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
What 5 investigations should be ordered if a Mallory Weiss Tear is suspected?
Upper GI Endoscopy (Gold Standard)
- Depending on the Glasgow-Blatchford Score
- Usually shows a single (or multiple) longitudinal tear in the mucosa at the gastrooesophageal junction
FBC- assess for anaemia
U&Es- UREA will be raised in an UPPER GI BLEED
LFTs- mostly normal but may be DERANGED if it is a VARICEAL BLEED
Erect CXR- to rule out Oesophageal Perforation or Perforated Peptic Ulcer
What Glasgow Blatchford Score suggests the patient needs to be admitted for a bleed?
Anything above 0
What is the 2 step management for a Mallory Weiss Tear?
Usually a Mallory Weiss Tear is self-limiting so treatment is not needed unless the bleeding is persistent or significant
First line (3) Upper GI Endoscopy - Clipping with or without ADRENALINE - Thermal Coagulation with ADRENALINE - Sclerotherapy with ADRENALINE
High-dose IV Protein Pump Inhibitor (like Pantoprazole)- give it Post-Endoscopy to reduce the chances of rebleeding- Do NOT give before the endoscopy
Offer Long Term PPI if there is evidence of G.O.R.D.
Second line-
Surgical repair or IV radiology if first line treatments have failed
What are Oesophageal Varices?
They are dilated submucosal veins within the Lower Third of the Oesophagus that develop as a consequence of Portal Hypertension- as the lower third of the oesophagus drains into the Portal Vein via the Left gastric Vein
What is the most common cause of Portal Hypertension, and therefore most common cause of Oesophageal Varices?
Liver Cirrhosis
What are the 3 risk factors for an Oesophageal Varices bleed?
Decompensated Liver Cirrhosis
Portal Hypertension
Large Varices
What are the 6 signs of an Oesophageal Varices bleed?
Melaena
Haematemesis
Symptoms of blood loss (4)
- Light-headedness
- Dyspnoea
- Chest pain
- Syncope
Features of Chronic Liver Disease (4)
- Leukonychia
- Palmar Erythema
- Spider Telangiectasia
- Gynecomastia
Features of Decompensated Liver Disease (3)
- Jaundice
- Ascites
- Encephalopathy
Splenomegaly due to Portal Hypertension
What 4 investigations should be ordered if an Oesophageal Varices bleed is suspected?
FBC- Anaemia
LFTs and Coagulation Profiles- assess the severity of liver disease and bleeding risk
U&Es- UREA is RAISED in an upper GI bleed (protein in RBCs is digested into urea basically)
ABG- Raised Lactate indicates Poor Tissue Perfusion and therefore indicates a Significant Bleed
What is the 8 step management for an Oesophageal Varices bleed?
ABCDE- patient should be resuscitated prior to endoscopy
IV Fluids- useful if the patient is in shock but do not overhydrate as this causes HAEMODILUTION
If PLTS<50x10^9 then Transfusion is needed, also transfuse if clotting is deranged OR Vitamin K is abnormal
Terlipressin- it is an ADH analogue and causes Splanchnic Vasoconstriction which reduces blood flow into the portal vein and reduces the Portal Pressure
- OCTREOTIDE is an alternative but is less effective
Prophylactic Antibiotics like Quinolones must be given to all patients
Balloon Tamponades (The Sengstaken-Blakemore Tube) are a temporary measure to be given until the surgery
Definitive Management (3)
- Oesophageal varices- Endoscopic Variceal Band Ligation
- Gastric varices- Endoscopic Scleropathy
- Transjugular Intrahepatic Portosystemic Shunt (TIPS) for a variceal bleed if endoscopy fails
Prophylaxis (2)
- Non-selective Beta Blocker- PROPANOLOL- to reduce the Portal Pressure
- Endoscopic Variceal Band Ligation with a Protein Pump Inhibitor
What are the 7 risk factors for Peptic Ulcers?
H Pylori (most common cause)
NSAIDs
Other Drugs (Corticosteroids, SSRIs, Bisphosphonates)
Smoking and Alcohol
Raised Intracranial Pressure- promotes Vagal Stimulation which increases Acid Production- these are called Cushing’s Ulcers
Severe Burn- these are called Curling’s Ulcer
Having a Blood Type O
What are the 8 signs of Peptic Ulcer Disease?
Pallor if Anaemic
Evidence of bleeding-
- Hypotension and Tachycardia
- Meleana on Rectal Examination
- Haematemesis
- Pain Relieved by Eating- Duodenal Ulcer
- Pain Worsened by Eating- Gastric Ulcer
- Reduced Appetite and Weight Loss
- Epigastric Tenderness
What investigations should be ordered if Peptic Ulcer Disease is suspected with No Active Bleeding (2) and Active Bleeding (5)?
No Active Bleeding-
- H Pylori Breath Test and/or Stool Antigen
- Upper GI Endoscopy and Biopsy- not routinely performed
Active Bleeding-
- FBC- Anaemia
- U&Es- UREA raised in Upper GI bleeds
- LFTs and Coagulation- assess the severity of the liver disease
- ABG- raised Lactate is a sign of poor tissue perfusion and indicates a Significant Bleed
- All Gastric Ulcers should be BIOPSIED
What is the management of Peptic Ulcer Disease with No Active Bleeding (4) and Active Bleeding (6)?
No Active Bleeding (3,1)- Check their H. Pylori First
- Stop NSAIDs
- If H. Pylori is negative= give a PPI like Omeprazole
- If H. Pylori is positive= give Omeprazole, Clarithromycin and Amoxicillin (or Metronidazole instead if they are allergic to Penicillin)
Second Line- Switch to the alternate strategy (give H. Pylori Treatment to the H. Pylori Negative Patients)
Active Bleeding (5,1)
- IV Crystalloid
- Blood Transfusion if Significant Blood Loss
- Upper GI Endoscopy
1. Clipping with or without ADRENALINE
2. Thermal Coagulation with ADRENALINE
3. Sclerotherapy with ADRENALINE - High-dose IV Protein Pump Inhibitor (like Pantoprazole)- give it Post-Endoscopy to reduce the chances of rebleeding- Do NOT give before the endoscopy
- Offer Long Term PPI if there is evidence of G.O.R.D.
Second line-
- Surgical repair or IV radiology if first line treatments have failed
What region does Ulcerative Colitis typically affect? (3)
It affects the Rectum (Proctitis) which spreads Proximally and affects the length of the continuous colon
It Never Spreads beyond the Ileocaecal Valve and is confined to the Large Bowel
It does not Affect the Anus
Which cellular layers does Ulcerative Colitis affect? And What kinds of Abscesses does it form?
It causes Mucosal and Submucosal Ulceration
And it causes Crypt Abscesses through Neutrophil Infiltration
What are 4 risk factors for Ulcerative Colitis?
Being a Non-Smoker
HLA-B27
Caucasian
Family History of Ulcerative Colitis
What are the 6 signs of Ulcerative Colitis (aside from the Entraintestinal malformations)?
Blood and Mucus in Stools with Fresh Blood on Rectal Examination
Fever
Abdominal Tenderness (Specifically in the Left Lower Quadrant)
Urgency and Tenesmus
Diarrhoea
Weight Loss (Although this is more common in Crohn’s)
What 8 Investigations should be ordered if Ulcerative Colitis is Suspected?
Colonoscopy and Biopsy (5)
- Red and Raw Mucosa with Widespread Shallow Ulceration
- No inflammation beyond the Mucosal Layer
- Pseudopolyps- The mucosa next to the ulcers is preserved and makes them look like Polyps
- Crypt Abscesses- Due to Neutrophil migration through the gland walls
- Goblet Cell Depletion
FBC-
- Leukocytosis during the Flare Up
- Anaemia from PR Bleeding
Faecal Calprotectin- will be Raised in Ulcerative Colitis and Crohn’s
CRP/ ESR- raised during Flares
LFTs- Low Albumin suggests Protein-losing Enteropathy (Like Ulcerative Colitis)
Abdominal Xray- Toxic Megacolon (Leadpipe Appearance)
Barium Enema- loss of Haustrations- widespread superficial Ulcerations and Pseudopolyps demonstrate a Leadpipe Appearance
Serum Antibody Markers-
- pANCA- associated with Ulcerative Colitis
- ASCA- associated with Crohn’s Disease
What are the 5 different treatment options for Ulcerative Colitis (3 points each- 1st line, 2nd line, 3rd line)?
Proctitis Only
- Topical ASA (Mesalazine is the ASA used)
- Add Oral ASA
- Topical or Oral Corticosteroid
Goes up to Splenic Flexure
- Topical ASA
- Add Oral ASA, or Oral ASA and Topical Corticosteroid
- Oral ASA and Topical Corticosteroid
Beyond Splenic Flexure
- Topical ASA and High-Dose Oral ASA
- Oral ASA and Topical Corticosteroid
Severe Disease (4)- HR>90, Pyrexial, Anaemic, ESR>30
- IV Corticosteroid (Or Ciclosporin if steroids are contraindicated)
- IV Ciclosporin (or IV Infliximab if Ciclosporin is contraindicated)
- Colectomy
If more than 2 exacerbations in the past year or if the remission is not maintained by ASAs-
- Oral Azathioprine or Oral Mercaptopurine
What are the 7 differences between Ulcerative Colitis and Crohn’s Disease?
There are Aphthous Ulcers in Crohn’s Disease, Not in Ulcerative Colitis
Crohn’s consists of Skip Lesions and does not involve the rectum usually. Ulcerative Colitis never spreads into the small bowel or anus
Crohn’s disease is most common in the Terminal Ileum and Ulcerative Colitis involves the Rectum
The Ulcers in Ulcerative Colitis consists of Shallow Ulcers with Pseudopolyps. The Ulcers in Crohn’s Disease are Deep Ulcers with Skip Lesions, Mucosal Inflammation and Cobblestone Mucosa
Ulcerative Colitis consists of only Mucosal and Submucosal Ulceration and has Crypt Abscesses with Neutrophil Infiltration. Crohn’s Disease consists of Transmural Inflammation with Granulomas and Goblet Cells
Ulcerative Colitis can involve Primary Sclerosing Cholangitis and Cholangiocarcinoma (which can happen in Crohn’s but is Rare). Crohn’s Disease can involve Gall Stones due to Bile Reabsorption and Calcium Oxalate Renal Stones
Ulcerative Colitis has a Toxic Megacolon on Colonoscopy. Crohn’s Disease consists of (3) Fissures, Fistulas and Strictures on Colonoscopy
