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N5315 Advanced Pathophysiology
Endocrine
Core Concepts and Objectives with Advanced Organizers
Endocrine Anatomy and Physiology Analyze the anatomy and physiology of the endocrine system:
- Examine the production and action of hormones produced by the thyroid, pancreas, and adrenal glands. a. Thyroid : ▪ Regulated by TSH ▪ Low thyroid hormone level release of thyroid-releasing factor release of TSH release of more T3 and T ▪ T3 and T4 : - Increase metabolism - Affect RR and oxygen utilization - Regulates body heat production ▪ Conditions may cause heart failure ▪ Possible to have been in thyroid failure x3 months before symptoms occur d/t storage of hormones ▪ Calcitonin : - Decrease serum calcium - Prevent PTH’s effect on bone resorption (pulling Ca) - Lowers serum phosphate levels - Reduces absorption of calcium and phosphorus from the gut b. Pancreas : ▪ Glucagon - Antagonizes insulin - Released during times of fasting ▪ Gastrin ▪ Somatostatin ▪ Pancreatic polypeptide ▪ Insulin - C-peptide levels may be measured to determine amount of insulin secreted ▪ Amylin - Suppresses glucagon secretion and delays gastric emptying c. Adrenal glands: ▪ Adrenal cortex - Glucocorticoids, mineralocorticoids, gonadocorticoids - Stimulated by ACTH - Aldosterone : increase sodium and decrease potassium o RAAS ▪ ACE inhibitors= hyperkalemia ▪ Adrenal medulla - Catecholemines
o Epi, norepi, and dopamine
- Discuss the effects of aging on the thyroid gland, adrenal gland and the pancreas. a. Thyroid: atrophy and fibrosis; TSH increases b. Pancreas: decline in B cell function= glucose intolerance/ diabetes c. Adrenal: fibrous, circulating levels of cortisol are elevated
Examine the pathologic basis of adult and pediatric disorders which affect the
endocrine system:
Obesity
- Explain the pathologic basis and consequences of obesity in the adult and child. a. Patho: white adipose tissue (WAT)- store triglycerides and secrete adipokines b. Visceral obesity: abdomen and upper body c. Peripheral obesity: pear shape Thyroid Disorders
- Differentiate between the etiology, clinical manifestations, pathophysiology and complications of thyroid disorders. a. Differentiate between the production, target tissues, control mechanisms, and functions of the hormones produced by the thyroid. b. Analyze the meanings of primary, secondary and subclinical thyroid disorders. Disease Definition Primary Thyroid Disorders Subclinical Thyroid Disease Secondary Thyroid Disorders c. Differentiate between the etiology, clinical manifestations, pathophysiology of thyrotoxicosis, grave’s disease, nodular hyperthyroidism, and thyrotoxic crisis. Disease Etiology Clinical Manifestations Pathophysiology Thyrotoxicosis Grave’s Disease Autoimmune hyperthyroidis m Goiter, exophthalmos, perioribital edema, extraocular muscle weakness, strabismus, diplopia Antibodies attach to thyroid cells and mimic function of TSH
Gestational Hyperglycemia during pregnancy Obesity, fam hx, high maternal age
b. Interpret diagnostic test results used to screen for diabetes mellitus and assign the correct diagnosis. Laboratory Test What does it measure? What value is consistent with a diagnosis of diabetes mellitus? What parameter is consistent with an increased risk for developing diabetes mellitus? Hemoglobin A1c
Fasting Plasma Glucose
Oral Glucose Tolerance Test (OGTT)
Random plasma Glucose
c. Differentiate between the initial presentation and clinical manifestations of diabetes mellitus type 1, type 2 and gestational diabetes. Diabetes Mellitus Initial Presentation Clinical Manifestations Type 1 Fluctuating glucose levels, ketosis, muscle and fat breakdown weight loss, DKA, polyphagia Type 2 Polydipsia polyphagia polyuria, no DKA BS much higher than type I; fatigue, recurrent infections, neuropathy, visual changes Gestational Hyperglycemia during pregnancy Child hypoglycemic after birth d. Describe how the difference in the pathophysiology between diabetes mellitus type I and type II impacts the treatment you prescribe to treat each diagnosis. e. Differentiate between the persons at risk, risk factors, timing of onset, clinical manifestations, laboratory results, and the pathophysiology of hypoglycemia, diabetic ketoacidosis, and hyperosmolar hyperglycemic syndrome. Disease Persons at Risk Risk Factors Timing of Onset Clinical Manifestations Lab Results Pathophysiology Hypoglycemia On insulin Not eating Pallor, anxiety, tachy, diaphoresis, irritable, confusion *beta blockers can block s/s Glucose <47 in newborns and < in children/ adults Diabetic Need IVF, IV Glucose Insulin
Disease Stroke Peripheral Arterial Disease Infection Adrenal Disorders
- Evaluate the etiologies, clinical manifestations, and the pathophysiology of cushing disease and addison disease. Disease Etiology Clinical Manifestations Pathophysiology Cushing Disease Over- secretion of cortisol; steroid use, over- secretion of ACTH d/t pituitary tumor, adrenal adenoma Hyperglycemia, insulin resistance, type2DM, truncal obesity, moon face, buffalo hump, bleed easily, hirsutism (increased hair growth), acne Addison Disease Decreased cortisol and aldosterone; autoimmune Hypoglycemia, weakness, fatigue, anorexia, Addisonian traid: hyperkalemia, hyponatremia, hypotension Crisis: hypotension, fluid loss, lack of cortisol/ aldosterone
- Evaluate the etiology, clinical manifestations and pathophysiology of anorexia of aging. Disease Etiology Clinical Manifestations Pathophysiology Anorexia of Aging Decrease in appetite or food intake Malnourished state Reduced energy requirements, decrease sense of smell/ taste
Musculoskeletal Disorders
- Differentiate between the etiology, pathophysiology and clinical manifestations for osteoporosis, osteoarthritis, sarcopenia and muscular dystrophy. Disorder Etiology Pathophysiology Clinical Manifestation Osteoporosis Low bone mineral density/ strength Insidious; only know after you’ve gotten a fracture Spontaneous fractures Osteoarthritis Aging/ mechanical stress *degeneration of articulating cartilage Loss of smooth joint Destruction of joint capsule Pain and stiffness; joint swelling; tenderness; deformity Worsened with weightbearing and relieved with rest Sarcopenia Loss of muscle mass d/t aging Muscular dystrophy x-linked disorder **mainly affects boys Deletion of one or more exons on DMD gene Age 3-4= gait abnormalit ies Toe walk Frequent falls Calf muscle hypertroph y Gower sign, unable to ambulate by age 12- 15 Absence of dystrophin= muscle fibers are torn apart during contraction= calcium enters cells and cell death and necrosis= increased levels of CK
