GASTROINTESTINAL Flashcards
What is it inflammatory bowel disease? What is seen in it?
It’s umbrella term for two main diseases causing inflammation of the GI tract: Ulcerative Colitis and Crohn’s disease.
Mucosal immune system exerts an inappropriate response to luminal antigens (such as bacteria)
which may enter the mucosa via a leaky epithelium
causes fibrous cobblestone scarring
Outline the epidemiology behind Crohn’s disease
Highest incidence and prevalence in Northern Europe, UK and North America
F>M
Presents mostly at 20-40
Where does Crohn’s affect? Where does it most commonly affect?
Affects any part of gut from mouth to anus – commonly ileum and colon
What genetic mutations have been seen to cause Crohns?
CARD15/NOD2 mutation
What pathogens can cause Crohn’s?
Escherichia coli, Mycobacterium avium paratuberculosis, C.Difficile
What are some risk factors for Crohns
- Family history
- Smoking
- NSAIDs may exacerbate
- Stress and depression
Outline the pathophysiology behind Crohn’s
A foreign pathogen triggers the immune system, which are able to get through the gut wall due a defect in the epithelium
This triggers a large and uncontrolled immune response - These immune cells invade deep into the mucosa and organise themselves into granulomas
This leads to ulcers forming throughout all layers, hence Crohn’s being said to be transmural, and cobblestone in appearence
the ileum is the most commonly affected site of crohns
Pathophysiology behind Crohn’s what are immune cells seen in it? In what way are the ulcers arranged at what is this called?
What is the most commonly affected site in Crohns?
T helper cells release cytokines which attract cells such as macrophages which release substances like proteases, platelet activating factor and free radicals
Ulcers occurs in patches known as skip lesions
the ileum is the most commonly affected site of crohns
Normal physiology - what are the layers of the GI tract?
Mucosa
Submucosa
Muscularis Externa
Serosa
(mostly, Sam Makes Eleanor Sick)
picture - taken from macmillan.org
How can Crohn’s lead to
a) Blood in Stool
b) Malabsorption
Blood may appear in stools due to damaged intestinal walls and due to the damage, the intestines lose their ability to absorb water, causing diarrhoea.
If the small intestine is affected, it loses its ability to absorb nutrients, leading to malabsorption.
What are the signs of Crohn’s?
Abdominal tenderness
Fever
Mouth ulcers
Rectal examination will show blood, skin tags, fissures and fistulas
eye problems - uveitis
What are the symptoms of Crohn’s?
Weight loss
Diarrhoea
Abdominal pain (most common in RLQ where the ileum is)
Lethargy and malaise also symptom
What are some first line investigations for Crohn’s?
Faecal calprotectin (released by intestines when inflamed)
C-reactive protein is a good indication of current inflammation
FBC:leukocytosis during a flare;anaemia due to vitamin B12, folate or iron deficiency
Stool sample to rule out infectious diseases
- U&Es: to assess for electrolyte disturbance and signs of dehydration
- Coeliac serology: to exclude coeliac disease
What is the gold standard test of Crohn’s?
What would you see, and what would you see with a biospy?
Colonoscopy will show mucosal inflammation (deep ulcers, skip lesions and cobblestone appearance)
Histology will show transmural inflammation with granulomas and increased number of goblet cells
What are some first line treatment options for Crohns?
Oral corticosteroids e.g. budesonide and prednisolone, as well as an elemental diet - pre-digested nutrients
What are some second line treatments to consider in Crohns, and what would you give in flairups?
IV hydrocortisone in severe flare ups
Add anti-TNF antibodies e.g. Infliximab if no improvement
Consider adding other immunosuppressive drugs
Surgery – doesn’t cure disease
What are some immunosuppressants used to treat Crohn’s?
azathioprine or methotrexate to remain in remission if there are frequent exacerbations.
Thiopurine methyltransferase level should be measured before using
Name some complications of Crohns.
- Peri-anal abscess:
- Anal fissure:a small tear in the lining of the anus
- Anal fistula:an abnormal connection between 2 epithelial surfaces, e.g. from the anal canal to skin surface
- Strictures and obstruction:
- Perforation:chronic inflammation can weaken the bowel wall and predispose to subsequent perforation
- Malignancy: colorectal cancer and small bowel cancer
- Osteoporosis
- Anaemia and malnutrition
What are the key things to remember for Crohn’s?
NESTS
N- No blood or mucus
E- entire GI tract
S- Skip lesions
T- Terminal ileum and transmural
S- Smoking is a big risk factor
What is Ulcerative colitis?
A type of IBD that typically involves the rectum and variable lengths of the colon. Will never spread beyond the ileocecal valve, and does not affect the anus
What age groups/races to ulcerative colitis effect the most?
bimodal age distribution, 15-25 and 55-70 years of age.
- Highest incidence and prevalence in Northern Europe, UK and North America
- Affects caucasians and eastern European Jews most
What are some risk factors (including genes) for getting ulcerative colitis?
- Family history
- HLA-B27 gene - codes for a protein assossicaated with autoimmune conditions like UC
- Caucasian
- Non-smoker
- NSAIDs- associated with flares
- Chronic stress and depression - associated with flares
picture taken from netters illustrated human pathology
Outline pathophysiology behind ulcerative colitis?
High levels of what substance is thought to correlate with exacerbations
Not well understood, however thought to be Autoimmune
Bacteria/dietary antigens pass into lamina propria
Picked up by antigen presenting cells, in lamina propria
Cytotoxic T cells destroy the epithelial lining of the colon, leaving behind ulcers.
UC seen more in people with higher sulphide producing bacteria ==> often high sulphide production is correlated with periods of active inflammation
What antibodies are found in patients with UC?
Antibodies found - p-ANCAs - Perinuclear antineutrophilic cytoplasmic antibodies.
just remember anti neutrophilic antibodies
antibodies that target antigens in the body’s own neutrophil
Maybe party due to immune reaction to gut bacteria that have to structural similarity to own neutrophils == cross react.
What are some general signs of UC?
Abdominal tenderness
Fever - in acute UC
Tachycardia - in acute severe UC
Fresh blood on rectal examination
picture taken from netters illustrated human pathology
What are some cutaneous, muscoskeletal and eye features you may see in a patient with Ulcerative collitis?
Erythema Nodosum - inflamed subcutaneous fat (see picture)
Pyoderma gangrenosum - rapidly enlarging, very painful ulcer.
- Osteoporosis and arthritis
- Clubbing
- Uveitis - eye inflammation
- Conjunctivitis
taken from netters illustrated human pathology
What are some symptoms of ulcerative colitis?
- Diarrhoea
- Blood and mucus in stool
- Urgency and tenesmus (cramping rectal pain)
- Abdominal pain: particularly in left lower quadrant
- Weight loss and malnutrition
- Fever and malaise during attacks
State some histological features that will be seen in ulcerative colitis
Pseudopolyps
Crypt abscess
Goblet cell depletion,
Infrequent granulomas
Increased plasma cells in lamina propria
What are some initial investigations for UC?
Stool studies for infective pathogens - rule out infection
Faecal calprotectin: will be raised, helps differentiate between irritable bowel disease
pANCA antibodies - often a feature of UC
FBC - may show leukocytosis, thrombocytosis, and anaemia
LFTs - check every 6 to 12 months for surveillance of primary sclerosing cholangitis.
Lead pipe appearance on a barium enema - indicative of chronic UC
What is the gold standard investigation for UC? What would you see on it?
Colonoscopy -
- Red and raw mucosa with widespreadshallow ulceration
- No inflammation beyond the submucosa, unless fulminant disease
- Pseudopolyps: mucosa adjacent to ulcers is preserved, which has the appearance of polyps - They are caused by mucosal repair after chronic inflammation.
- Crypt abscessesdue to neutrophil migration through gland walls
- Goblet cell depletion, withinfrequentgranulomas
picture taken from netters illustrated human pathology
What scoring criteria is used in UC? What does it look at, and what is it guaging?
truelove and witts
gauges mild, Moderate, Sever UC.
Looks at
Motions/day
Rectal Bleeding,
Temperature at 6am
Resting pulse
haemoglobin
picture from https://www.openmed.co.in/2022/03/truelove-and-witts-criteria-for.html
What is the management for inducing remission in mild UC?
First line: Anti-inflammatories such as Aminosalicylates (like mesalazine or sulfasalazine)
Second line corticosteroid (prednisolone)
(THINK SALAZINES)
Anti-TNF drugs - infliximab
What is the management in severe Ulcerative collitis?
Hospital admission + A high-dose intravenous corticosteroid, eg
hydrocortisone
What are the surgical options for UC?
PANPROCTOCOLECTOMY = Removal of the colon and rectum
Left with ileostomy or or J-pouch this is where small intestine is used to make rectum
Surgery will be curative
What is a complication of UC?
STI of stoma
Toxic megacolon - mass dilation of part of the colon
Perforation
Colonic adenocarcinoma
taken from netters illustrated human pathology
What are the key things to remember for UC?
ESCALOP
E- EXCRETE BLOOD AND MUCUS
S - SMOKING PROTECTS
C - CONTINOUS INFLAMMATION
A - AMINOSALICYLATE
L - LIMITED TO COLON AND RECTUM
O - ONLY SUPERFICIAL
P - PRIMARY SCLEROSING CHOLANGITIS
What are some extra intestinal signs of Inflammatory bowel disease?
- Conjunctivitis
- Arthritis
- Pyoderma gangrenosum
- Erythema nodosum
- Sclerosing cholangitis
- Clubbing
Name some differences between Crohns and Ulcerative collitis
Smoking is protective for UC, risk factor for Crohns!
picture taken from osmosis
Crohns -
Whole GI Tract
Skip lesions
Smoking is risk factor
Grannulomas present
Surgery doesn’t cure
Transmural
No blood in poo
UC
Only Rectum and Colon
Continuous inflammation
Smoking is protective
Surgery can cure
Crypts present
Blood in poo
What is irritable bowel syndrome?
A chronic condition characterised by pain associated with bowel dysfunction It is a functional bowel disorder
What are the 3 types of IBS?
IBS-C- with constipation
IBS-D with diarrhoea
IBS-M with both
What are the groups of people most likely affected with Irritable bowel syndrome
- It is very common and occurs in up to 20% of the population.
- Common, in western world around 1 in 5 report symptoms consistent with IBS
- It affects women more than men
- More common in younger adults <40 years
What is the pathophysiology behind irritable bowel syndrome?
For people With IBS, what can eating FODMAPs do?
Pain:
Dysfunction in the brain-gut axis results in disorder of intestinal motility and/or enhances visceral sensitivity - nerve endings in GI wall have abnormally strong response to stimuli like stretching during/after a meal
Abnormal motility:
Eating FODMAPs (fermentable oligo-, di-, mono-saccharides and polyols) can bring water into GI tract,
===> excess water can cause smooth muscle lining in GI tract to spasm, can lead to diarrhoea if the excess water is not reabsorbed
Recurrent abdominal pain with NO inflammation
What can alter the gut reactivity seen in IBS?
environmental (personal life stresses or abuse)
luminal (certain foods, bacterial overgrowth or toxins, or gut distension or inflammation)
What are some signs and symptoms of Irritable bowel syndrome?
- Signs
- General abdominal tenderness may be felt.
- Symptoms
- Fluctuating bowel habit
- Diarrhoea
- Constipation
- Urgency
- Mucus PR
- Abdominal pain
- Pain worse after eating
- Improved by opening bowels
- Bloating
image source - unknown
What is the diagnostic criteria for Irritable bowel syndrome?
Abdominal pain / discomfort:
- Relieved on opening bowels, or
- Associated with a change in bowel habit
AND 2 of:
- Abnormal stool passage
- Bloating
- Worse symptoms after eating
- PR mucus
When suspecting Irritable bowel syndrome in a patient you need to exclude other diseases. What diseases would these be and what tests would you do?
- Normal FBC, ESR and CRP blood tests
- Faecal calprotectinnegative, excludes inflammatory bowel disease
- Negative coeliac disease serology (IgA tissue transglutaminase antibodies)
- Cancer is not suspected or excluded if suspected: colonoscopy
What are some differentials for irritable bowel syndrome?
- Crohn’s disease
- Ulcerative colitis
- Coeliac disease
- Malignancies
What is some lifestyle advice given in the management of IBS?
- Adequate fluid intake
- Regular small meals
- Reduced processed foods
- Limit caffeine and alcohol
- Low “FODMAP” diet (ideally with dietician guidance)
- Increase fibre if constipation, reduce fibre if diarrhoea
- Reduce stress
- Increase activity
- Weight loss if obese or overweight
What Pharmalogical management options are there for IBS?
- Loperamidefor diarrhoea
- Laxatives for constipation - Linaclotideis a specialist laxative, 2nd line
- Antispasmodics for cramps e.g.hyoscine butylbromide(Buscopan)
- Second line
- Tricyclic antidepressants (i.e. amitriptyline 5-10mg at night), reduce pain, help mood, CBT may also be offered
What is coeliac disease?
State of heightened immunological responsiveness to ingested gluten in genetically susceptible individuals. Ingestion of gluten stimulates immune system to attack small intestine
Suspect in all with diarrhoea, weight loss & anaemia
What are the most common ages to see Coeliac disease? What diseases is it associated with?
Most common age for presentation is 4th to 6th decade
For every paediatric case diagnosed there are 9 adult cases
Presentation is at any age but typically presents infancy (after weaning on to gluten-containing foods) and in adults aged 40-49
Other autoimmune conditions e.g. T1DM and thyrotoxicosis
Outline the pathophysiology that leads to coeliac disease - what does Gliadin do and what happens to it?
A-Gliadin is in gluten, binds to IgA in mucosal membrane
Taken to Lamina propria, where it gets deaminated
Deaminated Gliadin gets taken up by macrophages, and expressed on MHC II Complex
==> T helper cells release inflammatory cytokines and stimulate B cells
pathophysiology that leads to coeliac disease - what is a consequence of the immune response by T helper cells responding to gliadin?
What will some with coeliac disease experience as a result?
T helper cells release inflammatory cytokines and stimulate B cells
This causes villous atrophy, crypt hyperplasia and intraepithelial lymphocyte infiltration
🡪 reduced SA to absorb nutrients 🡪 B12, folate and iron cannot be absorbed 🡪 anaemia
picture taken from zerotofinals
What are some classical clinical presentations of Coeliac disease?
Suspect in all with diarrhoea, weight loss & anaemia
Villous atrophy leads to malabsorption
Steatorrhoea (fat in stools) & stinking stools - due to Inability to properly absorb fat from diet
Anaemia - Due to inability to absorb B12, folate, iron
Weight loss
Fatigue & weakness
Diarrhoea
Abdominal pain
Bloating
Nausea + vomiting
What are some non classical presentations of coeliac disease?
Aphthous ulcers
Angular stomatitis
Osteomalacia
Decreased absorption of Vitamin D
Failure to thrive (children)
erythematous lesions on elbows
Dermatitis herpetiformis:
Raised red patches of skin, and blisters - due to Deposition of IgA in skin (normally on abdomen)
taken from https://www.verywellhealth.com/dermatitis-herpetiformis-photos-562325
What are some first line investigations for coeliac disease?
Serum antibody testing
IgA tissue transglutaminase (tTG),
Endomysial antibodies (EMAs),
Deaminated gliadin peptides antibodies (anti-DGPs), Very high sensitivity & specificity
Need to be on a gluten diet for testing!!
However, in patients with IgA deficiency there is a risk of false negatives, as the total IgA count will remain low —> So test total IgA count as well, and IgG version of anti-TTG or anti-EMA antibodies!!
What are some other investigations you could do for coeliac disease? (Genetics?)
HLA-DQ2 & HLA-DQ8 genotyping
Full Blood Count (FBC)
Low Hb
Low folate
Low ferritin
Low B12
~50% have mild anaemia
What is the gold standard test for diagnosing coeliac disease? What would you see?
Endoscopically
Required for definite diagnosis
+ve Findings:
Villous atrophy
Crypt hyperplasia
Increased epithelial WBCs
What is the management for coeliac disease?
Lifelong gluten-free diet
Avoid foods containing wheat, barley, rye, oats
Gluten-free food are now more available
Poor compliance is the main reason for recurrence
Symptoms & serology used to monitor response & compliance
Correct vitamin deficiencies
Pneumococcal vaccine given
Hyposplenism
What is gastritis?
Gastritis refers to inflammation of the lining of the stomach associated with mucosal injury.
image source - unknown
Define Gastropathy . What is its most common cause?
Gastropathy refers to epithelial cell damage and regeneration WITHOUT inflammation - commonest cause is mucosal damage associated with Aspirin/NSAIDs
Name some causes/Risk factors for getting Gastritis.
H. Pylori infection – most common
Autoimmune gastritis – the cause of pernicious anaemia associated with antibodies to gastric parietal cells and IF
Viruses e.g. CMV and HSV
Crohn’s disease
Mucosal ischaemia
Increased acid
Aspirin and NSAIDs e.g. naproxen
Alcohol
taken from Netters illustrated human pathology
Pathophysiology - how can H. Pylori lead to Gastritis?
H.pylori produces urease - which converts urea to ammonia and CO2
Ammonia reacts with H+ (from HCl) to form toxic ammonium
Ammonium damages gastric mucosa -leads to less mucous production
- Causes severe inflammatory response, Gastric mucus degradation and increased mucosal permeability
Treat with a H+ pump inhibitor , to raise the pH (Bacteria won’t like a higher pH) eg like Lansoprazole
image taken from https://drjockers.com/gastritis/
What is seen in Autoimmune gastritis?
Where does it affect?
Autoimmune gastritis damages the fundus and body of the stomach 🡪 atrophic gastritis and loss of parietal cells with IF deficiency resulting in pernicious anaemia (low RBCs due to low B12)
image taken from teach me anatomy
How can Aspirin and NSAIDs lead to gastritis?
e.g. naproxen – inhibits prostaglandins (which stimulate mucus production) via inhibiting COX-1 = resulting in less mucus production and therefore gastritis
image taken from https://www.researchgate.net/figure/NO-and-H-2-S-gastroprotection-against-NSAID-induced-gastric-damage_fig4_277179160
What are some common clinical manigestations of Gastritis?
- Nausea or recurrent upset stomach
- Vomiting
- Abdominal bloating
- Epigastric pain
- Indigestion
- Haematemesis/ malaena
What are some first line tests when investigating gastritis?
Helicobacter pylori urea breath test
H pylori faecal antigen test –both will be postive in H . pylori infection
Before testing, stop PPI for at least 2 weeks; antibiotics for 4 weeks
- Look for anti-IF (intrinsic factor) antibody and anti-parietal cell antibodies
- Raised gastrin levels, reduced pepsinogen
What is the gold standard test for gastritis?
- Endoscopy - will be able to see gastritis
- Biopsy
How would you treat gastritis not caused by H.Pylori?
- Remove causative agents such as alcohol/NSAIDs
- Reduce stress
- H2 antagonists e.g. ranitidine or cimetidine - to reduce acid release
- PPIs e.g. lansoprazole or omeprazole - to reduce acid release
- Antacids - neutralise acid to relieve symptoms
How do you treat a H.Pylori infection that is causing gastritis?
Triple threat (PPI and 2 antibiotics) - ‘CAP’ for 14 days. =
clarithromycin + amoxicillin + PPI - eg Omeprazole
If penicillin allergy then give metronidazole 400mg instead
What are the complications of gastritis?
Peptic ulcers
Bleeding and anaemia
MALT lymphoma (mucosa-associated lymphoid tissue)
Gastric cancer
normal physiology - Give some differences in the location, nerve innervation and sensation of the Parietal and visceral peritoneum
Parietal:
- Covers the abdominal wall
- Somatic innervation
- Sensation is well localised
Visceral:
- On organs e.g. stomach, liver and colon
- Autonomic innervation
- Sensation is poorly localised
from teach me anatomy
name some pathogens that can cause a spontaneous bacterial peritonitis.
E coli, Klebsiella, Staphylococcus Aureus, Enterococci
What is primary peritonitis caused by?
- Primary peritonitis - inflammation caused by spontaneous bacterial peritonitis. This is the most common type of peritonitis
- e.g. E.coli, klebsiella, staphylococcus aureus, Enterocci
What is secondary peritonitis caused by?
Secondary peritonitis - caused by something else e.g. chemical such as:
Bile
Ischaemia
Trauma
Familial Mediterranean Fever
Name some paths through which the peritoneum can become infected
GI perforation, eg **Perforated ulcer, Appendix, Diverticulum
Transmural Translocation no perforation eg Pancreatitis, Primar bacterial peritonitis
Female Gential tract infection, aka pelvic inflammatory disease
Haemoatogenous spread aka sepsis
from netter illustrated human pathology
What are the clinical features of localised peritonitis?
Signs and Symptoms of Underlying conditions
Pain
nausea and vommitng
Fever
Tachycardia
Localised Guarding and rebound tenderness
- Pain relieved by resting hands on abdomen - thereby stopping movement of peritoneum and thus pain
- Lying still - people with peritonitis want to stay still
- Prostration - lying stretched out on the ground
Infrequent bowel sounds, or ceasing of bowel sounds
Tender rectal/vaginal pain in pelvic peritontis
What are some general investigations for Peritonitis?
- To monitor/confirm infection - raised white cell count and CRP
- Serum amylase to exclude acute pancreatitis
- Human Chorionic Gonadotrophin (HCG) to exclude pregnancy as cause
- Erect CXR - may see free air under diaphragm
- Abdominal X-ray to exclude bowel obstruction and foreign body as cause of abdominal pain
- CT abdomen to exclude ischaemia as cause of pain
taken from OHCM 9th edition
What are some investigations you would do for suspected Spontaneous bacterial peritonitis?
- Ascitic tap - high white cell count
- Blood cultures
What are some first line management for Peritonitis?
What antibiotic would you use?
Broad spectrum antibiotics - metronidazole
Fluid resuscitation – IV fluids and electrolytes
Urinary catheter
Surgery
Laparotomy i.e. big cut
Laparoscopy i.e. key-hole surgery
Define GORD
Reflux of stomach contents into the oesophagus, due to pressure of the LOS getting lower = so the reflux persists for longer, becoming pathological
Where is GORD most common, What % of population here is thought to be affected by GORD?
Highest In Western European and Northern American populations, the estimated prevalence is as high as 10-20%.
What are some risk factors for getting GORD?
- High BMI
- Genetic association
-
Pregnancy
Male - Smoking
-
NSAIDs, caffeine & alcohol
Hiatus hernia – LOS sphincter can’t close properly - Other medication (may lower LOS pressure)
What medications have been known to lower LOS pressure and hence lead to GORD?
antihistamines, calcium channel blockers, antidepressants, benzodiazepines, and glucocorticoids
What are the two main types of hiatus hernia?
Sliding hiatus hernia (80%) is where the gastro-oesophageal junction slides up into the chest
Rolling hiatus hernia (20%) is where the gastro-oesophageal junction remains in the
abdomen but a bulge of stomach herniates up into the chest alongside the oesophagus
from OHCM, 9th edition
What type of Hiatus hernia is associated with GORD?
Sliding Hiatus hernia - Acid reflux often happens as the lower oesophageal sphincter becomes
less competent in many cases.
In Rolling, the gastro-oesophageal junction remains intact, gross acid reflux is uncommon.
Outlien the pathophysiology behind GORD.
An increase in transient lower oesophageal sphincter relaxations (due to reduced tone of LOS) results in reflux of gastric acid, pepsin, bile and duodenal contents back into the oesophagus
Lower oesophageal sphincter relaxes independently of a swallow, allowing gastric acid etc. to flow back into the oesophagus
What are some signs and symptoms of GORD?
Symptoms
Heart burn – burning chest pain
Odynophagia – painful swallowing
Hoarse throat
Wheezing
Regurgitation
Acidic taste in mouth
Signs
Chest pain aggravated by bending, stooping and lying
Nocturnal asthma – due to aspiration of gastric contents into lungs
What are some differential diagnosis for GORD?
- Eosinophilic oesophagitis
- Peptic ulcer disease
- Non-ulcer dyspepsia
- Malignancy
- Pericarditis
- Ischaemic heart disease
What first line investigation would you do in suspected GORD?
Prescribe an 8 week trail of a PPI - and suspect GORD if symptoms improve - first line
Also can do
ambulatory pH monitoring - insertion of pH capsule at gastro-oesophageal junction during endoscopy. === demonstrate abnormal exposure to oesophageal acid in the absence of oesophagitis
What are some red flags that you may see in a patient with GORD like symptoms?
• Anaemia
• Loss of weight
• Anorexia (loss of appetite)
• Recent onset of progressive symptoms
• Masses / Melena (black stools) → or bleeding from any part of GI tract
• Swallowing difficulties (Dysphagia)
• + > 55 y/o, new onset dyspepsia
ALARMS - (also nausea, raised platelet count)
If you see any red flag symptoms in GORD, what investigation would you do? What complications of GORD are you looking for
Endoscopy
oesophagitis, Barrett’s oesophagus or an alternative diagnosis (i.e. oesophageal/gastric malignancy).
Oesophageal adenocarcinoma
How can you classify GORD? Give some points of reference within the grading
-Los Angeles classification
- Grade A: ≥1 mucosal break, each ≤ 5mm
Grade B: ≥1 mucosal break > 5mm. Not continuous between top of mucosal folds.
Grade C: ≥1 mucosal break, continuous between top of mucosal folds, not circumferential
Grade D: mucosal breaks involving more thanthree quartersof luminal circumference.
What are lifestyle changes for managing GORD?
Weight loss
Reduce alcohol intake
Eat smaller meals
Avoid eating before going to bed (no food 2 hours before bed)
What are the medical managements for GORD
PPI- this will lower acid production within the stomach
H2 receptor antagonist e.g., ranitidine reduces stomach acid
Antacids e.g., Gaviscon
surgery - Nissen Fundoplication
What is the surgical management for GORD?
Nissen fundoplication: wrapping the fundus of the stomach around the lower oesophagus to tighten the sphincter
taken from Mayo Clinic
What is Barret’s oesophagus defined as?
Barrett’s oesophagus describes metaplasia (transformation of one cell type to another)
lower oesophageal lining from stratified squamous epithelium to mucous secreting columnar epithelium with goblet cells.
It can be the precursor to Oesophageal adenocarcinoma
Normal physiology - what can the inner wall of the GI tract (the mucosa) be divided into?
three cell layers.
- The innermost epithelial layer absorbs and secretes mucus and digestive enzymes.
- The middle lamina propria contains blood and lymph vessels.
- The outermost muscularis mucosa, a layer of smooth muscle that contracts and helps break down food.
normal physiology - what cell would you find in the Cardia of the stomach, and what would they secrete?
The cardia contains mostly foveolar cells that secrete mucus
normal physiology - what cell would you find in the Fundus and Body of the stomach, and what would they secrete?
The fundus and the body have mostly parietal cells that secrete hydrochloric acid and IF and chief cells that secrete pepsinogen, an enzyme that digests protein.
Normal physiology - what cell would you commonly find in the Antrum, and what would do they secrete?
The antrum has mostly G cells that secrete gastrin in response to food entering the stomach. (These G cells are also found in the duodenum and the pancreas). Gastrin stimulates the parietal cells to secrete hydrochloric acid, and more broadly stimulates the growth of glands throughout the stomach.
Normal physiology - what Glands do you find in the duodenum? What do they secrete?
The duodenum also contains Brunner glands which secrete mucus rich in bicarbonate ions, to neutralise the acid.
blood flowing to the stomach and duodenum brings in even more bicarbonate which helps neutralise the hydrochloric acid
The stomach and duodenum also secrete prostaglandins. What does this lead to?
- stimulate mucus and bicarbonate secretion,
- vasodilate nearby blood vessels allowing more blood to flow
- promote new epithelial cell growth,
- inhibit acid secretion.
Define what an ulcer is. Are Gastric or Duodenal ulcers more common ?
A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter. Duodenal ulcers are more common than gastric ulcers.
Outline the overacrhing pathophysiology leading to peptic ulcers.
What is the appearance of peptic ulcers?
A result of an imbalance between factors promoting mucosal damage (gastric acid,H. pylori, NSAIDs) and those promoting gastroduodenal defence (prostaglandins, mucus, bicarbonate).
Appear as small, round “punched out” holes in the mucosa.
What is the main cause of PUD? What % of Gastric and Duodenal ulcers is it responsible for?
H.Pylori is responsible for 95% of duodenal ulcers and 75% of gastric ulcers
What drugs can cause PUD?
NSAIDs inhibit COX enzyme which is needed for prostaglandin synthesis
SSRIs, steroids and bisphosphonates can also cause as they break down the protective layer
What lifestyle factors can cause PUD?
Smoking and alcohol: may lead to increased acid.
Caffeine: may lead to increased acid.
Stress: may lead to increased acid.
What other health conditions can cause PUD?
Zollinger-Ellison syndrome: a gastrinoma (tumour) that secretes too much gastrin, leading to numerous ulcers
Blood type O
Raised intracranial pressure: causes vagal stimulation which increases acid production (Cushing’s ulcer).
Severe burn: hypovolaemia secondary to a burn = reduced perfusion of stomach, = necrosis (Curling ulcer)
What are the signs of PUD?
- Evidence of bleeding
- Hypotension and tachycardia (shock)
- Melaena on rectal examination
- Epigastric tenderness
- Pallor, if anaemic
What are the symptoms of PUD?
-
‘Burning’ epigastric pain
- Pain relieved by eating and worse when hungry:duodenal ulcer
- Pain worsened by eating:gastric ulcer
- Nausea and vomiting
- Haematemesis or melaena
- Dyspepsia (indigestion)
- Reduced appetite and weight loss
- Anaemia: due to bleeding
- Fatigue
What are some alarm signs you need to be aware of in peptic ulcer disease? What should you do if you see any of these?
Alarm symptoms:
Anaemia (iron deficiency);
loss of weight;
anorexia;
recent onset/progressive symptoms;
melaena/haematemesis;
swallowing difficulty
If you see any of these, or patient is under 55 to Do upper GI endoscopy
What are some investigations you would do for Peptic ulcer disease, if there is no evidence of bleeding
-
H. pyloribreath test and/or stool antigen
- Breath test: measures CO2 in breath after ingesting C-urea
- Stool antigen: monoclonal antibodies for detection of H. pylori
Fasting gastrin level: if suspected Zollinger-Ellison syndrome
Endoscopy with Biopsy - not routinely done if no evidence of bleeding
What is the management for non bleeding peptic ulcers?
- Conservative:treat risk factors e.g. cease NSAIDs/ other drugs, smoking and alcohol
-
H. pylorinegative: - . lansoprazole and omeprazole
H2 antagonists e.g. cimetidine to reduce acid release
H. pyloripositive:triple eradication therapy -
CAP
Clarithromycin
Amoxicillin
PPI e.g. omeprazole
Outline the pathophysiology behind appendicitis
Normally occurs due to luminal obstruction
As the appendix continues to secrete mucus the fluid and mucus build up = increasing pressure = makes appendix get bigger
= and push on the visceral nerve fibres causing pain
Bacteria now trapped and able to multiply resulting in invasion of gut organisms into the appendix wall
This leads to oedema, ischaemia, necrosis, perforation and inflammation
What signs and symptoms would you see in acute appendicitis?
Describe the pain seen
- Periumbilical pain (referred pain) which migrates to the right iliac fossa (McBurney’s point)
- Low-grade fever: > 38°C suggests alternative pathology e.g. mesenteric adenitis
- Reduced appetite and anorexia
- Nausea and vomiting: persistent vomiting is unusual
- Diarrhoea: rare but may occur in pelvic appendicitis or due to a pelvic abscess
What signs would you see in someone with acute appendicits? What examinations would you do?
- Right iliac fossa tenderness: rebound tenderness (pain when pressure is taken off) or percussion tenderness (pain during percussion) suggests localised peritonism
- Guarding
- Rovsing’s sign: pain in the right iliac fossa is worsened by pressing on left iliac fossa
- Psoas sign: pain is worsened by extending the hip
- Obturator sign: pain is worsened by flexing and internally rotating the hip
Tachycardia, hypotension and generalised peritonism: suggests perforation
What are some investigations of someone with acute appendicitis?
FBC – raised WBC count
Elevated CRP and ESR
Ultrasound – especially in women and children
aperistaltic or non-compressible structure with outer diameter >6 mm
Abdominal CT with contrast
Urinalysis (exclude UTI)
Pregnancy test - exclude pregnancy
What are Diverticula?
Outpouching of the colon wall, most frequently in the sigmoid colon.
Define Diverticulosis
Diverticulosis:the presence of diverticula (out-pouching) in an asymptomatic patient
Define Diverticulitis
Diverticulitis:where diverticula become inflamed and infected, typically causing severe lower abdominal pain, fever, general malaise, and occasionally rectal bleeding
How do Diverticula form, leading to diverticulosis?
Areas in the large intestine where the smooth muscle is penetrated by blood vessels are weaker than normal.
Increased pressure in the lumen causes a gap to form in this muscle, allowing the mucosa to herniate through.
It happens in areas that are not covered by teniae coli
Where is the most common area for the formation of diverticula?
Mainly form in sigmoid colon but can also affect right colon
When would you use a colonoscopy when investigating diverticulitis? Why do you need to be cautious using it?
Colonoscopy: should generally be avoided in acute diverticulitis due to the risk of perforation, and is used if the diagnosis is unclear or alternative pathology is suspected
What would you offer in symptomatic diverticular disease?
1ST LINE –
dietary and lifestyle modifications
CONSIDER –
analgesia - Paracetamol, avoid NSAIDs
CONSIDER –
antispasmodic - dicycloverine
What surgical procedure would be performed for diverticulitis?
Hartmann’s procedure- removing the affected section of the bowel and creating an alternative path for faeces to be passed
leads to stoma
What area/tissue layers are affected in a Mallory Weiss tear?
Longitudinal lacerations limited to the mucosa and submucosa
at the border of the gastro-oesophageal junction.
What is the classic presentation of someone with a Mallory Weiss tear?
The classic history of a Mallory Weiss tear is a patient with a background of alcohol excess presenting with episodes of violent retching or vomiting, followed by vomiting a small or moderate amount of fresh blood.
What is the management for C Diff Diarrohea due to antibiotic use?
map classification of C difficle
Treat: Metronidazole, stop antibiotics
C.difficle is a gram positive ANAEROBIC BACILLI -
Met has good anaerobic cover
Name some causes of small bowel obstruction.
Can be mechanical (obstruction) or functional (lack of contraction)
Adhesions (75%) from previous abdominal/ gynaecological surgeries
Hernias (10%)
Crohn’s (strictures) narrowing of intestines from scar tissue
Malignancy
Gallstone ileus - gallstone within lumen of small bowel
Bowel obstructions - name some things that can lead a functional (failure of peristalsis) bowel obstruction.
- Occurs post abdominal surgery
- Can occur due to electrolyte imbalances, particularly hypokalemia and hypercalcaemia
- Infection/ inflammation e.g. peritonitis, pancreatitis, appendicitis.
- Spinal injury
- Drugs e.g. TCAs
What is the pathophysiology behind the issues/symptoms that a mechanical Small bowel obstruction causes?
Mechanical obstruction leads to symptoms eg abdominal pain, distention, and absolute constipation. This is through it causing Dilation of the proximal bowel which leads to compression of mesenteric vessels
Leads to oedma in mucosa, which causes transudation of large volumes of electrolyte-rich fluid into the bowel.
Eventually, as arterial supply is compromised, bowel ischaemia occurs with risk of perforation and subsequent faecal peritonitis and sepsis
What are some signs and symptoms of a small bowel obstruction?
Colicky abdo pain (pain higher up)
Abdominal distension/tenderness (less severe than LBO)
Vomiting first (bilious), followed by constipation
Hyperresonant bowel
‘Tinkling’ bowel sounds
-
Tachycardia and hypotension:
- Third-spacing of fluid
- Significant hypotension may indicate ischaemia, perforation or sepsis
- Nausea and vomiting: early symptoms in SBO and a late sign in LBO
- Abdominal bloating
- Constipation (may be absolute in distal obstruction):
What investigations would you do for a small bowel obstruction? What is first line and what is gold standard?
1st line: Abdo XRay (dilation of the small bowel >3 cm, coiled-spring appearance)
- FBC:elevated white cell count with neutrophilia
- U&Es:assess for pre-renal acute kidney injury secondary to hypovolaemia (third spacing). Additionally, hypokalaemia is a cause of ileus
Gold standard: CT abdomen and pelvis with contrast
What is the management in unstable patients with severe SBO and LBO?
Surgical
Treat according to cause
Laparotomy - incision in abdominal wall, done if - Evidence of bowel ischaemia regardless of the cause, or there’s a non-adhesional cause (e.g. strangulated hernia)
Adhesiolysis for adhesions
Hernia repair
Bowel resection
Intestinal obstruction: what is volvulus?
Volvulus is a
twist/rotation in the bowel; and its a type of closed loop obstruction = two points of obstruction along the bowel; meaning that there is a middle section sandwiched between two points of obstruction.
There is a risk of necrosis. Most likely to happen to free floating areas of the bowel aka bowel with mesentery
What is Hirschprungs disease? What can it be a cause of?
- Neonates are born without complete innervation of colon to rectum
- Results in gut dilatation and the filling of faeces which remains since no ganglion cells to result in peristalsis and movement of contents - resulting in obstruction
Can cause a large bowel obstruction
What is the first line and gold standard investigation for large bowel obstructions?
1st line: Abdo XRay
Dilation of the large bowel >6cm
Dilation of the caecum >9cm
Gold standard: CT of the abdomen and pelvis with contrast
Abdo xray of someone with sigmoid volvulus - Coffee bean sign
What is the pathophysiology of achalasia?
The nerves in the LOS don’t work properly. This means the LOS can’t relax leading to an obstruction
Dysphagia: unable to swallow BOTH solids and liquids
Heartburn
Food regurgitation → aspiration pneumonia
name some investigations for achalasia. What is first line and what is gold standard?
The first line investigation for Achalasia is Upper GI Endoscopy to
exclude malignancy
Barium swallow: ‘bird’s beak’ sign
Manometry = GOLD - tube passed through nose, and measures strength of LOS
What part of the body is most commonly affected by ischaemic collitis? What part of gut is most resistant?
Splenic flexure most commonly affected, despite dual supply from SMA and IMA, as it is the most distal
Rectum is resistant to ischaemia due to dual supply from IMA and internal iliac artery
Where in the oesophagus do squamous cell carcinomas and adenocarcinomas most often occur?
Squamous cell carcinoma - upper two thirds
Adenocarcinoma - lower third
Ties in with risk factors for it!
Outline the pathophysiology behind squamous cell carcinomas of the oesophagus
epithelium is repeatedly exposed to risk factors like alcohol, cigarette smoke, or hot fluids, it gets damaged, so the squamous cells divide to replace the old damaged cells.
With each division there is a risk of mutation, which specifically can occur in tumour suppressor genes or proto-oncogenes.
this happens, squamous cells start dividing uncontrollably, and more mutations accumulate
Eventually, these mutations might make the cells malignant.
Outline the pathophysiology behind adenocarcinomas of the oesophagus
Most frequently, adenocarcinoma develops as a consequence of GORD
With GORD, the lower oesophageal sphincter is weaker than normal, and it allows acid from the stomach to go back up into the oesophagus after meals.
The presence of acid in the oesophagus can lead to Barrett’s oesophagus, which is when the squamous epithelium lining the oesophagus undergo metaplasia.
Over time, mutations might accumulate in either tumour suppressor genes or proto-oncogenesthat control the division of thesemetaplastic cells, ultimately resulting in a malignant tumour.
What is the first-line investigation for SSC/adenocarcinoma of oesphagus?
Upper GI endoscopy (OGD) and biopsy: first-line investigation and allows for visualisation of masses and biopsy
What test would be used to determine the severity of the cancer (oesophageal)?
CT/MRI of the chest and abdomen (staging and metastases)
Tumour, Nodal involvement, Metastasis
What cell does gastric adenocarcinoma arise from?
Where is it most common
Gastric adenocarcinomas arise from columnar glandular epithelium (adeno = gland)
Most common in the antrum
*MOST COMMON TYPE OF GASTRIC CANCER
What would you see on histology for intestinal type 1 gastric adenocarcinoma?
Well-differentiated
Tubular
What would you see on histology for diffuse type 2 gastric adenocarcinoma?
Poorly differentiated
Signet ring cells
they look like a signet ring because the cytoplasm has giant vacuoles that push the nucleus to the edge of the cell.
outline the pathophysiology behind diffuse type 2 gastric adenocarcinoma
a mutation of what gene is it commonly caused by?
Appear in any part of the stomach
Mostly related to genetic mutations in the CDH1 gene
Leads to E-cadherin not working properly,
cells detach and starts dividing uncontrollably.
causes gastric linitis plastica, === the stomach wall grows thick and hard resembles a leather bottle, as the cancer invades the connective tissue of the submucosa.
What are some signs and symptoms for gastric cancer?
Signs and symptoms
Virchow’s node (left supraclavicular)
Weight loss
Nausea & Vomiting
Haematemesis/melaena
Dysphagia
Anorexia
Epigastric pain
Red flags (ALARMS)
What is FAP?
Familial adenomatous polyposis (FAP)
Is an autosomal dominant condition involving the tumour suppressor gene APC
-
Adenomatous polyposis coli gene (APC) mutations:
- APC is a tumour suppressor gene. Normally, the APC protein identifies when a cell is accumulating a lot of mutations and forces it to undergo apoptosis, or programmed cell death.
- When the APC gene is mutated, the mutated bowel cells don’t die, and instead some start dividing uncontrollably, giving rise to polyps.
Outline the pathophysiology behind bowel cancer. What are they nearly all?
Pathology
Progression
Normal epithelium 🡪 adenoma 🡪 colorectal adenocarcinoma 🡪 metastatic colorectal adenocarcinoma
Nearly all are adenocarcinoma
Polypoid mass with ulceration
Spreads by direct infiltration through the bowel wall then spread to lymphatic and blood vessels and metastasise to liver and lung
Outline what TNM is.
Tumour, Node, Metastasis
Most solid organ cancers are staged using the TNM system,
which is based on the extent of tumour (T), the extent of spread to lymph nodes (N), and the presence of metastases (M)
What is assessed in the tumour part of TMN?
Tx- unable to asses size
T1- submucosa involvement
T2- Involvement of the muscle
T3- involvement of the subserosa and serosa (outer layer), but not through the serosa
T4- Spread through the serosa and reaching other tissues and organs
What is assessed in the node part of TMN?
NX- unable to asses
N0- No nodal spread
N1- spread 1-3
N2- spread to more than 3 nodes
What is assessed in the metastasis part of TMN?
M0- no metastasis
M1- Metastasis
What is Zenker’s diverticulum?
he outpouching into the pharynx causing food to become stuck
What are the symptoms of Zenker’s diverticulum?
pseudo-choking + bad breath + infection
outline what meckel’s diverticulum is
The distal ileum contains embryonic remnants of gastric
and pancreatic tissue. There may be gastric acid secretion, causing GI pain & occult bleeding.
symptoms for it mainly seen in children - can be a differential for appendicitis
Normal physiology - What is the dentate line?
a line which divides the upper two-thirds and lower third of the anal canal.
What are the four grades of internal haemorrhoids?
Grade I: no protrusion outside the anal canal.
Grade II: protrusion outside the anus during bowel movement, but they retract spontaneously.
Grade III: prolapsed haemorrhoids that don’t retract spontaneously, but they can be pushed back in manually.
Grade IV: prolapsed haemorrhoids that cannot be manually pushed back in.
What are the investigations for haemorrhoids?
External haemorrhoids are visible on inspection
Internal haemorrhoids can sometimes be felt on a digital rectal exam
GOLD STANDARD proctoscopy is required for proper visualisation and inspection (its a hollow tube with light on the end
What do internal haemorrhoids look like with proctoscopy?
Internal haemorrhoids look like bulging purplish-blue veins
Prolapsed internal haemorrhoids appear dark pink, glistening, and are sometimes tender masses at the anal margin
Outline some management for haemorrhoids.
Stool softeners
Topical Hydro cortisol
High fibre diet, good fluid intake
For 1st and 2nd degree:
Rubber band ligation
Infrared coagulation
Injection scleropathy
Bipolar diathermy
Surgical management
For 3rd and 4th degree:
Hemorrhoidectomy
Stapled haemorrhoidectomy
Haemorrhoidal artery ligation
What are some common causes of anal fistulas?
Anorectal abscess (70%)
Crohn’s ulcerations (30%)
TB
What is an anorectal abscess? What are the symptoms of it?
Infection in anorectal tissue
Perianal pain
Perianal swelling
Fever
What is a pilonidal sinus/abscess? How do you treat it?
Ingrown hair → inflammation → hole (sinus) in skin → infected (abscess)
Keep area clean + Abx
What is an anal fissure?
What are causes of it?
Tear in lower anal canal (distal to dentate line), usually due to trauma
Constipation
Anal trauma
Rarely: crohns, TB
What would you see on biopsy for someone with gastric infection of cyrptomegalovirus?
When would you see an infection like this
Would see OWLE EYE INCLUSION BODIES in CMV infection
CMV is an AIDS DEFINING ILLNESS, you only see it in immunocompromised people
