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GI Flashcards

1
Q

What is the pathophysiology of coeliac disease?

A
  • Autoantibodies created in response to gluten
  • These target epithelial cells of the small intestine (particularly the jejunum) -> inflammation
  • Inflammation results in atrophy of intestinal villi -> malabsorption
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2
Q

What 3 autoantibodies are related to coeliac disease?

A
  • Anti-tissue transglutaminase antibodies (anti-TTG)
  • Anti-endomysial antibodies (Anti-EMA)
  • Anti-deamidated gliadin peptide antibodies (anti-DGP)
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3
Q

A patient presents with a itchy blistering rash on their abdomen. What is this called? What is it be caused by?

A
  • Dermatitis herpetiformis
  • Caused by coeliac disease
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4
Q

What neurological symptoms can coeliac disease present with?

A
  • Peripheral neuropathy
  • Cerebellar ataxia
  • Epilepsy
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5
Q

What are differentiating features of Crohn’s disease?

A

Crows NESTS

  • No blood or mucus (PR can still occur in few cases)
  • Entire GI affected
  • Skip lesions on endoscopy
  • Terminal ileum most effected and Transmural inflammation (full thickness)
  • Smoking is a risk factor

Crohns is also associated with strictures and fistulas

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6
Q

What are differentiating features of UC?

A

You see (UC) CLOSEUP

  • Continuous inflammation
  • Limited to the colon and rectum
  • Only superficial mucosa affected
  • Smoking may be protective
  • Excrete blood and mucus
  • Use aminosalicylates
  • Primary sclerosis cholangitis
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7
Q

What are the first and second line blood tests for coeliac disease? What do you do if these are positive?

A

First line:
- Total immunoglobulin A levels
- Anti-tissue transglutaminase antibodies (anti-TTG)

Second line:
- Anti-endomysial antibodies (anti-EMA)

Patients with a positive antibody test are referred to a gastroenterologist for endoscopy and jejunal biopsy

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8
Q

What are the first and second line options for inducing remission in mild to moderate UC?

A
  • First line -> Aminosalicylate (mesalazine)
  • Secondline -> corticosteriods (pred)
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9
Q

How do you induce remission in severe UC?

A
  • First line -> IV steroids (hydrocortisone)
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10
Q

What are the first and second line options for maintaining remission in UC?

A
  • First line -> aminosalicylate (mesalazine)
  • Second line -> azathioprine/mercaptopurine
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11
Q

How do you induce remission in Crohn’s disease?

A
  • First line -> oral/IV steriods
  • Enteral nutrition
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12
Q

What are the first and second line options for maintaining remission in Crohn’s disease?

A
  • First line -> azathioprine/mercaptopurine
  • Second line -> methotrexate
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13
Q

Which are the more common peptic ulcers?

A

Duodenal ulcers

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14
Q

What drugs increase the risk of bleeding from a peptic ulcer?

A
  • NSAIDs
  • Aspirin
  • Anticoagulants
  • Steroids
  • SSRIs
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15
Q

How do gastric and duodenal ulcers present differently?

A

Gastric:
- Eating worsens pain
- Lose weight due to fear of pain when eating

Duodenal:
- Pain improves after eating and worsens after 2-3 hours
- Weight is stable or increases

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16
Q

What are signs of an upper GI bleed?

A
  • Haematemesis
  • Coffee ground vomit
  • Melaena
  • Fall in Hb on FBC
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17
Q

How can H pylori be diagnosed on endoscopy?

A

Rapid urease test (CLO test)

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18
Q

What are the core management aspects of treating peptic ulcers?

A
  • Stop NSAIDs
  • Treat H pylori
  • PPI
  • Repeat endoscopy in 4-8 wks to ensure ulcer heals
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19
Q

What are complications of peptic ulcers?

A
  • Bleeding
  • Perforation -> acute abdo pain and peritonitis
  • Scarring and strictures -> gastric outlet obstruction
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20
Q

How does gastric outlet obstruction present? What is the management?

A
  • Early fullness
  • Abdominal distention
  • Vomiting after eating

Treated with balloon dilatation during endoscopy/surgery

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21
Q

What are possible causes of an upper GI bleed? Which is the most common?

A
  • Peptic ulcers (most common)
  • Mallory-Weiss tear
  • Oesophageal varices
  • Stomach cancers
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22
Q

What score is used at initial presentation of a suspected upper GI bleed? What does it indicate? What score is significant?

A
  • Glasgow-Blatchford Bleeding score
  • Estimates the risk of the patient having an upper GI bleed
  • A score above 0 = high risk for an upper GI bleed
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23
Q

Why do patients with an upper GI bleed get high blood urea?

A
  • Urea is one of the break down products of blood
  • It is absorbed into the intestines causing a rise in blood urea
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24
Q

When is the Rockall Score used?

A
  • Upper GI bleed
  • Used after endoscopy to estimate the risk of rebleeding and mortality
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25
Q

What is the initial management of an upper GI bleed?

A

ABATED mnemonic

  • ABCDE
  • Bloods
  • Access (2 x large bore cannula)
  • Transfusions
  • Endoscopy (within 24 hrs)
  • Drugs (stop anticoagulants and NSAIDs)
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26
Q

What additional steps are important in the management of an upper GI bleed due to varices?

A
  • Terlipressin
  • Broad spec antibiotics
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27
Q

When treating a patient with an upper GI bleed what features determine the type of transfusion?

A
  • Massive bleed -> FFP (blood, platelets and clotting factors)
  • Active bleeding + thrombocytopenia -> platlets
  • Active bleeding + taking warfarin -> prothrombin complex concentrate
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28
Q

According to NICE, what is required to diagnose IBS?

A
  1. 6 months of abdominal pain
  2. At least one of:
    - Pain relieved by opening bowels
    - Bowel habit abnormality
    - Stool abnormalities
  3. At least two of:
    - Straining
    - Bloating
    - Worse after eating
    - Passing mucus
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29
Q

What is dyspepsia?

A

An unspecific term used to describe indigestion

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30
Q

What is a hiatus hernia?

A

Herniation of the stomach through the diaphragm

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31
Q

What are the 4 types of hiatus hernia?

A
  • Type 1 - slidling
  • Type 2 - rolling
  • Type 3 - combination of both
  • Type 4 - large opening with additional abdominal organs entering the thorax
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32
Q

A patient presents with dyspepsia, how should you manage them?

A
  • Exclude red flags
  • Address possible triggers
  • Offer 1 month trial of PPI
  • Consider H pylori testing
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33
Q

What are the investigations for H pylori?

A
  • Stool antigen test
  • Urea breath test
  • H pylori antibody test
  • Rapid urease test (CLO test) during endoscopy
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34
Q

What is H pylori (specifically)?

A

Gram -ve aerobic bacteria

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35
Q

How does H pylori cause gastric mucosal damage?

A
  • Produces ammonium hydroxide -> neutralises stomach acid
  • It also produces toxins
  • Together the ammonia and toxins damage the epithelial lining resulting in gastritis and ulcers
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36
Q

What happens in Barrett’s oesophagus? What is this process called?

A
  • Oesophageal endothelium changes from squamous to columnar
  • Metaplasia
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37
Q

What is the difference between dysplasia and metaplasia?

A
  • Metaplasia = change in the type of cell
  • Dysplasia = presence of abnormal cells
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38
Q

What is Barrett’s oesophagus a significant risk factor for?

A

Oesophageal adenocarcinoma

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39
Q

What’s the management of Barrett’s oesophagus?

A
  • Endoscopic monitoring for progression to adenocarcinoma
  • PPI
  • Endoscopic ablation (destroying abnormal columnar epithelial cells)
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40
Q

What is Zollinger-Ellison syndrome?

A
  • Rare condition where a duodenal or pancreatic tumour secretes excessive gastrin
  • Gastrin is a hormone that stimulates acid production
  • Results in severe dyspepsia, diarrhoea and peptic ulcers
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41
Q

What’s are the two most common types of oesophageal cancer? How do they differ? Include RF for each

A
  1. Adenocarcinoma
    - Most common
    - Lower 1/3 of oesophagus
    - RF - GORD, BO, smoking, obesity
  2. Squamous cell carcinoma
    - Most common in developing world
    - Upper 2/3 of oesophagus
    - RF - smoking, alcohol. achalasia
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42
Q

How do you investigate + diagnose oesophageal cancer?

A
  • Endoscopy with biopsy - diagnosis
  • Endoscopic US - loco regional staging
  • CT-TAP - initial staging
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43
Q

What is the management of oesophageal cancer?

A
  • Surgical resection where possible - Ivor-Lewis type oesophagectomy is most common procedure
  • Adjuvant chemo
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44
Q

What are RF for gastric cancer?

A
  • Age >75
  • M>F
  • H Pylori
  • Atrophic gastritis
  • Diet - salt, nitrates
  • Smoking
  • Blood group A
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45
Q

How do you investigate gastric cancer?

A
  • OGD with biopsy - diagnosis, signet ring cells may be seen (higher numbers = worse prognosis)
  • CT-TAP - staging
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46
Q

What is the management of gastric cancer?

A
  • Surgery - endoscopic mucosal resection, partial/total gastrectomy
  • Chemo
47
Q

How does appendicitis present?

A

Central abdominal pain that localises at McBurney’s point

48
Q

Where is McBurney’s point?

A

1/3rd the distance from the anterior superior iliac spine to the umbilicus

49
Q

What examination features indicate appendicitis? What suggests peritonitis indicating rupture?

A
  • Rovsing’s sign
  • Guarding

Peritonitis:
- Rebound tenderness in the RIF
- Percussion tenderness

50
Q

What conditions are risk factors for bowel cancer?

A
  • IBD
  • Familial adenomatous polyposis (FAP)
  • Hereditary nonpolyposis colorectal cancer (also called Lynch syndrome)
51
Q

What is familial adenomatous polyposis?

A
  • AD
  • Malfunctioning of tumour suppressor genes that results in polyps (adenomas) developing along the large intestine
  • These have the potential to become cancerous (normally <40 years)
  • Patients have their entire large intestine removed prophylactically
52
Q

What is Lynch syndrome?

A
  • Hereditary nonployposis colorectal cancer
  • AD
  • Increases patients risk of a number of cancers - particularly colorectal cancer
53
Q

What does a FIT test look for?

A

The amount of Hb in the stool

54
Q

What is the bowel cancer screening program in England?

A
  • Adults are 60-74 sent a FIT test every 2 years
  • +ve result -> colonoscopy
55
Q

What is the tumour marker for bowel cancer? How is it used?

A
  • Carcinoembryonic antigen (CEA)
  • Used for predicting relapse in patients previously treated for bowel cancer
56
Q

What investigations are used for bowel cancer? When are they indicated?

A
  • Colonoscopy - gold standard
  • Sigmoidoscopy - rectal bleeding
  • CT colonography - CT scan w bowel prep, considered in pts less fit for a colonoscopy
  • Staging CT scan (CT TAP) - metastasis, excluding other cancers if vague symptoms
57
Q

How can you define constipation?

A

Defecation that is unsatisfactory due to infrequent stools (<3 times weekly), difficult stool passage, seemingly incomplete defecation

58
Q

What is the management of constipation?

A
  • Exclude secondary causes of constipation
  • Lifestyle measures - fibre, hydration, activity levels
  • Oral laxatives:
    1. Bulk forming (1st line) e.g. ispaghula
    2. Add or switch to an osmotic e.g. macrogol
    3. If stools are soft but difficult to pass/inadequate emptying add a stimulant e.g. Senna

Advise gradually reduce and stop laxatives once they are producing soft, formed stool without straining >3 times/week

59
Q

When should you not prescribe bulk forming laxatives?

A
  • If opioid induced constipation
  • Offer osmotic + stimulant
60
Q

How do you manage chronic constipation that has not responded to the usual management?

A
  • If at least 2 laxatives (diff classes) have been tried at the highest doses for 6 months, consider tx with prucalopride
  • Its a serotonin agonist that stimulates GI motility
61
Q

How do you manage facial impaction?

A
  1. Hard stools - oral macrogol
  2. Soft stools/no response ^ - oral stimulant laxative
  3. If slow/inadequate response consider:
    - Suppository - glycerol +/- bisacodyl (hard stool), bisacodyl (soft stool)
    - Mini enema - docusate (softener + stimulant), sodium citrate (osmotic)
  4. If still inadequate response:
    - Sodium phosphate/arachis oil retention enema
62
Q

What are secondary causes of constipation?

A

VITAMIN C DEF
1. Vascular
2. Inflammatory/infective
3. Trauma - anal fissures, strictures, haemorrhoids, spinal cord injury
4. Autoimmune - DM, hypothyroid, hyperparathyroidism
5. Metabolic - DM
6. Iatrogenic - drugs
7. Neoplastic - obstructive mass, spinal cord tumours
8. Congenital - hirsprungs’s disease
9. Degenerative - PD, MS
10. Endocrine/envirnoment - hypercalcaemia, Hypermagnesaemia, hypokalaemia, uraemia
11. Functional - IBS

63
Q

What is a diverticulum?

A

A pouch/pocket in the bowel wall (range from 0.5-1cm)

64
Q

What is diverticulosis?

A

The presence of diverticula (without inflammation or infection)

65
Q

What is diverticular disease?

A

When pts experience symptoms of diverticulosis?

66
Q

What is diverticulitis?

A

Inflammation and infection of diverticula

67
Q

How do diverticula form?

A
  • The wall of the large intestine contains a layer of muscle called the circular muscle
  • The points where this muscle layer is penetrated by blood vessels are areas of weakness
  • Increased pressure inside the lumen over time, can cause a gap to form in these areas of the circular muscle
  • These gaps allow the mucosa to herniate through the muscle layer and form diverticula
68
Q

Why do diverticula not form in the rectum?

A
  • It has an outer longitudinal muscle layer that completely surrounds the diameter of the rectum, adding extra support
  • Longitudinal muscle is present in the rest of the colon (tenure coli) by it doesn’t surround the full diameter and the areas that aren’t covered are vulnerable
69
Q

What are RF for diverticulosis?

A
  • Increased age
  • Low fibre diet
  • Obesity
  • NSAIDs
70
Q

What are symptoms of diverticular disease?

A
  • Left lower abdo pain
  • Constipation
  • Rectal bleeding
71
Q

What is the management of diverticular disease?

A
  • Diet - increase fibre
  • Bulk forming laxative e.g. ispaghula husk
    • Note: avoid stimulant laxatives
  • Surgery - resection where there is significant symptoms
72
Q

How does acute diverticulitis present?

A
  • Pain + tenderness in the left iliac fossa
  • Fever
  • Diarrhoea
  • N+V
  • Rectal bleeding
  • Palpable abdo mass if abscess has formed
73
Q

What is the management of acute diverticulitis?

A

Uncomplicated diverticulitis:
- Can manage in primary care
- Oral co-amox
- Analgesia
- Clear liquids only until symptoms resolve (2-3 days)
- FU within 2 days to r/v symptoms

Pts with severe pain/complications:
- Nil by mouth/clear fluids only
- IV abx
- IV fluids
- Analgesia
- Urgent surgery for complications

74
Q

What are possible complications of acute diverticulitis?

A
  • Perforation
  • Peritonitis
  • Peridiverticular abscess
  • Large haemorrhage requiring transfusions
  • Fistula (between colon + bladder/vagina)
  • Ileus/obstruction
75
Q

What are haemorrhoids?

A

Enlarged anal vascular cushions

76
Q

What causes haemorrhoids?

A
  • Not entirely clear
  • Often associated with constipation and straining
  • RF - pregnancy, obesity, increased age, increased intra-abdominal pressure (weightlifting/chronic cough)
77
Q

How can haemorrhoids be classified?

A
  • 1st degree: no prolapse
  • 2nd degree: prolapse when straining and return on relaxing
  • 3rd degree: prolapse when straining, does not return on relaxing but can be pushed back
  • 4th degree: prolapsed permanently
78
Q

How do haemorrhoids present?

A
  • Painless, bright red bleeding (blood NOT fixed with stool)
  • Sore/itchy anus
  • Feeling a lump in/around anus
79
Q

What examination findings are seen in haemorrhoids?

A
  • External (prolapsed) haemorrhoids - visible on inspection
  • Internal haemorrhoids - felt on PR exam
  • Prolapsed haemorrhoids when the pt bears down

Proctoscopy is required for proper visualisation and inspection (inserting hollow tube into anal cavity to visualise the mucosa

80
Q

What are the general management options for haemorrhoids?

A
  • Topical treatments - for symptomatic relief and to reduce swelling
  • Non-surgical options
  • Surgical options
81
Q

What are examples of topical treatments for haemorrhoids?

A
  • Anusol (contains chemicals to shrink haemorrhoids)
  • Anusol HC (+ hydrocortisone)
  • Germoloids cream (contains lidocaine)
  • Proctosedyl ointment (containscinchocaine + hydrocortisone)
82
Q

What are non-surgical options for haemorrhoids ?

A
  • Rubber band ligation
  • Injection sclerotherapy (injection of phenol oil into the haemorrhoid to cause sclerosis and atrophy)
  • Infra-red coagulation (infra-red light is applied to damage the blood supply)
  • Bipolar diathermy (electrical current applied directly to the haemorrhoid to destroy it)
83
Q

What are surgical options for haemorrhoids?

A
  • Haemorrhoidal artery ligation
  • Haemorrhoidectomy
  • Stapled haemorrhoidectomy
84
Q

What are thrombosed haemorrhoids? How do they present?

A
  • Caused by strangulation at the base of the haemorrhoid -> thrombosis
  • V painful
  • Purplish, swollen lumps around the anus
  • A PR examination is unlikely due to pain
85
Q

What is a hernia?

A

A protrusion of an organ or the fascia of an organ through the wall of the cavity that normally contains it

86
Q

What are RF for abdominal wall hernia?

A
  • Obesity
  • Ascites
  • Increasing age
  • Surgical wounds
87
Q

What are features of abdominal wall hernias?

A
  • Palpable lump
  • Lump may be reducible
  • Lump may protrude on coughing/straining
  • Aching/pulling/dragging sensation
88
Q

What are the key complications of hernias?

A
  • Incarceration - hernia is irreducible and the bowel is trapped in the hernia. Can lead to the next 2
  • Obstruction - hernia causes a blockage in the passage of faeces through the bowel
  • Strangulation - hernia is irreducible and the base becomes tight and cuts of the blood supply -> ischaemia. Strangulation is a surgical emergency
89
Q

What are the general management options for abdominal hernias?

A
  • Conservative management - if hernia has wide neck/pt is not for surgery
  • Tension-free repair - placing mesh over the defect
  • Tension repair - suturing muscles and tissue on either side of the defect back together, less common due to complications (pain, reoccurrence)
90
Q

What are the different types of abdominal wall hernias?

A
  • Inguinal hernia
  • Femoral hernia
  • Umbilical hernia
  • Paraumbilical hernia
  • Epigastric hernia
  • Incisional hernia
  • Obturator hernia
  • Spigelian hernia - rare
  • Richter hernia - rare
91
Q

Where are inguinal hernias located?

A

Superior and medial to the pubic tubercle

92
Q

What are direct vs indirect hernias?

A
  • Indirect - bowel herniates through the inguinal canal
  • Direct - hernia protrudes directly through abdominal wall through Hesselbach’s triangle
93
Q

What is are key structures that pass through the inguinal canal in men and women?

A
  • Men - spermatic cord
  • Women - round ligament
94
Q

Where are femoral hernias located?

A

Below and lateral to the pubic tubercle

95
Q

Are femoral hernias more common in men or women?

A

Women (particularly multiparous ones)

96
Q

What is the management of femoral hernias?

A

Surgical repair is necessary

97
Q

What is the issue with femoral hernias?

A

Hernia protrude through the femoral ring which is a narrow opening -> high risk of obstruction and strangulation

98
Q

What are incisional hernias?

A

Hernias the occur at the site of an incision from previous surgery

99
Q

What type of hernia is suggested by a symmetrical bulge under the umbilicus?

A

Umbilical hernia

100
Q

What type of hernia is suggested by a lump between the umbilicus and xiphisternum?

A

Epigastric hernia

101
Q

What is a hiatus hernia?

A

Herniation of the stomach up through the diaphragm

102
Q

What are the 4 types of hiatus hernia?

A
  • Type 1 - sliding
  • Type 2 - rolling
  • Type 3 - mixed
  • Type 4 - large opening with abdo organs entering thorax
103
Q

What are risk factors for hiatus hernias?

A
  • Obesity
  • Increasing age
  • Pregnancy
104
Q

How do hiatus hernias present?

A
  • Heart burn
  • Acid reflux
  • Burping
  • Bloating
105
Q

What is the management of hiatus hernias?

A
  • Conservative
  • Surgery - laparoscopic fundoplication (tying the fundus of the stomach around the lower oesophagus to narrow the oesophageal sphincter)
106
Q

What is mesenteric adenitis?

A

Inflamed lymph nodes within the mesentery

107
Q

What normally proceeds mesenteric adenitis?

A

Recent viral infection

108
Q

What is a key differential of mesenteric adenitis?

A

Appendicitis - often difficult to distinguish between the two

109
Q

What is the management of mesenteric adenitis?

A

Needs no treatment

110
Q

What are the functions of B12?

A
  • Mainly used for RBC development
  • Maintenance of the nervous system
111
Q

How is B12 absorbed?

A

Binds to intrinsic factors (secreted from parietal cells in the stomach) and actively absorbed in the terminal ileum

112
Q

What are causes of B12 deficiency?

A
  • Pernicious anaemia (most common)
  • Past gastrectomy
  • Vegan/poor diet
  • Disorders of terminal ileum (Crohn’s)
  • Metformin (rare)
113
Q

How can B12 deficiency present?

A
  • Sore tongue and mouth
  • Loss of vibration sense + joint position
  • Diastal paraesthesia
  • Neuropsychiatric symptoms (mood disturbances)
114
Q

What’s the management of B12 deficiency?

A
  • If no neurological involvement - 1mg IM hydroxocobalamin 3x/week for 2 weeks then once/3 months
  • If pt is deficient in folic acid then treat B12 FIRST to avoid subacute combined degeneration of the cord

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