BGDB End-of-Course Tutorial

Sam and Arty
 Approaching the End of Course Exams
 Gastroenteritis
 Gut Physiology
 Thyroid Physiology
 Depression
 Normal Development
 GIT Embryology
 Wrap-up and Questions
Approaching the End of Course Exam
 Read the question
 Define key concepts
 Structure (Logical Flow)
 Tables & Diagrams
 Dot points
 Completely lost? Write what you know
A 5 yro child presents to the ED with symptoms of
diarrhoea, vomiting and nausea.
 What is gastroenteritis?
 What are the common causative agents of
 How would you make a diagnosis?
 How would you manage this case?
Defining Gastroenteritis
 Inflammation of the GIT.
 Involving stomach/SI
 Diarrhoea, vomiting, malaise, nausea, abdominal
Causative Agents-viral
 In Australia: viruses, bacteria, parasites
 Norovirus: most common in adults.
 Rotavirus: Second most common in children. Vaccine.
 Adenovirus: Most common in children
 Astrovirus, picornavirus, parvovirus, sapovirus
Causative Agents - bacterial
 Campylobacter jejuni: most common in Aust.
Zoonotic potential.
Salmonella non-typhoid: second most common. Food
Salmonella typhoid: s. Typhi, s. Paratyphi. Longer
lasting, systemic
Shigella: very low infectious dose. faecal/-oral, sexual
Vibrio cholera: ‘rice water stools’
Causative agents - parasites
 Giardia Lamblia: protozoan.
 Symptoms - flatulence, foul smelling stools, weight
loss, diarrhoea, constipation.
 Exclude other possibilities (eg. medications)
 Blood tests – FBC, inflammatory markers(CRP, ESR)
 Stool sample: microscopy & culture
 If bacterial/parasite microscopy & culture will help
 Diet/Nutrition
 Rehydration
 Adsorbents: eg. activated charcoal
 Antimotility drugs: eg. loperamide, atropine
 Bismuth subsalicylate: anti-inflammatory
 Intestinal flora modifers
 Anti-microbials: shigella, severe cholera, typhoid
Sample Question
 Antony 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
What are the components of the
 Digestion
 Mouth (Salivary Amylase)
 Pancreas (Pancreatic Amylase)
 Small Intestine (Disaccharidases)
 Absorption (transport across the enterocyte into the
 Salivary amylase breaks down complex sugars (eg.
starch) into simple sugars
 Pancreatic amylase further breaks down complex
 Disaccharidases break down disaccharides into
 Lactase (Lactose  Glucose + Galactose)
 Maltase (Maltose  2 * Glucose)
 Sucrase (Sucrose  Glucose + Fructose)
 Across the enterocyte apical membrane
 Na+/Glucose Co-Transporter (SGLT1) for Glucose and
 GLUT5 for Fructose
 Across the enterocyte basal membrane
 Gradients maintained by the Na+/K+ ATPase
Thyroid Physiology
Effects of Thyroid Hormone
 Increase basal metabolic rate: glycogenolysis,
gluconeogenesis, lipolysis, protein synthesis. Heat
generation, increased energy usage, oxygen
 Growth effects: with GH
 Cardiac effects: increase contractility
 Developmental effects: neonatal CNS
Thyroid – clinical perspectives
 A 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 hypothyroidism
 How would you manage a patient with
fatigue, muscle weakness, cold intolerance,
bradycardia, hypoglycaemia, constipation
 Increase basal metabolic rate: glycogenolysis,
gluconeogenesis, lipolysis, protein synthesis.
Heat generation, increased energy usage, oxygen
 Growth effects: with GH
 Cardiac effects: increase contractility, HR
 Developmental effects: neonatal CNS
Causes of Hypothyroidism
 Definition –abnormally low level of TH
 3-5% of the population. Women, age
 Hashimotos thyroiditis: inherited autoimmune
 Pituitary or hypothalamic disease
 Thyroid destruction
 Medications
 Severe iodine deficiency
Managing Hyperthyroidism
 Surgery
 Radioactive iodine
 Anti-thyroid drugs
Anti-Thyroid Drugs
 Carbimazole – inhibits thyroid peroxidase
 Propyl-Thiouracil (PTU) – inhibits thyroid peroxidase
& blocks de-iodination of T4 to T3
 More T4 produced. But T3 more potent at target
 Anhedonia
 Sleep Changes
 Appetite and weight changes
 Dysphoria (low mood)
 Fatigue
 Agitation (psychomotor)
 Concentration (loss of)
 Esteem (decreased self-esteem)
 Suicidal Ideation
 Mrs X is a 55-year-old South Sydney Rabbitohs
supporter, who has come in complaining of a fourweek 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?
Answering the Example Question
 Work through ASADFACES!
 Establish Chronicity!!
 Discuss risk factors if relevant
 Non-pharmacological methods!
 Pharmacological agents (name, class, mechanism of
action, side effects)
 Electroconvulsive therapy
Pharmacological Management of
 Selective Serotonin Reuptake Inhibitors (SSRIs)
 Monoamine Oxidase Inhibitors (MAOIs)
 Other (Venlafaxine, Buproprion)
Developmental Milestones
 A 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
 Is this normal? Why/why not?
 What is developmental delay? What could cause it?
 How would you assess this case?
Domains of Normal Development
 Gross Motor
 Fine Motor
 Cognitive (Piaget’s Theory)
 Personal/Social
 Speech/Language
Normal Developmental Milestones
 6weeks: primitive reflexes
 9months: sit alone, object permanence
 By 12months: pull to stand, precise pincer grip, first
 By 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 instructions
 6years: skip, bounce and catch ball, write first name,
know address.
Michael’s development
 Down syndrome – can delay development
 Michael’s case: reaching his milestones later
 Need to assess cases individually, and realise some
range is normal
Developmental delay and its
 The failure to meet developmental milestones at
expected periods. Global or Domain-Specific.
Mental retardation, CNS problems (meningitis)
In Utero: infection in womb, FAS, trauma
Chronic infection: deafness/glue ear (gentamicin)
Hormonal problems-eg. thyroid
Genetic/Family history-eg. DS, Turner
Nutritional problems
Assessing developmental delay
 observe child
 detailed history
 check milestones
 physical neurological exam
 developmental screening: eg. parents evaluation of
developmental status (PEDS),
How to learn GIT Embryology
 By time points
 By organs
 Pay attention to abnormalities mentioned in the
GIT Embryology Time Points
 Week 3 – GASTRULATION (formation of the three
germ cell layers) and FOLDING (around the
 Week 4 – Segmentation of Mesoderm (Paraxial,
Intermediate, Lateral Plate – Splanchnic + Somatic),
Formation of Foregut, Midgut and Hindgut
 Week 5 – 8 Recanalization.
 Weeks 8-10 Intestinal Rotation
GIT by Organ
 Liver
 Stomach (including rotation)
 Pancreas
 Spleen
 Learn about which germ cell layer, and key phrases (eg.
Dorsal mesogastrium for spleen, septum transversum
for liver)
GIT Abnormalities
 Oesophageal atresia (recanalization)
 Meckel’s diverticulum (improper closure of the
vitelline duct)
Wrap Up & Questions

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