Adrenal Gland Hormones PDF

## Adrenal Gland Hormones **What are the four zones of the adrenal gland and what types of hormones do each section release?** - Zona glomerulosa → mineralocorticoids - Zona fasciculata → glucocorticoids - Zona reticularis → androgens - Zona medulla → catecholamines **T/F: in cows the zona fascic...

## Adrenal Gland Hormones **What are the four zones of the adrenal gland and what types of hormones do each section release?** - Zona glomerulosa → mineralocorticoids - Zona fasciculata → glucocorticoids - Zona reticularis → androgens - Zona medulla → catecholamines **T/F: in cows the zona fasciculata is divided into two regions** True - inner and outer regions **What type of hormone is cortisol?** Glucocorticoid **What type of hormone is aldosterone?** Mineralocorticoid **What are examples of catecholamines?** - Epinephrine - Norepinephrine **What are androgens?** Sex hormones **Draw out and describe the hypothalamus-pituitary-adrenal axis** The brain detects stress in the environment, inducing a response in the HPA. This begins in the hypothalamus. The hypothalamus releases corticotropin releasing hormone (CRH) to stimulate the anterior pituitary. The pituitary releases adrenocorticotropic hormone (ACTH) to stimulate the adrenal cortex. The adrenal cortex releases cortisol for the stress response. Cortisol is a negative feedback to the pituitary and the hypothalamus to stop the production of ACTH and CRH respectively. **How are mineralocorticoids stimulated?** - Mainly by kidneys, but also by the hypothalamus and pituitary. **How are glucocorticoids stimulated?** - Hypothalamus and pituitary **How are catecholamines stimulated?** - Sympathetic nervous system **Hormones produced by the adrenal cortex are derived by what?** Cholesterol **What are the steps that cholesterol needs to undergo in order to become our steroid hormones?** Cholesterol → pregnenolone → aldosterone/cortisol **What is the role of mineralocorticoids and where/what do they act on?** Mineralocorticoids influence salt and water balance. They act on the distal tubules of the kidney by actively reabsorbing sodium ($Na^+$), actively secreting potassium ($K^+$), secreting protons ($H^+$), and passively reabsorbing water. **You will see aldosterone linked with what response/system?** Renin-angiotensin-aldosterone system (RAAS) **Aldosterone that is bound is either: bioactive or not bioactive?** Not bioactive **What is the half-life of aldosterone?** 20 minutes **T/F: aldosterone has a strong binding with plasma transport proteins** False, it weakly binds to plasma transport proteins **What are the type of receptors that accept aldosterone?** - Cytoplasm and nuclear receptors **What affect would we generally see with a patient on spironolactone?** Spironolactone is a diuretic that is also a potassium-sparing diuretic. This means it inhibits the transcription of new $K^+$ secretion and $Na^+$ absorption. **What are glucocorticoids involved in?** Metabolic (carbohydrate) and immunologic (anti-inflammatory) responses ## Cortisol **What is the most important glucocorticoid?** Cortisol **T/F: cortisol naturally fluctuates throughout the day, with higher concentrations in the morning than the afternoon/evening** True **What parts of the brain regulate cortisol and what is it in response to?** Cortisol is regulated by the HPA axis. The HPA axis is stimulated by low blood glucose and other stressors (physical and physiological). **What can influence that axis?** - Glucocorticoids - Stress - Diurnal rhythm **What can we expect to see on carbohydrate metabolism influenced by cortisol?** - Increased gluconeogenesis - Decreased glucose use by cells - Antagonize insulin **What about protein metabolism?** - Increased catabolism of proteins - Mobilization of amino acids from muscles **Fat metabolism?** - Decreased peripheral fat while increasing abdominal fat - Increased lipolysis - Shift of metabolism from glucose to fat **What are the affects of cortisol on the immune system?** - Suppressant: - Decrease pro-inflammatory factors - Increase anti-inflammatory factors (inhibits inflammation) - Inhibits secondary functions (growth/reproduction) **What is cortisol bound to within the blood?** - Transcortin and albumin **What is the half-life of cortisol?** 66 minutes **Where is cortisol metabolized and how is it secreted?** - It is metabolized by the liver and secreted in the urine. **How are androgens produced from cholesterol?** Cholesterol → pregnenolone → DHEA → androgen **What do androgens act on?** - Testis/ovaries to produce testosterone and estrogen **What cells secretes catecholamines?** - Chromaffin cells/neuroendocrine cells **Highlight how they are stimulated:** An action potential comes down the sympathetic neuron and releases acetylcholine. Acetylcholine binds to nicotinic receptors on chromaffin cells. This increases intracellular $Ca^2+$ concentration. The increase releases epinephrine, norepinephrine, and dopamine. **Which is the primary, secondary, and minimal secreted between epinephrine, norepinephrine, and dopamine?** - Epinephrine - primary - Norepinephrine – secondary - Dopamine – trace amounts **T/F: catecholamines only have long-term stress response** False. Catecholamines have short-term stress responses, while mineralocorticoids and glucocorticoids have longer-term effects. **List the six temporary solutions/short term stress responses from the adrenal medulla** - Increased HR - Increased BP - Glycogenolysis/increase BG - Dilate bronchioles - Decrease digestive activity - Reduce urine output - Increase metabolic rate **What type of response is this?** Fight or flight/parasympathetic **List the five prolonged stress responses from the HPA axis** - Retention of $Na$ and $H_2O$ by kidneys - Increased blood volume and BP - Gluconeogenesis proteins and fats - Increased BG - Suppression of immune system/responses **How are the catecholamines synthesized?** Tyrosine converts to DOPA (dopamine), epinephrine, and norepinephrine. **What is the physiological effect of the flight or fight response?** The flight or fight response increases energy availability and overall metabolism. **What are the types of adrenergic receptors and what do they do?** - Alpha 1 - smooth muscle contraction, mydriasis - Alpha 2 - mixed smooth muscle effects - Beta 1 - increase cardiac chronotropic and intropic effects - Beta 2 - bronchodilation **What are the half-lives of epinephrine and norepinephrine?** - Epinephrine: < 2 min - Norepinephrine: ~ 2 min **What are the common disorders of the adrenal gland (common and scientific names)?** - Cushing's (hyperadrenocorticism) - Conn's (hyperaldosteronism) - Pheochromocytoma - Addison's (hypoadrenocorticism). **How many types of hyperadrenocorticism are there?** Two, primary and secondary **Which is the most common?** Secondary **Where is the primary hyperadrenocorticism located? The secondary?** - Primary: adrenal gland - Secondary: pituitary gland **Explain the cause and mechanism of Cushing's disease** Cushing's disease is caused by a tumor on the pituitary gland. The tumor secretes ACTH, stimulating overproduction of cortisol. **T/F: Cushing's is extremely common in diabetic cats** False - it is common in dogs, rare in cats **Describe the mechanism behind Addison's disease** Addison's, also known as hypoadrenocorticism, occurs when there is dysfunction of the adrenal gland or pituitary gland. This leads to a decrease in the production of glucocorticoids and mineralocorticoids. The problem can be located to either the adrenal gland or the pituitary, and will present with either increased (adrenal) or decreased (pituitary) endogenous plasma ACTH. **Conn's** is an adrenal gland disease that is a result of excess aldosterone production. The adrenal gland produces a large amount of aldosterone because it is resistant to normal negative feedback and has a reduced response to exogenous ACTH. **Which of those types described above is primary and which is secondary?** - Primary = adrenal - Secondary = pituitary **What type of patient do you normally expect to see with Addison's?** Young to middle aged dogs, and occasionally horses. **You have a hyperaldosteronism patient coming in. What will the species most likely be?** Cat **What is a classic physical sign?** Arched neck **List the three electrolyte changes of a patient with Conn's syndrome** - Hypokalemia (inc K+) - Hypernatremia (inc Na+) - Metabolic alkalosis **T/F: Conn’s Syndrome is extremely rare** True **What is pheochromocytoma?** A neoplasm of adrenal medullary chromaffin cells that secretes catecholamines. This is also known as a catecholamine-secreting tumor. **List the signs that can be seen in these patients:** - Hypertension - Collapse - Tachypnea - Arrhythmia **T/F: sings can be absent or sporadic** True ## Thyroid Gland Hormones **What makes up the thyroid and what do they synthesize?** - Thyroid follicles: thyroid hormone - Parafollicular cells: calcitonin **What are the follicles filled with and describe it.** Colloid, fluid rich in thyroglobulin and a storage of thyroid hormones and components **Highlight how thyroid hormones are synthesized** Iodide from the diet is actively taken up and oxidized to iodine. Iodination of tyrosine on thyroglobulin then occurs, leading to the catalysis of MIT and DIT. **How is iodide getting into the cells?** Na+/I- cotransporter (secondary active transport) **What are the thyroid hormones and what are they composed of?** - **T3 (triiodothyronine):** 1 DIT and 1 MIT, 3 iodine molecules - **T4 (thyroxine):** 1 DIT and 1 DIT, 4 iodine molecules **What is the major source of T3?** Peripheral deiodination of T4 (free T4) **T/F: thyroid hormones remain attached to thyroglobulin molecule and stored in the colloid until secretion** True **How are the thyroid hormones secreted out of the follicular cells?** Thyroglobulin is digested by hydrolytic enzymes and free thyroid hormones diffuse out of the epithelial cells. **How are the thyroid hormones transported throughout the body?** The thyroid hormones are transported in plasma attached to proteins, such as TBG and albumin. A small amount of hormones freely circulate. **How are the thyroid hormones regulated?** This is controlled by Hypothalamus pituitary thyroid axis. The hypothalamus produces TRH, which stimulates the pituitary gland to produce TSH. TSH then stimulates the thyroid gland to produce T3 and T4. **What is the role of deiodinase?** Deiodinase converts T4 to T3 in peripheral tissues. **T/F: cats produce both T3 and T4 in their thyroid** False. Cats lack D1 in their thyroid, so they just produce T4 in the thyroid. T3 is produced peripherally. **What type of actions do you expect from thyroid hormones?** Thyroid hormones control metabolism, bind to nuclear receptors and initiate transcription of mRNA. They increase the basal metabolic rate of cells, stimulate carbohydrate metabolism and fat metabolism, aid in growth and development of the nervous system and long bones, increase blood flow and cardiac output, increase HR, and increase GI motility and appetite/food intake. **Define basal metabolic rate** The minimal energy expenditure per unit time at rest **Do we expect to see an increase or decrease in BMR when carbohydrate metabolism and fat metabolism are stimulated?** Increase in BMR **Will we see vasodilation or vasoconstriction with an increased blood flow and cardiac output?** Vasodilation **T/F: sometime hyperthyroid animals will have diarrhea due to thyroid hormones effects on GI motility.** True **Is hyperthyroidism an increase or decrease in thyroid stimulating hormones?** Decrease **What are the types of hypothyroidism and define them.** - **Primary:** thyroid gland dysfunction - **Secondary:** pituitary gland dysfunction **Congenital:** thyroid gland hyperplasia reported in foals as a result of flares not having enough iodide in their diet during pregnancy. **Hyperthyroidism:** increased or decreased thyroid hormones? Increased **Is this disorder mostly seen in dogs or cats?** This is a more common feline endocrine disorder, rare in dogs. **A patient is hyperthyroid, what do you expect to see in the body weight and metabolism?** Increased metabolism and decreased body weight **What type of heart rate do you expect to see with a hyper vs hypothyroid animal?** Increased **What are two clinical signs of hypothyroidism in dogs?** - Lethargy - Weight Gain **List three causes of hypothyroidism in dogs** - Primary: destruction of the thyroid gland - Lymphocytic thyroiditis (autoimmune disease) - Idiopathic atrophy **What happens to the thyroid follicles in lymphocytic inflammation?** Collapse and replaced with fibrotic or connective tissue **What happens to the thyroid follicles in idiopathic atrophy?** Collapse and replace with adipose or fatty tissue **You have a dog come in that you are suspecting of being hypothyroid. What type of tests do you run, and how would you treat him?** You would run a test for total T4/free T4. The treatment for hypothyroidism is thyroxine, which is given daily for the rest of the patient's life. **What are some clinical signs in a patient with hyperthyroidism?** - Weight loss - Increased HR - Tremors - Vomiting - Weakness - Eating/drinking excessively **What is the most common etiology?** Thyroid adenoidal or benign adenomatous hyperplasia. **What are some treatment options for these animals?** - Medication - Surgical ablation - Radioactive iodine ablation