Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
pharm
Adrenal & thyroid
| Question | Answer |
|---|---|
| adrenal glands are located | on top of each kidney |
| the medulla of the adrenal gland | the inside or 'Middle' releases NE |
| the cortex of the adrenal gland | the outside releases corticosteroids |
| layers of the cortex | zona golmerulosa zona fasciculata zona reticularis |
| zona golmerulosa | outer most later releases mineral-corticoids (ex: aldosterose) |
| zona fasciculata | middle layer releases Glucocorticoids (ex: cortisol, corticosterone, cortisone) to regulate glucose metabolism |
| zona reticularis | inside most layer releases androgens (ex: dehydroepiandrosterone) to stimulate masculinization |
| adrenal medulla releases which hormones? | stress hormones to stimulate sympathetic ANS epi and NE |
| cortisol release is controlled by...? | positive and negative feedback |
| hypothalamus releases what | CRH corticotrophin-releasing hormone |
| CRH stimulates what | stimulates the anterior pituitary gland to produce hormones |
| when stimulated, the anterior pituitary gland releases what | ACTH adrenocorticotrophic hormon |
| ACTH does what | ACTH travels through the blood to stimulate the adrenal glands |
| once stimulated, the adrenal glands secrete... | cortisol mineralocorticoids and Glucocorticoids |
| cortisol = | stress hormone |
| mineralocorticoid effects | K+ secretion and Na+ retention maintains blood pressure |
| Glucocorticoid is | anti-inflammatory |
| Glucocorticoid effects | creates energy substances dampens inflammatory and immune response |
| how do Glucocorticoids create energy substances? | they increase gluconeogenesis, proteolysis, and lipolysis |
| how do Glucocorticoids dampen inflammatory and immune response? | they reduce production of prostaglandins and interleukins and also inhibit T-lymphocytes |
| increased levels of cortisol= | increased risk of infections or disease |
| endogenous cortisol | levels rise to a peak in the morning (6am to 8am) levels decline throughout the day, reaching 0 around midnight |
| endogenous cortisol makeup of anti-inflam. and mineralocorticoid | endogenous cortisol has a 1:1 anti-inflammatory: mineralocorticoid activity |
| glucocorticoid medication routes | topical, systemic, inhaled, nasal |
| mineralocorticoid routes | systemic only - fludrocortisone |
| prototype corticosteroid drugs | Hydrocortisone, methylprednisolone, predisone, dexamethasone, fludrocortisone |
| hydrocortisone clinical pearl | SAME efects (1:1) on endogenous cortisol |
| predisone clinical pearl | inactive prodrug that is converted into its active form, prednisolone, by liver enzymes. |
| when is predisolone preferred? | pts with severe liver disease |
| dexamethasone spectrum of activity | pure glucocorticoid activity useful for severe inflammation/nausea |
| predisone(PO) or methylprednisone (IV) spectrum of activity | high glucocorticoid activity useful for immunological flares |
| hydrocortisone spectrum of activity | equal action of glucocorticoid and mineralocorticoid useful for adrenal insufficency |
| fludrocortisone spectrum of activity | only synthetic mineralocorticoid useful for addison's disease to treat hyperkalemia and hypotension |
| adverse effects of Supraphysiological doses of glucocorticoids short term use | Na retention, water retention, psychosis, mood changes, poor wound healing, insomnia, hyperglycemia, ulcers (GI upset), increased appetite (weight gain) |
| adverse effects of Supraphysiological doses of glucocorticoids long term use | hypertension, hyperlipidemia, weight gain, HPA axis suppression, cataracts, osteoporosis, acne, elevated insulin (fat accumulation) |
| pts receiving Supraphysiological doses of glucocorticoids >2 weeks | CANNOT suddenly stop the dose!!! dose should be tapered down slowly over several days/weeks/months to prevent HPA axis suppression |
| adrenal gland disorders: Cushing Syndrome | Hyperfunction of the adrenal gland Supraphysiological concentrations of glucocorticoids |
| possible causes of Cushing Syndrome: endogenous | endogenous excess production of cortisol -Cushing DISEASE (pituitary adenoma) -ectopic secretion of ACTH by non-pituitary tumor -adrenocortical adenoma or carcinoma |
| possible causes of Cushing Syndrome: iatrogenic | Supraphysiological administration of exogenous glucocorticoids |
| Cushing disease | ONE TYPE of Cushing syndrome |
| CM of Cushing syndrome | increased calcium reabsorption from bone glucose intolerance Truncal obesity Buffalo Hump Bruising Broad purple Striae |
| what does increased calcium reabsorption from bone mean in cushing? | osteoporosis and increased risk of fractures |
| what does glucose intolerance mean in cushing? | hyperglycemia, often seen w diabetes |
| Tx of cushing syndrome (when causes by endogenous)- first line | surgery (resection of tumor), chemo, or radiation |
| Tx of cushing syndrome (when causes by endogenous)- pharacotherapy | -stabilize pts prior to surgery -pts waiting for potential response to chemo or radiation -used if surgery is ineffective |
| Pharmacotherapy option | -drugs to inhibit adrenal hormone synthesis -drugs to destroy adrenocortical cells -drugs that inhibit ACTH secretion -glucocorticoid receptor antagonists |
| drugs to inhibit adrenal hormone synthesis example | ketoconazole they block the pathway |
| drugs to destroy adrenocortical cells example | mitotane kill adrenal gland= cortisol deficiency + need exogenous |
| drugs that inhibit ACTH secretion example | pasireotide |
| glucocorticoid receptor antagonists exmaple | mifepristone cant cause cushing syndrome w receptors blocked |
| adrenal gland disorders- hypofunction of the adrenal gland | can be either primary adrenal insufficiency or secondary adrenal insufficiency |
| primary adrenal insufficiency | Addison's disease primary= target organ w the problem (adrenal gland) |
| Addison's disease | damage to adrenal glands themselves effects both glucocorticoid and mineralocorticoid production |
| secondary adrenal insufficiency | low ACTH cause reduces cortisol effects JUST glucocorticoid production; aldosterone is normal secondary =problem with either hypothalamus or pituitary |
| CMs of adrenal insufficiency | decreased CO, dehydration, weakness/fatigue, hypoglycemia, craving salt, postural dizziness |
| what other CM does women get w adrenal insufficiency | diminished axillary and pubic hair (men do not have these effects bc androgens produced in testes) |
| Adrenal Crisis CM | GI symptoms (N/V and abd pain) hyponatremia hyperkalemia hypotension |
| what other CM is associated with primary adrenal insufficiency (Addisons disease) | Increased melanin level= darkening of skin pigmentation darkens especially in the palmar creases, nail beds, and mucous membranes |
| why does melanin increase with Addison's disease | pituitary produces more ACTH in response to cortisol deficiency |
| Tx of addison's disease | Glucocorticoid + mineralocorticoid replacement |
| Tx Secondary or Tertiary Adrenal Insufficiency | Glucocorticoid Replacement |
| Glucocorticoid replacement | Physiologic Doses (not Supraphysiologic Dose) |
| hydrocortisone | initial dosing schedule: AM and then 8 hours later can be used 2 or 3 times daily |
| hydrocortisone goal | establish lowest effective dose while mimicking the normal diurnal adrenal rhythm |
| what to monitor with hydrocortisone | body weight, postural BP, enegery levels, signs of glucocorticoid excess q6-8 weeks to assess proper replacement |
| indicators of adequate glucocorticoid replacement | disappearance of hyperpigmentation and the resolution of electrolyte abnormalities |
| adrenal crisis is triggered by | triggered by anything that increases adrenal requirements dramatically (stressful situations, surgery, infection, and trauma) |
| what other main thing can cause adrenal crisis? | abrupt withdrawal of chronic glucocorticoid use will cause HPA-axis suppression |
| prevention of Adrenal Crisis | -additional 5-10 mg of hydrocortisone shortly before strenuous activities (exercise). - pts would be told to double dose during severe physical stress. |
| severe physical stress examples | febrile illness or injury |
| prevention of Adrenal Crisis- major trauma | for major trauma, surgery, or critically ill pts, larger doses (up to 10x the usual) may be required |
| what to do when pt is going for surgery in adrenal crisis? | double dose of cortisol to get through the surgery |
| mineralocorticoid Replacement | *only need for primary adrenal deficiency (Addison's)* Fludrocortisone acetate 0.05 to 0.2 mg once per day |
| mineralocorticoid Replacement- Fludrocortisone acetate adverse effects | adverse effects must be monitored closely and include gastric upset, edema, hypertension, hypokalemia, insomnia, excitability, and diabetes mellitus. |
| mineralocorticoid Replacement- Fludrocortisone acetate what else should be monitored? | pt weight, BP, and EKG should be monitored regularly |
| Euthyroid | normal thyroid function |
| TRH | thyrotropin-releasing hormone |
| TSH | thyroid-stimulating hormone also called thyrotropin |
| what does the production of thyroid hormones depend on? | thyroid hormone production depends on presence of iodine and tyrosine |
| makeup of thyroid hormone | iodine and tyrosine |
| T4 | thyroxine (4 atoms of iodine) prohormone ONLY source is secretion from Thyroid |
| what does pro-hormone mean for T4 | its inactive form but gets converted to T3 (active form) |
| T3 | Triiodothyronine (3 atoms of iodine) less than 20% produced in thyroid more potent than T4 more rapid onset but shorter duration of action |
| how is majority of T3 formed | from breakdown of T4 in peripheral tissue |
| when TH is HIGH... | TRH is LOW |
| when TH is LOW... | TRH is HIGH |
| role of thyroid hormone | -affects function of every organ system -critical for normal growth and development in childhood -maintains metabolic stability in adults * affects ALL body systems- look at slide 28* |
| Hyperthyroid | overproduction of thyroid hormone by thyroid gland |
| hyperthyroidism levels | High T3 and T4 |
| if primary hyperthyroidism... | Grave's Disease TSH will be LOW (bc of negative feedback) |
| if secondary hyperthyroidism... | due to pituitary tumor TSH may be high |
| thyrotoxicosis | caused by tissue exposure to excessive levels to T3 and T4 wayyy too much TH...messes up everything |
| thyrotoxicosis symptoms | heat intolerance/sweating, palpitatons, fatigue/weakness, weight loss w inc appetite |
| thyrotoxicosis signs | tachycardia (Afib), tremor of tongue or hands, thyromegaly/goiter |
| Grave's disease CM only | Ophthalmopathy/ exophthalmos bulging EYES |
| Tx of hyperthyroidism | reduce amount of thyroid tissue reduce thyroid hormone synthesis- antithyroid meds reduce symptoms |
| Tx of hyperthyroidism- reduce amount of thyroid tissue | radioactive iodine (taken up by the thyroid and kills it) thyroidectomy (removal of thyroid) |
| Tx of hyperthyroidism- antithyroid meds: ADVANTAGES | non-invasive, low initial cost, low risk of permanent hypothyroidism, possible remission due to immune effects |
| Tx of hyperthyroidism- antithyroid meds: DISADVANTAGES | low cure rate (40-50%), adverse drug rxns, adherence |
| Tx of hyperthyroidism- reduce symptoms | beta blockers |
| antithyroid medication- thionamide class | methimazole (MMI) or Propylthiouracil (PTU) |
| methimazole (MMI) | first line pharmacology once a day dosing long half life |
| Propylthiouracil (PTU) | second line pharmacotherapy use limited by hepatotoxicity requires dosing 3-4 times per day preferring first trimester of pregnancy (less teratogenic) |
| MOA for antithyroid medications | inhibit both the organification of iodine to tyrosine...new formation of TH. PTU also inhibits peripheral conversion of T4 to T3 |
| when do therapeutic effects occur with anti-thyroid meds? | therapeutic effect in 1-2 weeks, but euthyroid state may not occur for 6-8 weeks |
| Antithyroid meds adverse effects | S/S of hypothyroidism benign transiet leukopenia (WBC<4,000) pruritic maculopapular rash arthralgias fever Agranulocytosis |
| Agranulocytosis | serious! discontinue therapy and contact provider for flu-like symptoms (fever/malaise/sore throat) and get labs |
| Beta blockers | used for Beta-adrenergic mediated symptoms |
| Beta-adrenergic mediated symptoms | palpitations, anxiety, tremor, heat intolerance |
| Beta blockers- propanolol | dose: 20-40mg q6-8hrs 240-480mg/day for younger/severely toxic pts atenolol preferred by some for once daily dosing |
| beta blockers contraindications | decompensated HF unless caused solely by tachycardia sinus bradycardia MAOI or TCA therapy spontaneoug hypoglycemia |
| beta blockers side effects | N/V, anxiety, insomnia, light-headedness, bradycardia, hematological disturbances |
| hypothyroidism | elevated TSH and LOW T4 and T3 |
| symptoms of hypothyroidism | dry skin, cold intolerance, weight gain, constipation, weakness |
| signs of hypothyroidism | periorbital puffiness bradycardia speech: slowed and hoarse reversible neuro syndromes goiter |
| why do pts w hypothyroidism get a goiter? | due to overstimulation of TSH |
| Tx of hypothyroidism | replacement of thyroid hormone is cornerstone of treatment |
| hypothyroidism Tx drug of choice | levothyroxine (synthetic T4) |
| levothyroxine half life | approx. 7 days (very long) stable pool of pro-hormone once daily dosing |
| how does food affect levothyroxine administration | food impairs absorption of T4 take 30 minutes before breakfast/other meds |
| when is levothyroxine administered | administered on empty stomach to INC absorption |
| reformulation of levothyroxine | new forms of the drug allow for better bioavailability: about 80% if a pts TSH is stable on a dose taken w meals, do not chance time of admin. |
| where is levothyroxine metabolized and excreted? | metabolized in the liver and excreted in urine |
| side effects of levothyroxine | S/S of hyperthyroidism |
| formulations of levothyroxine | oral and IV |
| levothyroxine drug interactions: decreased absorption | acid suppression w antacids, histamine blockers and PPIs ferrous sulfate sucralfate |
| levothyroxine drug interactions: increased clearance | rifampin, carbamazepine, phenytoin due to P450 issue w metabolism in the liver |
| levothyroxine drug interactions: block conversion of T3 to T4 | amiodarone, selenium deficiency |
| Levothyroxine lab monitoring | gradual dose increases until symptoms relieved and TSH is normal. we dont want it to be too high too fast! |
| Levothyroxine lab monitoring- checking TSH and T4 | check TSH and T4 no sooner than every 6 weeks after dose changes to assess effectiveness. this allows for a steady state |
Created by:
ago24