Alimentary 2 Sachini Ranasinghe - PowerPoint Presentation

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Alimentary 2

Sachini

Ranasinghe

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Slides available:

https://muslimmedics.co.uk/year-1/

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Topics to be covered:

Appetite Regulation

Immunology

Cancer of the gut

Nutrition/

Clinical Nutrition

Obesity

Control of Function

Hydration

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Learning Objectives

1-LSS-ALI-MECH-05: Appetite control: recall the hormones (hypothalamic, leptin, ghrelin, peptide YY) and neuronal populations involved in the regulation of appetite; explain how mutations disrupting these systems can influence energy balance and theories which aim to explain the obesity epidemic

1-LSS-ALI-IMM-01: MALT and GALT: Define mucosa-associated lymphoid tissue (MALT) and gut-associated lymphoid tissue (GALT)

1-LSS-ALI-IMM-02: Peyer's patches: recall the structure and function of Peyer's patches

1-LSS-ALI-IMM-03: IgA: define the role of IgA in the gastrointestinal tract

1-LSS-ALI-IMM-04: Lymphocyte circulation: explain the circulation of lymphocytes within the alimentary system

1-LSS-ALI-PATH-18: Irritable bowel syndrome: explain the role of dietary management to treat irritable bowel syndrome

1-LSS-ALI-PATH-19: Coeliac disease: recall the pathophysiology and dietary management of coeliac disease

1-LSS-ALI-PATH-17:  Inflammatory bowel disease: explain the dietary management and nutritional significance of inflammatory bowel disease 

1-LSS-ALI-PAN-05: Pancreatitis: define acute and chronic pancreatitis; recall causes, symptoms and signs, investigations and complications

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1-LSS-ALI-PATH-07: Gastrointestinal cancer: list the common sites of cancer in the gastrointestinal system, recall associated cell types, explain clinical features and investigation of gastrointestinal cancer, including oesophageal, bowel and pancreatic

1-LSS-ALI-PATH-11: Nutritional screening: Recall how nutritional screening is performed and its significance

1-LSS-ALI-PATH-12: Malnutrition assessment: Recall how to assess for malnutrition clinically

1-LSS-ALI-PATH-14: Malnutrition management: recall how to manage malnutrition with nutritional support interventions

1-LSS-ALI-PATH-13: Refeeding syndrome: explain the pathophysiology of refeeding syndrome

1-LSS-ALI-PATH-14: Malnutrition management: recall how to manage malnutrition with nutritional support interventions

1-LSS-ALI-PATH-15: Critical care: compare enteral and parenteral feeding and associated problems, and identify reasons for the use of tracheotomy within ICU

1-LSS-ALI-PATH-16: Short bowel syndrome: identify the nutritional consequences and management options of short bowel syndrome

1-LSS-ALI-PATH-10: Health eating guidelines: Recall the healthy eating guidelines

1-LSS-ALI-PATH-08: Energy requirements: identify the energy requirements in exercise and how exercise in extreme conditions impacts on requirements

1-LSS-ALI-PATH-09: Fuel sources: distinguish between fuel sources for different exercise types and evaluate uses and limitations of supplements

1-LSS-ALI-PATH-21: Cancer: identify changes that contribute to the development malnutrition in cancer patients

1-LSS-ALI-PATH-06: Alcohol: recall the biochemistry and metabolism of ethanol, recall the physiological effects of alcohol and the pathophysiological mechanisms of alcohol induced disease, demonstrate awareness of the impact of alcohol on individuals and society and recommended limits of consumption

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Appetite Regulation

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Appetite control: recall the hormones (hypothalamic, leptin, ghrelin, peptide YY) and neuronal populations involved in the regulation of appetite; explain how mutations disrupting these systems can influence energy balance and theories which aim to explain the obesity epidemic

HYPOTHALAMUS

Arcuate Nucleus

Paraventricular Nucleus

Incomplete BBB



access to brain

NPY/

Agrp

(Medial)*POMC (Lateral)  

*MC4R  when activated decreases food intake.Axons from arcuate nucleus release neuropeptides that bind to receptors in the Paraventricular nucleus. 

Appetite regulation largely involves the following:HormonesHypothalamus

Paraventricular Nucleus:Alpha-MSH acts as an agonist to MC4R Agrp binds to MC4R and acts as an antagonist, blocking the satiety signal from α-MSH

*Known mutations

 obesity

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Long term regulation of Food Intake

Adipostat Mechanism

Hormone produced by fatHypothalamus detects concHypothalamus increases/decrease food intakeCAN LEAD TO OBESITY!!

Leptin (as a specific example)

Made by adipocytes (fat)Circulates in the bloodReaches hypothalamus  appetite and thermogenesis controlMORE FAT, MORE LEPTIN

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Leptin and Obesity

If you have no leptin you will not decrease appetite or increase energy expenditure = FATNormal leptin levels but the system just isn’t working – FATFat people can have leptin but cannot respond to it (receptor defect) = FAT

*Leptin is only effective as a therapy in congenital leptin deficiency – NOT as a weight loss drug.

If leptin decreases appetite how is it an issue relating to obesity?

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Short term regulation of food intake

Peptide YY:

Post-prandial hormone Released in proportion to how much you eatDECREASES APPETITE

Ghrelin:

Peptide hormone with a fatty acid at position 3

Basically the opposite of PYY – it is released before a meal

INCREASES APPETITE

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SBA

Which of the following hormones decreases appetite?

Ghrelin

PYY

Insulin

Sodium

Orexin

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SAQ

Explain 3 mechanisms in which leptin regulation can cause obesity? (6 marks)

Explain how ghrelin works (3 marks)

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Immunology

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Quick Recap!

Lots of microbiota in the gutThe epithelium of the gut is an EXTERNAL environmentThe gut has a massive SA – why is this good?Bacteria recap:Millions in mouthNot many in stomach – why??Not many in the SIMassive beyond ileocaecal valve (into LI)

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1-LSS-ALI-IMM-01: MALT and GALT: Define mucosa-associated lymphoid tissue (MALT) and gut-associated lymphoid tissue (GALT)

Mucosa associated lymphoid tissue

Found mainly in the mouth e.g. tonsils (M cells) which can initiate an immune response

MALT is a umbrella term for many immunological tissues

Gut associated lymphoid tissue

Organised – Peyer’s patches

Found in the small intestines and lymphocytes in the lymph nodes

Disorganised

Lamina

propria

lymphocytes



IgA secreting B cells

Intraepithelial cells



lymphocytes below basolateral membrane of the epithelium of the gut

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1-LSS-ALI-IMM-02: Peyer's patches: recall the structure and function of Peyer's patches

What are Peyer’s patches?Found in the ileum of the small intestine (highest conc is distally)Aggregated lymphoid tissueMucus  B cells and T cellsHow is mucosal epithelium specialised?No goblet cellsNo secretory IgALack microvilli

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1-LSS-ALI-IMM-03: IgA: define the role of IgA in the gastrointestinal tract

Steps in formation of secretory IgA:2 IgA molecules are bound by a J chain in the plasma cellThis is secreted into the interstitial spaceThe dimer binds to a pIgR receptor on the basolateral surface of enterocytesThis receptors Is the secreteory component which binds to IgA  SIgA.SIgA is endocytosed into the epithelial cell and eventually exocytosed into the gut.

TAKE HOME MESSAGE: The secretory component is very important because it protects the antibody dimer from acidic/enzymatic degradation. This means

SIgA

can bind to pathogens.

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1-LSS-ALI-IMM-04: Lymphocyte circulation: explain the circulation of lymphocytes within the alimentary system

Mucosal lymphocytes in Peyer's patches, once stimulated by an antigen, migrate into the local mesenteric lymph nodes and drain into the lymphatic system.

They re-the systemic circulation via the thoracic duct and travel in the blood.

Lymphocyte homing occurs



lymphocytes remain in the blood until activated by tissue-specific endothelial adhesion molecules, which enable migration of the lymphocytes into the gut mucosa.

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1-LSS-ALI-PATH-18: Irritable bowel syndrome: explain the role of dietary management to treat irritable bowel syndrome

What is it?Describes a pattern of recurrent bouts of abdominal pain in abnormal bowel motility – diarrhoea/constipation. Abdo pain relieved after poopingNB: NOT the same as IBD because IBD has the same symptoms + ulcers.

Features?

Lactose or fructose, often trigger the symptomsDiarrhoea or Constipation!Flatulence due to fermentation of sugars (Farting basically)

Treatments

Diet modifications



avoiding foods e.g. cauliflower, apples

Constipation meds

 laxatives

Spasms and pain  anti-diarrheal meds

Control stress and anxiety!

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1-LSS-ALI-PATH-19: Coeliac disease: recall the pathophysiology and dietary management of coeliac disease

An immune system mediated disorder where gluten triggers the body’s immune cells to attack self-cells in the small intestine.

The main problem is gluten specifically a 33 aa peptide called gliadin. Gliadin is very hard to breakdown!

MOST DAMAGE OCCURS IN THE DUODENUM – crypt hyperplasia and villus atrophy

Symptoms

Bloating

Diarrhoea

In children



abdo

distension and failure to thrive

Treatment

Dietary management



gluten-free diet (duh) and medication

Note: cross contamination at home and holidays, lifestyle and eating out can affect compliance

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Why is gliadin a problem?

Gliadin gets into SI via

SIgA

in the mucosal membrane

Normally anything bound to

SIgA

is destroyed by immune cells however gliadin binds up to transferrin receptors (these are overexpressed in CD patients)

The complex is

transcytosed

into the lamina

propriae

(lining of the gut wall) – basically through the enterocyte

Tissue transglutaminase (TTG) cleaves an amide group from gliadin

Deamidated

gliadin is consumed by macrophages and presented on MHC II

Presented to immune cells

CD4+ T helper cells recognise this and release inflammatory cytokines (IFN-gamma and TNF)



destruction of villi in SI.

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Learn the characteristics of both conditions by using this easy table!

1-LSS-ALI-PATH-17:  Inflammatory bowel disease: explain the dietary management and nutritional significance of inflammatory bowel disease 

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Crohns Disease

This is an inflammatory bowel disease that causes inflammation in the bowel – classified as an immune related disorder

Pathogenesis:

Triggered by a foreign pathogen in the GI tract e.g. listeria

This activates the immune system by antigen presentation.

T helper cells release cytokines (TNF /IFN )



inflammatory response.

Cytokines recruit macrophages which release even more inflammatory mediators which contribute to inflammation

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Continued..

Facts:

genetic influence

Unregulated inflammation



massive tissue destruction (usually transmural from mucosa to serosa)

Cobbled appearance – inflammation isn’t continuous

**ILEUM AND COLON MOST AFFECTED**

Treatments:

Immunosupressants

Antibiotics

Diet



liquid diet, low fibre, restriction of diet basically

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Ulcerative Colitis

A type of inflammatory bowel disease that specifically refers to inflammation in the colon or the large intestineCharacterised by ulcers in the large intestine and rectumMost common IBD

Symptoms:

Patients experience pain in the Left Lower Quadrant (rectum location)Severe and frequent diarrhoea +/- blood!

Treatments:

Dietary manipulation to minimise diarrhoea

Pre/probiotics: to treat and prevent

pouchitis

and helps remission of ulcerative colitis. Prebiotics may cause ab-

dominal

pain, bloating diarrhoea and flatulence

Diarrhoea: drink fluid, nutritious drinks, replace salt.

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SAQ

What is the characteristic histological feature of Coeliac Disease? (2 marks)

Name 2 specific inflammatory bowel conditions (2 marks)

State 4 differences between

Crohns

Disease and Ulcerative Colitis (4 marks)

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Cancer

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1-LSS-ALI-PAN-05: Pancreatitis: define acute and chronic pancreatitis; recall causes, symptoms and signs, investigations and complications

Pancreatitis is inflammatory disease of pancreas

 acute or chronic

Acute Pancreatitis:

Is an acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems.

Causes = alcoholism and

cholelithiasis

Diagnosis = upper

abdo

pain, vomiting and

abdo

tenderness. Ecchymosis on the body wall. Increased amylase/lipase/pancreatic enzymes. Increased bilirubin/liver enzymes/RBCs

MRCP = non invasive investigation of bile duct

ERCP = In patients thought to have severe biliary pancreatitis secondary to gallstones

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Chronic Pancreatitis

Same definition – just long term

Causes = alcoholism,

microlithisasis

(sludge) and idiopathic causes. Rare causes - hereditary pancreatitis, hyperparathyroidism, and obstruction of the main pancreatic duct

Diagnosis = amylase, lipase are both normal. Inflammatory markers increase. Pancreatic calcifications on X-Ray

Treatment = similar to acute pancreatitis + fluids and diet restriction (less fat and protein).

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1-LSS-ALI-PATH-07: Gastrointestinal cancer: list the common sites of cancer in the gastrointestinal system, recall associated cell types, explain clinical features and investigation of gastrointestinal cancer, including oesophageal, bowel and pancreatic

OESOPHAGEAL CANCER

Adenocarcinoma

Squamous cell carcinoma

Metaplastic columnar epithelium

Lower 1/3

Acid reflux

Common in Developed countries

Oesophageal squamous epithelium

Upper 2/3Acetaldehyde pathwayDeveloping countries

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Colon Cancer

Investigations (tests for diagnosis)Abdominal X-RayComputer Tomography (CT)Barium enemaColonoscopyCT virtual colonscopyEpidemiology14% in men, 12% in women30000 new cases per year

! RISK FACTORS !

Family history

Uncontrolled

uclerative

colitis

Age

Previous Polyps

Specific inherited conditions

e.g

FAP or HNPCC

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Pancreatic Cancer

SILENT KILLER  symptoms not easily detected and therefore late diagnosis.Probably the worst cancer you can get5 year survival is 2% (very very low!)Symptoms:DepressionAbdo painGlucose intoleranceWeight loss Jaundice Ascites (accumulation of fluid)

! RISK FACTORS !

Smoking

Drinking

Obesity

Family History e.g. MEN

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SBA

Which of the following cancers is known as a ‘silent killer’?

Stomach cancer

Kidney cancer

Liver cancer

Pancreatic cancer

Lung cancer

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SAQ

State two differences between Adenocarcinoma of oesophagus and squamous cell carcinoma of the oesophagus? (2 marks)List 3 causes of chronic pancreatitis? (3 marks)What does ERCP stand for and what can it be used for? (2 marks)

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Nutrition/Malnutrition

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1-LSS-ALI-PATH-12: Malnutrition assessment: Recall how to assess for malnutrition clinically

Largely through asking the right questions and in conjunction with nutritional screeningNeed to be aware that malnutrition costs the NHS billions of £££ - so it’s a massive clinical issueAssociated with:Reduced mobilityIncreased risk of fallsInfectionsConfusionIncreased hospital admissionsNB treatment = nutritional support e.g. high energy food drinks

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1-LSS-ALI-PATH-11: Nutritional screening: Recall how nutritional screening is performed and its significance

Nutritional screening is used to assess a patient’s nutritional status and identify those with malnutrition using scores/flowcharts.

For example;

Calculating BMI

Assessing special diets/reduced appetite/supplements

GI symptoms (pain/diarrhoea/ constipation)

history of diabetes

functional impairment (exercise tolerance/lethargy/daily activities).

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1-LSS-ALI-PATH-13: Refeeding syndrome: explain the pathophysiology of refeeding syndrome

Refeeding syndrome



A syndrome consisting of metabolic disturbances that occurs when nutritional support is reinstated in severely malnourished/starved patients

Characteristics:

Hypokalaemia

hypomagnesaemia

Hypophosphataemia

thiamine deficiency

salt and water retention

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Fasting

Depleted electrolyte stores

Refeeding

Increased insulin driving synthesis

Uptake of PO4-, K+ and Mg2+  further depletion  low levels of PO4-, K+ and Mg2+

Cardiac arrythmias and cardiac failure, confusion, convulsions, coma and fatality

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Treatment for Refeeding syndrome

Monitoring:Urea / electrolytesBone profile (calcium and phosphate)Magnesium levels dailyAdditional measures:Parenteral feeding, nasogastric feeds, nil by mouthDehydration and electrolyte imbalanceMany elderly patients admitted are malnourished

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1-LSS-ALI-PATH-15: Critical care: compare enteral and parenteral feeding and associated problems, and identify reasons for the use of tracheotomy within ICU

In intensive care we need to provide nutrition for patients who cannot eat on their own - either

enterally

or parenterally.

Enteral = via GI tract

Parenteral = bypasses GI tract e.g. through the blood

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Enteral nutrition (EN)

Parenteral nutrition (PN)

Route of delivery

A tube is placed into GI tract to deliver liquid food.

e.g.

nasooesophageal

, nasogastric,

nasoduodenal

; 

percutaneously e.g. oesophagostomy, gastrostomy,

jejunostomy

Preferred for most

A micronutrient-rich solution is adminstered slowly directky intro the blood through a venous catheter.

Necessary for some

Type of patient

Upper GI problem e.g. dysphagia or trauma

Dysfunction GI tract that is unable to digest, absorb or excrete appropriately (e.g. mid-GI blockage)

Complications

Low risk of complications:

Nausea

Vomition

Aspiration

High risk of serious complications:

Blood clots

Infection

Liver failure

Technical requirements

Requires basic training only to administer and maintain

Requires specialist training

Effect on GI tract

Maintains the internal structure and function of GI tract

Causes atrophy of gastrointestinal structures through underuse.

Cost

Much cheaper than PN.

Expensive!

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Tracheotomy

an incision made in the trachea to enable breathing e.g. for patients with obstruction or patients in intensive care

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1-LSS-ALI-PATH-16: Short bowel syndrome: identify the nutritional consequences and management options of short bowel syndrome

Short bowel syndrome is when a patient undergoes significant removal of the bowel which leaves less than 100 cm of functional intestinal tract. Usually for conditions: Crohn’s disease, cancer, ischaemia, ulcerative colitis, irradiationConsequences:dehydrationmalnutrition malabsorptionManagement: To provide adequate nutrition for patientsTo ensure adequate water and electrolytes to maintain homeostasisCorrection and prevention of acid base imbalance

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1-LSS-ALI-PATH-10: Health eating guidelines: Recall the healthy eating guidelines

Health eating is about reaching nutritional potential.

The definition of depends on the context:- In developing countries: Nutritional security - In developed countries: Limiting the development of chronic disease in the developed countries 

Healthy eating is largely to encourage the public to change their feeding habits in order to target the following:

Obesity

CHD

Diabetes

Veg consumption

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1-LSS-ALI-PATH-08: Energy requirements: identify the energy requirements in exercise and how exercise in extreme conditions impacts on requirements1-LSS-ALI-PATH-09: Fuel sources: distinguish between fuel sources for different exercise types and evaluate uses and limitations of supplements

Energy requirements of exercise depend on the intensity, duration and type of the exercise being conducted.

Different fuel sources are utilised at varying levels to produce energy in the form of ATP. 

Types:

Anaerobic exercise:

glycogen



ATP by glycolysis

Phosphocreatine lasts for 20secs of max activity

Lactic acid is produced (by product)

Aerobic exercise:

Oxidation of CO and fats produce ATP – the amount produced depends on how intense the exercise is

Low intensity



fat is the preferred substrate

High intensity



CHO is the preferred substrate

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Muscles

Muscle Anabolism:

balancing the breakdown and synthesis of muscle proteins can affect the muscle mass.

Muscle protein synthesis > Muscle protein breakdown for hypertrophy/muscle gain

Creatine

supplementation:

often taken by athletes to increase the contraction time of muscles.

The risks include fluid retention and therefore increased body mass. Can also affect blood flow.

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1-LSS-ALI-PATH-21: Cancer: identify changes that contribute to the development malnutrition in cancer patients

Weight change is a common presenting complaint in patients who are ultimately diagnosed with cancer. It is a predictor for outcome in cancer.

Reasons for malnourishment in cancer patients:

Iatrogenic



decreased food intake/increased energy expenditure

Chemotherapy



fatigue/nausea/vomiting

Poor symptom control



loss of appetite, D/N/V

Increased metabolic rate in cancer patients

Cancer cachexia =

metabolic response due to the presence of a tumour resulting in catabolic action

(this is why cancer patients are anorexic and weak).

Nutritional support cannot completely reverse this.

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1-LSS-ALI-PATH-06: Alcohol: recall the biochemistry and metabolism of ethanol, recall the physiological effects of alcohol and the pathophysiological mechanisms of alcohol induced disease, demonstrate awareness of the impact of alcohol on individuals and society and recommended limits of consumption

3 routes of metabolism:Ethanol  acetaldehyde  acetateEthanol  Acetaldehyde via CYP2E1 Ethanol  Acetaldehyde via NAD+

Metabolism can be influenced by genetics (polymorphisms) and race

e.g

Asian flush

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Effects of Alcohol

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Effects of Alcohol

Physical

Physiological

CNS –

Wernickes

encephalopathy

CVS – Hypertension

GIT – OesophagitisGUT – Glomerulonephritis Endocrine & Reproduction

Drug addiction and mental illness

See previous slide (Venn Diagram)

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Continued…

Obesity is a GLOBAL problem – not just prevalent in the UK. Obesity rates are increasing across all ages – particularly in childhood. In the UK the highest in age group is 55-64 year olds

You need to understand that there is some genetic contribution to obesity but it only explains 5% of all obesity cases

Important receptors and molecules you should be aware of: Leptin receptor, POMC, MC4R, NPY, AGRP and MCH molecules

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Complications

Healthcare costs!! MASSIVE burden on the NHS ~ £3.7bnHealth effects  increased risk of ischaemic heart disease, hypertension, diabetes, cancer, strokeWaist circumference or omental fat can be a marker of obesity e.g. pear shaped body is better than an apple shaped body/

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Management of Obesity

Clinical Management:

Diet

Exercise

Behavioural therapy

Drugs

Surgery if morbidly obese

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Obesity

Obesity can only occur when energy intake remains higher than energy expenditure for an extended period of time.BMI levels: 18.5 – 24.5 kg/m2 is HEALTHY25-29.9 kg/m2 OVERWEIGHT>30 OBESE

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SAQ

What is short bowel syndrome? What can it result in? (2 marks)

List 4 ways in which an obese person can manage their condition? (4 marks)

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Control of Function

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1-LSS-ALI-MECH-06 - Enteric nervous system: explain the major features of the enteric nervous system and how it interacts with the autonomic nervous system

The wall of the GI tract has millions of neurons – it technically is a mini brain which controls the GI tract function.

Plexi

are local networks of nerves and cells which are interconnected.

Enteric Nervous system (ENS) is an INTEGRATING CENTRE for coordinating function. Afferent

 Integration  efferent signals.

NB: The following can cause dysfunction of the ENS:

Inflammation e.g.

Crohns

Disease

IBS

Ageing  constipation

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1-LSS-ALI-MECH-06 - Enteric nervous system: explain the major features of the enteric nervous system and how it interacts with the autonomic nervous system

Myenteric plexus (Auerbach’s plexus)  between the circular and longitudinal smooth muscle layers. MOTILITY!Submucosal plexus ( Meissner’s plexus)  in the submucosal layer. SENSE ENVIRONMENT AND CHANGE BLOOD FLOW/ENDOCRINE FUNCTION!

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1-LSS-ALI-MECH-06 - Enteric nervous system: explain the major features of the enteric nervous system and how it interacts with the autonomic nervous system

Efferent

Function

Description

Secretion

controlling the secretion of enzymes, paracrine signals and endocrine hormones to regulate local and non-local gut functions.

Perfusion

blood flow needs to be carefully controlled to ensure high perfusion in regions of the gut that are working

Absorption

carefully controlling the absorption of nutrients, vitamins, minerals and ions

Motility

smooth muscle cells in the circular and longitudinal muscle layers can contract and relax to cause effective gut transit. It may be desirable to accelerate this or stop it completely

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1-LSS-ALI-MECH-06 - Enteric nervous system: explain the major features of the enteric nervous system and how it interacts with the autonomic nervous system

You should already know that there are 3 types of neurones (sensory, motor and interneurons).

The autonomic nervous system (ANS)

 regulates smooth muscle, cardiac muscle and glands.

SYMPATHETIC = fight/flight

PARASYMPATHETIC = rest and repair

NB: neurotransmitters and structures of these two branches of the ANS are very different!

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Sympathetic NS

Parasympathetic NS

Cell Bodies

Preganglionic

Postganglionic

 

 

T&L spinal cord

Pre paravertebral ganglia

 

Brainstem and Sacral spinal cord

Close to targets

Length

Preganglionic

Postganglionic

 

 

SHORT

LONG

LONG

SHORT

Innervation

Thoracic splanchnic



FOREGUT+MIDGUT

Lumbar splanchnic



HINDGUT

Mostly CN X (Vagus)

From duodenum pelvic

Major Neurotransmitter

Norepinephrine

Acetylcholine

Effect

Decrease Function

Increase function

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TAKE HOME MESSAGES

The myenteric plexus communicates directly with the submucosal plexus to make 'local' decisions based on 'local' signals

The ANS typically inputs into the enteric nervous system, allowing integration with local afferent signals to provide a coordinated response

With the exception of sympathetic innervation of vascular smooth muscle.

The enteric nervous system is very INDEPENDENT!

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Gut Hormones (quick recap)

This should be covered in another alimentary tutorial but extra notes I made last year are in the notes section of the slides.

Next few slides are just some summary tables of each hormone you need to know!

Make sure you learn these table at least if you want to pass – worst case scenario you’ll get the basic info if you don’t have time to learn the deeper detailed bits



Slide65

Most endocrine hormones are released from enteroendocrine cells (submucosa/mucosa of gut)3 specific functions:Glucose regulation (e.g. insulin & glucagon)Appetite regulation (e.g. ghrelin & peptide YY)Gut function regulation (e.g. somatostatin and secretin to name a few)

NB: You can also get paracrine control of the gut e.g. hormones released from the stomach such as histamine released from enterochromaffin-like cells.

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Gastrin and Secretin

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Somatostatin, Cholecystokinin, GDIP

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Hydration

Slide69

1-LSS-ALI-MECH-04: Water control: recall the hormonal control of water balance, and explain the role of angiotensin II in the perception of thirst

KEY CONCEPTS:

Brain, gut and kidney are vital organs involved in regulation of thirst

Osmolality is very important to tightly control – if this is messed up – your entire body will go into disarray!!

Osmoreceptors

detect the solute concentration (found in organs with incomplete BBB) e.g. Hypothalamus within OVLT and SFO

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1-LSS-ALI-MECH-04: Water control: recall the hormonal control of water balance, and explain the role of angiotensin II in the perception of thirst

Vasopressin or ADH is produced by hypothalamus and neurohypophysis

ADH involved in:

Inserting AQP2 into collecting ducts of nephrons (water retention)

Stimulate vasoconstriction

These functions act to maintain blood volume and therefore INCREASE blood pressure.

They also stimulate

thirst

to allow us to drink more water.

Slide71

1-LSS-ALI-MECH-04: Water control: recall the hormonal control of water balance, and explain the role of angiotensin II in the perception of thirst

Angiotensin II has 5 primary effects:

It binds to receptors on vascular smooth muscle cells to stimulate

vasoconstriction

It

upregulates activity of the sympathetic nervous system

, which largely promotes vasoconstriction

It stimulates

aldosterone secretion

, which

increases sodium reabsorption

in the nephron, which creates an osmotic gradient for water reabsorption

It

directly influences sodium reabsorption

, causing water reabsorption

It stimulates

ADH release and stimulates thirst

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1-LSS-ALI-MECH-04: Water control: recall the hormonal control of water balance, and explain the role of angiotensin II in the perception of thirst

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SBA

Which of the following has an incomplete blood brain barrier?

Subfornical

Organ

Lateral terminalis

Lateral Hypothalamus

Neurohypophysis

Entire brain

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scr15@ic.ac.uk for any questions about Y1 

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Next tutorial info

LSS and LCRS Revision Day

James Moss and Chris John

Wednesday 6

th

June – 2pm–5pm

CX,

Glenister

LT

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Feedback link

https://goo.gl/eHjFe9https://www.brainscape.com/profiles/2683619

Brainscape

link