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
How is coeliac’s disease managed?
Gluten free diet - adherence is a problem
Annual review – assess compliance, weight & symptoms, bone health, vaccine status, annual blood test – hypothyroidism and type 1
What is non-responsive Coeliac Disease?
Ongoing symptoms 12 months after gluten free diet implemented
Things to think about…
* Is the patient compliant to the GFD
* Some people may take up to 2 years to heal their intestinal mucosa - slower responder
* Associated conditions, mimics or refractory coeliac - repeat endoscopy and biopsy - no atrophy or atrophy - look for alternatives
What is refractory coeliac disease?
Persistent or recurrent malabsorptive symptoms and villous atrophy despite strict adherence to a gluten-free diet (GFD) for at least 6–12 months in the absence of other causes
What are the two types of refractory coeliac’s disease?
Refractory coeliac disease – take samples from small bowel to decipher whether it is type 1 or 2 – rare – less than 1% with coeliac
Type 1 – no abnormal clonality of lymphocytes (intra-epithelial cytosis) – treat with dietitian, budesonide – steroids – 5 year survival is more than 90% – 10% will progress to Type 2
Type 2 – lymphocytes in the epithelium are aberrant – treat as a pre-malignant condition – stage as a cancer, steroids and aggressive immunosuppression
What are infectious enteropathies? What are some different examples?
Infectious causes of malabsorption are important, as they are relatively common and relatively easy to treat.
Examples
1. Tropical Sprue - travel + whole small bowel affected
2. Whipple’s disease - middle aged farmers - intestine covered in foamy macrophages – diagnoses by biopsy
3. Giardiasis - Malabsorption can be significant – weight loss - Easy to diagnose with stool ELISA
What are some other examples of enteropathies that may cause malabsorption?
- Drug induced – main one in Scotland = NSAIDs
- Autoimmune enteropathy
- Radiation enteropathy
- Crohn’s disease - normally isolated to the ileum – B12 deficiency – surgery can result in rapid intestinal transit – no-ileal brake
Malabsorption - What is small intestinal bacterial overgrowth (SIBO)? What can it be caused by?
SIBO – normally not much bacteria in the small bowel – balance is lost and there is overgrowth
Present with maldigestion, bloating, diarrhea and B12 deficiency with folate being normal or high
Causes:
1. Stasis – blind loop/post-UGI surgery (shown on the right) - causes stasis
2. Stricture
3. Diverticulum in the small bowel
4. Dysmotility – diabetes and Parkinson’s
5. Systemic immunodeficiency
6. Local mucosal disease - Coeliacs, Crohn’s and NSAIDs.
How is SIBO diagnosed?
- Diagnoses with glucose/hydrogen breath test – rise of 20ppm over baseline
- Look for anatomical abnormalities, test for risk factors and secondary causes
Treatment – Rifaxamin
Malabsorption - What is pancreatic exocrine insufficiency?
PEI - Insufficient secretion or function of pancreatic enzymes or sodium bicarbonate for normal digestion
This and coeliacs are the most common causes of malabsorption
Associated with significant morbidity and mortality
What are some different causes of pancreatic enzyme insufficiency?
Many different causes…
1. Not making enough
2. Not secreting/block route
3. Pancreas not being stimulated enough
4. Desynchrony in digestion due to dysmotility or abnormal anatomy (timing)
It is found most commonly in patients with chronic pancreatitis, pancreatic cancer, pancreatic resection or cystic fibrosis.
How is a diagnosis for pancreatic enzyme insufficiency made?
Multi-pronged approach to diagnosis
1. History and risk factors
2. Fecal elastase is the main test - less than 200 is positive (will misclassify 10% of people)
3. Nutritional blood test - look for signs of malnutrition
4. Pancreatic imaging to check for any abnormalities – cross-sectional imaging
How is a pancreatic enzyme insufficiency treated?
- Pancreatic enzyme replacement therapy (PERT) - Well tolerated - 80% of patients respond clinically
- Refer to a dietitian
- Dietary modification - No!
- Smoking and alcohol cessation
- Monitor response
What is the definition of anaemia? What is the definition of iron deficiency? What is iron deficiency anaemia?
Anaemia – where serum haemoglobin levels are 2 standard deviations below the normal
Iron deficiency– when the total body iron is low as a result of absorption not matching demand.
Iron deficiency anaemia - low iron leading to low RBC production - microcytic anaemia
What are the causes of iron deficiency anaemia?
- Poor intake of dietary iron
- Reduced absorption (malabsorption) e.g coeliac, post surgical
- Increased iron (blood) loss e.g. menstruation, cancer
- Increased demand e.g. pregnancy, adolescence
What are the signs and symptoms associated with iron deficiency anaemia?
- Often none (asymptomatic)
- Common symptoms: tiredness, dyspnoea, headache
- Common signs: pallor, atrophic glossitis
- Rarer signs: koilonychia, leuconychia, tachycardia, angular cheilosis
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 are some factors that increase or decrease iron absorption?
Iron absorption enhanced by vitamin C, fructose, sorbitol and alcohol
Iron absorption inhibited by tannins, oxalates, polyphenols, phylates, egg and pulse proteins, etc.
Where is iron absorbed in the small intestine?
Iron is absorbed in the duodenum and upper jejenum
Iron is used in multiple places – muscle, liver, bone and spleen
Different destinations include…
* Haemoglobin
* Myoglobin
* Enzymes
* Sotrage
* Excreted
What is haemochromatosis?
Haemochromatosis – too much iron absorbed (no mechanisms for excretion) - disorder located on the enterocyte surface
What protein is used for iron storage? What protein is used for iron transport?
Body stores iron in the cell as ferritin – marker of total body iron stores (not plasma iron)
Transferrin is used to transport iron around
If a patient is anaemic and has low ferritin what does that mean?
If ferritin is low = total body iron is low = iron deficiency anemia
But there is no single good test for iron deficiency anaemia if the ferritin is normal - ferritin might be elevated – acute phase reactant
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 are the local guidelines for defining iron deficiency anaemia?
Iron deficiency anaemia is defined as a low haemoglobin in the presence of either
* Low ferritin (best diagnostic marker)
* Low serum iron in the presence of transferrin >3.0 (high)
If someone has iron deficiency anaemia, what is one test that everyone should get?
Test for coeliac disease!
If a young healthy women, with no history or family history of GI conditions, presents with iron deficiency anaemia, what test(s) should we perform?
Young fit women with no history or family history – only needs coeliac serology
But if there is GI symptoms or family history – we need to perform further investigation
If a elderly women, with asymptomatic iron deficiency anaemia presents, what test(s) should we perform?
Gold standard – man of any age or non-menstruating women – endoscopy (well tolerated – even in this case) or colonoscopy
What are the two ways that an standard endoscopy is performed?
Two ways
1. Topical lidocaine spray to the back of the throat – awake and aware
2. Topical lidocaine and some sedation (midazolam) – we want conscious sedation
What is transnasal endoscopy?
Ultra-thin scopes
Positives – better tolerated, less sedation, biopsy standard equivalency
Negative – unable to perform most therapeutic procedures
Pros and Cons of standard colonoscopy? What is an alternative?
Gold standard
How good the bowel has been cleared out is important – better view
Advantages – take biopsies and can remove polyps (polypectomy)
Negatives
1. Invasive
2. Uncomfortable – liquid diet and strong laxatives
3. Complications – bleeding and perforation
7-10% of cancers are missed in colonoscopies
4. Majority of lesions are in the right colon – poor prep for this region and harder to see lesions (flatter)
Alternative - CT colonoscopy - Tube inserted into their anus and bowel is inflated
What is capsule endoscopy?
Capsule endoscopy - minimal patients – small bowel
Camera on a pill – takes pictures
Takes pictures and uploaded wirelessly
After a Iron deficiency anaemia patient has got a endoscopy and colonoscopy that look normal, what happens next?
Once upper and lower GI have been assessed no further GI needed
Remember to check renal blood loss using dipstick
No formal diagnosis is common – we think it is usually is diet
Investigate small bowel if recurrent IDA
What is the standard treatment for iron deficiency anaemia?
- Optimize diet
- Iron tablets for three months – after iron deficiency is corrected
- Main side is constipation, GI upset and dark stools
If unable to tolerate that alternative daily dosing is effective
If unable – IV iron is now safe and quick – not used in the majority of cases – risk of iron overload as there is no excretion
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
Are variceal bleeds common in liver cirrhosis patients? Are they dangerous?
Occurs in 30% of cirrhotic patients
* 1/3 of episodes are fatal
* Amongst suvivors 1/3 will re-bleed within 6 months
* Only 1/3 will survive over 1 y
Don’t over transfuse with blood – as this increases pressure too much increasing risk of a bleed
How should variceal bleeds be dealt with?
- Endoscopy should be performed early (6-12 h)
- Endotracheal intubation /critical care management (often needed to avoid aspiration)
- OESOPHAGEL VARICES: Banding ligation preferred
- GASTRIC/ ECTOPIC VARICES: histoacryl or thrombin injection
- iv antibiotics and iv terlipressin ( medication to reduce portal pressure)
Where can peptic ulcers be found? What layer of the GI tract wall does it penetrate?
Location The oesophagus and/or Stomach (gastric) and/or Duodenum
It penetrates the muscularis mucosae - can be acute or chronic
What are the two main causes of peptic ulcers?
- H.Pylori (>90% DU’s, >70% GU’s)
- NSAID’s (Non-Selective NSAIDs deplete mucosal defense)
Other - Stress – Burn injury/Sepsis/prolonged hospitalization
Smoking – causes increased risk / delayed healing
How can we test for H. Pylori?
- Breath test
- Stool Antigen test
- Antibody measurement - serology
- Endoscopic biopsy - CLO test or histology
How do NSAIDs cause peptic ulcers?
Results in the depletion of mucosal prostaglandins resulting in mucosal injury
What are the emergency scenerios associated with peptic ulcers?
Emergency
* Perforation
* Bleeding
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 are signs of an upper GI bleed due to peptic ulcers?
30-50% of cases are due to peptic ulcer
Mortality remains 6-10%
Hematemesis (vomiting blood) or melaena (black stools) or both
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
Things to consider when managing an upper GI bleed.
- Assess the need for blood transfusion
- Timely endoscopy
How can a peptic ulcer bleed be dealt with? How can we ensure that the ulcer heals and clot stabilizes post-endoscopy?
Use tools to stop bleeding – clip vessels or coagulate vessels
e.g. Hemospray – cause immediate hemostasis (stop the bleed) to stop the bleed
When endoscopy fails – use angiography and embolization - insertion of a coil
Post-endoscopy…
We need to heal the ulcer and have the clot stabilise (needs a higher pH to stabilize) – bring the pH of the stomach from 2 to 6 or 7 – how? – use high dose PPIs
Don’t forget to stop NSAIDs and check for H. Pylori
What is acute pancreatitis? What are the most common causes?
Pancreatitis is inflammation of the pancreas
Causes…
* Commonest cause is Gallstones – blocks pancreatic duct – enzymes can leave and start digesting the pancreas
* Second most common - Alcohol
* Post ERCP pancreatitis – iatrogenic following the removal of gallstones
* Drug induced - azathioprine, steroids
How does acute pancreatitis present? How is it diagnosed?
Symptoms
* Severe abdominal pain
* Nausea, vomiting (75%)
* Collapse or hypotension
* Fever, tachycardia
* Obstructive Jaundice (30%) – pancreas gets swollen obstructing the flow of bile – causing jaundice
Diagnosis - measuring amylase in the blood – spill over into the blood – more than 3x normal
How does pain in acute appendicitis present?
Belly button migrating to the lower right side
Pain, sharp and constant – worsening with movement
What is the treatment for acute appendicitis?
Treatment
* Fluids
* Broad spectrum antibiotics – remove risk of appendix bursts
* Remove inflamed appendix – appendectomy
* Pain management
What is the definition of an acute abdomen?
An abdominal condition of abrupt onset associated with severe abdominal pain (resulting from inflammation, obstruction, infarction, perforation, or rupture of intra-abdominal organs).
What three conditions should you of if someone presents with generalised peritonitis?
Acute abdomen – go through three conditions –
1. Perforated ulcer
2. Colonic perforation
3. Perforated appendix
Don’t forget amylase – acute pancreatitis
What four conditions should you of if someone presents with localised peritonitis?
- ACUTE APPENDICITIS
- ACUTE DIVERTICULITIS
- ACUTE CHOLECYSTITIS
- RUPTURED OVARIAN CYST-OVARIAN TORSION
What is the definition of malnutrition?
Malnutrition is a state of nutrition in which a deficiency or excess (or imbalance) of energy, protein and other nutrients causes measurable adverse effects on tissue / body form (body shape, size and composition) and function and clinical outcome.
The term malnutrition does include obesity
What is the MUST nutrition screening tool?
MUST - Malnutrition Universal Screening Tool
Includes…
1. BMI – where patient is now
2. Recent weight loss – where patient has come from
3. Starvation in presence of acute disease – where patient is going
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
What are the 5 factors that we consider in a nutritional assessment?
- A – Anthropometry - BMI, waist circumference, skinfold thickness, etc.
- B - Biochemical Data
- C - Clinical presentation/picture
- D - Diet History and Dietary Intake
- E – Environmental/social factors
Summary - What are the four main causes of malabsorption?
Main causes of malabsorption
* Coeliac disease
* Pancreatic insufficiency
* SIBO
* Crohn’s Disease
Summary - The absorption of what metal is particularly affected by coeliac’s disease?
Iron - hence why it is always important to check for coeliac’s disease if someone presents with iron deficiency anaemia.
Summary - What histological changes do we observe in coeliac’s disease?
- Villous atrophy
- Crypt hyperplasia
- Intraepithelial lymphocytes
Summary - What are the main symptoms associated with coeliac’s disease?
- Diarrhea
- Anemia
- Abdo Pain and bloating
- Weight loss
Dermatitis herpetiformis (itchy/blistering skin) – common in coeliac disease but not necessarily found
How is coeliac’s disease diagnosed?
Serological markers
* Anti-tissue transglutaminase antibody (IgA) (TTG) Sensitivity and specificity >95%
* Anti-endomysial antibody (IgA)
* Anti-gliadin antibody (IgA, IgG)
Small intestinal biopsy (D2 biopsies – endoscopy)
