General GI Flashcards
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What are the four layers that make up the wall of the GI tract (general terms)?
The wall of the GI tract is formed of 4 layers:
- Mucosa - the lining of the GI tract. Itself comprises 3 layers, inc a thin layer of muscle
- Submucosa – connective tissue. This is where blood vessels and nerves lie
- Muscularis – Layers of smooth muscle and enteric nervous system
- Serosa – this is the visceral layer of the peritoneum
Note some parts of the GI tract have modifications to these standard layers
What are the functions of the mouth in the GI tract?
Mouth - oral/buccal cavity
Key for mastication, speech, start digestion (salivary amylase), some absorption (some absorption not subjected to first pass metabolism)
Comprises:
1. Lips, cheeks, soft and hard palates
2. Tongue (skeletal muscle) with taste buds on papillae
3. Salivary glands: submandibular, parotid and sublingual (secrete salivary amylase)
4. Teeth
What are the parts of the pharynx and what function does it play?
The pharynx is typically divided into 3:
1. Nasopharynx
2. Oropharynx
3. Laryngopharynx
Function - Swallowing involves the moving of a food bolus from the buccal cavity to the oesophagus through the pharynx.
Pharyngeal or Esophageal dysphagia – most common cause strokes/neurological
What are the relevant anatomical features in oesophagus?
First segment of true digestive tract
Extends from pharynx to stomach (C6-T10), traverses the diaphragm
Lined with stratified SQUAMOUS EPITHELIUM until last 1cms (entry to stomach) when COLUMNAR EPITHELIUM - Barret’s oesophagus converts squamous epithelium into columnar epithelium.
Muscles in the oesophagus
1. Muscle are voluntary (striated) in upper third
2. Middle - mixed (striated and smooth) in the middle
3. Lower third involuntary smooth muscles
Sphincters
* Upper oesophageal sphincter – Stops air getting into the gut.
* Lower oeosphageal sphincter – comprises a thickened muscular layer in the lower oesophagus and cardia of the stomach (intrinsic) and the diaphragm (extrinsic).
What is a hiatus hernia?
A hiatal hernia occurs when the upper part of your stomach bulges through your diaphragm into your chest cavity.
What are the key cells present in the lining of the stomach?
- Mucous Cells: secrete mucous which protects the mucosa from the acid environment of the stomach
- Chief cells: secrete enzymes
- of gastric juice (pepsin)
- Parietal Cells: secrete hydrochloric acid and intrinsic factor (imp for b12 absorption)
- Endocrine cells: secrete grelin (hormone which promotes appetite) and gastrin (digestive hormone)
What are the functions of the stomach?
Food reservoir: stores food until ready to be digested
Digestion: started by gastric acids and juices and physically broken down by churning
Secretes intrinsic factor: allows b12 absorption
Some absorption: water, alcohol, some drugs
Endocrine: ghrelin and gastrin secretion
What is the definition of the lower GI tract?
Definition varies but it is acceptable, as in this case to define it as the GI tract that is beyond the pylorus
What are the four parts of the duodenum? When does it transition into the jejenum?
Split into 4 sections
Sections
* D1- superior
* D2 (pancreatic juices and bile comes out) - descending
* D3 - horizontal
* D4 - ascending
Transitions into the jejunum at the DJ flexure (when abruptly turns)
What are the cells the line the small intestine?
- Surface cells – enterocytes – have microvilli this is known as the ‘brush border’
- Mucus secreting goblet cells
- Enteroendocrine cells
- Stem cells - Found in deep crypts adjacent to villi
What are the cells the line the large intestine?
- Large intestine lined by enterocytes
- Multiple mucus secreting glands - goblet cells
- No villi but crypts
What are the arrows pointing at?
What is the gut hormone that stimulates bile release?
Gallbladder - triggered by gut hormone - CCK - it empties
Cholecystokinin
How is the exocrine portion of the pancreas arranged?
Exocrine portion - majority of the tissue
* Have an acinar arrangement like the liver
* Complex ductal collecting system that ends at the pancreatic duct which empties into the duodenum
* Secrete pancreatic juice i.e. Digestive enzymes and sodium bicarbonate
What are the endocrine subunits of the pancreas called? What are the key cells?
Islands of endocrine cells ‘islet of langerhans’
Most important is insulin (from beta cells) and glucagon (from alpha cells)
What innervates the esophagus?
Innervation – vagus nerves and sympathetic fibres
What part of the diaphragm helps to prevent acid-reflux?
Right crus of the diaphragm – forms a sphincter like sling – prevent acid reflux
What are the three main areas of esophageal constriction?
Esophageal constrictions – narrowing
* Superior – level of the cricoid cartilage – juncture with pharynx
* Middle – where the aorta cross and left man bronchus
* Inferior – diaphragmatic sphincter
What are the differ layers of the esophageal wall?
Layers divided into…
1. Mucosa (Stratified squamous epithelium – non-keratinizing, lamina propria, muscularis mucosae)
2. Submucosa
3. Muscularis externa
4. Adventitia (no serosa)
How do we distinguish between T1-T4 tumours in the oesophagus?
- T1 - Mucosa, muscularis mucosa and submucosa – three layers - any tumour invading these layers is a T1
- T2 - reaches the muscularis propria
- T3 - reaches the adventitia
- T4 - reaches passed the adventia into nearby organs
Metastases – mainly to the liver and lungs
We can use an endoscopic ultrasound to stage an esophageal tumour
What are common lymph node sites where esophageal tumours spread?
Esophagus tends to metastasize into certain lymph area
- Bifurcation of the trachea – common area
- Lymph nodes between aortic arch and pulmonary artery
- Further down towards the diaphragm or higher up
Why may a patient with an oesophageal tumour present with hoarse voice?
Left recurrent laryngeal nerve innervates the vocal cords – passes underneath aortic arch – hence compression/invasion in this area can influence the vocal cords.
Dysphagia and hoarse voice – indicates an advanced tumour
Outline how portal hypertension results in varices formation.
- Liver cirrhosis – liver becomes nodular and stiff – portal system pressure increase – blood flow slows down
- Collateral circulation forms – shunting of blood through the coronary vein (reversal of flow) - entering the peri-esophageal plexus forming the esophageal varices
- This blood drains then into the hemiazygous and azygous system – ultimately entering into the superior vena cava and into systemic circulation
- Furthermore, back flow into the splenic vein results in collateral circulation formation – creating gastric varices that connect with the peri-esophageal plexus
What are some other causes of oesophageal varices formation.
When vessels leading into portal triad become obstructed – e.g. clot in the portal vein (thrombosis) - we see varices formation
For example…
Acute pancreatitis – clot in splenic vein blood redirected – forming collaterals – draining via the fundus of the stomach – segmental portal hypertension
Inflammation of the small bowel – clot in the superior mesenteric – collaterals/anastomoses with nearby vessels
How are esophageal and gastric varices treated?
Esophageal - band ligation - cutting off blood blood - thromboses the tissue - falls off
Gastric varices – bigger in diameter than esophageal - Inject a thrombotic agent causing thrombosis
What are the different layers that make up the stomach wall?
What are the different zones that make up the stomach? What cells types are found in all zones and what cells are found paritcularly in the fundus?
Zones - Cardia, Fundus, Body and Pylorus
All zones have glands with mucous cells and enteroendocrine cells
Fundus and particularly in the corpus/body we have…
* Parietal - HCL and instrinsic factor
* Chief - pepsinogen, renin and lipases
* Mucous neck cells
* Enteroendocrine (gastrin – acid secretion, CCK – bile secretion, secretin, etc..)
Why is the gastroduodenal artery clinically relevant?
Gastroduodenal artery - branch from common hepatic, which is a branch of the celiac trunk
Supplies the bulb/1st part of the duodenum, particularly the posterior aspect
Posterior aspect of duodenum and stomach often gets ulcers, therefore it is not uncommon for gastroduodenal artery to be invaded by these ulcers resulting in bleeding
If lymph nodes in the coeliac axis become invaded by esophageal tumour, is it considered a metastasis?
If the coeliac axis lymph nodes are invaded by tumours in the context of esophageal cancers – it is considered a metastasis
How does common bile duct obstruction by gallstones and tumours (pacreatic/ampullary) differ?
Gallstones - Gall bladder is an area where stones form – can cause obstruction resulting in colicky pain (muscle spasms) and bile spills over into the blood resulting in jaundice
Tumour - gall bladder becomes enlarged as the the tumour is slowly growing – results in painless jaundice with weight loss
What is abdominal angina? What is it causes by?
Superior mesenteric can narrow (not uncommon) - ischemia can develop in the small bowel – causing abdominal angina
Typically after eating (a lot of blood needs to enter into this area)
What is the artery joining the inferior and superior mesenteric in the colon?
Marginal artery – inferior and superior mesenteric supply anastomose
What is the most important organ for digestive enzyme production?
Exocrine pancreas is the most important organ when it comes to digestive enzyme production
What nutrients are absorbed in the different areas of the small intestine?
The vast majority of absorption takes place in the distal duodenum and jejunum.
Duodenum
Iron and calcium is best absorbed in acidic conditions and this takes place in the proximal duodenum (D1 and D2 area) – more acidic environment as the contents have just left the stomach
Duodenum and Jejenum
Simple sugars and fats are also easily absorbed in the proximal small bowel, along with fat soluble vitamins.
Ileum
The terminal ileum is a specific site of absorption of vitamin B12 - unique site for B12 absorption
Note that iron and B12 absorption require a functioning stomach - Acidic environment and intrinsic factor
What is the definition of malabsorption? How does it relate to maldigestion?
Malabsorption is the inadequate absorption of fluid, macro or micronutrients to maintain health
- Problems at any site of nutrient absorption
- Most commonly relating to loss of absorptive surface area
Can be due to maldigestion, as the nutrients are not in a suitable form for absorption - Most commonly relating to digestive enzyme insufficiency or inefficiency
What are 7 different potential causes of malabsorption?
- Reduction of absorptive capacity – most common villous atrophy (biggest cause coeliac disease) – can also have reduced absorptive area due mucosal damage, small bowel resection, small bowel bypass and infiltration
- Enzyme deficiencies – pancreatic exocrine insufficiency – reduced lipases and proteases
- Enzyme dysfunction – even though you have the right enzyme you need the right environment – e.g. Zollinger Ellison Syndrome (acidity inactivates enzymes), menetriere disease (too much mucus) and Orlistat (inactivates pancreatic enzymes)
- Bile acid deficiency – obstruction, bile acid malabsorption (reabsorb 95%) resulting in deficiency and deconjugation of bile acids by small bacterial overgrowth
- Competition for nutrients – parasites
- Dysmotility/desynchrony – rapid transit – not enough time for enzymes to do the work, slow transit – predisposition to small intestine bacterial overgrowth and anatomical dyssynchrony – e.g. in by-pass which is the intended outcome
- Impaired transport
How does malabsorption present?
GI symptoms
* Diarrhoea - Steatorrhoea (lack of fat absorption)
* Bloating
* Abdominal distension
* Flatulence
* Borborygmi - rumblingorgurglingnoise made by the movement of fluid and gas in theintestines
* Abdominal pain
Malnutrition
* Global - Weight loss & Failure to Thrive
* Specific - hypoalbuminaemia, anaemia (proximal small bowel affected – iron deficiency, distal small bowel affected – B12 deficiency)
Is hypoalbuminaemia a specific marker for malabsorption or GI loss?
It is not a specific marker for malnutrition or GI protein loss.
It is low in chronic liver disease, cardiac failure, renal failure, nephrotic syndrome, and acute and chronic inflammatory states from any cause, including cancer.
How do we perform a diagnosis for malabsorption?
Better off performing a clinical diagnosis looking at symptoms, risk factors, physical/biochemical evidence of malnutrition in sufficient dietary intake, exclusion of other explanations and some specific tests for diseases causing malabsorption
How do we manage malabsorption?
Find the cause - address that
Find a dietitian
Nutritional Support - replacement of fluids and electrolytes, mitigate risk of refeeding syndrome (refeeding to quickly after a period of undernutrition) and restoration of nutritional status.
Improve symptoms - normalising digestion and absorption will provide relief, consider a diary free diet – secondary lactose intolerance is very common
Consider their other medications - malabsorbing nutrients, likely malabosrbing drugs.
What is coeliac disease?
Chronic autoimmune-mediated gluten-sensitive enteropathy - leads to destruction of intestinal mucosa
Caused by exposure to cereal prolamins (especially wheat - gluten - gliadin) in genetically susceptible individuals
Environmental triggers also described – H. Pylori and after surgery
How does coeliac’s disease present?
GI - symptoms of malabsorption - Chronic or intermittent diarrhoea, bloating, weight loss, fatigue, failure to thrive, lactose intolerance
‘Coeliac crisis’ - rare – significant fluid and electrolyte losses – need intensive care
Extra GI symptoms – iron deficiency is the most common (iron requires the acidic environment in D1 an D2 – area where gluten is first presented to, hence in the worst condition), neurological, dermatitis, raised liver enzymes, etc.
How do most patients with coeliac disease present?
Most patients don’t know they have coeliacs
Many are asymptomatic or have symptoms at the milder end of malabsorption syndrome, similar to IBS
Therefore, a very low threshold for testing should be used, particularly in Caucasions.
How is a diagnosis for coeliac’s performed?
Diagnosis can’t be made in someone that is already excluding gluten – Before we test we ask the patient to take more than 2 slices or 4 digestives per day for 4 week
Accurate serological test – TTG IgA test – 98% sensitive and 90% specific
IgA deficiency present in 0.5% and 2% of coeliac – normally tested for
Biopsies should be taken from D2 (4 biopsies) and D1 (2), as the changes are patchy - histological diagnosis – there has to be a intra-duodenal lymphocytosis to diagnose coeliacs (inflammation)
Note when TTG is very high we can diagnose without a biopsy
Outline how iron is absorbed (Fe2+ and Fe3+)
Two forms
* Ferrous – 2+ – highly absorbed – found in red meat and seafood – preferred form
* Ferric – 3+ - needs to be converted to Fe2+ in order to be absorbed – some Fe3+ (ferric) can be absorbed but at much lower rate
Vegan on a PPI - high pH (low reduction potential) and low ferrous 2+ ingested - not a good combo.
What is anaemia of chronic disease? What are the mechanisms driving anaemia?
Anemia of chronic disease – looks very similar to iron deficiency anaemia on a hematological test
Anemia of chronic disease – occurs when the body is in a state of chronic inflammation
1. Increase levels of hepcidin – reduces release of iron from the reticular endothelial system
2. Reduces EPO production
3. Reduced erythroid proliferation
4. Augmentation of hemophagocytosis
Giving more iron won’t help as there is already enough
How can we tell the difference between iron deficinecy anaemia and anaemia of chronic disease?
IDA
* Low ferritin
* High Transferrin - body is low in iron the body will make more transferrin to help with transport
ACD
* Ferritin will be normal
* Transferiin will either be low or normal
What is transnasal endoscopy?
Ultra-thin scopes
Positives – better tolerated, less sedation, biopsy standard equivalency
Negative – unable to perform most therapeutic procedures
What are the main types of bariatric surgery?
What are the most common causes of an upper GI bleed?
- Peptic ulcer disease – commonest cause of upper GI bleed
- Bleeding from varices in liver cirrhosis
How do NSAIDs cause peptic ulcers?
Results in the depletion of mucosal prostaglandins resulting in mucosal injury
How does GI perforation due to peptic ulcers present?
- Peritonitis - Inflammation of the peritoneum
- Septic Shock
- Sudden severe pain
- Shoulder tip pain
- Air under the diaphragm (bilateral)
MORTALITY 10%
EMERGENCY SURGERY
What blood vessel is commonly affected by duodenal ulcers?
Gastroduodenal artery – gives blood supply to the duodenum
Duodenum is thin making it susceptible to ulceration and given that his artery passes behind the duodenum, this artery is often eroded
Other - Right gastric artery can be eroded in the body of the stomach
What scoring system is used to assess the severity of a bleed?
Rockall score – make a decision about the severity of the bleed
Factors - Age, shock, comorbidities, diagnosis and stigmata of haemorrhage
When using the MUST score, what adjustments need to be in our BMI calculation?
Always consider the patients estimated dry weight and account for variables including oedema and ascites.
Depending on the level of oedema and ascites we add remove different amounts from the bodyweight.
How much does each BMI category add to the MUST score?
How do we calculate the weight loss score when using MUST?
How do we take into account acute disease effect into the MUST score?
What scores are we adding together when using MUST and how do we use that to guage the risk of malnutrition? What do we do if there is a risk of malnutrition?
Implement local policy plan and refer to dietitian
Summary - What histological changes do we observe in coeliac’s disease?
- Villous atrophy
- Crypt hyperplasia
- Intraepithelial lymphocytes
