Gastrointestinal Flashcards
What is the pathophysiology of Achalasia?
It is the inability of the Lower Oesophageal Sphincter to relax when swallowing
This is due to the loss of INHIBITORY NEURONS which secrete VIP and NO within the AUERBACH PLEXUS
Also there is a lack of Peristalsis
so the Lower Oesophageal Sphincter is constantly contracted and the Oesophagus above is dilated
What are the two risk factors for Achalasia?
Algrove Syndrome
Infection- specifically with Trypanosoma Cruzi (Chagas Disease)
What are the 5 signs of Achalasia?
Dysphagia of both solids and liquids
Regurgitation which may lead to coughing
Cachexia- extreme weight loss and muscle wasting
Coughing when laying down
Retrosternal chest pain (Heartburn)
What 3 investigations should be ordered if Achalasia is suspected?
Upper GI Endoscopy- to exclude a potential malignancy
Barium Swallow- which shows a Bird’s Beak Appearance
Oesophageal Manometry- to assess for (2)
- Oesophageal aperistalsis
- Incomplete relaxation of the Lower Oesophageal Sphincter
What is the 4 step Management Plan for Achalasia?
Calcium Channel Blockers (Nifedipine and Verapamil) and Nitrates (Isosorbide Dinitrate) reduces pressure and relaxes the Lower Oesophageal Sphincter- This is USUALLY INEFFECTIVE and is done while waiting for the other treatments
Laparoscopic Heller’s Cardiomyotomy- This is the Most Effective and the First Line for Achalasia
Endoscopic Pneumatic Dilation- a balloon is expanded to relax the Lower Oesophageal Sphincter- but this carries a risk of PERFORATION. This can also be conducted First Line
Botox Injection into the Lower Oesophageal Sphincter- Can be done if the other two are not possible
What is the pathophysiology of Coeliac Disease?
Gliadin is a component of Gluten that underlies Coeliac Disease
Gliadin is deamidated by Tissue Transglutaminases (tTG) once absorbed
In patients with Coeliac Disease, the deamidated Gliadin molecules are presented by Antigen-Presenting Cells through the HLA-DQ2 and HLA-DQ8 molecules to T Helper Cells and thsi triggers an immune response
The immune activation results in (3) Villous Atrophy, Lymphocyte Accumulation and Intestinal Crypt Hyperplasia which leads to Malabsorption
What are the 2 risk factors for Coeliac Disease?
HLA-DQ2 and HLA-DQ8
IgA Deficiency- which allows for increased gluten peptides to circulate the submucosa
What are the 8 signs of Coeliac Disease?
Persistent Abdominal Symptoms
- Indigestion
- Diarrhoea (watery) or steatorrhoea (pale, floating stools)
- Abdominal bloating or Discomfort
- Constipation
Unexplained Iron, Vitamin B12 or Folate Deficiency
TYPE 1 Diabetes Mellitus
Unexplained Weight Loss
Autoimmune Thyroid Disease
Mouth Ulcers
Dermatitis Herpetiformis (Associated with this due to IgA Deposition)
What 6 investigations should be ordered if Coeliac Disease is suspected? What should be done before the patient is investigated?
First, put the patient on a gluten-free diet for 6 weeks before the investigations
Tissue Transglutaminase Antibodies and Total IgA should be measured= First Line (Total IgA should be measured to make sure patients are not IgA deficient)
Endomysial Antibodies= Second Line if Anti-tTG is weakly positive
Anti-tTG, Gliadin or Endomysial (IgG) Antibodies should be measured if the patients turn out to be IgA deficient
Anti-Casein Antibodies
Duodenal Biopsy (The Gold Standard)- Refer any patient with positive serology (4)
- Villous Atrophy
- Crypt Hyperplasia
- Increase in Intraepithelial Lymphocytes
- Lamina Propria infiltration with Lymphocytes
FBC- Microcytic Anaemia
What is the 4 step Management Plan for Coeliac Disease?
Gluten-Free Diet (4). Avoid-
- Wheat (Breads etc.)
- Rye
- Barley (including Beer)
- Oats
Supplements if the diet is inefficient
Vaccinations- due to Functional Hyposplenism
- Pneumococcal Vaccination with Booster every 5 years
Referral to specialist if symptoms persist
What are the 5 main complications of Coeliac Disease?
Dermatitis Herpetiformis
Calcium and Vitamin D Deficiency
Increased risk of Osteoporosis
Anaemia
Lactose Intolerance
Which gene mutation is thought to underlie Crohn’s Disease?
CARD 15/ NOD 2
Which two regions are commonly affected in Crohn’s Disease? (even though it affects all regions)
The Terminal Ileum and the Colon
Describe the inflammation in Crohn’s
It is a Transmural Inflammation with Granuloma Formation that occurs in ALL Layers down to the serosa
Involves (3) Fistulas, Strictures and Adhesions
Which antigen indicates the presence of Crohn’s Disease and Ulcerative Colitis?
HLA B27
What are the 8 signs of Crohn’s Disease? (Excluding the extra-intestinal malformations)
Diarrhoea
Abdominal pain
Bloody stools (although this is more common in Ulcerative Colitis)
Weight loss and Lethargy
Fever
Aphthous Mouth Ulcers
Delayed Puberty
Rectal Examination reveals (7)
- Blood
- Skin
- Tags
- Erythema
- Fissures
- Fistulas
- Ulceration
What are the Cutaneous (2), Musculoskeletal (5), Hepatobiliary (2) and Eye-related (2) extra-intestinal malformations in Crohn’s Disease and Ulcerative Colitis?
Cutaneous-
- Erythema Nodosum
- Pyoderma Gangrenosum (requires Steroid Therapy)
Musculoskeletal-
- Pauci-articular Arthritis (Asymmetrical)
- Polyarticular Arthritis (Symmetrical)
- Axial Arthritis
- Clubbing
- Osteoporosis
Hepatobiliary (more common in Ulcerative Colitis than Crohn’s Disease)-
- Primary Sclerosing Cholangitis
- Autoimmune Hepatitis
Eyes
- Episcleritis (more common in Crohn’s than Ulcerative Colitis)
- Uveitis (more common in Ulcerative Colitis than Crohn’s Disease)
What 12 investigations should be considered if Crohn’s Disease is suspected?
Colonoscopy is the investigation of choice (4)
- Mucosal Inflammation
- Deep Ulcers
- Skin Lesions
- Cobblestone Mucosa
Faecal Calprotectin- Raised in Crohn’s
Coeliac Serology- Make sure it isn’t Coeliac Disease
Barium Fluoroscopy (3)-
- Kantor’s ‘string sign’- suggests strictures
- Rose Thorn Ulcers
- Proximal Bowel Dilatation and Fistulae may be present
FBC- (3)
- Leukocytosis during a flare
- Anaemia due to low Vitamin B12
- Folate or Iron Deficiency
CRP/ ESR
B12, Folate, Ferritin and Vitamin D may be Low
LFTs- Low Serum Albumin= Protein-losing Enteropathy
U&Es- Electrolyte Disturbance and signs of Dehydration
Stool Microscopy- to exclude Infective Gastritis or Pseudomembranous Colitis (including Clostridium Difficile)
CTAP- demonstrates inflammatory bowel changes and their distribution, as well as the presence of fistulae or abscesses
Serum Antibodies-
- pANCA- Ulcerative Colitis
- ASCA- Crohn’s Disease
What is the 4 step management plan for the induction of remission in Crohn’s Disease?
What is the 3 step plan for the maintenance of remission?
First Presentation (3)
- Give Glucocortoids (PO Prednisolone or IV Hydrocortisone)
- Aminosalicylate (Mesalazine)
- Distal Ileal or Ileocaecal Disease (Budesonide)
Two or More Exacerbations a Year or the Glucocorticoids are not working-
- Add Azathioprine or Mercaptopurine (Measure their Thiopurine Methyltransferase levels before doing so)
- Then add Methotrexate
Severe (unresponsive to medications and >3 loose stools a day)
- Infliximab or Adalimumab
Surgery
Maintenance of Remission
- Azathioprine or Mercaptopurine
- Methotrexate
- Post surgery- Azathioprine with or without Methotrexate
What are the 4 indications for surgery in Crohn’s Disease?
Poor response to conventional treatment
Strictures (the narrowing of the intestine)
Abscesses (collections of pus) and Fistulae (incorrect passageway formed by abscesses)
Delayed growth in children (steroid treatment and malabsorption can lead to delayed growth or delayed puberty)
Malignancy
What is the main surgical option for Crohn’s and 4 alternative options if the disease invades the large bowel? State a fact about each
Ileocaecal Resection
If the large bowel is affected-
Partial Right Hemicolectomy
- If the right side of the colon is affected, the disease portion of the bowel is removed and reattached to the rest of the colon
Colectomy with Ileostomy
- If a significant portion of the colon is affected, it will need to be removed and a stoma will need to be put in
Colectomy with Ileorectal Anastomosis
- Appropriate if Healthy Rectum but the Colon is affected- do NOT perform in Rectal Disease or if the Anal Muscles are affected
Panproctocolectomy and Ileostomy
- If the rectum is also affected, the entire colon and anal canal is removed and an ileostomy can be formed
What is the pathophysiology of Mallory-Weiss Tears?
A tear caused by a sudden increase in the Intra-abdominal and Transmural Pressure across the gastrooesophageal junction- secondary to Vomiting and Retching in the presence of a pre-existing damaged gastric mucous membrane
Often related to alcoholism
What is the difference between a Mallory Weiss Tear and Boerhaave’s Syndrome?
In a Mallory Weiss Tear, only the mucosa and submucosa are affected, whereas in Boerhaave’s Syndrome all layers of the oesophageal wall are ruptured and surgery is needed ASAP
What are the 4 signs of a Mallory Weiss Tear?
Background of alcohol excess, presenting with vomiting and retching
Melaena (rare)
Preceding retching and vomiting
Vomiting blood