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Adrenal Disease Normal Anatomy and Physiology Adrenal Disease Objectives: 1. To increase students’ working knowledge of adrenal anatomy, physiology and pathology 2. To incorporate this working knowledge into patient assessment and clinical decision making Adrenal glands: cortex medulla Adrenal: Normal Physiology 1. Adrenal medulla: - ganglion of the sympathetic nervous system - secretes catecholamines: epinephrine and norepinephrine Adrenal: Normal Physiology 1. Adrenal medulla: Catecholamine (epinephrine and norepinephrine) secretion in response to sympathetic stimulation: fight or flight response Adrenal: Normal Physiology 2. Adrenal cortex: secretes steroid based hormones a. sex steroids b. mineralocorticoids c. glucocorticoids Adrenal: Normal physiology a. Sex steroids (testosterone) supplemental to gonadal production … not crucial to life Adrenal: Normal physiology b. Mineralocorticoids: control of Na / K / H20 … blood pressure renin / angiotensin / aldosterone CRUCIAL TO LIFE Adrenal: Normal physiology Regulation of Renin / Angiotensin / Aldosterone 1. Renin secreted by JGA in response to BP or chronic Na depletion 2. Renin catalyses the production of angiotensin I (a decapeptide) from a circulating protein 3. Angiotensin converting enzyme (ACE) in the lungs cleaves off 2 more amino acids to form Angiotensin II (an octapeptide) Adrenal: Normal physiology Renin / Angiotensin / Aldosterone 4. Angiotensin II : is a potent vasoconstrictor and it stimulates the release of aldosterone by the adrenal cortex 5. Aldosterone acts on the collecting tubule to increase the reabsorption of Na (and, therefore H2O) Adrenal: Normal physiology c. Glucocorticoids: -control of CHO / protein / fat metabolism -maintenance of vascular reactivity -anti-inflammatory -maintenance of homeostasis in response to stress (surgery, infection, starvation, etc.) CRUCIAL TO LIFE Adrenal: Normal physiology c. Glucocorticoids: control of CHO / protein / fat metabolism insulin antagonist ( serum glucose) hepatic glucose output initiates lipolysis and proteolysis gluconeogenesis Adrenal: Normal physiology c. Glucocorticoids: maintenance of vascular reactivity “primes” blood vessels to respond to catecholamine driven vasoconstriction Adrenal: Normal physiology c. Glucocorticoids: anti-inflammatory inhibits lysosome, prostaglandin, eicosanoid, and cytokine release inhibits endothelial cell adhesion Adrenal: Normal physiology c. Glucocorticoids: maintenance of homeostasis in response to physiologic stress (surgery, infection, starvation, etc.) Adrenal: Normal physiology Steroid hormone mechanism of action: 7 H 1 H 2 3 H 4 5 6 1. cell entry 2. cytoplasmic receptor binding 3. migration to nucleus 4. DNA transcription 5. mRNA migration to cytoplasm 6. mRNA translation 7. regulation of receptor number or activity Adrenal: Normal physiology c. Steroid mechanism of action: requires multiple steps for effect therefore, requires time to have an effect … 2 to 4 hours Adrenal: Normal physiology c. Glucocorticoids: regulation • Normal diurnal variation (highest in AM): • Daily average of approximately 20 mg Adrenal: Normal physiology c. Glucocorticoids: regulation • Increased secretion in response to physiologic stress (up to 200 mg) • Decreased secretion in response to exogenous steroids, eg Prednisone Adrenal: Normal physiology c. Glucocorticoids: regulation EXOGENOUS STEROID OR INCREASING CORTISOL STRESS OR DECREASING CORTISOL CRH = corticotropin releasing hormone hypothalamus CRH anterior pituitary ACTH cortisol adrenal cortex Adrenal: Disease Hyperadrenalism Hypoadrenalism Patients taking or have taken oral steroids Will have 50 in 2000 patient practice Adrenal: Disease (hyper) Hyperadrenalism: (Cushingoid) Cushing’s disease: excess of cortisol production (eg pituitary or adrenal tumour) with signs and symptoms of excess steroid Adrenal: Disease (hyper) Hyperadrenalism: (Cushingoid) Cushing’s syndrome: Signs and symptoms of excess steroid secondary to chronic use Adrenal: Disease (hyper) Cushingoid side effects from excess long term steroids: - adrenocortical suppression - weight gain, moon face, buffalo hump - abdominal striae, acne Adrenal: Disease (hyper) Cushingoid side effects from excess long term steroids: - hypertension, heart failure - osteoporosis, growth suppression - diabetes, impaired healing, peptic ulcers - depression, psychosis Adrenal: Disease (hypo) a. Adrenal insufficiency: Primary: Addison’s disease (loss of >90% of adrenal cortex) due to autoimmune, hemorrhage, infection, tumour, surgery, etc. Cortisol and Aldosterone deficiency Adrenal: Disease (hypo) a. Adrenal insufficiency: Secondary: hypothalamic or pituitary disease or exogenous steroid causing suppression of the hypothalamic / pituitary axis leading to atrophy of the adrenal cortex Cortisol deficiency only Adrenal: Pharmacology b. Glucocorticoids: steroids indicated for inflammatory conditions such as: - rheumatoid arthritis (RA) systemic lupus erythematosis (SLE) asthma inflammatory bowel disease (IBD) prevention of organ transplant rejection many others Adrenal: Pharmacology b. Glucocorticoids: equivalents Cortisol 20 mg = Prednisone = Solumedrol = Decadron 5 mg 4 mg .75 mg Adrenal: Disease (hypo) c. Secondary Adrenal insufficiency: IS caused by chronic oral steroid use: > 5 mg of Prednisone / day (> 20 mg of cortisol) for > 2 wks within the last year IS NOT caused by inhaled, nasal or topical steroid use Adrenal: Disease (hypo) c. Secondary Adrenal insufficiency: Strategies used to minimize suppression: • minimize oral dosage to 20 mg/day equivalent of cortisol or less • every other day dosing • tapering dosage to complete course Adrenal: Disease (hypo) d. Adrenal insufficiency: Problems • impaired CHO / protein / fat metabolism • hypoglycemia • hypovolemia / hyperkalemia / acidosis • hypotension Adrenal: Disease (hypo) d. Adrenal insufficiency: Signs and symptoms • excess pigmentation • postural hypotension (dizziness) • muscular weakness • nausea, anorexia, weight loss Adrenal: Disease (hypo) d. Adrenal insufficiency: diagnosis • Signs and symptoms • Lab values: difficult to do and interpret • CRH stimulation • ACTH stimulation • 24 hour urine cortisol Adrenal: Disease (hypo) d. Adrenal insufficiency: treatment • Treat the cause (tumour / infection) • Hormone replacement: • mineralocorticoid • glucocorticoid Adrenal: Pharmacology d. For mineralocorticoid insufficiency: - fludrocortisone (Florinef) - 0.05 to 0.1 mg daily Adrenal: Pharmacology d. For glucocorticoid insufficiency: - Cortisol: 20 mg AM / 10 mg PM - Prednisone: 5 mg AM / 2.5 mg PM (divided doses to reflect normal diurnal cycle) Adrenal: Crisis e. Acute Adrenal insufficiency: crisis • • • • • • medical emergency inability to tolerate physiologic stress acute refractory hypotension, diaphoresis dehydration, dyspnea, hypothermia, hypoglycemia, circulatory collapse, death less likely with secondary AI Adrenal: Crisis prevention e. Acute Adrenal crisis prevention: 1. Recognition of patient at risk: Addison’s disease Has taken suppressive dose Is taking low suppressive dose (Prednisone 10 mg or less) Adrenal: Crisis prevention e. Acute Adrenal crisis prevention: 2. Supplement: day before / day of / day after 100 mg cortisol = 20 mg Prednisone or double the existing dose if 10 mg of Prednisone or less Adrenal: Crisis treatment e. Acute Adrenal crisis treatment: • Hydrocortisone 100 mg IV bolus • Hospital setting for fluid and electrolyte replacement • Correction of hypoglycemia • Continued IV steroid Adrenal: Dental concerns 1. Assess compliance with steroids 2. Assess need for supplementation: complexity of surgery versus degree of adrenal suppression 3. Discontinue Ketoconazole and barbiturates if possible Adrenal: Dental concerns 4. AM procedures 5. Anxiety reduction eg N2O / O2 6. Good intra- and post-op pain control avoid NSAIDs (Peptic ulcers) 7. Monitor blood pressure 8. Cushingoid patients prone to fractures Questions???? Thyroid Disease Normal Anatomy and Physiology Thyroid Disease Objectives: 1. To increase students’ working knowledge of thyroid anatomy, physiology and pathology 2. To incorporate this working knowledge into patient assessment and clinical decision making Thyroid gland: Thyroid: Normal Physiology Thyroid gland produces 3 hormones: T3: triiodothyronine T4: thyroxine Calcitonin: controls Calcium levels in conjunction with parathyroid hormone and Vitamin D Thyroid: Normal Physiology T3: triiodothyronine: more potent form of thyroid hormone … 20% formed by the thyroid, 80% by deiodination in the periphery T4: thyroxine: produced in the thyroid Thyroid hormone formation is iodine dependant The Great Lakes area is endemically deficient in iodine, for this reason iodine is added to the table salt. Thyroid: Normal Physiology Thyroid hormone … distribution: produced and stored (3 to 4 month reserve) in the thyroid gland secreted and transported bound to thyroid globulin Thyroid: Normal Physiology Thyroid hormone … effects: controls oxidative metabolism and basic metabolic rate growth and maturation of tissues Thyroid: Normal physiology Thyroid hormone mechanism of action: 7 H 1 H 2 3 H 4 5 6 1. cell entry 2. cytoplasmic receptor binding 3. migration to nucleus 4. DNA transcription 5. mRNA migration to cytoplasm 6. mRNA translation 7. regulation of receptor number or activity Thyroid: Normal physiology Thyroid hormone: regulation • Increased secretion in response to physiologic stress (cold, illness, etc) • Decreased secretion in response to increased thyroid hormone levels Thyroid: Normal physiology Thyroid hormone: regulation INCREASING THYROID HORMONE STRESS / COLD OR DECREASING THYROID HORMONE TRH = thryroid releasing hormone hypothalamus TRH anterior pituitary TSH Thyroxine thyroid gland Thyroid: Assessment Serum TSH • Elevated in hypothyroidism • Decreased in hyperthyroidism • Most commonly performed screening test Thyroid: Disease Hyperthyroidism Hypothyroidism Thyroid masses: benign / malignant Hyperthyroidism (thyrotoxicosis) Causes: • • • • • • autoimmune (Graves’ disease) multinodular goitre thyroid adenoma subacute thyroiditis ingestion of TH (OD / factitial / food) anterior pituitary disease Hyperthyroidism (thyrotoxicosis) Graves’ disease: autoimmune - stimulatory anti-TSH receptor antibodies resulting in continual stimulation of thyroid hormone production - 7:1 female to male ratio Hyperthyroidism (thyrotoxicosis) Signs and symptoms: - nervousness, irritability, tremour fatigue, heat intolerance, weight loss, rosy complexion - tachycardia, palpitations, atrial fibrillation, angina Hyperthyroidism (thyrotoxicosis) Signs and symptoms: - myxedema…red, raised, puffy areas - dyspnea due to muscle weakness - diarrhea - wide stare, lid lag Hyperthyroidism (thyrotoxicosis) Signs and symptoms: - Graves’ ophthalmopathy: - edema and inflammation of the extraocular muscles - increase in orbital connective tissue and fat - may be persistent and lead to loss of vision Hyperthyroidism (thyrotoxicosis) Treatment: - Medical: propylthiouracil … blocks hormone synthesis in the thyroid and conversion of T4 to T3 in the periphery - B-blocker (propranolol) to control adrenergic symptoms Hyperthyroidism (thyrotoxicosis) Treatment: - Radioiodine ablation - Surgery: thyroidectomy Radio ablation will and surgery might make the patient hypothyroid Thyrotoxic crisis (thyroid storm) Acute hyperthyroid crisis: risk factors • more likely in patients who have long standing or poorly treated disease and in patients with goiter and eye signs • precipitated by trauma, infection or surgery Thyrotoxic crisis (thyroid storm) Acute hyperthyroid crisis: S & S • • • • • extreme restlessness nausea, vomiting, abdominal pain fever, diaphoresis tachycardia, arrythmia pulmonary edema, congestive heart failure • stupor, coma, hypotension … death Thyrotoxic crisis (thyroid storm) Acute hyperthyroid crisis: treatment • • • • • • propylthiouracil (Propyl-Thyracil) potassium iodide (Thyro-Block) propranolol (Inderal) glucorticoids IV glucose, Vitamin B complex wet packs, ice packs, fans Hyperthyroidism (thyrotoxicosis) Dental concerns: - be aware of signs and symptoms - assess compliance with medications - in poorly controlled or newly diagnosed: - avoid epinephrine Hyperthyroidism (thyrotoxicosis) Dental concerns: - refer to MD if concerns exist - prevent and manage infection - be alert to S&S of thyroid storm - treat as normal if well controlled Hypothyroidism Causes: • • • • • • • congenital agenesis or hypoplastic autoimmune (Hashimoto’s thyroiditis) iodine deficiency with goitre iodine excess post-radio ablation post-surgical ablation anterior pituitary disease Hypothyroidism Signs and symptoms: - Congenital: Neonatal cretinism - Slowing of mental and physical activity, weakness - Cold intolerance - Constipation, weight gain Hypothyroidism Signs and symptoms: - Dry skin, dry and brittle hair - Loss of outer 1/3 of the eybrows - Puffy eyelids - Hoarse voice - Myxedema Hypothyroidism Treatment: - T4 (L-thyroxin, Synthroid) - Titrated until patient has normal TSH Hypothyroid crisis Myxedematous Coma: risk factors - Seen in untreated or non-compliant patients - Precipitated by cold, trauma, surgery, infections and CNS depressants - More common in winter Hypothyroid crisis Myxedematous Coma: S & S - severe myxedema - bradycardia - severe hypotension Hypothyroid crisis Myxedematous Coma: treatment - IV T4 - Steroids - CPR Hypothyroidism Dental Concerns: - be aware of signs and symptoms - assess compliance with medications - in poorly controlled or newly diagnosed: - use CNS depressants (sedatives and narcotics) with caution Hypothyroidism Dental Concerns: - refer to MD if concerns exist - prevent and manage infection - be alert to S&S of myxedematous coma - treat as normal if well controlled Thyroid masses Benign: - goitre due to iodine deficiency enlargement due to Graves’ disease thyroiditis thyroglossal duct cyst benign adenoma Thyroid masses Malignant - follicular carcinoma papillary carcinoma anaplastic carcinoma other carcinomas Thyroid masses Malignant: increased risk for cancer if nodule is found - in patients of a young age - in a male - with a history of radiation exposure - with concommitant dysnea, dysphagia or dysphonia (hoarseness) Thyroid masses Malignant: increased risk for cancer if nodule is found to - be a hard fixed lump - be a single nodule - have demonstrated rapid growth Thyroid masses Assessment: - history - clinical examination - thyroid function tests - thryroid scan - fine needle aspiration biopsy Thyroid cancer Treatment: - radio ablation with 131I * - thyroidectomy +/- neck dissection - external beam radiotherapy for persistent disease * * Does not cause osteoradionecrosis of the jaws Questions????