GI AND LIVER Flashcards

(412 cards)

1
Q

what is achalasia?

A

-oesophageal aperistalsis and impaired relaxation of the lower oesophageal sphincter

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2
Q

what are the risk factors for developing achalasia?

A
  • Allgrove syndrome (achalasia, alacrima, adrenal insufficiency).
  • Viral infection.
  • Autoimmune disease such as multiple sclerosis and Sjogren’s syndrome.
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3
Q

what are the clinical features of achalasia?

A
  • Intermittent dysphagia for both solids and liquids from the onset.
  • Retrosternal chest pain due to oesophageal spasm.
  • Regurgitation of food.
  • Aspiration pneumonia.
  • Gradual weight loss.
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4
Q

what is the first line investigation for achalasia and what does it show?

A
  • upper GI endoscopy:
  • -Obscured mucosa
  • -Dilated oesophagus
  • -Food debris.
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5
Q

what is seen on barium swallow in achalasia?

A
  • Lack of peristalsis

- bird beak appearance of lower end of oesophagus.

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6
Q

which investigation is diagnostic of achalasia and what does it show?

A
  • manometry
  • Incomplete relaxation of the lower oesophageal sphincter
  • oesophageal peristalsis.
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7
Q

how is achalasia treated?

A
  • nifedipine or verapamil.
  • pneumatic dilatation or laparoscopic cariomyotomy
  • botox
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8
Q

what are the complications of acute pancreatitis?

A
  • haemorrhage
  • hyperglycaemia
  • hypocalcaemia
  • pancreatic pseudocyst
  • fistulas
  • pancreatic abscess
  • ARDS
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9
Q

what are the causes of acute pancreatitis in adults?

A
  • Idiopathic
  • Gallstones.
  • Ethanol.
  • Trauma.
  • Steroids.
  • Mumps.
  • Autoimmune.
  • Scorpion bites.
  • Hypertriglyceridaemia, hypercalcaemia, or hypothermia.
  • ERCP.
  • Drugs such as bendroflumethiazide, allopurinol, azathioprine and tetracyclines.
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10
Q

what are the causes of acute pancreatitis in children?

A
  • blunt abdominal trauma (RTA)
  • viral infection (mumps, Hep A, coxsackie B)
  • multisystem disease such as SLE, Kawasaki, HUS, IBD and hyperlipidaemia)
  • drugs and toxins (thiopurines, metronidazole, cytotoxic drugs)
  • pancreatic duct obstruction (e.g. cystic fibrosis, choledochal cysts or tumours)
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11
Q

what are the symptoms of acute pancreatitis?

A
  • Severe epigastric pain that radiates to the back. It is sudden onset, continuous, and worse with movement.
  • Nausea and vomiting.
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12
Q

what are the signs of acute pancreatitis?

A
  • Abdominal tenderness and distension.
  • Stony dull percussion due to pleural effusion.
  • Bluish discolouration around the Umbilicus (Cullen’s sign) or over both flanks (Grey Turner’s sign) due to haemorrhagic pancreatitis.
  • Facial spasm due to hypocalcaemia (Chvostek’s sign).
  • Tachycardia, hypotension, oliguria, sweating due to hypovolaemic shock.
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13
Q

what investigations should be performed for suspected acute pancreatitis and what is seen?

A
  • Amylase or lipase: 3x upper limit of normal
  • transabdominal USS: may see gallstones
  • FBC: neutrophils raised
  • CRP: raised
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14
Q

what three criteria should be met to diagnose acute pancreatitis?

A
  • Upper abdominal pain.
  • Serum lipase or amylase is greater than 3x the upper limit.
  • Radiological changes (USS, CT) consistent with pancreatitis.
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15
Q

what are the poor prognostic factors in pancreatitis?

A
  • PaO2 < 8.0 kPa
  • Age > 55 years.
  • Neutrophilia > 15 x 109/L
  • Calcium < 2 mmol/L
  • Renal Function: urea > 16 mmol/L
  • Enzymes: Serum LDH > 600 U/L
  • Albumin < 30 g/L
  • Sugar: Blood glucose > 10 mmol/L
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16
Q

how is acute pancreatitis managed?

A
  • fluid resus
  • supportive care e.g. analgesia, supplemental oxygen, antiemetic and calcium/magnesium replacement therapy
  • establish normal feeds when tolerable
  • ERCP for gallstones
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17
Q

how is pancreatic necrosis managed?

A
  • Administer intravenous antibiotics (imipenem).
  • Perform percutaneous catheter drainage.
  • Perform a necrosectomy if catheter drainage is unsuccessful.
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18
Q

what are the causes of chronic pancreatitis?

A
  • alcohol excess
  • hereditary pancreatitis
  • autoimmune pancreatitis
  • ductal adenocarcinoma
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19
Q

what are the complications of chronic pancreatitis?

A
  • pancreatic pseudocyst formation
  • pleural effusion
  • jaundice
  • fat necrosis
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20
Q

what are the symptoms of chronic pancreatitis?

A
  • An intermittent dull epigastric pain that radiates to the back, that is relieved by leaning forward, and worsened by eating.
  • Steatorrhoea.
  • Weight loss.
  • Malnutrition.
  • Bloating, abdominal cramps, excessive flatus.
  • Nausea and vomiting.
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21
Q

what are the signs of chronic pancreatitis?

A
  • Signs of chronic liver disease.
  • Epigastric tenderness.
  • Jaundice.
  • Abdominal distension due to a pseudocyst.
  • Skin nodules due to disseminated fat necrosis.
  • Shortness of breath due to a pleural effusion.
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22
Q

how is chronic pancreatitis managed?

A
  • lifestyle changes such as smoking and alcohol cessation, smaller, more frequent meals and minimising sugar intake.
  • analgesia (paracetamol) for pain relief.
  • pancreatin and fat soluble vitamins for exocrine insufficiency.
  • endoscopic drainage of pseudocysts if there is persistent pain or complications
  • biliary decompression if there is a two-fold elevation in ALP that persists for more than 1 month.
  • pancreatic ductal decompression for pain relief if other medications fail.
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23
Q

what is a mallory-weirs tear?

A

rupture of the oesophageal mucosa

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24
Q

what is Boerhaave syndrome?

A

perforation of the whole thickness of the oesophageal wall

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25
what are the risk factors for the Mallory-weiss/Boerhaave syndrome?
- Significant alcohol use. - History of food poisoning, gastroenteritis, gallstones, cholecystitis etc. - Chronic cough e.g. bronchiectasis, COPD, lung cancer. - Hiatus hernia.
26
what are the clinical features of Mallory-weiss/Boerhaave syndrome?
- Haematemesis following second episode of vomiting, it may have a ‘coffee-ground’ appearance or bright-red bloody haematemesis. - Dizziness and postural hypotension. - Severe retrosternal pain (Boerhaave syndrome).
27
how should suspected mallory-weiss tear investigated and what does it show?
- oesophagogastroduodenoscopy | - Red longitudinal defect.
28
how should boerhaave syndrome be investigated?
water double contrast enema (Gastrografin) to localise the lesion.
29
how is boerhaave syndrome managed?
-Early recognition and surgical management within 12 hours of rupture
30
what is mesenteric adenitis?
inflamed lymph glands in the abdomen
31
what are the clinical features of mesenteric adenitis?
- abdominal pain - following a sore throat or cold - fever and generally unwell - nausea and diarrhoea
32
how is mesenteric adenitis diagnosed?
- clinically | - by excluding other causes of abdominal pain
33
what are the clinical features of alpha-1-antitrypsin deficiency?
- Productive cough. - Shortness of breath on exertion. - Wheezing. - Chest hyperinflation. - Jaundice. - Asterixis.
34
how is Alpha-1-Antitrypsin deficiency diagnosed?
- Measure plasma AAT level: < 20 mmol/L. - Perform pulmonary function testing: Reduced FEV1, FVC and FEV/FVC; Increased TLC. - Perform CXR: Large lung volumes and emphysema.
35
how is Alpha-1-Antitrypsin deficiency managed?
- lifestyle advice such as smoking cessation. - hepatitis A and B vaccination. - For pulmonary manifestations: Offer bronchodilators, inhaled steroids and antibiotics. - For hepatic manifestations: Offer diuretics for ascites, endoscopy to detect and manage varices, and liver transplantation in decompensated cirrhosis.
36
when does infant colic present?
first few months of life
37
what are the clinical features of infant colic?
- Paroxysmal, inconsolable crying or screaming - accompanied by drawing up of the knees - passage of excessive flatus - takes place several times a day, particularly in the evening.
38
what are the symptoms of appendicitis?
- Anorexia - Vomiting and nausea - Fever - Abdominal pain, initially central and colicky (appendicular midgut colic), but then localising to the right iliac fossa (from localised peritoneal inflammation)
39
what are the signs of appendicitis?
- low-grade fever - Abdominal pain aggravated by movement - Persistent tenderness with guarding in the right iliac fossa (McBurney’s point). - Rovsing’s sign – palpation of the left lower quadrant increases pain in the right lower quadrant - Psoas sign – passive extension of the right thigh with the person in the left lateral position elicits pain in the RLQ, suggestive of a retrocaecal appendix
40
what is seen on FBC and CRP in appendicitis?
- neutrophil dominant leucocytosis | - Elevated CRP
41
how is appendicitis managed?
- supportive therapy - NBM, IV fluids and analgesia - Laparoscopic appendicectomy - postoperative antibiotics (e.g. amoxicillin + metronidazole) for complicated appendicitis where there is suspected perforation.
42
what is intussusception?
-invagination of proximal bowel into a distal segment.
43
what are the clinical features of intussusception?
- Paroxysmal, severe colicky pain - pallor - May refuse feeds - may vomit, which may become bile-stained depending on the site of the intussusception - sausage shaped mass palpable in the abdomen - passage of redcurrant jelly stool - abdominal distention - shock
44
what is seen on ultrasound in intussusception?
target sign
45
how is intussusception managed?
- Perform fluid resuscitation with 0.9% NaCl. - Give clindamycin and gentamicin if sepsis is suspected. - Perform pneumatic reduction (air insufflation) as first line management in patients who are clinically stable. - Perform surgical reduction if pneumatic reduction fails.
46
what is a volvulus?
a twist in the bowel that occludes its lumen.
47
what are the clinical features of volvulus?
- Absolute constipation. - Crampy abdominal pain. - Bilious vomiting (caecal volvulus) - If ischaemia is present: - --Severe acute abdominal pain. - --Tachycardia. - --Tachypnoea. - --Acidosis. - --Guarding and rebound tenderness.
48
what is seen on AXR in volvulus?
- Inverted U shaped loop in sigmoid volvulus | - Coffee bean share in caecal volvulus.
49
what is seen on upper GI contrast series in volvulus?
- Bird-beak sign in sigmoid volvulus | - Corkscrew sign in caecal volvulus.
50
how is sigmoid volvulus managed?
- Perform therapeutic flexible sigmoidoscopy with insertion of a rectal tube if there is no peritonitis or mucosal gangrene. - Perform surgical resection if there is peritonitis or mucosal gangrene.
51
how is caecal volvulus managed?
- Perform surgical resection as first line. - Offer supportive care including nasogastric tube, IV fluid resuscitation and prophylactic antibiotics. - If ischaemia is not present, gram positive cover is required e.g. cefazolin. - If ischaemia is present, gram negative cover is required e.g. cefoxitin.
52
what is meckel's diverticulum?
blind-ended outpouching of the ileum on the antimesenteric border approximately 60 cm from the ileocaecal valve
53
what are the clinical features of Meckel's diverticulum?
- Haematochezia | - intractable constipation
54
how is Meckel's diverticulum diagnosed?
- Order a technetium-99m pertechnetate scan: Ectopic focus. | - Perform surgical exploration of the abdomen: Identify Meckel’s diverticulum.
55
how is Meckel's diverticulum managed?
- Perform a laparoscopic resection. - Give urgent blood transfusion if bleeding. - Remove any adhesive bands if obstruction. - Perform small bowel segmental resection and give cefotaxime and metronidazole if perforation and peritonitis.
56
what are the risk factors for developing gallstones?
- Crohn’s disease. - Diabetes mellitus. - Diet high in triglycerides, refined carbohydrates, and low in fibre. - Female gender. - Hispanic and Native-American ethnicity. - Increasing age. - Octreotide, a somatostatin analogue, due to impaired gallbladder motility. - GLP-1 analogies. - Ceftriaxone, due to precipitation of bile. - Non-alcoholic fatty liver disease. - Obesity.
57
what are the clinical features of biliary colic?
-Severe epigastric and RUQ pain - lasting several hours - associated with nausea and vomiting.
58
what is seen on abdominal ultrasound in biliary colic?
- gallstones in gallbladder | - stones in the bile duct
59
what are the risk factors for acute cholecystitis?
- Trauma. - Burns. - Immobility. - Starvation. - Sepsis. - Acute renal failure. - Diabetes mellitus. - Vascular disease. - Total parenteral nutrition. - Narcotic analgesics.
60
what are the clinical features of acute cholecystitis?
- Sudden-onset, constant, severe pain in the upper right quadrant. - Referred pain in the shoulder or intrascapular region. - Tenderness in the upper right quadrant, with or without Murphy’s sign. - Nausea and vomiting. - Fever.
61
what is seen on serum LFTs in acute cholecystitis?
- Raised aminotransferases | - raised ALP.
62
what is seen on abdominal ultrasound in acute cholecystitis?
- Distended gallbladder | - Gallstones.
63
following ultrasound, which diagnostic investigations can be used?
MRCP and ERCP
64
how is acute cholecystitis managed?
- Provide fluid resuscitation, analgesia and antibiotics to all patients. - Refer for laparoscopic cholecystectomy preferably within a week of onset. - Refer for percutaneous cholecystectomy to manage gallbladder empyema for patients unfit for general anaesthesia and surgery, and who do not improve after fluid resuscitation, analgesia, and antibiotics.
65
what are the risk factors for ascending cholangitis?
- Above the age of 50. - History of cholelithiasis. - History of primary or secondary sclerosing cholangitis. - Surgical, endoscopic or radiological intervention of bile ducts.
66
what are the clinical features of ascending cholangitis?
- Charcot’s triad: Fever, jaundice, right upper quadrant pain. - Reynold’s pentad: Charcot’s triad, in addition to hypotension and confusion, which are indicative or sepsis.
67
what is seen on serum LFTs in ascending cholangitis?
- Raised ALT - raised ALP - hyperbilirubinaemia.
68
what are the diagnostic criteria for ascending cholangitis?
- A: Systemic inflammation: - --Fever (>38 degrees celsius) and or shaking chills. - --Laboratory data: Raised WCC. - B: Cholestasis: - --Jaundice. - --Laboratory data: Abnormal LFTs. - C: Imaging: - --Biliary dilation. - --Evidence of aetiology: Stones.
69
how is ascending cholangitis managed?
- Give intravenous antibiotics: - --Initially give piperacillin with tazobactam. - --Give metronidazole with ciprofloxacin as an alternative for patients with a penicillin allergy. - Perform biliary decompression: - --Perform ERCP with sphincterectomy, as first-line therapy. - --Perform percutaneous trans-hepatic cholangiography (PTC) for patients who are poor ERCP candidates. - --Perform laparoscopic choledochotomy with T tube - --Perform endoscopic lithotripsy for stones that are large or difficult to remove. -Offer opioid analgesia (morphine, pethidine, fentanyl).
70
What are the risk factors for development of fulminant hepatic failure?
- Chronic alcohol use - Poor nutritional status - Female sex - Age >40 years - Pregnancy - Chronic hepatitis B - Narcotics e.g. paracetamol - Hepatotoxic medication
71
what are the clinical features of fulminant hepatic failure?
- jaundice - hepatomegaly - abdominal pain with RUQ tenderness - malaise - encephalopathy - drowsiness, confusion, coma - hypotension - hypoglycaemia - cerebral oedema
72
what is seen on LFTs and clotting in fulminant hepatic failure?
- Hyperbilirubinaemia - Prolonged PT > 30 seconds - Elevated INR > 1.5.
73
how is paracetamol overdose managed?
- Admit to ICU if blood paracetamol concentration is greater than > 700 mg/L, associated with coma and elevated lactate level. - Administer activated charcoal if the patient presents within 1 hour of ingestion. -Additionally, administer intravenous acetylcysteine (140 mg/kg orally) within 8 hours for paracetamol toxicity. o
74
in which cases should acetylcysteine be given immediately?
- There is uncertainty about the time of overdose, but it is potentially toxic - The overdose was staggered over a time period longer than an hour - The plasma-paracetamol level is over the treatment line on the treatment graph - The overdose was taken 8-36 hours before presenting
75
how should an anaphylactoid reaction to acetylcysteine be managed?
-If anaphylactoid reaction to acetylcysteine occurs, stop the infusion, give nebulised salbutamol, then re-commence infusion at a lower rate.
76
what are the clinical features of alcoholic fatty liver?
- often no symptoms or signs. - Vague abdominal symptoms of nausea, vomiting and diarrhoea are due to the more general effects of alcohol on the gastrointestinal tract. - Hepatomegaly, sometimes huge, can occur together with other features of chronic liver disease.
77
what are the clinical features of alcoholic hepatitis?
- Right upper quadrant pain. - Hepatomegaly. - Jaundice. - Ascites
78
what are the clinical features of alcoholic cirrhosis?
- Ascites. - Varices. - Hepatic encephalopathy. - Hepatocellular carcinoma.
79
what is seen on LFTs in alcoholic liver disease?
- Raised AST and ALT - AST:ALT > 2 - Elevated GGT.
80
how is alcoholic liver disease managed?
- Recommend alcohol abstinence, weight reduction and smoking cessation. - Recommend bed rest with a diet high in protein and vitamin supplements. - Recommend the influenza and pneumococcal vaccine. - Offer prednisolone to patients with alcoholic hepatitis with a Maddrey’s Discriminant Function score of 32 or more. - Offer furosemide and spironolactone for patients with less severe ascites. - Consider liver transplantation in patients with end-stage disease.
81
what autoantibodies are present in type 1 autoimmune hepatitis?
- Antinuclear antibody (ANA) - smooth muscle antibody (SMA) - soluble liver antibody (SLA) positive.
82
what autoantibodies are present in type 2 autoimmune hepatitis?
-Anti-liver/kidney microsomal-1 (ALKM1).
83
what are the clinical features of autoimmune hepatitis?
- Fatigue. - Anorexia. - Abdominal discomfort. - Hepatomegaly. - Jaundice. - Pruritus. - Arthralgia. - Nausea. Fever.
84
what is seen on LFTs in autoimmune hepatitis?
- Raised AST and ALT - Mild elevation of ALP and GGT - Raised bilirubin - Low serum albumin.
85
what are the criteria for initiating management in autoimmune hepatitis?
- Raised aminotransferase levels greater than 10-fold the upper list. - Raised gamma-globulin level at least twice the upper limit of normal. - Bridging necrosis on liver histology.
86
how is autoimmune hepatitis managed?
- prednisolone and azathioprine - ursodeoxycholic acid in addition to initial management for patients with autoimmune hepatitis - primary biliary cholangitis overlap syndrome. - liver transplant
87
what are the clinical features of Budd-Chiari syndrome?
- Right upper quadrant pain. - Tender hepatomegaly. - Ascites - Splenomegaly due to underlying myeloproliferative disease. - Leg oedema due to obstruction of the inferior vena cava. - Jaundice and hepatic encephalopathy with acute liver failure
88
what is seen on doppler ultrasonography in Budd-chiari syndrome?
- Thrombosis | - stenosis.
89
how is budd-chiari syndrome treated?
- Perform thrombolysis for symptomatic patients presenting within 72 hours. - Offer anticoagulation (enoxaparin or dalteparin) if the patient presents after 72 hours. - Perform hepatic angioplasty as the second line treatment. - Perform surgical shunting as the third line treatment. - Perform liver transplant as the fourth line treatment, or as an emergency procedure in patients with fulminant disease.
90
what is compensated cirrhosis?
the liver can still function effectively, and there are no or few clinical symptoms.
91
what is decompensated cirrhosis?
the liver is damaged to the point that it cannot function adequately and overt clinical complications.
92
what are the risk factors for the development of cirrhosis?
- Alcohol misuse. - Hepatitis B and C (unprotected sex and intravenous drug use). - Obesity. - Autoimmune disease (autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis). - Genetic conditions (haemochromatosis, Wilson’s disease, alpha-1 antitrypsin deficiency).
93
what are the clinical features of cirrhosis?
- Presence of stigmata of chronic liver disease - Spider naevi. - Palmar erythema. - Leukonychia
94
what are the clinical features of variceal haemorrhage?
- Haematemesis | - Melaena.
95
what are the clinical features of ascites?
- Abdominal swelling. - Mild generalised abdominal pain. - Deterioration suggests spontaneous bacterial peritonitis.
96
what are the clinical features of hepatic encephalopathy?
- Fetor hepaticus (sweet smell to breath). - Asterixis. - Decreased mental function. - Coma.
97
what is seen on LFT in cirrhosis?
- Raised AST and ALT - Raised GGT - Prolonged PT (most sensitive and specific finding for liver cirrhosis).
98
how is ascites managed?
- Initially give spironolactone. - Offer large volume paracentesis for symptomatic tense ascites or when diuretic therapy is insufficient to control accumulation of fluid. - Offer intravenous cefotaxime and human albumin solution for spontaneous bacterial peritonitis.
99
how are oesophageal varies managed?
- Offer a beta blocker for prophylaxis for variceal haemorrhage. - Offer terlipressin with suspected oesophageal variceal haemorrhage. - Perform endoscopic band ligation if bleeding does not stop following terlipressin. - Consider transjugular intrahepatic portosystemic shunt (TIPSS) if bleeding is not controlled by band ligation.
100
how is cirrhosis treated?
liver transplant
101
what are the risk factors for coeliac disease?
- Family history of coeliac disease. - Type 1 diabetes. - Autoimmune thyroid disease. - Gluten exposure. - Down’s syndrome.
102
what are the clinical features of coeliac disease?
- Diarrhoea. - Bloating. - Abdominal discomfort. - Anaemia. - Fatigue. - Weight loss. - Failure to thrive. - Depression and anxiety. - Peripheral neuropathy. - wasted buttocks
103
what is seen on coeliac serology?
- Elevated titre of IgA-tissue Transglutaminase | - Elevated titre of IgG endomysial antibodies.
104
what is the gold standard investigation in coeliac disease and what does it show?
- endoscopy | - subtotal villous atrophy and crypt hyperplasia
105
how is coeliac disease managed?
- Advise long-term adherence to a gluten free diet. The usual cause for failure to respond to the diet is poor compliance. - Offer supplementation (iron, folic acid, calcium, vitamin D) if needed. - Offer pneumococcal vaccinations once every 5 years due to hyposplenism
106
how is coeliac crisis treated?
- Rehydrate and correct electrolyte abnormalities. | - Offer a short course of glucocorticoid therapy (budesonide).
107
what is dermatitis herpetiformis?
uncommon blistering subepidermal eruption of the skin associated with a gluten-sensitive enteropathy
108
what are the clinical features of tropical sprue?
- diarrhoea - anorexia - abdominal distension - weight loss.
109
how is tropical sprue diagnosed?
- Acute infective causes of diarrhoea must be excluded, particularly Giardia - Malabsorption should be demonstrated, particularly of fat and B12. - The jejunal mucosa is abnormal, showing some villous atrophy (partial villous atrophy).
110
how is tropical sprue treated?
- folic acid - tetracycline - Severely ill patients require resuscitation with fluids and electrolytes for dehydration, and nutritional deficiencies should be corrected. - Vitamin B12 (1000 μg) is also given to all acute cases.
111
what are the clinical features of gut bacteria overgrowth\?
- diarrhoea and steatorrhoea - b12 deficiency - high folate
112
how is gut bacteria overgrowth diagnosed?
-hydrogen breath test
113
how is gut bacterial overgrowth treated?
- correct underlying lesion | - rotating courses of antibiotics, such as metronidazole, a tetracycline or ciprofloxacin.
114
which factors predispose to adenocarcinoma of the small bowel?
- coeliac disease | - Crohn's
115
which factors predispose to lymphoma of the small bowel?
- coeliac disease | - IPSID
116
how are small bowel adenocarcinomas treated?
-segmental resection
117
how is immunoproliferative small intestinal disease treated?
- if there is no evidence of lymphoma, antibiotics, e.g. tetracycline, should be tried initially. - In the presence of lymphoma, combination chemotherapy is used
118
how is lymphoma of the small bowel treated?
- surgery | - radiotherapy with chemotherapy
119
where do carcinoid tumours arise from?
enterochromaffin cells in the small intestine
120
what are the clinical features of carcinoid syndrome?
- Diarrhoea. - Flushing. - Palpitations. - Abdominal cramps. - Telangiectasia. - Peripheral oedema. - Elevated JVP. - Cardiac murmurs. - Hepatomegaly. - Wheeze
121
how should suspected carcinoid syndrome be investigated?
- Measure serum chromogranin A: Elevated. - Measure urinary 5-hydroxyindoleacetic acid: Elevated. - Perform an CT scan of the chest, abdomen and pelvis: Location of primary tumour and liver metastases.
122
how is carcinoid syndrome managed?
- Perform surgical resection of localised disease with no evidence or lymph node involvement or distant metastases. - Give a somatostatin analogue (octreotide or lanreotide) which controls symptoms of flushing, diarrhoea, and wheeze.
123
what are the risk factors for developing colon cancer?
- Increasing age. - A diet high in animal fat and red meat. - Obesity. - Smoking. - Hereditary non-polyposis colorectal cancer (HNPCC) (Lynch syndrome) - Familial adenomatous polyposis (FAP) - Peutz-Jeghers syndrome - IBD
124
what are the clinical features of colon cancer?
- Rectal bleeding. - Looser and more frequent stools. - Tenesmus. - Symptoms of anaemia. - Rectal mass on DRE, and occasionally, a palpable abdominal mass on examination. - Weight loss and anorexia are associated with advanced disease.
125
what is seen on blood tests in colon cancer?
- Perform a FBC: Anaemia suggestive of right sided colorectal cancer. - Measure LFTs: May be abnormal in liver metastases. - Measure U&Es: May be abnormal in renal metastases or diarrhoea.
126
which patients with suspected colon cancer should be referred on a 2 week wait?
- Aged 40 and over with unexplained weight loss and abdominal pain. - Aged over 50 with unexplained rectal bleeding. - Over 60 with iron deficiency anaemia or change in bowel habit.
127
what is the diagnostic investigation for colon cancer?
colonoscopy with biopsy
128
which cancer antigen is measured in colon cancer?
serum carcinoembryonic antigen (CEA)
129
how is colon cancer managed?
- surgery - chemotherapy - lifestyle advice (smoking cessation and reduced intake of red meat)
130
what are the risk factors for developing crohn's disease?
- Family history of Crohn’s disease. - Smoking. - Infectious gastroenteritis. - Appendicectomy. - Drugs such as NSAIDs.
131
what are the symptoms of Crohn's disease?
- Unexplained and persistent diarrhoea (frequent loose stools for more than 4 - 6 weeks), including nocturnal diarrhoea. - Abdominal pain or discomfort. - Perianal pain or tenderness. - Non-specific symptoms such as fatigue, malaise, anorexia, fever.
132
what are the signs of Crohn's disease?
- Pallor. - Clubbing. - Aphthous mouth ulcers. - Abdominal tenderness or mass, for example in the right lower quadrant. - Signs of malnutrition and malabsorption such as weight loss, faltering growth or delayed puberty.
133
what are the extra-intestinal manifestations of Crohn's disease?
- Pauci-articular or polyarticular arthritis. - Erythema nodosum usually on the anterior tibial area or extensor surfaces of the arms or legs. - Uveitis and episcleritis, both of which produce a red eye, but the formed is painful and is associated with blurred vision, photophobia, headache - Metabolic bone disorders such as osteoporosis, osteopenia, osteomalacia. - sacroiliitis causing buttock pain, or spondylitis causing back pain. - Pyoderma gangrenosum. - Psoriasis - Hepatobiliary conditions such as primary sclerosing cholangitis.
134
how do fistulas present in Crohn's disease?
- Recurrent urinary tract infections, passing gas or faeces through the urine or vagina. - Perianal discharge of mucus or pus. - Partial bowel obstruction presents as abdominal colicky pain and distension. - Complete bowel obstruction presents as severe abdominal pain, vomiting, no flatus, complete constipation.
135
what is seen on blood tests in crohn's?
- anaemia, either microcytic or normocytic - raised ESR and CRP - hypoalbuminaemia in severe disease - pANCA negative
136
what is seen on stool tests in Crohn's?
-Faecal calprotectin and lactoferrin are raised in active colonic disease
137
what are the macroscopic changes on colonoscopy in Crohn's disease?
- skip lesions - cobblestone appearance - deep ulcers and fissures
138
what are the microscopic changes on colonoscopy in Crohn's disease?
- transmural inflammation | - non-caseating granulomas
139
how is remission induced in Crohn's?
- nutritional therapy in children - corticosteroids - aminosalicylate
140
how is remission maintained in Crohn's?
- thiopurine - methotrexate - TNFa inhibitor (infliximab or adalimumab) if no response to conventional therapy
141
how is a fistula treated in Crohn's?
- Offer colorectal surgery in patients with complicated perianal or internal fistulas or fistulas that fail to respond to optimal medical treatment. - Offer a thiopurine to maintain remission. - Offer 3-months post operative metronidazole to control infection.
142
what are the risk factors for developing UC?
- Family history. - No appendicectomy. - Drugs such as NSAIDs. - Not smoking.
143
what are the symptoms of UC?
- Bloody diarrhoea persisting for more than 6 weeks. - Rectal bleeding. - Faecal urgency and or incontinence. - Nocturnal defecation. - Tenesmus (persistent, painful urge to pass stool even when rectum is empty). - Abdominal pain, particularly in the left lower quadrant. - Pre-defecation pain that is relieved on passage of stool. - Non-specific symptoms such as fatigue, malaise, anorexia, or fever. - Weight loss, faltering growth, or delayed puberty
144
what are the signs of UC?
- Pallor - Clubbing. - Abdominal distension, tenderness or mass, for example in the left lower quadrant. - Signs of malnutrition or malabsorption.
145
what is seen on blood tests in UC?
- iron deficiency anaemia - raised WCC - raised platelets - Raised ESR and CRP - hypoalbuminaemia - positive pANCA
146
what is seen on colonoscopy in UC?
- superficial inflammation that is continuous - the mucosa looks reddened, inflamed and bleeds easily (friability). - In severe disease there is extensive ulceration with the adjacent mucosa appearing as inflammatory (pseudo) polyps. - In ulcerative colitis, the mucosa shows a chronic inflammatory cell infiltrate in the lamina propria. - Crypt abscesses and goblet cell depletion are also seen.
147
how is mild-moderate UC treated to induce remission?
- a topical aminosalicylate - oral aminosalicylate - corticosteroids - ciclosporin
148
how is remission maintained in UC?
- thiopurine - methotrexate intravenous TNF-alpha inhibitor (infliximab or adalimumab)
149
what are the risk factors for the development of diverticula?
- Genetic factors. - Increasing age. - Low-fibre diet. - Smoking. - Obesity. - Drugs such as NSAIDs.
150
what are the clinical features of diverticular disease?
- Intermittent abdominal pain in the left lower quadrant, which may be triggered by eating and relieved by the passage of stool or flatus. - Constipation, diarrhoea or occasional large rectal bleeds. - Bloating and passage of mucus rectally. - Tenderness in the left lower quadrant.
151
how should diverticular disease be investigated?
colonoscopy
152
how is diverticular disease managed?
-Arrange urgent admission if the patient has significant rectal bleeding and is haemodynamically unstable (a pulse greater than 150 bpm, and a systolic blood pressure lower than 90 mmHg). - Offer lifestyle advice to patients who do not need admission: - --Recommend a healthy balanced diet contains whole grains, fruits, and vegetables. - --Recommend drinking an adequate fluid intake with a high-fibre diet. - Consider prescribing a bulk-forming laxative (Ispaghula husk) if a high fibre diet is insufficient, or if symptoms of constipation or diarrhoea persist. - Offer paracetamol for pain relief. Advise the patient to avoid NSAIDs and opiate analgesia.
153
what are the clinical features of uncomplicated diverticulitis?
- Constant abdominal pain, usually severe and starting in the hypogastrium before localising in the left lower quadrant. - Fever. - Change in bowel habit. - Significant rectal bleeding. - Nausea, vomiting, dysuria, urinary frequency. - Tenderness in the left lower quadrant.
154
what are the clinical features of complicated diverticulitis?
-Abscess formation suggested by abdominal mass on examination. -Perforation and peritonitis suggested by abdominal rigidity, guarding, and rebound tenderness. - Sepsis suggested by skin discolouration, raised or lowered temperature, rigors, change in conscious level, confusion, rapid pulse, reduced urination. - Fistula formation: Faecaluria, pneumaturia. - Intestinal obstruction suggested by colicky abdominal pain, vomiting, inability to pass flatus, abdominal distension.
155
how is acute uncomplicated diverticulitis managed?
- Offer paracetamol for pain relief. - Advise the patient to avoid NSAIDs and opiate analgesia. - Offer co-amoxiclav for patients who are systemically unwell, but do not meet the criteria for suspected complicated acute diverticulitis.
156
how is acute complicated diverticulitis managed?
- Arrange urgent hospital admission if there is suspected acute diverticulitis: - --Offer intravenous antibiotics (co-amoxiclav or metronidazole + cefuroxime), fluid replacement, and analgesia. - Consider percutaneous drainage of an abscess that is greater than 3 cm. - Offer laparoscopic lavage or Hartmann’s procedure (sigmoid colectomy with formation of an end colostomy) for patients with faecal peritonitis or who fail to respond to antibiotic therapy.
157
what are the risk factors for the development of eosinophilic oesophagitis?
- Family history of eosinophilic oesophagitis. - Male sex. - Atopic disease (asthma, atopic dermatitis, allergic rhinitis / sinusitis, food allergies). - Children and young adults. - White ancestry.
158
what are the clinical features of eosinophilic oesophagitis?
- Dysphagia. - Food avoidance and modification behaviours. - Regurgitation. - Heartburn. - Oesophageal pain. - Nausea and vomiting. - Failure to thrive.
159
how is eosinophilic oesophagitis diagnoses
- OGD | - Oesophageal biopsy
160
how is eosinophilic oesophagitis treated?
- Offer a corticosteroid (budesonide or fluticasone) for 8 weeks. - Offer dietary elimination therapy for 6 weeks. - Offer endoscopic oesophageal dilation (wire-guided bougie) in patients with severe oesophageal narrowing. - Emerging therapy includes mepolizumab, a monoclonal antibody against IL-5.
161
what are the risk factors for squamous carcinoma of the oesophagus?
- alcohol | - tobacco
162
what are the risk factors for adenocarcinoma of the oesophagus?
- barrett's oesophagus | - hiatus hernia
163
what are the clinical features of oesophageal cancer?
- Progressive dysphagia for solids (meat and bread) and then liquids within weeks. - Odynophagia. - Weight loss. - Anorexia. - Lymphadenopathy.
164
how is oesophageal cancer diagnosed?
-OGD with biopsy
165
how is stage 0 and 1a oesophageal cancer managed?
-endoscopic resection.
166
how is stage 1b and 2a oesophageal cancer managed?
- oesophagectomy | - chemoradiotherapy
167
how is stage 2b and 3 oesophageal cancer managed?
Perform oesophagectomy with preoperative chemoradiotherapy
168
how is stage 4 oesophageal cancer managed?
Offer chemoradiotherapy (cisplatin, fluorouracil and radiotherapy) and offer endoscopic ablation and stenting for symptom relief
169
what are the risk factors for developing gastric cancer?
- Pernicious anaemia. - H.pylori. - N-nitroso compounds. - Smoking. - Family history. - Male sex. - Age 50 to 70 years.
170
what are the symptoms of gastric cancer?
- Epigastric pain. - Weight loss. - Vomiting. - Dysphagia.
171
what are the signs of gastric cancer?
- Anaemia from occult blood loss. - Virchow’s node. - Sister Mary Joseph’s nodule. - Acanthosis nigricans. - Dermatomyositis. - Thrombophlebitis.
172
how is gastric cancer managed?
- Perform surgical resection and perioperative chemotherapy (epirubicin + cisplatin + fluorouracil) in patients with early localised disease in a surgical candidate. - Offer chemoradiotherapy (fluorouracil + radiotherapy) in patients with early localised disease who are not surgical candidates. - For advanced and metastatic disease: - --Offer chemotherapy (ECF). - --Offer palliative gastrectomy.
173
what are the risk factors for development of pancreatic cancer?
- Cigarette smoking is the most important risk factor. - Type II diabetes mellitus. - Chronic pancreatitis. - Family history: Hereditary pancreatitis, Peutz-Jeghers syndrome, Lynch syndrome. - Increasing age. - Male gender.
174
what are the clinical features of pancreatic cancer in the head of the pancreas?
- Obstructive jaundice. - Characteristic stretch marks secondary to cholestasis. - Painless palpable gall-bladder. - Epigastric mass is a sign of advanced disease.
175
what are the clinical features of pancreatic cancer in the body and tail of the pancreas?
- Dull abdominal pain that radiates through the back, that is partially relieved by sitting forward. - Anorexia. - Weight loss. - Thromboembolic phenomena. - Polyarthritis. - Skin nodules.
176
how is suspected pancreatic cancer investigated?
- transabdominal ultrasound showing dilated bile ducts and pancreatic mass - CT scan - FDG-PET and ERCP if ambiguous CT - CA19-9 biomarker
177
how is pancreatic cancer managed with resectable disease?
- Pancreaticoduodenectomy (Whipple procedure). - Preoperative endoscopic stent insertion. - Neoadjuvant chemotherapy (5-fluorouracil).
178
how is pancreatic cancer managed with unresectable disease?
- Endoscopic stent insertion - Offer gemcitabine based combination chemotherapy or FOLFIRINOX. - Opioid analgesia or percutaneous neurolytic coeliac plexus block for pain relief.
179
what are the risk factors for developing GORD?
- Stress and anxiety. - Smoking and alcohol. - Trigger foods, such as coffee and alcohol. - Obesity, pregnancy, hiatus hernia. - Family history. - Drugs such as alpha blockers, anticholinergics, benzodiazepines, NSAIDs. - Children with cerebral palsy or other neurodevelopmental disorders - Preterm infants, particularly with coexistent bronchopulmonary dysplasia
180
What are the clinical features of GORD?
- Heartburn, which is aggravated by bending over or lying down, worsened after food, hot drinks, alcohol, and relieved by antacids. - Acid regurgitation mainly after meals. - Dysphagia is uncommon. - Posseting and poor feeding in children
181
what lifestyle measures can improve symptoms of GORD?
- Lose weight if the patient is overweight or obese. - Avoid trigger foods and eat smaller meals. - Stop smoking and reduce alcohol consumption. - Sleep with the head of the bed raised (bricks under head of bed if practical). - Relaxation strategies for stress and anxiety. - Stopping drugs that may exacerbate symptoms.
182
How is GORD managed?
-PPI
183
How is GORD managed in children?
- thickening agents (carobel) - acid suppression (gaviscon or PPI) - Nissen fundoplication with complications
184
what are the clinical features of Zollinger-Ellison syndrome?
- Recurrent peptic ulcer disease. - Diarrhoea. - Epigastric abdominal pain. - Gastro-oesophageal reflux disease. - Steatorrhoea.
185
how is Zollinger-Ellison syndrome diagnosed?
- Measure fasting serum gastrin: Elevated. - Perform a secretin infusion test: Increase in fasting serum gastrin. - Measure serum calcium: Raised suggest MEN1 syndrome. - Consider a GI endoscopy: Prominent gastric folds.
186
how is Zollinger-Ellison syndrome treated?
- Offer a proton pump inhibitor (omeprazole 60 mg) to control gastric acid hypersecretion. - Offer surgery for localised disease if the primary site is causing symptoms. - Offer a somatostatin analogue (octreotide) and everolimus for liver metastases to limit tumour growth and symptoms. - Offer chemoradiotherapy for extrahepatic metastatic disease.
187
what are the risk factors for hereditary haemochromatosis?
- Middle age. - Male gender (the reduced incidence in women is probably explained by physiological blood loss and a smaller dietary intake of iron). - White ancestry. - Family history. - Supplemental iron.
188
what are the clinical features of hereditary haemochromatosis?
- Fatigue, weakness, lethargy. - Arthralgia. - Impotence and loss of libido. - Arrhythmia and heart failure (uncommon). - Bronze skin pigmentation due to excess melanin deposition. - Hepatomegaly.
189
what is seen on iron profile in hereditary haemochromatosis?
- Raised ferritin - raised serum transferrin - reduced total iron binding capacity
190
how is hereditary haemochromatosis managed?
- Perform venesection 500 mL twice weekly for 2 years. - Offer iron chelation therapy with desferrioxamine for patients who cannot tolerate venesection. - Patients should avoid iron and vitamin C containing supplements.
191
what are the clinical features of Hirschprung's disease?
- Delay of passage of meconium. - Vomiting which can be bilious. - Abdominal distension. - Constipation. - Explosive passage of liquid and foul stools. - Fever and failure to thrive associated with enterocolitis.
192
how should suspected Hirschprung's disease be investigated?
- Perform an AXR initially: Air-fluid levels present and dilated colon. - Perform a contrast enema which is the most useful diagnostic test: Contracted distal bowel and dilated proximal bowel. - Perform a rectal biopsy which allows for definitive diagnosis: Absence of ganglion cells.
193
how is Hirschprung's disease managed?
- Perform bowel irrigation as the initial treatment prior to surgery. It allows evacuation of gas and liquid stool through the tube. - Perform a pull through procedure surgery (Swenson procedure) within the first week of life for segmental disease. - Administer intravenous metronidazole for enterocolitis. - Perform a total colectomy and ileostomy for total colon aganglionosis.
194
what are the clinical features of ileus?
- Decreased bowel sounds. - Nausea and vomiting. - Abdominal distension. - Constipation.
195
what are the causes of ileus
- GI surgery - electrolyte imbalances - release of inflammatory agents - dysregulation of sympathetic and parasympathetic input to GI tract - analgesia and anaesthesia
196
how is ileus managed?
- Patient should be nil by mouth. - Administer intravenous hydration with normal saline. - Reduce opioid analgesia.
197
what is pyloric stenosis?
hypertrophy of the pyloric muscle
198
what are the risk factors for pyloric stenosis?
- 2 and 7 weeks of age - males - first born - family history on maternal side
199
what are the clinical features of pyloric stenosis?
- projectile, non-bilious vomiting - Hunger after vomiting until dehydration leads to loss of interest in feeding - Weight loss if presentation is delayed. - Tachycardia - Dry mucous membranes - Palpable pylorus - A hypochloraemic metabolic alkalosis with a low plasma sodium and potassium occurs as a result of vomiting stomach contents.
200
how is pyloric stenosis diagnosed?
-Ultrasound examination is helpful if the diagnosis is in doubt, showing pyloric muscle thickness >4mm
201
how is pyloric stenosis managed?
- The initial priority is to correct any fluid and electrolyte disturbance with intravenous fluids (0.45% saline and 5% dextrose with potassium supplements). - pyloromyotomy
202
what are the risk factors for developing IBS?
- Psychosocial factors include stress, anxiety, depression. - Genetic factors. - Gastroenteritis. - Inflammatory bowel disease. - Dietary factors such as alcohol, caffeine, spicy and fatty foods. - Antibiotics.
203
what are the clinical features of IBS?
- Abdominal pain. - Bloating. - Change in bowel habits. - Lethargy. - Nausea. - Back pain. - Bladder symptoms such as nocturia.
204
what are the Rome IV criteria for the diagnosis of IBS?
- Recurrent abdominal pain, at least 1 day per week in the last 3 months: - Relieved by defecation. - Associated with a change in frequency of stool. - Associated with a change in appearance of stool.
205
how is IBS managed?
- Provide advice and reassurance. - Encourage stress management such as exercise or yoga. - Advise the patient to maintain a healthy, balanced diet: - Low FODMAP diet (low fermentable carbohydrate diet, avoiding fruits, artificial sweeteners, and some green vegetables). - Reduce intake of fibre if diarrhoea. - Fibre supplements or foods high in fibre if constipation. - Reducing caffeine, alcohol, spicy and fatty foods. - Adequate fluid intake. - Consider probiotics for a minimum of four weeks. - Offer loperamide for diarrhoea.
206
how should constipation in IBS be managed?
- Offer a bulk forming laxative (ispaghula husk). | - Offer linaclotide if constipation persists for over 12 months or if laxatives are poorly tolerated
207
how should abdominal pain and spasm be managed in IBS?
- Offer an antispasmodic agent (mebeverine hydrochloride). - Consider amitriptyline if abdominal pain persists. - Consider an SSRI (citalopram) if the patient is constipated, as TCAs can cause constipation, or where a TCA is ineffective, contra-indicated or not tolerated
208
what are the risk factors for developing Hep A?
- Travelling to countries where the virus is highly endemic. - Men who have sex with men, and people with risky sexual behaviours. - People with clotting factor disorders. - Intravenous drug use. - People at occupational risk such as laboratory workers, and sewage workers.
209
what are the prodromal features of Hep A?
- Flu-like symptoms, including fatigue, malaise, joint and muscle pain, low-grade fever. - Gastrointestinal symptoms, such as nausea, vomiting, anorexia, right upper quadrant discomfort. - Accompanying headache, cough, sore throat, or urticaria
210
what are the icteric features of Hep A?
- Pruritus. - Fatigue, anorexia, nausea, vomiting. - Hepatomegaly, splenomegaly, lymphadenopathy.
211
what are the convalescent features of Hep A?
- Malaise. - Anorexia - Muscle weakness. - Hepatic tenderness.
212
what is seen on LFTs in Hep A?
- Elevated ALT and AST (usually between 500 and 10,000 IU/L). - Low ALT in fulminant hepatitis - Elevated bilirubin - Prolonged PT.
213
which serological result suggests acute Hep A infection?
- Positive HAV-IgM | - positive HAV-IgG
214
which serological result suggests past Hep A infection with immunity?
- Negative HAV-IgM | - positive HAV-IgG
215
which serological result suggests a false positive for Hep A?
- Positive HAV-IgM | - negative HAV-IgG
216
who should Hep A vaccination be given to?
- People travelling to high-risk areas. - People with chronic liver disease. - People receiving plasma-derived clotting factors to treat haemophilia. - IV drug users. - Men who have sex with men with multiple sexual partners. - People at occupational risk.
217
what supportive symptomatic treatment should be offered in Hep A?
- Advise paracetamol or ibuprofen for pain relief. - Prescribe metoclopramide (for 5 days) or cyclizine for nausea. - Prescribe chlorphenamine for pruritus.
218
what are the risk factors for the development of Hep B?
- Sharing of drug injecting equipment. - Travelling to areas of high prevalence. - Receiving regular blood or blood products (such as people with haemophilia). - Occupational hazards including needle stick injuries or direct exposure of mucous membranes to infected blood. - Tattoos, body piercing, or acupuncture. - Sexual transmission via mucous membranes. Having sex unprotected sex or having multiple sexual partners produces the greatest risk. - Transmission during childbirth (perinatal transmission).
219
what are the clinical features of acute Hep B?
- Prodromal illness that includes fever, arthralgia or a rash. - Right upper quadrant abdominal pain. - Jaundice with dark urine or pale stools. - Extrahepatic manifestations, including glomerulonephritis, vasculitis, polyarteritis.
220
what are the clinical features of chronic Hep B?
- Spider naevi. - Finger clubbing. - Jaundice. - Hepatosplenomegaly. - In severe cases: thin skin, bruising, ascites, liver flap, encephalopathy.
221
what is seen on LFTs in acute Hep B?
- Elevated ALT and AST - Elevated ALP - Elevated bilirubin - Prolonged PT
222
which hepatitis B serology result suggests acute infection?
- A positive HBsAg and IgM | - negative IgG
223
which hepatitis B serology result suggests chronic infection?
- A positive HBsAg and IgG | - a negative IgM
224
what symptomatic care should be given in acute Hep B infection?
- paracetamol, ibuprofen, or a weak opioid for pain relief. - Metoclopramide for nausea. - Chlorphenamine for pruritus
225
Which patients should be given antiviral therapy for Hep B?
- Aged 30 years and older. - HBV DNA greater than 2000 IU/L and an ALT greater than 30 IU/L. - Evidence of necroinflammation or fibrosis on liver biopsy.
226
which antiviral should be given for: a) acute Hep B infection b) chronic Hep B infection?
a) entecavir or tenofovir | b) peg-interferon alpha-2a
227
what are the risk factors for developing Hep C?
- Unsafe medical practices. - Intravenous drug use. - HIV. - Prisoners. - Multiple sexual partners, men who have sex with men. - Infected mother, especially if the mother is co-infected with HIV.
228
what are the clinical features of Hep C?
- Fatigue. - Myalgia. - Arthralgia. - Signs of advanced liver disease include ascites and signs of hepatic encephalopathy, including confusion, altered consciousness, and coma
229
which patients with Hep C should be given direct acting anti-virals first line?
- For patients with acute hepatitis in whom there is no spontaneous resolution (HCV RNA after 6 months). - For patients with chronic hepatitis.
230
what are the clinical features of acute mesenteric colitis?
- Peri-umbilical severe abdominal pain. | - Rapid forceful bowel evacuation.
231
what are the clinical features of chronic mesenteric colitis?
- Poorly localised abdominal pain after meals. - Sitophobia and associated weight loss. - Nausea and vomiting. - History of smoking.
232
what are the clinical features of ischaemic colitis?
- Peripheral severe abdominal pain and tenderness. | - Frequent bloody stools, characteristic maroon or red blood.
233
what are the x-ray features of ischaemic colitis?
-thumbprint sign
234
how is acute mesenteric ischaemia managed?
- Offer adequate fluid resuscitation and oxygenation. - Offer empirical antibiotics (ceftriaxone and metronidazole). - Perform endovascular therapy. - Perform exploratory laparotomy if there is infarction, perforation or peritonitis.
235
how is chronic mesenteric ischaemia managed?
-Consider endovascular treatment
236
how is ischaemic colitis managed?
- Most cases resolve spontaneously and only supportive care is needed. - Perform segmental colectomy for severe disease if there is generalised peritonitis or perforation.
237
what are the causes of large bowel obstruction?
- colorectal malignancy - Colonic volvulus (sigmoid or caecal). - Benign stricture (diverticulum). - Pelvic abscess. - Endometriosis.
238
what are the clinical features of large bowel obstruction?
- Colicky abdominal pain. - Tympanic abdomen. - Hard faeces. - Recent weight loss (suggests underlying malignancy). - Rectal bleeding (suggests underlying malignancy).
239
what is seen on Abdominal X-ray in large bowel obstruction?
- Gaseous distension of large bowel | - Coffee bean shape in volvulus
240
what are the causes of small bowel obstruction?
- adhesions from previous surgery - Appendicitis. - Intestinal malignancy. - Crohn’s disease. - Inguinal hernia.
241
what are the clinical features of small bowel obstruction?
- Cramping abdominal pain. - Nausea and vomiting. - Abdominal distension. - Constipation.
242
how is small bowel obstruction managed?
- Offer supportive care with fluid resuscitation and analgesia. - Perform nasogastric decompression for complete or complicated small bowel obstruction. - Declare the patient nil by mouth.
243
what are the clinical features of liver abscess?
- Fever. - Malaise - Right upper quadrant pain. - Anorexia. - Vomiting.
244
what is seen on contrast-enhanced CT in liver abscess?
Hypo-dense liver lesion.
245
how is a liver abscess treated?
- Offer piperacillin with tazobactam and fluid resuscitation for haemodynamically unstable patients - Offer metronidazole and ciprofloxacin for patients who are haemodynamically stable. - Offer metronidazole in patients with suspected amoebic abscess. -Perform ultrasound guided percutaneous drainage in all patients in addition to antibiotic therapy. -Offer anticandidal therapy (caspofungin) when liver abscess is diagnosed in an immunocompromised patient.
246
what are the risk factors for non-alcoholic fatty liver disease?
- Obesity, hypertension, type 2 diabetes and hyperlipidaemia - Hypertension - Medications including amiodarone, corticosteroids, diltiazem, methotrexate, tamoxifen
247
what are the symptoms of non-alcoholic fatty liver disease?
- Typically asymptomatic - Fatigue - Malaise - Pruritus - Hepatosplenomegaly - RUQ pain
248
what is seen on LFTs in non-alcoholic fatty liver disease?
- Elevated ALT and AST - Elevated ALP and GGT - Elevated bilirubin - Decreased serum albumin.
249
what is seen on liver biopsy in non-alcoholic fatty liver disease?
-steatosis
250
how is non-alcoholic fatty liver disease managed?
- Offer lifestyle advice on gradual weight loss (rapid weight loss is a risk factor for NAFLD) through diet and exercise. - Offer metformin for patients with diabetes. - Offer a statin for patients with hyperlipidaemia. - For patients with advanced liver disease: - --Monitor for hepatocellular cancer using ultrasound scans and alpha-fetoprotein. - --Offer vitamin E or pioglitazone for advanced liver fibrosis. - --Refer for liver transplantation.
251
what is gastritis?
- inflammation associated with mucosal injury
252
what is gastropathy?
- epithelial cell damage and regeneration without inflammation.
253
what are the clinical features of peptic ulcer disease?
- Recurrent, burning epigastric pain which the patient can identify with a single finger. - Pain on hunger and at night suggests duodenal ulcer. - Pain worsened by eating suggests gastric ulcer. - Back pain suggests a penetrating duodenal ulcer into the pancreas. - Persistent vomiting suggests gastric outlet obstruction. - Haematemesis and melaena suggests haemorrhage. - Examination reveals epigastric tenderness on palpation.
254
how is H.pylori diagnosed?
- carbon-13 urea breath test | - stool antigen test
255
which patients should be referred of OGD with suspected peptic ulcer disease?
- older than 55 | - have alarm symptoms such as dysphagia, weight loss, vomiting, anorexia, haematemesis or melaena.
256
what lifestyle advice can improve the symptoms of peptic ulcer disease?
- Lose weight if overweight or obese. - Avoid trigger food such as coffee, chocolate, tomatoes, fatty or spicy foods. - Eat smaller meals and avoid eating an evening meal 3 - 4 hours before bed. - Smoking cessation and reduced alcohol consumption. - Relaxation strategies if stress or anxiety. - Avoid NSAIDs, bisphosphonates, and corticosteroids.
257
what regimes can be used for h.pylori eradication?
- Offer omeprazole 20 mg twice daily, amoxicillin 1 g twice daily, and clarithromycin 500 mg twice daily. - Offer metronidazole 400 mg twice daily in place of amoxicillin in patients who are allergic to penicillin. - Offer tetracycline hydrochloride 500 mg four times daily in place of clarithromycin in patients who have had previous exposure to clarithromycin.
258
what are the risk factors for primary biliary cholangitis?
- Female (F:M ratio of 10:1). - Increasing age (peak incidence between 45 and 60). - Family history of PBC or autoimmune disease. - Smoking. - Urinary tract infection.
259
what are the clinical features of primary biliary cholangitis?
- Pruritus. - Fatigue. - Dry eyes and mouth (associated Sjogren’s syndrome). - Sleep disturbance. - Postural dizziness. - Hepatomegaly.
260
which antibodies are present in primary biliary cholangitis?
- anti-mitochondrial antibody - ANA - anti-M2
261
what are the diagnostic features of primary biliary cholangitis?
- raised ALP | - presence of AMA.
262
how is early stage primary biliary cholangitis treated?
- Offer a bile acid analogue (ursodeoxycholic acid) to modify disease progression. - Offer cholestyramine for pruritus.
263
how is end stage primary biliary cholangitis treated?
liver transplant
264
what are the risk factors for primary sclerosing cholangitis?
- Male sex. - Inflammatory bowel disease. - Genetic predisposition.
265
what are the clinical features of primary sclerosing cholangitis?
- Right upper quadrant pain. - Pruritus (excoriations on examination). - Fatigue. - Fever. - Jaundice
266
which autoantibodies are present in primary sclerosing cholangitis?
-ANCA
267
how is early stage primary sclerosing cholangitis treated?
- Offer lifestyle advice such as maintaining a healthy diet and weight, and limiting alcohol consumption. - Offer cholestyramine for pruritus.
268
how are acutely ill patients with primary sclerosing cholangitis treated?
- Refer for ERCP and balloon dilatation of the structure. | - Offer percutaneous transhepatic cholangiogram if ERCP is unsuccessful
269
what are the risk factors for hepatocellular carcinoma?
- Cirrhosis. - Chronic hepatitis B infection. - Chronic hepatitis C infection. - Chronic heavy alcohol use. - Diabetes. - Obesity.
270
what are the clinical features of hepatocellular carcinoma?
- Weight loss. - Anorexia. - Fever. - Stigmata of chronic liver disease. - Clinical features of the complications of cirrhosis. - Examination reveals an enlarged, irregular tender liver.
271
which tumour marker is raised in hepatocellular carcinoma?
serum alpha-fetoprotein
272
how is hepatocellular carcinoma treated?
- Offer liver transplantation for early disease (BCLC stage A). - Offer trans-arterial chemoembolisation (TACE) in intermediate disease (BCLC stage B). - Offer sorafenib or lenvatinib for advanced disease (BCLC stage C). - Offer hospice care for end-stage disease (BCLC stage D).
273
what are the risk factors for cholangiocarcinoma?
- Increasing age. - Choledocholithiasis. - Primary sclerosing cholangitis. - Ulcerative colitis.
274
which serum tumour markers may be raised in cholangiocarcinoma?
- serum CA19-9 | - serum CEA
275
how is resectable cholangiocarcinoma treated?
- Perform partial liver resection for intrahepatic tumours. - Perform surgical excision of extrahepatic tumours. - Offer pre-operative portal vein embolisation.
276
how is unresectable cholangiocarcinoma treated?
- Offer liver transplant and chemoradiotherapy. | - Offer palliative care.
277
what are the clinical features of Wilson's disease?
- Hepatitis. - Behavioural. - Tremor. - Dysarthria. - Dystonia. - Incoordination. - Sloppy or small handwriting. - Dysdiadochokinesia. - Abnormal extraocular movement. - Kayser-Fleischer ring, which appears as a greenish brown pigment at the corneoscleral junction. - neuropsychiatric features are more common in those presenting from second decade onwards
278
how is Wilson's disease treated?
- Offer lifelong treatment with penicillamine. - Offer trientine or zinc if patient experiences severe adverse effects with penicillamine such as nephropathy, lupus like syndrome and bone marrow depression. - Offer liver transplantation for fulminant hepatic failure or decompensated cirrhosis.
279
how is Wilson's disease diagnosed?
- >100mcg urinary copper - Reduced blood caeruloplasmin - >250mcg copper on liver biopsy
280
how can constipation be self-managed?
- increase fibre, fruits high ins orbital and veg - increase fluid intake - develop a toilet routine
281
how should short duration constipation be managed?
- manage secondary causes - increase fibre, fluid and activity - bulk-forming laxative (ispaghula) - osmotic laxative (macrogol or lactulose) - stimulant laxative
282
how is chronic constipation managed?
increase fibre, fluid and activity - bulk-forming laxative (ispaghula) - osmotic laxative (macrogol or lactulose) - consider prucalopride
283
how should faecal loading/impaction be managed?
- with hard stool give macrogol - with soft stool give stimulant laxative - if laxative response is inadequate, give bisacodyl suppository or mini docusate/sodium citrate enema - if response is still inadequate, give sodium phosphate or arachis oil retention enema overnight before giving sodium phosphate or sodium citrate enema - regular laxatives
284
how is constipation managed in children?
- disimpaction regimen of stool softeners, initially with a macrogol osmotic laxative, e.g. polyethylene glycol + electrolytes (Movicol Paediatric Plain). - An escalating dose regimen is administered over 1–2 weeks or until impaction resolves. - If this proves unsuccessful, a stimulant laxative, e.g. senna, or sodium picosulphate, may also be required. - If the polyethylene glycol + electrolytes is not tolerated, an osmotic laxative can be substituted.
285
what are the clinical features of travellers' diarrhoea?
- Abdominal pain - Cramps - Nausea - Vomiting - Dysentry
286
when should a stool sample be sent with suspected gastroenteritis?
- systemically unwell - blood or pus in the stool. - Persistent diarrhoea with suspected giardiasis. - Patient is immunocompromised.
287
which antibiotic can be used in camplyobacter?
erythromycin
288
how should salmonella be treated?
ciprofloxacin
289
how should shigella be treated?
ciprofloxacin
290
what are the clinical features of cholera?
- incubation of few hours to 6 days. - profuse painless diarrhoea - vomiting - rice-water stools - hypovolaemic shock - muscle cramps
291
how is cholera diagnosed?
- clinical - rapid dipstick test - stool and rectal swabs for culture
292
how is cholera treated?
-oral rehydration
293
what are the clinical features of amoebiasis?
- chronic, with mild intermittent diarrhoea and abdominal discomfort - may progress to bloody diarrhoea with mucus
294
what are the features of Amoebic liver abscess?
- Tender hepatomegaly - high swinging fever - profound malaise
295
how is amoebiasis diagnosed?
-microscopic examination or colonic exudate obtained at sigmoidoscopy
296
how is amoebiasis diagnosed?
- metronidazole or tinidazole | - bowel should then be cleared of parasites with diloxanide furoate
297
what are the clinical features of giardiasis?
- diarrhoea, often watery - nausea - anorexia - abdominal discomfort - bloating - steatorrhoea - weight loss
298
how is giardiasis diagnosed?
- stool examination | - duodenal aspirate
299
how is giardiasis treated?
- metronidazole | - Alternative drugs include tinidazole, mepacrine and albendazole.
300
what are the risk factors for C.diff?
- Increasing age (more than 65 years old). - Antibiotic treatment. - Hospitalisation or residence in a nursing home. - History of C.difficile-associated disease. - Use of acid suppressing drugs. - Inflammatory bowel disease. - Solid organ or haematopoietic stem cell transplant recipients. - Chronic kidney disease. - HIV infection.
301
what are the clinical features of C.diff?
- Clinical features commence anything from 2 days to some months after antibiotics. - Mild diarrhoea to profusely, water, haemorrhagic diarrhoea. - Abdominal pain. - Fever. - Abdominal tenderness. - Hypotension (suggests life-threatening infection).
302
how is c.diff diagnosed?
-Measure stool PCR or ELISA which is diagnostic: Toxin A or B present
303
how is c.diff managed?
- oral metronidazole for 10 days for mild/moderate infection - oral vancomycin for severe infection
304
what is failure to thrive?
sub-optimal weight gain in infants and toddlers.
305
what are the non-organic causes of inadequate intake failure to thrive?
- feeding problems - insufficient or unsuitable foods - lack of regular feeding - infant difficult to feed - conflict over feeding - intolerance of normal feeding behaviour - problems with finances - low socioeconomic status - poor maternal-infant interaction - maternal depression - poor maternal education - neglect or child abuse
306
what are the organic causes of inadequate intake failure to thrive?
- oromotor dysfunction - neurological disorder - cleft palate
307
what are the inadequate retention causes of failure to thrive?
- vomiting | - severer GORD
308
what are the malabsorption causes of failure to thrive?
- coeliac - CF - cow's milk protein allergy - cholestatic liver disease - short gut syndrome - post-NEC
309
what are the failure to utilise nutrients causes of failure to thrive?
- syndromes - chromosomal disorders - IUGR - extreme prematurity - congenital infection - metabolic disorders
310
what are the increased requirement causes of failure to thrive?
- thyrotoxicosis - CF - malignancy - chronic infection - CHD - chronic renal failure
311
what are the thresholds for concern in faltering growth?
- a fall across 1 or more weight centile spaces, if birth weight was below the 9th centile. - a fall across 2 or more weight centile spaces, if birth weight was between the 9th and 91st centiles. - a fall across 3 or more weight centile spaces, if birth weight was above the 91st centile. - when current weight is below the 2nd centile for age, whatever the birth weight.
312
when is enteral nutrition used?
-when the digestive tract is functioning
313
what are the clinical features of marasmus?
- weight for height more than -3 standard deviations from the median - wasted, wizened appearance - withdrawn and apathetic
314
what are the clinical features of kwashiorkor ?
- a ‘flaky-paint’ skin rash with hyperkeratosis (thickened skin) and desquamation - a distended abdomen and enlarged liver (usually due to fatty infiltration) - angular stomatitis - hair which is sparse and depigmented - diarrhoea, hypothermia, bradycardia and hypotension - low plasma albumin, potassium, glucose and magnesium.
315
how is severe acute malnutrition managed in children?
- Hypoglycaemia–common; correct urgently, particularly if coma or severely ill. - Hypothermia–wrap, especially at night. - Dehydration–correct, but avoid being overzealous with intravenous fluids, as may lead to heart failure. - Electrolytes–correct deficiencies, especially potassium. - Infection–give antibiotics; fever and other signs may be absent. Treat oral candida if present. - Micronutrients–give vitamin A and other vitamins - Initiate feeding–small volumes, frequently, including through the night.
316
what are the causes of rickets?
- northern latitudes - dark skin - decreased exposure to sunlight - poor diet - intestinal malabsorption
317
what are the clinical features of rickets?
- misery - failure to thrive - frontal bossing of skull - craniotabes - delayed closure of anterior fontanelle - delayed dentition - rickety rosary - harrison sulcus - expansion of metaphases - bowing of legs - hypotonia - seizures
318
how is rickets diagnosed?
- dietary history - low serum calcium - low phosphorus - plasma alkaline phosphatase - low 25-hydroxyvitamin D - elevated PTH
319
how is rickets managed?
- advice about a balanced diet - correction of predisposing risk factors - daily administration of vitamin D3 (cholecalciferol).
320
what are the clinical features of vitamin A deficiency?
- blindness - xerophthalmia - increased susceptibility to measles
321
what are the causes of vomiting in infants?
- GORD - Feeding problems - infection - dietary protein intolerance - intestinal obstruction - inborn errors of metabolism - congenital adrenal hyperplasia - renal failure
322
what are the causes of vomiting in pre-school children?
- gastroenteritis - infection - appendicitis - intestinal obstruction - raised ICP - coeliac - renal failure - inborn errors of metabolism - testicular torsion
323
what are the causes of vomiting in school aged and adolescents?
- gastroenteritis - infection - peptic ulceration and H.pylori - appendicitis - migraine - raised ICP - coeliac - renal failure - DKA - alcohol and drug use - cyclical vomiting syndrome - Eating disorder - pregnancy - testicular torsion
324
what are the clinical features of gingivitis?
- Reddening and swelling of the gum margins | - Bleeding of gums with toothbrushing, flossing, gentle probing or eating hard foods such as an apple
325
what are the clinical features of periodontitis?
- Halitosis - Foul taste in the mouth - Drifting/loosening of teeth causing difficulty in eating - Periodontal abscess which may cause pain - Bleeding, pus and debris expressible from gingival pockets - Loosening or drifting of teeth - Periodontal abscess
326
what are the clinical features of acute necrotising ulcerative gingivitis?
- Intensely painful gums, particularly when brushing teeth - Bleeding gums with no or minimal trauma - Severe halitosis - Anorexia - Malaise or fever - Punched out gingival ulcers covered with a white, yellowish or grey pseudomembrane - Cervical lymphadenopathy
327
how is gingivitis and periodontitis managed?
- Advise routine regular review by a dentist - Give advice on oral hygiene - Smoking cessation
328
how is acute necrotizing ulcerative gingivitis managed?
- Urgently see a dentist - Give metronidazole 400mg three times daily for 3 days in adults, or 200-250mg 3 times daily for 12-18 year olds - Give amoxicillin 500mg three times daily for 3 days if metronidazole inappropriate - Paracetamol or ibuprofen for pain relief - Chlorhexidine or hydrogen peroxide - Regular review by a dentist - Give advice on oral hygiene
329
what are the clinical features of IgE-mediated food allergy?
- urticaria - facial swelling - anaphylaxis - usually occurring 10–15 min after ingestion of a food.
330
what are the clinical features of non-IgE-mediated food allergy?
- diarrhoea - vomiting - abdominal pain - failure to thrive - colic - eczema
331
how is IgE mediated food allergy diagnosed?
- skin prick tests | - RAST
332
what are the clinical features of rotavirus?
- vomiting - fever - diarrhoea - metabolic consequences of water and electrolyte loss.
333
how is rotavirus diagnosed?
- PCR for genome detection | - ELISA for antigen detection in faeces
334
what are the clinical features of yellow fever?
- 3-6 day incubation period - high fever - headache - Retrobulbar pain - myalgia - arthralgia - flushed face - suffused conjunctivae - epigastric pain - vomiting - relative bradycardia - jaundice - hepatomegaly - ecchymosis, bleeding from the gums, haematemesis and melaena - coma
335
what is seen on liver histology in yellow fever?
- mid-zone necrosis | - eosinophilic degeneration of hepatocytes (Councilman bodies)
336
how is yellow fever diagnosed?
-serology
337
what are the clinical features of scarlet fever?
- regional lymphadenopathy - fever - rigors - headache - vomiting - blanching rash, which initially occurs on the neck but rapidly becomes punctate, erythematous and generalised - typically rash is absent from the face, palms and soles - circumoral pallor - strawberry tongue - raspberry tongue
338
how is scarlet fever treated?
penicillin V - amoxicillin - clarithromycin - for 10 days.
339
what is seen on blood tests in haemolytic jaundice?
- raised urinary urobilinogen - raised bilirubin - normal serum ALP, AST, ALT and albumin
340
what are the clinical features of Gilbert's syndrome?
- asymptomatic | - raised bilirubin
341
how are Dubin-johnson and rotor syndromes inherited?
autosomal recessive
342
how does the liver appear in dubin-johnson syndrome?
-black due to melanin deposition
343
what are the clinical features of biliary atresia?
- jaundice - pale stools and dark urine - hepatomegaly
344
what is seen on investigation of suspected biliary atresia?
- fasting abdominal USS shows contracted or absent gallbladder - Radioisotope scan with iminiodiacetic acid derivatives shows good uptake but no excretion into the bowel
345
how is biliary atresia treated?
- surgical bypass of the fibrotic ducts - hepatoportoenterostomy (Kasai procedure), in which a loop of jejunum is anastomosed to the cut surface of the porta hepatis, facilitating drainage of bile from any remaining patent ductules.
346
how do choledochal cysts present?
- abdominal pain - a palpable mass - jaundice - cholangitis.
347
how are choledochal cysts diagnosed?
ultrasound or radionuclide scanning
348
how are choledochal cysts managed?
surgical excision of the cyst with the formation of a Roux-en-Y anastomosis to the biliary duct
349
what are the clinical features of galactosaemia?
- poor feeding - vomiting - jaundice - hepatomegaly when fed milk. - Liver failure, cataracts and developmental delay are inevitable if galactosaemia is untreated. - A rapidly fatal course with shock, haemorrhage and disseminated intravascular coagulation, often due to Gram-negative sepsis, may occur.
350
how is galactosaemia diagnosed?
- prolonged (persistent) jaundice, by detecting galactose, a reducing substance, in the urine. - measuring the enzyme galactose-1-phosphate-uridyl transferase in red cells.
351
how is galactosaemia treated?
galactose-free diet
352
what are the features of vitamin E deficiency?
- peripheral neuropathy - haemolysis - ataxia
353
how can pruritus associated with liver disease in children be treated?
- Loose cotton clothing, avoiding overheating - Emollients or evening primrose oil - Phenobarbital to stimulate bile flow - cholestyramine - ursodeoxycholic acid
354
what are the indications for liver transplant in children?
- Severe malnutrition unresponsive to intensive nutritional therapy - Recurrent complications (bleeding varices, resistant ascites) - Failure of growth and development - Poor quality of life.
355
what liver disease is seen in cystic fibrosis?
- hepatic steatosis is the most common | - cirrhosis and portal hypertension develop in some
356
what are the clinical features of portal hypertension?
- Haematemesis or melaena from rupture of gastro-oesophageal varices or portal hypertensive gastropathy - Ascites - Breathlessness due to pulmonary hypertension or hepatopulmonary syndrome - splenomegaly - haemorrhoids - caput medusae
357
what are the causes of haemorrhoids?
- Constipation with prolonged straining is a key factor - Diarrhoea - Effects of gravity due to posture - Congestion from a pelvic tumour, pregnancy, portal hypertension - Anal intercourse
358
how are haemorrhoids classified?
- 1st - Remain in rectum - 2nd - Prolapse through the anus on defecation but spontaneously reduce - 3rd - Prolapse but can be reduced manually - 4th - Remain persistently prolapsed - external haemorrhoids originate the dentate line
359
how do haemorrhoids present?
- Bright red rectal bleeding (since blood from capillaries) that often coats stools, seen on tissue or drips into toilet - Mucus discharge and pruritus ani (itchy bottom) - Severe anaemia may occur - Weight loss and change in bowel habit should prompt thoughts of pathology
360
how are haemorrhoids diagnosed?
-Abdominal examination to rule out other disease - PR (per rectum) exam: - --Prolapsing piles are obvious - --Internal haemorrhoids are not palpable - Proctoscopy (rectal scope) to see internal haemorrhoids - Sigmoidoscopy to see rectal pathology higher up
361
how are first degree haemorrhoids treated?
- Increase fluid and fibre | - Topical analgesic and stool softener
362
how are second and third degree haemorrhoids treated?
- Rubber band ligation: Cheap, produces an ulcer to anchor the mucosa (side effects are bleeding, infection and pain) - Infra-red coagulation: Locally coagulates vessels and tethers mucosa to subcutaneous tissue
363
how are fourth degree haemorrhoids treated?
- Excisional haemorrhoidectomy - excision of piles | - Stapled haemorrhoidopexy
364
how are prolapsed or thromboses piles treated?
- analgesia - ice packs - stool softeners
365
what is an anal fistula?
• An abnormal connection between the epithelised surface of the anal canal and skin
366
what are the causes of an anal fistula?
- Perianal sepsis - Abscesses - Crohn’s - TB - Diverticular disease - Rectal carcinoma
367
what are the clinical features of anal fistulas?
- Pain - Discharge (bloody or mucus) - Pruritus ani (itchy bottom) - Systemic abscess if it becomes infected
368
how are anal fistulas diagnosed?
- MRI: To exclude sepsis and to detect associated conditions e.g. Crohn’s or TB - Endoanal ultrasound: To determine tracks location and underlying causes
369
how are anal fistulas treated?
- Surgical - Fistulotomy and excision - Drain abscess with antibiotics if infected
370
what are the causes of anal fissures?
- Hard faeces - Spasm may constrict the inferior rectal artery resulting in ischaemia which makes healing difficult and perpetuates the problem - Syphilis - Herpes - Trauma - Crohn’s - Anal cancer
371
how do anal fissures present?
- Extreme pain especially on defecation - Bleeding - Anal spasm and a tearing sensation on passing stool
372
how are anal fissures treated?
- Increase dietary fibre and fluids to make stools softer - Advise that sitting in a shallow warm bath several times a day may help relieve pain - lidocaine ointment for extreme pain on defecation - GTN ointment for those with symptoms for 1 week without improvement - If anal fissure is unhealed after 6-8 weeks, prescribe topical diltiazem ointment - Surgery if medication fails
373
what are the clinical features of perianal abscess?
- Painful swellings - Tender - Discharge
374
how are peri-anal abscesses diagnosed?
- MRI | - Endoanal ultrasound
375
how are perianal abscesses treated?
- drainage | - antibiotics
376
what are the risk factors for developing pilonodal sinus?
- Obese caucasians and those from Asia, Middle East and Mediterranean are at increased risk - Large amount of body hair - Sedentary job - Occupation involving sitting or driving - Family history
377
how do pilonodal sinuses present?
- Painful swelling over days - Pus filled with foul smell from abscess - Systemic signs of infection
378
how are acute pilonodal sinuses treated?
- Arrange for urgent same day incision and drainage - Offer paracetamol for pain - Following I and D, advise meticulous hygiene and buttock hair removal
379
what are the adverse effects of alginates and antacids?
- Magnesium salts cause diarrhoea | - Aluminium salts cause constipation.
380
with which drugs do alginates and antacids interact with?
- Reduce serum concentration of --ACE inhibitors - -antibiotics - -bisphosphonate - -digoxin - -levothyroxine - -proton pump inhibitors.
381
what are the adverse effects of PPIs?
- GI disturbances - Headache - Hypomagnesaemia leading to tetany and ventricular arrhythmias
382
in which patients should PPIs be used with caution?
- Caution in patients presenting with ‘red-flag features’ of gastric cancer as PPIs can disguise symptom - Caution in patients at risk of osteoporosis due to increased risk of fractures
383
with which drugs do PPIs interact?
- Increases anticoagulant effect of warfarin | - Decreases anti-platelet effect of clopidogrel.
384
what are the adverse effects prostaglandin analogues such as misoprostol?
- Nausea and vomiting - Diarrhoea - Abdominal cramps - Uterine constrictions.
385
what are the adverse effects of bismuth chelate?
- Black tongue and faeces | - Nausea and vomiting.
386
in which patients should bismuth chelate be avoided?
- Avoid in children due to risk of Reye’s syndrome | - Caution in clotting disorders and gout.
387
what are the indications for macrolide antibiotics?
- Eradication of H.pylori in peptic ulcer disease - Respiratory and skin infections when penicillin is contraindicated by allergy - Severe pneumonia added to penicillin to cover Legionella pneumophilia and Mycoplasma pneumoniae.
388
what are the adverse effects of macrolide antibiotics?
- Nausea and vomiting and less frequently antibiotic-associated colitis - cholestatic jaundice - prolongation of QT syndrome - ototoxicity.
389
with which drugs do macrolide antibiotics interact?
- Increased risk of bleeding with warfarin - increased risk of myopathy with statins - increased risk of prolonging QT interval with amiodarone, antipsychotics, SSRIs.
390
what are the indications for broad spectrum penicillins?
- Eradication of H.pylori in peptic ulcer disease - Pneumonia caused by gram positive (S.pneumonia) or gram negative (H.influenza) - urinary tract infections (mostly E.coli) - combination treatment for hospital acquired infection or sepsis - combination treatment for peptic ulcers (H.pylori).
391
what are the adverse effects of broad spectrum penicillins?
- Nausea and diarrhoea and less frequently antibiotic-associated colitis - penicillin allergy presenting as a IgG-mediated skin rash or less commonly IgE mediated anaphylactic reaction - cholestatic jaundice with co-amoxiclav.
392
with which drugs do broad spectrum penicillins interact?
- Reduced renal excretion of methotrexate, increasing risk of toxicity - Enhance anticoagulant effect of warfarin by killing gut flora that synthesise vitamin K.
393
what are the indications for D2 antagonist anti-emetics?
- Prophylaxis and treatment of nausea and vomiting due to reduced gut motility - GORD in patients who do not respond to proton pump inhibitors and H2-receptor antagonists.
394
what are the adverse effects of D2 antagonist anti-emetics?
- Diarrhoea - Acute dystonias (metoclopramide) - QT prolongation (domperidone).
395
in which patients should D2 antagonist anti-emetics be avoided?
- Avoid with GI obstruction, perforation, haemorrhage or recent surgery - Avoid domperidone with long QT syndrome - Caution with metoclopramide in patients under 20 and epilepsy.
396
with which drugs do D2 antagonist anti-emetics interact?
- Dopaminergic agents - Antipsychotics - Drugs that prolong the QT interval (e.g. clarithromycin, fluconazole, diltiazem).
397
what are the adverse effects of H1 antagonist antiemetics?
- Drowsiness due to H1 antagonism | - Dry mouth, blurred vision, urinary retention and constipation due to antimuscarinic effects.
398
in which patients should H1 antagonist antiemetics be avoided?
- patients with prostatic hypertrophy and hepatic encephalopathy - in neonates.
399
what are the indications for antimuscarinics such as hyoscine?
- Irritable Bowel Syndrome - Bradycardia - Reducing respiratory secretions.
400
what are the adverse effects of anti-muscarinics?
- dry mouth - tachycardia - urinary retention - blurred vision - drowsiness - confusion.
401
in which patients should anti-muscarinics be avoided?
- Caution in angle-closure glaucoma | - Caution with arrhythmias.
402
what are the adverse effects of aminosalicylates?
- GI disturbances - Headache - Leucopenia and thrombocytopenia - Renal impairment - Oligospermia - Hypersensitivity reactions.
403
with which drugs do aminosalicylates interact?
- Reduced efficacy with drugs that alter gut pH (PPIs in stomach, lactulose in gut) - Increased risk of leucopenia with azathioprine, mercaptopurine.
404
what is a direct inguinal hernia?
pierces the posterior abdominal wall and the abdominal contents are forced through a defect in the inguinal canal.
405
what is an indirect inguinal hernia?
does not pierce the posterior abdominal wall and the abdominal contents pass through the deep inguinal ring.
406
what are the risk factors for developing inguinal hernias?
- Male sex. - Old age. - Smoking. - Family history. - Abdominal aortic aneurysm. - Marfan’s syndrome or Ehlers-Danlos syndrome.
407
what are the clinical features of inguinal hernias?
- Groin discomfort or pain with bulge. - Groin mass. - Abdominal discomfort and pain is uncommon. - Acute abdomen and an irreducible abdomen suggests strangulation.
408
how is an inguinal hernia managed?
- Refer for urgent surgical repair if the hernia is irreducible which suggests a strangulated hernia. - Refer urgently to a paediatric surgeon (preferably to be seen within 2 weeks) if an infant or young boy presents with a hernia. - Refer all others for routine surgical repair unless: - --They have minimally symptomatic hernias. - --They have significant comorbidity. - --They do not wish to have surgery. -Cefazolin prophylaxis for repair
409
what are the clinical features of angiodysplasia?
- Chronic, painless, low-grade, intermittent bleeding | - Symptoms of anaemia
410
what is seen on OGD and colonoscopy in angiodysplasia?
- Abnormal epithelium - small lesions with irregular edges - a draining vein
411
how are haemodynamically unstable patients with angiodysplasia managed?
- Upper GI endoscopy employing electrocautery, photocoagulation, clips and adrenaline to treat a lesion - If upper GI endoscopy is negative, mesenteric angiogram with or without embolisation, and supportive care - If angiography unavailable, perform colonoscopy employing electrocautery, photocoagulation, clips and adrenaline, or subtotal hemicolectomy if large bleed
412
how are haemodynamically stable patients with angiodysplasia managed?
- Perform interventional endoscopy, angiography with embolisation or wireless capsule enteroscopy as needed - Surgery may be required if the above techniques are unavailable - If the patient is not a surgical candidate, consider octreotide, conjugated oestrogens or thalidomide.