Liver and GI (& GU!) Flashcards

1
Q

Why does physiological neonatal jaundice occur?

A
  • foetal Hb broken down as it is replaced by adult Hb
  • liver metabolic pathways are immature and unable to conjugate bilirubin
  • bilirubin accumulates in the blood
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2
Q

What are some causes of unconjugated hyperbilirubinaemia?

A
  • haemolysis
  • impaired hepatic uptake
  • impaired conjugation
  • physiological newborn jaundice
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3
Q

What can cause impaired hepatic uptake of bilirubin?

A
  • drugs

- right heart failure causing hepatic venous congestion

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4
Q

What can cause impaired conjugation of bilirubin?

A
  • Gilbert’s syndrome - decreased UGT enzyme activity

- Crigler Najjar disease - mutation in UGT causing impairment or absence of the enzyme

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5
Q

Appearance of urine and stool in unconjugated hyperbilirubinaemia?

A
  • normal urine and stool
  • unconjugated bilirubin cannot be excreted via urine therefore urine not dark
  • stercobilin is not obstructed to stool is a normal colour
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6
Q

Appearance of urine and stool in conjugated hyperbilirubinaemia?

A
  • dark urine and pale stool
  • excessive conjugated bilirubin can be excreted in urine so urine is dark
  • obstruction of stercobilin / less bilirubin entering gut to become stercobilin (as it’s excreted in urine) causes pale stools
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7
Q

What is indicated by AST/ ALT to ALP ratio?

A
  • raised AST/ALT indicates hepatocellular disease

- raised ALP indicates cholestasis

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8
Q

What are some intra-hepatic causes of jaundice?

A
  • viruses
  • pregnancy
  • cirrhosis
  • alcohol
  • drugs
  • liver mets
  • metabolic syndromes
  • right heart failure
  • toxins
  • fungi
  • swelling
  • bile excretion abnormalities
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9
Q

What is the most common cause of peptic ulcers?

A

H. Pylori

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10
Q

Gram stain appearance of H. Pylori?

A

Gram negative.

Curved rods.

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11
Q

Treatment of H. Pylori?

A

Clarithromycin / metronidazole.
Amoxicillin.
PPI (omeprazole / lansoprazole).

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12
Q

What are some causes of peptic ulcers?

A
  • H. Pylori
  • increased stomach acid production
  • recurrent NSAID use
  • mucosa ischaemia
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13
Q

What are some risk factors for GORD?

A
  • obesity
  • hiatus hernia
  • smoking
  • pregnancy
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14
Q

What type of pain is characteristic of duodenal ulcers?

A

They cause pain several hours after eating and the pain gets better when eating.

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15
Q

Smoking and IBD?

A

Ulcerative colitis - protective.

Crohn’s - risk factor.

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16
Q

Risk factors for oesophageal cancer?

A
  • achalasia
  • alcohol
  • obesity
  • smoking
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17
Q

Where are the majority of colon cancers found?

A

Distal colon.

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18
Q

Causes of diverticulum (diverticulosis)?

A
  • low fibre diet
  • obesity
  • NSAIDs
  • smoking
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19
Q

What is shown on duodenal biopsy of a patient with coeliac disease?

A

Villous atrophy and crypt hyperplasia.

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20
Q

Causes of AKI?

A
  • acute tubular necrosis
  • hypovolaemia
  • nephrotoxins
    - prostate hyperplasia
  • sepsis
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21
Q

What is stage 1 CKD?

A

eGFR > 90 ml/min with evidence of tissue damage.

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22
Q

What is stage 2 CKD?

A

eGFR 60 - 89 ml/min.

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23
Q

What is stage 3a CKD?

A

eGFR 45 - 59 ml/min.

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24
Q

What is stage 3b CKD?

A

eGFR 30 - 44 ml/min.

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25
What is stage 4 CKD?
eGFR 15 - 29 ml/min.
26
What is stage 5 CKD?
eGFR < 15 ml/min.
27
What are some risk factors for CKD?
- diabetes - family history - old age - recurrent UTIs
28
Most common cause of pyelonephritis?
E. Coli
29
First-line treatment of lower UTI in pregnant women?
Nitrofurantoin
30
When should nitrafurantoin be avoided in pregnant women?
At term due to risk of neonatal haemolysis.
31
Which antibiotic is contraindicated for UTI treatment in pregnant women?
Trimethoprim - teratogenic effects.
32
Patient presenting with conjunctivitis, urethritis and arthritis?
Reiter’s syndrome (reactive arthritis).
33
Inheritance of polycystic kidney disease?
Autosomal dominant.
34
What are some complications of polycystic kidney disease?
- cardiovascular disease - kidney stones - polycystic liver disease - subarachnoid haemorrhage (due to Berry aneurysms)
35
Are granulomas found in Crohn's or UC?
Crohn's
36
Are crypt abscesses found in Crohn's or UC?
Crohn's and UC
37
Are goblet cells depleted in Crohn's or UC?
UC
38
Does Crohn's or UC have a cobblestone appearance?
Crohn's
39
What condition is likely if a patient has more difficulty swallowing solid food compared to liquids?
Achalasia
40
CXR findings in achalasia?
Very dilated oesophagus. | Small / absent gastric bubble.
41
Complication of achalasia?
Aspiration pneumonia.
42
Investigations for achalasia?
- CXR | - barium swallow
43
Complications of coeliac disease?
- osteoporosis | - dermatitis herpetiformis
44
How to distinguish between gastric and duodenal ulcers?
- gastric ulcer pain is worse with eating | - duodenal ulcer pain is relieved by eating
45
What is haematochezia?
Blood in stool.
46
Risk factors for oesophageal cancer?
- achalasia - barret's oesophagus - corrosive oesophagitis - diverticulitis - oesophageal web - familial - GORD - hiatal hernia - alcohol & smoking
47
Viral cause of diarrhoea?
- norovirus | - rotavirus
48
Bacterial cause of diarrhoea?
- E. coli - Salmonella (non-typhoidal) - campylobacter
49
What is diverticulosis?
herniation of the mucosa and submucosa through the muscular layer of the colonic wall
50
What is the pathophysiology of diverticulosis?
Colonic smooth muscle over-activity.
51
What is diverticulitis?
Inflammation of diverticula, may be caused by infection.
52
Risk factors for diverticulosis / diverticulitis?
- ageing - low fibre diet - obesity - smoking - sedentary lifestyle
53
How is diverticulitis managed?
Uncomplicated - oral antibiotics and liquid diet. | Complicated - IV antibiotics, abscess drainage, surgical resection.
54
When is surgery indicated in diverticulitis?
- complicated disease - recurrent disease - immunocompromised
55
First line treatment of C. diff infection?
Vancomycin (125mg orally 4x per day for 10 days).
56
Most likely cause of bowel obstruction in a child?
Intussusception
57
What are some causes of mechanical bowel obstruction?
- post-surgery adhesions - hernia - volvulus - intussusception
58
What are some causes of functional bowel obstruction?
- post-operative ileus - appendicitis - peritonitis - hypothyroidism - hypokalaemia - hypercalcaemia
59
What is the difference between mesenteric ischaemia and ischaemic colitis?
Mesenteric ischaemia - narrowed / blocked arteries restrict blood flow to the small intestine. Ischaemic colitis - temporary restriction of blood supply to the large intestine due to vasoconstriction or low pressure flow.
60
Risk factors for ischaemic colitis?
- clotting abnormalities (e.g. factor V leiden) - high cholesterol - reduction of blood flow (heart failure, low BP) - previous abdominal surgery - heavy exercise - surgery involving the aorta
61
Causes of oesophageal varices?
- liver cirrhosis - hepatitis - primary biliary cholangitis - parasitic infection (schistosomiasis) - thrombosis of portal / splenic veins
62
How is a Mallory-Weiss tear managed?
- most self-resolve in a few days - endoscopic therapy (coagulation) - transfusions if Hb is low - surgical repair - PPI
63
What is indicated if AST > ALT with a 2:1 ratio?
Alcoholic liver disease
64
What part of the bowel is most commonly affected in Crohn’s disease?
Terminal ileum
65
What do testicular seminomas secrete?
ALP
66
Which type of testicular cancer secretes alpha fetoprotein?
Endodermal yolk sac tumour
67
Drug with prognostic benefit in prostate cancer?
5-alpha reductase inhibitor (e.g. finasteride)
68
Which antibodies are memory antibodies?
IgG
69
What is Korsakoff’s syndrome?
Long-term irreversible complication of Wernicke’s encephalopathy.
70
What is diapedesis?
Leucocyte extravasation
71
What is Beck’s triad?
Cardiac tamponade: - muffled heart sounds - hypotension - raised JVP
72
What is acute cholecystitis?
Inflammation of the gallbladder, usually occurs when a gallstone completely obstructs the gallbladder neck or cystic duct. There may be infection of the gallbladder.
73
What is acalculous cholecystitis?
Obstruction of the cystic duct causing inflammation of the gallbladder, without gallstones.
74
Signs and symptoms of acute cholecystitis?
- RUQ pain and tenderness - fever - nausea & vomiting - palpable gallbladder - Murphy's sign
75
What is Murphy's sign?
Pain on inspiration when the right subcostal area is palpated.
76
Where can pain be referred / radiate to in acute cholecystitis?
- right shoulder (due to phrenic nerve irritation) | - around the right side to the back (intercostal nerve irritation)
77
First line investigation for cholecystitis?
Abdominal ultrasound
78
Investigations for cholecystitis?
- abdominal ultrasound - MRCP (if ultrasound doesn't detect the stone) - blood cultures - FBC (elevated WCC) - LFTs (generally normal) - serum lipase / amylase (exclude pancreatitis)
79
Management of acute cholecystitis?
- analgesia - IV antibiotics - laparoscopic cholecystectomy
80
Complications of acute cholecystitis?`
- gallbladder perforation - gangrenous cholecystitis - sepsis
81
What is meant by cholelithiasis?
Gallstone formation in the gallbladder or other parts of the biliary tree.
82
What is meant by choledocholithiasis?
Gallstones in the common bile duct.
83
What is biliary colic?
Intermittent RUQ pain caused by gallstones irritating the bile ducts (worse after eating, particularly fatty foods).
84
What do gallstones consist of?
- 90% are cholesterol stones | - 10% are black / brown pigment stones
85
Risk factors for cholesterol gallstones?
- female - increasing age - diabetes / metabolic syndrome - obesity - pregnancy - rapid weight loss / prolonged fasting - medications (e.g. oestrogen, GLP-1 analogues)
86
What causes black pigment stones?
High bilirubin / red cell turnover states - i.e. haemolytic anaemia.
87
What causes brown pigment stones?
Stasis and infection.
88
How do cholesterol stones form?
- bile becomes supersaturated with cholesterol due to excessive amounts of cholesterol produced by the liver, compared with solubilising agents (bile salts and lethicin) - there is accelerated nucleation (crystallisation) - gallbladder hypomobility contributes to stone formation
89
Clinical manifestations of biliary colic?
- severe colicky epigastric / RUQ pain - often triggered by meals (particularly fatty meals) - lasts 30 minutes - 8 hours - may be associated with nausea & vomiting
90
Investigations for biliary colic / gallstones?
- abdominal ultrasound - LFTs (normal or elevated ALP/bilirubin if there is cholestasis) - MRCP (if common bile duct stones are suspected but have not been picked up on ultrasound)
91
Management of uncomplicated gallstone disease?
- avoid fatty foods - analgesia - laparoscopic cholecystectomy if symptomatic - clear bile duct stones (ERCP / laparoscopic cholecystectomy)
92
Complications of gallstone disease?
- biliary colic - acute cholecystitis - acute pancreatitis - acute cholangitis
93
What is ascending cholangitis?
Infection and inflammation of the biliary ducts - surgical emergency with high mortality from sepsis.
94
Most common infective organisms in ascending cholangitis?
- E. coli - Klebsiella - Enterococcus
95
Causes of ascending cholangitis?
- obstruction of the common bile duct | - infection introduced during ERCP
96
Risk factors for ascending cholangitis?
- cholelithiasis - benign / malignant strictures - injury to the bile ducts (e.g. surgical, endoscopic, radiological) - history of primary sclerosing cholangitis
97
Pathophysiology of ascending cholangitis?
- obstruction of the common bile duct leads to bacterial seeding and contamination of the biliary tree - sludge formation provides a growth medium for bacteria - bile duct pressure increases as the obstruction progresses, promoting extravasation of bacteria into the bloodstream - this leads to sepsis if untreated
98
Clinical manifestations of ascending cholangitis?
- Charcot's triad (jaundice, fever, RUQ pain) - pale stools - pruritus
99
Gold standard investigation for ascending cholangitis?
endoscopic retrograde cholangiopancreatography
100
Investigations for ascending cholangitis?
- ERCP - abdominal ultrasound - FBC (raised WCC) - ABG (raised lactate, metabolic acidosis) - LFTs (raised ALP, bilirubin, and transaminases) - blood cultures
101
Differentials for ascending cholangitis?
- acute cholecystitis - acute pancreatitis - acute appendicitis - acute pyelonephritis
102
Management of ascending cholangitis?
- sepsis 6 - ERCP for biliary decompression (with sphincterotomy / stent placement) - elective laparoscopic cholecystectomy in stabilised patients
103
What is the sepsis 6?
3 in, 3 out: - O2 to target saturations - IV fluids - IV antibiotics - blood cultures - serial lactates - monitor urine output
104
Complications of ascending cholangitis?
- sepsis | - acute pancreatitis
105
What is primary biliary cholangitis?
Chronic autoimmune disease of the small intra-hepatic bile ducts. Obstruction of the bile ducts results in chronic inflammation and fibrosis.
106
Epidemiology of PBC?
- peak incidence 45-60 - affects females much more than males (10:1) - associated with other autoimmune conditions (rheumatoid arthritis, Sjogren's)
107
Pathophysiology of PBC?
- T lymphocyte-mediated damage to bile duct epithelial cells, with autoantibody involvement - cholestasis occurs as a result of autoimmune bile duct damage - this leads to bile acid retention, causing further liver damage and progressive loss of bile ducts - this results in liver fibrosis and eventually cirrhosis - bile acids, bilirubin, and cholesterol build up in the blood
108
Signs and symptoms of PBC?
- pruritus - jaundice - xanthelasma (cholesterol deposits on eyelids) - xanthoma (cholesterol deposits on in) - GI disturbance - abdominal pain - pale stools - signs of liver cirrhosis
109
Investigations for PBC?
- raised ALP - raised bilirubin and transaminases (later in disease course) - autoantibodies (AMA are most specific, ANA may also be seen) - liver biopsy (usually not required as raised ALP and presence of specific autoantibodies normally sufficient for diagnosis) - imaging (abdominal ultrasound / MRCP) to exclude bile duct lesion or PSC
110
Differentials for PBC?
- obstructive bile duct lesion | - PSC
111
Management of PBC?
- ursodeoxycholic acid (reduces intestinal cholesterol absorption) - obeticholic acid (bile acid analogue, decreases circulating bile acids) - cholestyramine (bile acid sequestrant, binds bile in the GI tract to prevent its absorption) - prednisolone / azathioprine - liver transplant
112
Complications of PBC?
Hepatocellular carcinoma
113
What is primary sclerosing cholangitis?
Intra- or extra-hepatic bile ducts become strictured and fibrotic, causing cholestasis. Chronic bile obstruction eventually leads to liver inflammation, fibrosis and cirrhosis.
114
Epidemiology of PSC?
affects males more than females
115
Cause of PSC?
Immune-mediated condition with a genetic component.
116
Risk factors for PSC?
- male - history of IBD - first degree relative with PSC
117
Signs and symptoms of PSC?
- pruritus - jaundice - RUQ pain - vitamin deficiency (ADEK) - hepatomegaly - signs of liver cirrhosis - fever
118
Investigations for PSC?
- LFTs - elevated ALP (transaminases and bilirubin elevated as the disease progresses) - autoantibodies (ANA, ANCA) - MRCP ('beads on a string' appearance)
119
Management of PSC?
- cholestyramine (bile acid sequestrant to relieve pruritus) - ERCP to dilate and stent strictures - liver transplant
120
Complications of PSC?
- hepatocellular carcinoma - cholangiocarcinoma - cirrhosis and liver failure
121
What is acute pancreatitis?
Inflammation of the pancreas, presenting with rapid onset of inflammation (both local and systemic) and symptoms.
122
Most common causes of acute pancreatitis?
- gallstones (50%) | - alcohol (25%)
123
Causes of acute pancreatitis?
- idiopathic - gallstones - ethanol - trauma - steroids - mumps - autoimmune - scorpion venom - hyperlipidaemia - ERCP - drugs (azathioprine)
124
Pathophysiology of acute pancreatitis?
- inflammation damages acinar cells, resulting in the release of digestive enzymes - this is due to abnormal intra-cellular calcium accumulation which activates intra-cellular proteases, releasing stored digestive enzymes - proteases cause autodigestion and lipases cause fatty necrosis
125
What causes acute lung injury in acute pancreatitis?
Systemic inflammation and the release of pancreatic proteases results in lung damage.
126
Signs and symptoms of acute pancreatitis?
- severe epigastric pain - pain radiates to back - pain improves leaning forward - nausea & vomiting - anorexia - abdominal tenderness - hypovolaemia - pleural effusion
127
Signs of hypovolaemia?
- hypotension - oliguria - dry mucous membranes - tachycardia - decreased skin turgor
128
Gold standard investigation for acute pancreatitis?
Serum amylase / lipase - greater than 3 times the upper limit of the normal range.
129
Investigations for acute pancreatitis?
- serum amylase / lipase - FBC (elevated WCC and haematocrit) - CRP elevated - creatinine may be elevated - LFTs - CXR - abdominal ultrasound (gallstones) - CT abdomen (for complications) - ERCP / MRCP
130
Differentials for acute pancreatitis?
- abdominal aortic aneurysm - ascending cholangitis - acute cholecystitis - MI - mesenteric ischaemia
131
Management of acute pancreatitis?
- IV fluids - nil by mouth - analgesia - anti-emetics - ERCP / cholecystectomy for gallstones - IV antibiotics for infection - drain abscess
132
Complications (and likelihood) in acute pancreatitis?
High - acute renal failure. Medium - sepsis / acute lung injury. Low - chronic pancreatitis.
133
What is chronic pancreatitis?
Chronic inflammation in the pancreas, resulting in fibrosis and loss of pancreatic function.
134
What is the most common cause of chronic pancreatitis in adults?
Alcohol
135
What is the most common cause of chronic pancreatitis in children?
Cystic fibrosis
136
Risk factors for chronic pancreatitis?
- alcohol - repeated episodes of acute pancreatitis - family history - coeliac disease
137
Signs and symptoms of chronic pancreatitis?
- dull epigastric pain - pain worse around 30 minutes after eating - pain radiates to the back - steatorrhoea - weight loss and malnutrition - jaundice - nausea and vomiting - diabetes mellitus / glucose intolerance
138
Investigations for chronic pancreatitis?
- CT / MRI abdomen - shows pancreatic calcifications, enlargement, and dilation of ducts - endoscopic ultrasound - secretin-enhanced MRCP - demonstates abnormal exocrine function - biopsy and histology - shows fibrosis, loss of acini
139
Management of chronic pancreatitis?
- alcohol and smoking cessation - dietary supplementation - pancreatic enzyme replacement therapy - blood glucose monitoring - analgesia - ERCP for duct stenting and stricture dilatation
140
Complications of chronic pancreatitis?
- exocrine insufficiency - diabetes mellitus - osteoporosis - pancreatic cancer
141
Pathophysiology of alcoholic liver disease?
- ethanol is directly toxic to the liver, resulting in the development of steatosis due to altered lipid metabolism - steatosis initially develops in hepatocytes surrounding the central vein - there is progression to hepatitis with activation of Kupffer cells (and hepatic stellate cells )which induce inflammation - Mallory-Denk bodies are seen within hepatocytes - fibrosis and cirrhosis develop following deposition of extracellular matrix proteins by hepatic stellate cells
142
Signs and symptoms of alcoholic liver disease?
- fatigue, malaise, nausea, anorexia - abdominal pain - jaundice - hepatomegaly - spider naevi - ascites - caput medusae - asterixis
143
What are caput medusae?
Engorged superficial epigastric veins.
144
Investigations for alcoholic liver disease?
- LFTs (AST:ALT ratio >2 is strongly suggestive) - increased prothrombin time - liver ultrasound - CT/MRI abdomen - liver biopsy - endoscopy (assess for oesophageal varices)
145
Differentials for alcoholic liver disease?
- non-alcoholic steatohepatitis - acute / chronic viral hepatitis - Wilson's disease - autoimmune hepatitis
146
Management of alcoholic liver disease?
- stop drinking alcohol - smoking cessation - liver transplant - corticosteroids for alcoholic hepatitis - treat complications
147
Complications of alcoholic liver disease?
- ascites - hepatic encephalopathy - portal hypertension - oesophageal varices - hepatocellular carcinoma
148
Why does hepatic encephalopathy occur?
Decreased ammonia metabolism by the damaged liver results in build-up of ammonia in the blood.
149
Pathophysiology of portal hypertension?
Increased resistance in the liver as a result of fibrosis / cirrhosis, results in an increase in blood pressure in the portal vein.
150
Gold standard investigation for portal hypertension?
Pressure measurement - catheterisation via the internal jugular vein.
151
Investigations for portal hypertension?
- catheterisation via internal jugular vein and blood pressure measurement - doppler ultrasound - upper GI endoscopy (for oesophageal varices)
152
Surgical intervention for portal hypertension?
TIPSS - transjugular intrahepatic portal systemic shunt.
153
Medication for prevention of varices bleeding?
Propanolol
154
Medication for ruptured varices?
Terlipressin (vasopressin analogue) causes vasoconstriction and slows bleeding.
155
Endoscopic intervention for oesophageal varices?
- elastic band ligation | - injection scleropathy (to cause clotting)
156
What type of virus is hep A?
Single-stranded RNA virus.
157
How is hep A transmitted?
Faecal-oral (contaminated food and water).
158
Gold standard investigation for hep A?
IgM anti-hepatitis A serology.
159
How is hep A managed?
- supportive care (analgesia) | - resolves in 1-3 months
160
Signs and symptoms of hep A?
- nausea and vomiting - anorexia - jaundice - dark urine and pale stools - hepatomegaly - fever - RUQ pain
161
What type of virus is hep B?
DNA virus
162
How is hep B transmitted?
Contact with blood or bodily fluids (needle-sharing, sexual intercourse).
163
Clinical presentation of acute hep B?
70% of patients are asymptomatic.
164
Clinical presentation of chronic hep B?
Patients are asymptomatic until they develop chronic liver disease.
165
Signs and symptoms of hep B?
- jaundice - hepatomegaly - fever - nausea and vomiting - fatigue - RUQ pain - signs of cirrhosis
166
What does serum hep B surface antigen indicate?
Active infection
167
What does serum hep B e antigen indicate?
Marker of viral replication, indicates high infectivity.
168
What does serum antibody to the hep B surface antigen indicate?
- vaccination - previous infection - current infection (if other markers are also present)
169
What does serum antibody to the hep B core antigen indicate?
Past or current infection.
170
What does serum hep B DNA indicate?
Direct measure of viral load.
171
Management of hep B?
- supportive care and antiviral therapy | - liver transplant
172
Complications of hep B?
- hepatocellular carcinoma - liver cirrhosis - liver failure
173
Hep B prognosis?
- over 95% achieve seroconversion without treatment within 2 months - some patients become chronic hep B carriers (viral DNA integrated into their own DNA)
174
What type of virus is hep C?
Single stranded RNA (positive-sense)
175
How is hep C transmitted?
- IVDU - sexual transmission is uncommon - contaminated blood transfusion / medical equipment
176
Clinical manifestations of acute hep C?
Patients usually asymptomatic
177
Clinical manifestations of chronic hep C?
- fatigue, myalgia, anorexia - jaundice - ascites - hepatic encephalopathy
178
Investigations for hep C?
- hep C antibody (current / past infection) - hep C RNA PCR (current infection) - serum aminotransferases elevated
179
Management of hep C?
- direct acting antiviral treatment for 8-12 weeks | - liver transplant
180
Prognosis for hep C?
- some young, healthy patients develop an immune response that eradicates the virus - the majority of infected patients have chronic infection and progressive liver damage
181
What type of virus is hep D?
Single stranded RNA virus (negative sense).
182
How does hep D survive in the host?
Attaches itself to the hep B surface antigen.
183
What type of virus is hep E?
RNA virus
184
How is hep E transmitted?
Faecal-oral
185
Clinical manifestations of hep E?
Normally produces a mild illness that clears in a month without treatment. Rare to progress to chronic hepatitis and liver failure.
186
What is autoimmune hepatitis?
Chronic inflammatory disease of the liver - characterised by the presence of circulating autoantibodies, inflammatory changes on liver histology, and response to immunosuppressive treatment.
187
Aetiology of autoimmune hepatitis?
- genetic predisposition | - environmental triggering agents (viruses, drugs, etc)
188
HLA association with autoimmune hepatitis?
HLA-DR3 and HLA-DR4 are associated with type 1 AIH.
189
Pathophysiology of autoimmune hepatitis?
T-cell mediated response against hepatocytes, with auto-antibody involvement. This leads to chronic inflammation and liver fibrosis.
190
Signs and symptoms of AIH?
- fatigue, malaise, anorexia - abdominal pain - hepatomegaly / splenomegaly - jaundice - encephalopathy - pruritus - fever - nausea - ascites - spider naevi
191
Investigations for AIH?
- LFTs (greater increase in aminotransferases than ALP and bilirubin) - serum autoantibodies - serum immunoglobulin concentration - liver biopsy
192
What autoantibodies are present in AIH?
- ANA - anti smooth muscle antibody - pANCA - anti soluble liver / pancreas antigens - anti liver-kidney microsome 1 antibody - anti liver cytosol antibody
193
Management of AIH?
- corticosteroid (prednisolone) - plus immunosuppressant if necessary (azathioprine) - liver transplant
194
Complications of AIH?
- steroid complications - hepatocellular carcinoma - liver failure
195
What is haemochromatosis?
Autosomal recessive iron storage disorder resulting in excessive total body iron, and iron deposition in tissues.
196
Aetiology of haemochromatosis?
Autosomal recessive mutation in the human haemochromatosis protein (HFE) on chromosome 6.
197
What does the human haemochromatosis protein do?
Regulates the expression of hepcidin.
198
Pathophysiology of haemochromatosis?
- hepcidin expression is too low - hepcidin is a negative regulator of iron, so this results in ongoing duodenal absorption of iron despite adequate iron stores - there is also continued release of iron from macrophages (from erythrophagocytosis) - serum iron and transferrin saturation is high - this leads to iron accumulation in multiple organisms
199
Clinical presentation of haemochromatosis?
Usually presents after 40 (later in females due to iron loss from menstruation).
200
Signs and symptoms of haemochromatosis?
- chronic fatigue - bronze / grey skin discolouration - joint pain - hypogonadism (impotence, loss of libido) and erectile dysfunction - memory and mood disturbance - hepatomegaly - diabetes mellitus - arrhythmias - congestive heart failure
201
Investigations to diagnose haemochromatosis?
- serum ferritin elevated - total iron binding capacity reduced (fasting transferrin saturation) - genetic testing confirms Dx - LFTs may be normal
202
Investigations to assess iron deposition in haemochromatosis?
- liver biopsy with Perl's stain - fasting blood glucose - ECG and echocardiogram
203
Management of haemochromatosis?
- phlebotomy | - manage complications
204
What are some complications of haemochromatosis?
- type 1 diabetes - liver cirrhosis - hepatocellular carcinoma - infertility - congestive heart failure - bone loss
205
What is Wilson's disease?
Autosomal recessive disease causing copper accumulation in tissues.
206
What is the genetic cause of Wilson's disease?
Mutation in the ATP7B copper-binding protein on chromosome 13.
207
Pathophysiology of Wilson's disease?
- ATP7B normally produces a protein involved in the excretion of excess copper in the bile, where it is subsequently eliminated in the stool - faulty ATP7B production results in high levels of free copper, causing toxicity by oxidant damage - this leads to cell injury, inflammation, and death - excess copper is stored in the liver, which causes hepatitis and eventually fibrosis due to inflammation and cell injury - the basal ganglia and movement co-ordination areas of the brain are most sensitive to copper accumulation
208
Clinical manifestations of Wilson's disease?
Patients present with either hepatic problems, or neurological / psychiatric problems.
209
What is the transport protein for copper?
Ceruloplasmin
210
Where is ceruloplasmin synthesised?
Liver
211
Hepatic manifestations of Wilson's disease?
- jaundice - RUQ tenderness - spider naevi - ascites - GI bleeding (varices)
212
Neurological manifestations of Wilson's disease?
- behavioural abnormalities - tremor - dysarthria - dysphagia - incoordination - ophthalmoplegia - dysdiadochokinesia
213
What is dysdiadochokinesia?
Slowness in alternating hands from prone to supine position.
214
What are Kayser-Fleischer rings?
Brown circles surrounding the iris. Seen in Wilson's disease due to copper deposition.
215
Gold standard investigation for Wilson's disease?
Liver biopsy
216
Investigations for Wilson's disease?
- liver biopsy - 24 hour urine copper - serum ceruloplasmin (low) - LFTs (raised transaminases and bilirubin, low albumin)
217
Management of Wilson's disease?
- trientine (copper chelator) - zinc (blocks copper absorption) - dietary restriction of liver and shellfish - liver transplant
218
What is the mechanism of action for trientine?
Copper chelator, enhances urinary excretion of copper.
219
Complications of Wilson's disease?
- liver failure | - oesophageal varices
220
What is alpha 1 antitrypsin deficiency?
Autosomal co-dominant disorder in which there is insufficient production of A1AT, resulting in lung and liver damage.
221
Genetic cause of A1AT deficiency?
Allele mutations in the SERPINA1 gene.
222
What is the inheritance pattern of A1AT deficiency?
Autosomal co-dominant.
223
Pathophysiology of A1AT deficiency?
- A1AT is made in the liver, and nomally inhibits neutrophil elastase (enzyme that digests connective tissues) - deficiency results in lung damage because excess protease enzymes attack connective tissue - liver damage occurs because the abnormal A1AT protein becomes trapped and accumulates, leading to fibrosis over time
224
Signs and symptoms of A1AT?
- productive cough - shortness of breath on exertion - hepatomegaly - ascites - hepatic encephalopathy - jaundice / scleral icterus
225
What are the lung manifestations of A1AT deficiency?
Bronchiectasis and emphysema.
226
Investigations for A1AT deficiency?
- serum A1AT - genetic testing for A1AT gene - liver biopsy - CT chest - LFTs (elevated transaminases, ALP, and bilirubin)
227
Management of A1AT deficiency?
- stop smoking - short / long acting bronchodilators - inhaled corticosteroids - pulmonary rehabilitation - lung transplant - liver transplant - manage hepatic complications
228
Complications of A1AT deficiency?
Hepatocellular carcinoma
229
Risk factors for hepatocellular carcinoma?
- chronic hep B / C infection - alcoholic liver disease - non-alcoholic steatohepatitis - haemochromatosis - A1AT deficiency - PBC / PSC
230
How is hep B directly carcinogenic?
Causes methylation of the P16 gene, leading to hepatocellular carcinogenesis.
231
Signs and symptoms of hepatocellular carcinoma?
- weight loss - anorexia - abdominal pain - nausea & vomiting - jaundice - pruritus - cirrhosis (ascites, spider naevi, caput medusae, varices, asterixis)
232
Investigations for HCC?
- alpha fetoprotein - liver ultrasound - CT / MRI abdomen - liver biopsy
233
Is conventional chemotherapy / radiotherapy effective for HCC?
No, HCC is generally considered resistant to chemotherapy and radiotherapy.
234
Summary of HCC management?
- surgical resection of individual tumours - liver transplant - kinase inhibitors - transcatheter arterial embolisation - radiofrequency ablation
235
What are kinase inhibitors?
Inhibit cancer cell proliferation (e.g. sorafenib).
236
What is Budd-Chiari syndrome?
Rare disorder characterised by narrowing and occlusion of hepatic veins.
237
Signs and symptoms of paracetamol overdose?
- nausea & vomiting - RUQ pain - jaundice - hepatomegaly - altered consciousness level & asterixis (due to hepatic encephalopathy) - loin pain
238
What causes loin pain in paracetamol overdose?
AKI
239
Investigations for paracetamol overdose?
- serum paracetamol - LFTs (raised transaminases) - serum creatinine elevated - ABG (lactic acidosis)
240
Blood glucose in paracetamol overdose?
Hypoglycaemia
241
Management of paracetamol overdose?
- activated charcoal (within 1 hour) - acetylcysteine to prevent liver damage - refer to psychological support
242
First-line treatment for mild UC?
Aminosalicylate - e.g. mesalazine.
243
What is nephrolithiasis?
Calculi form in the renal pelvis before travelling down the ureters. They may be symptomatic until they irritate or become stuck in the ureters.
244
Where do renal stones commonly become stuck?
Vesico-ureteric junction
245
Most common type of renal stone?
Calcium based - calcium oxalate (more common) - calcium phosphate
246
Types of renal stone?
- calcium oxalate / calcium phosphate - uric acid - struvite - cystine
247
Causes of struvite stones?
Produced by bacteria, associated with infection.
248
Causes of cystine stones?
Cystinuria - autosomal recessive disease.
249
What is a staghorn calculus?
Complex renal stone occupying the majority of the renal collecting system - associated with high risk of sepsis.
250
Most common cause of staghorn calculus?
Upper UTI - bacteria hydrolyse the urea in urine to ammonia, producing struvite.
251
Risk factors for renal stones?
- UTI - obesity - excessive uric acid intake - dehydration - previous renal stones - hyperparathyroidism - anatomical urinary tract abnormalities
252
Signs and symptoms of renal colic?
- acute severe spasmodic flank pain radiating to the ipsilateral groin - nausea and vomiting - urinary frequency / urgency - haematuria - costovertebral angle and flank tenderness - restlessness - fever (if infection)
253
What pain is characteristic of renal colic?
Acute severe spasmodic flank pain, radiating to the ipsilateral groin.
254
Investigations for renal stones?
- urine dipstick (haematuria, nitrites & leucocytes if UTI) - non-contrast CT KUB (renal ultrasound in pregnant patients) - U&Es - X ray KUB - shows calcification
255
Differentials for renal stones?
- acute appendicitis - ectopic pregnancy - ovarian cyst - bowel obstruction
256
When is urgent intervention indicated in a patient with a renal stone?
Obstruction with or without infection.
257
Urgent management of renal stone?
- decompression (ureteric stent or percutaneous nephrostomy tube) - antibiotics for infection - stone removal after drainage complete and infection cleared
258
Supportive care for renal stone?
- analgesia (strong - e.g. diclofenac) - anti-emetic - hydration
259
Management of renal stones without obstruction or infection?
``` Stone less than 10mm - consider watchful waiting. Stone greater than 10mm: - tamsulosin - shock wave lithotripsy - ureteroscopy - percutaneous nephrolithotomy ```
260
Prevention of uric acid renal stones?
Oral alkalinisation therapy - potassium citrate.
261
What is AKI?
An acute drop in kidney function leading to a rise in serum creatinine or a fall in urine output.
262
NICE criteria for AKI?
- creatinine rise > 25 micromol/L in 48 hours - creatinine rise > 50% from baseline in 7 days - urine output < 0.5 ml/kg/hour for > 6 hours
263
Pre-renal causes of AKI?
- hypovolaemia / haemorrhage - sepsis - third-spacing of fluid (acute pancreatitis) - heart failure - hepatorenal syndrome - renal artery stenosis
264
Intrinsic causes of AKI?
- acute tubular necrosis - rapidly progressive glomerulonephritis - interstitial nephritis - thrombosis - haemolytic uraemic syndrome
265
Post-renal causes of AKI?
- strictures - tumour - prostate hyperplasia - renal calculi - ascending UTI - urinary retention
266
Risk factors for AKI?
- underlying renal disease - sepsis - IV iodinated contrast - hypovolaemia - pancreatitis - renal stones - older age - nephrotoxic drugs
267
Causes of acute tubular necrosis?
- ischaemia - drug-induced - contrast-induced
268
Pathophysiology of post-renal AKI?
- obstruction increases intratubular pressure | - this causes tubular ischaemia and atropy
269
Examples of nephrotoxic drugs?
- ibuprofen - lithium - antibiotics (cefotaxime, gentamicin, vancomycin) - immunosuppressants (methotrexate, sulfasalazine) - ACE inhibitors and ARBs
270
Investigations for AKI?
- U&Es (hyperkalaemia) - serum creatinine - urine output - renal tract ultrasound for obstruction
271
Management of AKI?
STOP AKI - screen for and treat sepsis - toxins - stop nephrotoxic drugs - optimise volume status and BP - prevent harm: treat underlying cause and complications (hyperkalaemia) Emergency renal replacement therapy if not responding to treatment.
272
What is CKD?
Reduction in kidney function present for more than 3 months.
273
Units for GFR?
ml/min/1.73m^2
274
Risk factors for CKD?
- diabetes - hypertension - older age - glomerulonephritis - polycystic kidney disease - nephrotoxic drugs - obstructive uropathy - SLE - AKI
275
How does CKD lead to bone disease?
- kidney no longer activates vitamin D, leading to hypocalcaemia - hypocalcaemia stimulates increased PTH secretion, increasing bone resorption - bones become brittle and weak due to mineral loss
276
How does CKD lead to hypertension?
Low rate of blood flow through the glomerulus results in increased renin secretion.
277
Management of CKD?
- treat underlying cause (diabetes, hypertension, glomerulonephritis) - reduce CVD risk - atorvastatin 20 mg - manage complications (vitamin D and iron supplementation) - dialysis and transplant
278
Complications of CKD?
- AKI - hypertension - cardiovascular disease - anaemia - bone disease - metabolic acidosis - arrhythmias (hyperkalaemia) - uraemic pericarditis
279
What is renal cell carcinoma?
Adenocarcinoma arising from the kidney tubules, most common form of renal cancer.
280
Most common subtype of RCC?
Clear cell renal carcinoma
281
What is Wilms' tumour?
Specific kidney tumour affecting young children.
282
Risk factors for RCC?
- smoking - obesity - hypertension - end-stage renal failure - von-hippel lindau - haemodialysis
283
What is Von-Hippel Lindau?
Rare genetic multi-system disorder characterised by the development of benign tumours, with potential for malignant transformation.
284
Signs and symptoms of RCC?
- haematuria - loin pain - weight loss - fatigue - anorexia - night sweats - renal mass
285
Local spread of RCC?
Within the renal fascia, renal vein, inferior vena cava.
286
Common presentation of metastatic RCC?
Cannonball lung metastases
287
Paraneoplastic syndromes associated with RCC?
- polycythaemia (unregulated EPO) - hypercalcaemia (secretion of PTH mimicking hormone) - hypertension - Stauffer's syndrome
288
What is Stauffer's syndrome?
Paraneoplastic syndrome seen in RCC. Causes abnormal LFTs without liver metastasis.
289
First line investigation for RCC?
Abdominal / pelvic ultrasound.
290
Gold-standard investigation for RCC staging?
CT thorax, abdomen, pelvis.
291
Investigations for RCC?
- abdominal / pelvic ultrasound - CT thorax, abdomen, pelvis - biopsy (or pathology post-resection) - FBC - increased haematocrit - LFT derangement - serum creatinine - elevated - urinalysis - haematuria / proteinuria
292
Management of RCC?
Surgical resection (partial or radical nephrectomy). Other options are arterial embolisation or radiofrequency ablation. Chemotherapy / radiotherapy.
293
Most common type of bladder cancer?
Transitional cell carcinoma
294
Risk factors for bladder cancer?
- smoking - increased age - aromatic amine exposure (dye and rubber industries) - pelvic irradiation - bladder stone (chronic inflammation)
295
Clinical presentation of bladder cancer?
Painless haematuria
296
Gold standard investigation for bladder cancer?
Cystoscopy and biopsy.
297
Management of bladder cancer?
- transurethral resection of bladder tumour - post-TURBT intravesical chemotherapy - radical cystectomy - intravesical BCG - chemotherapy / radiotherapy
298
Most common type of prostate cancer?
Adenocarcinoma
299
Risk factors for prostate cancer?
- increasing age | - family history
300
Local invasion of prostate cancer?
- seminal vesicles - peri-prostatic tissue - bladder neck
301
Sites of metastasis of prostate cancer?
- bone - liver - lungs
302
Grading system of prostate cancer?
Gleason score
303
Clinical manifestations of prostate cancer?
- LUTS - erectile dysfunction - lethargy, anorexia, weight loss - haematuria - asymmetric, firm, nodular prostate on DRE
304
What is PCA3?
Urinary marker of prostate cancer.
305
Gold standard investigation for prostate cancer?
Prostate biopsy (guided by ultrasound / MRI).
306
Differentials for prostate cancer?
- benign prostatic hyperplasia | - chronic prostatitis
307
What options are there to actively treat prostate cancer?
- radical prostatectomy - radiotherapy - androgen deprivation therapy - brachytherapy (insertion of radioactive source into prostate)
308
Risk factors for testicular cancer?
- undescended testes - male infertility - family history
309
Clinical presentation of testicular cancer?
``` Usually painless lump on the testicle. - non-tender - hard - irregular - not fluctuant - no transillumination Gynaecomastia may be present. ```
310
Investigation to confirm testicular cancer?
Scrotal ultrasound
311
Which type of testicular cancer causes raised alpha fetoprotein?
- teratoma | - yolk sac tumour
312
Which type of testicular cancer causes raised beta-hCG?
- seminoma | - choriocarcinoma
313
Staging system for testicular cancer?
Royal Marsden
314
Management of testicular cancer?
- radical orchidectomy - chemotherapy - radiotherapy
315
Long term treatment side effects of testicular cancer?
- infertility - hypogonadism - secondary cancers
316
Function of PSA?
Liquefies semen
317
How does BPH present?
LUTS - urinary frequency - urinary urgency - urine retention - hesistancy - terminal dribbling - weak flow - incomplete empyting
318
Investigations for BPH?
- DRE | - serum PSA (normal)
319
Management of BPH?
1. tamsulosin (alpha blocker). | 2. finasteride (5-alpha reductase inhibitor).
320
What is a testicular varicocele?
Abnormal enlargement of testicular veins within the pampiniform plexus.
321
Presentation of testicular varicocele?
'Bag of worms' appearance.
322
Investigations for testicular varicocele?
Doppler ultrasound
323
What side do varicoceles most commonly occur on?
Left side
324
Management of testicular varicocele?
- usually conservative | - surgical intervention if symptomatic
325
What is a hydrocele?
Fluid in the tunica vaginalis causing scrotal swelling.
326
Presentation of testicular hydrocele?
- soft - non-tender - transluminous
327
Management of hydrocele?
Conservative
328
Testicular torsion vs epididymitis?
Prehn's sign is positive in epididymitis, negative in testicular torsion.
329
What is Prehn's sign?
Relief of pain on elevation of the affected testicle.
330
Management of epididymitis?
IM ceftriaxone and oral doxycycline.
331
What is testicular torsion?
Rotation of the testicle around the spermatic cord. Without intervention, leads to ischaemia and loss of the testis.
332
Clinical presentation of testicular torsion?
- sudden severe pain in scrotum and lower abdomen on affected side - swelling, redness, tenderness of testicle - upward retraction of testicle
333
Management of testicular torsion?
Immediate surgical detorsion.
334
Most common cause of scrotal swelling?
Epididymal cyst (lump on posterior aspect of testicle) - self-resolves.
335
Defining features of nephritic syndrome?
- haematuria - oliguria - proteinuria (sub-nephrotic range) - hypertension (due to fluid overload)
336
Causes of nephritic syndrome?
- SLE - post streptococcal glomerulonephritis - small vessel vasculitis (granulomatosis with polyangiitis) - anti-GBM disease (Goodpasture's) - IgA nephropathy
337
Gold standard investigation for nephritic syndrome?
Kidney biopsy
338
Management of nephritic syndrome?
- treat underlying cause - blood pressure control (ACEi / ARB) - corticosteroids to reduce kidney damage
339
Most common cause of nephritic syndrome in the UK?
IgA nephropathy
340
What is IgA nephropathy?
Glomerulonephritis caused by IgA immune deposits in the mesangium.
341
What is Henoch-Schonlein purpura?
IgA vasculitis
342
Common presentation of IgA nephropathy?
Asymptomatic with microscopic haematuria.
343
What is post-streptococcal glomerulonephritis?
Glomerulonephritis occuring 1-3 weeks after a beta haemolytic strep infection (strep pyogenes). Presents with nephritic syndrome.
344
Pathophysiology of post-strep GN?
Immune complexes of streptococcal antigens, antibodies, and complement proteins get stuck in the glomeruli and cause inflammation.
345
Blood markers for strep pyogenes infection?
Anti-streptolysin antibodies.
346
What is haemolytic uraemic syndrome?
Thrombosis occurs in small vessels throughout the body, usually triggered by the shiga toxin.
347
Classic triad of HUS?
- haemolytic anaemia - AKI - thrombocytopenia
348
Which pathogens produce the Shiga toxin?
- E. coli | - shigella
349
What causes haemolytic anaemia in HUS?
Shearing forces created by blood clots.
350
What causes AKI in HUS?
Impaired blood flow through the kidney, due to blood clots.
351
Typical clinical presentation of HUS?
Symptoms manifest around 5 days after gastroenteritis (with bloody diarrhoea). - oliguria - haematuria - abdominal pain - confusion (uraemia) - bruising - pallor
352
Investigations for HUS?
- FBC (anaemia and thrombocytopenia) - peripheral blood smear (schistocytes) - serum creatinine (elevated) - stool culture on sorbitol MacConkey (E. coli O157 does not ferment sorbitol) - PCR for shiga toxin from stool samples
353
Management of HUS?
Supportive care: - anti-hypertensives - blood transfusions - haemodialysis
354
What is Goodpasture's syndrome?
Anti-GBM disease - a rare small vessel vasculitis. Anti-GBM antibodies target type IV collagen in the kidneys and lungs, leading to life-threatening glomerulonephritis or pulmonary haemorrhage.
355
What is vasculitis?
Inflammation of blood vessels.
356
Signs and symptoms of Goodpasture's syndrome?
- constitutional features (lethargy, anorexia, weight loss, myalgia / arthralgia) - renal manifestations (nephritic syndrome) - pulmonary manifestations: cough, dyspnoea, haemoptysis, pulmonary haemorrhage
357
Investigations for Goodpasture's syndrome?
- serum anti-GBM antibodies - renal biopsy (crescentic glomerulonephritis) - CXR / CT chest
358
Management of Goodpasture's syndrome?
- plasmapheresis - immunosuppression - steroids and cyclophosphamides - haemodialysis - supportive pulmonary measures (intubation and ventilation)
359
What is rapidly-progressive glomerulonephritis?
GN often occuring secondary to Goodpasture's syndrome.
360
Clinical presentation of rapidly-progressive GN?
Very acute illness with rapid deterioration in renal function. Presents with nephritic syndrome.
361
Investigations for rapidly-progressive glomerulonephritis?
Renal biopsy shows crescentic glomerulonephritis.
362
Management of rapidly-progressive glomerulonephritis?
- immunosuppression - plasmapheresis - haemodialysis - anti-hypertensives
363
How does Henoch-Schonlein purpura present?
- purpuric rash on legs - nephritic syndrome - joint pain (due to IgA deposition)
364
How is Henoch-Schonlein purpura managed?
- corticosteroids | - ACE inhibitor / ARB for hypertension control
365
Why does nephrotic syndrome occur?
Problem with the glomerular filtration barrier, primarily involving the podocytes. This results in the classic triad of proteinuria, hypoalbuminaemia, and oedema.
366
Nephrotic proteinuria?
> 3g per 24 hours.
367
Primary causes of nephrotic syndrome?
- minimal change disease - focal segmental glomerulosclerosis - membranous nephropathy
368
Secondary causes of nephrotic syndrome?
- diabetes - drugs - autoimmune - neoplasia - infection
369
Signs and symptoms of nephrotic syndrome?
- oedema | - frothy urine (due to proteinuria)
370
Investigations for nephrotic syndrome?
- urinalysis - 24 hour urinary protein (> 3 g/day) - urine protein:creatinine ratio - renal biopsy - U&Es - lipid profile (hyperlipidaemia)
371
Why does hyperlipidaemia occur in nephrotic syndrome?
Loss of albumin increases cholesterol formation.
372
Management of nephrotic syndrome?
- fluid and salt restriction - loop diuretics (for oedema) - treat underlying cause - ACE inhibitor / ARB to reduce proteinuria - statin for hyperlipidaemia
373
Complications of nephrotic syndrome?
Venous thromboembolism due to increased clotting factors.
374
How is VTE managed in nephrotic syndrome?
Anticoagulation (e.g. LMWH)
375
Causes of focal segmental glomerulosclerosis?
Primary FSGS, or secondary to severe obesity or reflux nephropathy.
376
Pathophysiology of primary FSGS?
- circulating factor damages podocytes, leading to podocyte foot process effacement - this causes them to spread out and reduces the effectiveness of the filtration barrier
377
Management of FSGS?
Primary - immunosuppression with steroids. Secondary - treat underlying cause. Blood pressure control (ACE inhibitor).
378
What is membranous nephropathy?
Glomerular basement membrane thickening in the absence of significant cellular proliferation, leading to nephrotic syndrome.
379
What causes membranous nephropathy?
Can be primary or secondary to SLE, viral hepatitis, prostate cancer, NSAID use.
380
Pathophysiology of primary membranous nephropathy?
- autoimmune reaction against antigens in the filtration barrier, with autoantibody development and immune complex deposition - this leads to thickening of the glomerular basement membrane
381
What antibodies are seen in primary membranous nephropathy?
Anti-phospholipase A2 receptor antibodies.
382
Investigations for primary membranous nephropathy?
- serum anti-phospholipase A2 receptor antibodies | - renal biopsy
383
Management of membranous nephropathy?
- blood pressure control (ACE inhibitor) - primary: immunosuppression - secondary: treat underlying cause
384
What is minimal change disease?
Most common cause of nephrotic syndrome in children.
385
Causes of minimal change disease?
Majority of cases are idiopathic, but drugs, infection, or malignancy may be causes.
386
Pathophysiology of minimal change disease?
Immune dysfunction leads to the production of a permeability factor that disrupts the filtration barrier. This leads to the fusion of podocyte foot processes.
387
Management of minimal change disease?
Prednisolone
388
How many adult cases of nephrotic syndrome are caused by minimal change disease?
25%
389
Microscopy appearance in minimal change disease?
Normal
390
Most common cause of nephrotic syndrome in adults?
Focal segmental glomerulosclerosis.
391
Does nephritic or nephrotic syndrome impact GFR more?
Nephritic syndrome
392
Where does bladder cancer spread?
- iliac and para-aortic lymph nodes - liver - lungs
393
What is a UTI?
Infection of any part of the urinary tract (kidney to urethra). Presents with characteristic symptoms and bacteriuria.
394
What is an upper UTI?
Pyelonephritis
395
What is a lower UTI?
Infection of the bladder / urethra.
396
UTIs are considered uncomplicated in what group of patients?
Healthy, non-pregnant females.
397
What factors complicate a UTI?
- male - diabetes - infant < 3 months - catheters - pregnancy
398
Most common cause of UTI?
E. coli
399
Causes of UTI?
- klebsiella pneumoniae - e. coli - enterococci - proteus mirabilis - staphylococcus saprophyticus
400
Which organism commonly causes renal stone associated UTI?
Proteus mirabilis
401
Which organism commonly causes catheter associated UTI?
Klebsiella pneumoniae
402
Which organism commonly causes UTI in young women?
Staphylococcus saprophyticus
403
Risk factors for UTI?
- recent sexual intercourse - diabetes - history of UTIs - catheters
404
Why are UTIs uncommon in men?
- longer urethra - anti-microbial properties of prostatic secretions - drier periurethral area
405
Typical signs and symptoms of UTI?
- dysuria (burning pain) - increased urinary frequency - urgency - incontinence
406
What signs and symptoms of UTI indicate pyelonephritis?
- nausea & vomiting - fever - flank pain and costovertebral angle tenderness - pyuria
407
Red flags for urosepsis?
- haemodynamic instability (tachycardia and hypotension) - tachypnoea - changes to mental status - reduced urine output - pyrexia
408
Investigations for UTI?
- midstream urine MC&S - urine dipstick - leucocytes and nitrites, haematuria - U&Es (renal function may be impaired) - ultrasound - may show obstruction
409
Antibiotic course length for females vs males in uncomplicated lower UTI?
Females - 3 days | Males - 7-14 days
410
Antibiotics for lower UTI?
Trimethoprim / nitrofurantoin / cefalexin
411
Antibiotics for uncomplicated pyelonephritis?
Oral ciprofloxacin (14 days)
412
Empirical treatment for urosepsis?
Piperacillin / tazobactam
413
Antibiotics for complicated cystitis / pyelonephritis?
IV co-amoxiclav
414
Management of urosepsis?
3 in: - oxygen - antibiotics - fluids 3 out: - serial lactates - blood cultures - urine output
415
What symptom indicates cystitis?
Suprapubic tenderness / discomfort.
416
Most common cause of prostatitis?
E. coli
417
How does acute bacterial prostatitis present?
- very tender prostate on DRE - fever, chills, malaise - voiding symptoms (dysuria)
418
Investigations for acute bacterial prostatitis?
- urinalysis (haematuria, leucocytes) - midstream urine MC&S - blood cultures in febrile patients
419
Management of acute bacterial prostatitis?
Ciprofloxacin (14 days).
420
Most common bacterial STI?
Chlamydia (caused by chlamydia trachomatis).
421
Second most common bacterial STI?
Gonorrhoea (caused by neisseria gonorrhoea).
422
How does chlamydia present?
Males - testicular pain, dysuria. | Females - vaginal discharge, dysuria.
423
How is chlamydia diagnosed?
Nucleic acid amplification testing.
424
How is chlamydia managed?
- 1g single oral dose of azithromycin OR | - 7 day course of doxycycline BD
425
How does gonorrhoea present?
Males - dysuria, frequency, discharge. | Females - pelvic pain, dysuria, vaginal discharge.
426
Investigations for gonorrhoea?
- nucleic acid amplification testing | - swab of infected areas for microscopy and culture
427
Treatment for gonorrhoea?
Single dose of IM ceftriaxone.
428
First line investigation for renal stones?
KUB X ray
429
Gold standard investigation for renal stones?
Non-contrast CT-KUB
430
Common locations for renal stones?
- vesico-ureteric junction - pelvic brim - pelvico-ureteric junction
431
What is autosomal dominant polycystic kidney disease?
Common genetic disorder characterised by the development of multiple renal cysts and progressive renal impairment.
432
What two gene mutations cause PKD?
PKD1 and PKD2
433
Most common gene mutation of ADPKD?
PKD1
434
Investigations for polycystic kidney disease?
- ultrasound (multiple bilateral cysts) - LFTs - MR angiography for cerebral aneurysm screening - genetic testing - urine protein:creatinine ratio
435
Management of PKD?
- blood pressure control with ACE inhibitors - cyst decompression - nephrectomy - renal transplant if CKD - treat complications (infected cysts)
436
Complications of PKD?
- polycystic liver disease - pancreatic cysts - cerebral aneurysms
437
Functions of the kidney?
- EPO secretion - acid-base balance - waste product excretion - activation of vitamin D - regulation of BP (RAA system) - fluid volume balance
438
Medical emergency most associated with acute kidney injury?
Hyperkalaemia
439
2 week wait referral criteria for bladder cancer?
Over 45 with unexplained visible haematuria with no UTI / haematuria persists after resolution of UTI.
440
How can you identify a true scrotal mass?
You can palpate above a true mass.
441
Conditions associated with erectile dysfunction?
- diabetes mellitus - hypertension - pelvic fracture - prostatectomy - liver disease - renal failure
442
What is Crohn's disease?
Inflammatory bowel disease involving the full thickness of the intestinal wall. Affects discrete parts of the GI tract, leaving normal areas in between ('skip lesions').
443
Is Crohn's autoimmune?
Not auto-immune, but immune-mediate. Caused by environmental trigger in genetically susceptible individuals.
444
Risk factors for Crohn's?
- family history - genetics (NOD2 mutation) - smoking - infectious gastroenteritis
445
Signs and symptoms of Crohn's?
- diarrhoea (may be bloody) - right lower quadrant pain (terminal ileum) - fatigue, malaise, weight loss, anorexia - aphthmous mouth ulcers - joint pains - inflammatory eye disease
446
Gold standard investigation for Crohn's?
Colonoscopy - take multiple samples for biopsy.
447
Investigations for Crohn's?
- colonscopy and biopsy - upper GI endoscopy (if upper GI symptoms) - FBC (anaemia) - faecal calprotectin
448
Differentials for Crohn's?
- ulcerative colitis - pseudomembranous colitis - diverticulitis - coeliac disease - IBS
449
Management of Crohn's?
- corticosteroids / immunosuppressants (azathioprine) / anti-TNF agents - surgery for fissures and strictures - bowel resection - stop smoking - vitamin & mineral supplements
450
Complications of Crohn's?
- intestinal strictures - GI haemorrhage - osteoporosis - GI dilatation and perforation - anaemia - bowel cancer
451
What is ulcerative colitis?
Chronic inflammatory disease of the GI tract. Characterised by diffuse, continuous inflammation of the large bowel, limited to the mucosa. Affects the rectum with a variable length of colon involved proximally.
452
Subtypes of UC?
- proctitis - proctosigmoiditis - left-sided colitis - pancolitis
453
Aetiology of UC?
Immune mediated disease, possibly initiated by inflammation in response to colonic bacteria. Occurs in genetically susceptible people in response to environmental triggers.
454
Risk factors for UC?
- family history - non-smoker - NSAIDs
455
What is seen on histology in UC?
- crypt abscesses filled with granulocytes - continuous inflammation involving the intestinal mucosa - goblet cell depletion
456
Signs and symptoms of UC?
- persistent diarrhoea (may contain blood / mucus) - abdominal pain (usually left lower quadrant) - increased frequency of defecation - faecal urgency / incontinence - tenesmus - fatigue, malaise, anorexia, weight loss - pallor - aphthous mouth ulcers - eye / joint / skin involvement
457
What is tenesmus?
Persistent painful urge to pass stool even when the rectum is empty.
458
Extra-intestinal manifestations of UC?
- arthritis - erythema nodosum - uveitis - primary sclerosing cholangitis
459
Gold standard investigation for UC?
Colonoscopy (or flexible sigmoidoscopy) with biopsy.
460
Investigations for UC?
- colonoscopy with biopsy - stool microscopy & culture (negative) - FBC (anaemia) - faceal calprotectin
461
Investigation for UC presenting with acute abdomen?
AXR - exclude toxic megacolon, bowel obstruction, perforation.
462
Differentials for UC?
- Crohn's disease - pseudomembranous colitis - diverticulosis - coeliac disease - IBS
463
Drugs for mild UC?
Aminosalicylates (mesalazine). | Second line - add corticosteroid.
464
Drugs for moderate / severe UC?
- systemic corticosteroids - methotrexate - anti-TNF agent
465
When is surgery indicated in UC?
- if pharmacological management of moderate / severe UC is ineffective - acute severe UC if IV corticosteroids are ineffective - acute severe UC with toxic megacolon / bowel perforation
466
Complications of UC?
- toxic megacolon - bowel obstruction - bowel perforation - anaemia - fistulas & strictures - colorectal cancer - PSC
467
What is IBS?
Chronic functional bowel disorder characterised by abdominal pain and altered bowel habits.
468
What meant by a functional GI disorder?
Disorder not associated with structural or biochemical abnormalities. Symptoms are thought to be the result of dysregulation between the gut and the brain.
469
Risk factors for IBS?
- female - young - stressful life events - anxiety / depression
470
Signs and symptoms of IBS?
- abdominal pain - diarrhoea (not nocturnal) - tenesmus - constipation - bloating & distention - nausea
471
Criteria for IBS diagnosis?
Rome IV: recurrent abdominal pain occurring on average at least one day per week over the last 3 months (6 months since symptom onset). - pain related to defecation - associated with a change in stool frequency / form
472
Investigations for IBS?
Investigations for exclusion: - faecal calprotectin - FBC - CRP - coeliac serology - endoscopy
473
Differentials for IBS?
- Crohn's disease - ulcerative colitis - colorectal cancer - coeliac disease
474
Management of IBS?
- dietary changes (low FODMAP diet, avoid lactose / gluten, avoid excaerbating foods) - laxatives / loperamide - CBT - tricyclic antidepressants
475
What is functional dyspepsia?
Functional GI disorder, characterised by: - bothersome post-prandial fullness - bothersome early satiation - bothersome epigastric pain / burning
476
Management of functional dyspepsia?
After failure of PPI trial - tricyclic antidepressant / psychotherapy.
477
What is coeliac disease?
Systemic autoimmune disease condition triggered by dietary gluten peptides, causing inflammation and damage to the small intestine.
478
Genetic associations in coeliac disease?
- HLA-DQ2 | - HLA-DQ8
479
Example of a prolamin?
Gliadin
480
Pathophysiology of coeliac diease?
- gliadin enters the lamina propria, where it is deaminated by tissue transglutaminase - deaminated gliadin is more immunogenic, and it binds to antigen-presenting immune cells - T helper cells are activated and secrete pro-inflammatory cytokines, and activate B cells - B cells produce auto-antibodies (anti-tTG and anti-endomysial) - immune system activation leads to chronic inflammation and damage, resulting in intra-epithelial lymphocyte activation, villous atrophy, and crypt hyperplasia
481
Signs and symptoms of coeliac disease?
- weight loss - fatigue - loose stools - steatorrhoea - mouth ulcers & angular stomatitis - anaemia - dermatitis herpetiformis
482
Features of dermatitis herpetiformis?
Blistering, itchy rash on extensor surfaces.
483
Gold standard investigation for coeliac disease?
Small bowel endoscopy with biopsy (multiple samples from both the duodenal bulb and distal duodenum).
484
Histological findings in coeliac disease?
- intra-epithelial lymphocytes - villous atrophy - crypt hyperplasia
485
Investigations for coeliac disease?
- elevated IgA-tTG - anti-endomysial antibodies - skin biopsy shows granular IgA deposits in dermatitis herpetiformis - FBC (anaemia) - HLA typing
486
Management of coeliac disease?
- gluten-free diet | - steroids & immunomodulatory drugs if refractory coeliac disease
487
How is dermatitis herpetiformis treated?
Dapsone (oral sulphonamide antibiotic) and topical steroid cream.
488
What is GORD?
Reflux of stomach contents into the oesophagus, characterised by symptoms of heartburn and acid regurgitation.
489
Risk factors for GORD?
- high BMI - smoking - pregnancy - hiatus hernia
490
Pathophysiology of GORD?
Inappropriate relaxation of the lower oesophageal sphincter, allowing stomach contents to wash back into the oesophagus. Acidity of stomach contents results in damage to the oesophageal epithelium over time.
491
Signs and symptoms of GORD?
- heartburn - regurgitation - dyspepsia - cough - hoarse voice - dysphagia - nausea and vomiting
492
Investigations for GORD?
- pH monitoring via nasal tube | - gastroscopy (may be normal or show oesophagitis, Barrett's oesophagus)
493
Pharmacological management of GORD?
- PPIs - histamine receptor antagonists - antacids
494
How do PPIs work?
Inhibit H+/K+ ATPase in parietal cells, preventing gastric acid production.
495
Example of histamine receptor antagonist?
Ranitidine
496
What is erosive oesophagitis?
Inflammation caused by reflux of stomach contents into the oesophagus, resulting in ulcer formation, bleeding, and peptic strictures.
497
What is Barrett's oesophagus?
Metaplasia in the cells of the lower portion of the oesophagus - stratified squamous epithelium replaced by simple columnar epithelium with goblet cells.
498
What cancer is Barrett's oesophagus associated with?
Oesophageal adenocarcinoma
499
Risk factors for Barrett's oesophagus?
- GORD - smoking - obesity - male - older age - hiatus hernia
500
Investigation for Barrett's oesophagus?
Endoscopy with tissue biopsy.
501
Management of Barrett's oesophagus?
- PPIs - stop NSAIDs - weight loss - reduce alcohol intake - smoking cessation - Nissen fundoplication - regular endoscopies to monitor progression
502
What is a Nissen fundoplication?
Fundus of stomach is wrapped and stapled around the lower oesophagus - used to treat GORD / Barrett's oesophagus.
503
What are the two main types of oesophageal cancer?
- squamous cell carcinoma | - adenocarcinoma
504
Most common type of oesophageal cancer in the UK?
Adenocarcinoma
505
Risk factors for oesophageal cancer?
- older age - radiotherapy - smoking - obesity - Barrett's oesophagus - GORD
506
Where does squamous cell carcinoma most commonly occur?
Middle third of the oesophagus.
507
Where does adenocarcinoma of the oesophagus most commonly occur?
Distal third of the oesophagus.
508
Signs and symptoms of oesophageal cancer?
- weight loss - dysphagia - persistent indigestion / heartburn - retrosternal pain - food regurgitation - persistent cough - hoarse voice - haematemesis - dark stool
509
Investigations for oesophageal cancer?
- endoscopy and biopsy - CT - PET-CT
510
Management of oesophageal cancer?
- chemotherapy - radiotherapy - endoscopic mucosal resection - oesophagectomy - oesophageal stent
511
Stomach cancer typical type?
Adenocarcinoma
512
Most common histological type of stomach cancer?
Intestinal (also has better prognosis than diffuse).
513
Anatomical classification of stomach cancer?
Distal - antrum / pylorus. | Proximal - cardia.
514
What type of stomach cancer is more associated with H. pylori infection?
Distal
515
Which type of stomach cancer is commonly seen in countries with high incidence?
Distal (proximal more likely in countries with low incidence).
516
Risk factors for stomach cancer?
- smoking - high salt intake - low fruit and vegetable intake - H. pylori infection - EBV - family history
517
How does H. pylori increase risk of stomach cancer?
Causes inflammation, and secretes CagA into host cells (oncogenic protein).
518
Signs and symptoms of stomach cancer?
- anorexia, lethargy, weight loss, malaise - dyspepsia - nausea and vomiting - haematemesis - melaena - early satiety and post-prandial fullness (due to obstruction) - lymphadenopathy (Virchow node) - Sister Mary Joseph nodule
519
Paraneoplastic syndromes associated with stomach cancer?
- acanthosis nigricans (skin hyperpigmentation) - dermatomyositis - erythma gyratum repens (ring-shaped appearance, involves limbs and trunk)
520
Gold standard investigation for stomach cancer?
Gastroscopy and biopsy.
521
Common sites of metastasis of stomach cancer?
- liver - lung - peritoneum - bone
522
Management of stomach cancer?
- resection (endoscopic submucosal dissection / gastrectomy) - chemotherapy (adjunct or primary treatment for non-operable cancer) - trastuzumab
523
Which immunological therapy can be used to treat stomach cancer?
Trastuzumab (herceptin)
524
Risk factors for bowel cancer?
- family history - familial adenomatous polyposis - hereditary nonpolyposis colorectal cancer - IBD - increased age - diet (low fibre, high red / processed meat intake) - obesity - smoking & alcohol - sedentary lifestyle
525
Two hereditary risk factors for bowel cancer?
- familial adenomatous polyposis | - hereditary nonpolyposis colorectal cancer
526
What is familial adenomatous polyposis?
- autosomal dominant - malfunctioning of tumour suppressor genes results in development of adenomas along the colon - adenomas have the potential to become cancerous
527
What is hereditary nonpolyposis colorectal cancer?
- autosomal dominant - increases risk of a number of cancers - does not cause adenomas, tumours develop in isolation
528
Red flags for bowel cancer?
- change in bowel habit (diarrhoea) - unexplained weight loss - rectal bleeding - unexplained abdominal pain - IDA - abdominal / rectal mass
529
Acute presentation of bowel cancer?
Bowel obstruction - vomiting, abdominal pain, absolute constipation.
530
Screening for bowel cancer?
FIT tests (faecal immunochemical tests).
531
What do FIT tests detect?
Human Hb in stool (to detect bleeding).
532
Investigations for bowel cancer?
- colonoscopy and biopsy - CT colonography - CT chest, abdomen, pelvis - serum CEA (carcinoembryonic antigen)
533
Gold standard investigation for bowel cancer?
Colonoscopy and biopsy.
534
Tumour marker for bowel cancer?
CEA (carcinoembryonic antigen).
535
Management of bowel cancer?
- surgical resection (with end-to-end anastomosis or stoma) - chemotherapy - radiotherapy
536
Complications of bowel resection?
- nerve damage - bladder / ureter / bowel damage - post-operative ileus - failure of anastomosis - incisional hernia - intra-abdominal adhesions
537
What is Hartmann's procedure?
Proctosigmoidectomy with creation of Hartmann's pouch (sealed remnant of rectum). Remaining colon is redirected to a colostomy. May be reversed later/
538
What is peptic ulcer disease?
The development of gastric and duodenal ulcers - characterised by dyspepsia, abdominal discomfort, and nausea.
539
Erosion vs ulcer?
Erosion - superficial or partial break within the epithelium or mucosal surface. Ulcer - deep break through the full thickness of the epithelium or mucosal surface.
540
Causes of PUD?
- H. pylori (95% duodenal ulcers, 70-80% gastric ulcers). - drugs (NSAIDs, corticosteroids) - alcohol - Zollinger-Ellison syndrome - malignancy
541
What is Zollinger-Ellison syndrome?
Hyper-secreting gastrinoma in the pancreas leads to hypergastrinaemia. This leads to peptic ulcer development.
542
How do NSAIDs cause ulcers?
- inhibition of COX-1 enzymes | - COX-1 enzymes have a protective effect on the gastric mucosa
543
H. pylori microscopy?
Gram negative, spiral-shaped bacterium with flagella.
544
What area of the stomach does H. pylori predominantly colonise?
Antrum
545
How does H. pylori lead to ulcer formation?
- urease (converts urea into water and ammonia) buffers gastric acid and raises pH - H. pylori bind strongly to the gastric epithelium and secrete effector molecules into host cells via their type IV secretion system (CagA and VacA - disrupt tight junctions and induce apoptosis)
546
Signs and symptoms of peptic ulcers?
- epigastric pain - dyspepsia - heartburn - distention and bloating - upper GI bleed (haematemesis, melaena)
547
Complications of peptic ulcers?
- upper GI haemorrhage - perforation - gastric outlet obstruction
548
Presentation of GI perforation (peptic ulcer disease)?
- acute severe abdominal pain and tenderness - abdominal guarding - features of shock
549
Presentation of gastric outlet obstruction?
- nausea & vomiting - upper abdominal pain and tenderness - early satiety - distention - succussion splash
550
Gold standard for diagnosis of PUD?
Upper GI endoscopy and biopsy
551
Investigations for PUD?
- upper GI endoscopy and biopsy - FBC (anaemia) - ECG (exclude cardiac pathology) - H. pylori testing
552
What are some tests for H. pylori?
- urea breath test - serum IgG against H. pylori - stool antigen test - histology & culture from biopsy
553
Management of non H. pylori-associated PUD?
4-8 weeks PPI treatment.
554
Management of H. pylori-associated PUD?
Eradication therapy - 7 day course: - PPI - amoxicillin - clarithromycin / metronidazole
555
Causes of appendicitis?
- faecolith (hard collection of stool) - lymphoid hyperplasia - fibrous stricture - carcinoid tumour
556
Pathophysiology of appendicitis?
- obstruction of lumen causes stasis and bacterial overgrowth - increase in intra-luminal pressure causes peri-umbilical pain - increased pressure causes venous and lymphatic congestion, and eventually compromises arterial blood supply to the appendix - results in gangrene, perforation and generalised peritonitis
557
What is Rovsing's sign?
Pain in the right iliac fossa on palpation of the left. Indicates appendicitis.
558
Investigations for appendicitis?
- pregnancy test - abdominal ultrasound - contrast-enhanced abdominal CT / abdominal MRI in pregnant women
559
Differentials for appendicitis?
- intussusception - peptic ulcer disease - ectopic pregnancy - ovarian torsion - cholecystitis
560
Management of appendicitis?
- pre-operative antibiotics (co-amoxiclav) - laparoscopic appendicectomy - temporary drain insertion in some cases
561
What is the Rockall score?
Gives the risk of adverse outcomes following upper GI bleeding.
562
What is achalasia?
Oesophageal motility disorder characterised by oesophageal aperistalsis and insufficient lower oesophageal sphincter relaxation in response to swallowing.
563
Named signs seen in acute appendicitis?
- Rovsing - psoas - obturator
564
Gold standard for appendicitis?
CT scan
565
Risk factors for hernia?
- muscle weakness (abdominal wall surgery) - older age - pregnancy - increased intra-abdominal pressure (cough, constipation, weight lifting)
566
Management of reducible vs non-reducible hernia?
Reducible - watch and wait. | Non-reducible - surgery.
567
Complications of hernia?
- bowel obstruction | - strangulation hernia (compression of blood supply)
568
Sliding vs paraoesophageal hiatus hernia?
Sliding - stomach moves upwards and slides over the oesophagus. Paraoesophageal - stomach moves upwards alongside the oesophagus.
569
Diagnosis of hiatal hernia?
Barium swallow.
570
Direct vs indirect inguinal hernia?
Direct - via defect in the posterior wall of the inguinal canal. Indirect - via inguinal ring.
571
Is a femoral hernia more common in females or males?
Females
572
What is an anal fissure?
Small tear in the skin of the distal anal canal, caused by passage of hard stool.
573
Symptoms of anal fissure?
- severe pain during defecation - bright red blood - constipation - may be itchy
574
Management of anal fissure?
- stool softeners - leave to heal - sphincterectomy is gold standard
575
What is a perianal abscess?
Infection in anal gland.
576
Risk factors for perianal abscess?
- immunosuppression - IBD - diabetes
577
Symptoms of perianal abscess?
- fever and chills - constant anal pain - pus in stool
578
Management of perianal abscess?
Surgical removal and drainage.
579
Signs of an anal fistula?
- visible fistula - blood - pus
580
Treatment of anal fistula?
- drain infection | - surgical repair
581
What are haemorrhoids?
Bulging veins in anus.
582
Risk factors for haemorrhoids?
- constipation | - increased abdominal pressure
583
Investigation for haemorrhoids?
Endoscopy - DRE not helpful.
584
Symptoms of haemorrhoids?
- bulging pain in anus - feeling of incomplete emptying - itchy - bleeding
585
Treatment of haemorrhoids?
Gold standard is rubber band ligation. Also stool softeners.
586
Symptoms of pseudomembranous colitis?
- watery diarrhoea - fever - dehydration
587
Investigations for C. diff infection?
Stool sample MC&S
588
What is Meckel's diverticulum?
Congenital outpouching of all three layers of the small bowel, highly vascular so causes bleeding.
589
Blood marker for ovarian cancer?
CA-125
590
Blood marker for pancreatic cancer?
CA 19-9
591
What is Zenker's diverticulum?
Pharyngeal pouch
592
Signs and symptoms of pharyngeal pouch?
- dysphagia - halitosis - regurgitation of undigested food - hoarseness - chronic cough
593
What does mesenteric ischaemia affect?
Small bowel
594
What is a Mallory Weiss tear?
Haematemesis from tear in the oesophageal mucosa.
595
Causes of Mallory Weiss tear?
- bulimia - alcoholism - hyperemesis gravidarum - chronic cough - gastroenteritis
596
Management of Mallory Weiss tear?
- terlipressin - banding / clipping - thermocoagulation
597
Investigations for Mallory Weiss tear?
- Rockall score - ECG - endoscopy
598
What is Boerhaave syndrome?
Oesophageal rupture. | Characterised by vomiting, chest pain and subcutaneous emphysema.
599
What is Mackler's triad?
Vomiting, chest pain, subcutaneous emphysema - oesophageal rupture.
600
What is gastritis?
Inflammation of the stomach mucosa.
601
Causes of gastritis?
- autoimmune - H. pylori - bile reflux - NSAIDs - stress
602
Presentation of gastritis?
- epigastric pain - nausea and vomiting - dyspepsia
603
Investigations for gastritis?
- H. pylori testing | - endoscopy and biopsy
604
Management of gastritis?
- treat underlying cause | - H. pylori eradication
605
Cause of Meckel's diverticulum?
Incomplete obliteration of the vitelline duct.
606
Complications of Meckel's diverticulum?
- intussusception - volvulus - hernia
607
Rule of 2s for Meckel's diverticulum?
- 2 years old - 2 ft from ileocaecal valve - 2 inches long - 2% of the population
608
Where are diverticula most likely to occur?
Sigmoid colon (smallest luminal diameter and highest pressure).
609
Presentation of diverticulitis?
- LIF pain and tenderness - LIF mass - constipation - tachycardia - fever - nausea
610
Investigations for diverticulitis?
Bloods - raised WCC, ESR & CRP. | Imaging - CXR, AXR, CT
611
Imaging findings in diverticulitis?
- pneumoperitoneum - dilated bowel loops - obstruction - abscess
612
Causes of peritonitis?
- bacterial infection of ascitic fluid - bowel perforation - pelvic inflammatory disease - peritoneal dialysis infection - gall bladder perforation - appendicitis
613
Management of diverticulitis?
- antibiotics (oral / IV ciprofloxacin or metronidazole) - analgesia - liquid diet - surgical resection in rare cases
614
Histological appearance of intestinal type stomach cancer?
Glandular
615
Histological appearance of diffuse type stomach cancer?
Poorly differentiated, signet ring cells.
616
2 week wait criteria for stomach cancer?
Upper abdominal mass AND - dysphagia (any age) - over 55 with weight loss and upper abdominal pain / reflux / dyspepsia
617
Top 3 sites for bowel cancer?
1. rectum 2. sigmoid colon 3. descending colon
618
Staging system for colon cancer?
Dukes'
619
Dukes' Stage A
Cancer confined to the submucosa.
620
Dukes' Stage B
Invasion through muscularis without lymph node involvement.
621
Dukes' Stage C
Invasion through muscularis with lymph node involvement.
622
Dukes' Stage D
Distant metastasis
623
Causes of mechanical small bowel obstruction?
- surgical adhesions - tumour - strangulated hernia - volvulus - intussusception - inflammatory strictures - gallstone ileus
624
Causes of mechanical large bowel obstruction?
- volvulus (sigmoid) - tumour - diverticular disease - strictures
625
Clinical presentation of bowel obstruction?
- abdominal pain - nausea and vomiting (early in SBO, late in LBO) - constipation (early in LBO, late in SBO) - distention - tinkling bowel sounds / absent bowel sounds - resonant percussion
626
Conservative management of bowel obstruction?
- decompression with NG tube aspiration - IV fluids - antibiotics
627
Surgical management of bowel obstruction?
- endoscopic decompression of volvulus | - bowel resection (with anastomosis or stoma formation)
628
In diverticulosis, are the diverticula true or false?
False - acquired diverticula only involve outpouching of the mucosa and submucosa, not all three layers. True diverticula are congenital.
629
Investigations for diverticulosis?
- colonoscopy | - barium enema
630
What are the watershed areas in the bowel?
- splenic flexure | - rectosigmoid junction
631
Cause of acute vs chronic mesenteric ischaemia?
Acute - embolus, low perfusion (heart failure), thrombus. | Chronic - atherosclerosis.
632
Signs and symptoms of intestinal ischaemia?
- abdominal pain disproportionate to examination findings (widespread as ischaemia progresses) - nausea & vomiting - diarrhoea - rectal bleeding - abdominal distention (later in presentation)
633
Risk factors for intestinal ischaemia?
- atherosclerosis - age - smoking - AF - hypercoagulability - chronic organ failure
634
Investigations for intestinal ischaemia?
- FBC (leucocytosis) - ABG (elevated lactate) - CT with IV contrast (oedematous bowel, progressing to pneumatosis) - CT angiography
635
Management of intestinal ischaemia?
Supportive care - IV fluids, oxygen, analgesia, antibiotics, blood transfusion. Interventions - endovascular thrombectomy, exploratory laparascopy, bypass, excision of necrotic bowel. Treat underlying cause of low perfusion.
636
Complications of intestinal ischaemia?
- bowel necrosis | - bowel perforation
637
Why are patients with chronic liver disease more prone to infection?
Reticulo-endothelial dysfunction.