Thyroid Gland PDF

**Thyroid Gland ** - Located in the anterior portion of the neck in front of the trachea (butterfly shaped)  - It consists of 2 encapsulated lobes connected by a narrow isthmus  - Highly vascular (for hormone distribution) and is regulated by thyroid stimulating hormone (TSH) which...

**Thyroid Gland ** - Located in the anterior portion of the neck in front of the trachea (butterfly shaped)  - It consists of 2 encapsulated lobes connected by a narrow isthmus  - Highly vascular (for hormone distribution) and is regulated by thyroid stimulating hormone (TSH) which is secreted by the anterior pituitary gland - Hormones produced from the thyroid gland:  - Triiodothyronine (T3) - more potent + influence metabolism  - Thyroxine (T4) - more abundant but needs to be converted to T3 to have metabolic affect  - Calcitonin\* - regulates calcium levels \[not as important\]  ***Triiodothyronine (T3) & Thyroxine (T4) *** - The major function of the thyroid gland is the production, storage and release of T4 and T3  - T4 = most abundant thyroid hormone, and accounts for more than 90% of the hormone produced by the thyroid gland  - T4 = largely inactive and is converted into the more active T3 → happens in kidneys + liver  - T3 = most powerful - most potent of thyroid hormones  - Iodine is necessary for the thyroid gland to synthesize thyroid hormones  ***Effects of T3 & T4 on the body *** - Metabolic rate  - Caloric requirements  - Oxygen consumption → enough to function properly  - Carbohydrate & lipid metabolism → blood sugar levels + fat storage  - Growth & development → critical in children  - Brain function → cognitive ability + neurological health  - Nervous system activity ***TRH→ TSH→ T4/T3 thyroid hormones*** - Regulated by negative feedback loop  - Once reaching certain level T3/T4 will inhibit release of TRH + TSH  **[Hyperthyroidism ]** - Hyperthyroidism is a sustained increase in the synthesis and release of thyroid hormones by the thyroid gland  - Most common cause is Graves' disease  - Other causes include toxic nodule goiter, thyroiditis, pituitary tumors, thyroid cancer  ***Toxic Nodular Goiter*** ***- Plummer's Disease *** - Characterized by nodules that secrete thyroid hormones  - Term toxic refers to overproduction of thyroid hormones, leading to hyperthyroidism  - Causes: environmental, genetic, or chronic iodine deficiency (Get more nodules bc trying to capture more iodine from bloodstream → thyroid or more over production) ***Thyrotoxicosis *** - Thyrotoxicosis is the clinical state that results from inc levels of T3, T4 or both  - Can be acute or sustained increase  - Hyperthyroidism & thyrotoxicosis usually occur together  - Thyrotoxicosis manifestations may include:  - anxiety  - tachycardia; arrhythmias  - Weight loss; increased appetite  - Heat intolerance; excessive sweating  - Tremors  - Symptoms can vary in severity and duration  - Manifestations will depend on underlying cause  ***Graves' Disease *** - Autoimmune disease of unknown cause where the thyroid gland is enlarged, and thyroid hormones (T3/T4) are secreted and released in increased amounts  - Accounts for 90% of cases of hyperthyroidism  - Graves' disease is characterized by remissions and exacerbations, even when treated - Graves' disease (overstimulation of thyroid) may lead to destruction of the thyroid tissue → can cause ***hypo***thyroidism  ***Graves' Disease: Pathophysiology *** 1. TSIs that mimic TSH develop  2. TSIs attach to the TSH receptors of the thyroid (TSIs gain control of the pathway) 3. TSIs stimulate the thyroid to release T3/T4  4. Thyrotoxicosis (excess of thyroid hormones)  5. Thyroid enlargement  - Unlike TSH, which is regulated by negative feedback, TSIs continuously stimulate the thyroid gland  - \*TSI = Thyroid-Stimulating Immunoglobulins which are abnormal antibodies  ***Graves' Disease: Clinical Manifestations *** - Nervousness , shaking increased nervousness, irritability  - Increased sensitivity of nervous system - Tremors (especially in hands)  - Tachycardia, palpitations  - Feeling hot  - Weight loss  - Fatigue, feeling exhausted  - Increased metabolic activity  - More frequent bowel movements  - Increased GI activity  - Shorter or lighter menstrual periods  - Affect balance of reproductive hormones  - Goiter - bulge in neck where thyroid is  - Exophthalmos - bulging eyes  - Pretibial myxedema - lumpy rash on shins  - Specific to Graves' disease  ***Ophthalmopathy *** - Exophthalmos: excessive accumulation of fluid behind the eyes  - The tissue and muscles behind the eyes becomes inflamed and edema occurs, pushing the eyeballs forward away from the orbits  - If eyelids are unable to close, exposed cornea becomes dry and irritated - could lead to corneal abrasions & corneal ulcers  - Usually bilateral, but can be unilateral as well  ***Pretibial myxedema *** - Fluid can also accumulate under the skin (on lower legs) and is termed pretibial myxedema  - It looks like a lumpy rash on the shins  - Can spread to the feet, and if untreated, to other parts of the body  - Incidence is rare  ***Hyperthyroidism complication: Thyrotoxic crisis (aka thyroid storm) *** - Acute rare condition where all of the hyperthyroid manifestations are intensified  - Rapid increase in T3 and T4 secretion  - Heart and nervous system are more sensitive to catecholamines (epinephrine and norepinephrine)  - Cause: stressor such as infection, trauma, surgery in patient with hyperthyroidism  - Thyrotoxic crisis = medical emergency that requires immediate treatment  ***Thyrotoxic crisis manifestations *** **REQUIRE IMMEDIATE TREATMENT ** - Severe tachycardia - exceeds 140 bpm - Heart failure - from inc cardiac workload  - Shock - unable to keep up with cardiac demand  - Hyperthermia (up to 40.7 degrees C) → inc metabolic rate  - Restlessness & agitation  - Seizures  - Abdominal pain, nausea, vomiting, diarrhea - Delirium  - Coma  ***Thyrotoxic crisis: Treatment *** - Decrease the amount of circulating hormones (e.g. antithyroid meds, iodine solutions, beta blockers, corticosteroids)  - Supportive care (to manage hyperthermia, maintain fluid and electrolyte balance, and ensure adequate nutrition) - Management of stressor (i.e. treat the underlying cause)  ***Hyperthyroidism: Evaluation*** - History and physical assessment  - Lab values to look out for  - TSH - decreased  - Negative feedback loop will lower TSH levels but TSI's are unaffected by this so they continue stimulating T3/T4 release + synthesis  - Free T4 - increased  - Will exceed protein binding capacities so free T3/T4 remain unbound + responsible for manifestations  - Free T3 - increased  - Free T3 will inc sooner and to a larger extent than T4 → note: Total T3 and T4 levels include bound hormones. Only free hormone is biologically active  ***24-hour radioactive iodine uptake (RAIU) *** - 24-hour radioactive iodine uptake (RAIU) test can be used to differentiate Graves' disease from other forms of thyroiditis  - Graves' disease: uptake of 35-90%  - Thyroiditis: uptake less than 20%  - Thyroid inflamed + damaged so has reduced ability to take up iodine  - Nodular goiter: high normal range  - Uptake rate is dependent on nodule size  - Normal result is 3-16% at 6 hours and 8-25% at 24 hours ***Pharmacotherapy for Hyperthyroidism*** - Overall goals are to:  - Block the AE of the thyroid hormones  - Stop the over-secretion of thyroid hormones  - Three main treatment options are:  - Antithyroid meds (thionamides)  - Radioactive iodine therapy  - Subtotal thyroidectomy (surgical)  ***Thionamides *** - Inhibit the enzyme thyroid peroxidase (TPO), which is crucial for the synthesis of thyroid hormones  - Used long term or short term (i.e. prior to thyroid surgery)  - Improvement usually within 2 weeks with therapeutic results in 4-8 weeks, and up to 12 weeks to see significant lab result changes  - Therapy continued for 6 mths to 2 yrs  - Drugs are not curative, pt can go into remissions & exacerbations  - AE: agranulocytosis (severely low levels of WBCs) - caused by bone marrow suppression and immune response targeting neutrophils + granulocytes  - fever and sore throat may be early indicators - **Methimazole** - Inhibits TPO  - Preferred for long-term management  - Has less adverse effects  - Lower risk of agranulocytosis and hepatotoxicity than PTU  - Generally avoided in 1st trimester but safer in later trimesters of pregnancy; avoid with lactation  - **Propylthiouracil (PTU)** - Inhibits TPO but also blocks conversion of T4 to T3  - Used in specific situations (i.e. 1st trimester of pregnancy) or acute cases  - Higher risk of agranulocytosis and hepatotoxicity  ***Iodine Therapy *** - Iodine therapy: Can be used in combo with antithyroid drugs  - Not as common  - Rapidly inhibits synthesis of T3 and T4 and blocks their release into circulation  - It also decreases the vascularity of the thyroid gland making surgery safer and easier  - Maximum effect is seen within 1-2 weeks & therapeutic effect lessens  - **Signs of toxicity ** - Swelling of buccal mucosa & other mucous membranes  - Excessive salivation  - N&V  - Skin rxns - Iodine should be stopped if there is toxicity  ***β-Blockers *** - Symptomatic relief of β-adrenergic receptor stimulation (seen in thyrotoxicosis)  - Will lead to reduction of palpitations, tremors, anxiety, heat intolerance & tachycardia - Slows down HR and reduces metabolic activity  - Propranolol is the most common type of β-adrenergic blocker given  - Non-selective; targets β1 + β2 receptors  - Atenolol preferred in pts with asthma  A diagram of a patient\'s flow Description automatically generated ***Radioactive Iodine Therapy (RAI) *** - Treatment of choice for most postpubertal adolescents and young adults  - Delayed response  - Should not be used in pregnancy or lactation  - Avoid in young children  - AE: dryness & irritation of the mouth and throat, high incidence of post-treatment hypothyroidism  ***Subtotal Thyroidectomy*** - Involves removal of whole lobe, isthmus + some of the remaining lobe (about ⅘ grams left behind)  - Indications  - Large goiter compressing the trachea (breathing difficulties or positional dyspnea) - No response to meds  - Thyroid cancer  - Not a candidate for RAI  - Typically treated w meds prior to surgery to achieve euthyroid state (state of having normal thyroid gland function) and to manage symptoms  ***Postoperative management*** - Assess for complications:  - S&S of hypothyroidism  - Hypocalcemia, secondary to damage to parathyroid glands  - Parathyroid glands have active role in calcium level regulation - Hemorrhage  - Damage to laryngeal nerve  - Thyrotoxic crisis  - Movement or removal of thyroid can release large amts of stored thyroid hormones causing a surge  - Infection  ***Nutrition (Hyperthyroidism) *** - May need high calorie diet  - Inc protein allowance  - GI tract may be hyperactive - avoid high fibre (already have diarrhea or go to the bathroom more frequently) - May be more sensitive to effects of caffeine