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Phase 1c: Conditions > Gastroenterology > Flashcards

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
Q

What are the risk factors for coeliac disease?

A

Family history
IgA deficiency
Type 1 diabetes
Autoimmune thyroid disease
Down’s syndrome

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26
Q

What investigations are considered for coeliac disease?

A

Immunoglobulin A-tissue transglutaminase (IgA-tTG) - some patients may be seronegative
Quantitative IgA
FBC (iron deficiency anaemia)
Small bowel endoscopy and biopsy

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27
Q

What does the small bowel endoscopy and biopsy show in coeliac disease?

A

Atrophy and scalloping of mucosal folds
Nodularity and mosaic pattern of mucosa
Presence of intra-epithelial lymphocytes
Villous atrophy
Crypt hyperplasia

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28
Q

How is the biopsy of coeliac disease assessed?

A

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.

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29
Q

How is coeliac disease treated?

A

Gluten-free diet
Vitamin and mineral supplemenation

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30
Q

How does a coeliac crisis present?

A

Hypovolaemia
Severe watery diarrhoea
Acidosis
Hypocalcaemia
Hypoalbuminaemia
Patients may have a precipitating major medical event, e.g. recent abdominal surgery

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31
Q

How is a coeliac crisis treated?

A

Parenteral fluid replacement
Correction of electrolyte abnormalities
Corticoseroid (budesonide or prednisolone)

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32
Q

what are the complications of coeliac disease?

A

anaemia: iron, folate and B12 deficiency
hyposplenism
osteoporosis, osteomalacia
lactose intolerance
subfertility
enteropathy associated T-cell lymphoma

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33
Q

What are the symptoms of acute pancreatitis?

A

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

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34
Q

What is the acid-base abnormality in acute pancreatitis?

A

Hypokalaemic metabolic alkalosis
Also hypocalcaemia

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35
Q

How does acute pancreatitis present on examination?

A

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)

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36
Q

What are the signs of hypovolaemia?

A

Hypotension
Oliguria
Dry mucous membranes
Decreased skin turgor
Sweating
In extreme cases, may be tachycardic or tachypnoeic

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37
Q

What are the most common causes of acute pancreatitis?

A

Gallstones and excessive alcohol consumption

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38
Q

What are the causes of acute pancreatitis?

A

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)

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39
Q

What blood tests are considered for acute pancreatitis?

A

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)

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40
Q

What investigations are considered for acute pancreatitis?

A

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)

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41
Q

What does an ultrasound show in acute pancreatitis?

A

Swollen pancreas, dilated common bile duct, free peritoneal fluid
Can show gallstones

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42
Q

What are the other causes of raised amylase?

A

Renal failure
Ectopic pregnancy
Diabetic ketoacidosis
Perforated duodenal ulcer
Mesenteric ischaemia/infarction

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43
Q

How is acute pancreatitis treated?

A

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)

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44
Q

How is the severity of acute pancreatitis assessed?

A

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

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45
Q

What are the systemic complications of pancreatitis?

A

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

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46
Q

What are the local complications of acute pancreatitis?

A

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

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47
Q

How is infected pancreatic necrosis discovered?

A

Rising CRP suggests necrosis
Confirmed by dynamic CT

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48
Q

How is infected pancreatic necrosis treated?

A

Fine needle aspiration and culture
IV antibiotics (imipenem)
Percutaneous/endoscopic catheter drainage
Necrosectomy

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49
Q

How does acute appendicitis present commonly?

A

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)

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50
Q

What are the uncommon symptoms of acute appendicitis?

A

Hypotension and tachycardia (signs of shock/sepsis - suggests perforated appendix)
Palpable mass
Loose stool
Constipation
Psoas sign (flexed right hip, retrocaecal appendicitis)

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51
Q

What investigations are considered for acute appendicitis?

A

FBC (leukocytosis with neutrophilia)
CRP (elevated)
Abdominal ultrasound
Contrast-enhanced abdominal CT
Urinalysis to exclude UTI

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52
Q

How is appendicitis risk scored?

A

Appendicitis Inflammatory Response (AIR) or the Adult Appendicitis Score (AAS)

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53
Q

How is acute appendicitis treated?

A

Laparoscopic appendicectomy with prophylactic IV antibiotics
Antibiotics (amoxicillin) if unfit for surgery

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54
Q

Differentiate between diverticulosis, diverticular disease and diverticulitis

A

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

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55
Q

What are the risk factors for diverticular disease?

A

Low dietary fibre intake
Age >50 years
Marfan’s/Ehler’s-Danlos syndrome

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56
Q

How does diverticular disease present?

A

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)

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57
Q

What investigations are considered for diverticular disease?

A

FBC, U&Es, CRP for suspected diverticulitis
Colonoscopy
Contrast CT scan

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58
Q

How is symptomatic diverticular disease treated?

A

Dietary and lifestyle modifications (high-fibre diet)
Consider analagesia (paracetamol - NSAIDs increase risk of diverticular perforation)
Consider antispasmodic (dicyloverine) - abdominal cramping

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59
Q

What are true and psuedo/false diverticula?

A

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

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60
Q

How is acute diverticulitis treated?

A

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

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61
Q

What are the key diagnostic factors of large bowel obstruction?

A

Intermittent abdominal pain
Abdominal distension
Nausea and faeculent vomiting (late stage)
Changes in bowel habits
Tinkling bowel sounds

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62
Q

What does hard faeces indicate on DRE?

A

Faecal impaction

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63
Q

What does soft stools indicate on DRE?

A

Partial obstruction

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64
Q

What does an empty rectum indicate on DRE?

A

Proximal obstruction

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65
Q

What are the risk factors for large bowel obstruction?

A

Colorectal adenomas or polyps
Current or previous malignancy
IBD
Diverticular disease
Hernias
Previous abdominal surgery (postoperative adhesions, strictures, volvulus)

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66
Q

How is bowel obstruction investigated?

A

Abdominal XR
CT - abdominal USS for contraindications of CT
FBC
U&Es (deranged electrolytes, low potassium)
CRP

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67
Q

What are the key diagnostic factors of small bowel obstruction?

A

Cramping, intermittent abdominal pain
Nausea and bilious vomiting
Abdominal distension and tenderness
Constipation

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68
Q

How is bowel obstruction treated?

A

IV fluids
NBM and NG tube
Nasogastric decompression to remove built-up fluid and gases
Laparotomy if complications of symptoms don’t improve

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69
Q

What is chronic mesenteric ischaemia?

A

Narrowing of the mesenteric blood vessels by atherosclerosis - causes ischaemia

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70
Q

What is acute mesenteric ischaemia?

A

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)

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71
Q

What are the risk factors for intestinal ischaemia?

A

Smoking
Hypertension
Diabetes mellitus
Hypercholesteraemia
Increased age
Family history

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72
Q

How does chronic mesenteric ischaemia present?

A

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)

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73
Q

How is chronic mesenteric ischaemia investigated?

A

CT angiography
Amylase (possibly elevated)
U&Es, FBC (anaemia), ABG and serum lactate

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74
Q

How is chronic mesenteric ischaemia treated?

A

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)

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75
Q

How does acute mesenteric ischaemia present?

A

Generalised abdominal pain out of proportion to clinical signs
Diffuse and constant pain
Non-specific tenderness
Nausea and vomiting

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76
Q

How is acute mesenteric ischaemia investigated?

A

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)

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77
Q

What are the key diagnostic factors of cholecystitis?

A

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)

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78
Q

What are the risk factors for cholecystitis?

A

Gallstones (lodged in cystic duct, causes gallbladder inflammation)
Diabetes
Total parenteral nutrition

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79
Q

How is cholecystitis investigated?

A

Abdominal ultrasound
CT if sepsis is suspected
FBC (neutrophilic leukocytosis), CRP
LFTs (ALP may be elevated if stone in CBD)

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80
Q

How is cholecystitis treated?

A

Analgesia (paracetamol)
Fluid resuscitation
Consider antibiotics
Laparoscopic cholecystectomy

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81
Q

What are the risk factors for cholelithiasis?

A

Female
Obesity
Pregnancy
Middle age

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82
Q

What are the symptoms of biliary colic?

A

Abdominal pain - epigastric or RUQ, radiates to right shoulder
Nausea and vomiting
Pain occurs after meal, sudden onset - recurrent attacks of constant pain

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83
Q

How is biliary colic treated?

A

Analgesia (paracetamol)
If recurrent, cholecystectomy

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84
Q

How does cholelithiasis present?

A

Often unnsymptomatic
Can develop biliary colic or cholecystitis

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85
Q

What are the key diagnostic of GORD?

A

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)

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86
Q

What are the risk factors for GORD?

A

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

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87
Q

What are the complications of GORD?

A

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

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88
Q

How is GORD investigated?

A

PPI trial (with GORD, symptoms improve)
X-rays with barium contrast for complications (oesophageal stenosis, ulcers)
Endoscopy and biopsy for Barrett’s oesophagus/cancer

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89
Q

How is GORD treated?

A

PPIs (omeprazole or lansoprazole) - lowest effective dose
Lifestyle changes (weight loss, smoking cessation, head-of-bed elevation)

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90
Q

How is PPI-unresponsive GORD treated?

A

1st line: continued standard-dose PPI inhibitor
2nd line: surgery (Nissen fundoplication) or transoral incisionless fundoplication

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91
Q

What are the symptoms of peptic ulcer disease?

A

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

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92
Q

What are the complications of peptic ulcer disease?

A

GI bleeding (haematemesis, melaena) - ulcer erodes into blood vessel
GI perforation (hypotension or septic shock)
Gastric outlet obstruction

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93
Q

What are the risk factors for peptic ulcer disease?

A

H. pylori infection (most common)
Zollinger-Ellison syndrome (excessive gastrin secretion)
Drugs (NSAIDs, SSRIs, corticosteroids, bisphosphonates)
Smoking
Increasing age
Family history

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94
Q

How is peptic ulcer disease diagnosed?

A

Upper GI endoscopy
H. pylori carbon-13 urea breath test

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95
Q

How is H. pylori positive peptic ulcer disease treated?

A

H. pylori eradication therapy (triple therapy: PPI, clarithromycin, amoxicillin - metronidazole if allergic to penicillin)

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96
Q

How is H. pylori negative peptic ulcer disease treated?

A

Treat underlying cause and stop NSAID use
Full dose PPI therapy
2nd line: H2 antagonist (famotidine, nizatidine)

97
Q

How is an active bleeding ulcer treated?

A

Urgent evaluation and blood transfusion
Endoscopy

98
Q

What are the symptoms of gastritis?

A

Dyspepsia/epigastric discomfort
Nausea, vomiting and loss of appetite
Fever

99
Q

How is hepatitis A transmitted?

A

Via the faecal-oral route - contaminated food or water

100
Q

What are the symptoms of hepatitis A?

A

Fever, malaise
Nausea and vomiting
Jaundice
Hepatomegaly and RUQ pain
Dark urine and pale stools

101
Q

What are the risk factors for hepatitis A?

A

Travel to endemic region
Close contact with infected person
Men who have sex with men
Illegal drug use

102
Q

How is hepatitis A investigated?

A

LFTs (high transaminases - AST/ALT, proportionally less ALP)
Bilirubin (elevated)
HAV IgM antibody (positive, indicates infection)

103
Q

How is hepatitis A treated?

A

Vaccination
Resolves without treatment in 1-3 months (basic analgesia)

104
Q

How is hepatitis B transmitted?

A

Transfer of bodily fluids, e.g. sex, sharing needles, childbirth

105
Q

How does hepatitis B present?

A

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
Q

How is hepatitis B investigated?

A

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
Q

How is acute hepatitis B treated?

A

Vaccination for prevention
Antiviral therapy (entecavir)
Assess for liver transplantation

108
Q

How is hepatitis C transmitted?

A

Via blood and bodily fluids
Mostly progresses to chronic hepatitis

109
Q

How is hepatitis D transmitted?

A

Only survives in patients with pre-existing HBV infection - increases severity of HBV

110
Q

How is hepatitis E transmitted?

A

Via faecal-oral route

111
Q

How is hepatitis E transmitted?

A

Via faecal-oral route

112
Q

what are the features of autoimmune hepatitis?

A

signs of chronic liver disease
acute hepatitis: fever, jaundice
amenorrhoea
ANA/LKM1 antibodies, raised IgG

113
Q

How is autoimmune hepatitis treated?

A

Corticosteroids (prednisolone)
Azathioprine (immunosuppressant)
If patients are resistant, liver transplant

114
Q

How is autoimmune hepatitis investigated?

A

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
Q

What are the symptoms of colorectal carcinoma?

A

Rectal bleeding
Change in bowel habits
Weight loss
Abdominal pain
Iron deficiency anaemia

116
Q

What are the risk factors for colorectal carcinoma?

A

Non-modifiable: elderly, male, IBD
Modifiable: smoking, obesity, lack of fibre
Disorders: hereditary non-polyposis colorectal carcinoma more common, familial adenomatous polyposis

117
Q

What are the features of right-sided colon cancers?

A

Abdominal pain
Iron-deficiency anaemia
Palpable mass in RIF
Presents late

118
Q

What are the features of left-sided colon cancers?

A

Rectal bleeding
Change in bowel habit
Tenesmus
Palpable mass in LIF

119
Q

How is colorectal cancer diagnosed?

A

Colonoscopy with biopsy
CT scan (distant metastases and local invasion)
FBC (microcytic anaemia)
CEA to monitor disease progression

120
Q

How is colorectal cancer treated?

A

Surgical resection
Chemotherapy
Radiotherapy for rectal cancer

121
Q

What are the risk factors for pancreatic cancer?

A

Smoking
Obesity
Dietary factors (high red meat, low fibre)
Chronic pancreatitis
Liver cirrhosis
FHx
Male, elderly, African American

122
Q

What are the symptoms of pancreatic cancer?

A

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
Q

How is pancreatic cancer investigated?

A

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
Q

How is head of pancreas cancer treated?

A

Whipple’s procedure with regional lymphadenopathy

125
Q

How is tail of pancreas cancer treated?

A

Distal pancreatectomy +/- splenectomy, with regional lymphadenectomy

126
Q

What are the most common causes of cirrhosis?

A

Alcoholic liver disease
Non Alcoholic Fatty Liver Disease
Hepatitis B
Hepatitis C

127
Q

What are the symptoms of cirrhosis?

A

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
Q

How is cirrhosis investigated?

A

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
Q

What are the complications of cirrhosis?

A

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
Q

How are stable varices treated?

A

Propranolol (reduces portal hypertension)
Elastic band ligation of varices
Injection of sclerosant (less effective than band ligation)
Transjugular Intra-hepatic Portosystemic Shunt (TIPS)

131
Q

How are bleeding varices treated?

A

Vasopressin analogues (terlipressin) - vasoconstriction and slows bleeding
Vitamin K and FFP
Elastic band ligation of varices

132
Q

What are the features of spontaneous bacterial peritonitis?

A

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
Q

How is spontaneous bacterial peritonitis investigated?

A

Diagnostic paracentesis - ascitic fluid culture
FBC (leukocytosis, anaemia suggests GI bleeding)

134
Q

What organisms commonly cause spontaneous bacterial peritonitis?

A

E. coli
Klebsiella pneumoniae
Gram positive - Staphylococcus and Enterococcus

135
Q

How is spontaneous bacterial peritonitis treated?

A

IV cephalosporin (cefotaxime) for 5-7 days

136
Q

How is hepatic encephalopathy treated?

A

Lactulose (laxatives - promotes excretion of ammonia)
Oral rifaximin (antibiotic - reduces number of intestinal bacteria producing ammonia)

137
Q

What are the causes of ascites?

A

Portal hypertension (cirrhosis, congestive heart failure, constrictive pericarditis, Budd-Chiari syndrome)
Hypoalbuminaemia (nephrotic syndrome)
Pancreatitis
TB
Bowel obstruction
Intra-abdominal malignancy

138
Q

How is ascites investigated?

A

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
Q

How is ascites managed?

A

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
Q

What are the risk factors for volvulus?

A

Neuropsychiatric disorders, e.g. Parkinson’s
Nursing home residents
Chronic constipation
High fibre diet
Pregnancy
Adhesions

141
Q

How does volvulus present?

A

constipation
abdominal bloating
abdominal pain
nausea/vomiting

142
Q

How is volvulus investigated?

A

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
Q

How is volvulus managed?

A

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
Q

What are haemorrhoids?

A

Enlarged anal vascular cushions (specialised submucosal tissue that contain connections between the arteries and veins)

145
Q

What are the risk factors for haemorrhoids?

A

45-65 years
History of constipation
Pregnancy
Pathological pelvic lesions, e.g. ovarian cysts

146
Q

What are the symptoms of haemorrhoids?

A

May be asymptomatic
Painless, bright red bleeding - not mixed in with stool
Sore, itchy anus
Tender palpable perianal lesion
Palpable anal mass

147
Q

How are haemorrhoids investigated?

A

Anascopic examination (protoscopy)
FBC for anaemia if extensive bleeding
Colonoscopy to exclude other pathology, e.g. cancer

148
Q

How are haemorrhoids treated?

A

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
Q

What are the types of haemorrhoids?

A

External: originate below the dentate line, prone to thrombosis, may be painful
Internal: originate above the dentate line, do not generally cause pain

150
Q

How are haemorrhoids classified?

A

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
Q

What are the complications of a hernia?

A

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
Q

How are thrombosed haemorrhoids treated?

A

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
Q

What are the risk factors for an inguinal hernia?

A

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
Q

What are the symptoms of an inguinal hernia?

A

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
Q

What are direct inguinal hernias?

A

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

156
Q

What are indirect inguinal hernias?

A

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

157
Q

How are inguinal hernias diagnosed?

A

Clinical diagnosis
USS if diagnosis uncertain
CT imaging for patients with features of obstruction or strangulation

158
Q

How are symptomatic inguinal hernias treated?

A

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
Q

Where are femoral hernias located?

A

Inferolateral to the pubic tubercle - high risk of strangulation

160
Q

What are the risk factors for a femoral hernia?

A

Female
Pregnancy
Raised intra-abominal pressure
Increasing age

161
Q

how can a direct and indirect inguinal hernia be differentiated?

A

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
Q

What is a hiatus hernia?

A

Protrusion of an organ from the abdominal cavity into the thorax through the oesophageal hiatus (typically the stomach)

163
Q

What are the risk factors for a hiatus hernia?

A

Obesity
Increased age
Previous gastro-oesophageal procedure

164
Q

How do hiatus hernias present?

A

Most cases are asymptomatic
Bowel sounds in chest
Heartburn or regurgitation
Chest pain
Dysphagia or odynophagia
Haematemesis
Cough
Shortness of breath

165
Q

How are hiatus hernias investigated?

A

barium swallow (most sensitive test)
also OGD

166
Q

How is hiatus hernia managed?

A

PPI (omeprazole) - symptom control
Lifestyle changes - smoking cessation, weight loss, reduced alcohol intake, dietary changes
Surgery - cruroplasty or laparoscopic fundoplication

167
Q

When is surgery indicated for hiatus hernia?

A

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
Q

What are the risk factors for squamous cell carcinoma of the oesophagus?

A

Smoking
Excessive alcohol consumption
Chronic achalasia
Low vitamin A levels
Iron deficiency

169
Q

What are the risk factors for adenocarcinoma of the oesophagus?

A

Obesity
Long-standing GORD
High fat intake

170
Q

What are the symptoms of oesophageal cancer?

A

Dysphagia and odynophagia
Weight loss
Hoarseness
Hiccups
Postprandial/paroxysmal cough

171
Q

How is oesophageal cancer investigated?

A

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

172
Q

How are squamous cell carcinomas of the oesophagus treated?

A

Difficult to operate on
Chemo-radiotherapy

173
Q

How are adenocarcinomas of the oesophagus treated?

A

Neoadjuvant chemotherapy or chemo-radiotherapy
Oesophageal resection

174
Q

What are the signs of peritonitis?

A

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
Q

What are the types of peritonitis?

A

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

176
Q

What are the symptoms of acute cholangitis?

A

Charcot’s triad: RUQ pain, fever, jaundice (raised bilirubin)
Pale stools
Hypotension and confusion

177
Q

What are the causes of acute cholangitis?

A

Obstruction in bile ducts stopping bile flow, e.g. gallstones in CBD
Infection introduced during ERCP procedure

178
Q

What are the most common causative organisms of acute cholangitis?

A

E. coli
Klebsiella species
Enterococcus species

179
Q

How is acute cholangitis diagnosed?

A

FBC (raised WCC)
CRP (raised)
ERCP (removal of stones)
Abdominal USS (dilated bile duct with stones, first line)

180
Q

How is acute cholangitis treated?

A

NBM
IV antibiotics
ERCP to remove stones

181
Q

What are the symptoms of alcoholic hepatitis?

A

Abdominal pain
Anorexia and fatigue
Nausea and vomiting
Jaundice
RUQ pain and hepatomegaly
Ascites

182
Q

How is alcoholic hepatitis investigated?

A

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
Q

How is alcoholic hepatitis treated?

A

Prednisolone for acute alcoholic hepatitis
Pentoxifylline if glucocorticoid contraindicated (e.g. TB, hepatitis B)
Alcohol abstinence

184
Q

what are the risk factors for C. difficile infection?

A

Antibiotics
PPIs

185
Q

what are the features of C. difficile infection?

A

abdominal pain
diarrhoea
raised WCC
if severe, toxic megacolon

186
Q

how is C. difficile investigated?

A

C. difficile toxin in stool
C. difficile antigen only shows exposure to the bacteria, rather than current infection

187
Q

How is C. difficile treated?

A

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
Q

What are the symptoms of haemochromatosis?

A

early symptoms include fatigue, erectile dysfunction and arthralgia
‘bronze’ skin pigmentation
diabetes mellitus
liver cirrhosis
hypogonadotrophic hypogonadism
cardiac failure secondary to dilated cardiomyopathy

189
Q

How is haemochromatosis investigated?

A

ferritin and transferrin saturation (both raised)
low total iron binding capacity
low transferrin
genetic testing for HFE mutation - autosomal recessive condition

190
Q

How is haemochromatosis managed?

A

1st line: venesection
2nd line: desferrioxamine

191
Q

What are the risk factors for gastric cancer?

A

H. pylori infection
Atrophic gastritis
Diet (salt and salt-preserved foods, nitrates)
Smoking
Blood group

192
Q

What are the symptoms of gastric cancer?

A

Abdominal pain
Weight loss and anorexia
Nausea and vomiting
Dyspepsia
Dysphagia
Spread to Virchow’s node and Sister Mary Joseph’s nodule

193
Q

How is gastric cancer diagnosed?

A

OGD and biopsy (signet ring cells)
CT staging

194
Q

How is gastric cancer managed?

A

Surgery (partial/total gastrectomy, endoscopic mucosal resection)
Chemotherapy

195
Q

What are the causes of B12 deficiency?

A

Insufficient dietary intake
Pernicious anaemia (autoimmune antibodies against IF or parietal cells)
Post-gastrectomy
Disorders/surgery of terminal ileum (e.g. Crohn’s)

196
Q

What are the symptoms of B12 deficiency?

A

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
Q

How is B12 deficiency treated?

A

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
Q

What is mesenteric adenitis?

A

Inflamed lymph nodes within the mesentery - often follows a recent viral infection

199
Q

What are the symptoms of mesenteric adenitis?

A

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
Q

How is mesenteric adenitis treated?

A

Often self-limiting and doesn’t require treatment
Paracetamol or ibuprofen for fever and pain
Antibiotics if caused by bacterial infection

201
Q

What are the symptoms of a perianal abscess?

A

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
Q

What are the common causative organisms of perianal abscess?

A

E. coli
S. aureus

203
Q

What are the risk factors for perianal abscess?

A

IBD, esp Crohn’s
Diabetes Mellitus
Underlying malignancy

204
Q

How is perianal abscess investigated?

A

Clinical diagnosis
HbA1c to check for DM
MRI (gold standard) or anal ultrasound if complications or part of more serious underlying process

205
Q

How is perianal abscess treated?

A

Incision and drainage of abscess under local anaesthetic
Intra-operative protoscopy to check for fistula in-ano

206
Q

What is a perianal fistula?

A

Abnormal connection between perianal skin and anal canal

207
Q

What are the risk factors for a perianal fistula?

A

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
Q

What are the symptoms of perianal fistula?

A

Recurrent perianal abscess
Intermittent or continuous discharge onto the perineum

209
Q

How is perianal fistula investigated?

A

MRI pelvis

210
Q

How is perianal fistula treated?

A

Fistulotomy
Placement of a seton through the fistula
Oral metronidazole for Crohn’s patients with symptomatic fistulae

211
Q

What are the risk factors for cholangiocarcinoma?

A

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
Q

what are the features of achalasia?

A

dysphagia of both liquids and solids
heartburn
regurgitation of food - leads to cough, aspiration pneumonia
malignant change in small number of patients

213
Q

how is achalasia investigated?

A

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
Q

how is achalasia treated?

A

pneumatic (balloon) dilation
Heller cardiomyotomy if recurrent or persistent symptoms
intra-sphincteric botulinum toxin if patients are high surgical risk

215
Q

what are the features of Wilson’s disease?

A

liver: hepatitis, cirrhosis
neuropsychiatric disorder
Kayser-Fleischer rings
renal tubular acidosis
haemolysis
blue nails

216
Q

how is Wilson’s disease investigated?

A

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
Q

how is Wilson’s disease treated?

A

penicillamine (chelates copper)

218
Q

what are the features of GI perforation?

A

rapid onset severe abdominal pain
features of peritonism (guarding, rebound tenderness)
haemodynamic instability
malaise, vomiting, lethargy

219
Q

how is GI perforation diagnosed?

A

CT scan with IV contrast (gold standard)
erect CXR (Rigler’s sign, free air under diaphragm)

220
Q

how is GI perforation treated?

A

IV fluids, NBM, IV antibiotics

221
Q

what is Boerhaave’s syndrome?

A

spontaneous rupture of the oesophagus due to repeated episodes of vomiting

222
Q

what are the features of Boerhaave’s syndrome?

A

sudden onset of severe chest pain following vomiting - worse on swallowing
signs of shock
little/no haematemesis
subcutaneous emphysema

223
Q

how is Boerhaave’s syndrome diagnosed?

A

CT contrast swallow

224
Q

how is Boerhaave’s syndrome managed?

A

IV fluids and antibiotics
thoracotomy and lavage

225
Q

what are the features of pellagra?

A

B3 (niacin) deficiency
dermatitis
diarrhoea
dementia

226
Q

what are the features of alcoholic ketoacidosis?

A

metabolic acidosis
raised anion gap
elevated serum ketone levels
normal or low glucose concentrations

227
Q

how is alcoholic ketoacidosis treated?

A

infusion of saline and thiamine

228
Q

what are the features of primary sclerosing cholangitis?

A

cholestasis: jaundice, pruritus, raised bilirubin + ALP
RUQ pain
fatigue

229
Q

how is primary sclerosing cholangitis investigated?

A

ERCP or MRCP: ‘beaded’ appearance
p-ANCA may be positive

230
Q

what are the side effects of PPIs?

A

hyponatraemia, hypomagnasaemia
osteoporosis
increased risk of C. difficile infections

231
Q

what are the side effects of metoclopramide?

A

extrapyramidal effects - acute dystonia e.g. oculogyric crisis
diarrhoea
hyperprolactinaemia
tardive dyskinesia
parkinsonianism
should be avoided in bowel obstruction!

232
Q

what are the risk factors for primary biliary cholangitis?

A

Sjogren’s syndrome
rheumatoid arthritis
systemic sclerosis
thyroid disease
middle-aged women

233
Q

what are the features of primary biliary cholangitis?

A

early: may be asymptomatic (raised ALP), fatigue, pruritus
cholestatic jaundice
hyperpigmentation
RUQ pain
xanthelasmas
clubbing, hepatosplenomegaly

234
Q

how is primary biliary cholangitis investigated?

A

raised IgM
anti-mitochondrial antibodies
MRCP or ultrasound to exclude extrahepatic biliary obstruction

235
Q

how is C. difficile investigated?

A

C. difficile toxin in stool
C. difficile antigen only shows exposure to the bacteria, rather than current infection

236
Q

what are the features of hepatocellular carcinoma?

A

tends to present late
jaundice
ascites
RUQ pain
pruritus
splenomegaly
raised alpha-fetoprotein

237
Q

what are the features of constipation?

A

<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
Q

what organisms commonly cause bloody diarrhoea?

A

campylobacter jejuni (gram negative)
haemorrhagic e. coli (gram negative)
entamoebe histolytica
salmonella
chigella

Phase 1c: Conditions (18 decks)

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