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Phase 2a > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is the mortality risk for upper GI bleeds?

A

10%

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2
Q

What are the possible causes of an upper GI bleed?

A

50% due to peptic ulcers
oesophageal varices

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3
Q

What is considered an upper GI bleed?

A

bleeding from anywhere above the ligament of treitz

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4
Q

What does low Hb and high urea indicate?

A

bleeding

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5
Q

What is melaena?

A

black stools due to GI bleeding

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6
Q

What is the Glasgow-blatchford score?

A

a scoring system to grade risk of death for patients with upper GI bleeding

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7
Q

What is ABCDE?

A

Airway
Breathing
Circulation
Disability
Exposure

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8
Q

What is the difference between variceal bleeds and non-variceal bleeds?

A

variceal is due to bursting oesophageal varies

suspect variceal bleeds in patients with history of liver disease or alcohol excess, they have a higher mortality rate than non-variceal bleeds

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9
Q

What do patients with variceal bleeds die of?

A

sepsis

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10
Q

How are variceal bleeds treated?

A

antibiotics- to prevent sepsis
terlipressin
endoscopy within 12 hours
band ligation of varices

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11
Q

How are non-variceal bleeds treated?

A

proton pump inhibitors
endoscopy within 24 hours
cauterise/ clip ulcers that are bleeding

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12
Q

What are the causes of intraluminal obstruction?

A

tumour (carcinoma, lymphoma)
diaphragm disease
meconium ileum
gallstone ileus

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13
Q

What are the causes of intramural obstruction?

A

inflammatory (Crohn’s, diverticulitis)
tumours
neural (Hirschsprung’s)

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14
Q

What are the causes of extraluminal obstruction?

A

adhesions
volvulus
tumour (peritoneal deposits)

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15
Q

What are the causes of small bowel obstruction?

A

adhesions
hernia
cancer

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16
Q

What investigations can confirm a diagnosis of small bowel obstruction?

A

FBC
U+E
lactate
C-reactive protein
CT scan

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17
Q

What do we CT scan for small bowel obstructions?

A

localise site of obstruction
indicated cause
tells you if bowel is ischemic (poor enhancement, free fluid, twisted mesentery)

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18
Q

What is coeliac disease?

A

Inflammation of the mucosa of the upper small bowel that improves when gluten is withdrawn from the diet and relapses when gluten is reintroduced

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19
Q

Which protein causes coeliac disease?

A

prolamin intolerance (component of gluten protein)

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20
Q

Describe the pathophysiology of coeliac disease.

A
  1. a-Gliadin is resistant to digestion from protease enzymes (pepsin and chymotrypsin) in small intestine lumen
  2. passes through damaged epithelial wall and into cells
  3. deaminated by tissue transglutaminase
  4. interacts with antigen-presenting cells via HLA- DQ2
  5. These activate gluten-sensitive CD4+ T cells
  6. T-cells produce pro-inflammatory cytokines, leading to inflammatory cascade
  7. causes villous atrophy and crypt hyperplasia
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21
Q

What % of the population are affected by Coeliac disease?

A

~1%
but only ~25% of these people are diagnosed

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22
Q

What are the risk factors for coeliac disease?

A

other autoimmune conditions
IgA deficiency

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23
Q

What are the signs and symptoms of coeliac disease?

A

GI:
- weight loss
- fatigue and weakness
- diarrhoea
- abdominal pain
- bloating
- nausea and vomiting
- steatorrhoea and odorous stools

Dermatological:
- apthous ulcers (canker sore)
- angular stomatitis (redness at sides of mouth)
- dermatitis herpetiformis (raised red patches of skin and blisters due to deposition of IgA in skin)

  • anemia
  • failure to thrive in children
  • osteomalacia
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24
Q

Why can coeliac disease present as osteomalacia?

A

decreased absorption of vitamin D due to malabsorption

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25
Q

Why can coeliac disease cause anaemia?

A

malabsorption leads to inability to absorb B12, folate and iron

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26
Q

What is dermatitis herpetiformis?

A

raised red patches of of skin and blisters due to deposition of IgA in skin (caused by coeliac disease)

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27
Q

What are the potential complications of coeliac disease?

A
  • anaemia
  • osetoporosis
  • hyposplenism
  • neuropathies
  • malnutrition
  • pregnancy complications

INCREASED RISK OF MALIGNANCY
- T- cell lymphoma
- Gastric, oesophageal, small bowel and colorectal cancer

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28
Q

Why does coeliac disease increase the risk of T-cell lymphoma?

A

There is an increased number of T-cells in the GI wall due to the autoimmune response

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29
Q

Why does coeliac disease increase the risk of gastric, oesophageal, small bowel and colorectal cancer?

A

due to increase cell turnover

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30
Q

What is first line and gold standard investigations for coeliac disease?

A

first line = serum antibody testing
gold standard = duodenal biopsy

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31
Q

What investigations are used to diagnose coeliac disease?

A
  1. Serum antibody testing- first line
    positive result will show IgA tissue transglutaminase
    IgA high in most cases, but IgA deficiency also possible
  2. Duodenal biopsy - gold standard
    This is do endoscopically and is required for definite diagnosis
    positive findings will show villous atrophy, crypt hyperplasia, increase epithelial WBCs
  3. FBC
    low Hb, folate, ferritin and B12
    ~50% have mild anaemia
  4. Stool
    used to exclude giardiasis
    may show stool cysts and antibodies
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32
Q

What is the management for coeliac disease?

A
  • LIFE-LONG GLUTEN FREE DIET
  • pneumococcal vaccine given due to hyposplenism
  • correct vitamin deficiencies
  • prescribe dapsone (sulphonamide antibiotic) for dermatitis herpetiformis
  • monitor to check compliance with diet
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33
Q

What is inflammatory bowel disease?

A

Umbrella term for Crohn’s and Ulcerative Colitis

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34
Q

What is Crohn’s?

A

chronic inflammatory condition affecting whole GI tract (mouth to anus)

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35
Q

What is ulcerative colitis?

A

chronic inflammatory condition affecting colon and rectum

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36
Q

How does Crohn’s present on imaging?

A
  • transmural inflammation
  • cobblestone mucosa
  • “string sign” due to narrowed colon lumen
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37
Q

How does UC present on imaging?

A
  • mucosal and submucosal inflammation
  • ulceration
  • loss of haustra - “lead pipe” appearance
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38
Q

In what IBD condition do you expect the most bleeding?

A

bleeding more common in UC than in Crohn’s

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39
Q

Where will a patient with UC and Crohn’s feel pain?

A

Crohn’s: right upper quadrant pain
UC: left lower quadrant pain

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40
Q

Describe the pathophysiology of UC both macroscopically and microscopically.

A

MACROSCOPIC:
- affects colon only
- begins in rectum and extends proximally
- continuous involvement
- red mucosa (bleeds easily)
- ulcers and pseudopolyps (regenerating mucosa) in severe disease

MICROSCOPIC:
- mucosal and submucosal inflammation
- no granulomata
- goblet cell depletion
- crypt abscesses

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41
Q

Describe the pathophysiology of Crohn’s both macroscopically and microscopically.

A

MACROSCOPIC:
- affects any part of GI tract
- oral and perianal disease
- discontinuous involvement (skip lesion)
- deep ulcers and fistulas in mucosa (cobblestone appearance)

MICROSCOPIC:
- transmural inflammation
- granulomas present in 50% of cases

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42
Q

What is a protective factor of UC?

A

smoking

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43
Q

What are the risk factors of UC?

A
  • age (under 30)
  • race/ ethnicity - white, ashkenazi jew
  • family history
  • NSAIDS
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44
Q

What are the risk factors of Crohn’s?

A
  • age (under 30)
  • race/ ethnicity- white, ashkenazi jew
  • family history
  • cigarette smoking
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45
Q

What are the signs and symptoms of ulcerative colitis?

A

SIGNS:
- tender, distended abdomen
SYMPTOMS:
- bloody diarrhoea
- blood and mucus discharge
- abdominal discomfort
- tenesmus, faecal urgency
- systemic symptoms (diarrhoea, pyrexia, malaise, weight loss)

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46
Q

What is tenesmus?

A

feeling that you need to pass a stool even though your bowel is empty

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47
Q

What are the signs and symptoms of Crohn’s?

A

SIGNS:
- aphthous ulcers
- abdo tenderness
- right iliac fossa mass
- perianal abscess, fistula, tags
- anal, rectal structures
SYMPTOMS:
- diarrhoea (not bloody)
- abdo pain
- systemic symptoms (diarrhoea, pyrexia, malaise, weight loss)

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48
Q

What are the investigations for ulcerative colitis?

A
  1. BLOOD TEST
    - raised WCC
    - raised platelets
    - raised c-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)
    - potentially normocytic anaemia of chronic disease
    - LFTs may show low albumin in severe disease
    - pANCA may be positive (negative in Crohn’s)
  2. STOOL SAMPLE
    - used to exclude c.diff, campylobacter and other infections
  3. FAECAL CALPROTECTIN
    - indicates IBD if raised, doesn’t differentiate between UC and Crohn’s
  4. ABDOMINAL X-RAY
    - excludes chronic dilatation
    - also useful when UC is too severe for colonscopy
  5. COLONOSCOPY AND BIOPSY- gold standard
    - sigmoidoscopy for diagnosis
    - full colonoscopy to determine extent once controlled
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49
Q

What investigations are used for Crohn’s disease?

A
  1. BLOOD TEST
    - raised WCC
    - raised platelets
    - raised c-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)
    - anaemia (folate, iron and B12 deficiency)
    - LFTs may show low albumin in severe disease
  2. STOOL SAMPLE
    - used to exclude c.diff, campylobacter and other infections
  3. FAECAL CALPROTECTIN
    - indicates IBD if raised, doesn’t differentiate between UC and Crohn’s
  4. IMAGING
    - capsule endoscopy
    - potentially use MRI to find structures and fistulae
  5. COLONOSCOPY AND BIOPSY- gold standard
    - sigmoidoscopy for diagnosis
    - full colonoscopy to determine extent once controlled
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50
Q

What is gastritis?

A

inflammation of the stomach

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51
Q

What is the proper term for indigestion?

A

dyspepsia

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52
Q

What drugs reduce stomach acid?

A

H2 blockers
proton pump inhibitors

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53
Q

How does the stomach lining protect itself from gastric acid?

A

epithelium lined with buffering mucin

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54
Q

Where is the stomach does helicobacter live?

A

in the mucin lining the stomach epithelium

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55
Q

What are the causes of malabsorption?

A

insufficient intake
defective intraluminal digestion
insufficient absorptive area
lack of digestive enzymes
defective epithelial transport
lymphatic obstruction

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56
Q

What causes defective intraluminal digestion?

A
  • pancreatic insufficiency (pancreatitis, cystic fibrosis)
  • defective bile secretion (biliary obstruction, ileal resection)
  • bacterial overgrowth
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57
Q

What is the most common type of gallstone?

A

cholesterol stone

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58
Q

What are the symptoms of gallstones?

A

pain
fever
jaundice
dietary upset

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59
Q

What is colicky pain?

A

usually a sharp, localized gastrointestinal or urinary pain that can arise abruptly, and tends to come and go in spasmlike waves

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60
Q

What is the management for ulcerative colitis?

A

aim is to induce remission

  1. AMINOSALICYCLATES
    used in mild/ moderate cases
    given orally as first line for left sided/ extensive, given rectally for proctitis (inflammation of rectal lining)
  2. MILD/ MODERATE
    oral prednisolone- second line if they don’t respond to 5-ASA
  3. MAINTING REMISSION
    - 5-ASA
    - Azathioprine - if still relapsing on 5-ASA
  4. SEVERE WITH SYSTEMIC FAILURE
    - IV hydrocortisone
    - ciclosporin
    - inflaximab
  5. SURGERY- for severe cases with no response to treatment
    COLECTOMY - whole bowel removed and ilestomy (stoma) attached
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61
Q

What is the management for Crohn’s?

A

Aim to induce remission

  1. MILD/ MODERATE
    oral prednisolone- first line
    smoking cessation
    correct iron/ folate/ B12 deficiences
    antibiotics for perianal disease
    liquid enteral nutrition
  2. SEVERE
    IV hydrocortisone
  3. IF NOT RESPONSIVE TO STEROIDS:
    Anti-TNF antibodies (infliximab, adalimumab)
  4. MAINTAINING REMISSION
    azathioprine (if intolerant- methotrexate)
    infliximab, adalimumab (if resistant to immunosuppressives)
  5. SURGERY
    up to 80% patients require 1+ surgery, never fully cures
    resection of worst affected areas of bowel
    surgery kept to a minimum
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62
Q

Why is surgery for Crohn’s kept to a minimum?

A
  • recurrence is almost inevitable in the remaining bowel
  • short bowel syndrome is life long and includes diarrhoea and malabsorption
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63
Q

What is an alternative option to resection surgery in Crohn’s disease?

A

temporary ileostomy to allow time for affected areas to rest and heal

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64
Q

What are the indications of surgery for Crohn’s?

A

failure of medical therapy
obstruction from structures
fistulae, abscesses, perianal disease
toxic dilatation and perforation

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65
Q

What kind of drug is prednisalone?

A

glucocorticoid steroid

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66
Q

What is the active component in aminosalicyclates?

A

5-aminosalicyclic acid (5-ASA)

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67
Q

What are the 3 most commonly prescribes 5-ASAs?

A

sulfasalazine
mesalazine
oslalazine

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68
Q

What is proctitis?

A

inflammation of rectal lining

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69
Q

What are the complications of ulcerative colitis?

A

toxic megacolon
bleeding
malignancy
structures (leading to obstruction)
venous thrombosis

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70
Q

What are the complications of Crohn’s?

A

fistulae
structures
abscesses
malabsorption

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71
Q

What is IBS?

A

irritable bowel syndrome- mixed group of abdominal symptoms with no organic cause

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72
Q

What are the 3 types of IBS?

A

IBS-C: with constipation
IBS-D: with diarrhoea
IBS-M: mixed, with alternative constipation and diarrhoea

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73
Q

What is the age of onset for IBS?

A

under 40 years old

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74
Q

What sex is more susceptible to IBS?

A

females

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75
Q

How many people in the western world have IBS?

A

1 in 5

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76
Q

What are the theories for pathophysiology of IBS?

A

disorders of intestinal motility
enhanced visceral perception
disfunction of brain-gut axis
microbial dysbiosis (imbalance)

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77
Q

What are the potential causes/ triggers for IBS?

A

depression/ anxiety
psychological stress/ trauma
GI infection
sexual/ physical/ verbal abuse
eating disorders

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78
Q

What are the risk factors for IBS?

A

female
previous severe diarrhoea
high hyperchondrial anxiety and neurotic score at time of initial illnesses

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79
Q

When should IBS be considered?

A

if patient reports any of (ABC):
Abdo pain/ discomfort
Bloating
Change in bowel habit

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80
Q

What is the diagnostic criteria for IBS?

A

abdominal pain/ discomfort with 2+ of:
- relieved by defecation
- altered stool form
- altered bowel frequency

other symptoms include:
- urgency
- incomplete evacuation
- mucus in stool
- worsening symptoms after food

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81
Q

What’s the exclusion criteria for IBS?

A

> 40 yrs old
bloody stool
anorexia
weight loss
diarrhoea at night

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82
Q

As IBS is a multisystem disorder, what other symptoms can it trigger?

A

painful periods
bladder symptoms
back pain
joint hypermobility
fatigue
nausea

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83
Q

What exacerbates the symptoms of IBS?

A

stress
menstruation
gastroenteritis
food

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84
Q

What is the differential diagnosis for IBS?

A

coeliac disease
lactose intolerance
bile acid malabsorption
IBD
colorectal cancer
GI infection
pancreatic insufficiency

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85
Q

When a patient presents with IBS symptoms, what are the red flag symptoms indications a possible colon cancer?

A

unexplained weight loss
bleeding on defaecation/ wiping
abdo/ rectal mass
raised inflammatory markers
anaemia
family history
aged over 50
nocturnal symptoms

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86
Q

What is the aim of investigations for IBS?

A

process of elimination, investigations used to rule out differentials

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87
Q

What are the investigations for IBS?

A

process of elimination

FBC- rule out anaemia
ESR+CRP - rule out inflammation
tTG/EMA- coeliac
faecal calproctetin - raised in IBD
colonoscopy - IBD, colorectal cancer

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88
Q

What is the management for IBS?

A

exclusion diets
bulking agents for constipation and diarrhoea
antispasmodics for colic/ bloating
CBT

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89
Q

What is acute appendicitis?

A

sudden inflammation of the appendix

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90
Q

What is a vestigial organ?

A

retention of an organ that has lost some or all ancestral function, e.g. appendix

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91
Q

Where is the appendix?

A

at McBurney’s point- 2/3rds of the way from the umbilicus to the anterior superior iliac spine

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92
Q

In what age is acute appendicitis most common?

A

~ 10-20 yrs

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93
Q

What is the most common surgical emergency?

A

acute appendicitis

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94
Q

What causes appendicitis?

A

usually due to an obstruction:
- faecoliths (stoney mass of compacted faeces)
- lymphoid hyperplasia (post-infection)
- tumour (caecal carcinoma, carcinoid)
- worms (ascaris lumbiciodes, schisto)

obstruction of the appendix results in invasion of gut organisms into the appendix wall, this leads to inflammation, necrosis and eventually perforation

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95
Q

What is the largest cavity in the body?

A

peritoneal cavity

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96
Q

What are the 2 parts of the peritoneum?

A

visceral and parietal peritoneum

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97
Q

What is the function of the peritoneum?

A

in health:
visceral lubrication
fluid and particulate absorption

in disease:
pain perception
inflammatory and immune responses
fibrinolytic activity

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98
Q

What is peritonitis?

A

inflammation of the peritoneum

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99
Q

What is the peritoneum?

A

a continuous membrane which lines the abdominal cavity and covers the abdominal organs

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100
Q

What is the nature of appendicitis abdominal pain?

A

EARLY INFLAMMATION:
- appendices irritation
- visceral pain not well localised
- umbilical pain

LATE INFLAMMATION:
- parietal peritoneum inflammation
- pain localised in right iliac fossa

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101
Q

What are the signs and symptoms of acute appendicitis?

A

abdominal pain (colicky)
anorexia
nausea (sometimes with vomiting)
pyrexia
constipation/ diarrhoea
tachycardia
guarding at McBurney’s point
tender mass in RIF
foetor oris (halitosis)
Rovsing’s sign
Psoas sign
Cope sign

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102
Q

What is Rovsing’s sign?

A

pressure in left iliac fossa causes more pain in right iliac fossa

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103
Q

What is Psoas sign?

A

pain on entending hip

104
Q

What is Cope sign?

A

pain on flexion and internal rotation on right hip

105
Q

What is the differential diagnosis for acute appendicitis?

A

acute crohn’s
ectopic pregnancy
UTI
diverticulitis
perforated ulcer
food poisoning
constipation
strangulated hernia

106
Q

What are the investigations of acute appendicitis?

A

CT- gold standard

BLOOD TEST
raised WCC
raised CRP+ESR

ULTRASOUND
can detect inflamed appendix
may show appendiceal mass

pregnancy test to exclude ectopic
urinalysis to exclude UTI

107
Q

What is the management for acute appendicitis?

A
  • appendicectomy GOLD STANDARD
    usually laparoscopic (keyhole) but can be laparotomy (open)
  • IV antibiotics + fluids (pre and post operatively)
  • analgesia
108
Q

What are the complications of acute appendicitis?

A

perforation
appendix mass
appendices abscess
adhesions
pelvic inflammatory disease

109
Q

Why can acute appendicitis cause an appendix mass?

A

the small bowel and the momentum adhere to the appendix

110
Q

What are the types of bowel obstruction?

A
  • small bowel
  • large bowel
  • pseudo-obstruction
111
Q

What is a bowel obstruction?

A

arrest of onward propulsion of intestinal contents

112
Q

Describe the pathophysiology of small bowel obstructions

A
  • obstruction of bowel leads to distension above the blockage due to a build-up of fluid and contents
  • this causes increased pressure which pushes on the blood vessels within the bowel wall causing them to become compressed
  • these compressed vessels cannot therefore supply blood resulting in ischaemia and necrosis, and eventually perforation
113
Q

What are the causes of small bowel obstruction?

A

adhesions (60%) of cases
hernias
malignancy
Crohn’s

114
Q

Adhesions can cause small bowel obstructions. What his the likely cause of an adhesion forming?

A

usually due to previous abdominal/ pelvic surgery
can also be due to previous abdominal infections (e.g. peritonitis)

115
Q

How do hernias cause small bowel obstructions?

A

intestinal contents can’t pass through a strangulated loop of hernia

116
Q

Describe signs and symptoms of SBOs.

A
  • pain which is colicky and then diffuses, higher in abdomen than LBO
  • profuse vomiting following pain, occurring earlier than an LBO
  • less abdominal distension than LBO
  • tenderness suggests strangulation/ risk of perforation
  • constipation with no passage of gas occurring at a late stage in SBO
  • increased bowel sounds (tinkling)
117
Q

Describe the investigations for SBOs.

A

1st line = abdominal x-ray
- shows central gas shadows that completely cross the lumen
- no gas is seen in large bowel
- there will be distended loops proximal to the obstruction
- may see fluid level within bowel

FBC

Examination of hernia orifices and rectum

Gold Standard = CT (non-contrast)
- accurately localises obstruction

118
Q

What is the management for SBOs and LBOs?

A

SAME FOR BOTH

  • aggressive fluid resuscitation
  • decompression of bowel: “drip and suck”, IV fluids and NG tube
  • analgesia and anti-emetics for symptoms
  • antibiotics
  • surgery to remove obstruction (usually laparotomy)
119
Q

What are anti-emetics?

A

anti-sickness medication used to prevent nausea and vomiting

120
Q

What are the most common used anti-emetics?

A

Dopamine agonists such as:
- metoclopramide
- domperidone
- chlorpromazine

121
Q

What are the causes of large bowel obstruction?

A

malignancy (90% of cases in western world)
volvulus (most common in Africa)
diverticulitis
Crohn’s
intussusception

122
Q

What is volvulus?

A

rotation/ twisting of the bowel on it’s mesenteric axis
most commonly occurs in sigmoid colon

123
Q

What is intussusception?

A

bowel rolls inside itself
almost exclusively occurs in neonates/ infants as they have “softer” bowels

124
Q

Why is large bowel obstruction rarer than small bowel obstruction?

A

the lumen of the larger bowel is bigger and can distend more, therefore harder to block

125
Q

What are the signs and symptoms of a large bowel obstruction?

A
  • abdominal pain (more constant than SBO and lower in abdomen)
  • much more abdominal distension than SBO
  • normal bowel sounds initially then increased and eventually silent as no movement
  • palpable mass (most commonly in LIF)
  • vomiting occurs much later than in SBO, may be absent
  • constipation earlier than SBO
126
Q

What investigations are used for large bowel obstructions?

A

Digital rectal exam (DRE) shows:
- empty rectum
- hard, compacted stools
- might be blood

FBC:
- low Hb
- signs of chronic occult blood loss

CT gold standard

Abdo x-ray first line
- peripheral gas shadows proximal to blockage, but doesn’t show re tum hence why DRE is essential
- caecum and ascending colon will be distended

127
Q

What are pseudo bowel obstructions?

A

when the clinical picture mimics SBO or LBO with no mechanical cause

128
Q

What are the causes of pseudo bowel obstruction?

A

intra-abdominal trauma
pelvic/ spinal/ femoral fractures
post-operative fractures
intra-abdominal sepsis
pneumonia
drugs (opiates, antidepressants)
metabolic disorders

129
Q

What is the management of pseudo bowel obstruction?

A

treat underlying cause
IV neostigmine

130
Q

What is the difference between acute and chronic diarrhoea?

A

acute diarrhoea < 2 weeks
chronic diarrhoea > 2 weeks

131
Q

What are the causes of diarrhoea?

A

BACTERIAL:
campylobacter jejuni
e.coli
salmonella
shigella

VIRAL (majority):
children = rotavirus
adults = norovirus

PARASITIC:
giardia lamblia
entamoeba histolytica
cryptosporidium

132
Q

What is the management of diarrhoea?

A
  • treat underlying causes (bacterial diarrhoea usually treated with metronidazole)
  • oral rehydration therapy (IV fluids if very severe)
  • anti-emetics e.g. metoclopramide
  • anti-motility agents, e.g. loperamide
133
Q

What are the main types of ischaemic bowel disease?

A

acute mesenteric ischaemia
chronic mesenteric ischaemia
ischaemic colitis

134
Q

What bacteria may cause bloody diarrhoea?

A

e.coli
salmonella
shigella

135
Q

Describe the blood supply to the gut.

A

foregut= coeliac artery
midgut= superior mesenteric artery
hindgut= inferior mesenteric artery

136
Q

Which part of the gut is affected by acute and chronic mesenteric ischaemia?

A

small bowel

137
Q

Which parts are the gut are most susceptible to ischaemia?

A

“watershed areas” such as the splenic flexure and caecum

138
Q

What are the causes of acute mesenteric ischaemia?

A
  • SMA thrombosis
  • SMA embolism
  • mesenteric vein thrombosis (typically young patients who are in hypercoaguable states)
  • non-occlusive disease (e.g. poor blood flow, poor cardiac output)
139
Q

What are the signs and symptoms of acute mesenteric ischaemia?

A

CLASSIC TRIAD:
- acute, severe abdominal pain (constant and central)
- no abdo signs on examination
- rapid hypovolaemia then shock

IF YOU SEE AF WITH SEVERE ABDO PAIN, THINK AMI

140
Q

What investigations are used for acute mesenteric ischaemia?

A

BLOODS:
- raised Hb (due to blood loss)
- raise WCC
- persistent metabolic acidosis (due to ischaemia)

ABDO X-RAY:
used to rule out an obstruction

LAPAROSCOPY:
used to visualise necrosis

CT/ MRI ANGIOGRAPHY:
non-invasive way to look at arteries to see blockages, however it is a difficult scan to perform

141
Q

What is the management of acute mesenteric ischaemia?

A

fluid resuscitation
antibiotics (metronidazole, gentamicin)
IV heparin (reduce clotting)
surgery to remove necrotic bowel

142
Q

What are the potential complications of acute mesenteric ischaemia?

A

sepsis
peritonitis

143
Q

What is ischaemic colitis?

A

occlusion of a branch of the superior mesenteric artery or interior mesenteric artery

144
Q

What are the causes of ischaemic colitis?

A

thrombosis
emboli
low flow states (low cardiac output/ arrhythmia)
surgery
vasculitis
coagulation disorders
oral contraceptive pill
idiopathic

145
Q

What are the signs and symptoms of ischaemic colitis?

A

sudden onset LIF pain
passage of bright red blood
signs of hypovolaemic shock

146
Q

What are the investigations for ischaemic colitis?

A

urgent CT to rule out perforation

flexible sigmoidoscopy with biopsy (will show epithelial apoptosis)

colonoscopy with biopsy gold standard- only done after patient has fully recovered to exclude formation of structures at the site and to confirm mucosal healing

barium enema

147
Q

What is the management of ischaemic colitis?

A
  • most patients with be fine with only symptomatic treatment
  • fluid resuscitation
  • antibiotics (reduce infection risks due to translocation of bacteria across the drying bowel wall)
  • structures common

gangrenous ischaemic colitis includes peritonitis and hypovolaemic shock which will require surgical intervention

148
Q

What is a Mallory Weiss tear?

A

a tear/ laceration along the right border of, or near, the gastro-oesophageal junction

149
Q

What are the risk factors for a Mallory Weiss tear?

A

alcoholism
forceful vomiting
eating disorders
male
NSAID use

150
Q

What are the signs and symptoms of a Mallory Weiss tear?

A

vomiting
haematemesis after vomiting
retching
postural hypotension
dizziness

151
Q

What investigations are used for a Mallory Weiss tear?

A

OGDoscopy

152
Q

What is an OGD biopsy?

A

Oesophagus Gastro Duodenal Biopsy

153
Q

What is the differential diagnosis for a Mallory Weiss tear?

A

gastroenteritis
peptic ulcer
cancer
oesophageal varices

154
Q

What is the management of a Mallory Weiss tear?

A

heals by itself over time
provide supportive care

155
Q

What is Barrett’s oesophagus?

A

metaplasia of the lower oesophageal mucosa (stratified squamous to simple columnar epithelium)

156
Q

What are the potential causes of Barrett’s oesophagus?

A

GORD
male (7:1)
caucasian
family history
hiatus hernia
obesity
smoking
alcohol

157
Q

What are the signs and symptoms of Barrett’s oesophagus?

A

classic history: middle-aged caucasian male with long history of GORD and dysphagia

158
Q

What investigations are used for Barrett’s oesophagus?

A

OGD and biopsy

159
Q

What is the management for Barrett’s oesophagus?

A

LIFESTYLE:
- weightloss
- smoking cessation
- reduce alcohol
- small regular meals
- avoid hot drinks/ alcohol/ eating < 3hrs before bed
- avoid certain drugs (nitrates, anticholinergics, TCAs, NSAIDS, K+ salts, alendronate)

160
Q

What are the types of oesophageal cancer?

A
  • squamous cell carcinoma: middle and upper third of oesophagus
  • adenocarcinoma: lower third of oesophagus
161
Q

What are the causes of oesophageal squamous cell carcinoma?

A
  • high levels of alcohol consumption
  • achalasia
  • tobacco use
  • obesity
  • smoking
  • not enough fruit and veg
162
Q

What is achalasia?

A

a condition in which the muscles of the lower part of the oesophagus fail to relax, preventing food from passing into the stomach

163
Q

What are the causes of oesophageal adenocarcinoma?

A
  • smoking
  • GORD
  • obesity
164
Q

What are the protective factors against oesophageal squamous cell carcinoma?

A

diets rich in fibre
carotenoids
folate
vitamin C

165
Q

What are the risk factors for oesophageal cancers?

A

alcohol
smoking
obesity
achalasia
diet low in vitamin C and vitamin A
Barrett’s oesophagus

166
Q

What are the signs and symptoms of oesophageal cancer?

A
  • progressive dysphagia (starts with solids, then onto liquids)
  • weight loss
  • lymphadenopathy
  • anorexia
  • pain
  • difficulty swallowing saliva, coughing and aspiration into lungs
  • if in upper third of oesophagus, hoarseness and coughing
167
Q

What is dysphagia?

A

difficulty swallowing

168
Q

How do benign oesophageal tumours present?

A
  • usually asymptotic, found incidentally in a barium swallow
  • dysphagia
  • retrosternal pain
  • food regurgitation
  • recurrent chest infections
169
Q

Why do oesophageal cancers cause pain?

A

due to impaction of food or infiltration of cancer into adjacent structures

170
Q

What investigations are used for oesophageal cancer?

A
  • oesophagoscopy with biopsy - confirms diagnosis
  • barium swallow to find structures
  • CT scan/ MRI/ PET for staging
171
Q

What type of scans best at detecting metastases?

A

PET scan

172
Q

How are benign oesophageal tumours diagnosed?

A
  • endoscopy
  • barium swallow
  • biopsy to rule out malignancy
173
Q

What is the management of oesophageal tumours?

A

to manage dysphagia:
- endoscopic insertion of expanding metal stent across tumour to ensure oesophageal patency
- laser and alcohol injections to cause tumour necrosis and increased lumen size

if cancerous:
- surgical resection
- chemo with potential radiotherapy for best outcome
- systemic chemo if incurable/ metastases

if benign:
- endoscopic removal of tumour
- surgical removal if tumour is large

174
Q

What is GORD?

A

gastrooesophageal reflux disease
when acid from the stomach leaks up into the oesophagus

175
Q

Describe the pathophysiology of GORD.

A
  • relaxation of gastro-oesophageal sphincter occurs after meals and is stimulated by fat in the duodenum
  • hiatus hernia makes this more common
  • mucosal damage is caused by the acid regurgitation, leading to oesophagitis
176
Q

What are the risk factors for GORD?

A

hiatus hernia
smoking
alcohol
obesity
pregnancy
drugs
iatrogenic

177
Q

What drugs are risk factors for GORD?

A

anti-muscarinics
nitrates
calcium channel blockers (CCBs)
TCAs

178
Q

What are the signs and symptoms for GORD?

A

OESOPHAGEAL:
- heartburn
- belching
- acid brash, water brash
- odonophagia
- dysphagia

EXTRA-OESOPHAGEAL:
- noturnal asthma
- chronic cough
- laryngitis/ sinusitis

179
Q

What is odonophagia?

A

painful swallowing

180
Q

Describe GORD-related heartburn?

A

worse lying down
related to meals
relieved by antacids

181
Q

What is water/ acid brash?

A

If you have acid reflux, stomach acid gets into your throat. This may make you salivate more. If this acid mixes with the excess saliva during reflux, you’re experiencing water brash.

182
Q

What investigations are used for GORD?

A

PPI trial, confirmed if symptoms relieved
endoscopy if any red flags

183
Q

What is the management of GORD?

A

CONSERVATIVE:
- weight loss
- raise head of bed
- small, regular meals not soon before bed
- smoking cessation/ alcohol reduction
- avoid hot drinks and spicy food
- stop NSAIDS, steroids, CCBs, nitrates

MEDICAL:
- OTC antacids
- PPI- lansoprazole

SURGICAL:
- nissen fundoplication

184
Q

What is Nissan fundoplication?

A

treatment for GORD

in this procedure, the surgeon wraps the top of the stomach around the lower esophagus. This reinforces the lower oesophageal sphincter, making it less likely that acid will back up in the oesophagus

185
Q

What are the complications of GORD?

A
  • oesophagus
  • infection
  • IBD
  • PUD
  • Barrett’s metaplasia- oesophageal adenocarcinoma
186
Q

What is PUD?

A

peptic ulcer disease
open sores in the lining of the stomach

187
Q

What are peptic ulcers?

A

open sores in stomach lining

188
Q

Describe the pathophysiology of duodenal ulcers.

A
  • chronic H.pylori infection
  • impaired secretion of somatostatin –> increased gastrin release
  • gastric acid hypersecretion

If Zollinger-Ellison syndrome: gastrin-secreting neurological-endocrine tumour stimulates high rates of gastric acid secretion

189
Q

Describe the pathophysiology of gastric ulcers?

A
  • chronic H.pylori infection and severe inflammation
  • gastric mucin degradation and disruption of tight junction between gastric epithelial cells
  • induction of gastric epithelium cell death
  • NSAIDS: cause injury directly and indirectly and increase bleeding risk
190
Q

Name the causes of acute peptic ulcers?

A

drugs (NSAIDS, steroids)
stress

191
Q

What are the causes of chronic peptic ulcers?

A

drugs
H. pylori
high calcium
Zollinger-Ellison

192
Q

Where are gastric ulcers and duodenal ulcers found specifically?

A

gastric ulcers- lesser curvature of gastric antrum
duodenal- usually 1st part of duodenum

193
Q

What are the risk factors for gastric ulcers?

A

H.pylori
smoking
drugs
delayed gastric emptying
stress

194
Q

What are the risk factors for duodenal ulcers?

A

H.pylori
smoking
drugs
NSAID, steroids
alcohol
blood group O
increased gastric emptying

195
Q

What is the presentation of gastric and duodenal ulcers?

A

Epigastric pain for both

For gastric:
- worse on eating
- relieved by antacids

For duodenal:
- occurs before meals and at night
- relieved by eating or drinking milk

196
Q

What are the investigations for gastric/ duodenal ulcers?

A
  • upper GI endoscopy, look for ulcers, may be able to detect cause
  • H.pylori C13 urea breath test, stool antigen test positive result if H.pylori present
  • FBC, may see microcytic anaemia or high platelets
197
Q

What is the management for gastric/ duodenal ulcers?

A

CONSERVATIVE:
lose weight
smoking and alcohol cessation
avoid hot drinks/ spicy food
stop drugs- NSAIDS, steroids

MEDICAL:
OTC antacids
H.pylori eradication
full or low dose acid suppression

198
Q

What are the possible complications of gastric/ duodenal ulcers?

A

haemorrhage
perforation
gastric outflow obstruction
malignancy

199
Q

What is gastritis?

A

inflammation of the stomach associated with mucosal injury

200
Q

What are the causes of gastritis?

A

H.pylori infection
autoimmune gastritis
viruses- CMV, HSV
duodenogastric reflux
Crohn’s
mucosal ischaemia
increased acid
NSAIDS
alcohol

201
Q

How does duodenogastric reflux cause gastritis?

A

bile salts can enter the stomach and damage mucin production leading to inflammation

202
Q

What are the signs and symptoms of gastritis?

A

nausea + vomiting
abdo bloating
epigastric pain
indigestion
haematemesis

203
Q

What investigations are used for gastritis?

A

endoscopy- can see inflammation
biopsy
H.pylori urea breath test
H. pylori antigen stool test

204
Q

What is the differential diagnosis for gastritis?

A

PUD
GORD
non-ulcer dysplasia
gastric lymphoma
gastric carcinoma

205
Q

What is the management for gastritis?

A

remove causative agents
reduce stress
H.pyori eradication (if positive)
H2 agonist/ PPIs to reduce acid release
antacids

206
Q

What is the definition of a diverticulum?

A

out pouching of gut mucosa
i.e. gaps in wall of gut where blood vessels can penetrate

207
Q

For what age group is diverticula common?

A

> 50yrs old

208
Q

What is diverticulosis?

A

presence of multiple diverticula

209
Q

What is diverticulitis?

A

inflammation/ infection of diverticulum

210
Q

What is diverticular disease?

A

when diverticula are symptomatic

211
Q

What is Meckel’s diverticulum?

A

common congenital abnormality of GI tract

true diverticula of all 3 layers of the small intestine caused by incomplete obliteration of the vitelline duct

usually asymptomatic

212
Q

What % of the population have Meckel’s diverticulum?

A

2-3%

213
Q

What is the difference between true vs false diverticula?

A

true- composed of complete wall
false- composed of mucosa only

214
Q

Why does bleeding occur in Meckel’s diverticulum?

A

painless bleeding occurs due ulcers caused by heterotypic gastric tissue

215
Q

How can Meckel’s diverticulum cause obstruction?

A

obstruction can be caused by intussusception, volvulus, hernia

216
Q

How is Meckel’s diverticulum diagnosed?

A

diagnosed via a nuclear medicine scan (AKA Meckel’s scan)
99m technetium pertechnetrate)

217
Q

Where are diverticula most likely to form?

A

sigmoid colon as it has the smallest luminal diameter and the highest pressure

218
Q

What are the causes of diverticulitis?

A

low fibre diet
obesity
smoking
NSAIDS

219
Q

What are the signs and symptoms of diverticulitis?

A

constipation
LIF pain with tenderness
LIF palpable mass
tachycardia
fever

220
Q

What are the investigations for diverticulitis?

A

BLOODS: raised WCC, ESP, CRP
IMAGING: chest x-ray, abdo x-ray, CT
imaging may show:
- pneumoperitoneum
- dilated bowel loops
- obstruction
- abscess

221
Q

What is the management for diverticulitis?

A

oral/ IV antibiotics- ciprofloxacin, metronidazole
analgesia

222
Q

How do polyps in the rectum or sigmoid colon present?

A

bleeding

223
Q

How do right sided colorectal carcinomas present?

A

usually asymptomatic until anaemia due to bleeding
may have a mass
weight loss
low Hb
abdo pain

224
Q

How do left sided colorectal carcinomas present?

A

change of bowel habit with blood and mucus in stool
alternating constipation and diarrhoea
thin/ altered stool

225
Q

How do rectal carcinomas present?

A

rectal bleeding and mucus
thinner stool and tenesmus when cancer grows

226
Q

What is tenesmus?

A

cramping rectal pain

227
Q

What is an emergency presentation of colorectal carcinomas?

A

obstruction

228
Q

What are the 4 cardinal signs of bowel obstruction?

A

absolute constipation
colicky abdominal pain
abdominal distension
faecal vomiting

229
Q

What is the location for diverticular disease?

A

sigmoid and descending colon

230
Q

What is diverticular disease?

A

symptomatic diverticulae

231
Q

What are the risk factors for diverticular disease?

A

low fibre diet
obesity
age > 40

232
Q

What is the presentation of diverticular disease?

A

altered bowel habit
abdo pain
bleeding PR

233
Q

What are the investigations for diverticular disease?

A

CT (if acute)
colonoscopy

234
Q

What is the management for diverticular disease?

A

high fibre diet and fluid +/- laxatives
surgery

235
Q

What are the types of gastric cancers?

A

TYPE 1
intestinal/ differentiated

TYPE 2
diffuse/ undifferentiated

236
Q

What proportions of gastric cancers ate type 1/ type 2?

A

Type 1: 70-80%
Type 2: ~20%

237
Q

What type of cancer accounts for most of gastric cancers?

A

most are gastric adenocarcinomas

238
Q

What is the exact location of type 1 and type 2 gastric cancers?

A

type 1- antrum and lesser curvature
type 2- anywhere especially the cardia

239
Q

What are the causes of gastric cancer?

A

smoking
H.pylori infection
diet (high salt and nitrates)
loss of p53 and APC genes
family history (CDH1 gene)
pernicious anemia

240
Q

What is the clinical presentation of gastric cancer?

A

often a late presentation

  • epigastric pain that is constant and severe
  • nausea
  • anorexia
  • weight loss
  • vomiting
  • dysphagia
  • anaemia
  • palpable lymph node in supraclavicular fossa
241
Q

What does severe vomiting as a symptom of stomach cancer indicate?

A

that the tumour has encroached on the pylorus

242
Q

What does dysphagia as a symptom of stomach cancer indicate?

A

that the tumour has encroached on the fundus

243
Q

Where can gastric cancer metastasise to?

A

liver (present with jaundice)
bone
lung
brain

244
Q

What are the investigations for gastric cancer?

A
  • gastroscopy taking 8-10 biopsies (histologically confirms adenocarcinoma)
  • endoscopic USS to evaluate depth of invasion
  • CT/MRI for staging
  • PET for mets
245
Q

What is the management for stomach cancer?

A

nutritional support
surgical resection
chemo

246
Q

What type of chemo is used for gastric cancer?

A

ECF therapy:

epirubicin
cisplantin
5-flurouracil

247
Q

What is the prognosis for gastric cancer?

A

60% survive 5 years

248
Q

What are the risk factors for small intestine cancer?

A

coeliac disease
crohn’s disease

249
Q

What are the signs and symptoms of small intestine cancer?

A

pain
diarrhoea
anorexia
weight loss
anaemia
palpable mass

250
Q

What are the protective factors of gastric cancer?

A

non-starchy vegetables
fruit
garlic
low salt

251
Q

What investigations confirm a diagnosis of small intestine cancer?

A

ultrasound
endoscopic biopsy

252
Q

Where does colon cancer occur most?

A

in the distal colon

253
Q

What is a colonic polyp?

A

abnormal growth of tissue projecting from colonic mucosa

254
Q

What is a colon adenoma?

A

type of polyp

is a benign dysplastic tumour of columnar epithelial cells/ glandular tissue

they are precursor legions in most cases for colon cancer

255
Q

What are the risk factors for colon cancer?

A

family history
IBD (UC)
low fibre high fat diet
obesity
alcohol
smoking
colorectal polyps/ adenomas

Phase 2a (18 decks)

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