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Phase 2A > Gastro > Flashcards

Gastro Flashcards

1
Q

What are the defence mechanisms of the GI microbiome?

A

Intestinal microflora:
- prevent infection by interfering and competing with pathogens
- produce its own antibacterial substances
Gastric acid kills most organisms that are swallowed
Bile has antibacterial properties

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2
Q

What is diarrhoea?

A

The passage of loose or watery stools, typically at least three times in 24hrs.

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3
Q

What are the types of diarrhoea?

A

Acute - 14 days or fewer in duration
Persistant diarrhoea - 14-30 days duration
Chronic diarrhoea - >30 days duration

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4
Q

What are the causes of diarrhoea?

A

Infective: intraluminal infection, systemic infections (sepsis, TSS, tropical infections, COVID)

Non-infective: cancer, chemical (poisoning, sweeteners, medications), IBD, IBS/malabsorption, endocrine (thyrotoxicosis), radiation

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5
Q

What are the characteristics and causes of watery diarrhoea?

A

Non-inflammatory
Infection in proximal small bowel
Bacteria implicated: vibrio cholerae, E. coli, Clostridium perfringens, Bacillus cereus (reheated rice), S. aureus, C. difficile
Viral causes: Rotavirus, norovirus
Parasitic: Giardia, Cryptosporidium

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6
Q

What condition is associated with rice water diarrhoea?

A

V. cholerae infection

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7
Q

What is dysentery?

A

bloody diarrhoea

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8
Q

What is H. pylori?

A

Gram -ve rod, commensal bacteria, usually asymptomatic acquisition

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9
Q

What conditions are caused by H. pylori?

A

Peptic ulcer disease (PUD), chronic gastritis, gastric adenocarcinoma, gastric mucosal lymphoma

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10
Q

What is the pathophysiology of H. pylori infection?

A
  • H. pylori synthesises urease, an enzyme which produces ammonia
  • Ammonia damages the gastric mucosa as well as neutralising the protective stomach acid which allows the organs, to survive in the stomach
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11
Q

What are the diagnostic tests for H. pylori infection?

A

Biopsy
Stool antigen
C-urea breath test

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12
Q

What is the treatment for H. pylori infection?

A

Triple therapy: clarithromycin, amoxicillin, PPI (lansoprazole, omeprazole)

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13
Q

What is E. coli?

A

Gram -ve rod, often commensal bacteria
Most strains are harmless but some serotypes are pathogenic:
- ETEC (EnteroToxigenic), EAEC (EnteroHaemorrhagic), EPEC (EnteroPathogenic) → watery diarrhoea
EHEC (EnteroHaemorrhagic) → bloody diarrhoea
Serotype 0157:H7 → Haemolytic Uremic Syndrome
( → haemorrhagic diarrhoea + nephritic syndrome)

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14
Q

What is the treatment for E. coli?

A

Amoxicillin, trimethoprim, nitrofurantoin

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15
Q

What is C. difficile?

A

Gram +ve spore-forming, toxin-producing bacteria
Mainly induced w/ antibiotics (ciprofloxacin, co-amoxiclav, cephalosporins, clindamycin)

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16
Q

What is the pathophysiology of C. difficile infection?

A

Causes pseudomembranous colitis
- Normal GIT flora killed by antibiotics and C. difficile replaces them
- Results in dangerous severe diarrhoea (very watery; ↑↑dehydration)
Highly infectious

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17
Q

What is the treatment for C. difficile?

A

Stop using C-antibiotics (ciprofloxacin, co-amoxiclav, cephalosporins, clindamycin)
Give vancomycin

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18
Q

Which bacteria cause dysentry?

A

C - Campylobacter
E - E. coli
S - Shigella
S - Salmonella

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19
Q

What factors are essential to refer to in the history for GI infections?

A

Onset/duration
Characteristics of stool
Food/drink
Travel
Immune status
Unwell contacts
Hobbies + fresh water
Animal contact
Medications

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20
Q

What are the indications for testing in GI infections

A

Severe illness: signs of hypovolemia, severe abdo pain, hospitalization
Bloody diarrhoea+ mucus
High-risk host: Age ≥70 years, immunocompromising condition , IBD , pregnancy
Symptoms persisting for more than one week
Public health concerns (eg, diarrhoeal illness in food handlers, HCW, individuals in day care centers)

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21
Q

What can be tested in a stool sample?

A

Microscopy
Culture
Multi-pathogen molecular panels (GE PCR panel)
Ova, cysts and parasites x3
Toxin detection (C difficile)

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22
Q

What is Acute Cholecystitis?

A

Gallbladder inflammation caused by cystic duct obstruction by gall stones

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23
Q

What are the symptoms of acute cholecystitis?

A

Right upper quadrant or epigastric pain, fever and leukocytosis

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24
Q

What is the diagnostic test for acute cholecystitis?

A

USS

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25
Q

What is the treatment for acute cholecystitis?

A

IV fluids, analgesia and antibiotics
Surgery: cholecystectomy

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26
Q

What is ascending cholangitis?

A

Obstruction of the common bile duct resulting in inflammation

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27
Q

What are the symptoms of ascending cholangitis?

A

Charcot’s triad: Fever, abdominal pain and jaundice

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28
Q

What is the management of ascending cholangitis?

A

Prompt admission + IV antibiotics
ERCP (Endoscopic retrograde cholangiopancreatography) - also used for diagnosis
Cholecystectomy

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29
Q

What is the most common cause of upper GI bleeding?

A

Peptic ulcer (50%)

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30
Q

what is the Glasgow-Blatchford score?

A

A scoring method to decide whether a patient presenting with upper GI bleeding should be admitted or sent home.

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31
Q

What factors are considered in the Glasgow-blatchford score?

A
  • Systolic blood pressure
  • Blood urea
  • Haemoglobin
  • Pulse ≥ 100
  • Melaena (black, tarry stools due to blood)
  • Syncope
  • Hepatic disease
  • Cardaic failure
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32
Q

What are the two types of upper GI bleeding?

A

Variceal and Non-variceal bleeding

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33
Q

When is variceal bleeding suspected?

A

In patients with a history of liver disease or alcohol excess

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34
Q

What is the first line treatment for variceal bleeding?

A

Antibiotics and terlipressin (inhibits portal circulation) reduce mortality

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35
Q

What is the endoscopic treatment for variceal bleeding?

A

Band ligation (within 12 hours)

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36
Q

When is non-variceal bleeding suspected?

A

In patient with a history of peptic ulcers, using certain medications; NSAIDs, anticoagulation or antiplatelets

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37
Q

What is the first line treatment for non-variceal bleeding?

A

Consider proton pump inhibitors

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38
Q

What are the causes of intraluminal obstruction of the GI tract?

A

tumour - carcinoma, lymphoma block lumen
diaphragm disease - diaphragm-like membranes of mucosa and submucosa form in bowel lumen creating pinhole lumen and subsequent obstruction
meconium ileus - meconium = first stool produced by neonate, in meconium ileus it gets stuck and blocks the ileum
gallstone ileus - impacted gallstone blocks lumen of small instestine

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39
Q

What are the causes of intramural GI obstruction?

A

inflammatory - Crohn’s, diverticulitis
tumours
neural - Hirschsprung’s disease - occurs in babies when the nerve cells do not migrate all the way down to the distal colon/rectum –> immobile distal colon/rectum so can’t pass stool

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40
Q

What are the causes of extramural bowel obstruction?

A

adhesions
volvulus
tumour (peritoneal deposits)

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41
Q

Where does volvulus occur most often?

A

Sigmoid colon

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42
Q

What are the 2 types of oesophageal cancer?

A
  • adenocarcinoma - lower 1/3 oesophagus, associated with Barrett’s oesophagus
  • squamous cell carcinoma - upper 2/3 oesophagus, smoking + alcohol
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43
Q

What are the risk factors for oesophageal cancer?

A

male
older age
smoking
alcohol use (SCC)
Barrett’s oesophagus (AC)
GORD (AC)
hiatus hernia (AC)
FHx

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44
Q

where are the typical sites of oesophageal cancer metastasis?

A

perioesophageal lymph nodes, liver, lungs

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45
Q

What are the key presentations of oesophageal cancer?

A

usually presents at advanced stage
anaemia
weight loss
anorexia
melaena
haematemesis
odynophagia (progressive difficulty swallowing)

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46
Q

What are the risk factors/causes of gastric carcinoma?

A

H. pylori infection
smkoing
CDH-1 mutation –> 80% risk
FHx
pernicious anaemia (autoimmune chronic gastritis)

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47
Q

What are the key presentations of gastric carcinomas?

A

severe epigastric pain
anaemia
weight loss
fatigue
progressive dysphagia

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48
Q

what are the signs of gastric carcinoma metastases?

A

jaundice (liver mets), Krukenberg tumour (ovarian mets)

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49
Q

what are the investigations for gastric carcinoma?

A

gastroscopy + biopsy
CT/MRI for staging, PET to ID mets

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50
Q

What is the chemotherapy for gastric carcinoma?

A

ECF - epirubicin, cisplatin, fluorouracil

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51
Q

Which 2 inherited conditions massively increase the risk of colorectal polyps?

A

Familial adenomatous polyposis (FAP)
- autosomal dominant APC gene (tumour suppressor) mutation
- 95% risk of corectal polyps by 50

Hereditary non-polyposis colon cancer/Lynch syndrome
- autosomal dominant MSH-1 mutation = DNA mismatch for repair gene
- rapidly increases progression, adenoma –> adenocarcinoma

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52
Q

What are the risk factors for colorectal polyps/cancer?

A

familial inherited genetic disposition
adenomas/polyps
alcohol
smoking
ulcerative colitis

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53
Q

what are the key presentations of colorectal polyps/cancer?

A

mostly in distal colon –> LLq pain, bloody mucousy stools, tenesmus

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54
Q

What are the investigations for colorectal polyps/cancer?

A

FIT test
Colonoscopy + biopsy

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55
Q

What is dyspepsia?

A

indigestion –> early satiation, epigastric pain + reflux, extreme fullness

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56
Q

What is achalasia?

A

oesophageal dysmotility (impaired peristalsis), LOS fails to relax

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57
Q

what are the key presentations of achalasia?

A

non-progressive dysphagia (difficulty swallowing anything)
substernal pain
food regurgitation
aspiration pneumonia (food or liquid breathed into the airways)

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58
Q

What are the investigations for achalasia?

A

1st line = upper GI endoscopy
GS = oesophageal manometry
other = barium swallow (bird’s beak sign)

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59
Q

What is the treatment for achalasia?

A

only curative option = surgery (balloon stenting)
nitrates + nifedipine can help pre-surgery to relax the LOS

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60
Q

What does achalasia increase the risk of?

A

oesophageal squamous cell lung cancer

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61
Q

What is ischaemic colitis?

A

ischaemia of colonic arterial supply (inferior mesenteric artery); colon inflamed due to hypoperfusion

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62
Q

What are the risk factors for ischaemic colitis?

A

> 60 yrs old
female
clotting problems
high cholesterol
heart failure
previous abdominal surgery

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63
Q

what are the most common sites affected by ischaemic colitis?

A

splenic flexure, sigmoid colon + cecum (watershed areas between the two major arteries supplying the colon - SMA/IMA)

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64
Q

what are the key presentations of ischaemic colitis?

A

LLQ pain + bright red bloody stool
signs of hypovolemic shock (pallor, agitation, confusion)

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65
Q

What is the gold standard test for ischaemic colitis?

A

colonoscopy + biopsy

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66
Q

What are the treatments for ischaemic colitis?

A

IV fluid + antibiotics (prophylactic)
Surgery only treatment if becomes gangrenous

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67
Q

What is pseudomembranous colitis?

A

infection of the colon caused by clostridium difficile

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68
Q

what are the risk factors for pseudomembranous colitis?

A

antibiotic exposure
advanced age
hospitalisation or residence in a nursing home
exposure to infected family member
IBD
CKD
HIV

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69
Q

What is the pathophysiology of pseudomembranous colitis?

A

C. difficile bacteria produce toxins which cause an inflammatory response in the large intestine, leading to increased vascular permeability and pseudomembrane (raised yellow and white plaques on inflamed mucosa made up of neutrophil, fibrin, mucin and cellular debris) formation.

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70
Q

What are the key presentations of pseudomembranous colitis?

A

diarrhoea
abdominal pain
fever
abdominal tenderness
nausea + vomiting
abdominal distension
shock symptoms

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71
Q

What are the investigations for pseudomembranous colitis?

A

FBC, stool sample (FIT, PCR, immunoassay)
Abdo XR
Sigmoidoscopy/colonoscopy

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72
Q

What is the management for pseudomembranous colitis?

A

antibiotics (fidaxomicin, vancomycin, metronidazole)
supportive care

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73
Q

what is mesenteric ischaemia?

A

ischaemia of the small intestine
AMI = acute attack
CMI = longer lasting (month +)

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74
Q

What are the risk factors for mesenteric ischaemia?

A

Older age
low/high bp
Heart disease
High cholesterol
Smoking
Clotting problem
Inflammatory problems e.g. pancreatitis, diverticulitis

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75
Q

What are the key presentations for mesenteric ischaemia?

A

triad:
1. acute severe pain in the central/right iliac fossa
2. No abdo signs on exam
3. rapid hypovolemic shock

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76
Q

What are the investigations for mesenteric ischaemia?

A

FBC + ABG = persistent metabolic acidosis
CT angiogram

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77
Q

What is the treatment for mesenteric ischaemia?

A

Fluid resuscitation, antibiotics, IV heparin
infarcted bowel –> surgery

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78
Q

What are haemorrhoids?

A

Swollen veins around anus disrupt anal cushions causing prolapse of parts of the anal cushions through the anal passage

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79
Q

what is the classification of haemorrhoids?

A

1st degree: no prolapse
2nd: prolapse when straining and return on relaxing
3rd: prolapse when straining, do not return on relaxing, but can be pushed back
4th: prolapsed permanently

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80
Q

What are the risk factors for haemorrhoids?

A

constipation
anal sex
age 45-65
pregnancy
pathological pelvic lesions

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81
Q

What are the 2 types of haemorrhoid presentation?

A

Internal - originate above internal rectal plexus (dentate line), less painful as has decreased sensory supply
external - originate below dentate line, so painful patient can’t sit down

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82
Q

What are the key presentations of haemorrhoids?

A

bright red fresh PR bleeding + mucousy bloody stool
bulging pain
pruritis ani

83
Q

What are the investigations for haemorrhoids?

A

PR exam for external
protoscopy for internal

84
Q

What is the management for haemorrhoids?

A

topical treatments for symptomatic relief
scleropathy (injection of phenol oil)
rubber band ligation

85
Q

What is a perianal abscess?

A

Walled off collection of pus resulting from infection of the soft tissues around the anus

86
Q

What are the risk factors for perianal abscesses?

A

Anal sex
Crohn’s disease
male
hard stool
21-40 yrs old

87
Q

What are the key presentations of perianal abscesses?

A

Pus in stool
Constant pain and tenderness
Perianal swelling
Low-grade fever
Tachycardia

88
Q

What is the management for perianal abscesses?

A

surgical removal + drainage

89
Q

What is an anal fistula?

A

Abnormal connection under the skin between the anal canal to the skin of the buttocks.

90
Q

What is the aetiology of anal fistulae?

A

Most often form in a reaction to an anal gland that has developed a pus-filled infection (abscess).
The abscess discharges (toxic substances) which aid fistula formation as abscess grows.

91
Q

What are the risk factors for anal fistulae?

A

Anal abscess → 50% chance of developing fistula
Crohn’s disease
Chronic diarrhoea
Radiation treatment for rectal cancer

92
Q

What are the key presentations of anal fistulae?

A

Pain + swelling
Fever
Malaise
Fatigue
Perianal redness, soreness, puruitis
Pus drainage
Bloody/mucousy discharge

93
Q

What are the investigations for anal fistulae?

A

Fistula probe (dye used to identify internal opening)
Anoscope
Imaging e.g. USS, MRI

94
Q

What is the management for anal fistulae?

A

Surgical removal + drainage
- Fistulotomy
- Fill the internal opening with special glue or plug
- Reconstructive surgery
- Seton placement (rubber band progressively tightened in fistula)
antibiotics if infected

95
Q

What is an anal fissure?

A

tear in anal skin lining below dentate line

96
Q

how common are anal fissures?

A

occur in 1 in 350 people

97
Q

what are the risk factors for anal fissures?

A

Hard stool/constipation
Pregnancy
Opiate analgesia (associated with constipation)
Crohn’s
Trauma such as childbirth

98
Q

What are the key presentations for anal fissures?

A

Very severe pain on defecation
Tearing sensation on passing stool
Fresh blood in stool
Anal spasm
Puruitis ani

99
Q

What are the treatment options for anal fissures?

A

Stool softening; increase fibre + fluid intake
Topical creams e.g. lidocaine ointment
Surgery

100
Q

What are pilonidal sinuses/abscesses?

A

Hair follicles get stuck in natal cleft (bum crack) which can form small tracts (sinuses) or get infected (abscesses)

101
Q

What are the risk factors for pilonidal sinuses/abscesses?

A

16-40 yrs old
Male
FHx
Stiff hair + hirsutism

102
Q

What is the pathophysiology of pilonidal sinuses/abscesses?

A

Broken hair is driven into the skin of the natal cleft by the rolling action of the buttocks.
This provokes a foreign body-type reaction and chronic inflammation results in a sinus..

103
Q

What is the presentation of a pilonidal sinus/abscess?

A

swollen, pus filled, odorous abscess on natal cleft

104
Q

What is the treatment for pilonidal sinuses/abscesses?

A

hair removal + local hygiene
Antibiotic therapy with infected abscess

105
Q

What are the symptoms of coeliac disease?

A

often asymptomatic
failure to thrive in young children
Diarrhoea
Steattorhoea
Fatigue
Weight loss
Mouth ulcers
Anaemia secondary to iron B12 or folate deficiency
Dermatitis herpetiformis (itchy, blistering abdominal rash)

106
Q

What is the gluten challenge?

A

6 week gluten containing diet
1g/day - 4 slices bread/day

for diagnosis of coeliac

107
Q

What are the investigations for coeliac disease?

A

serology: anti-ttG, ↑total IgA
duodenal biopsy; crypt hyperplasia + villous atrophy + epithelial lymphocyte infiltration

108
Q

What are the risk factors for coeliac disease?

A

Hashimoto’s thyroiditis
T1DM
Thyroid disease
PBC
PBS
Autoimmune hepatitis
Genetic

109
Q

What is the management for coeliac disease?

A

lifelong gluten-free diet = essentially curative
+ replace vitamins/mineral deficiency

110
Q

What are the complications of coeliac disease if left untreated?

A

vitamin deficiency, anaemia, osteoprosis, ulcerative jejunitis, enteropathy-associated T-cell lymphoma of the intestine, Non-Hodgkin Lymphoma, small bowel adenocarcinoma

111
Q

What are the Trueglove and Witts criteria?

A

> 6 bloody stools/day
tachycardia >90bpm
pyrexia >38oC
Hb >10.5 g/dL
ESR >30mm/h

112
Q

What is Crohn’s disease?

A

Transmural autoimmune inflammation affecting the whole GI tract, especially terminal ileum + proximal colon (usually rectum spared)

associated with skip lesions on endoscopy

113
Q

What is the aetiology of Crohn’s disease?

A

NOD-2 mutations + environmental; bacteria cause immune mediated response (T cells) → TNFa, IL-1, IL-6

114
Q

What are the risk factors for CD?

A

Smoking
Jewish
FHx

115
Q

What is the pathophysiology of Crohn’s?

A

Initial lesion starts as an inflammatory infiltrate around intestinal crypts that subsequently develops into ulceration of the superficial mucosa. This progresses to involve all layers of the intestinal wall and the mesentery and regional lymph nodes.

116
Q

What are the presentations of CD?

A

Pain in Right lower quadrant
Malabsorption (as SI affected, colon = only H2O absorbed)
+
B12/folate/iron deficiencies
Gallstones + kidney stones
Watery diarrhoea
Failure to thrive
Weight loss
Primary sclerosing cholangitis seen in 75% of CD patients
Extra GI: aphthous mouth ulcers, uveitis/episcleritis, erythema nodosum/pyoderma gangrenosum, spondyloarthritis (spine ache)

117
Q

What are the investigations for CD?

A

pANCA -ve (may be ASCA +ve)
Faecal calprotectin ↑
Biopsy = transmural inflammation with non-caseating granulomas
Endoscopy - skip lesions, cobblestoned appearance of GI tract, string sign (narrowing of GI tract)

118
Q

What are the characteristic features of Crohn’s seen on endoscopy?

A

skip lesions
cobblestone appearance
string sign (narrowed GI tract)

119
Q

What is the management for CD?

A

For flares: sulfasalazine + prednisolone
For remission: azathioprine + methotrexate
biologics : anti-TNFa: Infliximab, IL 12 + 23 inhibitor: Ustekenumab
* Surgery is not curative as entire bowel can be affected

120
Q

What are the complications of CD?

A

fistula, strictures, abscesses, small bowel obstruction

121
Q

What is Ulcerative Colitis?

A

Autoimmune colitis that presents with continuous inflammation only affecting the superficial mucosa and limited to the colon and rectum.

122
Q

What is the aetiology of Ulcerative Colitis?

A

Associated with HLAB27 gene + pANCA

123
Q

What are the risk factors of UC?

A

FHx
Jewish
Smoking = protective (reduces inflammation)

124
Q

What are the presentations of UC?

A

Pain in LLQ + tenesmus (rectal defecation pain)
Bloody mucosal watery diarrhoea
Extraintestinal signs: uveitis/episcleritis, pyoderma gangrenosum,/erythema nodosum, spondyloarthropathy, primary sclerosing cholangitis (90% UC pts have PSC)

125
Q

What are the investigations for UC?

A

pANCA +ve
Faecal calprotectin ↑ (non-specific)
Biopsy = mucosal inflammation with crypt hyperplasia
Colonoscopy = continuous, “lead pipe” sign (loss of haustrations)
Severity of flares are assessed by Trueglove + Witts scoring (mild/moderate/severe)

126
Q

What are the characteristic signs of UC seen on colonoscopy?

A

continuous lesions
pseudo-polyps
crypt abcesses
lead pipe sign (loss of haustrations)

127
Q

What is the management for UC?

A

Flares = sulfasalazine + prednisolone
For remission = azathioprine, methotrexate, cyclosporin (calcineurin inhibitor)
biologics : anti TNFa - Infliximab
Surgery (total/partial colectomy) → curative

128
Q

What is coeliac disease?

A

Autoimmune T4 hypersensitivity to gluten which causes inflammation in the small bowel

129
Q

What is the aetiology of coeliac disease?

A

HLADQ2 (90%) + HLA-DQ8

130
Q

What is the pathophysiology of coeliac disease?

A

Auto-antibodies are created in response to gluten exposure that target the epithelial cells of the intestine and lead to inflammation.
Anti-tissue transglutaminase (anti-TTG) and anti-endomysial (anti-EMA) are IgA antibodies related to disease activity and rise with more active disease.
Inflammation affects the small bowel, particularly the jejunum and causes atrophy of the intestinal villi which usually absorb nutrients from food passing through the SI. The inflammation causes malabsorption of nutrients and the symptoms of the disease.

131
Q

What is a functional gut disorder?

A

Chronic GI symptoms in the absence of organic disease to explain the symptoms
also termed “disorders of gut-brain interaction”

132
Q

What are the 2 most commonly recognised functional gut disorders?

A

IBS (bowel)
Functional dyspepsia (stomach)

133
Q

What are the indications of functional gut disorders?

A

visceral hypersensitivity
motility disturbances
altered mucosal and immune function
altered CNS processing
altered gut microbiota

134
Q

What is dyspepsia?

A

a symptoms or combination of symptoms which indicate an upper GI problem,
Typical symptoms: epigastric pain, early satiety, post-prandial fullness, bloating, nausea, burping, discomfort in upper abdomen

135
Q

What are the alarm features with functional gut disorders?

A

age >45 yrs
short hx of symptoms
documented unintentional weight loss
nocturnal symptoms
family history of GI cancer/IBD
GI bleeding
palpable abdominal mass or lymphadenopathy
evidence of iron deficiency anaemia on blood testing
evidence of inflammation on blood/stool testing

136
Q

What does a raised faecal calprotectin indicate?

A

Increased numbers of white blood cells in bloodstream which cross into gut lumen and release calprotectin –> sign of inflammation

137
Q

What is IBS?

A

Irritable Bowel Syndrome = functional chronic bowel disorder which can be characterised by constipation, diarrhoea or mixed symptoms

138
Q

What is the epidemiology of IBS?

A

affects around 17 % of adults in the UK
higher prevalence in women

139
Q

what is the aetiology of IBS?

A

thought to be multifactorial with a variety of possible causes which include:
- food poisoning/gastroenteritis triggers
- stress
- irregular eating or abnormal diet
- certain medications
- interaction between the brain and gut

140
Q

What are the risk factors for IBS?

A

Physical + sexual abuse
PTSD
Age <50 yrs
Female
Previous enteric infection
FHx
family/job stress

141
Q

What are the ABC symptoms which indicate IBS consideration in diagnosis?

A

Abdominal pain/discomfort
Bloating
Change in bowel habit

142
Q

What are the key presentations of IBS?

A

Abdo pain + bloating (relieved by defecation)
Altered stool form + frequency

143
Q

What are the investigations for IBS?

A

Diagnosis is by ruling out other conditions e.g. coeliac which is done through serology, faecal calprotectin, ESR/CRP/blood cultures

144
Q

What are the differentials for IBS?

A

coeliac, IBD, colorectal cancer, ovarian cancer

145
Q

What is the management for IBS?

A

Conservative = patient education (diet changes) + reassurance
Moderate = IBS-C → laxatives (e.g. senna), IBS-D → antimotility drug (loperamide)
Severe = TCA (tricyclic antidepressants e.g. amitriptyline) + consider CBT/GI referral

146
Q

What is appendicitis?

A

Inflammation of the appendix, usually due to lumen obstruction. Surgical emergency

147
Q

What is the peak age for appendicitis?

A

10-20 years

148
Q

What are the causes of appendicitis?

A

Faecolith (hard solidified faeces)
Lymphoid hyperplasia (seen in teens, peyer’s patches), filarial worms

149
Q

What are the risk factors for appendicitis?

A

Low dietary fibre
Good personal hygiene (due to reduced exposure/imbalance of GI microbial flora which can lead to a modified response to viral infection and trigger appendicitis
Smoking

150
Q

What is the pathology of appendicitis?

A

Blockage is typically infected with E.coli and as pressure inside the appendix increases, risk of rupture is increased (SBP)

151
Q

What are the key presentations of appendicitis?

A

Umbilical pain which localises to McBurney’s point + rebound tenderness of abdominal guarding
Pyrexia

152
Q

What are the clinical signs of appendicitis?

A

Rovsing’s sign (pressure on RLQ causes pain in LLQ)
Obturator sign (discomfort felt on slow internal movement of hip joint while right knee is flexed)
PSOAS sign (pain when lying on left side, extending right leg)

153
Q

What are the investigations for appendicitis?

A

FBC, CRP
CT abdomen + pelvis
Pregnancy test to rule out ectopic pregnancy, urinalysis

154
Q

What is the management for appendicitis?

A

Antibiotics then appendectomy (laparoscopic)
Drainage of abscesses as systemic antibiotics will be ineffective, follow with intra-abscess antibiotics

155
Q

What is gastritis?

A

Inflammation of the gastric mucosa

156
Q

What is the aetiology of gastritis?

A

Most commonly due to H. pylori infection
Can also be caused by NSAIDs, alcohol misuse, autoimmune (related to pernicious anaemia + anti-IF antibiotics), mucoid ischaemia, reflux of bile salts into stomach, campylobacter (Guillain Barre)

157
Q

What are the risk factors for gastritis?

A

NSAID use
Alcohol use/abuse
Previous gastric surgery
Autoimmune disease

158
Q

What is the pathophysiology of gastritis?

A

Severe inflammatory response to infection → gastric mucosa degradation, increased mucosal permeability and gastric epithelial cytotoxicity

159
Q

What are the key presentations of gastritis?

A

Epigastric pain with diarrhoea
N+V
Indigestion

160
Q

What are the investigations for gastritis?

A

If H. pylori suspected → stool antigen test/urea breath test
Endoscopy + biopsy

161
Q

What is the management for gastritis?

A

H. pylori = triple therapy (CAP - clarithromycin, amoxicillin, PPI)

162
Q

What is the major complication of H. pylori gastritis?

A

Peptic ulcer disease

163
Q

What is small bowel obstruction?

A

A form of intestinal failure where the gut is unable to absorb the necessary water, macronutrients (carbohydrates, proteins, fats), micronutrients, and electrolytes sufficient to sustain life.

164
Q

What is the aetiology of small bowel obstruction?

A

Adhesions (50%)
Hernia (15%) - groin (inguinal/femoral)
Cancer (10%)

165
Q

What are the key presentations of SBO?

A

Colic (sharp cramping pain)
Bilious vomiting (green vomit)
Hernia orifices
bloating/distension
Abdominal tenderness/peritonism

166
Q

What are the investigations for SBO?

A

FBC, U+Es, Lactate, C-reactive protein
CT scan

167
Q

What is the management for SBO?

A

Analgesia
IV fluids (for resuscitation)
Nasogastric tube, antiemetics (alleviate nausea)
Nasogastric tube, urinary catheter (assess fluid balance)
Operation (key hole or open)

168
Q

What is GORD?

A

Gastroesophageal reflux disease = reflux of gastric contents into the oesophagus resulting in symptoms and/or complications

169
Q

What percentage of people living in developed countries are affected by GORD?

A

10-20%

170
Q

What is the pathophysiology of GORD?

A

Abnormally frequent occurrences of transient lower oesophageal sphincter relaxation causing reflux of gastric contents into the oesophagus.
This causes damage to the oesophageal mucosa of varying severity depending on the duration of contact.

171
Q

What are the risk factors for GORD?

A

FHx
Older age
Hiatus hernia
obesity
Pregnancy
Drugs e.g. antimuscarinics
Scleroderma (scarring of lower oesophageal sphincter)

172
Q

What are the key presentations for GORD?

A

Heartburn
Regurgitation
*symptoms worse lying down as acid can reflux more easily
Dysphagia
Chronic cough + nocturnal asthma
bloating /early satiety

173
Q

What are the investigations for GORD?

A

Clinical diagnosis if no red flags
Red flags = dysphagia, haematemesis, weight loss
→ endoscopy (oesophagitis or Barrett’s oesophagus), oesophageal manometry (measures LOS pressure + gastric acid pH)

174
Q

What is the management for GORD?

A

Conservative = lifestyle changes (smaller meals, 3+ hrs before bed)
PPI, antacids, alginates (gaviscon)
Last resort = surgical tightening of LOS (Nissen fundoplication = wrapping of fundus around LOS externally to increase pressure)

175
Q

What are the potential complications of GORD?

A

Oesophageal sphincters: usually 60+ patients, progressively worsening dysphagia, Tx: oesophageal dilation + PPI
Barrett’s Oesophagus: 10% GORD patients develop, always involves hiatal hernia, metaplasia of oesophageal lining (SSNKE → simple columnar), ↑risk of adenocarcinoma

176
Q

What is a Mallory Weiss Tear?

A

Linear lower oesophageal mucosal tear due to sudden increase in intra-abdominal pressure

177
Q

What are the risk factors for Mallory Weiss tears?

A

Alcohol
Chronic cough
Bulimia
Hyperemesis gravidarum (pregnancy complication of severe N+V, weight loss, dehydration
No hx of liver disease or pulmonary hypertension (more likely to be oesophageal varices rupture)

178
Q

What are the key presentations for Mallory Weiss tears?

A

Haematemesis (after retching/vomiting Hx)
+ hypotensive if severe - often mild therefore this is unlikely

179
Q

What is the gold standard investigation for a Mallory Weiss tear?

A

oesophagogastroduodenoscopy

180
Q

What is the management for a Mallory Weiss tear?

A

Most spontaneously heal within 24hrs (80-90%)
Supportive treatment

181
Q

What is the management for a Mallory Weiss tear?

A

Most spontaneously heal within 24hrs (80-90%)
Supportive treatment

182
Q

What is PUD?

A

Peptic ulcer disease = break in the mucosal lining of the stomach or duodenum more than 5mm in diameter with depth to the submucosa
more commonly duodenal than gastric

183
Q

What are the risk factors for PUD?

A

Chronic use of NSAIDs
H. pylori infection
Smoking
Old age
FHx
Zollinger-ellison syndrome

184
Q

What is Zollinger Ellison Syndrome?

A

A digestive disorder where gastrin-secreting tumours cause this triad of symptoms: pancreatic tumours, gastric acid hypersecretion, widespread peptic ulcers

185
Q

What is the pathophysiology of PUD?

A

The ulcers result from an imbalance between factors promoting mucosal damage and those mechanisms promoting gastroduodenal defence (prostaglandins, mucus, bicarbonate, mucosal blood flow).

186
Q

What are the key presentations of PUD?

A

Epigastric pain (gastric PUD - worse on eating and better between meals, duodenal PUD - worse between meals and better with food)
Gastric PUD - typically weight loss, Duodenal PUD - typically weight gain
‘Pointing sign’ (patients can show the site of pain with one finger)

187
Q

What are the investigations for PUD?

A

Non invasive tests if no red flags (55+, haematemesis/melaena, anaemia, dysphagia): C-urea breath test, stool antigen test
If red flags - urgent endoscopy + biopsy

188
Q

What is the treatment for PUD?

A

Stop NSAIDs, if H. pylori +ve —> triple therapy (CAP - clarithromycin, amoxicillin, PPi)

189
Q

What are the potential complications of PUD?

A

Complications: bleeding, ruptured left gastric artery or gastroduodenal artery (more common)

190
Q

What is diverticular disease?

A

Outpouching of colonic mucosa
Diverticulum = outpouching at perforating artery sites
Diverticulosis = asymptomatic outpouching
Diverticular disease = symptomatic outpouch
Diverticulitis = inflammation of outpouch (infection)

191
Q

What are the risk factors of diverticular disease?

A

> 50 yrs
Low dietary fibre
Diet high in salt, meat, sugar
Obesity (BMI>30)
NSAID and opioid use
smoking

192
Q

What is the pathophysiology of diverticular disease?

A

A low fibre diet increases intestinal transit time and decreases stool volume resulting in increased intraluminal pressure and colonic segmentation, which predispose to diverticular formation. Precise mechanism is not fully understood.

193
Q

What are the key presentations of diverticular disease?

A

LLQ pain, guarding, tenderness
Constipation
Fresh rectal bleeding
Leukocytosis
Fever
bloating

194
Q

What is the gold standard investigation for diverticular disease?

A

CT abdo pelvis

195
Q

What is the management for diverticular disease?

A

Diverticulosis = nothing, watch and wait
Diverticular disease = bulk forming laxatives, surgery (gold standard)
Diverticulitis = antibiotics (co-amoxiclav) and paracetamol. IV fluid + liquid food, rarely surgery

196
Q

What is intestinal obstruction?

A

Mechanical bowel obstruction
Can be partial (allows passage of flatus and occasionally stool - not a surgical emergency and may resolve itself) or complete (emergency situation in which the lumen of the intestine is completely blocked resulting in failure to pass flatus and stool - generally associated with peritonitis - will not respond to non-operative treatment in most cases)

197
Q

What is the aetiology of partial intestinal obstruction?

A

Adhesions
Crohn’s
Strangulating hernias
Malignancy

198
Q

What is the aetiology of complete bowel obstruction?

A

Malignancy
Volvulus
Intussusception (bowel telescopes in on itself)

199
Q

What are the key presentations of partial intestinal obstruction?

A

First vomiting, then constipation
Mild abdominal distension + pain
Tinkling bowel sounds (hypersonant bowels on percussion in both SBO/LBO

200
Q

What are the key presentations of complete intestinal obstruction?

A

First constipation, then vomiting
Gross distension + pain
hyperactive, then normal, then absent bowel sounds

201
Q

What are the investigations for intestinal obstruction?

A

XR (dilated bowel loops + transluminal fluid-gas shadows *LBO → coffee bean sign (if sigmoid volvulus)
CT abdomen = GS

202
Q

What is the management for intestinal obstruction?

A

Fluid resuscitation
Nasogastric tube
Antiemetics + analgesia
Antibiotics
Surgery last resort

203
Q

What is Hirschsprung disease?

A

congenital malformation where the child is bron without a colonic nerve supply –> inability to pass stool often resulting in lower bowel obstuction

204
Q

What is pseudoobstruction of the bowel?

A

no mechanical obstruction, often a result of post-operative state (e.g. opiate induced paralytic ileus)

Phase 2A (18 decks)

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