Gastroenterology Flashcards

1
Q

What are the key diagnostic factors for IBS?

A

Abdominal discomfort (lower and/or mid abdomen)
Changes in bowel habits - passage of stool relieves abdominal pain
Abdominal bloating (improved with defecation/flatus)
Passage of mucus with stool
Urgency of defecation

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2
Q

What are the risk factors for IBS?

A

Age <50 years
Female sex
Previous enteric infection
Family history

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3
Q

How is IBS diagnosed?

A

Usually diagnosed from typical symptoms
FBC to exclude iron deficiency anaemia
ESR and CRP to indicate inflammation (not seen in IBS)
Faecal calprotectin (indicates IBD)

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4
Q

How is IBS treated?

A

Exercise and low FODMAP diet
Antispasmodics (e.g. dicycloverine) for abdominal pain
Linaclotide for constipation
Loperamide for diarrhoea
Tricyclic antidepressant (e.g. amitriptyline)

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5
Q

What are the symptoms of anal fissure?

A

Pain on defecation
Tearing sensation on passing stool
Fresh blood on stool or paper
Anal spasm
Fissure visible on retraction of buttock

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6
Q

What are the risk factors for anal fissure?

A

Hard stool
Pregnancy
Opiate analgesia (associated with constipation)

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7
Q

How is anal fissure treated?

A

High-fibre diet with adequate fluid intake
Topical analgesia
Bulk-forming laxatives
Topical glyceryl trinitrate (relaxes smooth muscle, reducing anal tone) for chronic anal fissure
Topical diltiazem (CCB causing vasodilation and smooth muscle relaxation, less headaches than GTN)
If persists after 8 weeks of topical GTN, consider sphincterectomy or botulinum toxin

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8
Q

How are resistant fissures treated?

A

Botulinum toxin injection
Surgical sphincterotomy (risk of faecal leakage and incontinence)
Anal advancement flap

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9
Q

What features are shared between Crohn’s and UC?

A

Diarrhoea
Arthritis
Erythema nodosum
Pyoderma gangrenosum

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10
Q

What features are specific to Crohn’s?

A

weight loss
non-bloody diarrhoea
abdominal pain
mouth to anus, skip lesions
inflammation in all layers
Goblet cells, granulomas
bowel obstruction, fistulae
abdominal mass inn RIF

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11
Q

How is Crohn’s disease investigated?

A

FBC (anaemia, leukocytosis, thrombocytosis?)
Serum B12 and folate (normal or low)
CRP and ESR (elevated)
Stool culture (absence of infectious elements)
Faecal calprotectin
MRI abdomen/pelvis (skip lesions, bowel wall thickening, surrounding inflammation, abscess, fistulae)
CT abdomen
Ileocolonoscopy and biopsies
Test for C. difficile (stool sample for toxin)

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12
Q

What are the main endoscopic findings for Crohn’s disease?

A

Aphthous ulcers
Cobblestone mucosa (normal tissue in between ulcers)
Discontinuous lesions
Inflammation in all layers from mucosa to serosa
Rose-thorn ulcers, fistulae or abscesses
Non-caseating granulomas
Mainly affects terminal ileum

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13
Q

what are the main endoscopic findings in UC?

A

widespread ulceration
‘pseudopolyps’

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14
Q

How is Crohn’s disease treated?

A

Smoking cessation
Prednisolone or IV hydrocortisone to induce remission-
Azathioprine or mercaptopurine to maintain remission (assess TPMT activity before)

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15
Q

What features are specific to UC?

A

Bloody diarrhoea
Primary sclerosing cholangitis
Uveitis
Colorectal cancer
Continuous disease from the ileocaecal valve to the rectum
No inflammation beyond submucosa, crypt abscesses

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16
Q

What extra-intestinal manifestations of ulcerative colitis are related to activity of the colitis?

A

Erythema nodosum
Aphthous ulcers
Episcleritis
Anterior uveitis
Acute arthropathy

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17
Q

What extra-intestinal manifestations of ulcerative colitis are NOT related to the activity of the colitis?

A

Sacroiilitis/ankylosing spondylitis
Primary sclerosing cholangitis

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18
Q

How is UC investigated?

A

FBC, U&Es, LFTs, ESR, CRP, iron studies, B12 and folate
Faecal calprotectin
Microbiological testing for C. difficile
Sigmoidoscopy/colonoscopy and rectal biopsy
Abdominal X-ray (to exclude colonic dilatation, toxic megacolon - shows thumbprinting sign)

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19
Q

How is acute severe UC treated?

A

IV hydrocortisone - consider ciclosporin or infliximab
Consider colectomy (especially for toxic megacolon, perforation)

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20
Q

How is moderate-to-severe UC treated?

A

Prednisolone or budenoside (oral corticosteroid)
Infliximab (biological)
Consider azathioprine or methotrexate (immunosuppressant)

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21
Q

How is mild UC treated?

A

Aminosalicylates (oral/topical mesalazine)

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22
Q

What are the differential diagnoses for a right iliac fossa mass?

A

Crohn’s disease
Appendix mass or abscess
Caecal carcinoma
Ovarian or renal mass
TB, Actinomycosis or amoebic abscess

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23
Q

What are the key diagnostic factors for coeliac disease?

A

Diarrhoea (chronic or intermitent)
Bloating
Abdominal pain/discomfort
Anaemia (iron deficiency, folate/B12)
IgA deficiency
Osteopenia or osteoporosis
Fatigue
Weight loss
Failure to thrive
Dermatitis herpetiformis

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24
Q

What skin changes are present in coeliac disease?

A

Dermatitis herpetiformis

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25
What are the risk factors for coeliac disease?
Family history IgA deficiency Type 1 diabetes Autoimmune thyroid disease Down's syndrome
26
What investigations are considered for coeliac disease?
Immunoglobulin A-tissue transglutaminase (IgA-tTG) - some patients may be seronegative Quantitative IgA FBC (iron deficiency anaemia) Small bowel endoscopy and biopsy
27
What does the small bowel endoscopy and biopsy show in coeliac disease?
Atrophy and scalloping of mucosal folds Nodularity and mosaic pattern of mucosa Presence of intra-epithelial lymphocytes Villous atrophy Crypt hyperplasia
28
How is the biopsy of coeliac disease assessed?
MARSH CRITERIA: 0: normal villous architecture with no increase in intra-epithelial lymphocytes I: normal villous architecture with increased intra-epithelial lymphocytes II: increased intra-epithelial lymphocytes and crypt hyperplasia with normal villi IIIa: increased intra-epithelial lymphocytes and crypt hyperplasia with partial villous atrophy IIIb: increased intra-epithelial lymphocytes and crypt hyperplasia with subtotal villous atrophy IIIc: increased intra-epithelial lymphocytes and crypt hyperplasia with total villous atrophy.
29
How is coeliac disease treated?
Gluten-free diet Vitamin and mineral supplemenation
30
How does a coeliac crisis present?
Hypovolaemia Severe watery diarrhoea Acidosis Hypocalcaemia Hypoalbuminaemia Patients may have a precipitating major medical event, e.g. recent abdominal surgery
31
How is a coeliac crisis treated?
Parenteral fluid replacement Correction of electrolyte abnormalities Corticoseroid (budesonide or prednisolone)
32
what are the complications of coeliac disease?
anaemia: iron, folate and B12 deficiency hyposplenism osteoporosis, osteomalacia lactose intolerance subfertility enteropathy associated T-cell lymphoma
33
What are the symptoms of acute pancreatitis?
Mid-epigastric or left upper quadrant pain that radiates to the back - sudden onset, worsens with movement Nausea and vomiting Signs of hypovolaemia Signs of pleural effusion Anorexia Dyspnoea? Jaundice in severe gallstone pancreatitis
34
What is the acid-base abnormality in acute pancreatitis?
Hypokalaemic metabolic alkalosis Also hypocalcaemia
35
How does acute pancreatitis present on examination?
Tender and distended abdomen with voluntary guarding Diminished bowel sounds (if ileus has developed - assessment of disease severity) Signs of pleural effusion? (localised reduced air entry and dullness to percussion, commonly on the left) Cullen's sign (bruising around umbilicus) - haemorrhagic pancreatitis Grey-Turner's sign (bruising around the flanks) - haemorrhagic pancreatitis Chvostek's sign (facial muscle spasm when facial nerve is tapped)
36
What are the signs of hypovolaemia?
Hypotension Oliguria Dry mucous membranes Decreased skin turgor Sweating In extreme cases, may be tachycardic or tachypnoeic
37
What are the most common causes of acute pancreatitis?
Gallstones and excessive alcohol consumption
38
What are the causes of acute pancreatitis?
GET SMASHED Gallstones Ethanol (alcohol) Trauma Steroids Mumps and other viruses (EBV, CMV) Auto-immune (SLE) Scorpion/snake bite ERCP Drugs (SAND: steroids and sulphonamides, azathioprine, NSAIDs, diuretics)
39
What blood tests are considered for acute pancreatitis?
Serum lipase (preferred) or amylase - lipase levels remain elevated for longer FBC (leukocytosis with left shift, elevated haematocrit indicates poor prognosis) CRP (early indicator of severity, monitors inflammation) Urea/creatinine (elevated in severe cases) LFTs (elevated ALTs shows gallstones as cause)
40
What investigations are considered for acute pancreatitis?
Erect CXR (pleural effusion, ARDS) Transabdominal ultrasound (identifies gallstones, if cause unknown) CT abdomen (if patients are not settling with conservative management after 48-72 hours) MRCP (gallstone pancreatitis) ERCP (to remove common bile duct stone) Amylase and lipase (lipase more specific)
41
What does an ultrasound show in acute pancreatitis?
Swollen pancreas, dilated common bile duct, free peritoneal fluid Can show gallstones
42
What are the other causes of raised amylase?
Renal failure Ectopic pregnancy Diabetic ketoacidosis Perforated duodenal ulcer Mesenteric ischaemia/infarction
43
How is acute pancreatitis treated?
IV fluids with NBM (NJ tube or total parenteral nutrition) Analgesia (ibuprofen or codeine phosphate or morphine) Antibiotics if necrotic pancreatitis or infected necrosis (imipenem)
44
How is the severity of acute pancreatitis assessed?
Modified Glasgow criteria (PANCREAS - score of 3 or more is severe) or CRP>200 PO2 <8kPa Age >55 years Neutrophilia (WCC >15) Calcium <2mmol/L Renal (urea >16mmol/L) Enzymes (elevated AST, LDH) Albumin <32g/L Sugar >10mmol/L
45
What are the systemic complications of pancreatitis?
Hypocalcaemia Hyperglycaemia SIRS (systemic inflammatory response syndrome) ARF (acute renal failure) ARDS (adult respiratory distress syndrome) DIC (disseminated intravascular coagulation) MOF (multi-organ failure) and death
46
What are the local complications of acute pancreatitis?
Pancreatic necrosis (+/- infected necrosis) Pancreatic abscess Pancreatic pseudocyst Haemorrhage secondary to arroded vessels (haemorrhagic pancreatitis in small vessels, pseudoaneurysm in large vessels) Thrombosis of splenic vein, SMV, portal vein - ascites, small bowel congestion and ischaemia Chronic pancreatitis Pleural effusions
47
How is infected pancreatic necrosis discovered?
Rising CRP suggests necrosis Confirmed by dynamic CT
48
How is infected pancreatic necrosis treated?
Fine needle aspiration and culture IV antibiotics (imipenem) Percutaneous/endoscopic catheter drainage Necrosectomy
49
How does acute appendicitis present commonly?
Central abdominal pain, which migrates to the right iliac fossa due to peritoneal involvement - worse on movement and coughing Anorexia Nausea and vomiting Localised tenderness, guarding and rebound tenderness in RIF Low-grade pyrexia Rovsing's sign (palpation pain in LLQ felt in RLQ)
50
What are the uncommon symptoms of acute appendicitis?
Hypotension and tachycardia (signs of shock/sepsis - suggests perforated appendix) Palpable mass Loose stool Constipation Psoas sign (flexed right hip, retrocaecal appendicitis)
51
What investigations are considered for acute appendicitis?
FBC (leukocytosis with neutrophilia) CRP (elevated) Abdominal ultrasound Contrast-enhanced abdominal CT Urinalysis to exclude UTI
52
How is appendicitis risk scored?
Appendicitis Inflammatory Response (AIR) or the Adult Appendicitis Score (AAS)
53
How is acute appendicitis treated?
Laparoscopic appendicectomy with prophylactic IV antibiotics Antibiotics (amoxicillin) if unfit for surgery
54
Differentiate between diverticulosis, diverticular disease and diverticulitis
Diverticulosis: presence of diverticula which are asymptomatic. Diverticular disease: diverticula associated with symptoms. Diverticulitis: evidence of diverticular inflammation (fever, tachycardia) with or without localised symptoms and signs
55
What are the risk factors for diverticular disease?
Low dietary fibre intake Age >50 years Marfan's/Ehler's-Danlos syndrome
56
How does diverticular disease present?
Left lower quadrant abdominal pain with guarding and tenderness Leukocytosis Fever Abdominal bloating Constipation/diarrhoea Pelvic tenderness on DRE Palpable abdominal mass (abscess) Rectal bleeding (uncommon)
57
What investigations are considered for diverticular disease?
FBC, U&Es, CRP for suspected diverticulitis Colonoscopy Contrast CT scan
58
How is symptomatic diverticular disease treated?
Dietary and lifestyle modifications (high-fibre diet) Consider analagesia (paracetamol - NSAIDs increase risk of diverticular perforation) Consider antispasmodic (dicyloverine) - abdominal cramping
59
What are true and psuedo/false diverticula?
True diverticula are outpouchings that include all layers of the intestine (mucosa, submucosa, muscle and serosa) Pseudo diverticula do not include the muscle layer - these are more commonn
60
How is acute diverticulitis treated?
analgesia - paracetamol (NSAIDs and opioids increase the risk of diverticular perforation) oral co-amoxiclav (metronidazole + trimethoprim if allergic) liquid diet if severe symptoms or >72 hours, IV antibiotics
61
What are the key diagnostic factors of large bowel obstruction?
Intermittent abdominal pain Abdominal distension Nausea and faeculent vomiting (late stage) Changes in bowel habits Tinkling bowel sounds
62
What does hard faeces indicate on DRE?
Faecal impaction
63
What does soft stools indicate on DRE?
Partial obstruction
64
What does an empty rectum indicate on DRE?
Proximal obstruction
65
What are the risk factors for large bowel obstruction?
Colorectal adenomas or polyps Current or previous malignancy IBD Diverticular disease Hernias Previous abdominal surgery (postoperative adhesions, strictures, volvulus)
66
How is bowel obstruction investigated?
Abdominal XR CT - abdominal USS for contraindications of CT FBC U&Es (deranged electrolytes, low potassium) CRP
67
What are the key diagnostic factors of small bowel obstruction?
Cramping, intermittent abdominal pain Nausea and bilious vomiting Abdominal distension and tenderness Constipation
68
How is bowel obstruction treated?
IV fluids NBM and NG tube Nasogastric decompression to remove built-up fluid and gases Laparotomy if complications of symptoms don't improve
69
What is chronic mesenteric ischaemia?
Narrowing of the mesenteric blood vessels by atherosclerosis - causes ischaemia
70
What is acute mesenteric ischaemia?
A blood clot forms in a mesenteric blood vessels, blocking blood flow - this may be a thrombus (developed inside artery) or an embolus (from another site)
71
What are the risk factors for intestinal ischaemia?
Smoking Hypertension Diabetes mellitus Hypercholesteraemia Increased age Family history
72
How does chronic mesenteric ischaemia present?
Postprandial central colicky abdominal pain Weight loss (food avoidance) Concurrent vascular co-morbidities, e.g. MI, stroke, PVD Changes in bowel habits Nausea and vomiting Abdominal bruits heard on auscultation Sitophobia (fear of eating, pain associated with food)
73
How is chronic mesenteric ischaemia investigated?
CT angiography Amylase (possibly elevated) U&Es, FBC (anaemia), ABG and serum lactate
74
How is chronic mesenteric ischaemia treated?
Reduce modifiable risk factors (smoking cessation) Secondary prevention (statins and antiplatelet medication) Revascularisation to improve blood flow to intestines - endovascular (percutaneous mesenteric artery stenting) or open (bypass grafting)
75
How does acute mesenteric ischaemia present?
Generalised abdominal pain out of proportion to clinical signs Diffuse and constant pain Non-specific tenderness Nausea and vomiting
76
How is acute mesenteric ischaemia investigated?
CT scan with IV contrast ABG and serum lactate (acidosis and raised lactate) FBC, U&Es, LFTs, clotting, amylase abdominal X-ray (gasless abdomen, thickening of bowel wall, pneumatosis)
77
What are the key diagnostic factors of cholecystitis?
Constant pain and tenderness in RUQ - can refer to right scapula/shoulder Positive Murphy's sign Fever Nausea and vomiting May have jaundice (if gallstone lodged in CBD)
78
What are the risk factors for cholecystitis?
Gallstones (lodged in cystic duct, causes gallbladder inflammation) Diabetes Total parenteral nutrition
79
How is cholecystitis investigated?
Abdominal ultrasound CT if sepsis is suspected FBC (neutrophilic leukocytosis), CRP LFTs (ALP may be elevated if stone in CBD)
80
How is cholecystitis treated?
Analgesia (paracetamol) Fluid resuscitation Consider antibiotics Laparoscopic cholecystectomy
81
What are the risk factors for cholelithiasis?
Female Obesity Pregnancy Middle age
82
What are the symptoms of biliary colic?
Abdominal pain - epigastric or RUQ, radiates to right shoulder Nausea and vomiting Pain occurs after meal, sudden onset - recurrent attacks of constant pain
83
How is biliary colic treated?
Analgesia (paracetamol) If recurrent, cholecystectomy
84
How does cholelithiasis present?
Often unnsymptomatic Can develop biliary colic or cholecystitis
85
What are the key diagnostic of GORD?
Heartburn - burning sensation in chest, worsened while lying down or bending over Acid regurgitation (sour or bitter taste) Bloating Dysphagia (if oesophageal stenosis) Chronic cough or hoarseness (if reflux enters respiratory tract) Enamel erosion (reflux of acid)
86
What are the risk factors for GORD?
Obesity and fat-rich diet Older age Family history Caffeine Alcohol and smoking Medications: hiatus hernia, scleroderma, Zollinger-Ellison syndrome Medications: antihistamines, CCBs, antidepressants, benzodiazepines, glucocorticoids
87
What are the complications of GORD?
Barrett's oesophagus (metaplastic change to columnar epithelium) Oesophagitis Oesophageal stenosis (scarring of oesophagus makes wall thicker and lumen smaller) Laryngitis or asthma (if reflux enters pharynx or larynx) Oesophageal adenocarcinoma
88
How is GORD investigated?
PPI trial (with GORD, symptoms improve) X-rays with barium contrast for complications (oesophageal stenosis, ulcers) Endoscopy and biopsy for Barrett's oesophagus/cancer
89
How is GORD treated?
PPIs (omeprazole or lansoprazole) - lowest effective dose Lifestyle changes (weight loss, smoking cessation, head-of-bed elevation)
90
How is PPI-unresponsive GORD treated?
1st line: continued standard-dose PPI inhibitor 2nd line: surgery (Nissen fundoplication) or transoral incisionless fundoplication
91
What are the symptoms of peptic ulcer disease?
Epigastric pain - in duodenal ulcers, pain may radiate to back due to penetration of ulcer posteriorly into pancreas Nausea and vomiting Early satiety Weight loss or anorexia Bloating, belching
92
What are the complications of peptic ulcer disease?
GI bleeding (haematemesis, melaena) - ulcer erodes into blood vessel GI perforation (hypotension or septic shock) Gastric outlet obstruction
93
What are the risk factors for peptic ulcer disease?
H. pylori infection (most common) Zollinger-Ellison syndrome (excessive gastrin secretion) Drugs (NSAIDs, SSRIs, corticosteroids, bisphosphonates) Smoking Increasing age Family history
94
How is peptic ulcer disease diagnosed?
Upper GI endoscopy H. pylori carbon-13 urea breath test
95
How is H. pylori positive peptic ulcer disease treated?
H. pylori eradication therapy (triple therapy: PPI, clarithromycin, amoxicillin - metronidazole if allergic to penicillin)
96
How is H. pylori negative peptic ulcer disease treated?
Treat underlying cause and stop NSAID use Full dose PPI therapy 2nd line: H2 antagonist (famotidine, nizatidine)
97
How is an active bleeding ulcer treated?
Urgent evaluation and blood transfusion Endoscopy
98
What are the symptoms of gastritis?
Dyspepsia/epigastric discomfort Nausea, vomiting and loss of appetite Fever
99
How is hepatitis A transmitted?
Via the faecal-oral route - contaminated food or water
100
What are the symptoms of hepatitis A?
Fever, malaise Nausea and vomiting Jaundice Hepatomegaly and RUQ pain Dark urine and pale stools
101
What are the risk factors for hepatitis A?
Travel to endemic region Close contact with infected person Men who have sex with men Illegal drug use
102
How is hepatitis A investigated?
LFTs (high transaminases - AST/ALT, proportionally less ALP) Bilirubin (elevated) HAV IgM antibody (positive, indicates infection)
103
How is hepatitis A treated?
Vaccination Resolves without treatment in 1-3 months (basic analgesia)
104
How is hepatitis B transmitted?
Transfer of bodily fluids, e.g. sex, sharing needles, childbirth
105
How does hepatitis B present?
Most cases are asymptomatic Jaundice Hepatomegaly and RUQ pain Ascites Fever, malaise Nausea/vomiting Only 20% of cases lead to chronic hepatitis (more common in young age) Can progress to cirrhosis and hepatocellular carcinoma!
106
How is hepatitis B investigated?
LFTs (elevated ALT/AST, bilirubin) HBcAb (core antibody, for previous infection) HBsAg (surface antigen, active infection or vaccination) HBcAb IgM - active infection, IgG indicates past infection where HBsAb is negative HBeAg indicates infectivity
107
How is acute hepatitis B treated?
Vaccination for prevention Antiviral therapy (entecavir) Assess for liver transplantation
108
How is hepatitis C transmitted?
Via blood and bodily fluids Mostly progresses to chronic hepatitis
109
How is hepatitis D transmitted?
Only survives in patients with pre-existing HBV infection - increases severity of HBV
110
How is hepatitis E transmitted?
Via faecal-oral route
111
How is hepatitis E transmitted?
Via faecal-oral route
112
what are the features of autoimmune hepatitis?
signs of chronic liver disease acute hepatitis: fever, jaundice amenorrhoea ANA/LKM1 antibodies, raised IgG
113
How is autoimmune hepatitis treated?
Corticosteroids (prednisolone) Azathioprine (immunosuppressant) If patients are resistant, liver transplant
114
How is autoimmune hepatitis investigated?
LFTs (elevated ALT/AST) Prothrombin time (prolonged in severe cases) Type 1 autoantibodies: ANAs, anti-smooth muscle antibodies - affects both adults and children Type 2 autoantibodies: ALKM-1, ALC1 - affects children only Diagnosis confirmed with liver biopsy
115
What are the symptoms of colorectal carcinoma?
Rectal bleeding Change in bowel habits Weight loss Abdominal pain Iron deficiency anaemia
116
What are the risk factors for colorectal carcinoma?
Non-modifiable: elderly, male, IBD Modifiable: smoking, obesity, lack of fibre Disorders: hereditary non-polyposis colorectal carcinoma more common, familial adenomatous polyposis
117
What are the features of right-sided colon cancers?
Abdominal pain Iron-deficiency anaemia Palpable mass in RIF Presents late
118
What are the features of left-sided colon cancers?
Rectal bleeding Change in bowel habit Tenesmus Palpable mass in LIF
119
How is colorectal cancer diagnosed?
Colonoscopy with biopsy CT scan (distant metastases and local invasion) FBC (microcytic anaemia) CEA to monitor disease progression
120
How is colorectal cancer treated?
Surgical resection Chemotherapy Radiotherapy for rectal cancer
121
What are the risk factors for pancreatic cancer?
Smoking Obesity Dietary factors (high red meat, low fibre) Chronic pancreatitis Liver cirrhosis FHx Male, elderly, African American
122
What are the symptoms of pancreatic cancer?
Obstructive jaundice Mid-epigastric pain that radiates to back - worse on lying flat Weight loss and anorexia Nausea, vomiting, fatigue Courvoisier's sign (painless palpable gallbladder) Trousseau sign of malignancy New onset diabetes (endocrine insufficiency)
123
How is pancreatic cancer investigated?
CT (gold standard for preliminary diagnosis, staging) Elevated LFTs FBC (anaemia or thrombocytopenia) Elevated CA19-9 (assess response to treatment) Abdominal ultrasound MRCP shows 'double duct' sign
124
How is head of pancreas cancer treated?
Whipple's procedure with regional lymphadenopathy
125
How is tail of pancreas cancer treated?
Distal pancreatectomy +/- splenectomy, with regional lymphadenectomy
126
What are the most common causes of cirrhosis?
Alcoholic liver disease Non Alcoholic Fatty Liver Disease Hepatitis B Hepatitis C
127
What are the symptoms of cirrhosis?
Jaundice Hepatomegaly - liver shrinks as it becomes more cirrhotic Splenomegaly (portal hypertension) Spider naevi Palmar erythema Gynaecomastia and testicular atrophy (endocrine insufficiency) Bruising (due to abnormal clotting) Ascites Caput Medusae (portal hypertension) Asterixis
128
How is cirrhosis investigated?
LFTs and GGT Serum albumin (decreased) U&Es (hyponatraemia, hyperkalaemia) Prothrombin time (prolonged) Paracentesis of ascitic fluid - to determine SAAG Ultrasound (screen for hepatocellular carcinoma every 6 months) FibroScan (every 2 years for patients at risk of cirrhosis) Upper GI endoscopy (identify and treat oesophageal varices, every 3 years) Liver biopsy (confirms cirrhosis diagnosis)
129
What are the complications of cirrhosis?
Malnutrition Portal Hypertension, Varices and Variceal Bleeding Ascites and Spontaneous Bacterial Peritonitis (SBP) Haemorrhoids Hepato-renal Syndrome Hepatic Encephalopathy - build up of ammonia Hepatocellular Carcinoma
130
How are stable varices treated?
Propranolol (reduces portal hypertension) Elastic band ligation of varices Injection of sclerosant (less effective than band ligation) Transjugular Intra-hepatic Portosystemic Shunt (TIPS)
131
How are bleeding varices treated?
Vasopressin analogues (terlipressin) - vasoconstriction and slows bleeding Vitamin K and FFP Elastic band ligation of varices
132
What are the features of spontaneous bacterial peritonitis?
Infection of the ascitic fluid - can be asymptomatic Fever, ascites, abdominal pain Nausea/vomiting Diarrhoea Altered mental status Hypotension and tachycardia Can show metabolic acidosis
133
How is spontaneous bacterial peritonitis investigated?
Diagnostic paracentesis - ascitic fluid culture FBC (leukocytosis, anaemia suggests GI bleeding)
134
What organisms commonly cause spontaneous bacterial peritonitis?
E. coli Klebsiella pneumoniae Gram positive - Staphylococcus and Enterococcus
135
How is spontaneous bacterial peritonitis treated?
IV cephalosporin (cefotaxime) for 5-7 days
136
How is hepatic encephalopathy treated?
Lactulose (laxatives - promotes excretion of ammonia) Oral rifaximin (antibiotic - reduces number of intestinal bacteria producing ammonia)
137
What are the causes of ascites?
Portal hypertension (cirrhosis, congestive heart failure, constrictive pericarditis, Budd-Chiari syndrome) Hypoalbuminaemia (nephrotic syndrome) Pancreatitis TB Bowel obstruction Intra-abdominal malignancy
138
How is ascites investigated?
Serum-Ascites Albumin Gradient (SAAG) If SAAG >11g/L, indicates portal hypertension (ascitic fluid is transudative, low protein) If SAAF <11g/L, other cause (ascitic fluid is exudative, high protein) Diagnostic paracentesis to detect peritoneal infections Abdominal ultrasound
139
How is ascites managed?
Reduce dietary sodium Fluid restriction if patient is hyponatraemic (<125mmol/L) Spiranolactone (loop diuretic sometimes added) Therapeutic paracentesis (drainage in tense ascites) - IV albumin if large volume paracentesis Prophylactic antibiotics (oral ciprofloxacin) to prevent bacterial peritonitis
140
What are the risk factors for volvulus?
Neuropsychiatric disorders, e.g. Parkinson's Nursing home residents Chronic constipation High fibre diet Pregnancy Adhesions
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How does volvulus present?
constipation abdominal bloating abdominal pain nausea/vomiting
142
How is volvulus investigated?
abdominal X-ray sigmoid volvulus: large bowel obstruction (large, dilated loop of colon, often with air-fluid levels) + coffee bean sign caecal volvulus: small bowel obstruction may be seen
143
How is volvulus managed?
NBM, NG tube, IV fluids sigmoid volvulus: rigid sigmoidoscopy with rectal tube insertion caecal volvulus: management is usually operative. Right hemicolectomy is often needed
144
What are haemorrhoids?
Enlarged anal vascular cushions (specialised submucosal tissue that contain connections between the arteries and veins)
145
What are the risk factors for haemorrhoids?
45-65 years History of constipation Pregnancy Pathological pelvic lesions, e.g. ovarian cysts
146
What are the symptoms of haemorrhoids?
May be asymptomatic Painless, bright red bleeding - not mixed in with stool Sore, itchy anus Tender palpable perianal lesion Palpable anal mass
147
How are haemorrhoids investigated?
Anascopic examination (protoscopy) FBC for anaemia if extensive bleeding Colonoscopy to exclude other pathology, e.g. cancer
148
How are haemorrhoids treated?
Increased fibre uptake and adequate fluids Grade I: topical corticosteroids Grade II and III: rubber band ligation Grade IV: surgical haemorrhoidectomy (removing the anal cushions may result in faecal incontinence)
149
What are the types of haemorrhoids?
External: originate below the dentate line, prone to thrombosis, may be painful Internal: originate above the dentate line, do not generally cause pain
150
How are haemorrhoids classified?
1st degree: no prolapse 2nd degree: prolapse when straining and return on relaxing 3rd degree: prolapse when straining, do not return on relaxing, but can be pushed back 4th degree: prolapsed permanently
151
What are the complications of a hernia?
Incarceration (hernia cannot be reduced back into proper position - leads to obstruction and strangulation) Obstruction - vomiting, generalised abdominal pain, absolute constipation Strangulation - significant pain and tenderness at hernia site, medical emergency
152
How are thrombosed haemorrhoids treated?
If patient presents within 72 hours, referral should be considered for excision Otherwise, patients can be managed with stool softeners, ice packs and analgesia Symptoms usually resolve within 10 days
153
What are the risk factors for an inguinal hernia?
Prior hernia Old age Chronically increased intra-abdominal pressure (e.g. constipation, chronic cough, heavy lifting) Smoking Male Marfan's/Ehler's-Danlos High BMI
154
What are the symptoms of an inguinal hernia?
Groin discomfort or pain (dull, heaviness) with bulge Groin mass - may or may not be reducible, superomedial to pubic tubercle Tender, distended abdomen with absent bowel sounds indicates strangulated hernia Nausea, vomiting, constipation if bowel obstruction
155
What are direct inguinal hernias?
Bowel enters the inguinal canal through a weakness in the posterior wall, termed Hesselbach's triangle More common in older patients, secondary to abdominal wall laxity or significant increase in intra-abdominal pressure Medial to inferior epigastric vessels
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What are indirect inguinal hernias?
Bowel enters the inguinal canal via the deep inguinal ring - caused by defect in abdominal wall, congenital More common in infants Lateral to inferior epigastric vessels
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How are inguinal hernias diagnosed?
Clinical diagnosis USS if diagnosis uncertain CT imaging for patients with features of obstruction or strangulation
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How are symptomatic inguinal hernias treated?
Open mesh repair for primary unilateral inguinal hernia Laparoscopic repair for primary bilateral or recurrent inguinal hernia - also if female or risk of chronic pain
159
Where are femoral hernias located?
Inferolateral to the pubic tubercle - high risk of strangulation
160
What are the risk factors for a femoral hernia?
Female Pregnancy Raised intra-abominal pressure Increasing age
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how can a direct and indirect inguinal hernia be differentiated?
both lie superomedial to the pubic tubercle reduce the hernia, place a finger on the deep inguinal ring and ask the patient to cough direct hernia will protrude, while an indirect hernia will remain reduced
162
What is a hiatus hernia?
Protrusion of an organ from the abdominal cavity into the thorax through the oesophageal hiatus (typically the stomach)
163
What are the risk factors for a hiatus hernia?
Obesity Increased age Previous gastro-oesophageal procedure
164
How do hiatus hernias present?
Most cases are asymptomatic Bowel sounds in chest Heartburn or regurgitation Chest pain Dysphagia or odynophagia Haematemesis Cough Shortness of breath
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How are hiatus hernias investigated?
barium swallow (most sensitive test) also OGD
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How is hiatus hernia managed?
PPI (omeprazole) - symptom control Lifestyle changes - smoking cessation, weight loss, reduced alcohol intake, dietary changes Surgery - cruroplasty or laparoscopic fundoplication
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When is surgery indicated for hiatus hernia?
Remaining symptomatic, despite maximal medical therapy Increased risk of strangulation/volvulus (e.g. rolling hiatus hernia) - should have. stomach decompressed via NG tube prior to surgery Nutritional failure (due to gastric outlet obstruction)
168
What are the risk factors for squamous cell carcinoma of the oesophagus?
Smoking Excessive alcohol consumption Chronic achalasia Low vitamin A levels Iron deficiency
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What are the risk factors for adenocarcinoma of the oesophagus?
Obesity Long-standing GORD High fat intake
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What are the symptoms of oesophageal cancer?
Dysphagia and odynophagia Weight loss Hoarseness Hiccups Postprandial/paroxysmal cough
171
How is oesophageal cancer investigated?
Upper GI endoscopy (OGD, urgent 2 week referral) Biopsy CT or PET-CT to identify metastases Endoscopic ultrasound Staging laparoscopy Fine needle aspiration biopsy of palpable cervical lymph nodes
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How are squamous cell carcinomas of the oesophagus treated?
Difficult to operate on Chemo-radiotherapy
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How are adenocarcinomas of the oesophagus treated?
Neoadjuvant chemotherapy or chemo-radiotherapy Oesophageal resection
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What are the signs of peritonitis?
Guarding: involuntary tensing of abdominal wall muscles when palpated Rigidity Rebound tenderness Coughing test: coughing results in pain in abdomen Percussion tenderness: pain on percussion
175
What are the types of peritonitis?
Localised peritonitis: caused by underlying organ inflammation, e.g. appendicitis, cholecystitis Generalised peritonitis: caused by perforation of an abdominal organ Spontaneous bacterial peritonitis: spontaneous infection of ascites in a patient with liver disease
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What are the symptoms of acute cholangitis?
Charcot's triad: RUQ pain, fever, jaundice (raised bilirubin) Pale stools Hypotension and confusion
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What are the causes of acute cholangitis?
Obstruction in bile ducts stopping bile flow, e.g. gallstones in CBD Infection introduced during ERCP procedure
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What are the most common causative organisms of acute cholangitis?
E. coli Klebsiella species Enterococcus species
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How is acute cholangitis diagnosed?
FBC (raised WCC) CRP (raised) ERCP (removal of stones) Abdominal USS (dilated bile duct with stones, first line)
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How is acute cholangitis treated?
NBM IV antibiotics ERCP to remove stones
181
What are the symptoms of alcoholic hepatitis?
Abdominal pain Anorexia and fatigue Nausea and vomiting Jaundice RUQ pain and hepatomegaly Ascites
182
How is alcoholic hepatitis investigated?
LFTs (ALT and AST raised more than GGT and ALP; AST:ALT ratio >2) Bilirubin (elevated conjugated bilirubin) Albumin (decreased) PT (raised) Liver ultrasound
183
How is alcoholic hepatitis treated?
Prednisolone for acute alcoholic hepatitis Pentoxifylline if glucocorticoid contraindicated (e.g. TB, hepatitis B) Alcohol abstinence
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what are the risk factors for C. difficile infection?
Antibiotics PPIs
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what are the features of C. difficile infection?
abdominal pain diarrhoea raised WCC if severe, toxic megacolon
186
how is C. difficile investigated?
C. difficile toxin in stool C. difficile antigen only shows exposure to the bacteria, rather than current infection
187
How is C. difficile treated?
1st line: oral vancomycin for 10 days 2nd line: oral fidaxomicin 3rd line or life-threatening: oral vancomycin and IV metronidazole withhold opioid medications!
188
What are the symptoms of haemochromatosis?
early symptoms include fatigue, erectile dysfunction and arthralgia 'bronze' skin pigmentation diabetes mellitus liver cirrhosis hypogonadotrophic hypogonadism cardiac failure secondary to dilated cardiomyopathy
189
How is haemochromatosis investigated?
ferritin and transferrin saturation (both raised) low total iron binding capacity low transferrin genetic testing for HFE mutation - autosomal recessive condition
190
How is haemochromatosis managed?
1st line: venesection 2nd line: desferrioxamine
191
What are the risk factors for gastric cancer?
H. pylori infection Atrophic gastritis Diet (salt and salt-preserved foods, nitrates) Smoking Blood group
192
What are the symptoms of gastric cancer?
Abdominal pain Weight loss and anorexia Nausea and vomiting Dyspepsia Dysphagia Spread to Virchow's node and Sister Mary Joseph's nodule
193
How is gastric cancer diagnosed?
OGD and biopsy (signet ring cells) CT staging
194
How is gastric cancer managed?
Surgery (partial/total gastrectomy, endoscopic mucosal resection) Chemotherapy
195
What are the causes of B12 deficiency?
Insufficient dietary intake Pernicious anaemia (autoimmune antibodies against IF or parietal cells) Post-gastrectomy Disorders/surgery of terminal ileum (e.g. Crohn's)
196
What are the symptoms of B12 deficiency?
Sore tongue and mouth Macrocytic anaemia Peripheral neuropathy with numbness or paraesthesia (pins and needles) Loss of vibration sense or proprioception Visual changes Mood or cognitive changes
197
How is B12 deficiency treated?
Insufficient dietary intake: oral replacement with cyanocobalamin Pernicious anaemia: 1mg IM hydroxycobalamin 3 times weekly for 2 weeks, then every 3 months TREAT B12 DEFICIENCY BEFORE FOLATE DEFICIENCY - otherwise can lead to subacute combined degeneration of the cord
198
What is mesenteric adenitis?
Inflamed lymph nodes within the mesentery - often follows a recent viral infection
199
What are the symptoms of mesenteric adenitis?
Abdominal pain - usually in RLQ, but may be more widespread General abdominal tenderness Fever Mesenteric lymph node enlargement May also have diarrhoea, nausea and vomiting
200
How is mesenteric adenitis treated?
Often self-limiting and doesn't require treatment Paracetamol or ibuprofen for fever and pain Antibiotics if caused by bacterial infection
201
What are the symptoms of a perianal abscess?
Severe pain in perianal region, worse with direct pressure (e.g. when sitting) Erythematous, fluctuant, tender perianal mass Purulent discharge Fever and malaise due to infection
202
What are the common causative organisms of perianal abscess?
E. coli S. aureus
203
What are the risk factors for perianal abscess?
IBD, esp Crohn's Diabetes Mellitus Underlying malignancy
204
How is perianal abscess investigated?
Clinical diagnosis HbA1c to check for DM MRI (gold standard) or anal ultrasound if complications or part of more serious underlying process
205
How is perianal abscess treated?
Incision and drainage of abscess under local anaesthetic Intra-operative protoscopy to check for fistula in-ano
206
What is a perianal fistula?
Abnormal connection between perianal skin and anal canal
207
What are the risk factors for a perianal fistula?
IBD, mainly perianal Crohn’s Disease Systemic diseases, typically Diabetes Mellitus History of trauma to the anal region Previous radiation therapy to the anal region
208
What are the symptoms of perianal fistula?
Recurrent perianal abscess Intermittent or continuous discharge onto the perineum
209
How is perianal fistula investigated?
MRI pelvis
210
How is perianal fistula treated?
Fistulotomy Placement of a seton through the fistula Oral metronidazole for Crohn's patients with symptomatic fistulae
211
What are the risk factors for cholangiocarcinoma?
History of gallstones/chronic cholecystitis Smoking Obesity Primary sclerosing cholangitis Ulcerative colitis/Crohn's colitis Oestrogens Occupational exposure (pesticides, radiation, heavy metals, vinyl chloride)
212
what are the features of achalasia?
dysphagia of both liquids and solids heartburn regurgitation of food - leads to cough, aspiration pneumonia malignant change in small number of patients
213
how is achalasia investigated?
oesophageal manometry - excessive LOS tone, which doesn't relax on swallowing barium swallow - 'bird beak' appearance (dilated oesophagus that tapers at oesophageal sphincter) CXR - wide mediastinum, fluid level
214
how is achalasia treated?
pneumatic (balloon) dilation Heller cardiomyotomy if recurrent or persistent symptoms intra-sphincteric botulinum toxin if patients are high surgical risk
215
what are the features of Wilson's disease?
liver: hepatitis, cirrhosis neuropsychiatric disorder Kayser-Fleischer rings renal tubular acidosis haemolysis blue nails
216
how is Wilson's disease investigated?
reduced serum caeruloplasmin reduced total serum copper free copper is increased increased 24h urinary copper excretion diagnosis is confirmed by genetic analysis of the ATP7B gene
217
how is Wilson's disease treated?
penicillamine (chelates copper)
218
what are the features of GI perforation?
rapid onset severe abdominal pain features of peritonism (guarding, rebound tenderness) haemodynamic instability malaise, vomiting, lethargy
219
how is GI perforation diagnosed?
CT scan with IV contrast (gold standard) erect CXR (Rigler's sign, free air under diaphragm)
220
how is GI perforation treated?
IV fluids, NBM, IV antibiotics
221
what is Boerhaave's syndrome?
spontaneous rupture of the oesophagus due to repeated episodes of vomiting
222
what are the features of Boerhaave's syndrome?
sudden onset of severe chest pain following vomiting - worse on swallowing signs of shock little/no haematemesis subcutaneous emphysema
223
how is Boerhaave's syndrome diagnosed?
CT contrast swallow
224
how is Boerhaave's syndrome managed?
IV fluids and antibiotics thoracotomy and lavage
225
what are the features of pellagra?
B3 (niacin) deficiency dermatitis diarrhoea dementia
226
what are the features of alcoholic ketoacidosis?
metabolic acidosis raised anion gap elevated serum ketone levels normal or low glucose concentrations
227
how is alcoholic ketoacidosis treated?
infusion of saline and thiamine
228
what are the features of primary sclerosing cholangitis?
cholestasis: jaundice, pruritus, raised bilirubin + ALP RUQ pain fatigue
229
how is primary sclerosing cholangitis investigated?
ERCP or MRCP: 'beaded' appearance p-ANCA may be positive
230
what are the side effects of PPIs?
hyponatraemia, hypomagnasaemia osteoporosis increased risk of C. difficile infections
231
what are the side effects of metoclopramide?
extrapyramidal effects - acute dystonia e.g. oculogyric crisis diarrhoea hyperprolactinaemia tardive dyskinesia parkinsonianism should be avoided in bowel obstruction!
232
what are the risk factors for primary biliary cholangitis?
Sjogren's syndrome rheumatoid arthritis systemic sclerosis thyroid disease middle-aged women
233
what are the features of primary biliary cholangitis?
early: may be asymptomatic (raised ALP), fatigue, pruritus cholestatic jaundice hyperpigmentation RUQ pain xanthelasmas clubbing, hepatosplenomegaly
234
how is primary biliary cholangitis investigated?
raised IgM anti-mitochondrial antibodies MRCP or ultrasound to exclude extrahepatic biliary obstruction
235
how is C. difficile investigated?
C. difficile toxin in stool C. difficile antigen only shows exposure to the bacteria, rather than current infection
236
what are the features of hepatocellular carcinoma?
tends to present late jaundice ascites RUQ pain pruritus splenomegaly raised alpha-fetoprotein
237
what are the features of constipation?
<3 stools per week abdominal pain rectal bleeding associated with hard stools faecal impaction causing overflow soiling - incontinence of loose smelly stools hard stools may be palpable in abdomen
238
what organisms commonly cause bloody diarrhoea?
campylobacter jejuni (gram negative) haemorrhagic e. coli (gram negative) entamoebe histolytica salmonella chigella