Curriculum Objective
Objective
General Objectives
General Objectives
Tutorial Cases
Curriculum Block
Part 3 / Medical Foundation 3
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Curriculum Block
Part 3
Medical Foundation 3
Curriculum Week
Part 3
Related Objectives
Parent Objective
Child Objectives
- Upon completion of this problem, students are expected to describe the key developmental milestones of the peri-pubertal stage and the nutritional requirements of the adolescent and the impact of extreme lifestyle behaviours on growth and nutritional health of adolescents. Students will describe common presentations of eating disorders.
- Upon completion of this problem, students will be able to describe the role of insulin in lipid, carbohydrate and protein metabolism in normal homeostasis and and appreciate the consequences of the pathophysiological condition of absolute insulin deficiency.
- Upon completion of this problem, students will explain how a genetic defect can disturb normal lipoprotein metabolism and increase risk of cardiovascular disease.
- Upon completion of this problem, students will describe the role of thyroid hormones in energy metabolism.
- Upon completion of this problem, students will be able to describe the regulation and function of the hypothalamic-pituitary-adrenal axis.
- Upon completion of this problem, students will identify genetic and environmental risk factors for childhood obesity and discuss prevention and treatment strategies at the individual and population level.
- Upon completion of this problem, students will outline the key hormones and organs or tissues involved in calcium homeostasis, as well as the causes and consequences of hypercalcemia. Students will also be able to describe the histological structure of bone, the physiology of bone formation and remodeling and the pathophysiology of osteoporosis.
- Upon completion of this problem, students will be able to describe normal pituitary structure and function and compare with the pathologic state of growth hormone excess.
- Upon completion of this problem, students should be able to describe the production of steroid hormones and to interpret the implications of steroidogenic enzyme deficiencies on embryologic development and postnatal health. Students will also have reviewed the inheritance of Congenital Adrenal Hyperplasia, discussed related genetic counselling, and considered a patient-centered approach to caring for intersex patients.
- Upon completion of this problem, students should be able to discuss the actions of testosterone and dihydrotestosterone on embryological development and sexual differentiation.
- Explain the genetics, embryology and physiology of the sexual differentiation of the reproductive organs.
- Outline the biochemistry of steroidogenesis in the adrenal gland and gonads, including the role of the key enzyme 21-hydroxylase.
- Explain the clinical consequences of primary adrenal insufficiency as they pertain to the infant.
- Explain the anatomic presentation of the female child with virilizing Congenital Adrenal Hyperplasia.
- Describe the actions of testosterone and dihydrotestosterone on the androgen receptor.
- Discuss the impact of androgen receptor mutations on the phenotypic display of sexual differentiation.
- Describe the anatomy, histology and function of the endocrine pancreas.
- Explain the metabolic effects of insulin at the level of muscle, liver and adipose tissue.
- Explain the pathophysiology of diabetic ketoacidosis.
- Describe how to diagnose diabetes.
- Describe the classification of diabetes mellitus types (type 1 , type 2, monogenic, etc.).
- Review the precipitants and management of diabetic ketoacidosis.
- Outline microvascular complications of diabetes mellitus.
- Discuss reasons for non-compliance to diabetes treatments.
- Describe the pathogenesis of type 2 diabetes.
- Outline the mechanism of action of non-insulin anti-hyperglycemic medications.
- Outline lipoprotein metabolism.
- Explain the genetic defect that causes Familial Hypercholesterolemia and how it results in elevated LDL levels and atherogenesis.
- Compare primary vs secondary prevention of cardiovascular disease.
- Describe the anatomy and physiology of the hypothalamic pituitary-adrenal axis.
- Contrast the physiological regulation and effects of adrenocortical steroids (glucocorticoids, mineral corticoids, adrenal androgens).
- Propose a diagnostic approach for patients with cortisol excess, illustrating the concept of dynamic testing as it applies to diagnosis.
- Establish a differential diagnosis of Cushing syndrome.
- Evaluate treatment modalities for Cushing syndrome (including surgery, pharmacology and radiation).
- Outline the regulation, production, release and function of thyroid hormone.
- Identify the signs and symptoms of thyroid disease, with a focus on Graves' disease.
- Describe the diagnostic principles and approach to thyrotoxicosis.
- Discuss treatment options for patients with Graves' disease.
- Identify the role of hormones, exercise and energy balance in the maintenance of energy homeostasis.
- Review the guidelines for the diagnosis of overweight and obesity in children and adolescents.
- Describe what laboratory and other tests may be useful in the investigation of obesity.
- Summarize current approaches to the treatment of obesity including diet, exercise, behavior modification, pharmacotherapy and bariatric surgery.
- Describe current population-based approaches to prevention and/or treatment of childhood obesity at regional, provincial or national levels.
- Describe the histology, function and control of osteoclasts, osteoblasts and osteocytes in bone remodeling with reference to their hormonal regulators.
- Define osteoporosis, describe changes to bone associated with osteoporosis and discuss the major secondary causes of osteoporosis.
- Review normal adolescent nutrient needs during pubertal growth spurt (i.e. the DRIs).
- Review the Dietary Reference Intakes (DRI) for North Americans (particularly for protein and energy) and explain how they are applied in clinical practice.
- Review optimal growth during childhood and adolescence using the WHO growth charts.
- Discuss the health risks of extreme dietary practices (e.g., poorly planned restrictive diets or ‘fad’ weight control diets) in adolescents, including disordered eating, and malnutrition.
- Discuss the unique features of the physician-patient relationship during adolescence including confidentiality and consent.
- List the hormones produced by the pituitary and outline their effects on body function.
- Describe the anatomy, regulation and function of the pituitary gland, with emphasis on the production and regulation of growth hormone.
- Outline the role of growth hormone during normal development.
- List and categorize common insulin preparations used in the treatment of diabetes mellitus.
- Upon completion of this problem, students should be able to describe the pathogenesis of insulin resistance and type 2 diabetes mellitus as well as discuss its epidemiology and management strategies.
- Recognize the epidemiological trends in type 2 diabetes mellitus in Canada and globally.
- Identify the major components of risk modification in diabetes mellitus (control of blood glucose, blood pressure and lipids) and associated treatment targets.
- Review the recommendations for screening for diabetic complications.
- Describe hormonal, physiological, and medical issues that arise in response to poor nutrition and excessive exercise.
- Describe the diagnosis and treatment of hypothyroidism.
- Describe the clinical findings associated with acromegaly and provide an approach to its diagnosis.
- Upon completion of this problem, students will be able to describe the anatomy and physiology of the adrenal gland. Students will be able to summarize the physiological role of catecholamines and the consequences of catecholamine excess.
- Describe the structure and function of the adrenal gland with reference to the three cortical layers as well as the medulla.
- Describe the clinical presentation, diagnostic evaluation (including genetic testing) and management of pheochromocytoma.
- List the various biological effects of cortisol.
- Describe the clinical presentation of individuals with glucocorticoid excess and deficiency.
- Describe and account for the internal and external reproductive anatomy in partial androgen insensitivity with reference to the hormonal control of embryological sexual differentiation.
- Calculate the risks to relatives of an individual with an X-linked genetic condition.
- Differentiate the forms of calcium, bound and unbound, found in the extracellular space.
- Delineate the interactions between hormones (parathyroid hormone, vitamin D and calcitonin) and relevant organs (parathyroid glands, bone, kidney and gastrointestinal tract) in maintaining calcium homeostasis.
- Explain the consequences of high levels of parathyroid hormone and of low levels of vitamin D.
- List common food sources of vitamin D and calcium and state the recommended daily intake for each.
- Upon completion of this problem, students will be able to outline the hormonal abnormalities involved in Multiple Endocrine Neoplasia Type 1 (MEN 1) and review the genetics of proto-oncogenes and tumour suppressor genes.
- List the hormonal abnormalities in MEN 1.
- Discuss treatment options for a parathyroid adenoma, including indications for parathyroidectomy.
- Describe the physiological control and function of prolactin.
- Outline the diagnosis and treatment of a prolactinoma.
- Explain how and why hyperprolactinemia causes amenorrhea.
- Summarize the clinical presentation and pathophysiology of a gastrinoma.
- Discuss the social determinants of health that influence control of food and energy intake, and the importance of system-level solutions.
- Describe the role of inter-disciplinary health care providers (physiotherapists, dietitians, psychologists, nurse practitioners) in the treatment of obesity.
- List medications used to lower lipid levels and outline their mechanisms of action.
- Detail the signs and symptoms of hypercalcemia and give a differential diagnosis for this electrolyte disturbance.
- Identify the genetic defect responsible for MEN1 and explain how this defect results in multiple hormonal abnormalities originating in distinct endocrine glands.