Endocrine Study Guide PDF

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Summary

This document provides a study guide on hyperthyroidism, covering symptoms, causes, and treatment. It delves into the condition, including Grave's disease as well as additional causes. The text also explains the physiological mechanisms and potential complications of the condition. It's designed to help students and medical professionals learn.

Full Transcript

Hyperthryoid A sustained increased in synthesis and release of thyroid hormones by thyroid gland Occurs more often in women Highest frequency between ages 20 to 40 years Low TSH (Thyroid Stimulating Hormone) Increased T4 and T3 levels (what are normal levels?) Mo...

Hyperthryoid A sustained increased in synthesis and release of thyroid hormones by thyroid gland Occurs more often in women Highest frequency between ages 20 to 40 years Low TSH (Thyroid Stimulating Hormone) Increased T4 and T3 levels (what are normal levels?) Most common forms is Grave’s Disease Other causes: Toxic nodular goiter, thyroiditis, excess iodine intake, pituitary tumors, thyroid cancer Hyperthyroidism Symptoms High/Fast Metabolism Increased HR and RR Increased appetite Increased thirst Tremors Nervous feeling Restless Weight loss Goiter (palpate large mass and may hear a bruit) Ophthalmopathy/exophthalmos Hyperthyroidism: Grave’s Disease Autoimmune disease Thyroid enlargement Increased Thyroid Hormone Secretion Develop antibodies to TSH receptors. Antibodies attach to the receptors stimulating the thyroid to release T3 and T4 Has periods of remission May eventually lead to hypothyroidism from the destruction of thyroid tissue Thyroid Storm Life threatening emergency Caused by stressors (infection, trauma, surgery… especially during thyroidectomy when hormones are released). Heart and nerve tissues become more sensitive to sympathetic nervous system activation Signs are severe tachycardia, heart failure, shock, hyperthermia, seizures, etc. Treatment aimed at reducing the amount of hormone circulating. Reduce or treat cause Hyperthyroidism Treatment Drug Therapy: Antithyroid drugs (PTU, Tapazole)-reduces hormone synthesis Iodine: inhibits release of T3/T4 B-adrenergic blockers: offset symptoms by blocking SNS Radioactive Iodine: Destroys thyroid tissue Surgery: Thyroidectomy: Partial or complete removal. Can result in hypothyroidism Hyperthyroid: Acute Care Thyroid Storm Post Surgical Assessment for Thyroidectomy Necessitates aggressive treatment Monitor for complications: Hypothyroidism, Give medications that block thyroid hormone hypocalcemia, hemorrhage, laryngeal production and SNS nerve damage, thyrotoxicosis, infection Monitor for dysrhythmias Post-op care: maintain patent airway, Ensure adequate oxygenation oxygen, suction and trach tray at bedside, Fluid and electrolyte replacement monitor for laryngeal stridor, iv calcium readily available Hypothyroidism Not enough circulating hormone Causes: Primary: destruction to thyroid tissue or Atrophy of thyroid gland defective hormone synthesis Iodine deficiency (not common in US) Secondary: R/T pituitary disease with a Surgical removal decrease in TSH secretion Drugs (lithium blocks hormone production) Hypothyroidism: Clinical Manifestations Signs of a decreased metabolism Low exercise intolerance d/t decreased Fatigue cardiac output and contractility Constipation SOB Weight gain Slow speech Depressed Confusion Anemia Hashimoto's Thyroiditis Autoimmune disorder in which your immune Risk Factors system creates antibodies that damage your 1. Sex- Women are much more likely thyroid gland 2. Age- More commonly occurs during middle Leads to underactive thyroid age 3. Heredity 4. Other autoimmune disease 5. Radiation exposure Hypothyroidism Complications: Myxedema Myxedema: Accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues Myxedema Coma: Impaired consciousness or coma, caused by drugs, trauma, infection etc. S/S: Hypotension (Decrease in cardiac output), subnormal temps, hypoventilation Treatment: Supportive care and IV thyroid replacement Hypothyroidism: Diagnostics TSH: High if thyroid is impaired… not responding to it! TSH: Low if pituitary or hypothalamus is impaired… Can’t make it! Free T4: Low… because its not being told to produce either way TPO (THYROPEROXIDASE): Test for Hashimotos Hypothyroidism: Treatment Thyroid Replacement With Synthroid Start with low dose Monitor for chest pain (Increased Myocardial O2 demand and/or Dysrhythmias), weight loss, nervousness, tremors, insomnia Increase dose in 4- to 6 week intervals as needed based on TSH levels Lifelong therapy Contact MD asap if they feel their heart bounding or any other cardiac signs Hypoparathyroidism Chvostek’s Sign: Hand flexes with BP Cuff inflation Trousseau’s Sign: Face twitches/spasms when tapping facial nerve Hypoparathyroidism/Secondary Thyroidectomy PTH maintains normal levels of Ca+ Causes: Accidental removal from a thyroidectomy, atrophy of gland, or severe hypomagnesemia Secondary Post Thyroidectomy Can cause hypocalcemia- leads to tetany, tingling in lips and extremities, tonic spasms of smooth and skeletal muscle, and dysphagia Nursing: Check for Chvotek’s sign or Trousseau’s sign, give IV calcium gluconate, monitor ECG Corticosteroids High= Cushing’s Low= Addison’s Cushing’s Syndrome Excess of Corticosteroids Causes 1. Administration of Prednisone 2. Adrenocorticotropic Hormone (ACTH)- secreting pituitary tumor 3. Adrenal tumors 4. Ectopic ACTH tumors (Lungs or Pancreas) Cushing’s Syndrome vs. Disease Cushing’s Syndrome refers to the general state characterized by excessive levels of cortisol in the blood Cushing’s syndrome is much more common than Cushing’s disease Cushing’s disease is used exclusively to describe the condition of excessive cortisol arising from a pituitary tumor secreting the hormone ACTH Cushing’s Syndrome- Manifestations Weight gain (accumulation of adipose tissue esp. In the truck, face, and cervical, spine) Hyperglycemia (glucose intolerance d/t cortisol-induced insulin resistance) Protein wasting-muscle weakness, osteoporosis, pathological fracture Loss of collagen: weaker skin, easily bruised, delayed wound healing. Neuro: mood disturbance, insomnia, etc. HTN: (secondary to fluid) Several more…. Cushing’s Syndrome Diagnostics Plasma Cortisol Increased 24 hour urine: cortisol levels> 100 mcg/24 hr Cushing’s Syndrome: Treatment Treatment depends on the cause! Prolonged use of corticosteroids? Gradually discontinue therapy (TAPER) Decrease dose Convert to an alternate-day dosing Tumor? Surgical removal or irradiation Excess Hormone Synthesis? Medicine to suppress synthesis Cushing’s Syndrome Acute Care Assess for drug toxicity Respiratory: issues with weight and fluid retention Neuro: mental changes Cardiac: From fluid retention, electrolytes, etc. Blood sugars Fractures, skin issues Emotional support Addison’s Disease All three of the adrenal corticosteroids are reduced (glucocorticoids, mineralocorticoids, and androgens) Causes: Autoimmune response, co-occurring endocrine conditions, tuberculosis, infections, AIDS, genetics, cancer Manifestations Progressive weakness Fatigue Weight loss Anorexia HYPERPIGMENTATION Orthostatic hypotension Low Na+, salt craving High K+ Addison’s Disease- Complications ADDISONIAN CRISIS Caused By: Stress Infection Trauma Sudden withdrawal of steroid treatment (needs to be tapered!!) After adrenal surgery, following sudden pituitary gland Signs: Hypotension, tachycardia, electrolyte issues, shock, fever, vomiting, pain in abdomen etc. Nursing Care VS EKG Monitoring (Various electrolyte abnormalities & arrhythmias) Fluid volume deficit Electrolyte replacement Daily weights Hydrocortisone Florinef (mineralocorticoid replacement… salt needs to be added to diet) NS and 5% dextrose for hypotension Daily labs or more frequently focusing on electrolytes ADH= Antidiuretic Hormone High= SIADH Low= DI SIADH: Syndrome of Inappropriate Antidiuretic Hormone Abnormal or sustained secretion of ADH ADH= Antidiuretic hormone Produced by the hypothalamus Stored in the pituitary ADH helps regulate fluid volume by promoting reabsorption of water in the renal tubules. Also called vasopressin (Potent vasoconstrictor) Patho of SIADH 1. Increase in ADH 2. This causes the increase in permeability of the renal (kidneys) distal tubules. 3. With this increased permeability, there is reabsorption of water. 4. This causes an increase in intravascular fluid (water in the body). 5. Plasma osmolality declines (blood is watered down from the excess volume the body is holding into) 6. GFR increases 7. Sodium levels decline (because the body has so much water it becomes diluted) Causes of SIADH Malignant tumors (small cell)... because these tumors produce ADH Some drugs Head injuries, brain tumors, etc. SIADH-Presentation Hyponatremia (Low Na+): Cramping, pain, and weakness, progresses to vomiting, muscle twitching, cerebral edema (leading to seizures, confusion, headache, lethargy, and coma. Thirst Low urine output (because the body is holding onto fluid) Weight gain (from the fluid) No edema.. Because this is NOT a third spacing issue, its a fluid retention issue Hyponatremia > 125 Asymptomatic 120-125 N/V, malaise 120-110 muscle cramps, weak, confusion, agitation, Delirium, lethargy, seizures

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