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Rx05.pdf

Name: Thyroglobulin (Proloid)
Name: Levothyroxine sodium (Synthroid, Levothroid, Levoxine)
Class: Thyroid Hormone
Class: Thyroid Hormone
Mech.: T3/T4 synergize w/GH effects, increase BMR, potentiate catecholamine
Mech.: Sodium salt of T4. T3/T4 synergize w/GH effects, increase BMR, potentiate
effects on heart, promote lipolysis, and decrease serum cholesterol.
catecholamine effects on heart, promote lipolysis, and decrease serum Absorption: Oral
Dist.: Poor placental transfer → okay for pregnant E. Little in milk (use cautiously).
Absorption: Incomplete oral absorption—30-40% recovered in stool.
Metab.: T
Dist.: Poor placental transfer → okay for pregnant E. Little in milk (use cautiously).
4 & T3 released by proteolysis after ingestion. Hepatic conjug. of T4/T3 Metab.: Hepatic conjug. w/glucuronic & sulfuric acids. Peripheral deiodination to
Excretion, : Bile; some lost in stool due to enterohepatic circulation.
Toxicity/S.E.s: Salicylates and dicumarol compete for albumin binding sites →
Excretion, : Bile; some lost in stool due to enterohepatic circ. 6-7 d.
Toxicity/S.E.s: Salicylates and dicumarol compete for albumin binding sites →
Utility: Treat hypothyroidism and goiter (not due to iodine deficiency or
Utility: Treat hypothyroidism and goiter (not due to iodine deficiency or
Special Features: 120-180 mg/d. Similar efficacy to levothyroxine sodium and
liothyronine sodium, although dose not standardized by Special Features: 200-300 µg/d. 1/4 the potency of liothyronine sodium, but same
Name: Liothyronine sodium (Cytomel)
Name: Propylthiouracil (PTU)
Class: Thyroid Hormone
Class: Antithyroid Drug (Thioamide)
Mech.: Sodium salt of T3. T3/T4 synergize w/GH effects, increase BMR, potentiate
Mech.: Blocks thyroid synthesis.
catecholamine effects on heart, promote lipolysis, and decrease serumcholesterol.
Absorption: Oral → 80-95% bioavailability.
Absorption: Oral → 95% absorption.
Dist.: 80% protein binding. Poor placental transfer. 10% transfer into milk.
Dist.: Poor placental transfer → okay for pregnant E. Little in milk (use cautiously).
Metab.: Conjugated to gluconamide.
Metab.: Hepatic conjug. w/glucuronic & sulfuric acids.
Excretion, : 35% excreted in urine, mostly as gluconamide. 1-2 hr.
Excretion, : Bile; some lost in stool due to enterohepatic circ. ≤ 2 d.
Toxicity/S.E.s: 3% freq. of untoward rxns. Most common = rash. 0.44% develop
Toxicity/S.E.s: Salicylates and dicumarol compete for albumin binding sites →
agranulocytosis. Occurs suddenly in first months of therapy, preceded by a sore throat and fever. Unusual bleeding and Utility: Preferred in treatment of myxedema coma. Treat hypothyroidism and
bruising may occur. C/i in nursing mothers, but can be used goiter (not due to iodine deficiency or hyperthyroidism).
(w/great caution) in pregnancy-complicated hyperthyroidism (maycause neonatal goiter).
Special Features: 50-75 µg/d. 4x the potency of levothyroxine sodium, but same
Utility: Treat hyperthyroidism, but relapse after single course ≥ 50%.
Special Features: 75-100 mg/8 hr (or higher).
Name: Methimazole (Tapazole)
Name: Iodide
Class: Antithyroid Drug (Thioamide)
Class: Antithyroid drug
Mech.: Blocks thyroid synthesis.
Mech.: High doses of iodide inhibit thyroid gland fxn. Effects decrease w/time,
Absorption: Oral → 80-95% bioavailability.
possible due to decrease in iodide transport.
Dist.: 0% protein binding. High placental transfer. 100% transfer into milk.
Absorption:
Metab.: Conjugated to gluconamide.
Excretion, : <10% excreted in urine, mostly as gluconamide. 3-5 hr.
Toxicity/S.E.s: 7% freq. of untoward rxns. Most common = rash. 0.12% develop
Excretion, :
agranulocytosis. Occurs suddenly in first months of therapy, preceded by a Toxicity/S.E.s:
sore throat and fever. Unusual bleeding and bruising may occur. C/i in Utility: Used in conjunction w/thioamides for preoperative preparation to diminish
nursing mothers, but can be used (w/great caution) in pregnancy-complicated vascularity and swelling of thyroid gland → reduced operative mortality.
hyperthyroidism (may cause neonatal goiter); PTU is safer.
Treatment of thyrotoxicosis. Blocks synthesis and release of thyroid Utility: Treat hyperthyroidism, but relapse after single course ≥ 50%.
Special Features: 5-10 mg/8 hr (or higher).
Special Features: No longer used very much.
Name: Radioactive Iodine
Name: Propranolol (Inderal)
Class: Antithyroid Drug
Class: Nonselective β-Blocking Agent
Mech.: Trapped by thyroid. β particles cause highly localized tissue destruction.
Mech.: Competitive blockade of β1 and β2 receptors. No α effect. Decreases conversion of
X-rays are diagnostically useful. I131 generally used due to short t½ (8 d).
T4 to T3 by inhibiting hepatic monodeiodinase.
Absorption: Good oral (>90%). But low bioavailability ~30%. Plasma levels vary 20x btwn.
Absorption: 90% ends up in thyroid or urine. 10% absorbed by the rest of the
Dist.:93% bound to protein. Enters CNS. Metab.: Hepatic Excret., : Short t½ (3.5-6 hr).
Dist.: Metab.:
Toxicity/S.E.s: CV—hypotension, bradycardia, c/i for CHF or AV block. Resp—c/i in
Excretion, : Urine. 8 d.
asthmatics, COPD, bronchitis, allergic rhinitis. Metab—caution w/diabetics (masks sign
Toxicity/S.E.s: High incidence of hypothyroidism (5-10% in 1-2 yr., eventually
of hypoglycemia: tachycardia). CNS—weakness, fatigue, nightmares, depression. GI
50%). May require multiple exposures—up to a year (thioamides usu. used n/v (uncommon). Hypersens—rash, hematologic disorders (rare).
to cover hyperthyroidism in the interim). C/i in pregnant E and kids.
Utility: Hypertension (↓ CO → ↓ BP; blocks renin release). Angina pectoris (prophylactic →
Utility: Treat hyperthyroidism w/o surgery. Indicated for old folk (esp. w/heart
↑ exercise tolerance due to ↓ O2 demand). Cardiac arrhythmias (esp. supravent.
disease), when subtotal thyroidectomy or thioamides have not worked, and tachyarrhyths). Acute MI (prophylaxis and reduction of infarct size and failure).
especially for some metastatic thyroid cancers where cells continue to take Pheochromocytoma (in comb. w/alpha blocker). Essential tremor. Migraine headache(prophylaxis). Performance anxiety. Thyrotoxicosis—Suppression of signs/symptoms of up iodide and respond to TSH. Used to evaluate thyroid fxn (e.g., thyrotoxicosis. Most effective drug for treatment of thyrotoxic crisis or thyroid storm (usu.
hypo/hyperthyroidism, goiter types, response to TSH/TRF.).
used in comb w/a thioamide and/or iodide. Can be used preop. for thyroid surg.
Special Features: Min. dose = 80-150 µCi/g thyroid or 4-10 mCi total. Estimate
Controversial Rx of hyperthyroid symptoms while awaiting effects of thioamides or iodide.
Special Features: Abrupt w/drawal may trigger MI.
Name: Calcium gluconate (Kalcinate)
Name: Calcium gluceptate
Class: Element
Class: Element
Absorption: Slow IV infusion.
Absorption: IV (IM if IV is infeasible).
Excretion, :
Excretion, :
Toxicity/S.E.s: Major = hypercalcemia (esp. during long-term therapy or co-admin.
Toxicity/S.E.s: Major = hypercalcemia (esp. during long-term therapy or co-admin.
w/vit. D). Hypercalciuria. Rapid infusion may cause cardiac arrhythmias.
w/vit. D). Hypercalciuria. More irritating than calcium gluconate. May cause Enhances action of digitalis. ∴ IV infusion may ppt arrhythmias. Drug mild local rxns (e.g., tingling). Metallic taste. Enhances action of digitalis. ∴ interactions—↓ bioavailability and/or oral absorption of some drugs (e.g., IV infusion may ppt arrhythmias. Drug interactions—↓ bioavailability and/or etidronate, tetracyclines, iron salts, atenolol, norfloxacin). Thiazide diuretic- oral absorption of some drugs (e.g., etidronate, tetracyclines, iron salts, induced hypercalcemias exacerbated by calcium supplementation.
atenolol, norfloxacin). Thiazide diuretic-induced hypercalcemias exacerbated Utility: DOC for severe hypocalcemia. Reduces/prevents bone loss in older
Utility: Treat hypocalcemia. Reduces/prevents bone loss in older women (800
Special Features: 9% calcium.
Special Features: 8% calcium.
Name: Calcium chloride
Name: Calcium carbonate (TUMS, etc.)
Class: Element
Class: Element
Absorption: IV. Never inject IM (highly irritating).
Absorption: Oral usu. → 15-20% (up to 50% w/maximal stimulation). Depends of
stomach acid for solubilization. ∴ Absorption is impaired in anchlorhydric or fasting patients. Absorption improved when taken Excretion, :
Toxicity/S.E.s: Major = hypercalcemia (esp. during long-term therapy or co-admin.
w/vit. D). Hypercalciuria. Enhances action of digitalis. ∴ IV infusion may ppt arrhythmias. High level of irritation (esp. IM). Drug interactions—↓ Excretion, :
bioavailability and/or oral absorption of some drugs (e.g., etidronate, Toxicity/S.E.s: Hypercalcemia, hypercalciuria. Drug interactions—↓ bioavailability
tetracyclines, iron salts, atenolol, norfloxacin). Thiazide diuretic-induced and/or oral absorption of some drugs (e.g., etidronate, tetracyclines, hypercalcemias exacerbated by calcium supplementation.
iron salts, atenolol, norfloxacin). Thiazide diuretic-induced Utility: Treat hypocalcemia. Reduces/prevents bone loss in older women (800
hypercalcemias exacerbated by calcium supplementation.
Utility: Treat mild hypocalcemia. Also maintenance after initial IV treatment.
Special Features: 27% calcium. Probably obsolete due to greater irritation
Provide 400-800 mg/d. Reduces/prevents bone loss in older women (800 (enteral or parenteral admin.) than other calcium preparations.
Special Features: 40% calcium.
Name: Calcium citrate (Citracal, etc.)
Name: Calcium glubionate (Neo-Calglucon)
Class: Element
Class: Element
Absorption: Oral usu. → 15-20% (up to 50% w/maximal stimulation).
Absorption: Oral usu. → 15-20% (up to 50% w/maximal stimulation).
Excretion, :
Excretion, :
Toxicity/S.E.s: Hypercalcemia, hypercalciuria. Drug interactions—↓ bioavailability
Toxicity/S.E.s: Hypercalcemia, hypercalciuria, diarrhea. Drug interactions—↓
and/or oral absorption of some drugs (e.g., etidronate, tetracyclines, bioavailability and/or oral absorption of some drugs (e.g., etidronate, iron salts, atenolol, norfloxacin). Thiazide diuretic-induced tetracyclines, iron salts, atenolol, norfloxacin). Thiazide diuretic- hypercalcemias exacerbated by calcium supplementation.
induced hypercalcemias exacerbated by calcium supplementation.
Utility: Treat mild hypocalcemia. Also maintenance after initial IV treatment.
Utility: Treat mild hypocalcemia. Also maintenance after initial IV treatment.
Provide 400-800 mg/d. Reduces/prevents bone loss in older women (800 Provide 400-800 mg/d. Reduces/prevents bone loss in older women (800 Special Features: 21% calcium. More soluble than calcium carbonate. Works
Special Features: 6.5% calcium. Probably obsolete due to large number of
Name: Calcium lactate
Name: Tribasic calcium phosphate
Class: Element
Class: Element
Mech.:
Absorption: Oral usu. → 15-20% (up to 50% w/maximal stimulation).
Absorption: Oral.
Excretion, :
Toxicity/S.E.s: Hypercalcemia, hypercalciuria. Drug interactions—↓ bioavailability
and/or oral absorption of some drugs (e.g., etidronate, tetracyclines, Excretion, :
iron salts, atenolol, norfloxacin). Thiazide diuretic-induced Toxicity/S.E.s: Ectopic calcification, kidney failure, death. Serum calcium and
hypercalcemias exacerbated by calcium supplementation.
phosphate should be monitored to avoid hypocalcemia and Utility: Treat mild hypocalcemia. Also maintenance after initial IV treatment.
Provide 400-800 mg/d. Reduces/prevents bone loss in older women (800mg/d).
Utility: Treat simultaneous hypocalcemia and hypophosphatemia.
Special Features: 13% calcium. Probably obsolete due to large number of tablets
Special Features: 39% tribasic calcium phosphate.
Name: Dicalcium phosphate
Name: Sodium phosphate oral solution
Class: Element
Class: Element
Absorption: Oral.
Absorption: Oral
Excretion, :
Excretion, :
Toxicity/S.E.s: Ectopic calcification, kidney failure, death. Serum calcium and
Toxicity/S.E.s: Ectopic calcification, kidney failure, death. Serum calcium and
phosphate should be monitored to avoid hypocalcemia and phosphate should be monitored to avoid hypocalcemia and Utility: Treat simultaneous hypocalcemia and hypophosphatemia.
Utility: Primarily reserved for patients w/X-linked familial hypophosphatemia or
Special Features: 23% dibasic calcium phosphate dihydrate.
other forms of osteomalacia featuring hypophosphatemia.
Special Features: Safer than IV sodium/potassium phosphate. Sodium-free
preparations are available (K-Phos Original, Neutra-Phos K).
Name: Sodium or potassium phosphate
Name: Vitamin D2/ergocalciferol (Deltalin, Drisdol, Calciferol)
Class
: Vitamin
Class: Element
Mech.: Increases intestinal absorption of calcium and phosphate. Stimulates bone
resorption by facilitating effects of PTH. Stimulates renal reabsorption of Absorption: IV
calcium and phosphate. Net result = ↑↑ calcium, ↑↑ phosphate.
Absorption: Oral usu → adequate absorption. Bile is essential for absorption.
Dist.: Stored in fat and muscle. Tightly bound to vitamin D-binding protein.
Metab.: Requires hydroxylation in liver and kidney for full activity.
Excretion, :
Excretion, : 1° = bile. Weeks.
Toxicity/S.E.s: Ectopic calcification, kidney failure, death. Serum calcium and
Toxicity/S.E.s: Excess accumulation in fat/muscle, hypervitaminosis D,
phosphate should be monitored to avoid hypocalcemia and hypercalcemia. Drug interactions—phenytoin and phenobarbital reduce sensitivity to vit. D and/or increase rate of inactivation ofcalcitriol.
Utility: Treat hypophosphatemia.
Utility: Treat nutritional rickets; prophylactic dose = 400 U/d, fully developed rickets
Special Features: More dangerous than sodium phosphate oral solution.
= 3,000-4,000 U/d. Ameliorates Type I vit. D-dependent rickets (4,000 U/d).
Supplement to estrogen and calcium to treat postmenopausal osteoporosis.
Treat hypoparathyroidism (25-100,000 U 3x/wk + oral calcium); use calcitriolor dihydrotachysterol for faster action or if hypervit. D develops.
Name: Vitamin D
Name: Calcifediol/25-OH-cholecalciferol
3/cholecalciferol (Delta-D)
Class: Vitamin
Class: Vitamin
Mech.: Increases intestinal absorption of calcium and phosphate. Stimulates bone resorption
Mech.: Increases intestinal absorption of calcium and phosphate. Stimulates bone resorption
by facilitating effects of PTH. Stimulates renal reabsorption of calcium and by facilitating effects of PTH. Stimulates renal reabsorption of calcium and phosphate. Net result = ↑↑ calcium, ↑↑ phosphate.
phosphate. Net result = ↑↑ calcium, ↑↑ phosphate.
Absorption: Oral usu → adequate absorption. Bile is essential for absorption.
Absorption: Oral usu → adequate absorption. Bile is essential for absorption.
Dist.: Stored in fat and muscle. Tightly bound to vitamin D-binding protein.
Dist.: Stored in fat and muscle. Tightly bound to vitamin D-binding protein.
Metab.: Requires hydroxylation in kidney for full activity.
Metab.: Requires hydroxylation in liver and kidney for full activity.
Excretion, : 1° = bile. Weeks.
Excretion, : 1° = bile. Weeks.
Toxicity/S.E.s: Excess accumulation in fat/muscle, hypervitaminosis D, hypercalcemia.
Toxicity/S.E.s: Excess accumulation in fat/muscle, hypervitaminosis D, hypercalcemia.
Drug interactions—phenytoin and phenobarbital reduce sensitivity to vit. D and/or Drug interactions—phenytoin and phenobarbital reduce sensitivity to vit. D and/or increase rate of inactivation of calcitriol.
increase rate of inactivation of calcitriol.
Utility: Treat osteomalacia 2° to liver disease. Treat renal osteodystrophy 2° to chronic renal
Utility: Treat nutritional rickets—prophylactic dose = 400 U/d, fully developed rickets =
disease—50-100 µg/d (larger dose necessary because kidney hydroxylation is 3,000-4,000 U/d. Ameliorates Type I vit. D-dependent rickets (4,000 U/d). Treat osteodystrophy 2° to malabsorption of vit. D and calcium—25-50,000 U 3x/wk + Special Features: Does not require liver activation. Fully activated in kidney. More effective
calcium. Supplement to estrogen and calcium to treat postmenopausal osteoporosis.
than calcitriol for increasing renal absorption of calcium and phosphate. Much less Treat hypoparathyroidism (25-100,000 U 3x/wk + oral calcium); use calcitriol or effective than calcitriol for increasing bone resorption and increasing intestinal dihydrotachysterol for faster action or if hypervit. D develops.
reabsorption of calcium and phosphate.
Special Features:
Name: Calcitriol/1,25-(OH)2-cholecalciferol (Rocaltrol)
Name: Dihydrotachysterol (Hytakerol, DHT)
Class: Vitamin
Class: Vitamin
Mech.: Increases intestinal absorption of calcium and phosphate. Stimulates bone
Mech.: Increases intestinal absorption of calcium and phosphate. Stimulates bone
resorption by facilitating effects of PTH. Stimulates renal reabsorption of resorption by facilitating effects of PTH. Stimulates renal reabsorption of calcium and phosphate. Net result = ↑↑ calcium, ↑↑ phosphate.
calcium and phosphate. Net result = ↑↑ calcium, ↑↑ phosphate.
Absorpt.: Oral usu → adequate absorption. Bile essential for absorpt. Parenteral.
Absorption: Oral usu → adequate absorption. Bile is essential for absorption.
Dist.: Stored in fat and muscle. Tightly bound to vitamin D-binding protein.
Dist.: Stored in fat and muscle. Tightly bound to vitamin D-binding protein.
Metab.: Requires hydroxylation in liver for full activity.
Excretion, : 1° = bile. Hours.
Excretion, : 1° = bile.
Toxicity/S.E.s: Excess accumulation in fat/muscle, hypervitaminosis D,
Toxicity/S.E.s: Excess accumulation in fat/muscle, hypervitaminosis D,
hypercalcemia. Drug interactions—phenytoin and phenobarbital reduce hypercalcemia. Drug interactions—phenytoin and phenobarbital reduce sensitivity to vit. D and/or increase rate of inactivation of calcitriol.
sensitivity to vit. D and/or increase rate of inactivation of calcitriol.
Utility: Vit. D metab. of choice for rapid action. Raises serum calcium in 1-2 d.
Utility: Treat X-linked hypophosphatemic rickets (+ phosphate salts). Treat renal
Treat X-linked hypophosphatemic rickets (0.25-1 µg/d + phosphate salts).
osteodystrophy 2° to chronic renal disease. Treat hypoparathyroidism (+ Treat renal osteodystrophy 2° to chronic renal disease. Ameliorates Type I vit. D-dependent rickets (0.25-0.5 µg/d). Treat hypoparathyroidism (+ Special Features: Does not require kidney activation. Liver hydroxylation
produces full activity. ¼ the price of calcitriol, but takes 1-2 wk. to increase Special Features: Does not require liver or kidney activation (fully activated).
serum calcium. Serum concentration not measurable.
Name: Synthetic parathyroid hormone (Teriparatide, Parathar)
Name: Human calcitonin (Cibacalcin, Calcimar)
Class
: Hormone
Class: Hormone
Mech.: Inhibition of both bone resorption and renal tubular reabsorption of calcium
Mech.: Mobilizes bone calcium by stimulating bone resorption. Increases renal
and phosphate. Secretion stim by ↑ serum calcium. Net result = absorption of calcium. Decreases renal absorption of phosphate. Increases synth. of calcitriol → ↑intest. absorption of calcium and phosphate. Net Absorption: SC, IM. Nasal is variable and often poor.
result = ↑↑calcium, ↓↓phosphate.
Absorption:
Dist.: Metab.: Inactivated by proteolysis.
Metab.: Inactivated by proteolysis in kidneys and blood.
Excretion, : Minutes.
Excretion, : Minutes.
Toxicity/S.E.s: Flushing of face and hands w/in min. of injxn (16-21%).
Toxicity/S.E.s:
Nausea/vomiting w/in 30 min. of use (14-21%); usu. diminishes w/continued Utility: Only used for differential diagnosis—hypoparathyroidism vs.
therapy. Bedtime admin. can minimize effects. Urinary frequency (5-10%) pseudohypoparathyroidism. There is less of an increase in urinary cAMP Utility: Initial treatment of hypercalcemia. Diseases characterized by increased
and phosphate in pseudohypoparathyroidism.
skeletal remodeling (e.g., Paget’s disease of bone). Recently approved for Special Features: Consists of active portion of PTH (1st 34 AAs on N-terminal).
treatment of postmenopausal osteoporosis.
Not used to treat hypoparathyroidism. Currently being
Special Features: Effects begin after several hours, persist for up to 10 hr.
investigated for treatment of osteoporosis. Intermittent therapy Salmon calcitonin has a longer t½ and duration and is 50x more potent.
However, 30-50% of long-term patients develop antibodies to salmon calcitonin.
Name: Sodium etidronate (Didronel)
Name: Pamidronate (Aredia)
Class: Bisphosphonate
Class: Bisphosphonate
Mech.: Structure sim. to inorganic pyrophosphate. Impairs formation and dissolution of
Mech.: Structure sim. to inorganic pyrophosphate. Impairs formation and
calcium phosphate crystals. Alters number/activity of osteoclasts (1° effect) → dissolution of calcium phosphate crystals. Alters number/activity of slowed bone resorption. Slows formation and dissolution of hydroxyapatite crystals.
osteoclasts (1° effect) → slowed bone resorption. Slows formation and Absorp.: Oral → very little absorp., but still effective. Oral absorp. varies w/dose. Further
dissolution of hydroxyapatite crystals.
reduced by food or divalent cations. IV → much higher blood levels.
Dist.: 50% of absorbed drug accum. in bone and turns over w/t½ of weeks.
Absorption: IV admin. only
Excretion, : 50% rapidly excreted unchanged by kidney.
Toxicity/S.E.s: Protracted or high-dose therapy → osteomalacia.
Excretion, :
Utility: Treat Paget’s disease of bone as well as or better than calcitonin—oral efficacy, lower
Toxicity/S.E.s:
cost, no antigenicity, longer remissions. However, chronic use → osteomalaciaw/↑risk of bone pain & fractures. Treat heterotopic ossification—given orally after Utility: DOC for mod.-severe hypercalcemia assoc. w/malignant neoplasms. Treat
total hip replacement or spinal injury. Treat hypercalcemia of malignancy (IV). Under Paget’s disease of bone. Must be used in conjnxn w/adequate hydration and testing for long-term intermittent therapy for vertebral osteoporosis (+ calcium and vit.
Special Features: 100x more potent than etidronate, more efficacious, and does
Special Features: Unlike pyrophosphate, resistant to enzymatic hydrolysis. Clinical failure of
not affect normal bone mineralization at normal therapeutic concentrations.
therapy often due to coadmin. w/calcium tablets or food.
Name: Alendronate (Fosamax)
Name: Prednisone
Class
: Corticosteroid (Glucocorticoid)
Class: Bisphosphonate
Mech.: ↑ PMNs in periph. blood, but decrease all other WBCs. Inhib. monocyte reactivity and
Mech.: Structure sim. to inorganic pyrophosphate. Impairs formation and
secretion of IL-1 & TNF. Inhib. T cell activation, IgE-med. rxns, inducible cyclooxygenase IIexpression. Induces lipocortin → inhibition of phospholipase A2.
dissolution of calcium phosphate crystals. Alters number/activity of Absorption: IV, IM, oral.
osteoclasts (1° effect) → slowed bone resorption. Slows formation and dissolution of hydroxyapatite crystals.
Absorption:
Excretion, :
Toxicity/S.E.s: Cataracts, hypertension, osteoporosis, myopathy, obesity, acne, hirsutism,
hyperglycemia, muscle atrophy/myopathy, convulsions, mood changes, derm. changes, ↓ cellular immunity. Glucocorticoid admin > equiv. of 20 mg hydrocortisone/d → suppression ofHPA axis. Sudden stop of chronic therapy → impaired physiologic homeostasis. Drug Excretion, :
Interactions—phenytoin, barbiturates, & rifampin induce catabolic enzymes; antacids → ↓ Toxicity/S.E.s:
bioavailability of prednisone; salicylate levels reduced; increased doses required for insulin,hypoglycemic agents, antihypertensives, and glaucoma meds; if hypokalemia occurs, Utility: Increases bone mass in spines and hips of postmenopausal women → ↓
Utility: Oral for asthma. Immunosuppression, anti-inflammatory actions, cytostatic actions against
some lymphocyte tumors, mgt. of allergic diseases.
Special Features: Efficacy maintained over at least 3 yr.
Special Features: Synth. agents have potent anti-inflamm. activity w/little (if any) mineralocorticoid
Name: Plicamycin (Mithracin, nee Mithramycin)
Name: Hydrocortisone/Cortisol
Class: Antibiotic (Cytotoxic)
Class: Corticosteroid (Glucocorticoid)
Mech.: Intercalates into DNA like actinomycin and blocks DNA, RNA, and protein
Mech.: ↑ PMNs in periph. blood, but decrease all other WBCs. Inhib. monocyte reactivity
synthesis. Supposedly decreases serum calcium levels by direct toxic and secretion of IL-1 & TNF. Inhib. T cell activation, IgE-med. rxns, inducible cyclooxygenase II expression. Induces lipocortin → inhibition of phospholipase A2.
Absorption:
Absorption: IV, IM, oral, topical.
Metab.: Excretion, : 8-12 hr.
Toxicity/S.E.s: Cataracts, hypertension, osteoporosis, myopathy, obesity, acne, hirsutism,
Excretion, :
hyperglycemia, muscle atrophy/myopathy, convulsions, mood changes, derm. changes, Toxicity/S.E.s: Less severe w/doses for hypercalcemia than for neoplasms.
↓ cellular immunity. Glucocorticoid admin > equiv. of 20 mg hydrocortisone/d → Sudden onset of thrombocytopenia followed by hemorrhage.
suppression of HPA axis. Sudden stop of chronic therapy → impaired physiologic Hepatic and renal toxicity. Hypocalcemia. Monitor platelet count, homeostasis. Drug Interactions—phenytoin, barbiturates, & rifampin induce catabolic liver/kidney fxn, and serum calcium. C/i for patients w/renal or enzymes; antacids → ↓ bioavailability of prednisone; salicylate levels reduced; increased hepatic disease, bone marrow disease, thrombocytopathy, doses required for insulin, hypoglycemic agents, antihypertensives, and glaucoma meds; coagulation disorders, or bleeding susceptibilities of other etiologies.
if hypokalemia occurs, increased toxicity of digoxin.
Utility: Treat severe hypercalcemia resulting from CA w/wo bony metastases.
Utility: IV/IM for asthma. Immunosuppression, anti-inflammatory actions, cytostatic actions
against some lymphocyte tumors, mgt. of allergic diseases.
Special Features: Use limited by toxicity.
Special Features: Rel. anti-inflamm potency = 1. Synth. agents have potent anti-inflamm.
activity w/little (if any) mineralocorticoid effect.
Name: Beclomethasone diproprionate (Beclovent)
Name: Triamcinolone acetonide (Azmacort)
Class: Corticosteroid (Glucocorticoid)
Class: Corticosteroid (Glucocorticoid)
Mech.: ↑ PMNs in periph. blood, but decrease all other WBCs. Inhib. monocyte reactivity
Mech.: ↑ PMNs in periph. blood, but decrease all other WBCs. Inhib. monocyte reactivity
and secretion of IL-1 & TNF. Inhib. T cell activation, IgE-med. rxns, inducible and secretion of IL-1 & TNF. Inhib. T cell activation, IgE-med. rxns, inducible cyclooxygenase II expression. Induces lipocortin → inhibition of phospholipase A2.
cyclooxygenase II expression. Induces lipocortin → inhibition of phospholipase A2.
Absorption: IM, aerosol, oral, topical, intraarticular.
Absorption: Aerosol, nasal pump spray, oral, topical.
Excretion, : 12-36 hr.
Excretion, :
Toxicity/S.E.s: Cataracts, hypertension, osteoporosis, myopathy, obesity, acne, hirsutism,
Toxicity/S.E.s: Cataracts, hypertension, osteoporosis, myopathy, obesity, acne, hirsutism,
hyperglycemia, muscle atrophy/myopathy, convulsions, mood changes, derm. changes, ↓ hyperglycemia, muscle atrophy/myopathy, convulsions, mood changes, derm. changes, ↓ cellular immunity. Glucocorticoid admin > equiv. of 20 mg hydrocortisone/d → cellular immunity. Glucocorticoid admin > equiv. of 20 mg hydrocortisone/d → suppression of HPA axis. Sudden stop of chronic therapy → impaired physiologic suppression of HPA axis. Sudden stop of chronic therapy → impaired physiologic homeostasis. Drug Interactions—phenytoin, barbiturates, & rifampin induce catabolic homeostasis. Drug Interactions—phenytoin, barbiturates, & rifampin induce catabolic enzymes; antacids → ↓ bioavailability of prednisone; salicylate levels reduced; increased enzymes; antacids → ↓ bioavailability of prednisone; salicylate levels reduced; increased doses required for insulin, hypoglycemic agents, antihypertensives, and glaucoma meds; if doses required for insulin, hypoglycemic agents, antihypertensives, and glaucoma meds; hypokalemia occurs, increased toxicity of digoxin. Aerosol—oral candidiasis, dysphonia.
if hypokalemia occurs, increased toxicity of digoxin. Aerosol—oral candidiasis, dysphonia.
Utility: Asthma. Intraarticular injxn. to reduce inflamm. Immunosuppression, anti-
Utility: Asthma, allergic rhinitis. Immunosuppression, anti-inflammatory actions, cytostatic
inflammatory actions, cytostatic actions against some lymphocyte tumors, mgt. of actions against some lymphocyte tumors, mgt. of allergic diseases.
Special Features: Synth. agents have potent anti-inflamm. activity w/little (if any)
Special Features: Rel. anti-inflamm. potency of 5. Synth. agents have potent anti-inflamm.
activity w/little (if any) mineralocorticoid effect.
Name: Dexamethasone (Decadron)
Name: Regular insulin
Class: Corticosteroid (Glucocorticoid)
Class: Insulin (Fast-Acting Insulin Injection)
Mech.: ↑ PMNs in periph. blood, but decrease all other WBCs. Inhib. monocyte reactivity
and secretion of IL-1 & TNF. Inhib. T cell activation, IgE-med. rxns, inducible Mech.: Interacts w/ insulin receptors on cell membranes → phosph/dephosph of
cyclooxygenase II expression. Induces lipocortin → inhibition of phospholipase A2.
enzymes→ glucose transport into cells (esp. fat & muscle), glycogen synth., Absorption: IV, IM, Oral, topical, intraarticular.
↓ FFA, ↑ triglyceride storage, K+ & Mg2+ uptake, protein synth. Regulation of Excretion, : 36-72 hr.
cell proliferation & differentiation. May activate cAMP (significance unknown).
Toxicity/S.E.s: Cataracts, hypertension, osteoporosis, myopathy, obesity, acne, hirsutism,
Absorption: Injection (usu. SC).
hyperglycemia, muscle atrophy/myopathy, convulsions, mood changes, derm. changes,↓ cellular immunity. Glucocorticoid admin > equiv. of 20 mg hydrocortisone/d → suppression of HPA axis. Sudden stop of chronic therapy → impaired physiologic Metab.: Rapidly metab. by liver, kidneys, and muscle.
homeostasis. Drug Interactions—phenytoin, barbiturates, & rifampin induce catabolic Excretion, : 5-6 min.
enzymes; antacids → ↓ bioavailability of prednisone; salicylate levels reduced; increased Toxicity/S.E.s: Most freq. = hypoglycemia → ANS hyperactivity, impaired CNS fxn
doses required for insulin, hypoglycemic agents, antihypertensives, and glaucoma meds; (confusion, bizarre behavior, coma). Skin rxns—transient urticaria, subcut.
if hypokalemia occurs, increased toxicity of digoxin.
Utility: Intraarticular injxn. to reduce inflamm. Immunosuppression, anti-inflammatory
fibrosis, localized atrophy of subcut. tissue. Allergic rxn. Insulin resistance— actions, cytostatic actions against some lymphocyte tumors, mgt. of allergic refractory receptors or anti-insulin antibodies (may require 200-1000 units/d).
Utility: Treat diabetes mellitus. Preprandial control of blood glucose.
Special Features: Rel. anti-inflamm. potency of 20-30. Synth. agents have potent anti-
Special Features: Rapid onset (0.5-1 hr). Short duration (5-8 hr). Amorphous.
inflamm. activity w/little (if any) mineralocorticoid effect.
Name: Isophane insulin suspension (NPH insulin)
Name: Insulin Zn (Lente insulin)
Class: Insulin (Intermediate-Acting Suspension)
Class: Insulin (Intermediate-Acting Suspension)
Mech.: Interacts w/ insulin receptors on cell membranes → phosph/dephosph of
Mech.: Interacts w/ insulin receptors on cell membranes → phosph/dephosph of
enzymes → glucose transport into cells (esp. fat & muscle), glycogen synth., ↓ enzymes → glucose transport into cells (esp. fat & muscle), glycogen synth., FFA, ↑ triglyceride storage, K+ & Mg2+ uptake, protein synth. Regulation of cell ↓ FFA, ↑ triglyceride storage, K+ & Mg2+ uptake, protein synth. Regulation of proliferation & differentiation. May activate cAMP (significance unknown).
cell proliferation & differentiation. May activate cAMP (significance unknown).
Absorption: Injection (usu. SC).
Absorption: Injection (usu. SC).
Metab.: Rapidly metab. by liver, kidneys, and muscle.
Metab.: Rapidly metab. by liver, kidneys, and muscle.
Excretion, : 5-6 min.
Excretion, : 5-6 min.
Toxicity/S.E.s: Most freq. = hypoglycemia → ANS hyperactivity, impaired CNS fxn
Toxicity/S.E.s: Most freq. = hypoglycemia → ANS hyperactivity, impaired CNS fxn
(confusion, bizarre behavior, coma). Skin rxns—transient urticaria, subcut.
(confusion, bizarre behavior, coma). Skin rxns—transient urticaria, subcut.
fibrosis, localized atrophy of subcut. tissue. Allergic rxn. Insulin resistance— fibrosis, localized atrophy of subcut. tissue. Allergic rxn. Insulin resistance— refractory receptors or anti-insulin antibodies (may require 200-1000 units/d).
refractory receptors or anti-insulin antibodies (may require 200-1000 units/d).
Utility: Treat diabetes mellitus. Basal control of blood glucose.
Utility: Treat diabetes mellitus. Basal control of blood glucose.
Special Features: 70% crystalline form (ultralente) + 30% amorphous form
Special Features: Equal concentrations of insulin and protamine. Intermediate
(semilente) of Zn-insulin complex. Zn forms rel. insoluble complex Name: Extended insulin zinc suspension (Ultralente insulin)
Name: Tolbutamide (Orinase)
Class
: Anti-Diabetes Agent (Oral Hypoglycemic) (Sulfonylurea) (First Generation)
Class: Insulin (Long-Acting)
Mech.: Interferes w/ATP-sensitive K+ channel. Reduced K+ conductance →
Mech.: Interacts w/ insulin receptors on cell membranes → phosph/dephosph of
depolarization & influx of Ca2+. Stim. of insulin release from pancreas, enzymes → glucose transport into cells (esp. fat & muscle), glycogen synth., ↓ ↓ glucagon, ↑ binding of insulin to target tissue receptors.
FFA, ↑ triglyceride storage, K+ & Mg2+ uptake, protein synth. Regulation of cell Absorption: Oral.
proliferation & differentiation. May activate cAMP (significance unknown).
Dist.: Largely bound to plasma proteins.
Absorption: Injection (usu. SC).
Metab.: Hepatic.
Metab.: Rapidly metab. by liver, kidneys, and muscle.
Excretion, : Short duration of action (~8 hr).
Toxicity/S.E.s: Severe side effects in 2-4%. Only 10% still use them after 6-9 yrs
Excretion, : 5-6 min.
of treatment. Sustained hypoglycemia up to 4-5 days after discontinued use.
Toxicity/S.E.s: Most freq. = hypoglycemia → ANS hyperactivity, impaired CNS fxn
Rash (rare), GI upset (3-4%), hematological disturbance—usu. leukopenia (confusion, bizarre behavior, coma). Skin rxns—transient urticaria, subcut.
(1%), inappropriate ADH release (→ hyponatremia), flushing, disulfiram action, fibrosis, localized atrophy of subcut. tissue. Allergic rxn. Insulin resistance— variability in steady state conc. Drug interactions—protein binding (alcohol, β refractory receptors or anti-insulin antibodies (may require 200-1000 units/d).
Utility: Treat diabetes mellitus. Basal control of blood glucose.
Utility: NIDDM—prevents acute hyperglycemic problems, may postpone
development of glucose intolerance, may delay thickening of capillary BM.
Special Features: Crystalline form of Zn-insulin complex—very insoluble → slow
Special Features:
Name: Chlorpropramide (Diabinese)
Name: Glyburide (Micronase)
Class: Anti-Diabetes Agent (Oral Hypoglycemic) (Sulfonylurea) (First Generation)
Class: Anti-Diabetes Agent (Oral Hypoglycemic) (Sulfonylurea) (Second Gen.)
Mech.: Interferes w/ATP-sensitive K+ channel. Reduced K+ conductance →
Mech.: Interferes w/ATP-sensitive K+ channel. Reduced K+ conductance →
depolarization & influx of Ca2+. Stim. of insulin release from pancreas, ↓ depolarization & influx of Ca2+. Stim. of insulin release from pancreas, ↓ glucagon, ↑ binding of insulin to target tissue receptors.
glucagon, ↑ binding of insulin to target tissue receptors.
Absorption: Oral.
Absorption: Oral.
Dist.: Largely bound to plasma proteins.
Dist.: Largely bound to plasma proteins.
Metab.: Hepatic.
Metab.: Hepatic.
Excretion, : Long duration of action (36+ hr).
Excret., : Intermed. duration of action (t½=1.5-5 hr), but duration of effect 24 hr.
Toxicity/S.E.s: Severe side effects in 2-4%. Only 10% still use them after 6-9 yrs of
Toxicity/S.E.s: Severe side effects in 2-4%. Only 10% still use them after 6-9 yrs
treatment. Sustained hypoglycemia (esp. likely) up to 4-5 days after discont. use.
of treatment. Sustained hypoglycemia up to 4-5 days after discontinued use.
Rash (rare), GI upset (3-4%), hematological disturbance—usu. leukopenia (1%), Rash (rare), GI upset (3-4%), hematological disturbance—usu. leukopenia inappropriate ADH release (→ hyponatremia), flushing, disulfiram action (highest (1%), inappropriate ADH release (→ hyponatremia), flushing, disulfiram action, incidence of the class), variability in steady state conc. C/i in the elderly. Drug variability in steady state conc. Drug interactions—protein binding (alcohol, β interactions—protein binding (alcohol, β blockers, MAO inhibitors).
Utility: NIDDM—prevents acute hyperglycemic problems, may postpone
Utility: NIDDM—prevents acute hyperglycemic problems, may postpone
development of glucose intolerance, may delay thickening of capillary BM.
development of glucose intolerance, may delay thickening of capillary BM.
Special Features: Highest incidence of S.E.’s in sulfonylurea group.
Special Features: More lipophilic and 100x more potent than first gen.
Name: Glipizide (Glucotrol)
Name: Metformin (Glucophage)
Class: Anti-Diabetes Agent (Oral Hypoglycemic) (Sulfonylurea) (Second Gen.)
Class: Anti-Diabetes Agent (Oral Hypoglycemic) (Biguanide)
Mech.: Interferes w/ATP-sensitive K+ channel. Reduced K+ conductance →
depolarization & influx of Ca2+. Stim. of insulin release from pancreas, ↓ Mech.: Decreases hepatic output → decreased plasma glucose. Does not directly
glucagon, ↑ binding of insulin to target tissue receptors.
Absorption: Oral.
Absorption: Oral → good absorption.
Dist.: Largely bound to plasma proteins.
Dist.: No protein binding.
Metab.: Hepatic.
Excret., : Intermed. duration of action (t½=1.5-5 hr), but duration of effect 18 hr.
Toxicity/S.E.s: Severe side effects in 2-4%. Only 10% still use them after 6-9 yrs
Excretion, : Excreted unmetabolized in urine. 8 hr.
of treatment. Sustained hypoglycemia up to 4-5 days after discontinued use.
Toxicity/S.E.s: Lactic acidosis (1:40,000-80,000), metallic aftertaste, nausea,
Rash (rare), GI upset (3-4%), hematological disturbance—usu. leukopenia (1%), inappropriate ADH release (→ hyponatremia), flushing, disulfiram action, Utility: Use alone or in combination w/sulfonylureas to treat NIDDM that doesn’t
variability in steady state conc. Drug interactions—protein binding (alcohol, β respond well to sulfonylureas alone.
Utility: NIDDM—prevents acute hyperglycemic problems, may postpone
Special Features: Only reduces blood glucose in the presence of hyperglycemia.
development of glucose intolerance, may delay thickening of capillary BM.
Has not been found to cause serious hypoglycemia.
Special Features: More lipophilic and 100x more potent than first gen.
Name: Acarbose (Precose)
Name: Troglitazone
Class: Anti-Diabetes Agent (Oral Hypoglycemic)
Class: Anti-Diabetes Agent (Oral Hypoglycemic)
Mech.: Inhibits α-glucosidase → ↓ conversion of carbohydrates to glucose in the
Mech.: ↑ glucose utilization and reduces production by ↑ receptor response to
small intestine → ↓ absorption of glucose → ↓ post-prandial glucose rise.
Does not stimulate insulin release or action. ∴ No hypoglycemia.
Absorption:
Absorption: Oral → poor absorption.
Excretion, :
Excretion, :
Toxicity/S.E.s:
Toxicity/S.E.s: Flatulence, diarrhea, abdominal cramping.
Utility: May help prevent development of NIDDM.
Utility: Treat NIDDM. Possible adjunct to insulin for IDDM.
Special Features:
Special Features:
Name: Thiazides
Name: Furosemide (Lasix)
Class: Diuretic
Class: Loop Diuretic
Mech.: ↓ reabsorption of Na+ in distal tubule by inhibition of a Na+/Cl- cotransporter
Mech.: Inhib. Na+/K+/Cl- cotransport of the luminal membrane in the ascending limb
on the luminal membrane. Promotes reabsorption of Ca2+ → ↓ Ca2+ in of the loop of Henle → ↓ reabsorption of Na+, K+, & Cl-. Increases conc. of Absorption:
Absorption:
Excretion, :
Excretion, :
Toxicity/S.E.s: Potassium depletion, hyperuricemia, volume depletion,
Toxicity/S.E.s: Ototoxicity, hyperuricemia, acute hypovolemia, potassium
hypercalcemia, hyperglycemia, hypersensitivity.
Utility: Treat hypertension, congestive heart failure, renal impairment,
Utility: DOC for reducing acute pulmonary edema of congestive heart failure.
Rapid onset, so useful in emergency situations. Treat hypercalcemia.
Special Features:
Special Features:

Source: http://web.utah.edu/umed/courses/year2/pharm/study/rx05.pdf

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