence on strong analgesics
322
Summarise the prognosis for patients with pancreatitis (acute and chronic).
Acute: - 20% follow severe fulminating course with high mortality - Infected pancreatic necrosis associated with 70% mortality - 80% run milder course (still 5% mortality) Chronic: - Difficult to predict as pain may improve, stabilise or worsen - Surgery improved symptoms in 60-70%, often not sustained results - Life expectancy reduced by 10-20 years.
323
Define peptic ulcer disease and gastritis.
Peptic Ulcer Disease: Ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin. Most common: gastric, duodenal, oesophagus, Meckel's diverticulum Gastritis: The histological presence of gastric mucosal inflammation.
324
Explain the aetiology / risk factors of peptic ulcer disease and gastritis.
Peptic Ulcer Disease: Imbalance between damaging action of acid and pepsin, and mucosal protective mechanisms. Risk factors: - Helicobacter pylori infection - NSAID use - Smoking - Older age Gastritis: Risk factors: - Helicobacter pylori infection - NSAID use - Alcohol use - Hiatus hernia - Atrohic gastritis - Granulomas - e.g. Crohn's, sarcoidosis - Cytomegalovirus - Zollinger-Ellison Syndrome - Menetrier's disease - Toxic ingestions - Previous gastric surgery
325
Summarise the epidemiology of peptic ulcer disease and gastritis.
Peptic Ulcer Disease: - 1-4 / 1000 = common - Males - Mean age 30s = duodenal ulcers - Mean age 50s = gastric ulcers - H.pylori usually acquired in childhood, prevalence is equivalent to age in years Gastritis: - Epigastric pain - Dyspepsia - indigestion - Fever - Severe emesis (vomiting)
326
Recognise the presenting symptoms of peptic ulcer disease and gastritis.
Peptic Ulcer Disease: - Epigastric abdominal pain - Nausea - Vomiting - Early satiety - Relieved by antacids - If worse soon after eating = gastric ulcers - If worse several hours later = duodenal ulcers Gastritis: - No suspicious features of malignancy - Epigastric pain - Fever - Severe emesis (vomiting)
327
Recognise the signs of peptic ulcer disease and gastritis on physical examination.
Peptic Ulcer Disease: - No physical findings - Epigastric tenderness - Weight loss or anorexia - Signs of complications - e.g. anaemia, succession splash in pyloric stenosis Gastritis: - Upper GI Endoscopy if suspicious features
328
Identify appropriate investigations for peptic ulcer disease and gastritis and interpret the results.
Peptic Ulcer Disease: 1. Bloods 2. Endoscopy 3. Rockall Scoring 4. H.pylori Test Bloods - FBC - for anaemia - Amylase - exclude pancreatitis - U&E - Clotting screen - if GI bleeding - LFT - Cross-match - if actively bleeding - Secretin test - if Zollinger-Ellison Syndrome is suspected (IV secretin causes rise in serum gastrin in ZE patients) Endoscopy - 4 quadrant gastric ulcer biopsies to rule out malignancy - Duodenal ulcers does not need to be biopsied Gastritis: - H. pylori urea breath test - H. pylori faecal antigen test - FBC - Endoscopy - H. pylori rapid urease test - Gastric mucosal histology - Serum VitB12 - H. pylori culture / PCR
329
Generate a management plan for peptic ulcer disease and gastritis.
Peptic Ulcer Disease: - Acute - resuscitation if perforated or bleeding (IV colloids / crystalloids), close monitoring of vital signs, endoscopic / surgical treatment - Upper GI bleeding --> IV PPI at presentation until cause of bleeding is confirmed (continue if actively bleeding ulcers or high-risk stigmata ulcers) - Switch to oral PPI if no rebleeding in 24h - Endoscopy - haemostasis by injection sclerotherapy, laser or electrocoagulation - Surgery - If perforated or ulcer-related bleeding cannot be controlled - H-pylori eradication - 1 PPI + 2 antibiotics (triple therapy for 1-2 weeks) - Not H-pylori - PPIs or H2 antagonists, stop NSAIDs, use misoprostol (PGE1 analogue) Gastritis: - Antibiotics - treat H.pylori (1 PPI + 2 antibiotics) - Antacids - calcium carbonate - H2 antagonist - e.g. ranitidine, reduce production of stomach acid
330
Identify the possible complications of peptic ulcer disease and gastritis and its management.
Peptic Ulcer Disease: - 1% major complication rate per year - Haemorrhage presenting as haematemesis, melaena, iron-deficiency anaemia - Perforation - Obstruction / pyloric stenosis - due to scarring, penetration, pancreatitis Gastritis: - Bleeding from an erosion or ulcer - Gastric outlet obstruction due to oedema - Dehydration from vomiting - Renal insufficiency
331
Summarise the prognosis for patients with peptic ulcer disease and gastritis.
Peptic Ulcer Disease: - Lifetime risk 10% - Ulcers associated with H.pylori can be cured by eradication Gastritis: - Lead to stomach ulcers - Lead to stomach bleeding - Chronic - stomach cancer risk increased
332
Define perineal abscesses and fistulae.
Fistula - an abnormal connection between two epithelial surface, that often close spontaneously, but will not in the presence of malignant tissue, distal obstruction, foreign bodies, chronic inflammation or formation of muco-cutaneous junctions (e.g. stoma) Anorectal/ Perineal/Perianal Abscesses - a cavity filled with pus around either the anus or anus and rectum. Can be perianal (45%), ischiorectal (<30%), intersphincteric (>20%), supralevator (5%).
333
Explain the aetiology / risk factors of perineal abscesses and fistulae.
Anorectal abscesses - caused by gut organisms. Risk factors: - Anal fistula - Crohn's disease - Male sex - Hard stools - Malignancy
334
Summarise the epidemiology of perineal bscesses and fistulae.
Anorectal Abscesses: | - M:F 1:8
335
Recognise the presenting symptoms of perineal abscesses and fistulae.
- Perianal pain - Perianal swelling - Fever - Chills - Urinary retention - Sepsis from associated necrotising soft-tissue infection - History of Crohn's disease - Change in bowel habits
336
Recognise the signs of perineal abscesses and fistulae on physical examination.
- Perianal pain - Anal fistula - Leukocytosis - Low-grade fever - Tachycardia
337
Identify appropriate investigations for perineal abscesses and fistulae and interpret the results.
- Physical examination (DRE) - CT scan - US - MRI - Fistulography - Bloods - e.g.WBC, glucose, electrolytes
338
Generate a management plan for perineal abscesses and fistulae.
- Incise and drain under general anaesthetic - Adjunctive antibiotics (aminoglycosides, broad-spectrum with anaerobic and gram -ve coverage) - for patients with diabetes, immunocompromise, chronic debilitation, older age, history of cardiac valvular disease, extensive cellulitis - Fistulotomy - for elderly, immuno-compromised, cardiac valvular disease, diabetes, cellulitis
339
Identify the possible complications of perineal abscesses and fistulae and its management.
- Fistula formation - Bacteraemia - Sepsis - Seeing of the infection to other areas by haematogenous spread - Fecal incontinence - Malignancy
340
Summarise the prognosis for patients with perineal abscesses and fistulae.
High morbidity Reoccurance and chronic pain in >30% patients Chronic fistulae is common if treated only by incision and drainage.
341
Define peritonitis.
Inflammation of the peritoneum, caused by bacterial infection either via the blood or after rupture of an abdominal organ. E.g. Perforation of peptic ulcer, duodenal ulcer, diverticulum, appendix, bowel, gallbladder Spontaneous bacterial peritonitis - seen in patients with cirrhosis, and is an infection of ascitic fluid that can't be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition
342
Explain the aetiology /risk factors of peritonitis.
Due to bacterial infection Risk factors: - Decompensated hepatic state - Low ascitic protein / complement - GI bleeding - Endoscopic sclerotherapy for oesophageal varices
343
Summarise the epidemiology of peritonitis.
The prevalence of SBP in patients with cirrhosis and ascitis at the time of hospital admission ranges from 10-27%.
344
Recognise the signs of peritonitis on physical examination.
- Prostration - the action of lying stretched out on the ground - Ascites - Fever - Shock - Lying still - +ve cough test - Tenderness- with/without rebound / percussion pain - Board-like abdominal rigidity - Guarding - No bowel sounds - Erect CXR may show gas under the diaphragm - Hypothermia - Hypotension - Tachycardia
345
Identify appropriate investigations for peritonitis and interpret the results.
NB: Always check serum amylase as acute pancreatitis also shows these symptoms!
346
Identify appropriate investigations for peritonitis and interpret the results.
NB: Always check serum amylase as acute pancreatitis also shows these symptoms! - Ascitic fluid lab tests - cell count, culture - Urine - look at leukocyte esterase - Defined by ascitic fluid absolute neutrophil count >250cells/mm^3 - Ascitic fluid pH and asterial blood PH - Ascitic fluid protein, glucose, lactate dehydrogenase - Bloos - FBC, creatinine
347
Generate a management plan for peritonitis.
- Antibiotics - beware of local resistance patterns - If sepsis, history of fluoroquinolone prophylaxis, nosocomial-acquired SBP, history of previous infections with resistant organisms --> broader initial empirical coverage - Albumin indicated in renal dysfunction patients - Continuous antibiotic prophylaxis if ascitic fluid protein concerntation <15g/L or previous episode of SBP
348
Identify the possible complications of peritonitis and its management.
- Dehydration - Sepsis - Multiple organ infection / failure - Hepatic encephalopathy - Hepatorenal syndrome - liver disease leading to increasing renal failure - Shock - Death
349
Summarise the prognosis for patients with peritonitis.
Depends on underlying cause or how rapidly the patient is effectively treated, especially for infectious bacteria. Ranges from good (appendicitis) to poor (hepatorenal syndrome).
350
Define pilonidal sinus.
A small hole or tunnel in the skin, filled with fluid or pus, causing teh formation of a cyst or abscess.
351
Explain the aetiology / risk factors of pilonidal sinus.
The forceful insertion of hairs into the skin of the natal cleft in the sacrococcygeal area. This promotes a chronic inflammatory reaction, causing an epithelialised sinus. May be multiple sinuses and communicate via a deep cavity. Chronic discharge usually occurs, infection may supervene and lead to an abscess. Risk factors: - Male sex - 16-40yrs - Family history of pilonidal disease - Stiff hair - Hirsuitism
352
Summarise the epidemiology of pilonidal sinus.
Common Young men of working age M:F 10:1 Obses Caucasians and those from Asia, Middle East, Mediterranean at higher risk
353
Recognise the presenting symptoms of pilonidal sinus.
- Sacrococcygeal discharge - Sacrococcygeal pain - Sacrococcygeal swelling - Sacrococcygeal sinus tracts - Histroy of prior rupture of fluid into natal cleft - Skin maceration - Acutely increased natal cleft pain and swelling
354
Recognise the signs of pilonidal sinus on physical examination.
- Sacrococcygeal discharge - Sacrococcygeal pain - Sacrococcygeal swelling - Sacrococcygeal sinus tracts
355
Identify appropriate investigations for pilonidal sinus and interpret the results.
Clinical - no diagnostic tests. | Phsyical examination & inspection
356
Generate a management plan for pilonidal sinus.
- Excision of the sinus tract with/without primary closure - Drainage - Pre-operative antibiotics - Complex tracks laid open and packed individually or skin flaps to cover the defect - Hygiene and hair removal advice - Endoscopic ablation - hair and infected tissue removed, sinus cleaned, heat seals sinus
357
Identify the possible complications of pilonidal sinus and its management.
- Systemic Infection - Abscess formation - requires urgent surgical drainage - Recurrence of the pilonidal cyst - Squamous cell carinoma - development of a form of skin cancer within the cyst
358
Summarise the prognosis for patients with pilonidal sinus.
Many can live asymptomatic and can be treated with conservative measures - e.g. phenol infection, simple excision and drainage
359
Define portal hypertension.
Increased pressure in portal venous system - normal being 10mHg.
360
Explain the aetiology / risk factors of portal hypertension.
Pre-hepatic - portal/splenic vein thrombosis Hepatic - cirrhosis, granulomata, schistomasomiasis Post-hepatic - Budd-Chiari syndrome (hepatic vein thrombosis), congestive cardiac failure, constritcive pericarditis Cirrhosis is the main cause of portal hypertension - risk factors for cirrhosis are IVDU, tattooing/piercing in unhygienic condition, needlestick injury, blood transfusion before1992, vrial hepatitis, unprotected sexual intercourse Also caused by hepatitis, alcohol abuse, autoimmune hepatits, primary sclerosing cholangitis, primary biliary cholangitis
361
Summarise the epidemiology of portal hypertension.
Incidence is 25,000 cases per 100,000 individuals with non-alcholic fatty liver disease. Cirrhosis (main cause) prevalence is 270 cases per 100,000 in the US.
362
Recognise the presenting symptoms of portal hypertenion.
- GI bleeding - e.g. black, tarry stools - Ascites - Cramping - Bloating - Shortness of breath
363
Recognise the signs of portal hypertension on physical examination.
- Black, tarry stools (melena) | - Ascites
364
Identify appropriate investigations for portal hypertension and interpret the results.
- Difficult to diagnose if symptoms aren't obvious - Doppler ultrasound - reveal condition of portal vein and how blood is flowing through it - Look at ALTs, ASTs, gamma-GT - CT - Elastography - measures how tissue responds when pushed or probed - Endoscopy - Portal vein catheter with blood pressure monitor
365
Generate a management plan for portal hypertension.
- Lifestyle - e.g. improving diet, avoiding alcohol, exercising regularly, quitting smoking - Beta-blockers - Propranolol - Isosorbide - Diuretics - reduce fluid levels in body - Sodium restriction - help reduce fluid retention - Sclerotherapy or banding - stops bleeding in blood vessels of liver, verices - Non-surgical transjugular intrahepatic portal-systemic shunt (TIPSS) - control acute bleeding
366
Identfiy the possible complications of portal hypertension and its management.
F1 Teaching: - There are junctions between portal veins and normal circulation veins where the portal veins look to offload high pressure blood. - Normal circulation veins are not equipped to deal with the high pressure of blood - Areas of anastamosis become enlarged, engorged and balloon - e.g. oesophageal varices, caput medusae (superficial epigastric veins) Complications: - Oesophageal varices - Caput medusae - Burst of oesophageal varices and blood loss - Portal hypertensive gastropathy - affects mucus membrane of stomach and enlarges blood vessels Risk Factors of Variceal Bleeds: - High portal pressure - Variceal size - Endoscopic features of variceal wall - Advanced liver disease
367
Summarise the prognosis for patients with portal hypertension.
Cannot reverse cirrhosis damage Lifestyle changes -dietary restrictions, abstain from alcohol and drugs As long as liver function is maintained, survival rates are high
368
Define primary biliary cirrhosis.
A chronic inflammatory liver disease involving progressive desturction of intrahepatic bile ducts, leading cholestasis and cirrhosis.
369
Explain the aetiology / risk factors of primary biliary cirrhosis.
Unknown aetiology. Autoimmune, genetic, environmental factors. E.g. infection, chemical, toxin - causes bile duct epithelial injury. T-cell mediated autoimmune response directed against bile duct epithelial cells. Risk factors: - Female - 45-60 years - Family history of PBC/autoimmune disease - Smoking
370
Summarise the epidemiology of primary biliary cirrhosis.
Prevalence is 10-20 in 100,000 in UK | Middle aged women - (W:M 9:1)
371
Recognise the presenting symptoms of primary biliary cirrhosis.
Insidious onset - Fatigue - Weight loss - Pruritis - itching of the skin - Right upper quadrant discomfort - Liver decompensation - e.g. jaundice, ascites, variceal haemorrhage - Associated conditions - e.g. Sjogren's syndrom (dry eyes, mouth), arthritis, Raynaud phenomenon
372
Recognise the signs of primary biliary cirrhosis on physical examination.
May be incidental finding on blood tests - e.g. high AlkPhos, high cholesterol Early - may be no signs Late: - Jaundice - Skin pigmentation - Scratch marks - Xanthomas - secondary to hypercholesterolaemia - Hepatomegaly - Ascites - Liver disease Signs of Chronic Liver Disease: - Palmar erythema - Clubbing - Spider naevi
373
Identify appropriate investigations for primary biliary cirrhosis and interpret the results.
1. Bloods 2. Ultrasound - exclude extrahepatic biliary obstruction by gallstones or stricture 3. Liver biopsy Bloods: - LFT - high AlkPhos, high GGT, high/normal bilirubin, normal transaminases at start followed by increase on disease progession and cirrhosis - Clotting - prolonged PT - Antimitochrondrial antibodies (AMA) - High IgM - High cholesterol - TFTs - associated with autoimmune thyroid disease - Plasma calcium phosphate - Plasma 25-hydroxyVitD Liver Biopsy - Chronic inflammatory cells and granulomas around intrahepatic bile ducts - Destruction of bile ducts - Fibrosis - Regenerating nodules of hepatocytes
374
Define primary sclerosing cholangitis.
Chronic cholestatic liver disease characterized by progressive inflammatory fibrosis and obliteration of intrahepatic and extrahepatic bile ducts.
375
Explain the aetiology / risk factors of primary sclerosing cholangitis.
Unknown. Immune, genetic predisposition, toxic or infective triggers. Close association with IBD, UC - present in 70%. 5% of those with UC will develop PSC. Risk factors: - Male sex (2:1) - Inflammatory bowel disease - Genetic predisposition
376
Summarise the epidemiology of primary sclerosing cholangitis.
2-7 in 100,000. | Presents between 25-40yrs.
377
Recognise the presenting symptoms of primary sclerosing cholangitis.
Asymptomatic or diagnosed after high AlkPhos. - Intermittent jaundice - Pruritis - itchiness - Right upper quadrant pain - Weight loss - Fatigue - Fever & rigors less common - caused by acute cholanitis - History of UC - Symptoms of complications
378
Recognise the signs of primary sclerosing cholangitis on physical examination.
- No signs - Jaundice - Heptosplenomegally - Spider naevi - Palmar erythema - Ascites Periductal infalmmation with periductal concentric fibrosis (onnion skin), portal oedema, bile duct proliferation, expansion of portal tracts, progressive fibrosis, development of biliary cirrhosis.
379
Identfiy appropriate investigations for primary sclerosing cholangitis and interpret the results.
1. Bloods 2. Serology 3. ERCP 4. MRCP - non-invasive imaging of biliary tree 5. Liver biopsy - diagnosis, staging Bloods - LFT - high AlkPhos, high GGT, mild high transaminases, low albumin, high bilirubin Serology - Immunoglobulin levels - high IgG in children, high IgM in adults - ASM and ANA - in 30% - AMA - absent - pANCA - in 70% ERCP - Stricturing and interspersed dilation (beading) or intrahepatic and extrahepatic bile ducts - Small diverticula on common bile duct
380
Define rectal prolapse.
The mucosa (partial/type 1) or all layers (complete/type 2) may protrude through the anus.
381
Explain the aetiology / risk factors of rectal prolapse.
- Lax sphincter - Prolonged straining - Chronic neurological and psychological disorders Risk factors: - Pregnancy - Previous surgery - Diarrhoea - Benign prostatic hypertrophy - COPD - Cystic fibrosis - Pertussis (whooping cough) - Pelvic floor dysfunuction - Parasitic infections - e.g. amebiasis, schistosomiasis - Neurologic disorders - lower back or pelvic trauma/lumbar disk disease, cauda equina syndrome, spinal tumours, multiple sclerosis - Disordered defecation - e.g. stool withholding
382
Summarise the epidemiology of rectal prolapse.
2.5 per 100,000
383
Recognise the presenting symptoms of rectal prolapse.
- Incontinence (75%) - Constipation - Rectal ulceration
384
Recognise the signs of rectal prolapse on physical examination.
- Rectal ulceration | - Rectal prolapse - full-thickness, mucosal or internal (internal intussusception)
385
Identify appropriate investigations for rectal prolapse and interpret the results.
- Physical examination (DRE) - Defecopgraphy - Anal manometry - Continence tests - Electromyography of anal sphincter, pelvic floor - Nerve stimulation tests - proctosigmoidoscopy - assess rectum for additional lesions (e.g. solitary rectal ulcers)
386
Define ulcerative colitis.
Chronic relapsing and remitting inflammatory disease affecting the large bowel.
387
Explain the aetiology / risk factors of ulcerative colitis.
Unknown - genetic susceptiility (Chr12,16), immune response to bacterial or self-antigens, environmental factors, altered neutrophil function, abnormality in epithelial cell integrity Risk Factors: - Positive family history of IBD - 15% - HLA-B27 - NSAIDs - Infection - High serum pANCA - Primary sclerosing cholangitis
388
Summarise the epidemiology of ulcerative colitis.
``` 1/1500 in developed world Higher in Ashkenazi Jews, Caucasians Uncommon before 10 years Peak onset 20-40yrs Equal sex ratio up to age 40, then higher in males ```
389
Recognise the presenting symptoms of ulcerative colitis.
- Bloody or mucous diarrhoea - stool frequency related to severity of disease - Tenesmus - recurrent inclination to evacuate bowels - Urgency - Crampy abdominal pain before passing stool - Weight loss - Fever - Symptoms of extra-GI manifestations
390
Recognise the signs of ulcerative coltis on physical examination.
- Iron-deficiency anaemia - Dehydration - Clubbing - Abdominal tenderness - Tachycardia - Blood, mucus and tenderness on PR examination - Signs of extra-GI manifestations
391
Identify appropriate investigations for ulcerative colitis and interpret the results.
1. Bloods 2. Stool 3. AXR 4. Flexible sigmoidoscopy or colonoscopy 5. Barium enema Bloods - FBC - low Hb, high WCC - High ESR - High CRP - Low albumin - Cross-match if severe blood loss - LFT Stool - Culture - infectious colitis is differential - Faecal calprotectin - marker for disease severity AXR - Rule out toxic megacolon Flexible -Oscopy - Determines severity, histological confirmation, detection of dysplasia Barium Enema - Musocal ulceration with granular appearance and filling defects (pseudo-polyps) - Featureless narrow colon - Loss of haustral pattern - leadpipe or hosepipe appearance - Colonoscopy and barium enema dangerous in acute exacerbations due to risk of perforation NB: Markers of Activity - low Hb - low albumin - high ESR or CRP - diarrhoea frequency - <4 is mild, 4-6 moderate, >6 severe - bleeding - fever
392
Generate a management plan for ulcerative colitis.
Acute Exacerbation: - IV rehydration - IV corticosteroids - Antibiotics - Bowel rest - Parenteral feeding - DVT prophylaxis - Monitor fluid balance and vital signs - Toxic megacolon --> low threshold for proctocolectomy and ileostomy as perforation has mortality of 30% - Mild disease --> oral, rectal 5-aminosalicyclic acid dervatives and rectal steroids - Moderate disease --> oral steroids, oral 5-aminosalicyclic acid, immunosuppression with azathioprine, cyclosporine, 6-mercaptopurine, infliximab (anti-TNF monoclonal antibodies) Advice: - Patient education and support - Treatmnet of complications - Regular colonoscopic surveillance Surgical - Indicated for failure of medical treatment,presence of complications or prevention of colonic carcinoma - Proctocolectomy with ileostomy or an ileo-anal pouch formation
393
Identify the possible complications of ulcerative colitis and its management.
GI: - Haemorrhage - Toxic megacolon - Perforation - Colonic carcinoma - in those with extensive disease for 10+ years - Gallstones - Primary sclerosing cholangitis Extra-GI Complications: - Uveitis - Renal calculi - Arthropathy - Sacroilitis - Ankylosing spondylitis - Erythema nodosum - Pyoderma gangrenosum - Osteoporosis - from steroid treatment - Amyloidosis
394
Summarise the prognosis for patients with ulcerative colitis.
A relapsing and remitting condition with normal life expectancy. ``` Poor prognostic factors (ABCDEF): A = Albumin <30g/l B = Blood PR C = CRP raised D = Dilated loops of bowel E = Eight or more bowel movements per day F = fever - >38 degrees in first 24h ```
395
Define folate deficiency.
Folate - found in green vegetables, nuts, yeast and liver Synthesised by the gut bacteria Body stores last for 4 months Maternal folate deficiency causes foetal neural tube defects. Is absorbed by duodenum and proximal jejunum.
396
Explain the aetiology / risk factors of folate deficiency.
Causes: - Poor diet - e.g. poverty, alcoholics, elderly - Increased demand - e.g. pregnancy, high cell turnover - seen in haemolysis, malignacy, inflammatory disease, renal dialysis - Malabsorption - e.g. coeliac disease, tropical sprue - Alcohol - Drugs - anti-epileptics (phenytoin, valproate), methotrexate, trimethoprim Risk factors: - Low dietary folate intake - Age >65 - Alcoholism - Pregnant or lactating
397
Summarise the epidemiology of folate deficiency.
Lower income economies - >20% | Higher income economies - <5%
398
Recognise the presenting symptoms of folate deficiency.
- Presence of risk factors - Prolonged diarrhoea - Headache - Loss of appetite - Weight loss - Fatigue
399
Recognise the signs of folate deficiency on physical examination.
- Presence of risk factors - Prolonged diarrhoea - Headache - Loss of appetite - Weight loss - Fatigue
400
Identify appropriate investigations for folate deficiency and interpret the results.
- Bloods - peripheral blood smear, FBC, reticulocyte count, serum folate, red blood cell folate, vitB12, LDH
401
Define volvulus.
When a loop of intestine twists around itself and the mesentery that supports it, resulting in a bowel obstruction.
402
Explain the aetiology / risk factors of volvulus.
The presence of a long mesentery with a narrow base of fixation to the retroperitoneum and elongated, redundant bowel predisposes to formation. - Develops in any portion of large bowel - Most common in sigmoid colon due to mesenteric anatomy - Less commonly - right colon, terminal ileum, cecum Risk factors: - Neuropsychiatric institutionalized patients or nuring home patients - Parkinson's disease - Multiple sclerosis - Spinal cord injury - Chronic ocnstipation - Excessive use of laxatives, cathartics and enemas - Megacolon - either congenital or Chagas disease acquired - Presence of pelvic mass - Pregnancy - Large ovarian tumours - Embryological abnormality (psychotropic drug interference with colonic motility)
403
Summarise the epidemiology of volvulus.
Responsibile for 5% of all cases of intestinal obstruction 10-15% of all cases of large bowel obstruction Most common sites are sigmoid colon (80%), cecum (15%), transverse colon (3%), splenic flexure (2%).
404
Recognise the presenting symptoms of volvulus.
- Vomiting bile - greenish-yellow digestive fluid - Drawing up the legs - Pain in the abdomen - Abdominal distention - Breathlessness - Bloody stools - Malnutrition
405
Recognise the signs of volvulus on physical examination.
- Drawing up the legs - Abdominal pain - Abdominal distention - Tachycardia - Tachypnoea
406
Identify appropriate investigations for volvulus and interpret the results.
- Upper GI contrast series - CT abdomen - with oral and IV contrast - Abdominal plain X-rays - FBC - US - Lower GI contrast series - ABG
407
Define Wilson's disease.
An autosomal recessive disorder characterized by reduced biliary excretion of copper and accumulation in the liver and brain, especially in the basal ganglia. Also known as hepatolenticular degeneration.
408
Explain the aetiology / risk factors of Wilson's disease.
Chr13 - codes for copper transporting ATPas (ATP7B) in hepatocytes Mutations interfere with transport of copper into the intracellular compartments for incorporation into caeruloplasmin (and secretion into plasma) or excretion into bile. Excess copper damages hepatocyte mitochondira, causing cell death and release of free copper into plasma, which is subsequently deposited in other tissues.
409
Summarise the epidemiology of Wilson's disease.
1 in 30,000 Carrier 1 in 100 Liver disease in children >5 years Neurological disease in adults (young)
410
Recognise the presenting symptoms of Wilson's disease.
Liver: - Hepatitis - Liver failure - Cirrhosis - Jaundice - Easy bruising - Variceal bleeding - Encephalopathy Neurological: - Dyskinesia - Rigidity - Tremor - Dystonia - Dysarthria - Dysphagia - Drooling - Dementia - Ataxia Psychiatric: - Conduct disorder - Personality change - Psychosis
411
Recognise the signs of Wilson's disease on physical examination.
Liver: - Hepatosplenomegaly - Jaundice - Ascites / oedema - Gynaecomastia Neurological: - Hepatosplenomegaly - Jaundice - Ascites / oedema - Gynaecomastia Eyes - Green or brown Kayser-Fleischer ring at the corneal limbus - Sunflower cataract (copper accumulation in the lens, seen with slit lamp)
412
Identify appropriate investigations for Wilson's disease and interpret the results.
1. Bloods 2. 24 hours urinary copper levels --> increased 3. Liver biopsy --> high copper content 4. Genetic analysis --> wide variety of mutations cause the disease, no simple genetic test, sequencing requires specialist genetic advice Bloods - LFT - high AST, ALT, AlkPhos (not usual Hepatic picture) - Serum caeruloplasmin and copper
413
Explain the aetiology / risk factors of Wilson's disease.
Chr13 - codes for copper transporting ATPas (ATP7B) in hepatocytes Mutations interfere with transport of copper into the intracellular compartments for incorporation into caeruloplasmin (and secretion into plasma) or excretion into bile. Excess copper damages hepatocyte mitochondira, causing cell death and release of free copper into plasma, which is subsequently deposited in other tissues. Risk factors: - ATP7B gene mutation - Non-vegetarian diet
414
Define viral hepatitis = A&E.
Hepatitis caused by infection with the RNA viruses, hepatitis A (HAV) and hepatitis E virus (HEV), that follow an acute course without progression to chronic carriage.
415
Explain the aetiology / risk factors of viral hepatitis = A&E.
``` HAV = picornavirus HEV = calcivirus ``` - Small - Non-enveloped - Single-stranded - Linear - RNA viruses - Transmission by faecal-oral route - Replicate in hepatocytes - Secreted into bile - Immune responses causes liver inflammation and hepatocyte necrosis = CD8+ T-cells, NK cells - Inflammatory cell infiltration of poral tracts = neutrophils, macrophages, eosinophils, lymphocytes - Zone 3 necrosis - Bile duct proliferation
416
Summarise the epidemiology of viral hepatitis = A&E.
HAV - Endemic in developing world, infection occurs sub-clinically - Better sanitation in developed world - age of exposure increases = more likely to be symptomatic 5000 cases (5% seroprevalence). HEV - Endemic in Asia, Africa and Central America
417
Recognise the presenting symptoms of viral hepatitis = A&E.
Incubation period of 3-6 weeks. Prodromal Period - Malaise - Anorexia - distate for cigarettes in smokers - Fever - Nausea - Vomiting Hepatitis - Dark urine - Pale stools - Jaundice lasting 3 weeks - Itching & prolonged jaundice in HAV - due to cholestatic hepatitis
418
Recognise the signs of viral hepatitis = A&E on physical examination.
- Pyrexia - Jaundice - Tender hepatomegaly - Palpable spleen in 20% - Absence of stigmata of chronic liver disease - Few spider naevi transiently
419
Identify appropriate investigations for viral hepatitis = A&E and interpret the results.
1. Bloods 2. Viral Serology 3. Urinalysis Bloods - LFT - High AST and ALT, High bilirubin, High AlkPhos - High ESR - Low albumin - High platelets Viral Serology - Hep A - anti-HAV IgM (during acute illness, disappears after 3-5 months), anti-HAV IgG (recovery phase, lifelong persistence) - Hep E - anti-HEV IgM (high 1-4 weeks after onset), anti-HEV IgG - Hep B & C - rule out Urinalysis - +ve for bilirubin - High urobilinogen
420
Generate a management plan for viral hepatitis = A&E.
- No specific management - Bed rest and symptomatic treatment - e.g. antipyretic, antiemetics - Colestyramine for severe pruritis Prevention: - Public health - e.g. safe water, sanitation, food hygiene, notifiable disease, personal hygiene, sensible dietary precautions when travelling - Immunization (HAV) - passive IM human immunoglobulin effective for short period, active attenuated HAV vaccine for travellers, high-risk individuals
421
Identify the possible complications of viral hepatitis = A&E and its management.
- Fulminant hepatic failure - 0.1% HAV cases, 1-2% HEV cases, 20% if pregnant - Cholestatic hepatitis with prolonged jaundice and pruritis after HAV infection - Post-hepatitis syndrome - continued malaise for weeks-months
422
Summarise the prognosis for patients with viral hepatitis = A&E.
3-6 weeks recovery Relapse during recovery occasionally No chronic sequelae Fulminant hepatic failure has 80% mortality
423
Define viral hepatitis = B&D.
Hepatitis caused by infection with hepatitis B virus (HBV), which may follow an acute or chronic (defined as viraemia and hepatic inflammation continuing >6 months) course. Hepatitis D virus (HDV), a defective virus, may only co-infect with HBV or superinfect persons who are already carriers of HBV.
424
Explain the aetiology / risk factors of viral hepatitis = B&D.
HBV - Enveloped - Partially double-stranded DNA virus - Sexual contact, blood and vertical transmission - Viral proteins produced - e.g. HBcAg, HBsAg, HBeAG = core, surface and e antigens HDV - Single-stranded RNA virus - Coated with HBsAG = surface antigen Antibody and cell-mediated immune responses to viral replication lead to liver inflammation and heptocyte necrosis. Mild-severe inflammation. Changes of cirrhosis. Risk Factors: - IV drug abuse - Unscreened blood and blood products - Infants of HBeAg-positive mothers - Sexual contact with HBV carrier - Younger individuals more likely to develop chronic carriage - Genetic factors - higher rates of viral clearance
425
Summarise the epidemiology of viral hepatitis = B&D.
Common 350 million worldwide infected with HBV 1-2million deaths annually Common in SE Asia, Africa, Mediterranean countries HDV found worldwide HBV uncommon in UK
426
Recognise the presenting symptoms of viral hepatitis = B&D.
- Incubation period of 3-6 months - 1-2 week prodrome - malaise, headache, anorexia, N&V, diarrhoea, RUQ pain - Serum-sickness-type illness - e.g. fever, arthralgia, polyarthritis, urticaria, maculopapular rash - Jaundice - Dark urine - Pale stools Recovery usually within 4-8 weeks - 1% may develop fulminant liver failure Chronic carriage diagnosed after routine LFT testing or if cirrhosis or decompensation develops.
427
Recognise the signs of viral hepatitis = B&D on physical examination.
Acute - Jaundice - Pyrexia - Tender hepatomegaly - Splenomegaly - Cervical lymphadenopathy (10-20%) - Urticaria - Maculopapular rash Chronic - No findings - Signs of chronic liver disease or decompensation
428
Identify appropriate investigations for viral hepatitis = B&D and interpret the results.
1. Viral Serology 2. PCR 3. LFT 4. Clotting 5. Liver biopsy Viral Serology - Acute - HBsAg positive, IgM anti-HBcAg - Chronic - HBsAg positive, igG anti-HBcAg, HBeAg positive or negative - HBV cleared or immunity - anti-HBsAg positive, IgG anti-HBcAg - HDV infection - detected by IgM or IgG against HDV PCR - Detection of HBV DNA - most sensitive measure LFT - High AST, ALT - High bilirubin - High AlkPhos Clotting - High PT in severe disease Liver Biopsy - Percutaneous - Transjugular if clotting is deranged or ascites present
429
Generate a management plan for viral hepatitis = B&D.
Prevention: - Passive immunization - HepB immunoglobulin (HBIG) - if acute exposure, neonates born to HBeAg-positive mothers - Active immunization - recombinant HBsAg vaccine - individuals at risk, neonates born to HBV-positive mothers, also protects against HDV Acute HBV Hepatitis: - Symptomatic treatment - e.g. bed rest, antiemetics, antipyretics, cholestyramine for pruritis - Notification of communicable disease Chronic HBV Heptaitis: - Indications for treatments with anti-virals = HBeAg-positive, HBeAg negative chornic hepatitis (dependents on ALT, HBV DNA), compensated cirrhosis and HBV DNA >2,000 IU/mL, decompensated cirrhosis and detectable HBV DNA by PCR - Interferon alpha - high half life - Nucleoside/nucleotide analogues - watch out for drug resistance - e.g. adefovir, entecavir, telbivudine, tenofovir, lamivudine Interferon Alpha - Cytokine - Augments natural antiviral mechanisms - SE: flu-like symptoms, fevers, chills,myalgia, headaches, bone marrow suppression, bone marrow depression
430
Identify the possible complications of viral heptaitis = B&D and its management.
- Fulminant hepatic failure - 1% - Chronic HBV infection (10% adults, higher in neonates) - Cirrhosis - Hepatocellular carcinoma - Extrahepatic immune complex disorders- e.g. glomerulonephritis, polyarteritis nodosa - Superinfection with DHV --> acute liver failure
431
Summarise the prognosis for patients with viral hepatitis = B&D.
10% of infections become chronic 20-30% of those will develop cirrhosis Factors of good response to inferferon: - High serum transaminases - Low HBV DNA - Active histological changes - Absence of complicating disease
432
Define viral hepatitis = HepC.
Hepatitis caused by infection with Hepatitis C (HCV), often following a chronic course. (80% cases).
433
Explain the aetiology / risk factors of viral hepatitis C.
HCV - Small - Eneveloped - Single-stranded RNA virus - Flavivirus family Poor fidelity of replication High mutation rates Different HCV genotypes - quasi-species Transmission: - Parenteral route - Recipients of blood and blood products prior to blood screening - IV drug users - Non-sterile acupuncture - Tattooing - Haemodialysis - Health care workers - Sexual and vertical transmission uncommon - 1-5%, increased risk in those co-infected with HIV Pathology - Hepatotropic - Not directly hepatotoxic - Humoural and cell-mediated response leads to hepatic inflammation and necrosis - Liver biopsy - chronic hepatitis - Lymphoid follicles in portal tracts - Fatty changes - Features of cirrhosis
434
Summarise the epidemiology of viral hepatitis C.
Common 0.5-2% in developed countries. Higher in certain areas due to poor sterilisation practices. Different HCV genotypes have different geographical prevalence.
435
Recognise the presenting symptoms of viral hepatitis C.
99% of acute infections = asymptomatic <10% jaundiced with flu-like illness Diagnosed after incidental abnormal LFT or in older individuals with complications of cirrhosis
436
Recognise the signs of viral hepatitis C on physical examination.
No signs of chronic liver disease in long-standing infection Les common: - Skin rash - due to mixed cryoglobulinaemia causing a small-vessel vasculitis - Renal dysfunction - due to glomerulonephritis
437
Identify appropriate investigations for viral hepatitis C and interpret the results.
1. Bloods 2. Liver Biopsy Bloods - HCV serology - anti-HCV antibodies (IgM acute, IgG past or chronic) - Reverse transcriptase PCR - detection of HCV RNA, confirm antibody testing - LFT - acute = high AST, ALT, chronic = 2-8x elevation of AST and ALT Liver biopsy - Assess degree of inflammation and liver damage as transaminase levels bear little correlation to histological changes - Diagnose cirrhosis - monitoring for hepatocellular carcinoma
438
Generate a management plan for viral heaptitis C.
Prevention - Screening of blood, blood products and organ donors - Needly exchange schemes for IV drug abusers - Instrument sterilization - No vaccine avaliable at present Medical Acute - No specific management and mainly supportive - e.g. anti-pyretics, anti-emetics, cholestyramine - Specific antiviral treatment delayed for 3-6 months Chronic - Combined treatment with pegylated interferon-alpha and ribavirin - Interferon-alpha = cytokine which auments natural antiviral mechanisms - Ribavirin = guanosine nucleotide analogue - HCV 1 or 4 = 24-48 weeks - HCV 2 or 3 = 12-24 weeks Monitoring of HCV load recommended after 12 weeks of treatment to determine efficacy of treatment. Regular ultrasound of liver may be necessary if the patient has cirrhosis.
439
Identify the possible complications of viral hepatitis C and its management.
- Fulminant hepatic failure in acute phase (0.5%) - Chronic HCV carriage - Cirrhosis - Hepatocellular carcinoma - Porphyria cuteanea tarda - Cryoglobulinaemia - Glomerulonephritis
440
Summarise the prognosis for patients with viral hepatitis C.
80% of exposed progress to HCV chronic. | 20-30% of these develop cirrhosis over 10-20 years.
441
Define vitamin deficiency (A, B, C, D, E, K)
A condition of a long-term lack of a particular vitamin. When caused by not enough vitamin intake it is classified as a primary deficiency, whereas when due to an underlying disorder such as malabsorption it is called a secondary deficiency.
442
Explain the aetiology / risk factors of vitamin deficiency (A, B, C, D, E, K).
Vitamin A : - Site of absorption = small intestine - Deficiency syndrome = Xerophthalmia Vitamin B: 1) B1 = Thiamine - small intestine --> Beriberi, Wenicke's 2) B2 = Riboflavin - proximal small intestine --> angular stomatitis, cheilitis 3) B6 = Pyridoxine - small intestine --> polyneuropathy 4) B12 - terminal ileum --> macrocytic anaemia, neuropathy, glossitis Vitamin C: - Site of absorption = proximal ileum - Deficiency syndrome = scurvy Vitamin D: - Site of absorption = jejunum - Deficiency syndrome = rickets, osteomalacia Vitamin E: - Site of absorption = small intestine - Deficiency syndrome = haemolysis, neurological deficit Vitamin K: - Site of absorption = small intestine - Deficiency syndrome = bleeding disorders Risk factors: - Impaired nutrient absorption capacity - e.g. GI disorders, IBD, coeliacs - Impaired vitamin B12 absorption in the elderly - Poor nutrient bioavaliability - Alcohol abuse - Anorexia Vitamin D Deficiency Risk Factors: - Having dark skin - Being elderly - Being overweight or obese - Not eating much fish or dairy - Living far form the equator where there is little sun year-round - Always using sunscreen when going out - Staying indoors
443
Summarise the epidemiology of vitamin deficiency (A, B, C, D, E, K).
The overall prevalence of deficiency of vitamins A, D, B1, B2, B6, and folate were 6%, 29%, 11%, 50%, 46%, and 32%, respectively. The prevalence of deficiency of vitamin B6 was 30% in the mild form and 16% in the severe form.
444
Recognise the presenting symptoms of vitamin deficiency (A, B, C, D, E, K).
Vitamin A Deficiency - e.g. Xeropthalmia - Dry conjunctivae and cornea - Oval / triangular spots on conjunctiva - Bitot's spots - Poor adaptation of vision to darkness Vitamin B1 (Thiamine) Deficiency - e.g. Beriberi - Leg swelling - Loss of feeling in hands and feet - Difficulty walking - Paralysis - Confusion - Pain - Tingling - Vomiting Vitamin B1 (Thiamine) Deficiency - e.g. Wernicke's - Confusion - Memory loss - Loss of muscle co-ordination - Nystagmus - Double Vision Vitamin B2 (Riboflavin) - e.g. Cheilitis, Angular Stomatitis - Pain and burning at the corners of the mouth - Bad taste in your mouth - Lips feeling dry or chapped - Difficulty eating as a result of the irritation Vitamin B6 (Pyridoxine) - e.g. Polyneuropathy - Weakness - Dizziness - Fatigue - Mood swings - Tingling and pain in hands and feet (peripheral neuropathy) Vitamin B12 - e.g. Macrocytic Anaemia, Neuropathy, Glossitis - Painful red tongue (glossitis) - Pins and needles (paraesthesia) - Changes in the way that you walk and move around - Disturbed vision - Irritabikity - Depression Vitamin C - e.g. Scurvy - Foul breath - Bleeding from gums, nose, hair follicles, into joints, bladder, gut - Muscle pain and weakness - Swelling (legs etc) Vitamin D - e.g. Rickets, Osteomalacia - Rickets - growth retardation, hypotonia, apathy, knock-kneed, bow-legged, deformities of the metaphyseal-epiphyseal junction, ill - Osteomalacia - bone pain, tenderness, fractures, proximal myopathy (waddling gait) Vitamin E - e.g. haemolysis, neurological defect - Loss of feeling in the arms and legs - Muscle weakness - Vision problems Vitamin K - e.g. bleeding disorders - Easy bruising - Oozing from nose or gums - Excessive bleeding from wounds, punctures, injection or surgical sites - Heavy menstrual periods - Bleeding from the GI tract - Blood in the urine and / or stool - Increased PT
445
Recognise the signs of vitamin deficiency (A, B, C, D, E, K) on physical examination.
Vitamin A Deficiency - e.g. Xeropthalmia - Oval / triangular spots on conjunctiva - Bitot's spots - Cloudy and soft cornea Vitamin B1 (Thiamine) Deficiency - e.g. Beriberi - Heart failure - General oedema (wet) - Neuropathy (dry) - Confusion - Nystagmus Vitamin B1 (Thiamine) Deficiency - e.g. Wernicke's - Nystagmus - Opthalmoplegia - Atrophy - Ataxia - Disorientation - Disturbance of memory Vitamin B2 (Riboflavin) - e.g. Cheilitis, Angular Stomatitis - Red or purple spots around the corners of the lips - Swelling or cracking at the corners of the lips - Dry, chapped lips around the corners of the mouth Vitamin B6 (Pyridoxine) - e.g. Polyneuropathy - Skin rash - seborrheic dermatitis - Cracked and sore lips - Glossitis - loss of papillae - Seizures Vitamin B12 - e.g. Macrocytic Anaemia, Neuropathy, Glossitis - Pale, yellow tinge to the skin - Glossitis - Mouth ulcers - Irritability - Vision changes - Muscle weakness - Ataxia - loss of physical co-ordination Vitamin C - e.g. Scurvy - Listlessness - Anorexia - Cachexia - Gingivitis - Loose teeth - Foul breath (halitosis) - Bleeding from gums, nose, hair follicles, joints, bladder, gut - Muscle pain / weakness - Oedema Vitamin D - e.g. Rickets, Osteomalacia - Rickets - growth retardation, hypotonia, apathy, knock-kneed, bow-legged, deformities of the metaphyseal-epiphyseal junction, ill - Osteomalacia - bone pain, tenderness, fractures, proximal myopathy (waddling gait) Vitamin E - e.g. haemolysis, neurological defect - Muscle weakness - Loss of body movement control - Weakened immune system Vitamin K - e.g. bleeding disorders - Easy bruising = ecchymosis - Oozing from nose or gums = epistaxis - Excessive bleeding from wounds, punctures, injection or surgical sites - Heavy menstrual periods - Bleeding from the GI tract - Blood in the urine and / or stool - Increased PT
446
Identify appropriate investigations for vitamin deficiency (A, B, C, D, E, K) and interpret the results.
- Bloods - check for Hb, RBC size, level of vitamins in the blood, level of folate in the blood - Identify the cause - Refer to haematologist, gastroenterologist and nutritionist - Erythrocyte thiamine pyrophosphate blood test - indicates body stores of thiamine - ABG - check for lactic acidosis, elevated lactate - Thyroid function tests - Brain MRI - check for complications etc.
447
Generate a management plan for vitamin deficiency (A, B, C, D, E, K).
Vitamin A Deficiency - e.g. Xeropthalmia - Vitamin A supplementation - per oral or inection - Antibiotics - prevention of secondary infections - Nutritional education - e.g. oils, fats, grains, milk, sugar, golden rice Vitamin B1 (Thiamine) Deficiency - e.g. Beriberi & Wenicke's - Thiamine supplements (Pabrinex) - 2 pairs of high potency ampoules IV/IM per 8h over 30 mins for 2 days, then 1 pair OD for a further 5d - Oral supplementation until no longer at risk (100mg OD) - Hypoglycaemia - give thiamine before glucose Vitamin B2 (Riboflavin) - e.g. Cheilitis, Angular Stomatitis - Dietary or supplement recommendations - Topical antifungal - Topical antiseptics - Topical steroid ointment - Filelr infections to reduce the creases at the corners of your mouth - Sipping water or sucking on a hard candy for dry mouth Vitamin B6 (Pyridoxine) - e.g. Polyneuropathy - Dietary or supplement recommendations - Exercise - Isonazid (30-450mg/d) and penicillamine (100mg/d) for prevention Vitamin B12 - e.g. Macrocytic Anaemia, Neuropathy, Glossitis - Dietary and supplement recommendations - e.g. meat, fish, eggs, dairy, yeast, green vegetables Vitamin C - e.g. Scurvy - Dietary education - Ascorbic acid >250mg/24 per oral Vitamin D - e.g. Rickets, Osteomalacia - Give Vitamin D - e.g. one calcium D3 forte tablet / 12h PO - Malabsorption or hepatic disease - give ergocalciferol (D2), up to 40,000 u daily, or parenteral calcitriol (7.5mg monthly) - Renal disease or Vitamin D resistance - give alfacalcidol (1-alpha-hydroxyvitamin D3) 250ng-1mcg daily, or calcitriol (1,25 VitD3) 250ng-1mcg daily - Adjust dose according to plasma calcium - Watch out for hypercalcaemia - Monitor nausea & vomiting Vitamin E - e.g. haemolysis, neurological defect - Oral Vitamin E dietary supplements Vitamin K - e.g. bleeding disorders - Phytonadione = Vitamin K1 per oral
448
Identify the possible complications of vitamin deficiency (A, B, C, D, E, K)and its management.
Vitamin A - e.g. Xeropthalmia - Corneal ulcers - Corneal scarring - Blindness - highest cause in Tropics Vitamin B1 (Thiamine) Deficiency - e.g. Beriber & Wernicke's - Korsakoff's Psychosis (85%) - Death (20%) Vitamin B2 (Riboflavin) - e.g. Cheilitis, Angular Stomatitis - Bacterial or fungal infection spreads to adjacent skin - Oral thrush ``` Vitamin B6 (Pyridoxine) - e.g. Polyneuropathy - High pyridoxine - neuropathy characterized by ataxia and burning pain in the feet, hypolacticemia in pregnancy, drop in BP ``` Vitamin B12 - e.g. Macrocytic Anaemia, Neuropathy, Glossitis - CNS disturbance & peripheral neuropathy - Stomach cancer - Infertilty - Tachycardia - Heart failure - Prognancy complications - Birth defects - e.g. neural tube defects such as spina bifida, anencephaly, encephalocele Vitamin C - e.g. Scurvy - Scurvy - Connective tissue defects - e.g. gingivitis, petechiae, rash, internal bleeding, impaired wound healing Vitamin D - e.g. Rickets, Osteomalacia - Osteomalacia - Osteoporosis - Rickets (children) - Seasonal affective disorder (SAD) - Depression - Increased susceptibility of infections and illnesses Vitamin E - e.g. haemolysis, neurological defect - Fragility of red blood cells - Deneration of neurones - peripheral axons, posterior column neurones - Disorientation - Vision problems Vitamin K - e.g. bleeding disorders - Significant bleeding - Poor bone development - Osteoporosis - Higher risk of CVD
449
Summarise the prognosis for patients with vitamin deficiency (A, B, C, D, E, K).
Bad prognosis for very advanced patients who do not recieve supplementation and pharmacological help. Significant public health problem in developing world, areas of war or natural disasters.