BGDB End-of-Course Tutorial

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BGDB End-of-Course Tutorial Sam and Arty

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BGDB End-of-Course Tutorial. Sam and Arty. Tonight…. Approaching the End of Course Exams Gastroenteritis Gut Physiology Thyroid Physiology Depression Normal Development GIT Embryology Wrap-up and Questions. www.medsoc.org.au. Approaching the End of Course Exam. Read the question - PowerPoint PPT Presentation

Transcript of BGDB End-of-Course Tutorial

BGDB End-of-Course Tutorial

BGDB End-of-Course TutorialSam and Arty1Approaching the End of Course ExamsGastroenteritisGut PhysiologyThyroid PhysiologyDepressionNormal DevelopmentGIT EmbryologyWrap-up and QuestionsTonight

www.medsoc.org.au2Read the questionDefine key conceptsStructure (Logical Flow)Tables & DiagramsDot pointsCompletely lost? Write what you knowApproaching the End of Course Exam

www.medsoc.org.auTeach the marker e.g. definitions, saying what shit isTactics to Answering Questions ceebs full sentences, using shorthand and abbreviations, tables, diagrams

3GastroenteritisA 5 yro child presents to the ED with symptoms of diarrhoea, vomiting and nausea.

What is gastroenteritis?What are the common causative agents of gastroenteritis?How would you make a diagnosis?How would you manage this case?

Defining GastroenteritisInflammation of the GIT. Involving stomach/SIDiarrhoea, vomiting, malaise, nausea, abdominal discomfort.

Causative Agents-viralIn Australia: viruses, bacteria, parasites

Norovirus: most common in adults. Rotavirus: Second most common in children. Vaccine. Adenovirus: Most common in childrenAstrovirus, picornavirus, parvovirus, sapovirusViruses generally less severe than bacterial causes. Vomiting/diarrhea/nausea. Waterborne, fecal oral, airborne (norovirus)6Causative Agents - bacterialCampylobacter jejuni: most common in Aust. Zoonotic potential. Salmonella non-typhoid: second most common. Food poisoning. Salmonella typhoid: s. Typhi, s. Paratyphi. Longer lasting, systemicShigella: very low infectious dose. faecal/-oral, sexualVibrio cholera: rice water stoolsUsually more severe. Bloody stools/cramps/fever/leukocytosisGram negative rods

7Causative agents - parasitesGiardia Lamblia: protozoan. Symptoms - flatulence, foul smelling stools, weight loss, diarrhoea, constipation. Metronidazole. Attach to intestinal mucosa with ventral sucking discCyst and trophozoite(disease causing form) stages8DiagnosisExclude other possibilities (eg. medications)Blood tests FBC, inflammatory markers(CRP, ESR)Stool sample: microscopy & culture

If bacterial/parasite microscopy & culture will help detect

ManagementDiet/NutritionRehydrationAdsorbents: eg. activated charcoalAntimotility drugs: eg. loperamide, atropineBismuth subsalicylate: anti-inflammatoryIntestinal flora modifersAnti-microbials: shigella, severe cholera, typhoid salmonellaLow fibre for diarrhoea, no lactose, avoid fats/milk/alcohol/tea, soft digestable foods, make sure nutrition isnt compromisedOral rehydration saltsAdsorbents: activated charcoal, kaolin, attapulgite. Coat wall of Git or bind toxin and eliminate. Firmer stools, dont help rehydrationAntimotility drugs opioids: side effects of urinary retention/constipation/respiratory depression/bradycardia/drowsy. Anticholinergics eg. atropine, hyoscine. Ach muscarinic antagonists dry mouth/tachycardia/increase transit time to absorbBismuth subsalicylate: protective effects on mucosa, anti-inflammatory, inhibits PG synthesesAntimicrobials: norfloxacillin

10Sample QuestionAntony has just eaten a sugar-heavy meal. Describe the mechanism by which the sugars in the food are broken down and absorbed across the gastrointestinal lining. 11What are the components of the process?DigestionMouth (Salivary Amylase)Pancreas (Pancreatic Amylase)Small Intestine (Disaccharidases)Absorption (transport across the enterocyte into the bloodstream)

12DigestionSalivary amylase breaks down complex sugars (eg. starch) into simple sugarsPancreatic amylase further breaks down complex sugarsDisaccharidases break down disaccharides into monosaccharidesLactase (Lactose Glucose + Galactose)Maltase (Maltose 2 * Glucose)Sucrase (Sucrose Glucose + Fructose)

13AbsorptionAcross the enterocyte apical membrane Na+/Glucose Co-Transporter (SGLT1) for Glucose and GalactoseGLUT5 for FructoseAcross the enterocyte basal membraneGLUT2Gradients maintained by the Na+/K+ ATPase

Diagrams!

Thyroid Physiology

Effects of Thyroid HormoneIncrease basal metabolic rate: glycogenolysis, gluconeogenesis, lipolysis, protein synthesis. Heat generation, increased energy usage, oxygen consumption. Growth effects: with GHCardiac effects: increase contractilityDevelopmental effects: neonatal CNS18Thyroid clinical perspectivesA 20yro patient presents with symptoms of fatigue, muscle weakness, cold intolerance, bradycardia, hypoglycaemia, constipation. Is this more likely to be hypothyroidism or hyperthyroidism? Why?Describe two causes of hypothyroidismHow would you manage a patient with hyperthyroidism?

fatigue, muscle weakness, cold intolerance, bradycardia, hypoglycaemia, constipationIncrease basal metabolic rate: glycogenolysis, gluconeogenesis, lipolysis, protein synthesis. Heat generation, increased energy usage, oxygen consumption. Growth effects: with GHCardiac effects: increase contractility, HRDevelopmental effects: neonatal CNS

20Causes of HypothyroidismDefinition abnormally low level of TH3-5% of the population. Women, ageHashimotos thyroiditis: inherited autoimmunePituitary or hypothalamic diseaseThyroid destructionMedicationsSevere iodine deficiency

Amiodarone-anti-arrythmic drugs21Managing HyperthyroidismSurgeryRadioactive iodineAnti-thyroid drugs

Lumen

Anti-Thyroid DrugsCarbimazole inhibits thyroid peroxidasePropyl-Thiouracil (PTU) inhibits thyroid peroxidase & blocks de-iodination of T4 to T3

More T4 produced. But T3 more potent at target

DepressionAnhedoniaSleep ChangesAppetite and weight changesDysphoria (low mood)FatigueAgitation (psychomotor)Concentration (loss of)Esteem (decreased self-esteem)Suicidal Ideation

27ExampleMrs X is a 55-year-old South Sydney Rabbitohs supporter, who has come in complaining of a four-week history of tiredness and just not feeling like doing anything. You suspect she may be depressed. What questions could you ask Mrs X in order to help support a diagnosis of depression?28Answering the Example QuestionWork through ASADFACES!Establish Chronicity!!Discuss risk factors if relevant29ManagementNon-pharmacological methods!Pharmacological agents (name, class, mechanism of action, side effects)Electroconvulsive therapy30Pharmacological Management of DepressionSelective Serotonin Reuptake Inhibitors (SSRIs)Monoamine Oxidase Inhibitors (MAOIs)Other (Venlafaxine, Buproprion)31Developmental MilestonesA mother brings in her 2yro son, Michael, who has Down Syndrome. He said his first word last week, and although can crawl and cruise, has not yet started to walk. Is this normal? Why/why not?What is developmental delay? What could cause it?How would you assess this case? Domains of Normal DevelopmentGross MotorFine MotorCognitive (Piagets Theory)Personal/SocialSpeech/Language

Normal Developmental Milestones6weeks: primitive reflexes9months: sit alone, object permanenceBy 12months: pull to stand, precise pincer grip, first wordBy 2years: run, two words at two. 3years: tricycle, upstairs, mature pencil grip, use scissors, tower of 9 blocks, cooperative play, know gender, draw circle, understand 3keyword instructions6years: skip, bounce and catch ball, write first name, know address. Michaels developmentDown syndrome can delay developmentMichaels case: reaching his milestones later Need to assess cases individually, and realise some range is normal

Developmental delay and its causesThe failure to meet developmental milestones at expected periods. Global or Domain-Specific. Mental retardation, CNS problems (meningitis)In Utero: infection in womb, FAS, traumaChronic infection: deafness/glue ear (gentamicin) Hormonal problems-eg. thyroidGenetic/Family history-eg. DS, TurnerIdiopathicNutritional problems36Assessing developmental delayobserve childdetailed historycheck milestonesphysical neurological examdevelopmental screening: eg. parents evaluation of developmental status (PEDS),

Others: Australian developmental screening test (ADST-2hrs), Ages and Stages Questionnaires(ASQ), 37How to learn GIT EmbryologyBy time pointsBy organsPay attention to abnormalities mentioned in the lecture!GIT Embryology Time PointsWeek 3 GASTRULATION (formation of the three germ cell layers) and FOLDING (around the notochord)Week 4 Segmentation of Mesoderm (Paraxial, Intermediate, Lateral Plate Splanchnic + Somatic), Formation of Foregut, Midgut and HindgutWeek 5 8 Recanalization.Weeks 8-10 Intestinal RotationGIT by OrganLiverStomach (including rotation)PancreasSpleenLearn about which germ cell layer, and key phrases (eg. Dorsal mesogastrium for spleen, septum transversum for liver)GIT AbnormalitiesOesophageal atresia (recanalization)Meckels diverticulum (improper closure of the vitelline duct)Wrap Up & Questions