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 are some investigations you would do for Peptic ulcer disease, if there is evidence of bleeding
-
Upper GI endoscopy and biopsy:
-
Gold standard diagnostic test for visualisation, and biopsy:
- Excludes malignancy
-
Gold standard diagnostic test for visualisation, and biopsy:
- FBC: assess the extent of anaemia
-
U&Es: urea is raised in an upper GI bleed
Erect CXR:if concerned about perforation, an erect CXR may demonstrate pneumomediastinum
All gastric ulcers should be biopsied as they can potentially be malignant
What scoring systems can you use in Peptic Ulcer disease?
When are they used
-
Glasgow Blatchford Score
Risk stratify patients with an upper GI bleed. If you score 0 can be discharged and return for an outpatient endoscopy. - Rockall ScoreCalculated after endoscopy, with the score including age, shock (BP and HR), comorbidities, and endoscopic findings. It is used to identify patients at risk of adverse outcomes following endoscopic treatment of an upper GI bleed.
What are some differentials of Peptic Ulcer disease?
- GORD
- Non-ulcer dyspepsia
-
Gastritis
Gastric malignancy
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
What is the management in bleeding peptic ulcers?
- IV crystalloid
- Blood transfusion: if significant acute blood loss suspected
-
Upper GI endoscopy- one of the following suggested;
- Mechanical therapy (e.g. clipping) +/- adrenaline
- Thermal coagulation with adrenaline
- Sclerotherapy (fibrin or thrombin injection) with adrenaline
High-dose IV PPI: administered post-endoscopy to reduce rebleeding.
Surgery or embolisation (blocking abnormal vessels)
What are some complications of Peptic Ulcer disease?
Ulcers can grow deeper until it hits an artery) 🡪 massive haemorrhage 🡪 shock
Perforation – requires immediate surgical consult
Obstruction
Peritonitis as acid enters peritoneum
Acute pancreatitis if ulcer reaches pancreas
Complications of Peptic ulcers - Which artery is perforated in gastric vs duodenal ulcers?
- Gastric ulcers typically affect the left gastric artery
- Duodenal ulcers typically affect the gastroduodenal artery
What are the signs of perforation in gastric vs duodenal ulcers?
Gastric= haematemesis and melena
Duodena= Melaena and haematochezia
Melena is the passage of black, tarry stools. Hematochezia is the passage of fresh blood per anus, usually in or with stools.
Compare the timings of pain experienced following a meal between gastric and duodenal ulcers.
Gastric Ulcers = worsen straight after eating
Duodenal Ulcers = Better 1-2 hours after eating (as pyloric sphincter is closed and food is being digested in stomach) and then worsen 2 hours after eating when food is in duodenum
What is appendicitis?
Acute appendicitis is an acute inflammation of the vermiform appendix, most likely due to obstruction of the lumen of the appendix.
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 are some causes of appendix obstruciton?
Faecolith – stones made of faeces
Filarial worms
Undigested seeds
Lymphoid hyperplasia – can obstruct tube and lymphoid follicles can grow during viral infection
Bacteria –
WHat are some bacteria that have been known to cause appendicitis?
Campylobacter jejuni, Yersinia, salmonella, bacillus cereus
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 is guarding and rebound tenderness?
Guarding - when abdominal muscles tense up
Rebound tenderness - pain when releasing pressure on palpation
What is the initial management for appendicitis?
Fluids:
- Analgesia: patients can be in considerable pain - Morphine, Paracetamol
- Antiemetics: can be given for nausea and vomiting e.g. ondansetron
- Preoperative IV antibiotics - Metronidazole 500mg/8h + cefuroxime 1.5g/8h
What is the definitive management for appendicitis?
Prompt appendicectomy:laparoscopic
Postoperative antibiotics
What are some complications of Appendicitis?
Perforation (15-20%): if left untreated, there is a significant risk of appendiceal rupture, which will lead to sepsis and death if untreated
Appendix Mass: occurs when theomentumsurrounds and sticks to the inflamed appendix, forming a mass in the right iliac fossa
Abscess: inflammation may cause the formation of a localised collection of pus in proximity to the appendix, which will require drainage.
-
Complications of Appendicectomy
- Bleeding, infection, pain and scars
- Damage to bowel, bladder or other organs
- Removal of a normal appendix
What are some differentials for appendicitis? (gynae, GI, GU)
Gynae: Ectopic pregnancy,
ovarian torsion, ruptured ovarian cyst
GI: IBD, diverticulitis, Meckel’s diverticulum
GU: Kidney stones, UTI, testicular torsion
Name some GI conditions associated with Dyspepsia.
GORD
Gastritis (inflammation of stomach)
Peptic Ulcer disease
Oesophageal Cancer
When would you refer for 2 week endoscopy? (upper GI)
Dysphagia (Swallowing difficulties) or Age ≥ 55yo with weight loss and 1 of the following:
- Upper Abdo pain
- Reflux
- Dyspepsia
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 Diverticular Disease
Diverticular disease: where diverticula cause symptoms, such as intermittent lower abdominal pain, without inflammation and infection
Define Diverticulitis
Diverticulitis:where diverticula become inflamed and infected, typically causing severe lower abdominal pain, fever, general malaise, and occasionally rectal bleeding
What are some risk factors for getting Diverticular disease/diverticulitis?
- Increasing age:> 50 years; peak age is 50-70 years old
- Low dietary fibre
- Obesity: particularly in younger people
-
Sedentary lifestyle
Connective tissue disorders like Maarfans - Smoking:increases the risk of complicated diverticular disease
- NSAIDs:increases the risk of perforation in diverticulitis
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
Why do diverticula not form in the rectum?
As the rectum has an extra layer of longitudinal muscle that surrounds it this adds extra support.
Where is the most common area for the formation of diverticula?
Mainly form in sigmoid colon but can also affect right colon
What causes Diverticulitis/diverticular disease?
Can happen due to erosion of the diverticular wall from higher luminal pressures.
Inflammation can happen when fecal matter, or fecaliths, become lodged in the diverticula (less common)
What are some symptoms of diverticular disease?
Bowel habits changed
Bloating / flatulence
Left lower quadrant pain
N&V
What are some symptoms of diverticulitis?
Symptoms of diverticular disease = aka
Bowel habits changed
Bloating / flatulence
Left lower quadrant pain
N&V
AND
+ FEVER
+ Blood in stool - Haematochezia
What are some initial investigations to consider for diverticulitis? What is gold standard?
FBC - would see polymorphonuclear leukocytosis - diverticulitis in older patients with abdominal pain and leukocytosis, because the presentation can be atypical in this group
C reactive protein/ESR - should be raised
U and Es - to check kidney function
Contrast CT scan gold standard, imaging modality of choice
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 treatment would you offer for asymptomatic diverticulosis?
Dietary and lifestyle modifications.
Offer laxatives if constipation
increasing dietary fibre, including fruit and vegetables
What would you offer in symptomatic diverticular disease?
1ST LINE –
dietary and lifestyle modifications
CONSIDER –
analgesia - Paracetamol, avoid NSAIDs
CONSIDER –
antispasmodic - dicycloverine
What management would you offer in acute diverticulitis, that’s uncomplicated?
1ST LINE –
analgesia
CONSIDER –
antispasmodic - dicycloverine
CONSIDER –
oral antibiotic - eg Amoxicillin/clavulanate (co amoxcilcav)
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 are the complications of diverticulitis?
Perforation
Peritonitis
Peridiverticular abscess
Large haemorrhage requiring blood transfusions
Fistula (e.g., between the colon and the bladder or vagina)
Ileus / obstruction
name some common cause of upper GI bleeding
- Peptic ulcers
- Mallory–Weiss tear
- Oesophageal varices
- Gastritis/gastric erosions
- Drugs (NSAIDS, aspirin,
steroids, thrombolytics,
anticoagulants) - Oesophagitis
- Duodenitis
- Malignancy
- No obvious cause
What is a mallory weiss tear
Linear mucosal tear occurring at the oesophagogastric junction and produced by a sudden increase in intra-abdominal pressure
What group does a Mallory Weiss tear most commonly effect?
More common in males
Mainly between 20-50
Mallory-Weiss Tear (MWT) accounts for 5% to 15% of patients with gastrointestinal (GI) bleed.
What are some common causes of a Mallory Weiss tear? What do these lead to
Common causes:
forceful vomiting (alcoholism, bulimia)
Chronic coughing
Weightlifting
Hiatus hernia
increases intra-abdominal pressure which forces stomach contents into the oesophagus, dilating it and causing a tear results in an upper GI bleed that is usually self-limiting
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 are some symptoms of a Mallory Weiss tear?
Vomiting
Abdominal pain
Haematemesis (blood in vomit)
Retching
Postural hypotension
Dizziness
Melena
What investigations would you order for a suspected Mallory weiss tear?
upper GI endoscopy (i.e., gastroscopy) (this is also gold standard) would see red longitudinal defect with normal surrounding mucosa
Other tests;
FBC: assess for anaemia secondary to bleeding; usually normal
LFTs -typically normal but if deranged may raise the possibility of a variceal bleed
Erect CXR: performed to rule out oesophageal perforation or perforated peptic ulcer
What scoring systems can you use in a Mallory Weiss tear?
Glasgow and Blathford score,
and the Rockall Score =
When is a Glasgow and Blatchford score used? What does it indicate?
Glasgow and Blathford score, = both used for Risk gauging in Upper GI bleeds a score of more than 0 = admission to inpatient endocscopy
looks at
Haemoglobin
Urea
Initial systolic blood pressure
Gender
Heart rate (tachycardia)
Melaena
History of syncope
Hepatic disease history
Cardiac failure present
What is the Rockall scoring system used for?
Used in GI bleeding, and done after endoscopy, It is used to identify patients at risk of adverse outcomes following endoscopic treatment of an upper GI bleed.
What are some differentails for a Mallory Weiss tear?
- Boerhaave’s syndrome: spontaneous perforation of the oesophagus, usually due to vomiting, which ruptures all the layers of the oesophageal wall (transmural). Boerhaave’s syndrome is a surgical emergency.
- Gastroenteritis
- Peptic ulcer
- Varices
- Cancer
MWT can be often be self-limiting, so mild bleeding doesn’t require treatment. If bleeding is persistent or significant, what would you do?
-
Upper GI endoscopy:diagnostic and therapeutic with one of the following suggested
- Mechanical e.g. clipping +/- adrenaline
- Thermal coagulation with adrenaline (use heat to seal off bleed)
- Sclerotherapy with adrenaline (delivers medication to the tear to stop bleeding)
- Variceal band ligation
High-dose IV proton pump inhibitor: administered post-endoscopy to reduce rebleeding; e.g. pantoprazole.
^^Same as oesophageal varices!!
Treat the cause! (aka CBT for bulaemia, Alcohol Cesscation)
What are some Complications for a MWT?
- Rebleeding: usually occurs within the first 24 hours, but is rare after endoscopy
- Hypovolaemic shock: only occurs with life-threatening, persistent bleeds, which are very rare following MWT
- Oesophageal perforation: a rare complication
Name some different types of diarrhoea
secretory, osmotic, exudative, inflammatory, dysentery
What is the most common cause of infective diarrhoea in
a) children
b) Adults
- Rotavirus - leading cause of diarrhoea illness in young children, affects nearly all children by the age of 4
- Norovirus - most common among adults. Associated with; cruise ships, hospitals, restaurants - close proximity of people
Both cause watery diarrhoea
Name 4 common bacteria that lead to bloody diarrhoea.
Campylobacter jejuni - most common
Verotoxigenic E. Coli - more common in children
Salmonella - more common in children
Shigella spp. - more common in children
lead to Bloody diarrhoea
Name 4 bacteria that cause watery diarrhoea. What are they each associated with?
Enterotoxigenic e.coli - Cause of Travellers diarrhoea
Bacillus cereus reheated rice
Staphylococcus aureus
^all with food poisoning
Vibrio cholerae
Name some antibiotics that can lead to Diarrhoea due to C.Difficle
antibiotics beginning with C can give rise to antibiotic
induced Clostridium difficile diarrhoea:
Clindamycin, ciprofloxacin (Quinolones), co-amoxiclav (Penicillins), cephalosporins
When can you see a Clostridium Difficile infection? How can it lead to Diarrhoea?
in general, antibiotics beginning with C can give rise to antibiotic
induced Clostridium difficile diarrhoea:
Clindamycin, ciprofloxacin (Quinolones), co-amoxiclav (Penicillins), cephalosporins
Clostridium difficile replaces normal gut flora that has died, causes necrosis giving rise to pseudomembranous colitis - diarrhoea
How is C difficile spread?
Faecal oral route through spores
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
What is the most common parasitic cause of diarrhoea, and how would you treat it?
- Giardia lamblia - most common -Treat: metronidazole
What are some investigations for Diarrhoea?
Stool Microscopy
Blood in stool suggests bacteria infection - E Coli/Shigella
If chronic, sigmoidoscopy and bloods:
- Raised white cell count if parasites
- Raised CRP, WCC and low albumin if C.diff
What is the management for Diarrhoea?
Underlying cause
Oral rehydration and avoid high-sugar drinks
Antiemetics to treat vomiting– metoclopramide
Antimotility – loperamide, Codeine Phosphate
Broad spectrum antibiotics – ciprofloxacin, ceftriaxone
Giardia lamblia (parasite)– metronidazole
Viral - supportive, ensure fluid and electrolyte replacement - dioralyte
What are some non infectious causes of Diarrhoea?
Cancer
Chemical, eg Poisoning sweeteners, medications
Inflammatory bowel disease, eg Crohns, ulcerative Collitis
IBS / malabsorption
Endocrine eg Thyrotoxicosis
Radiation
What is a bowel obstruction and what are the 3 types?
What is most common?
The interruption of passage through the bowel. Can be a surgical emergency
Small bowel obstruction (most common) (60-75% of all bowel obstructions)
Large bowel obstruction
Pseudo-obstruction
What is a small bowel obstruction? What is a large bowel obstruction?
Small bowel obstruction (SBO) is a mechanical or functional obstruction of the small intestine that prevents the normal passage of digestive contents.
It can be partial or complete.
Large bowel obstruction (LBO) occurs due to mechanical or functional obstruction of the large intestine that prevents the normal passage of contents.
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
What are the complications of SBO?
Bowel ischaemia
Sepsis
Aspiration pneumonia
Short gut syndrome
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
Give 3 common causes of small bowel obstruction in children.
Appendicitis.
Volvulus.
Intussusception. Intussusception is when part of the intestine invaginates into another section of the intestine
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 are the causes of LBO?
Colorectal cancer is the most common (90% of cases)
Volvulus- torsion of the colon around itself and the mesentery
Stricture
Diverticulitis
Intussusception (more common in children) is when the bowel fold within itself
Hirschprung’s disease:
Outline the pathophysiology behind large bowel obstructions
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 does the large intestine having a larger lumen as well as longitudinal and circular muscles implicate, regrading large bowel obstructions?
Large bowel has a larger lumen as well as circular and longitudinal muscles thus the ability of the large bowel to distend is much greater thus symptoms present slower and later than in SBO
What are some signs and symptoms of a large bowel obstruction?
Continuous abdominal pain
Severe abdominal distension
Constipation first, followed by vomiting (initially bilious, then faecal vomiting)
Absent bowel sounds
What is the first-line treatment for SBO and LBO? (done if patient is stable)
‘drip’ (IV fluids) and ‘suck’ (NG tube)
NBM
and also IV antibiotics (cefotaxime and metronidazole)
Analgesia and anti-emetics
Catheter (monitor urine output)
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
Define a what pseudo obstruction is
Clinical picture mimicking colonic obstruction but with no mechanical cause.
Also known as Ogilvie syndrome.
How do you manage pseudo obstructions?
- Treat underlying problem e.g. withdrawal of opiate analgesia
- Correct U&E
- IV Neostigmine - a cholinesterase inhibitor, may be given to encourage motility.
- Endoscopic colonic decompression
What are some causes of pseudo obstructions?
- Puerperium: the period after childbirth during which the mother’s reproductive organs return to their original non-pregnant condition.
- Postoperative states e.g. abdominal, pelvic, cardiothoracic, orthopaedic and neuro
- Intra-abdominal trauma
- Intra-abdominal sepsis
recap - what are the main causes of a
Small bowel obstruction
Large bowel obstruction
Small - adhesions - due to surgery
Large - malignancy - colorectal cancer
What is achalasia?
Degeneration of ganglions in Auerbach’s/myenteric plexus (in muscularis externa)
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 is ischaemic colitis?
Bowel ischaemia that affects the large bowel. Due to pathology in the inferior mesenteric artery.
What are some causes of ischaemic colitis?
non-occlusive
Heart failure
Septic shock
Vasopressors
Renal impairment
PVD
Cocaine use
occlusive
Atrial fibrillation major risk factor
IE- can cause in younger patient’s
Vasculitis-
What are the signs of Ischaemic collitis?
Abdominal tenderness and distension in left abdomen
Haemodynamic instability (Shock)
Abdominal bruit (turbulent blood flow)
What are some symptoms of ischaemic colltiis?
Colicky lower left side abdominal pain- worse after eating
Diarrhoea
Haematochezia- passage of fresh blood
Fever
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
What is acute mesenteric ischaemia?
Its a medical emergency - Blockage of mesenteric arteries/veins → bowel ischaemia
What are the causes of mesenteric ischaemia?
Superior mesenteric artery thrombosis – most common
Superior mesenteric artery embolism (e.g. due to AF)
Mesenteric vein thrombosis – common in younger patients with hypercoagulable states
Non-occlusive diseases
What are some signs and symptoms of acute mesenteric ischaemia?
CLASSIC TRIAD OF
- Central/RIF severe abdo pain
- NO abdo signs on exam (aka no gurading, rebound tenderness)
- Rapid Hypovolaemic shock
Also
Nausea and vomiting
Melena/ haematochezia
Increasing abdominal distension
What is the investigations you would do for acute mesenteric ischaemia?
Bloods: metabolic acidosis (raised lactate)
1st line = CT contrast/angiography
GOLD = colonoscopy
What is the supportive first line management of ischaemic collitis and acute mesenteric ischaemia?
Nil by mouth (NG tube potentially)
IV fluids
Broad spectrum antibiotics
Unfractionated heparin
What are the surgical treatments of ischaemic colitis and acute mesenteric ischaemia?
Embolectomy
Thrombolysis
Mesenteric angioplasty and stenting
Laparotomy and resection of ischaemic/ necrotic segments
Stoma formation
What are the differences between IC and mesenteric ischaemia?
The area that is affected, Acute mesenteric ischaemia - SMA, and it tends to be more serious
Ischaemic colitis is seen in the colon , the inferior mesenteric artery is affected
What are the two types of oesophageal cancer?
Adenocarcinoma and squamous cell carcinoma
What type of oesophageal cancer is more common in developing world, and what is more common in the developed world?
adenocarcinomas - In the developed world
squamous cell carcinomas - Developing world
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!
What are the risk factors for an adenocarcinoma of the oesophagis?
Barret’s oesophagus
Obesity
Male sex
Smoking
GORD
Coeliac disease
What are some risk factors for squamous cell carcinomas of the oesphagus?
- Smoking:more associated with SCC
- Alcohol
- Achalasia
- Plummer-Vinson syndrome: rare disease characterised by difficulty swallowing, iron-deficiency anaemia, glossitis, cheilosis and oesophageal webs.
- Hot beverages
- Caustic strictures: strictures caused by caustic ingestions e.g. household bleach
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 are some symptoms of Oesophageal cancer?
- Progressive dysphagia (solids then liquids): most common feature
- Regurgitation
- Pyrosis (heartburn)
- Pain in chest or back
- Weight loss and anorexia
- Hoarseness: with recurrent laryngeal nerve involvement
- Vomiting
Think
A NAEMIA
L - loss of weight
A - anorexia
R - recent/sudden worsening of symptoms
M - Melaena/haematemesis
S - Swallowing/progressive worsening of symptoms, unlike achalasia.
What are some signs of oesophageal cancer?
- Lymphadenopathy
- Vocal cord paralysis
- Melaena on digital rectal examination: due to bleeding oesophageal cancer
think
A NAEMIA
L - loss of weight
A - anorexia
R - recent/sudden worsening of symptoms
M - Melaena/haematemesis
S - Swallowing/progressive worsening of symptoms, unlike achalasia.
Regarding Dysphagia, how can you differentiate between achalasia and oesophageal cancer?
Dysphagia of solids + liquids suggests achalasia.
Progressive dysphagia (struggle with solids, then after time struggle with liquids too) suggests cancer
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 is the treatment for an localised adenocarcinoma/SSC?/advanced
Surgical resection and chemoradiotherapy
Advanced - largely palliative
What are the 4 types of gastric cancer?
adenocarcinoma (most common),
carcinoid tumour,
leiomyosarcoma;
lymphoma,
depending on the type of cells it originates from.
ACLL
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 are the two types of gastric adenocarcinoma cancer?
Adenocarcinomas are divided into
- intestinal, or well-differentiated adenocarcinoma;
and - diffuse, or undifferentiated adenocarcinoma.
Intestinal is the most common!
Outline the pathophysiology behind intestinal (well differentiated) gastric adenocarcinomas
Where in the stomach does it typically appear?
Most commonly caused by H.pylori
H.pylori releases virulence factors, such as cagA, that damage epithelium and lead to gastritis
overtime cells undergo metaplasia. these might accumulate mutations in tumour suppressor genes and proto-oncogenes, so metaplastic cells divide uncontrollably and may become malignant.
This type typically appears on the lesser curvature of the antrum as a large, irregular ulcer, with heaped up edges.
What are some risk factors for
a) Type 1 Intestinal gastric adenocarcinoma
b) Type 2 diffuse gastric adenocarcinoma
Mutations in what gene is a risk factor for Adenocarcinoma of the stomach?
Male, older age, H.pylori infection, chronic/atrophic gastritis
Female, younger age (<50yo), Blood type A, Genetic, H.pylori infection
Mutations in the Cadherin gene (CDH-1) gene is risk factor
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.
Normal physiology - what does CDH1 gene normally code for, and what does this do?
It’s a tumour suppressor gene that codes for a membrane adhesion molecule called E-cadherin.
Normally, E-cadherin helps epithelial cells stick to one another and it also transmits signals that control the progression of cell cycle.
mutations in this gene is a risk factor for gastric cancer
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 type of gastric adenocarcinoma is more dangerous?
What is more common
Intestinal = Better
Diffuse = Worse (5-year survival of 3-10%)
has an increased ability to spread and invade adjacent structures, so it’s way more aggressive than the intestinal type.
Prevalence
Type 1 (intestinal type) = 80%
Type 2 (diffuse type) = 20%
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 investigations would you do for gastric cancer?
Upper GI endoscopy (gastroscopy) + biopsy
Endoscopic ultrasound
CT/MRI of the chest and abdomen to be able to stage the cancer, and check for metastases
HER2 testing: patients with HER2-positive metastatic gastric cancer may be responsive to trastuzumab(Herceptin)
How common is bowel cancer?
The 4th most common cancer in the UK
What are the risk factors for developing bowel cancer?
Familial adenomatous polyposis (FAP)
Hereditary nonpolyposis colorectal cancer (HNPCC)/Lynch syndrome
IBD
Diet high in red and processed meat and low in fibre
Obesity
DM
Smoking
Alcohol
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.
What is HNPCC?
It is also known as Lynch syndrome. It is an autosomal dominant condition that results from mutations in mismatch repair genes (MMR).
- Patients are at higher risk of number of cancers and doesn’t develop adenomas
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
What are the signs and symptoms of bowel cancer?
Change in bowel habit
Unexplained weight loss
Rectal bleeding
Unexplained abdominal pain
Iron deficiency
Abdominal/rectal mass
Right side tumours are often asymptomatic and will only present with iron deficiency
When would you be referred for suspected bowel cancer?
Over 40 with abdominal pain and unexplained weight loss
Over 50 with unexplained rectal bleeding
Over 60 with iron deficiency anaemia or change in bowel habit
OLD PERSON WITH ANAEMIA = THINK COLORECTAL CANCER HAVE TO REFER FOR URGENT 2 WEEK HOSPITAL APPT
What is the blood test used for testing bowel cancer?
CEA tumour marker used not in screening but testing relapse
Carcinoembryonic antigen (CEA): a serum tumour marker used tomonitor disease progression; it isnotdiagnostic and should only be performed following confirmation of diagnosis
What is the gold standard test for bowel cancer?
Colonoscopy and biopsy.
What other investigations can you do for colon cancer?
What is the at home screening test for bowel cancer?
Digital Rectal exam
38% of colorectal cancers can be detected by DRE
Double contrast barium enema
Faecal immunochemical test looks for the amount of human haemoglobin in the stool
Test used to be faecal occult blood test which detected blood in stools but used to detect meat blood
Who are FIT tests sent to?
Sent every 2 years for people from 60-74
What sided colorectal tumours is anaemia seen in? In what side is bleeding more common?
Right sided, More asymptomatic, and anaemia is seen
Left sided, more associated with a rectal mass and rectal bleeding is more common
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
Name some differentials for bowel cancer?
- IBS
- Ulcerative colitis
- Crohn’s disease
- Haemorrhoids
- Anal fissure
- Diverticular disease
Outline some management for colorectal cancer. What type of therapy is commonly used in a) Colon b) rectal cancers?
- Colon cancer:chemotherapy
- Rectal cancer:radiotherapy (T3 and above) or chemoradiotherapy (rectal cancer is amenable to radiotherapy as it is an extraperitoneal structure)
- Surgical resection:for all stages of colorectal cancer
Iron replacement: should be started immediately for patients with iron deficiency anaemia whilst awaiting for further investigations
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
What are haemorrhoids?
Definition: Haemorrhoids are enlarged anal vascular cushions
Internal (Grade 1-4)
External
What are internal and external haemorrhoids?
Internal are above the dentate line and external are below the dentate line
Normal physiology - What is the dentate line?
a line which divides the upper two-thirds and lower third of the anal canal.
What are haemorrhoids?
swelling and inflammation of veins in the rectum and anus
What can cause haemorrhoids?
Straining during bowel movements
Chronic diarrhoea
Anal sex
Congestion from a pelvic tumour, pregnancy, congestive heart failure and portal hypertension
What are the symptoms haemorrhoids?
Usually asymptomatic
Can cause itching, burning and vague discomfort - pruritus ani
Painless passage of bright red blood not mixed in with the stools
Straining
Can be painful
Mucous discharge
Constipation
Lump around or inside the anus
What are the 2 main types of haemorrhoids, and outline features of them
Internal haemorrhoids: arise internally, are painless covered in mucus, they can also prolapse.
External haemorrhoids: Form at the anal opening, painful, covered with skin.
NB a max of 2 marks may be achieved from each type of haemorrhoid
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 is an anal fistula?
An abnormal connection between the epithelial surface of the anal canal and skin - it is essentially a track that communicates between the skin and anal canal/rectum
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 are some signs and symptoms of an anal fissure? What are the treatments?
Extreme pain on passing motion
Blood in stool / on wiping
Fluids + eat more fibres, stool softeners
What is pseudomembranous colitis? (PMC)
Inflammation of the colon due to a overgrowth of C.diff and a recent history of antibiotic use.
Can cause TOXIC MEGACOLOM
What are the risk factors for developing PMC?
Recent antibiotic use
Staying in a hospital/nursing home
older age
IBD
Use of PPI
Immunocompromised -eg AIDS
How do you treat PMC?
Stop causative agent
Start another antibiotic that is effective against C.difficile
Oral vancomycin, metronidazole
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
