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Sharon's Phase 2a Medicine Revision > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Define inflammatory bowel disease

A

Umbrella term for two main diseases causing inflammation of the GI tract:

  • Ulcerative Colitis
  • Crohn’s disease

They both involve inflammation of the walls of the GI tract and are associated with periods of remission and exacerbation.

Dermatological manifestation:

Erythema nodosum - related to active disease

Pyoderma gangrenosum - not related to disease acitivity

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2
Q

What are the features of Crohn’s disease?

A

NESTS

N - no blood or mucus

E - entire GI tract

S – “Skip lesions” on endoscopy.

T – Terminal ileum most affected and Transmural (all 4 layers) inflammation

S – Smoking is a risk factor (don’t set the nest on fire)

Crohn’s is also associated with weight loss, strictures and fistulas.

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3
Q

What is the aetiology of Crohn’s?

A

Still unclear, but genetic links have been found - particularly mutations in the NOD2 pathogen recognition proteins

Environmental factors possibly include smoking, oral contraceptive pill, poor diet, NSAIDs, exposure to antibiotics etc.

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4
Q

What is the pathophysiology of Crohn’s?

A

Thought to occur in genetically and immunologically susceptible individual.

  • Initial inflammatory infiltrate enter into intestinal crypts
  • This develops into ulceration of the superficial mucosa
  • Ulceration penetrates deeper and forms non-caseating granulomas through all layers
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5
Q

What are the risk factors for Crohn’s disease?

A
  • Jewish
  • Affects females more than males
  • Presentation mostly at 20-40 years
  • Lower incidence than UC
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6
Q

What signs and symptoms might a patient with Crohn’s disease present with?

A
  • Abdominal pain (right lower quadrant)
  • Prolonged diarrhoea (no blood/intermittent blood and mucus)
  • Weight loss
  • Perianal lesions
  • Fatigue
  • Fever
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7
Q

What investigations/tests would you carry out for a patient with suspected Crohn’s disease?

A
  • FBC - anaemia, leukocytosis
  • B12 and folate deficiency
  • Faecal calprotectin (released by the intestines when inflamed) - does not differentiate between CD or UC
  • GOLD STANDARD:
    Colonoscopy with ileoscopy and tissue biopsy is diagnostic - granulomatous transmural inflammation
  • C-reactive protein (CRP) indicates inflammation and active Crohn’s disease
  • Stool sample - rule out C.difficile infection.
  • Imaging with ultrasound, CT and MRI to detect fistulas, abscesses and strictures
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8
Q

What is the treatment/management for Crohn’s disease on first presentation or during a flare?

A

Firsr line: oral prednisolone which is a glucocorticoid steroid

If not effective, consider adding immunosuppressant meds such as Azathioprine and Mercaptopurine

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9
Q

What is the treatment/management for Crohn’s disease to maintain remission?

A

Talk to the patient, as it is reasonable not to take medication when the patient is well.

Otherwise azathioprine or mercaptopurine for maintenance treatment

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10
Q

When is surgery considered for a patient with Crohn’s disease?

A

When the disease only affects the distal ileum it is possible to resect this area and prevent further disease flares surgically.

However, Crohns typically involves the entire GI tract

Surgery can also be used to treat strictures and fistulas secondary to Crohn’s disease.

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11
Q

What are the possible complications of Crohn’s disease?

A

Fistulas, strictures (narrowing of intestine0, abscesses and small bowel obstruction

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12
Q

Oral prednisolone - glucocorticoid steroid

Describe:
1) Use
2) Mechanism of action
3) Main side effects

A

1) Crohn’s disease - first presentation or flare-up

2) Prednisolone exerts glucocorticoid effects with minimal mineralocorticoid effects

3) Increased appetite, mood swings, Cushing’s syndrome

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13
Q

What are the features of ulcerative colitis (UC)?

A

UC = CLOSEUP

C – Continuous inflammation

L – Limited to colon and rectum

O – Only superficial mucosa affected

S – Smoking is protective

E – Excrete blood and mucus

U – Use aminosalicylates (e.g. mesalazine)

P – Primary Sclerosing Cholangitis (inflammation of bile ducts)

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14
Q

What is the aetiology of UC?

A

Recognised as a multifactorial polygenic disease as exact aetiology is still unknown

Theories indicate that genetically susceptible individuals might develop UC in response to environmental triggers.

Likely an autoimmune disease initiated by an inflammatory response to colonic bacteria

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15
Q

What is the pathophysiology of UC?

A

Macroscopically:

  • Limited to the colons and rectum.
  • Starts at the rectum, and can progress as far as the ileocaecal valve (junction between small and large intestine)
  • Continuous inflammation – no skip lesions (as in CD)
  • Ulcers & pseudo-polyps in severe disease

Microscopically:

  • superficial mucosa inflamed – no deeper (not transmural)
  • Crypt abscesses
  • Depleted goblet cells
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16
Q

What are the risk factors for UC?

A
  • Jewish
  • Affects males & females equally
  • Presentation mostly at 20-40 years
  • Higher incidence than Crohn’s
  • Smoking protective against UC
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17
Q

What signs and symptoms might a patient with UC present with?

A
  • Abdominal pain (lower left quadrant)
  • Rectal bleeding
  • Diarrhoea
  • Blood in stool
  • Arthritis and spondylitis
  • Malnutrition
  • Abdominal tenderness
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18
Q

What are the risk factors for UC?

A
  • Family history of inflammatory bowel disease
  • Human leukocyte antigen-B27 (suggestive of autoimmune disease)
  • Non-steroidal anti-inflammatory drugs (NSAIDs)
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19
Q

What investigations/tests would you carry out for a patient with UC?

A
  • GOLD STANDARD!

1) Endoscopy with biopsy and negative stool culture is diagnostic.

  • Shallow ulceration
  • No inflammation beyond submucosa
  • Crypt abcesses and goblet cell depletion

2) Stool studies for infective pathogens - to rule out C.difficile

3) Faecal calprotectin - elevated (detects IBD but cannot differentiate between UC or CD)

4) FBC to check for anaemia, infection, thyroid, kidney and liver function

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20
Q

What is the treatment/management for a patient with first presentation or flare of mild to moderate UC?

A

To induce remission:

First line: oral or rectal aminosalicylate (e.g. sulfasalazine or mesalazine)

Second line: corticosteroids (e.g. prednisolone)

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21
Q

What is the treatment/management for a patient with first presentation or flare of sereve UC?

A

To induce remission:

Hospitalisation

First line: IV corticosteroids (e.g. hydrocortisone)

Second line: IV ciclosporin

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22
Q

What is the treatment/management for UC in order to maintain remission?

A
  • Oral or rectal aminosalicylate e.g. mesalazine
  • Immunosuppressants such as azathioprine or mercaptopurine
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23
Q

Ulcerative colitis: if conventional therapy fails, what treatment can we try?

A

Third-line treatment: biologics (TNF-alpha inhibitor e.g. infliximab) and Janus kinase inhibitors

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24
Q

Can surgery be considered for patients with UC?

A

Yes, as UC only affects the rectum and colon, removing them (panproctocolectomy) is curative. However, be aware of post-op complications

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25
Q

Name one complication of UC

A

Biliary tract carcinoma

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26
Q

Define irritable bowel syndrome (IBS)

A

Known as a functional bowel disease - no identifiable organic disease underlying the symptoms.

The symptoms result from the abnormal functioning of an otherwise normal bowel.

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27
Q

What are the risk factors for IBS?

A
  • Physical and sexual abuse
  • PTSD
  • Age <50 years
  • Female sex
  • GI infections
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28
Q

What are the 3 types of IBS?

A

IBS-C – with constipation
IBS-D – with diarrhoea
IBS-M – mixed, with alternating constipation & diarrhoea

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29
Q

What symptoms might a patient with IBS experience?

A
  • Diarrhoea
  • Constipation
  • Fluctuating bowel habit
  • Abdominal pain
  • Bloating
  • Pain worse after eating
  • Pain improved by opening bowels
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30
Q

What investigations/tests are used to diagnose IBS?

A

IBS is considered once other pathologies are ruled out:

  • Normal FBC, ESR (erythrocyte sedimentation rate - shows inflammation) and CRP blood tests
  • Faecal calprotectin negative to exclude inflammatory bowel disease
  • Negative coeliac disease serology (anti-TTG antibodies)
  • Cancer is not suspected or excluded if suspected
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31
Q

If the investigations/tests rule out other pathologies, what are the NICE criteria for a diagnosis of IBS?

A

Symptoms should suggest IBS:

  • Abdominal pain/discomfort:
  • Relieved on opening bowels, or
    Associated with a change in bowel habit

AND 2 of:

  • Abnormal stool passage
  • Bloating
  • Worse symptoms after eating
  • PR mucus (rectal discharge)
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32
Q

What is the conservative (non-medical) management plan for IBS?

A

Reassure patient that no serious pathology is present - important!

Lifestyle management:

  • adequate fluid intake
  • regular small meals
  • reduce processed foods
  • limit alcohol and caffeine
  • low “FODMAP” diet (ideally with dietitian guidance)
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33
Q

What are the medical management options for IBS?

A

First-line

  • IBS-D - loperamide for diarrhoea
  • IBS-C - laxatives for constipation. Not lactulose as it can cause bloating.
  • Antispasmodics for cramps e.g. hyoscine butylbromide (Buscopan)

Cognitive Behavioural Therapy (CBT) can help patients manage their IBS

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34
Q

Define coeliac disease

A

An autoimmune condition where exposure to gluten causes an autoimmune response that results in inflammation of the small bowel.

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35
Q

What is the pathophysiology of coeliac disease?

A
  1. Autoantibodies are produced in response to dietary gluten peptides
  2. Main two autoantibodies are anti-tissue transglutaminase (anti-TTG) and anti-endomysial (anti-EMA)
  3. They attack the epithelial cells lining the small intestine - causing inflammation, particularly in the jejunum
  4. Villous atrophy and hyperplasia of the intestinal crypts
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36
Q

What is the aetiology of coeliac disease?

A

Almost all people with coeliac disease carry one of two major histocompatibility complex class-II molecules (human leukocyte antigen):

  • HLA-DQ2 gene (90%)
  • HLA-DQ8 gene
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37
Q

What signs and symptoms might a patient with coeliac disease present with?

A

Often asymptomatic - low threshold for diagnosis

  • Failure to thrive in young children
  • Diarrhoea
  • Fatigue
  • Weight loss
  • Mouth ulcers
  • Anaemia secondary to iron, B12 or folate deficiency
  • Dermatitis herpetiformis (an itchy blistering skin rash typically on the abdomen)
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38
Q

Why do we test patients newly diagnosed with T1DM for coeliac disease?

A

Coeliac disease and T1DM are closely associated and often occur together

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39
Q

What other conditions is coeliac disease associated with?

A

Several other autoimmune diseases:

  • Type 1 Diabetes
  • Autoimmune thyroid disease (e.g. Grave’s)
  • Autoimmune hepatitis
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40
Q

What investigations/tests are used to diagnose coeliac disease?

A

Anti-TTG ( tissue-transglutaminase) and anti-EMA are IgA antibodies.

  • Total IgA to exclude IgA deficiency before checking for coeliac disease-specific antibodies:
  • Raised anti-TTG antibodies (first choice)
  • Raised anti-endomysial antibodies

Endoscopy and intestinal biopsy show:

  • Crypt hypertrophy
  • Villous atrophy
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41
Q

What is the treatment/management for coeliac diease?

A
  • Lifelong gluten-free diet is curative
  • However relapse will occur if patient introduces gluten into their diet again
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42
Q

Define gastroenteritis

A

Acute gastritis is inflammation of the stomach.

Px = nausea and vomiting.

Enteritis is inflammation of the intestines

Px = diarrhoea

Gastroenteritis is inflammation of the stomach to the intestines

Px = nausea, vomiting and diarrhoea.

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43
Q

Define gastritis

A

The histological presence of gastric mucosal inflammation.

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44
Q

What are the most common causes of gastritis?

A
  • Helicobacter pylori infection
  • Non-steroidal anti-inflammatory drugs (NSAIDs)
  • Alcohol
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45
Q

What is the pathophysiology of gastritis caused by H.pylori infections?

A

Gastritis is characterised by acute and chronic inflammation and gastric mucosal protective layer disruption.

H. pylori infection induces a severe inflammatory response with degradation of the protective gastric mucosa layer, increased mucosal permeability, followed by gastric epithelial cell death

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46
Q

What is the pathophysiology of gastritis caused by NSAIDs?

A
  • NSAIDs inhibit COX-1 (cyclo-oxygenase-1)
  • COX-1 needed for prostaglandin production
  • Prostaglandins stimulate gastric mucus production
  • Reduced mucosal defence
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47
Q

What signs and symptoms might a patient with gastritis present with?

A
  • Dyspepsia/epigastric discomfort (non-specific gastritis)
  • Nausea
  • Vomiting
  • Loss of appetite

Make sure there are no red flag symptoms indicating malignancy

  • GI bleeding, anaemia, early satiety, unexplained weight loss (>10% body weight), progressive dysphagia, or persistent vomiting
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48
Q

How is gastritis diagnosed?

A
  • Check for presence of risk factors (H.pylori infection, NSAID use, alcohol use)
  • H. pylori urea breath test
  • H. pylori faecal antigen test
  • FBC
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49
Q

How is gastritis caused by H.pylori treated?

A

H.pylori eradication therapy

Triple therapy with
- PPI (e.g. omeprazole)
- Two antibiotics (amoxicillin/metronidazole & clarithromycin)

7 day course

Stop NSAIDs if patient are using them

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50
Q

Define peptic ulcer disease (PUD)

A

Peptic ulcer disease involve ulceration of the mucosa of the stomach (gastric ulcer) or the duodenum (duodenal ulcer).

Duodenal ulcers are more common

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51
Q

What is the aetiology of peptide ulcer disease?

A

Two main causes:

  • Gram-negative H.pylori infection (95% duodenal and 75% gastric ulcers)
  • Aspirin and NSAID use

There are suggestions that the two causes are associated with each other

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52
Q

What is the pathophysiology of peptic ulcer disease?

A

The stomach and duodenum has a protective layer comprised of mucus and bicarbonate - secreted by the stomach mucosa.

The stomach and duodenal mucosa is prone to ulceration from:

  • Breakdown of the protective layer of the stomach and duodenum by H. pylori, NSAIDs or steroids
  • Increase in stomach acid (stress, smoking, alcohol, caffeine, spicy food)
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53
Q

What signs and symptoms might a patient with peptic ulcer disease present with?

A
  • Epigastric discomfort or pain
  • Nausea and vomiting
  • Dyspepsia (ingestion without cause)
  • Bleeding causing haematemesis, “coffee ground” vomiting and melaena
  • Iron deficiency anaemia (due to constant bleeding)
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54
Q

What symptom experienced by the patient can help differentiate between a possible gastric or duodenal ulcer?

A

Eating - worsens pain caused by a gastric ulcer, and improves pain caused by a duodenal ulcer.

Common SBA question

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55
Q

What investigations/tests would you carry out for a patient with suspected peptic ulcer disease?

A
  • Upper gastrointestinal endoscopy - diagnostic for peptic ulcer
  • Helicobacter pylori breath test (patient must be free from PPI 2 weeks and Abx 4 weeks)
  • Helicobacter pylori stool antigen test (patient must be free from PPI 2 weeks and Abx 4 weeks)
  • FBC- microcytic anaemia or high platelet count
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56
Q

What are some differential diagnoses for peptic ulcer disease?

A
  • Oesophageal cancer
  • Stomach cancer
  • Gastro-oesophageal reflux disease
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57
Q

What is the management for H.pylori negative peptic ulcer disease?

A

If no active bleeding ulcers:

Proton pump inhibitors (reduce acid secretion in the stomach + allows ulcers to heal)
- Omeprazole
- Lansoprazole

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58
Q

What is the treatment/management for peptic ulcer disease caused by H.pylori infection?

A

H.pylori eradication therapy + PPI or H2 receptor antagonist for ulcer healing

Triple therapy with
- PPI (e.g. omeprazole)
- Two antibiotics (amoxicillin/metronidazole & clarithromycin)

7-day course

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59
Q

What treatment would you prescribe for a patient with peptic ulcer disease caused by NSAID or aspirin use?

A
  • Consider stopping causative medication use, discuss with specialist as aspirin as secondary prevention for CVD might need to continue
  • PPI or H2 receptor antagonist
  • Follwoed by H.pylori eradication therapy
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60
Q

What treatment would you prescribe for a patient with peptic ulcer disease caused by NSAID or aspirin use?

A
  • Consider stopping causative medication use, discuss with specialist as aspirin as secondary prevention for CVD might need to continue
  • Proton pump inhibitor
  • Followed by H.pylori eradication therapy
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61
Q

What monitoring is carried out for patients with peptic ulcer disease?

A

Endoscopy - ensure ulcer healing and to detect further ulcer development

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62
Q

What are possible complications that can arise from a gastric ulcer?

A

Upper GI bleeds - low level > chronic anaemia.

Large haemorrhage > life threatening!

Perforation - ulcer creates a hole in the stomach > “acute abdomen” and peritonitis > urgent surgical repair

Scarring and strictures of the muscle and mucosa > narrowing of the pylorus > difficulty with gastric emptying, known as pyloric stenosis.

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63
Q

What are possible complications that can arise from a duodenal ulcer?

A
  • Upper GI bleeds - low level > chronic anaemia.
  • Gastroduodenal artery erosion and rupture if ulcer is deeply penerating - DANGER!
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64
Q

Define gastro-oesophageal reflux disease (GORD)

A

GORD is defined as ‘the condition in which the reflux of gastric contents into the oesophagus results in symptoms and/or complications

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65
Q

What is the aetiology of GORD?

A

Causes include:

  • Increased intraabdominal pressure - e.g. obesity, pregnancy
  • Smoking
  • Alcohol use
  • Hiatus hernia (part of the stomach pushes through the diaphragm)
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66
Q

What is the pathophysiology of GORD?

A

GORD is a condition where there is reflux of gastric contents back into the oesophagus.

Normally, two mechanisms prevent reflux at gastro-oesophageal junction (GOJ):

  • Lower oesophageal sphincter
  • Diaphragmatic sphincter

GORD occurs when there is:

  • Increased sphincter relaxation
  • Rasied intragastic pressure (beyond what the sphincter can cope with) - e.g. Obesity
  • Reduced sphincter tone e.g. CCB
  • Anatomical abnormalities of GOJ e.g. hiatus hernia
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67
Q

What signs and symptoms might a patient with GORD present with?

A

Dyspepsia is a non-specific term used to describe indigestion. It covers the symptoms of GORD:

  • Heartburn - retrosternal burning chest pain
  • Acid regurgitation
  • Retrosternal or epigastric pain
  • Bloating
  • Nocturnal cough
  • Hoarse voice
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68
Q

What investigations/tests are used to diagnose GORD?

A

Endoscopy - assess for peptic ulcers, oesophageal or gastric malignancy.

Patients with evidence of a GI bleed (i.e. melaena or coffee ground vomiting) need admission and urgent endoscopy.

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69
Q

GORD: What red flag symptoms indicate cancer (urgent referral needed - 2-week wait)?

A
  • Dysphagia (difficulty swallowing) at any age
  • Aged over 55
  • Weight loss
  • Upper abdominal pain/reflux
  • Treatment resistant dyspepsia
  • Nausea and vomiting
  • Low haemoglobin
  • Raised platelet count
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70
Q

What is the treatment/medical management for GORD?

A

Acid-neutralising medication when required:

  • Gaviscon
  • Rennie

PPI

  • Omeprazole
  • Lansoprazole

Surgery - laparoscopic (Nissen’s) fundoplication.

This involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.

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71
Q

What lifestyle advice is provided for patients with GORD?

A

Lifestyle advice

  • Reduce tea, coffee and alcohol
  • Weight loss
  • Avoid smoking
  • Smaller, lighter meals
  • Avoid heavy meals before bed time
  • Stay upright after meals rather than lying flat
  • Also provided to patients with Barrett’s oesophagus
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72
Q

What are some possible complications that can arise from GORD?

A

Barrett’s oesophagus - metaplasia of oesophageal epithelium from stratified squamous to columnar epithelium like in the stomach

  • Premalignant condition as it is a risk factor for developing adenocarcinoma of the oesophagus (3 - 5% lifetime risk)
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73
Q

What are the risk factors for developing Barrett’s oesophagus?

A
  • GORD
  • Male (7:1)
  • Caucasian
  • FHx
  • Hiatus hernia
  • Obesity
  • Smoking
  • Alcohol
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74
Q

A 45-year-old male with a history of GORD and non-compliance with his PPIs presents with severe dysphagia.

What is the most likely diagnosis?
How would you investigate this?

A

Ix = upper GI endoscopy with biopsy (diagnostic - abnormal epithelium characteristic of Barrett’s oesophagus)

Dx = Barrett’s oesophagus

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75
Q

What is the treatment for Barrett’s oesophagus?

A

Treatment of underlying reflux:

  • PPIs (e.g. omeprazole)
  • Lifestyle changes: weight loss, smoking cessation, alcohol abstinence

Low grade dysplasia:

  • Repeat surveillance endoscopy every 5 years

High-grade dysplasia

  • Ablation treatment during endoscopy using photodynamic therapy

Ablation treatment destroys epithelium so that it is replaced with normal cells

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76
Q

How are patients with Barrett’s oesophagus monitored?

A

Patients are monitored for adenocarcinoma by regular endoscopy.

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77
Q

Define Mallory Weiss tear

A

Tear in the oesophageal mucosa resulting in haematemesis (vomiting blood)

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78
Q

What are the aetiology/risk factors of Mallory Weiss tear?

A
  • Recurrent forceful episodes of coughing or vomiting
  • Bulimia
  • Alcohol
  • Acute abdominal blunt trauma
  • Hyperemesis gravidarum (severe N+V in pregnancy)
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79
Q

What is the pathophysiology of Mallory Weiss tear?

A

Pathophysiology not fully understood

Most cases seem to occur due to a sudden rise in abdominal pressure or pressure gradient across the gastro-oesophageal junction with a corresponding low intrathoracic pressure. When these forces are high enough to cause distention in this area, an oesophageal tear may occur

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80
Q

What signs and symptoms might a patient with Mallory Weiss tear present with?

A

Haematemesis, melaena, symptoms of hypovolemic shock

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81
Q

What investigations/tests would you carry out to diagnose Mallory Weiss tear?

A
  1. Upper GI endoscopy: gold standard to assess for tear appearing as red longitudinal defect
  2. FBC - assess for anaemia secondary to bleeding; usually normal
  3. U&Es: urea is raised in an upper GI bleed (protein in RBCs is digested into urea in the GI tract)
  4. LFTs: typically normal but if deranged may raise the possibility of a variceal bleed
  5. Erect CXR: performed to rule out oesophageal perforation or perforated peptic ulcer

After endoscopy: Rockall score - assess the severity of upper GI bleed pre- and post-endoscopy: <3 = low risk)

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82
Q

What is the treatment/management for Mallory Weiss tear?

A
  1. Resuscitation with ABCDE + adrenaline
  2. Acute treatment: Terlipressin (vasopressin analogue for hypotension) + Urgent Endoscopy
  3. Rockall Score + Inpatient Observation
  4. Clip insertion/band ligation to stop bleeding
  5. Thermocoagulation - using heat to destroy bleeding tissue

Most MWTs resolve spontaneously after 24 hours!

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83
Q

Define oesophageal varices

A

Oesophageal varices are the dilation of veins in the oesophagus that develop as a complication of portal hypertension, usually in cirrhosis.

They can rupture and cause life-threatening bleeds.

Varices can occur anywhere in the GI tract, but most common in stomach and oesophagus

84
Q

Define oesophageal varices

A

Oesophageal varices are the dilation of veins in the oesophagus that develop as a complication of portal hypertension, usually in cirrhosis.

They can rupture and cause life-threatening bleeds.

Varices can occur anywhere in the GI tract but most common in the stomach and oesophagus

85
Q

What are the aetiology/risk factors for oesophageal varices?

A
  1. Prehepatic - portal vein
    thrombosis/obstruction
  2. Hepatic - Cirrhosis (most common)
  3. Post hepatic - Right-sided heart failure, constrictive pericarditis, compression
86
Q

What signs and symptoms might a patient with bleeding oesophageal varices present with?

A
  • Haematemesis (vomiting blood)
  • Melaena (black, foul-smelling stools)
  • Haematochezia (rectal bleeding)
  • Epigastric Discomfort
  • Sudden Collapse - symptom of haemodynamic instability
87
Q

What investigations/tests are used to diagnose oesophageal varices?

A
  • Urgent GI endoscopy - diagnostic
  • FBC - microcytic anaemia and/or thrombocytopenia
  • U&E- elevated urea, hyponatraemia
  • Clotting (INR) - normal or elevated, indicating liver cirrhosis
  • LFTs - elevated liver enzymes indicate cirrhosis
  • Venous blood gas - check for Hb and lactate levels (indicate significant bleed)
88
Q

What is the treatment/management for oesophageal varices?

A

For bleeding varices:

  • Resus using ABCDE + blood transfusion
  • Acute treatment: Terlipressin (ADH analogue)
  • Prophylactic Antibiotics (Ciprofloxacin)
  • Definitive first line: Endoscopic band ligation
  • Rockfall Score (Prediction of rebleeding and mortality)
89
Q

DDx for oesophageal varices

A
  • Hiatal hernia
  • Gastric varices
  • Mallory-Weiss tear
90
Q

Define appendicitis

A

Inflammation of the appendix

91
Q

What is the epidemiology of appendicitis?

A

Peak incidence between 10 - 20 years of age. Less common in younger children and adults > 50

92
Q

What is the aetiology of appendicitis?

A

The appendix is a long, thin tube arising from the caecum and it is where the three teniae coli (longitudinal muscles running along the colon) meet

Obstruction of the appendix lumen is the main cause of acute appendicitis.

Obstruction most commonly caused by:

  • Faecolith (a hard mass of faecal matter)
  • Normal stool
  • Lymphoid hyperplasia
93
Q

What is the pathophysiology of appendicitis?

A
  • Obstruction of appendix > build-up of mucus and resident bacteria > inflammation and infection.
  • Increasing pressure leading to engorgement and congestion of the appendix
  • Inflammation spreads to the parietal peritoneum (tissue covering the abdominal cavity) > classic LRQ pain

Gangrene + rupture > bacteria and faecal matter leak out > peritonitis

94
Q

What are the signs and symptoms of appendicitis?

A

The main presenting symptom is abdominal pain that starts centrally and then localises to the right iliac fossa (RIL) after 24 hours.

Tenderness on palpation at Mcburny’s point - a specific area 1/3 of the distance from the anterior superior iliac spine (ASIS) to the umbilicus

Other classic features are:

  • Loss of appetite (anorexia)
  • Nausea and vomiting
  • Low-grade fever
  • Rovsing’s sign (palpation of the left iliac fossa causes pain in the RIF)
  • Guarding on abdominal palpation
  • Rebound tenderness in the RIF (sudden release of deep palpation increases pain)
  • Percussion tenderness (pain and tenderness when percussing the abdomen)
95
Q

What does rebound tenderness indicate?

A

Peritonitis, potentially indicating a ruptured appendix.

96
Q

What investigations/tests would you carry out to diagnose appendicitis?

A

Usually, a clinical diagnosis - which is made based on signs and symptoms

Gold standard: CT scan useful if alternative diagnosis likely

Ultrasound for female patients to exclude ovarian or gynaecological pathology

97
Q

What are the key DDx for appendicitis?

A
  • Ectopic pregnancy - serum/urine human chorionic gonadotropin (hCG) to exclude pregnancy
  • Ovarian cyst
  • Meckel’s diverticulum - malformation of distal ileum
98
Q

What is the treatment/management for appendicitis?

A

Suspected appendicitis = emergency admission to the hospital under the surgical team.

Appendicectomy is the gold standard management for acute appendicitis.

Laparoscopic surgery = fewer risks and faster recovery compared to open surgery.

IV antibiotics & fluids pre & post-operatively:
Metronidazole, Cefuroxime

99
Q

What are the possible complications of appendicitis?

A
  • Perforation
  • Appendix mass - small bowel & omentum adhere to appendix
  • Appendiceal abscess
  • Adhesions
  • Pelvic inflammatory disease (PID)
100
Q

Define diverticulum

A

A diverticulum is an outpouching of the gut mucosa (gaps in the gut wall where blood vessels penetrate)

101
Q

Define diverticulosis

A

The presence of multiple diverticula, without inflammation or infection

102
Q

Define diverticular disease

A

Refers to the condition when patients experience symptoms from diverticula

103
Q

Define diverticulitis

A

Inflammation and infection of diverticula

104
Q

Define Merkel’s diverticulum

A
  • Congenital abnormality of GI tract - malformation of the distal ileum
  • Affects ~2% of the population
  • Usually asymptomatic
105
Q

What is the pathophysiology of diverticular disease?

A

Circular muscle layer in the wall of the large intestine have gaps where blood vessels penetrate

Increased pressure over time allow mucosa to herniate through the circular muscle layer and form pouches (diverticula)

The colon (except rectum) has longitudinal muscles forming ribbons called teniae coli

The areas that are not covered by teniae coli are vulnerable to the development of diverticula.

Rectum - outer longitudinal muscle surrounds it completely > extra support protecting it from diverticula

106
Q

What is the aetiology of diverticular disease?

A

Multifactoral disease - genetic and environmental factors

  • Low dietary fibre diet (most common in the west)
  • Decreased physical activity
  • Obesity
  • Increased red meat
  • Smoking, alcohol and caffeine
  • NSAIDs
107
Q

What are the risk factors for developing diverticular disease?

A
  • Age >50 years
  • Low dietary fibre
  • Diet rich in salt, meat, and sugar
  • Obesity (BMI >30)
108
Q

How might a patient with acute diverticulitis present (signs and symptoms)?

A

Inflammation in the diverticula presents with:

Symptoms

  • Pain and tenderness in the left iliac fossa / lower left abdomen
  • Fever
  • Diarrhoea
  • Nausea and vomiting
  • Rectal bleeding

Signs

  • Palpable abdominal mass (if an abscess has formed)
  • Raised inflammatory markers (e.g., CRP) and white blood cells
109
Q

What investigations/tests would you carry out for a patient with suspected diverticulitis?

A
  • FBC: anaemia, leukocytosis and neutrophilia
  • U&Es: pre-renal acute kidney injury if significantly dehydrated or septic
  • CRP: elevated
  • Venous blood gas: raised lactate in significant PR bleed
  • Group and save: if PR bleeding is a feature, to ensure that crossmatching is possible if required
  • Blood cultures: if sepsis suspected
  • CT abdomen/pelvis with contrast: gold standard for suspected acute diverticulitis and would demonstrate thickened bowel wall
110
Q

What is the treatment/management for uncomplicated diverticulitis?

A

Primary care mamangement

  • Oral co-amoxiclav (at least 5 days)
  • Analgesia (avoiding NSAIDs and opiates, if possible)
  • Clear liquids, no solid food until symptoms improve (usually 2-3 days)

Follow-up within 2 days to review symptoms

111
Q

What is the treatment/management for patients with severe pain and complications of diverticulitis?

A

Admission to hospital, management same as any patient with acute abdomen or sepsis

  • Nil by mouth or clear fluids only
  • IV antibiotics
  • IV fluids
  • Analgesia
  • Urgent investigations (e.g., CT scan)
  • Urgent surgery may be required for complications
112
Q

What section of the colon is most often affected by diverticular disease?

A

Sigmoid colon due to small diameter

113
Q

What signs and symptoms might a patient with diverticular disease present with?

A
  • Altered Bowel Habit
  • Abdominal Pain
  • PR bleeding
114
Q

What investigations/tests are used to diagnose diverticular disease?

A
  • Gold standard - CT abdomen/pelvis scan with contrast for patients with suspected acute diverticulitis + raised inflammatory markers
  • Colonoscopy - when acute diverticulitis diagnosis is unclear and bowel cancer/ischaemia is suspected
115
Q

What is treatment/management for patients with asymptomatic diverticular disease (diverticulosis)

A

Lifestyle change: high fibre diet, exercise, weight loss, stop smoking

116
Q

What is treatment/management for patients with symptomatic diverticular disease?

A
  • Lifestyle change: high fibre diet, exercise, weight loss, stop smoking
  • Anaglesia e.g. paracetamol
  • Antispasmodic
117
Q

What are some possible complications of diverticular disease?

A
  • Perforation
  • Peritonitis
  • Peridiverticular abscess
  • Large haemorrhage requiring blood transfusions
  • Fistula (e.g., between the colon and the bladder or vagina)
118
Q

Define bowel obstruction

A

A bowel obstruction refers to when the passage of food, fluids and gas, through the intestines becomes blocked.

Small bowel obstruction (60 - 75%) is more common than large bowel obstruction.

119
Q

What are the three different types of bowel obstruction?

A
  • Small bowel obstruction
  • Large bowl obstruction
  • Pseudo-obstruction

All can be serious and life-threatening

120
Q

What are the main causes of bowel obstruction?

A

The “big three” causes account for around 90% of cases:

  • Adhesions (small bowel) - scar tissue that binds the abdominal content together
  • Hernias (small bowel)
  • Malignancy (large bowel)
121
Q

What is the pathophysiology of bowel obstruction?

A

Obstruction of the bowel leads to distension above the blockage due to a build-up of fluid & contents.

This creates back-pressure, resulting in vomiting and dilating the intestines proximal to the obstruction.

The increased pressure, which compresses blood vessels in the bowel wall

Ischaemia & necrosis, and eventually perforation and peritonitis.

Bowel obstruction is a surgical emergency.

122
Q

What are small bowel adhesion usually caused by?

A
  • Previous abdominal/pelvic surgery with the formation of intra-abdominal adhesions
  • Previous infection e.g., peritonitis
123
Q

What are the signs and symptoms of small bowel obstruction?

A
  • Vomiting (particularly green bilious vomiting) - occurs early and profusely following pain
  • Abdominal distension
  • Diffuse abdominal pain
  • Absolute constipation and lack of flatulence
  • “Tinkling” bowel sounds may be heard in early bowel obstruction
124
Q

The signs and symptoms of large bowel obstruction can be similar to small bowel obstruction. What are some difference seen in the presentation of LBO compared to SBO?

A
  • Abdominal pain is more diffuse (widespread) and constant
  • Vomiting is less profuse and presents later than in SBO, even might be absent
  • Much more abdominal distension than in SBO
  • Constipation presents earlier in LBO compared to SBO
125
Q

What investigations/tests are used to diagnose small bowel obstruction?

A

Abdominal x-ray is 1st line

Finding = distended loops of bowel (> 3cm small bowel)

Non-contrast CT abdomen is the gold standard for locating the obstruction accurately

FBC - WBC count >10,000/mm3 = non-specific marker of inflammation, low haematocrit

126
Q

What investigations/tests are used to diagnose large bowel obstruction?

A

AxR = 1st line

Finding = distended loops of bowel (> 6 cm colon, > 9 cm caecum)

  • Caecum & ascending colon will be distended

Abdominal CT with contrast = gold standard > accurately locates the obstruction.

FBC - WBC count >10,000/mm3 = non-specific marker of inflammation, low haematocrit

127
Q

What is the initial treatment/management for small or large bowel obstruction?

A

Resuscitation with ABCDE (Airway, Breathing, Circulation, Disability, Exposure) if patient haemodynamically unstable

The initial management - “drip and suck”:

  • Nil by mouth (don’t put food or fluids in if there is a blockage)
  • IV fluids to hydrate the patient and correct electrolyte imbalances
  • Nasogastric (NG) tube with free drainage to allow stomach contents to drain and reduce the risk of vomiting and aspiration
128
Q

What is the management for small or large bowel obstruction after stabilising the patient?

A
  • Once the patient is stable, surgery might be needed to remove the obstruction
  • Pre- and post-op antibiotics
  • Analgesia & anti-emetics for symptoms
129
Q

What is pseudo-bowel obstruction?

A

Pseudo-bowel obstructions usually caused by an abnormality in the nerves or muscles of the gut, which leads to altered and inefficient contractions (peristalsis) of the digestive tract, so gut content does not pass through
properly.

It presents identically to LBOs or SBOs, dependent on the location. Occasionally, the entire bowel is obstructed so it presents as both at the same time.

130
Q

What is pseudo-bowel obstruction?

A

Pseudo-bowel obstructions present identically to LBOs or SBOs, dependent on the location. Occasionally, the entire bowel is obstructed so it presents as both at the same time.

131
Q

What are the main causes of pseudo-bowel obstruction?

A
  • Intra-abdominal trauma
  • Post-operative states eg. paralytic ileus
  • Intra-abdominal sepsis
  • Drugs eg. opiates, antidepressants
  • Electrolyte imbalances
132
Q

What is the best way to manage pseudo-bowel obstruction?

A

Treat underlying cause! See main causes card.

133
Q

Define diarrhoea

A

3 or more loose/watery stools a day and/or stools that are more frequent than what is normal for the individual

  • Acute = 14 days or less
  • Persistent = between 14 to 28 days
  • Chronic = more than 28 days
134
Q

What are the bacteria that most commonly cause diarrhoea?

A
  • Campylobacter jejuni (undercooked chicken)
  • Salmonella (contaminated meat/eggs)
  • Shigella (common in children attending daycare centres)
  • Escherichia coli (travellers from contaminated food)
  • Clostridium difficile (infection after Abx use)
135
Q

What are some common viral causes of diarrhoea?

A

Rotavirus = children (common children who attend daycare centres)

Norovirus = adults (consumption of contaminated food)

136
Q

Which bacteria are associated with bloody diarrhoea?

A
  • E.coli
  • Salmonella
  • Shigella
137
Q

What is the most common parasitic cause of diarrhoea?

A

Giardia lamblia

138
Q

What is the treatment/management of mild diarrhoea?

A

Viral diarrhoea is usually self-limiting, so no treatment is needed unless severe

Bacterial diarrhoea - Loperamide or bismuth subsalicylate (antacid)

Loperamide is an anti-motility agent that controls cramping and diarrhoea.

Consider rehydration therapy

139
Q

What is the treatment/management of moderate diarrhoea?

A

Viral = usually self-limiting, oral rehydration therapy

Bacterial:
- Loperamide or antibiotics therapy
- Rehydration therapy

140
Q

What is the treatment/management of severe diarrhoea?

A

Viral = IV rehydration therapy

Bacterial:
- 1st line is antibiotics therapy
- Rehydration therapy
-Loperamide

141
Q

Define oesophageal cancer

A

Most oesophageal cancers are neoplastic mucosal lesions that originate in the epithelial cells lining the oesophagus.

Oesophageal cancers are usually squamous cell carcinomas or adenocarcinomas.

142
Q

Where in the world is oesophageal adenocarcinoma most common?

A

Developed world

143
Q

Where in the world is oesophageal squamous cell carcinomas most common?

A

Developing world

144
Q

What are the aetiology/risk factors for oesophageal adenocarcinoma?

A
  • Male
  • Older age
  • Tobacco use
  • Barrett’s oesophagus
  • GORD
  • Hiatus hernia
145
Q

What are the aetiology/risk factors for oesophageal squamous cell carcinoma?

A
  • Male
  • Older age
  • Tobacco use
  • Repeated drinking of very hot drinks
  • Excess alcohol
  • Family history
146
Q

Where in the oesophagus does adenocarcinoma and SCC occur?

A

Adenocarcinoma - Lower 1/3 (Near the GO junction)

SCC - Upper 2/3 of oesophagus

147
Q

What is the pathophysiology of oesophageal cancer?

A

Arises in the mucosa of the oesophagus

It then progresses locally to invade the submucosa and the muscular layer

Metastasis typically occurs to the per (surrounding)i-oesophageal lymph nodes, liver, and lungs.

148
Q

What symptoms might a patient with oesophageal cancer present with?

A

Mnemonic: ALARMS

Anaemia
Loss of weight
Anorexia
Recent onset progressive symptoms
Melaena / haematemesis
Swallowing difficulties e.g. dysphagia

149
Q

What symptoms might a patient with oesophageal cancer present with?

A

Mnemonic: ALARMS

Anaemia
Loss of weight
Anorexia
Recent onset progressive symptoms
Melaena / haematemesis
Swallowing difficulties e.g. dysphagia

150
Q

What investigations/tests would you carry out to diagnose oesophageal cancer?

A

Oesophagogastroduodenoscopy (OGD) (endoscopy) with biopsy - 1st line

CT thorax and abdomen & endoscopic ultrasound - staging

151
Q

What is the treatment/management plan for oesophageal cancer?

A

Suitable for surgery:

  • Endoscopic therapy
  • Surgery (oesophagectomy) - removing the affected part of oesophagus

Unsuitable for surgery:

  • Chemotherapy + adjuvant (immunotherapy)
  • If metastatic - consider palliative chemotherapy or immunotherapy
152
Q

Define gastric (stomach) cancer

A

Stomach cancer is a neoplasm that can develop in any portion of the stomach and may spread to the lymph nodes and other organs. Most tumours are adenocarcinomas

153
Q

What is the Lauren classification for gastric cancer?

A

This classification system divides stomach cancer into two types:

  • Intestinal/differentiated (70 - 80%) - better prognosis
  • Diffuse/undifferentiated (20 - 30%)
154
Q

What are the main risk factors for gastric cancer?

A
  • Pernicious anaemia
  • Helicobacter pylori
  • N-nitroso compounds (additive in cured meats)
  • Diet (high nitrate, high salt, pickling, low vitamin C)
  • Smoking
155
Q

Where does the intestinal/differentiated type of gastric cancer most often occur?

A

Antrum and lesser curvature

156
Q

Where does the diffuse/undifferentiated type of gastric cancer most often occur?

A

Anywhere but especially cardia - associated with CDH-1 mutation

157
Q

What red flag symptoms for gastric cancer should you look out for in a patient?

A
  • Dysphagia of any age
  • Anaemia

Aged ≥ 55yr + weight loss with any of the following:

  • Upper abdominal pain/(or)
  • Reflux/ (or)
  • Dyspepsia

If above symptoms are present, refer patient for 2-week wait endoscopy (urgent referral)

158
Q

What signs suggest metastatic gastric cancer?

A
  • Epigastric mass
  • Hepatomegaly, jaundice > liver mets
  • Ascites
  • Large left supraclavicular node = Virchow’s node > lymph node spread
  • Kruckenberg tumour > ovarian met
159
Q

What investigations/tests would you carry out to diagnose gastric cancer?

A
  • Upper gastrointestinal endoscopy with biopsy - diagnostic
  • FBC - assess for iron-deficiency anaemia
  • LFT + renal function - assess suitable therapeutic options
160
Q

What is the treatment/management for gastric cancer?

A

Localised- suitable for surgery = gastrectomy (removal of part or whole of the stomach) + adjuvant chemo/radiotherapy

Localised - unsuitable for surgery = chemoradiotherapy

Metastatic/advanced disease = chemo and/or immunotherapy + palliative care

161
Q

Define large bowel/colorectal cancer

A

Cancer of the colon or rectum - majority are adenocarcinomas derived from epithelial cells.

Small bowel or anal cancer is rare

162
Q

What is the epidemiology of colorectal cancer?

A

4th most common in the UK behind breast, prostate and lung cancer

  • 66% arise in the colon (43% in the proximal colon and 23% in the distal colon)
  • 30% occur in the rectum
163
Q

What are the main risk factors for developing colorectal cancer?

A
  • Family history of bowel cancer:
    • Familial adenomatous polyposis (FAP)
    • Hereditary nonpolyposis colorectal cancer (HNPCC), also known as Lynch syndrome
  • Inflammatory bowel disease (Crohn’s or ulcerative colitis)
  • Increased age
  • Diet (high in red and processed meat and low in fibre)
  • Obesity and sedentary lifestyle
  • Smoking
  • Alcohol
164
Q

What is Familial adenomatous polyposis (FAP)?

A

Autosomal dominant condition involving malfunctioning of the tumour suppressor genes called adenomatous polyposis coli (APC).

Many polyps (adenomas) develop along the large intestine > can become cancerous, usually < 40 years old

Patients have their whole large intestine removed to prevent the development of colorectal cancer (panproctocolectomy).

165
Q

What is Lynch syndrome?

A

Autosomal dominant condition caused by mutations in DNA mismatch repair (MSH2/MLH1) genes.

Patients are at a higher risk of several types of cancers, particularly colorectal cancer at a younger age.

Unlikely FAP, it does not cause adenomas and tumours develop in isolation.

166
Q

What are the red flag symptoms of colorectal cancer?

A
  • Change in bowel habit (usually to more loose and frequent stools)
  • Unexplained weight loss
  • Rectal bleeding
  • Unexplained abdominal pain
  • Iron deficiency anaemia (microcytic anaemia with low ferritin)
  • Abdominal or rectal mass on examination
167
Q

A 40-year-old man presents to you with abdominal pain and unintentional weight loss over the last two weeks. You suspect colorectal cancer, what should you do next?

A

Urgent referral - 2-week wait to see a specialist for a colonoscopy and biopsy

NICE guideline recommendations for > 40s

168
Q

A 52-year-old man presents to you complaining that he has recently noticed blood in his stools and he is quite worried. What should you do?

A

Urgent referral - 2-week wait to see a specialist for a colonoscopy and biopsy

NICE guideline recommendations for > 50s

169
Q

A 65-year-old woman comes to you, her GP because she has noticed that her stools have become quite loose and more frequent. She also complains about feeling quite tired, you notice she has a pallor to her skin.

A blood test confirms iron-deficiency anaemia. You suspect colorectal cancer based on the signs and symptoms. What do you do?

A

Urgent referral - 2-week wait to see a specialist for a colonoscopy and biopsy

NICE guideline recommendations for > 60s

170
Q

What are the investigations/tests used to diagnose colorectal cancer?

A

Colonoscopy + biopsy is the gold standard investigation - demonstrate an ulcerating lesion, mucosal lesion that narrows the bowel lumen, or a polyp

Sigmoidoscopy = endoscopy of the rectum and sigmoid colon only.

Staging CT scan involves a full CT thorax, abdomen and pelvis (CT TAP). This is used to look for metastasis and other cancers.

171
Q

What screening for carried out for colorectal cancer?

A

Faecal immunochemical tests (FIT) looks for the amount of human haemoglobin in the stool.

Used in GP practices for specifics patients that do not meet criteria for 2-week wait referral, for example:

  • Over 50 with unexplained weight loss and no other symptoms
  • Under 60 with a change in bowel habit

FIT tests also used for the colorectal cancer screening programme in England > 60 - 74 years sent home kits every two years > positive = colonscopy

People with risk factors such as FAP, HNPCC or inflammatory bowel disease are offered a colonoscopy at regular intervals to screen for bowel cancer.

172
Q

What is the treament/management for colorectal cancer?

A
  • Mainstay treatment is surgical resection

Neoadjuvant treatment (pre-operative therapy)

  • Colon - chemotherapy
  • Rectal - radiotherapy or chemo radiotherapy (acceptable as extraperitoneal structure)
173
Q

Describe the TNM staging classification system

A

TNM staging determines size and spread of a tumour

T for Tumour:

TX – unable to assess size
T1 – submucosa involvement
T2 – involvement of muscularis propria (muscle layer)
T3 – involvement of the subserosa and serosa (outer layer), but not through the serosa
T4 – spread through the serosa (4a) reaching other tissues or organs (4b)

N for Nodes:

NX – unable to assess nodes
N0 – no nodal spread
N1 – spread to 1-3 nodes
N2 – spread to more than 3 nodes

M for Metastasis:

M0 – no metastasis
M1 – metastasis

174
Q

What are the different types of surgeries that can be performed to manage colorectal cancer?

A

Right hemicolectomy - removal of the caecum, ascending and proximal transverse colon.

Left hemicolectomy - removal of the distal transverse and descending colon.

High anterior resection - removing the sigmoid colon

Low anterior resection - removing the sigmoid colon and upper rectum but sparing the lower rectum and anus.

Abdomino-perineal resection (APR) - removes the rectum and anus and sutures over the anus. It leaves the patient with a permanent colostomy.

175
Q

Define Meckel’s diverticulum

A

Meckel’s diverticulum is a congenital malformation of the ileum. Affects around 2% of the population.

A pouch containing embryonic gastric and pancreatic tissue forms in the ileum.

Most people with Meckel’s diverticulum are asymptomatic

176
Q

What are the most common causes of symptomatic Meckel’s diverticulum?

A

Intestinal obstruction, gastrointestinal haemorrhage, and inflammation of the Meckel’s diverticulum (Meckel’s diverticulitis), with or without perforation.

177
Q

What is the epidemiology of symptomatic Meckel’s diverticulum?

A
  • Nearly 50% of patients with symptoms are
    < two years old
  • Males x2-3 more likely to experience symptoms
178
Q

What signs and symptoms might a patient with Meckel’s diverticulitis present with?

A
  • Passage of fresh blood PR (haematochezia)
  • Severe constipation (obstipation) - unable to pass stool/gas due to small bowel obstruction
  • Nausea +Vomitting
  • Abdominal cramps
  • Low abdominal pain
  • Diffuse abdominal tenderness - may indicate perforation
179
Q

What investigations/tests are used to diagnose Meckel’s diverticulum?

A
  • FBC - low haemoglobin and haematocrit
  • Technetium-99m pertechnetate scan (Meckel’s scan) - diagnostic and will show ectopic focus or ‘hot spot’; enhancement of diverticulum
  • CT scan of the abdomen and pelvis - can assess for MD and complication
  • Ultrasound of the abdomen
180
Q

What is the treatment/management for Merkel’s diverticulum?

A

If asymptomatic - no treatment is needed

If bleeding - diverticulum excision and opposing region of the ileum (as often bleeds from ulceration)

If bowel obstruction - diverticulum excision

Blood transfusion if the patient is hemodynamically unstable

Perforation/peritonitis - diverticulum excision or small bowel resection if very severe + pre- and post-op antibiotics

181
Q

Loperamide hydrochloride:

1) Use
2) MOA
3) Main side effects

A

1) Acute, symptomatic diarrhoea. Unlicensed use is facael incontinence for adults
2) Opioid receptor antagonist, reduces GI motility
3) Gastrointestinal disorders; headache; nausea

182
Q

A 24 year old woman presents with severe diarrhoea and has a history of IBS. She is taking the combined oral contraceptive pill, how would diarrhoea affect the effectiveness of the cOCP?

A

If the patient had diarrhoea, then these affected days should be counted as “missed” in terms of the cOCP, as diarrhoea reduces GI absorption of the medication. She should take extra precautions e.g. barrier method

183
Q

What is the MOA of the cOCP?

A

Suppresses GnRH release from anterior pituitary, therefore decreases levels of lutenizing hormone and follicle-stimulating hormone. (LH midcycle surge triggers ovulation, FSH thickens endometrium)

184
Q

What are the considerations for any woman when choosing a contraceptive?

A

Side effects - weight gain, mood swings, cancer risks

If can remember to take each day, or if comfortable with insertion of an intrauterine device

185
Q

What are the considerations for a doctor when helping a patient decide on a contraceptive?

A
  • medical history
  • if she smokes (can only like progesterone only pill)
  • if she wants kids in the future
186
Q

What scale is used to measure the consistency of faecal matter?

A

Bristol stool chart

187
Q

Define hernia

A

A hernia is the protrusion of viscera i.e an organ through a weakness in a surrounding muscle or tissue wall.

These predominantly occur within the abdomen which extends from the diaphragm down to the pelvis.

188
Q

What are the causes of a hernia?

A
  • Hernias can be either congenital or acquired.
  • Increasing age is the leading cause of progressive muscle degeneration and subsequent herniation.
189
Q

What are the three main complications of hernia?

A
  • Incarceration - hernia cannot be reduced back into the proper position (it is irreducible). The bowel is trapped in the herniated position. May lead to below.
  • Obstruction - hernia causes a blockage in the passage of faeces through the bowel. Patient presents with vomiting, generalised abdominal pain and absolute constipation (not passing faeces or flatus).
  • Strangulation - a hernia is non-reducible (it is trapped with the bowel protruding) and the base of the hernia becomes so tight that it cuts off the blood supply, causing ischaemia. This will present with significant pain and tenderness at the hernia site. Strangulation is a surgical emergency.
190
Q

What are the different types of hernia?

A
  • Inguinal - most common, can be direct or indirect
  • Femoral - herniation of the abdominal contents through the femoral canal below inguinal ligament, at top of thigh
  • Umbilical - hernia around the umbilicus due to a defect in the muscle around the umbilicus.
  • Incisional - site of an incision from previous surgery. Due to weakness of muscles and tissues at surgical site after incision
  • Epigastric - a hernia in the epigastric area (upper abdomen)
  • Hiatal - herniation of the stomach up through the diaphragm
191
Q

What is an indirect inguinal hernia?

A

where the bowel herniates through the inguinal canal.

Congenital indirect inguinal hernias = failure of the processus vaginalis to undergo regression

During fetal development, the processus vaginalis is a pouch of peritoneum that extends from the abdominal cavity through the inguinal canal to allow the testes to descend through the abdo cavity

192
Q

What is a direct inguinal hernia?

A

Direct inguinal hernias occur due to weakness in the abdominal wall at Hesselbach’s triangle. The hernia protrudes directly through the abdominal wall, through Hesselbach’s triangle.

Hesselbach’s triangle boundaries (RII mnemonic):

R – Rectus abdominis muscle – medial border
I – Inferior epigastric vessels – superior / lateral border
I – Inguinal ligament – inferior border

193
Q

What general signs and symptoms might a patient with a hernia present with?

A

Symptoms

  • Abdominal discomfort: at hernia site
  • Soft lump/mass protruding from hernia site
  • Nausea and vomiting: if strangulated or obstructed
  • Constipation: in bowel obstruction

Signs:

  • The lump may be/not reducible (it can be pushed back into the normal place)
  • The lump may protrude on coughing (raising intra-abdominal pressure) or standing (pulled out by gravity) and improves on lying down
194
Q

What investigations and tests are used to diagnose hernias?

A
  • Most hernias are a clinical diagnosis made by observation and palpation and do not require any further investigation.
  • CT abdomen if strangulation suspected
195
Q

What are the general management principles for hernias?

A

Depends on the type of hernia.

1) All strangulated or incarcerated hernia:

  • Urgent surgical repair
  • Prophylactic IV antibiotics

2) Small, asymptomatic inguinal hernia:

  • Watchful waiting
  • Avoidance of high-risk activity: heavy lifting

3) Large, symptomatic inguinal hernia and all femoral hernias:

  • Surgery: open-mesh repair vs laparoscopic repair

4) Small umbilical hernias (<1cm fascial defect) [6]:

  • Watchful waiting: will likely self-resolve by 5 years of age

5) Large umbilical hernias (>1.5-2cm fascial defect):

  • Elective surgical repair
196
Q

DDx for inguinal hernias

A
  • Femoral hernia, lymphadenopathy, undescended testes
197
Q

DDx for umbilical hernia

A

Epigastric hernia

198
Q

DDx for hiatus hernia

A
  • Angina pectoris (angina bought on by exertion)
  • GORD
  • Pneumonia
199
Q

What are the two main types of bowel ischaemia?

A
  • Mesenteric ischaemia -which affects the small bowel
  • Ischaemic colitis, which affects the large bowel

Both conditions occur due to narrowed or blocked blood vessels.

The diminished blood flow means that not enough oxygen or nutrients are able to supply the gastrointestinal tract.

200
Q

What artery does mesenteric ischaemia affect?

A

The superior mesenteric artery (SMA).

This artery supplies small bowel from major duodenal papilla (where the common bile duct and pancreatic drain into duodenum) to proximal 2/3 of transverse colon.

201
Q

What areas do ischaemic colitis affect?

A

The colon recieves blood supply from superior mesenteric and inferior mesenteric artery (IMA) (supplies last 3rd of the transverse colon to rectum)

Particularly affects ‘watershed’ (weak) areas e.g. splenic flexure

  • Causes acute, transient compromise in blood flow.
  • This leads to mucosal ulceration, inflammation, and haemorrhage.
202
Q

How would a patient with mesenteric ischaemia present?

A
  1. Acute (caused by thrombus or embolus): severe, sudden abdominal pain; pain is disproportionate to clinical findings
  2. Chronic (caused by narrowing of artery due to atherosclerosis):
  • Classic triad of colicky post-prandial (eating) abdominal pain, weight loss, abdominal bruit on auscultation (whooshing sound)
203
Q

How would a patient with ischaemic colitis present?

A

Transient, less severe abdominal pain, with bloody diarrhoea

204
Q

What is the diagnostic test for mesenteric ischaemia?

A

Acute: diagnostic contrast CT, ABG - metabolic acidosis with raised lactate

Chronic: CT abdominal angiogram or angiography (X-ray image is taken to visualize the inside of blood vessels)

205
Q

What is the diagnostic test for ischaemic colitis?

A

Colonoscopy: gold-standard

AXR: not diagnostic but may show ‘thumbprinting’ - sign of large bowel wall thickening, usually caused by oedema

206
Q

What is the management plan for mesenteric ischaemia?

A

Acute:

  • Surgical emergency: remove necrotic bowel tissue and remove thrombus/embolus through endovascular therapy, embolectomy, or bowel resection
  • Anticoagulation - IV LMWH

Chronic:

  • Managed by controlling cardiovascular risk factors and secondary prevention with statins, anti-platelets and may be suitable for elective endovascular or open procedures.
207
Q

What is the management plan for ischaemic colitis?

A

Conservative (IV Abx, nutrition support) - symptoms usually improve after 48 to 72 hrs and complete resolution by 1 - 2 weeks

Surgery: if conservative management fails or peritonitis, perforation, or ongoing bleeding

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