Alterations of Endocrine Function II Study Guide Questions PDF

**Alterations of Endocrine Function II -- Study Guide Questions** *[Instructions]: Use these questions to guide your learning and studying for the exam. You will [not] submit these study questions to be graded. Try to answer these questions without looking at your notes, then use your notes to corr...

**Alterations of Endocrine Function II -- Study Guide Questions** *[Instructions]: Use these questions to guide your learning and studying for the exam. You will [not] submit these study questions to be graded. Try to answer these questions without looking at your notes, then use your notes to correct and/or expand on your responses. Note -- we will not be posting 'answers' to these questions since the information is straight from your Class Notes and the lectures or online modules. You can post questions on the discussion board, email the TAs, or verify your responses during review sessions.* **Diseases of the Thyroid Gland** 1. What are the major causes of hyperthyroidism? Indicate whether the cause is primary or secondary and describe how they result in elevated T3/T4. a. Primary -- thyroid gland secretes more T3/T4 decreased TRH & TSH i. Genetic predisposition ii. Thyroiditis iii. Toxic nodular or multinodular goiter iv. Thyroid adenoma b. Secondary -- anterior pituitary gland secretes more TSH increased T3/T4 (no negative feedback) v. TSH-secreting pituitary adenomas 2. Compare and contrast the laboratory findings (i.e., T3/T4 and TSH) you would see with primary and secondary hyperthyroidism, as well as Graves' disease. Provide an explanation of the findings. c. Primary Hyperthyroidism -- A black arrow pointing to a black line Description automatically generated d. Secondary Hyperthyroidism -  e. Graves' Disease - A black text on a white background Description automatically generated 3. Describe the unique pathophysiology that causes hyperthyroidism in Graves' disease? f. Overproduction of thyroid autoantibodies called thyroid stimulating immunoglobulin (TSI) stimulate excess T3/T4 secretion TSH suppression g. Autoimmune disease and results from a form of type II hypersensitivity stimulation of the thyroid by autoantibodies directed against the TSH receptor. TSI stimulation of TSH receptors hyperplasia of the gland (goiter) and increased synthesis of T3/T4 TSH production by the pituitary is inhibited through the usual negative feedback loop 4. What unique clinical manifestations are seen in Graves' disease that do not occur with other types of hyperthyroidism? Why do these problems manifest? h. Goiter due to increased TSI effects on gland and accumulation of TSI in thyroid gland tissue i. Effects of thyroid stimulating immunoglobulins on ocular tissue -- degeneration of extraocular muscles and edematous fluid accumulation in orbit j. Exophthalmos - Orbital connective tissue accumulation, inflammation, and edema of the orbital contents k. Extraocular muscle dysfunction - infiltrative changes involving the orbital contents with enlargement of the ocular muscles; extraocular muscle weakness leading to diplopia (double vision) l. Retinal and optic nerve damage -- due to edema m. Tibial myxedmea -- characterized by subcutaneous swelling on the anterior portions of the legs and by indurated and erythematous skin 5. What are the major causes of hypothyroidism? Indicate whether the cause is primary or secondary and describe how they result in decreased T3/T4. n. Primary -- decreased T3/T4 production by thyroid gland (d/t loss of tissue) increased TSH vi. Iodine deficiency -- most common world-wide vii. Congenital lack of thyroid tissue viii. Hashimoto's thyroiditis: Autoimmune destruction of thyroid (most common in US) o. Secondary -- decreased TSH secretion from anterior pituitary gland decreased T3/T4 (failure of pituitary to secrete enough TSH) ix. Stroke to hypothalamus or pituitary x. Pituitary tumor (benign or cancerous) xi. Postpartum pituitary necrosis 6. Compare and contrast the laboratory findings (i.e., T3/T4 and TSH) you would see with primary and secondary hypothyroidism. Provide an explanation of the findings. p. Primary q. Secondary 7. What is myxedema? What symptoms of hypothyroidism are directly related to myxedema? r. Myxedema: collagen in connective tissues is replace by other proteins and muco-polysaccharides creating a complex that binds to water. s. Nonpitting, boggy edema, especially around the eyes, hands, and feet and in the supraclavicular fossae. The tongue and laryngeal and pharyngeal mucous membranes thicken, producing thick, slurred speech and hoarseness t. Coma - a diminished level of consciousness associated with severe hypothyroidism. xii. S/S: hypothermia without shivering, hypoventilation, hypotension, hypoglycemia, and lactic acidosis 8. Provide a brief explanation of the following manifestations of hyper- and hypothyroidism. +-----------------------+-----------------------+-----------------------+ | **Structure/System** | **Hyperthyroidism** | **Hypothyroidism** | +=======================+=======================+=======================+ | *Metabolic rate* | Heat | Cold | | | intolerance/weight | intolerance/weight | | | loss Hyperdynamic | gain Decreased | | | circulatory state and | metabolic demands and | | | increased catabolism | loss of regulatory | | | leads to the body\'s | and rate-setting | | | inability to meet its | effects of TH | | | metabolic needs | | +-----------------------+-----------------------+-----------------------+ | *Cardiovascular* | Hypertension dilates | Hypotension Decreased | | | resistance | metabolic demands and | | | arterioles, which | loss of regulatory | | | reduces systemic | and rate-setting | | | vascular resistance | effects of TH | | | increases cardiac | | | | output elevate | "increased peripheral | | | systolic blood | vascular resistance | | | pressure | to maintain systolic | | | | blood pressure can | | | "Increased cardiac | cause hypertension" | | | output and decreased | | | | peripheral | | | | resistance" | | +-----------------------+-----------------------+-----------------------+ | *Nervous system* | Hyperactive reflexes | Hypoactive reflexes | | | increased sensitivity | decreased metabolic | | | of nerve cells and | rate, which slows | | | muscle fibers | down nerve signal | | | | transmission, | | | | impacting the | | | | communication between | | | | nerves and muscles, | | | | resulting in weakened | | | | reflexes and muscle | | | | weakness | +-----------------------+-----------------------+-----------------------+ 9. Of the causes of hyperthyroidism listed in Question 1, which could result in the development of a goiter? Why? u. Grave's dz TSI stimulation of TSH receptors in the gland results in hyperplasia of the gland (goiter) **Diseases of the Adrenal Cortex** 10. What are the major causes of hypercortisolism? Indicate whether the cause is primary or secondary and describe how they result in elevated cortisol. v. Primary -- excess levels of cortisol due to hyperfunction of adrenal cortex or ectopic cortisol production xiii. Adrenal adenomas or carcinomas that secrete cortisol xiv. Non-adrenal tumors that secrete cortisol xv. Administration of cortisol-like medications w. Secondary Hypercortisolism -- excessive secretion of ACTH leads to increased cortisol secretion xvi. Pituitary adenomas with hypersecretion of ACTH xvii. Non-pituitary tumor synthesizes and secretes excessive amounts of ACTH 11. Compare and contrast the laboratory findings (i.e., cortisol and ACTH) you would see with primary and secondary hypercortisolism. Provide an explanation of the findings. x. Primary hypercortisolism --  y. Secondary hypercortisolism -- 12. You are seeing, for the first time, a 76-year-old patient with severe, chronic asthma who has been on prednisone for over 10 years. What would you expect the patient's physical appearance to be like? Explain why **excess cortisol** results in each clinical manifestation. z. Truncal obesity, moon face, buffalo hump a. Protein wasting is caused by the catabolic effects of cortisol thin extremities b. Cortisol has a specific tendency to encourage fat storage in the visceral (abdominal) cortisol binds to receptors in fat cells adipogenesis c. Moon fact fat redistribution and fluid retention 13. Explain why the following clinical findings are present in individuals with hypercortisolism. d. Hyperglycemia -- Glucose intolerance occurs because of cortisol-induced insulin resistance and increased gluconeogenesis and glycogen storage by the liver. e. Hypertension -- vascular sensitivity to catecholamines increases significantly, leading to vasoconstriction and hypertension f. increased risk for infection and sepsis -- cortisol acts as a potent immunosuppressant, directly inhibiting the function and development of immune cells, particularly lymphocytes, by downregulating key inflammatory pathways and reducing the production of important cytokines needed for immune responses; this leads to a weakened immune system 14. What are the major causes of hypocortisolism? Indicate whether the cause is primary or secondary and describe how they result in elevated cortisol. g. Primary (aka Addison Dz) -- Atrophy or destruction of adrenal cortex leads to decreased cortisol and aldosterone secretion xviii. Autoimmune destruction of adrenal cortex xix. Familial adrenal (glucocorticoid) insufficiency (autosomal recessive disease-causing mutations in the ACTH receptors or other factors affecting ACTH signaling) xx. Tuberculosis -- inflammatory response to the adrenals decreased cortisol production h. Secondary -- Decreased ACTH secretion leads to decreased cortisol secretion xxi. Anterior pituitary hypofunction (tumor, stroke\...) xxii. Special Case: Suppression of ACTH by exogenous glucocorticoids can lead to hypocortisolism when medications are discontinued abruptly 15. Explain why the following clinical findings are present in individuals with hypocortisolism. i. Hypoglycemia -- cortisol plays a crucial role in regulating glucose production in the liver, and without sufficient cortisol, the body cannot adequately produce glucose, resulting in low blood sugar levels j. Hypotension -- cortisol plays a crucial role in maintaining vascular tone by enhancing the body\'s response to other hormones like norepinephrine and angiotensin II; without sufficient cortisol, blood vessels become less responsive, causing blood pressure to drop k. bronze discoloration of the skin -- it triggers an increase in the production of adrenocorticotropic hormone (ACTH), which in turn stimulates melanocytes to produce more melanin, the pigment responsible for skin color, causing darkened patches on the skin l. fluid & electrolyte imbalances -- cortisol plays a crucial role in regulating sodium reabsorption in the kidneys, meaning when cortisol is deficient, the body loses excessive sodium in urine, causing dehydration and disrupting the balance of electrolytes like sodium and potassium 16. Compare and contrast the laboratory findings (i.e., cortisol and ACTH) you would see with primary and secondary hypocortisolism. Provide an explanation of the findings. m. Primary Hypocortisolism  n. Secondary Hypocortisolism A black arrow pointing to a red dot Description automatically generated