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FINALS > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

IBD
Comparing Crohn’s and ulcerative colitis, comment on the following for Crohn’s…

i) location?
ii) inflammation area?
iii) continuous?
iv) smoking?
v) goblet cells?
vi) histology?
vii) enema finding?

A

i) Mouth>anus, favours terminal ileum
ii) Transmural
iii) No – skip lesions
iv) Risk factor
v) Present
vi) Granulomas, cobblestone appearance on colonoscopy
vii) Fistula = string sign of Kantor

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2
Q

IBD
Comparing Crohn’s and ulcerative colitis, comment on the following for ulcerative colitis…

i) location?
ii) inflammation area?
iii) continuous?
iv) smoking?
v) goblet cells?
vi) histology?
vii) enema finding?

A

i) Colon only (never further than ileocaecal valve) + starts at rectum
ii) Mucosa only
iii) Yes
iv) Protective factor
v) Depletion
vi) Increased crypt abscesses, pseudopolyps
vii) Lead pipe colon = loss of haustrations

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3
Q

IBD
What is the clinical presentation of Crohn’s disease?
What are some extra-intestinal findings more related to Crohn’s disease?
What are some complications of Crohn’s disease?

A
  • Triad = abdominal pain (RLQ), diarrhoea (non-bloody) + weight loss
  • Gallstones due to reduced bile salt reabsorption in terminal ileum
  • Colorectal cancer, perianal disease (skin tags, fissures, abscesses, fistulas), strictures, bowel obstruction
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4
Q

IBD
What is the clinical presentation of ulcerative colitis?
What are some extra-intestinal findings more related to ulcerative colitis?
What are some complications of ulcerative colitis?

A
  • Triad = bloody diarrhoea, colicky LLQ pain + tenesmus
  • Primary sclerosing cholangitis
  • Toxic megacolon, colorectal cancer
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5
Q

IBD

What are some extra-intestinal features that are present in both types of inflammatory bowel disease (IBD)?

A
  • Arthritis
  • Erythema nodosum
  • Pyoderma gangrenosum
  • Uveitis + episcleritis
  • Finger clubbing
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6
Q

IBD

What initial investigations would you do for IBD and what might they show?

A
  • FBC = microcytic anaemia, raised WCC + platelets
  • LFTs = low albumin (malabsorption)
  • Raised ESR/CRP (inflammation)
  • Stool MC&S to exclude infection
  • Faecal calprotectin (released by intestines when inflamed, useful screen)
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7
Q

IBD
What is the diagnostic investigation for IBD?
What other investigations would you do?
What investigations would you not do in acute ulcerative colitis, why and what could you do instead?

A
  • Colonoscopy with biopsy
  • Barium enema, CT/MRI to check complications
  • Avoid barium enema/colonoscopy due to perforation risk, flexible sigmoidoscopy is preferred
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8
Q

IBD

How would you induce remission in Crohn’s disease?

A
  • Enteral feed 6–8w paeds if cautious of steroids
  • PO prednisolone/IV hydrocortisone 1st line, ?add azathioprine or mercaptopurine
  • Biologics like infliximab or adalimumab if fail to respond
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9
Q

IBD
How do you maintain remission in Crohn’s disease?
What investigation would you order first?

A
  • Azathioprine or mercaptopurine = 1st line, measure thiopurine methyltransferase (TPMT) activity first
  • If not methotrexate
  • Biologics infliximab, adalimumab
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10
Q

IBD

What surgery might you consider in Crohn’s disease?

A
  • Resections for complications (fistulae, abscess)
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11
Q

IBD

How do you classify the severity of ulcerative colitis?

A
  • Mild = <4 stools/day, small amount of blood
  • Moderate = 4–6 stools/day, varying blood, no systemic upset
  • Severe = >6 bloody stools/day + systemic upset (pyrexia, shock)
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12
Q

IBD
How do you induce remission in mild-moderate ulcerative colitis?
What is a side effect of the first line management?

A
  • First line = topical (PR) aminosalicylate (5-ASA) mesalazine if not PO
  • Second line = PO prednisolone
  • Sulfasalazine (lung fibrosis, anaemia), mesalazine (pancreatitis) + both (agranulocytosis)
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13
Q

IBD

How do you induce remission in severe ulcerative colitis?

A
  • Hospital admission
  • IV steroids
  • ?IV ciclosporin after 72h if still unwell
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14
Q

IBD
How do you maintain remission in ulcerative colitis if…

i) mild-moderate?
ii) severe relapse or ≥2/year?

A

i) PR/PO 5-ASA

ii) PO azathioprine or mercaptopurine

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15
Q

IBD

When would you consider surgery in ulcerative colitis and what’s the options?

A
  • Medical therapy fails to induce remission
  • Panproctocolectomy = curative as removes disease
  • Either permanent ileostomy or ileo-anal anastomosis (J-pouch) where ileum is folded back on itself + fashioned into a large pouch that functions as a rectum as it attaches to the rectum
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16
Q

COELIAC DISEASE

What is the pathophysiology of coeliac disease?

A
  • Autoimmune condition where response to alpha-gliadin portion of the protein gluten causes inflammation in small intestine, particularly jejunum
  • Autoantibodies in response to gluten exposure target intestinal epithelial cells leading to inflammation + atrophy of intestinal villi > malabsorption
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17
Q

COELIAC DISEASE
What is the genetic association with coeliac disease?
What conditions are associated with coeliac disease and would prompt screening?

A
  • HLA-DQ2 and HLA-DQ8

- T1DM, thyroid disease, Down’s syndrome, FHx

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18
Q

COELIAC DISEASE

What is the clinical presentation of coeliac disease?

A
  • Abnormal stools (smelly, floating, diarrhoea)
  • Abdo pain, distension + buttock wasting
  • Paeds = failure to thrive, weight loss
  • Dermatitis herpetiformis = itchy blistering skin rash often on abdomen
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19
Q

COELIAC DISEASE
What is crucial when investigating for coeliac disease?
What first line investigations would you do?

A
  • Gluten-containing diet for 6w for accuracy
  • IgA Ab = Anti-tissue transglutaminase (anti-TTG first line) and anti-endomysial as well as total IgA as deficiency can give false negative results
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20
Q

COELIAC DISEASE

What is the diagnostic investigation for coeliac disease and what will it show?

A
  • Endoscopic small intestinal biopsy

- Villous atrophy, crypt hyperplasia + increased intraepithelial lymphocytes

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21
Q

COELIAC DISEASE

What are some complications of coeliac disease?

A
  • Anaemia (iron/B12/folate)
  • Osteoporosis
  • Lymphoma (EATL)
  • Hyposplenism
  • Lactose intolerance
  • Subfertility
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22
Q

COELIAC DISEASE
What is the most important management in coeliac disease?
What other parts of the management is there?

A
  • Lifelong gluten free diet curative under dietician
  • ?Gluten challenge later if Dx <2y to ensure still intolerant
  • PCV vaccine with booster every 5y due to hyposplenism
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23
Q

OESOPHAGEAL CANCER
What are the two types of oesophageal cancer?
Where are they found?
What are the risk factors?

A
  • Adenocarcinoma = most common type in UK/US, lower third oesophagus, RF = GORD, Barrett’s, smoking, obesity, achalasia
  • Squamous cell = most common in developing world, upper two-thirds oesophagus, RF = smoking, alcohol, achalasia, Plummer-Vinson syndrome + nitrosamines (fish)
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24
Q

OESOPHAGEAL CANCER

What is the clinical presentation of oesophageal cancer?

A
  • Dysphagia = most common, often solids > liquids
  • Anorexia, vomiting, weight loss
  • Odynophagia, hoarseness
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25
Q

OESOPHAGEAL CANCER
What are the 2ww criteria for oesophageal cancer?
What is the first-line investigation?

A
  • Dysphagia OR ≥55y with weight loss and any of: upper abdo pain, reflux or dyspepsia
  • Upper GI endoscopy (OGD)
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26
Q

OESOPHAGEAL CANCER

What other investigations would you do in oesophageal cancer?

A
  • Staging CT chest, abdo + pelvis after endoscopy

- Endoscopic USS preferred method for regional staging

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27
Q

OESOPHAGEAL CANCER

What is Barrett’s oesophagus and some risk factors?

A
  • Intestinal metaplasia of lower oesophageal mucosa with the usual squamous epithelium being replaced by columnar
  • GORD = #1, male, smoking, obesity
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28
Q

OESOPHAGEAL CANCER

What is the management of Barrett’s oesophagus?

A
  • High dose PPI
  • Endoscopic surveillance + biopsies if metaplasia every 3–5y
  • Dysplasia detected of any grade = endoscopic mucosal resection or radiofrequency ablation
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29
Q

OESOPHAGEAL CANCER
What is the management of oesophageal cancer?
What is a complication of this?

A
  • Surgical resection and adjuvant chemotherapy

- Anastomotic leak > mediastinitis

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30
Q

GASTRIC CANCER
What are the two main types of gastric cancer and their different features?
What are the risk factors for gastric cancer?

A
  • Intestinal type adenocarcinoma = lesser curvature
  • Diffuse type adenocarcinoma = signet ring cells which high numbers are associated with worse prognosis
  • Helicobacter pylori, atrophic gastritis, smoking + nitrosamines
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31
Q

GASTRIC CANCER

What is the clinical presentation of gastric cancer?

A
  • Epigastric pain, dyspepsia + progressive dysphagia
  • Weight loss, N+V, early satiety
  • Lymphatic spread = left supraclavicular (Virchow’s node) and periumbilical (Sister Mary Joseph’s node)
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32
Q

GASTRIC CANCER

What are the investigations for gastric cancer?

A
  • OGD + biopsy

- CT/MRI for staging

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33
Q

GASTRIC CANCER

What is the management of gastric cancer?

A
  • Surgical = endoscopic mucosal resection, partial/total gastrectomy
  • Chemotherapy
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34
Q

COLORECTAL CANCER
What are the two broad aetiological groups for colorectal cancer?
What are some risk factors?

A
  • Sporadic (95%) and inherited autosomal dominant (5%)

- FHx, IBD, increased age, high red meat diet, obesity, smoking, alcohol

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35
Q

COLORECTAL CANCER

What are three inherited causes of colorectal cancer?

A
  • Hereditary non-polyposis colorectal carcinoma (Lynch syndrome) = #1
  • Familial adenomatous polyposis
  • Peutz-Jeghers syndrome
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36
Q

COLORECTAL CANCER
What is the pathology of lynch syndrome?
What other condition are individuals at risk of?

A
  • Mutation of mismatch repair genes

- Endometrial cancer

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37
Q

COLORECTAL CANCER
What is the pathology of familial adenomatous polyposis?
What is the management?

A
  • Mutation in APC gene > formation of hundreds of colonic polyps
  • Panproctocolectomy
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38
Q

COLORECTAL CANCER

What are the clinical features of Peutz-Jeghers syndrome?

A
  • Pigmented lesions on lips, oral mucosa, palms

- Multiple GI hamartomatous polyps

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39
Q

COLORECTAL CANCER

What is the clinical presentation of colorectal cancer?

A
  • Right sided = IDA + weight loss
  • Left sided = PR bleeding, altered bowel habit + bowel obstruction
  • Rectal = fresh bleeding, tenesmus, mass
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40
Q

COLORECTAL CANCER

What are the 2ww criteria for colorectal cancer and what investigation do they get?

A
  • ≥60 with change in bowel habit OR IDA
  • ≥50 with unexplained rectal bleeding
  • ≥40 with abdo pain AND unexplained weight loss
  • Gastroscopy and colonoscopy
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41
Q

COLORECTAL CANCER
Explain the screening programme for colorectal cancer
What else can it be used for?

A
  • Faecal immunochemical tests (FIT) for human Hb in stool replacing faecal occult blood test which gave false positives from blood in food
  • Every 2 years those 60–74y (can request after 74y) and if abnormal > colonoscopy
  • Also used if do not meet 2ww criteria
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42
Q

COLORECTAL CANCER

What investigations are used in diagnosing colorectal cancer?

A
  • Colonoscopy + biopsy = gold standard
  • CT colonography with bowel prep if less fit for colonoscopy
  • Staging CT with Dukes’ classification
  • Carcinoembryonic antigen (CEA) = tumour marker with role in monitoring/follow-up
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43
Q

COLORECTAL CANCER

What are the stages in the Dukes’ classification?

A
  • A = confined to bowel mucosa
  • B = extends through bowel wall
  • C = local lymph node spread
  • D = distant metastases
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44
Q

COLORECTAL CANCER
For the following colorectal cancer sites, state the type of resection and anastamosis…

i) caecal, ascending or proximal transverse colon?
ii) distal transverse or descending colon?
iii) sigmoid colon?
iv) upper rectum?
v) lower rectum?
vi) anal verge?

A

i) Right hemicolectomy = ileo-colic
ii) Left hemicolectomy = colo-colon
iii) High anterior resection = colo-rectal
iv) Anterior resection (total mesorectal excision, TME) = colo-rectal
v) Anterior resection (low TME) = colo-rectal ±defunctioning stoma
vi) Abdomino-perineal excision of rectum = none

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45
Q

COLORECTAL CANCER

What are some complications of colorectal cancer surgery?

A
  • Pain, infection and bleeding
  • Anastomotic leak
  • Post-op ileus
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46
Q

COLORECTAL CANCER

In an emergency situation where the bowel has perforated, what is the management?

A
  • Anastomosis risk so sigmoid colectomy with end colostomy which can be reversed later = Hartmann’s
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47
Q

PEPTIC ULCER DISEASE
What is the pathophysiology of peptic ulcer disease (PUD)?
What are some risk factors?

A
  • Breach in the mucosa due to breakdown of protective layer or increased acid
  • Stress, alcohol, caffeine, smoking, spicy foods = increased acid
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48
Q

PEPTIC ULCER DISEASE
What is the most common cause of PUD?
What are some other causes?

A
  • Helicobacter pylori (95% duodenal, 75% gastric)
  • Drugs = NSAIDs, SSRIs, corticosteroids + bisphosphonates
  • Zollinger-Ellison syndrome = rare gastrin-secreting tumour > excess gastrin
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49
Q

PEPTIC ULCER DISEASE

What is the mechanism by which NSAIDs cause PUD?

A
  • Reversible inhibitor of cyclo-oxygenase (COX1+2) > reduced prostaglandins = decreases mucus + bicarb secretion
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50
Q

PEPTIC ULCER DISEASE

What is the clinical presentation of PUD?

A
  • Epigastric pain with heartburn + nausea
  • Duodenal = PAIN when HUNGRY + RELIEVED by EATING
  • Gastric = PAIN when EATING + RELIEVED by HUNGER
  • Haematemesis = “coffee ground” vomit + melaena
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51
Q

PEPTIC ULCER DISEASE

What are some investigations for PUD?

A
  • H. pylori urea breath test or stool antigen test = first line
  • Endoscopy ± biopsies (gastric) ± rapid urease (CLO) test for H. pylori too
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52
Q

PEPTIC ULCER DISEASE

What are some potential complications of PUD?

A
  • Upper GI bleed = gastroduodenal artery
  • Perforation = acute abdo + peritonitis = erect CXR (free air under diaphragm)
  • Scarring and strictures > pyloric stenosis
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53
Q

PEPTIC ULCER DISEASE
What lifestyle advice would you give in PUD?
How do you manage H. pylori related PUD?
How do you manage H. pylori -ve PUD?

A
  • Stop smoking, alcohol, avoid acidic foods + NSAIDs
  • Triple eradication therapy = PO PPI + amoxicillin + metronidazole OR clarithromycin for 7d
  • High-dose PPI for 4–8w
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54
Q

UPPER GI BLEED

What are some causes of an upper GI bleed?

A
  • Peptic ulceration
  • Oesophageal varices (esp. if stigmata of liver disease)
  • Mallory Weiss tear = brisk small-mod bright red blood, after straining)
  • Malignancy
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55
Q

UPPER GI BLEED

What is the clinical presentation of an upper GI bleed?

A
  • Haematemesis = “coffee ground” vomit
  • Melaena = black, tarry stools
  • Shock
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56
Q

UPPER GI BLEED

What initial investigations would you do in an upper GI bleed?

A
  • FBC
  • U&E (high urea due to protein meal of blood)
  • LFTs and clotting
  • Crossmatch 4–6 units (O -ve if emergency activating major haemorrhage protocol)
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57
Q

UPPER GI BLEED
What 2 risk assessments are used in acute upper GI bleeds?
What are the various parameters?
How are they applied clinically?

A
  • Glasgow-Blatchford score at first assessment = Hb, urea, SBP + other parameters
  • Rockall score can be pre/post-endoscopy = age, shock, co-morbidities, endoscopic findings
  • For both >0 = inpatient OGD, 0 = urgent OP OGD
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58
Q

UPPER GI BLEED

What is the initial emergency management of an acute upper GI bleed?

A
  • A–E assessment
  • 2x wide bore IV access, NBM, IV fluids + blood transfusion if Hb <70g/L
  • Platelet transfusion if <50 + FFP in major haemorrhage
  • Anticoagulant reversal (e.g., IV vitamin K + PCC)
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59
Q

UPPER GI BLEED

What should be done after resuscitiation?

A
  • OGD offered immediately if severe bleed

- ALL patients should have OGD within 24h

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60
Q

UPPER GI BLEED

What is the management of a non-variceal bleed?

A
  • NICE do not recommend pre-endoscopy PPIs as can mask the bleed site
  • If further bleeding > repeat endoscopy, interventional radiology + surgery
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61
Q

UPPER GI BLEED

What is the management of a variceal bleed?

A
  • Terlipressin + prophylactic Abx before endoscopy
  • Endoscopic band ligation of varices
  • Transjugular intrahepatic portosystemic shunts (TIPS) if variceal bleeding not controlled with above
  • Uncontrolled variceal bleeding = ?Sengstaken-Blakemore tube
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62
Q

APPENDICITIS

What is the pathophysiology of appendicitis?

A
  • Faecolith causes obstruction of appendiceal lumen allowing gut organisms to invade the appendix wall > oedema, ischaemia ± perforation
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63
Q

APPENDICITIS
What is the classic presentation of appendicitis and why does it occur?
What other symptoms may the patient experience?

A
  • Central abdo pain initially (appendix is midgut structure) which migrates to RIF (localised parietal peritoneal inflammation)
  • Anorexia, N+V (often only 1–2x vomiting), fever
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64
Q

APPENDICITIS

What are some signs of appendicitis?

A
  • RIF tenderness
  • Rovsing’s sign
  • Guarding
  • Rebound/percussion tenderness
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65
Q

APPENDICITIS

What initial investigations would you do in appendicitis?

A
  • FBC (raised WCC, neutrophil dominant), VBG (lactate), U&E, LFTs, amylase, clotting, G&S for theatre + blood cultures if septic
  • Urinalysis (leukocytes)
  • Urine pregnancy test if childbearing age
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66
Q

APPENDICITIS

What imaging might you consider in appendicitis?

A
  • USS pelvis in women if ?gynae pathology

- CT abdomen = most sensitive imaging to Dx but not routinely used

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67
Q

APPENDICITIS

What are some potential complications of appendicitis

A
  • Perforation > faecal contents in peritoneal cavity > peritonitis = copious abdominal lavage
  • Local abscess
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68
Q

APPENDICITIS

What is the management of appendicitis?

A
  • Laparoscopic appendicectomy with prophylactic IV Abx prior

- If appendix mass (omentum), broad spectrum Abx + interval appendicectomy

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69
Q

SEPSIS

What is the difference between sepsis and septic shock?

A
  • Sepsis = life-threatening organ dysfunction (confusion, hypoxia, oliguria, metabolic acidosis) due to a dysregulated host response to infection
  • Septic shock = sepsis PLUS hypotension despite fluid resus or lactic acidosis
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70
Q

SEPSIS

What is the clinical presentation of sepsis?

A
  • Fever/sweats/chills, SOB, N+V, confusion

- Signs = shock (tachycardic, hypotensive), pyrexia, CRT >2s, hypoxia, high RR

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71
Q

SEPSIS

What is the initial management of sepsis

A
  • ABCDE and sepsis 6 BUFALO
  • Blood cultures + others (FBC, U&E, LFT, CRP, clotting)
  • Urine output (catheter)
  • Fluids IV crystalloids (if given 2L or pulmonary oedema = critical care)
  • Abx IV broad-spectrum (e.g., co-amox, tazocin)
  • Lactate (VBG/ABG)
  • Oxygen (high flow for >94% or 88–92% if COPD)
72
Q

SEPSIS

What other investigations would you do in sepsis to figure out the source?

A
  • Bedside = urinalysis + MC&S, pregnancy test, ECG, viral PCR
  • Imaging = CXR, abdominal USS
  • Lumbar puncture
73
Q

BOWEL OBSTRUCTION

What are the causes of small and large bowel obstruction?

A
  • Small = adhesion (prev surgery) #1, hernias

- Large = tumour #1 (may be initial presentation), volvulus, diverticular disease > strictures

74
Q

BOWEL OBSTRUCTION
What is the clinical presentation of bowel obstruction?
How might this differ in small vs. large bowel obstruction?

A
  • Abdominal pain + distension
  • N+V = EARLY + bilious/faeculent in SBO, LATE in LBO
  • Constipation (absolute = no flatus) = EARLY in LBO, LATE in SBO
  • Tinkling bowel sounds on auscultation
75
Q

BOWEL OBSTRUCTION
What investigations would you consider in bowel obstruction?
What is the first-line investigation you would request and what would you expect to see in bowel obstruction?

A
  • FBC, U&E, CRP, VBG
  • AXR (3-6-9 rule) = dilated loops of small bowel >3cm, large bowel >6cm + caecum >9cm diameter
  • CT abdomen = high sensitivity + specificity as well as identifying the aetiology
76
Q

BOWEL OBSTRUCTION

What is the initial management of bowel obstruction?

A
  • ABCDE
  • NBM
  • IV fluids
  • NG tube with free drainage
  • Avoid pro-kinetics like metoclopramide
77
Q

BOWEL OBSTRUCTION

What is the management of bowel obstruction?

A
  • Can settle with conservative, if not surgery (majority of LBO will need surgery)
78
Q

BOWEL OBSTRUCTION
What is a potential complication after bowel surgery?
How does it present?
How is it managed?

A
  • Post-op (paralytic) ileus = reduced bowel peristalsis = pseudo-obstruction
  • Presents as obstruction + deranged electrolytes can contribute
  • NBM, NG tube if vomiting, IV fluids ± electrolyte correction
79
Q

VOLVULUS

What is a volvulus?

A
  • Torsion of the colon around its mesenteric axis resulting in compromised blood flow + closed loop obstruction
80
Q

VOLVULUS

What are the two types of volvulus and how do they occur?

A
  • Sigmoid (80%) = LBO as sigmoid colon twists on sigmoid mesocolon
  • Caecal (20%) = retroperitoneal structure so not usually at risk of twisting but in minority there is failure of peritoneal fixation development
81
Q

VOLVULUS
What are some associations with…

i) sigmoid volvulus?
ii) caecal volvulus?

A

i) Older, chronic constipation, neuro (Parkinson’s)

ii) All ages, adhesions, pregnancy

82
Q

VOLVULUS

What is the clinical presentation of volvulus?

A
  • Abdominal pain + distension
  • Constipation
  • N+V
83
Q

VOLVULUS
What initial investigation would you do in volvulus and what would it show?
What other investigation would you do?

A
  • AXR – sigmoid volvulus = LBO + coffee bean sign, caecal volvulus = SBO may be seen
  • CT abdomen = confirm Dx + identify any other pathology
84
Q

VOLVULUS
What is the initial volvulus management?
How do you manage sigmoid volvulus?
How do you manage caecal volvulus?

A
  • NBM, IV fluids, NG tube (drip and suck)
  • Rigid sigmoidoscopy with rectal tube insertion
  • Operative, may require right hemicolectomy
85
Q

PERITONITIS

What are some causes of peritonitis?

A

Perforation of hollow viscus –
- Boerhaave syndrome = perf oesophagus
- Peptic ulcer perf
- Bowel perf = appendicitis, diverticulitis, obstruction
Infection = SBP (infected ascites in liver disease)

86
Q

PERITONITIS

What is the clinical presentation of peritonitis

A
  • Abdominal rigidity + guarding
  • Rebound + percussion tenderness
  • Shock, fever, vomiting
87
Q

PERITONITIS

What investigations would you do in peritonitis and what are you specifically looking for?

A
  • FBC, U&E, LFT, CRP, amylase, clotting, ABG/VBG, group + save, blood cultures
  • AXR = rigler’s sign (pneumoperitoneum > double wall sign)
  • ERECT CXR = air under the diaphragm (pneumoperitoneum)
88
Q

PERITONITIS

What is the management of peritonitis?

A
  • ABCDE + alert senior
  • NBM, IV fluids, NG tube
  • IV Abx (cefotaxime in SBP)
  • Laparotomy
89
Q

HIATUS HERNIA

What are the two types of hiatus hernia and how do they differ?

A
  • Sliding (95%) = gastroesophageal junction moves above the diaphragm
  • Rolling (paraoesophageal) = gastrooesophageal junction remains below diaphragm but separate part of stomach herniates through
90
Q

HIATUS HERNIA
What are some risk factors for a hiatus hernia?
What is the clinical presentaiton?

A
  • Obesity, increased intraabdominal pressure (ascites, multiparity)
  • Heartburn, dysphagia, regurgitation, chest pain
91
Q

HIATUS HERNIA

What are the investigations for hiatus hernia?

A
  • Barium swallow = Dx

- Given nature of Sx often have endoscopy first

92
Q

HIATUS HERNIA

What is the management of hiatus hernia?

A
  • Conservative = weight loss, avoid alcohol, smoking + acidic foods, avoid large meals before bed
  • Medical = PPI for 4–8w then assess
  • Surgery (Nissen’s fundoplication) if above fail
93
Q

INGUINAL HERNIA

What are the two types of inguinal hernias and how they are different?

A
  • Direct = protrudes directly through weakness in posterior wall of inguinal canal (older)
  • Indirect = protrusion through deep ring > inguinal canal > superficial ring (paeds, patent processus vaginalis)
94
Q

INGUINAL HERNIA

What are the causes of inguinal hernias?

A
  • Increased intra-abdominal pressure or abdominal muscle weakness = chronic cough, constipation, heavy lifting, obesity
95
Q

INGUINAL HERNIA

What is the clinical presentation of an inguinal hernia?

A
  • Painless groin lump, superior + medial to pubic tubercle
  • Indirect hernias may descend into scrotum
  • Unable to get ‘above’ it on examination
96
Q

INGUINAL HERNIA

How can you differentiate direct and indirect inguinal hernias on clinical examination?

A
  • Reduce hernia then pressure over deep ring (middle from ASIS-pubic tubercle)
  • Prevents indirect reappearing, no effect on direct
97
Q

INGUINAL HERNIA
How do you investigate an inguinal hernia?
What is the management of an inguinal hernia in adults and paeds?

A
  • USS abdomen/scrotum to confirm diagnosis
  • Open (unilateral) or laparoscopic (bilateral) mesh repair
  • Paeds in first few months = risk of strangulation so urgent, >1y = elective
98
Q

FEMORAL HERNIA
What is a femoral hernia?
Who is it more common in?
How does it present?

A
  • Abdominal viscus passes into femoral canal
  • Women
  • Groin lump (inferolateral to pubic tubercle), may be irreducible
99
Q

FEMORAL HERNIA

What are some potential complications of femoral hernias?

A
  • Incarceration = herniated tissue cannot be reduced
  • Strangulation risk higher = tender, non-reducible > surgical emergency
  • Bowel obstruction + ischaemia
100
Q

FEMORAL HERNIA

What is the management of a femoral hernia?

A
  • Urgent surgical repair due to high risk of strangulation compared to inguinal
101
Q

OTHER HERNIAS
What is an umbilical hernia?
What is it associated with?
How is it managed?

A
  • Symmetrical bulge under umbilicus
  • Paeds, Afro-Caribbean + down’s syndrome
  • No treatment + resolve by 3y, surgical mesh repair if large >1.5cm or if no closure by 4–5y
102
Q

OTHER HERNIAS
What is an incisional hernia?
What are some causes?

A
  • Hernia arises through a previously acquired defect

- Obesity, surgical technique, incision type or increased intra-abdominal pressure (cough, straining)

103
Q

GORD
What is gastro-oesophageal reflux disease (GORD)?
What are some risk factors?

A
  • Reflux of gastric contents into oesophagus due to a defective lower oesophageal sphincter
  • Obesity, alcohol, smoking, foods (coffee, spicy, citrus)
104
Q

GORD

What is the clinical presentation of GORD?

A
  • Dyspepsia + sense of acid regurgitation
  • Retrosternal chest pain
  • Globus
  • Nocturnal cough
105
Q

GORD
What investigations would you do in GORD?
What are some potential complications?

A
  • OGD > if -ve then ?24h oesophageal pH monitoring (gold standard)
  • Oesophagitis, benign strictures, Barrett’s oesophagus + oesophageal carcinoma
106
Q

GORD

What initial management would you trial in GORD?

A
  • Lifestyle = weight loss, dietary changes, elevate head of bed, avoid late night food
  • PPI (omeprazole) or H2 receptor antagonist (famotidine) to reduce stomach acid, antacids (Gaviscon) for symptomatic relief
107
Q

GORD

What are some potential adverse effects of PPIs?

A
  • Low Na + Mg
  • Osteoporosis
  • C. difficile risk
108
Q

GORD

If medical therapy for GORD fails, what option is available?

A
  • Nissen fundoplication
109
Q

CONSTIPATION
What is the clinical presentation of constipation?
What are some risk factor?

A
  • <3 bowel movements/week + often hard stool (type 1-2)
  • Tenesmus + excessive straining
  • Abdominal distension + masses
  • Advanced age, inactivity, low fibre diet, opioids, females
110
Q

CONSTIPATION

What investigations would you consider in constipation?

A
  • PR exam = hard stool or impaction
  • AXR if concerned about obstruction
  • Barium enema/colonoscopy for pathology
111
Q

CONSTIPATION

What are some complications with constipation?

A
  • Anal fissures
  • Haemorrhoids
  • Overflow diarrhoea
112
Q

CONSTIPATION

What is the process by which overflow diarrhoea occurs in constipation?

A
  • Prolonged faecal status = resorption of fluids = increase in size + consistency which can lead to rectal stretching + reduced sensation > overflow
113
Q

CONSTIPATION
What lifestyle advice can you give in constipation?
What are the main types of laxatives?

A
  • Increase dietary fibre, more water, increase exercise
  • Stimulant (senna, bisacodyl)
  • Osmostic (lactulose, macrogol)
  • Stool softeners (docusate sodium, glycerol suppositories)
  • Bulk-forming (ispaghula husk)
114
Q

CONSTIPATION
What is the mechanism of…

i) stimulant laxatives?
ii) osmotic laxatives?
iii) stool softener laxatives?
iv) bulk forming laxatives?

A

i) Increase intestinal motility > can lead to abdominal cramp, avoid in bowel obstruction
ii) Increase water in large bowel
iii) Increased penetration of intestinal fluid into the faecal mass
iv) Small hard stools + cannot increase dietary fibre

115
Q

CONSTIPATION

In adults, how do you manage constipation?

A
  • Bulk-forming laxatives initially (ensure adequate fluid intake)
  • Stools remain hard add/switch to osmotic laxatives
  • Stools soft but difficult to pass or tenesmus = stimulant laxatives
  • Enemas if impaction present (sodium citrate)
116
Q

CONSTIPATION

In paediatrics, how do you manage constipation?

A
  • First line = macrogols (e.g., Movicol)
  • Second line = add/switch to stimulant laxatives
  • Stools remain hard = lactulose or stool softener
117
Q

GASTROENTERITIS
How is diarrhoea defined?
What two sub-types can diarrhoea be put into?

A
  • ≥3 loose-watery stools within 24h
  • Acute food poisoning = staph. aureus, bacillus cereus
  • Traveller’s diarrhoea = E. coli, cholera
118
Q

GASTROENTERITIS

What are some causes of acute and chronic diarrhoea?

A
  • Acute <14d = gastroenteritis, diverticulitis, thyrotoxicosis
  • Chronic >14d = IBS, IBD, colorectal cancer, coeliac
119
Q

GASTROENTERITIS

What are some bacterial causes of gastroenteritis?

A
  • Escherichia coli = #1 traveller’s diarrhoea
  • Staph. aureus = eggs, dairy, meats
  • Bacillus cereus = reheated rice
  • Shigella = faeco-oral
  • Campylobacter = raw poultry, associated with GBS
  • Cholera (Vibrio cholerae) = faecal contaminated water
120
Q

GASTROENTERITIS
What is the clinical presentation of gastroenteritis caused by…

i) E. coli?
ii) Staph. aureus?
iii) Bacillus cereus?
iv) Shigella?

A

i) Watery stools, abdo pain, E. Coli 0157 > HUS
ii) Severe vomiting with short incubation period
iii) Vomiting within 6h then diarrhoeal illness after 6h
iv) Bloody diarrhoea + vomiting, HUS

121
Q

GASTROENTERITIS
What is the clinical presentation of gastroenteritis caused by…

i) campylobacter?
ii) cholera?

A

i) Flu-like prodrome, bloody diarrhoea, fever, abdo pain

ii) Profuse, rice-water diarrhoea, severe dehydration

122
Q

GASTROENTERITIS

What are some viral causes of gastroenteritis and their unique features?

A
  • Rotavirus = #1 in paeds, secretory D+V

- Norovirus = #1 overall, risks = nursing homes, cruise ships, hospitals

123
Q

GASTROENTERITIS

What are some parasitic causes of gastroenteritis and their unique features?

A
  • Giardiasis = resistant to chlorination so seen in swimming pools with fat malabsorption (greasy stools), prolonged
  • Amoebiasis = gradual onset bloody diarrhoea can last weeks
124
Q 
GASTROENTERITIS
What is Clostridium difficile?
What can cause it?
What are some risk factors?
How is it spread?
A
  • Gram +ve spore-forming anaerobic rod
  • C Abx = Cephalosporins, Clindamycin, Ciprofloxacin, Co-amoxiclav (penicillins)
  • Elderly, hospital admissions, PPIs
  • Faeco-oral from contaminated surfaces if people do not wash hands with soap + water
125
Q

GASTROENTERITIS
What is the clinical presentation of C. diff?
What investigations would you do?
What is a key complication?

A
  • Diarrhoea, pseudomembranous colitis, fever
  • Raised WCC (>15 severe), CDT (toxin infection, antigen exposure)
  • Toxic megacolon
126
Q

GASTROENTERITIS

What is the management of C. diff?

A
  • PO vancomycin first line
  • PO fidaxomicin second line (first-line if relapse <12w)
  • PO vancomycin PLUS IV metronidazole if life-threatening
127
Q

GASTROENTERITIS

What general investigations would you do in diarrhoea?

A
  • FBC, U&E, CRP, LFT, coeliac serology, stool MC&S and C. difficile toxin (CDT)
128
Q

GASTROENTERITIS

What are some post-gastroenteritis complications?

A
  • Lactose intolerance
  • IBS
  • GBS
  • Reactive arthritis
129
Q

GASTROENTERITIS
What is the conservative management for gastroenteritis?
What is the management in paeds?

A
  • Barrier nursing, strict handwashing with soap + warm water

- 50ml/kg oral rehydration solution

130
Q

GASTROENTERITIS
When would you consider antibiotics in gastroenteritis?
What antibiotics would you give for…

i) salmonella + shigella?
ii) campylobacter?
iii) cholera?

A
  • Systemically unwell, immunocompromised or elderly
    i) Ciprofloxacin
    ii) Macrolide (clarithromycin)
    iii Tetracycline like PO doxy but safe water + sanitation needed
131
Q

DIVERTICULAR DISEASE

What is a diverticulum?

A
  • Herniation of colonic mucosa through the muscular wall, often between the taenia coli where vessels pierce the muscle to supply the mucosa
132
Q

DIVERTICULAR DISEASE
What is meant by the following terms…

i) diverticulosis?
ii) diverticular disease?
iii) diverticulitis?

A

i) Presence of diverticular
ii) Symptomatic diverticulum
iii) Inflammation of diverticular

133
Q

DIVERTICULAR DISEASE
What is the classic location where diverticular disease is seen?
What are some risk factors?

A
  • Sigmoid colon

- Old age, lack of dietary fibre + obesity

134
Q

DIVERTICULAR DISEASE

What is the clinical presentation of diverticular disease?

A
  • Intermittent abdominal pain, usually LLQ

- Often constipation ± PR bleeding

135
Q

DIVERTICULAR DISEASE

What is the clinical presentation of acute diverticulitis?

A
  • Acute LLQ pain, tenderness + guarding
  • Pyrexia, N+V, urinary Sx
  • PR bleeding may occur
136
Q

DIVERTICULAR DISEASE

How would you diagnose diverticular disease?

A
  • Often incidental finding on CT abdomen or colonoscopy
137
Q

DIVERTICULAR DISEASE

What investigations would you do in acute diverticulitis?

A
  • FBC (raised WCC), raised CRP
  • Erect CXR if ?perforation, AXR if ?obstruction
  • CT abdomen = best modality in suspected abscesses
  • Colonoscopy = avoid initially due to increased risk of perforation
138
Q

DIVERTICULAR DISEASE

What are some complications of diverticulitis?

A
  • Abscess formation (drain CT/USS guided)
  • Perforation > peritonitis
  • Fistula formation e.g., colovesical > pneumaturia (bubbling) faecaluria + recurrent UTIs
139
Q

DIVERTICULAR DISEASE

What is the management of symptomatic diverticular disease?

A
  • Increase dietary fibre + fluids
  • Consider bulk-forming laxatives
  • Simple analgesia = avoid NSAIDs/opioids as perforation risk
140
Q

DIVERTICULAR DISEASE
What is the management of…

i) mild diverticulitis?
ii) severe or non-resolving diverticulitis?
iii) unresponsive to Abx or complications?
iv) recurrent severe diverticulitis?

A

i) PO co-amoxiclav + analgesia
ii) No improvement in <72h = NBM, IV Abx (cephalosporin + metronidazole) + IV fluids
iii) Surgery
iv) ?Elective colectomy

141
Q

ACUTE MESENTERIC ISCHAEMIA

What is the pathophysiology of acute mesenteric ischaemia?

A
  • Thrombus/embolism results in sudden occlusion of an artery supplying the small bowel, usually superior mesenteric artery in patients with AF
142
Q

ACUTE MESENTERIC ISCHAEMIA

What are some risk factors for acute mesenteric ischaemia?

A
  • Infective endocarditis
  • Atherosclerosis
  • Coagulopathy
143
Q

ACUTE MESENTERIC ISCHAEMIA

What is the clinical presentation of acute mesenteric ischaemia?

A
  • Severe, sudden onset abdo pain out-of-keeping with physical examination
  • PR bleeding + diarrhoea
  • Shock + signs of sepsis
144
Q

ACUTE MESENTERIC ISCHAEMIA

What investigations would you do in acute mesenteric ischaemia and what would they show?

A
  • FBC (high WCC), ABG (lactic acidosis)

- CT angiography for diagnosis

145
Q

ACUTE MESENTERIC ISCHAEMIA

What is the management of acute mesenteric ischaemia?

A
  • Immediate laparotomy esp. if signs of advanced ischaemia (peritonitis, sepsis)
146
Q

CHRONIC MESENTERIC ISCHAEMIA
What is the pathophysiology of chronic mesenteric ischaemia?
What are some risk factors?

A
  • ‘Intestinal angina’ result of mesenteric blood vessels affected by atherosclerosis where the blood supply cannot keep up with the demand
  • CVD risk factors = age, FHx, smoking, DM, HTN, raised cholesterol
147
Q

CHRONIC MESENTERIC ISCHAEMIA

What is the clinical presentation of chronic mesenteric ischaemia?

A
  • Central, colicky abdominal pain after eating
  • Weight loss secondary to food avoidance
  • Abdominal bruit on auscultation
148
Q

CHRONIC MESENTERIC ISCHAEMIA
How is chronic mesenteric ischaemia diagnosed?
What conservative management would you offer?

A
  • CT angiography

- Reduce modifiable risk factors (stop smoking) + secondary prevention (statins)

149
Q

CHRONIC MESENTERIC ISCHAEMIA

What is the definitive management of chronic mesenteric ischaemia?

A
  • Revascularisation either endovascular first line (percutaneous mesenteric artery stenting) or open surgery (endarterectomy, bypass grafting)
150
Q

ISCHAEMIC COLITIS
What is ischaemic colitis?
Where is it likely to occur?

A
  • Acute but transient compromise in the blood flow to the large bowel which can lead to inflammation, ulceration + haemorrhage
  • Watershed areas such as splenic flexure
151
Q

ISCHAEMIC COLITIS
What is the clinical presentation of ischaemia colitis?
What investigation might you consider?
What is the management?

A
  • Transient abdo pain, PR bleeding, diarrhoea
  • AXR = ‘thumbprinting’ due to mucosal oedema/haemorrhage
  • Supportive, surgery in minority (peritonitis, perf, haemorrhage)
152
Q

IRRITABLE BOWEL SYNDROME

What is irritable bowel syndrome (IBS)?

A
  • Functional bowel disorder thought to be related to neural gut-brain axis
153
Q

IRRITABLE BOWEL SYNDROME

What is the clinical presentation of IBS?

A
  • Abdominal pain (relieved on opening bowels)
  • Bloating
  • Change in bowel habit
  • Altered stool passage (straining, tenesmus) + PR mucus
  • Worse symptoms after eating
154
Q

IRRITABLE BOWEL SYNDROME

What investigations would you do in suspected IBS and what would they show?

A
  • Normal FBC, ESR + CRP
  • Faecal calprotectin + coeliac serology both negative
  • Exclude cancer if any red flags present
155
Q

IRRITABLE BOWEL SYNDROME

What is the lifestyle advice in IBS?

A
  • Adequate fluid intake
  • Low FODMAP diet
  • Regular small meals
  • Limit caffeine, alcohol + fresh fruit
156
Q

IRRITABLE BOWEL SYNDROME

What is the first line management of IBS?

A
  • Loperamide if diarrhoea
  • Laxatives if constipated (avoid lactulose > bloating)
  • Antispasmodics (hyoscine butylbromide) if cramps
157
Q

IRRITABLE BOWEL SYNDROME

What other management options are their in IBS?

A
  • Second line medical = TCA amitriptyline 5–10mg ON or if not SSRI
  • ?CBT or other psychological therapy if poor medication response
158
Q

HAEMORRHOIDS

What is the pathophysiology of haemorrhoids?

A
  • Anal cushions (3, 7 + 11 O’clock) expand + protrude outside the anal canal
  • External = originate BELOW dentate line, prone to thrombosis + can be painful
  • Internal = originate ABOVE dentate line, do NOT generally cause pain
159
Q

HAEMORRHOIDS

What is the clinical presentation of haemorrhoids?

A
  • Painless bright red PR bleeding on toilet tissue #1

- Pruritus, associated with constipation and straining

160
Q

HAEMORRHOIDS
How do you fully visualise haemorrhoids?
How are they graded

A
  • Proctoscopy
  • Grade I = do NOT prolapse out of anal canal
  • Grade II = prolapse on defecation but reduce spontaneously
  • Grade III = manually reduced
  • Grade IV = not manually reduced
161
Q

HAEMORRHOIDS
What is a key complication of haemorrhoids?
How does it present?

A
  • Thrombosed haemorrhoid
  • Significant pain
  • Exam = purple, oedematous, tender subcut perianal mass
162
Q

HAEMORRHOIDS

What is the management of a thrombosed haemorrhoid?

A
  • Presents <72h = referral for ?excision

- If not conservative = stool softeners, ice packs + analgesia

163
Q

HAEMORRHOIDS

What is the management for haemorrhoids?

A
  • Conservative = soften stools (increased fibre + fluids)
  • Topical local anaesthetics + steroids
  • O/P = rubber band ligation preferred to injection sclerotherapy
  • Surgery if large symptomatic which fail to respond to above
164
Q

PILONIDAL DISEASE

What is the pathophysiology of pilonidal disease?

A
  • Sinuses + cysts form near the upper part of the natal cleft of the buttocks thought to be due to hair debris collecting in intergluteal pores
165
Q

PILONIDAL DISEASE
What is the clinical presentation of pilonidal disease?
Epidemiology?

A
  • Presents when acute inflammation occurs leading to an abscess
  • Pain can be severe, purulent discharge + fluctuant swelling
  • More common in males
166
Q

PILONIDAL DISEASE

What is the management of pilonidal disease?

A
  • Asymptomatic = conservative, focus on local hygiene
  • Symptomatic acute = incision + drainage allowing to close by secondary intention
  • Symptomatic chronic/recurrent = excision of the pits + obliteration of underlying cavity
167
Q

ANAL FISSURES
What is an anal fissure?
What are some risk factors?

A
  • Tears of the squamous lining of the distal anal canal

- Constipation, IBD, STIs (HIV, syphilis, herpes)

168
Q

ANAL FISSURES

What is the clinical presentation of anal fissures?

A
  • Painful, bright red PR bleeding

- 90% on posterior midline (if elsewhere ?IBD)

169
Q

ANAL FISSURES

What is the management of an acute anal fissure?

A

<1w =

  • Soften stool = diet (high fibre + fluid) + bulk-forming laxatives (or lactulose)
  • Lubricants (petroleum jelly) before defecation
  • Topical anaesthetics + analgesia
170
Q

ANAL FISSURES

What is the management of a chronic anal fissure?

A
  • Topical GTN = first-line

- If not effective after 8w > secondary care referral to consider sphincterotomy or botulinum toxin

171
Q

ANAL FISTULA

What is an anal fistula?

A
  • Abnormal connection between ano-rectal canal + skin often secondary to anorectal abscess or Crohn’s
172
Q

ANAL FISTULA
What is the clinical presentation of anal fistula?
What investigation would you do?
What is the management?

A
  • Persistent anal discharge, pruritus ani + perianal pain
  • MRI
  • Fistulotomy + excision
173
Q

ANORECTAL ABSCESS
What is an anorectal abscess?
What are some risk factors?

A
  • Infection of one of the anal sinuses > inflammation + abscess formation
  • Anal fistulae + Crohn’s disease
174
Q

ANORECTAL ABSCESS

What is the clinical presentation of an anorectal abscess?

A
  • Fluctuant tender peri-anal swelling

- May have low grade pyrexia

175
Q

ANORECTAL ABSCESS

What is the management of anorectal abscess?

A
  • Early incision + drainage to prevent infection spread

FINALS (20 decks)

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