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111 Cards in this Set
- Front
- Back
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ketoconazole |
Antifungal and Antiandrogen at high doses inhibits side chain cleavage and CYP 17, leading to decreased synthesis of androgens/cortisone |
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finasteride |
inhibits 5 alpha reductase (prevents testosterone from being converted to DHT) - Treats Baldness and BPH |
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letrazole |
inhibits aromatase (decrease estrogens) -Tx: Estrogen R (+) breast cancer |
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metyrapone |
inhibits 11 Beta-Hydroxylase -decreases cortisol |
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desmopressin |
treatment of central diabetes insipidus - MOA: ADH replacement |
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HCTZ / drinking water |
treatment of nephrogenic diabetes insipidus - MOA: HCTZ helps secrete more salt |
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amiloride |
Tx of lithium induced nephrogenic DI -MOA: decrease Li++ in cell by blocking ENaC |
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Hypertonic Saline |
tx of SIADH -MOA: prevents hyponatremia |
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fluid restriction |
tx of SIADH -MOA: prevents excess secretion of salts with H2O |
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furosemide |
tx of SIADH -MOA: reduce medullary gradient |
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demeclocycline |
tx of SIADH -MOA: reduce responsiveness to ADH |
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tolvaptan |
tx of SIADH -MOA: V2 antagonists |
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Pitocin |
tx: induce/maintain labor post-partum hemorrhage -Oxytocin analog
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Ergot Alkaloids |
tx: post-partum hemorrhage migraines -oxytocic effects -Avoid: During/before pregnancy |
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Tocolytics |
tx: decrease uterine contractions delay pre-mature labor |
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ritodrine |
tocolytic (Beta 2 agonist) decrease uterine contractions |
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nifedipine |
tocolytic ( calcium channel blocker) decrease uterine contractions |
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atosiban |
tocolytic ( OT-R Blocker) decrease uterine contractions |
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Mg++ sulfate |
tocolytic (block LTCC, decrease MLCK) decrease uterine contractions |
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Dopamine R antagonists (antipsychotics / antiemetics) |
can cause hyperprolactinemia |
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cabergoline |
D2 agonist used to shrink a prolactinoma |
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bromocriptine |
D2 agonist used to shrink a prolactinoma |
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Somatropin |
recombinant growth hormone tx of GH deficiency |
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octreotide |
somatostatin analog tx of GH excess |
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pegvisomant |
GHR antagonist tx of GH excess |
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IGF-1 |
Used in tx of Laron Dwarfism caused by a defect in GH-R |
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Radio active Iodide Uptake Test (RAIU) |
Patient will have increased I* if there is increased TSH-R activity and if tumor cells active |
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Methimazole |
Tx: hyperthyroid Thioamide: inhibits thryroid peroxidase, decreasing T3/T4 synthesis--> may take weeks to work |
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Propylthiouracil (PTU) |
tx: hyperthyroid Thioamide: inhibits thryroid peroxidase, decreasing T3/T4 synthesis--> may take weeks to work |
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AE's of thioamides |
Agranulocytosis ( large decrease in WBC's) Increase risk of infection *let physician know if starting to feel sick |
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High Dose Idodine (250mg/day) |
tx: hypothyroid Build up excess I leading to decrease activity of NIS, Decrease TPO -> decrease new thyroid hormone, decrease release. (radioactive I- to kill tumor) * Works in 10-14 days |
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levothyroxine |
synthetic T4, tx hypothyroidism AE: -Causes cardiac stimulation: inc O2 consumption -arrhyhmias: A-fib - Insomnia: take in the morning (dont give with soy) |
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beta-blockers |
tx of symptoms of hyperthyroidism -B1block: dec cardiac toxicity (immediate) -B2 block: dec tremor (immediate) |
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Lithium |
tx of hyperthyroidism - dec ability for thryoid stimulation, dec t4 release, monitor thyroid levels |
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Amiodarone |
(37% iodine) -act similarly to high dose iodine - Can cause hypo, hyper, or no change in thyroid |
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cortisol |
Glucocorticoid stress hormone -stabilize (inc) BP, (inc) blood glucose, (dec) immune response - lypolysis, fat redistribution - inc bone resorption, dec bone formation -dec ACTH, dec reproductive function |
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addisons disease |
primary adrenocorticol insufficiency -cortisol deficiency -mineralocorticoid deficiency - adrenal androgen deficiency - increase in ACTH |
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cortisol deficiency |
hypoglycemia, hypotension, hyponatremia, weakness/fatigue, n/v, anorexia |
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mineralocorticoid deficiency |
salt wasting--> hypotension K retention--> hyperkalemia H+ retention--> metabolic acidosis |
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Adrenal androgen deficiency |
No large effects in men Female: decrease libido, dec axillary/pubic hair growth |
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Increase in ACTH |
can cause hyperpigmentation ( ACTH binding to MSH-R on skin |
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Congenital Adrenal Hyperplasia (CAH) cause |
Cause: 21 hydroxylase deficiency (cortisol pathway), dec cortisol biosynthesis, increase ACTH -> ZF/ZR hyperplasia |
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CAH clinical findings |
-cortisol deficiency (in cases of severe deficiency in enzyme --> dec mineralocorticoid activity) - Increase adrenal androgens ( fetus's) - inc 17 OH progesterone |
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Secondary Adrenocortical insufficiency causes |
Dec ACTH from anterior pituitary Pituitary damage exogenous glucocorticoid (chronic) --> ZF/ZR atrophy |
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2ndary Adrencortical insufficiency Clincical findings |
cortisol deficiency adrenal androgen deficiency ( No aldo deficiency - not dependent on ACTH) Low ACTH --> ZF/ZR atrophy |
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hydrocortisone |
glucocorticoid replacement high dose--> mineralocorticoid replacment |
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fludrocortisone |
mineralocorticoid replacements |
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Cushing's Syndrome causes |
Glucocorticoid excess ACTH dependent (inc): corticotroph tumor (Cushing's disease) or ectopic tumor
ACTH independent (dec): chronic glucocorticoid therapy (iatrogenic) or adrenal tumor |
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Cushings Syndrome clinicial findings |
central obesity, muscle wasting, skin changes, hypertension, hypokalemia, metabolic acidosis, dec reproductive function, inc infection risk, dec growth (kids), CNS effects, inc plasma glucose, inc peptic ulcers, inc cataracts/glaucoma, osteoporosis |
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ACTH dependent clinical findings |
skin hyperpigmentation, androgen excess (female = hirsutrium, acne, dec reproductive function) |
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dexamethasone suppression test |
diagnosis of Cushing's Syndrome -> inadequate suppression of cortisol |
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mineralocorticoid excess causes |
inc aldosterone (ZG tumor) inc 11DOC inc cortisol/cortisol effects MR agonists
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mineralcorticoid excess clinical findings |
hypertension, hypokalemia ( muscle weakness, cardiac arrythmias), metabolic alkalosis ( dec free Ca++)
Chronic stimuation--> cardiac remodeling |
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Conn's Syndrome |
primary aldosteronism from ZG tumor causing mineralocorticoid excess
Diagnosis: Inc plasma aldo / plasma renin |
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tx of mineralocorticoid excess |
CAH - replace cortisol MR receptor antag - spironolactone |
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exogenous glucocorticoids |
use: dec immune response, dec inflammation AE: same as cushing's syndrome ACTH indepenedent (ACTH low from feedback)
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osteoblasts |
formation of bone secrete osteoid (90% type 1 collagen, 10% ground substance) add Ca++ and PO4- to make bone |
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osteoclasts |
resorption of bone secrete proteases and H+ to digest matrix and dissolve minerals --> release Ca++ and PO4- |
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PTH synthesis |
parathyroid gland by chief cells |
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PTH actions (overall) |
receptor PTH-R1 (Gs, Gq) Increase plasma Ca++ Decrease plasma PO4- |
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PTH actions Bone |
High constant PTH = resorption normal intermittent PTH = formation |
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markers for osteoblast activity |
Alkaline phosphatase and BGLAP |
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markers for osteoclast activity |
CTX and NTX |
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Cortisol effects on bone |
decrease OPG and increase RANK-Ligand --> increased osteoclast activity |
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estrogen effects on bone |
increase OPG --> decreased osteoclast activity |
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PTH actions on kidney |
increase Ca++ resorption in DT (inc plasma Ca) Decrease PO4- resorption in PT (dec plasma PO4) vitamin D activation |
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Control of PTH release |
Calcium Sensing Receptors (CSR) (on parathyroid gland and thyroid gland) -high plasma Ca++ and high Vit D = Dec PTH - low Plasma Ca++ and high PO4 = inc PTH release
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Synthesis of calcitonin (CT) and tx |
thyroid C cells tx: hypercalcemia, Pagets Disease, 1st degree osteoporosis (decrease plasma Ca and decrease resorption) |
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Actions of CT (overall) |
Receptor: Calcitonin Receptor Decrease plasma Ca++ decrease plasma PO4- |
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Actions of CT on bone |
act on osteoclasts to inhibit resorption |
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actions of CT on kideny |
small dec in Ca++ reabsorption small dec in PO4 reabsorption |
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Control of CT |
Increase in Plasma Ca++ -> Inc CT release |
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Vit D Synthesis |
7 dehydrocholesterol --UV light--> D3 (cholecalciferol) --liver--> 25, OH D3 --Kindey--> 1,25 OH2 D3 (active calciferol) |
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Vit D Actions overall and tx |
Vitamin D Receptor = intracellular inc Ca++ plasma inc PO4- in plasma tx: hypocalcemia, rickets, osteomalacia, calcitriol for renal osteodystrophy, 1st degree osteoporosis
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Vit D actions GI tract |
inc Ca++ channels / calbindin /pumps = increase Ca++ absorption |
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Vit D actions Bone |
Osteoblasts inc RANK-L inc PTH sensitivity
Normal Vit D --> inc formation High Vit D --> inc resorption |
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Vit D actions Kidney |
small inc Ca++ reabsorption small inc PO4- reabsorption |
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Teriparatide |
Analog of PTH daily injections: inc bone formation AE: may cause osteosarcoma tx: hypocalcemia, 1st degree osteoporosis |
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Calcitonin |
made from salmon dec resorption dec overactive remodeling dec Ca++ plasma tx: hypercalcemia, Pagets disease, 1st degree osteoporosis |
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Alendronate |
bisphosphonate dec osteoclast activity dec resorption/ remodeling AE: esophagitis (drink water with and sit upright for 30 min after taking) jaw necrosis/ pain femur fractures tx: hypercalcemia, Pagets disease, osteoporosis |
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Raloxifene |
selective estrogen R modulator (SERM) Agonist: bones, lipid metabolism Antagonist - uterus, breast - dec resorption / inc formation - dec ER + breast cancer deaths - dec LDL tx: osteoporosis |
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cinacalcet |
Calcimimetic inc CSR activation --> dec PTH --> dec resorption, dec plasma Ca, dec plasma PO4, dec vit D tx: real osteodystrophy, hypercalcemia from adenoma |
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Furosemide |
diuretic dec renal Ca++ reabsoption tx: hypercalcemia
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HCTZ |
diuretic increase renal Ca++ reabsorption tx: hypocalcemia |
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Calcium carbonate calcium citrate |
increase Ca++ in body |
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Vit D replacements |
cholecalciferol (D3 inactive) ergocalciferol (D2 inactive) calcitriol (D3 active) |
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Densumab |
monoclonal antibody to RANK-L dec activation of osteoclasts --> dec resorption RANKL also in immune system --> inc infection?/malignancies? in animal models |
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things that increase the formation of bone |
mechanical load, Vit D, Ca++, Intermittant PTH, IGF-1, estrogens /androgens |
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things that decrease the formation of bone |
age, immobilization, smoking, excess EtOH |
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things that increase bone resorption |
calcitonin, denosumab, bisphosphonates, vit D, Ca++, estrogens/ SERMs |
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things that increase bone resorption |
immobilization, high constant PTH, high cortisol, high T3/T4, high Vit D, menopause |
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Effects of Hypercalcemia ( greater than 10.4 mg/dl) |
dec excitability, constipation, weakness, fatigue, dec DTR, depression, confusion, polyuria, kidney stones, arrthymias, dec QT interval, soft tissue calcification |
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Cause of Hypercalcemia (1) |
parathyroid adenoma --> increased PTH |
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Cause of hypercalcemia (2) |
Malignancy related: - tumor makes PTH-Related Peptide - tumor in bone expresses RANK-L (triggers osteoclast to chew bone) |
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Cause of hypercalcemia (3) |
Vit D excess, HCTZ, Li+--> inc PTH release, hyperthyroid (inc T3/T4) |
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Treatment of hypercalcemia |
treat cause - surgery -inhibit bone resorption: bisphosphonates, calcitonin, cinacalcet (useful for adenoma), denosumab (useful for ectopic tumor- high dose) -Increase Ca+ excretion: hydration, furosemide, calcitonin
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Effects of Hypocalcemia ( below 8.5 mg/dl) |
inc excitability, muscle spasms, tetany, inc DTR, inc QT interval, heart failure, seizures, hallucinations, dry skin/hair |
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Cause of Hypocalcemia (1) |
hypoparathyroidism -low PTH --> low Ca++, high PO4- |
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Cause of Hypocalcemia (2) |
pseudohypoparathyroidism - PTH receptor problem - high PTH but low Ca++, high PO4- |
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Cause of Hypocalcemia (3) |
Vitamin D deficiency - low kidney Ca abs - low GI Ca abs - low bone resorption |
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Cause of Hypocalcemia (4) |
Complex formation (binding of Ca++) -muscle damage --> release PO4- - blood transfusions --> stored blood has citrate and binds Ca+ |
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Treatment for Hypocalcemia |
Ca++/Vit D replacement Teriparatide (inc PTH) thiazides (HCTZ) |
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Rickets Osteomalacia |
inadequate mineralization of bone sx: rickets: short bones, deformities, fractures osteomalacica: bone pain, fractures |
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causes and tx of rickets, osteomalacia |
Vitamin D deficiency or decreased activity inadequate Ca++ or PO4- tx: give Vitamin D and Ca++ |
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Pagets Disease |
localized hyperactive remodeling excessive formation and resorption bone not compact= fluffy and swollen sx: fractures, pain, inc risk for osteosarcoma cause: unknown txL bisphosphonates, calcitonin ( dec resorption) |
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Renal Osteodystrophy |
renal failure leading to decreased vit D and PO4- retention. Overall leads to decreased free Ca+ and increased PTH and bone resorption |
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treatment for Renal osteodystrophy |
1) Ca++/ Calcitriol 2) Cinacalcet 3) Sevelemer (binds PO4 in GI) |
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Osteoporosis sx |
bone loss --> thin weak bones sx: fractures, vertebral --> dec height, back pain, kyphosis (curvature of spine) - affects hip and wrists |
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causes of osteoporosis |
1 degree- age, menopause 2nd degree - excess PTH/Cortisol/ T3,T4, immobilization, drugs ( anticonvulsant, heparin)
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Diagnosis of osteoporosis |
first degree: normal Ca++, PO4, PTH Bone Mineral Density Test (BMD) - measured by Dual Energy X-Ray absorptometry, (DexH, DxA)- test hip, wrist, back - T-score > -2.5 SD below normal --> osteoporosis - 2.5 > T > -1 SD below normal --> osteopenia |
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Treatment of 1st degree osteoporosis |
1) exercise, fall prevention 2) Ca++ (1200 mg/day) 3) Vit D 4) Bisphosphonates 5) estrogens / raloxifene 6) Calcitonin 7) teriparatide 8) low dose denosumab |
