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64 Cards in this Set
- Front
- Back
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Normal TSH
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TSH: 0.35-5 (ideally 1-2?)
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abnormal TSH with normal free T4 and free T3
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Euthyroid Sick
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Normal T3 and T4
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Free T3: 2.3-4.2
Free T4: 0.7-1.5 |
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Hypothyroid
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TSH >5
Free T4 <0.7 Free T3 <2.3 |
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Hypothyroid treatment
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Armour Thyroid
Liothyronine (T3) Levothyroxine (T4) |
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Hyperthyroidism
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TSH approaches 0 (suppressed)
Free T4 >1.5 Free T3 >2.3 |
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causes of hyperthyroidism
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Graves disease
Toxic multinodular goiter Autonomous nodule (hyper functioning) Thyroiditis |
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Treatment of Hyperthyroidism
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Beta blockers
Thionamides Steroids Cholystyramine (Questran) RAI Surgery |
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Thionamides
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Methimazole (Tapazole)
Propylthiouricil (PTU) Found in 1943 to inhibit thyroid hormone syntheses |
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Methimazole
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Half life 4-6 hours
Dose 5-60mg daily Can be given orally or rectally Usually not give in pregnancy, although probably safe Much higher intrathyroidal concentration than PTU |
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PTU
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Half life 75 minutes
Given in divided doses 3-4 times daily May need up to 1200mg/day PTU has advantage of inhibiting the 5´-monodeiodinase that converts thyroine (T4) to triiodothyronine (T3) in extrathyroidal tissue |
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side effects of PTU
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*Agranulocytosis- biggest one
Abnormal liver function tests Puritis Rash Urticaria Arthralgias Arthritis |
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Steroids
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Most work done with dexamethasone
Prevents peripheral conversion of T4-T3 Risk of adrenal insufficiency associated with long term use Usual dose 1mg bid-tid and tapered off |
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Cholystyramine (Questran)
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Usually for hypercholesterolemia
Works by inhibiting enterohepatic recycling of thyroid hormone Patients don’t like-gritty taste Dosed bid-tid Adjunct therapy, short-term use only |
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RAI (radioactive iodine)
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Radioactive iodine
Iodine is almost solely taken up by thyroid Destroys thyroid tissue See onset of effects 2-12 weeks post treatment Usually permanent-rarely need re-treatment Must be off T3 for at least 2 weeks, T4 for 4 weeks Essentially hypothyroid, treat with LT4 No IV contrast within 2-3 months-urine iodine level Don’t want you around immunosupressed, children, pregnancy- use own bathroom for awhile |
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Thyroiditis
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Inflammation of the thyroid
Often seen post-partum, following viral illness TSH suppressed, thyroid gland tender Thyroid scan: 0-1% uptake Treatment: analgesics, tincture of time, follow TFTs-FT3 and FT4 will normalize before TSH |
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Thyroid cancer TSH levels for papillary and medullary
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Suppressive LT4 (TSH <0.5) for papillary, “normal” TSH for medullary
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Can cause hypo or hyperthyroidism
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Amiodarone
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Gold standard for bone mineral density testing
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DEXA scan
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normal BMD
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BMD not > 1 SD below young adult mean
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BMD for osteopenia
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BMD 1-2.5 SD below young adult mean
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osteoporosis BMD
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BMD > 2.5 SD below young adult mean
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z-score
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compare to age-match population
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t-score
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compare to the norm, want to look at this
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2ndry causes of osteoporosis
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Cushing’s syndrome, glucocorticoid Rx
Multiple myeloma MGUS-not really sure what the significance is, but do know it leads to bone loss Anticonvulsants, heparin Malabsorption, gastric surgery Alcoholism Hypogonadism Primary hyperparathyroidism Hyperthyroidism COPD-rare (prob steroid) Idiopathic hypercalciuria Osteogenesis imperfecta Mastocytosis-rare Osteomalacia -rare |
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what level does calcium absorption plataeu at
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25(OH)D exceeds ~ 32 ng/ml (goal 30-40)
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HRT treatment for osteoporosis
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HRT does prevent bone loss and fractures but alternatives should be considered in view of WHI.
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RALOXIFENE (SERM)
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FDA approved - prevention and treatment (60 mg/d)
Increases BMD Decreases vertebral fx Issues - Hot flashes - ? Breast cancer - ? Cardiovascular |
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CALCITONIN
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FDA approved for treatment
Nasal or SQ Modest BMD effects Some vertebral fracture data (PROOF) Issues - Side effects (nasal, flushing, nausea) usually mild, allergy rare - ? Analgesic effects - ? Resistance due to antibody formation |
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Oral Bisphosphonates Alendronate/Risdronate/Ibandronate
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Increase BMD.
Decrease vertebral fractures in patients with osteoporosis. Decrease nonvertebral and hip fractures in patients with osteoporosis. Prevent bone loss in early PMP women. Prevent bone loss associated with corticosteroid therapy. weekly or monthly therapy. Fracture reduction with antiresorptives greater than predicted by BMD change.- PREVENTS further bone loss ONJ- osteonecrosis of the jaw- primarily of the injectable ones How to take meds:Taken on empty stomachs, water only, no other medications, 30-60 min need to stay upright |
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1st Generation Oral Agents for Diabetes
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Tolbutamide
Chlorpropamide Tolazemide |
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2nd generation oral agents for diabetes
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Glyburide (Micronase, Diabeta)
Glipizide (Glucotrol, Glucotrol XL) Glimepiride (Amaryl) |
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Glyburide
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Available as 1.25mg, 2.5mg and 5mg tablets
Max dose 20mg/day Micronized version available as 1.5mg and 3mg tablets Max dose 12mg/day Dosed qd-bid |
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Glipizide
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Excretion
Fecal: (extended release tablet), 10% Renal: (extended release tablet), 80%, less than 10% unchanged Dialyzable: no Elimination Half Life 2 h to 4 h |
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Only biguanide available currently
Mechanism of action: Reduction in glucose production, reduction in intestinal glucose absorption, increased insulin sensitivity Does NOT increase insulin secretion Dose NOT cause hypoglycemia in diabetic or non-diabetics Does NOT cause weight gain usually |
Metformin
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Contradindication to metformin
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CHF –contradindication
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Thiazolidinedione (TZDs)
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Actos (pioglitazone)
Avandia (rosiglitazone) |
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Meglitinide
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Nateglinide (Starlix)
Repaglinide (Prandin) |
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lowers blood glucose concentrations by stimulating the release of insulin from functioning beta cells of pancreatic islet tissue. Nateglinide interacts with the adenosine triphosphate (ATP)-sensitive potassium channel on pancreatic beta cells. The subsequent depolarization of the beta cell opens the calcium channel, producing calcium influx and insulin secretion.
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Nateglinide-MOA
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diabetic ketoacidosis
hypersensitivity to nateglinide type 1 diabetes |
Nateglinide-CI
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lowers blood glucose concentrations by stimulating the release of insulin from functioning beta cells of pancreatic islet tissue. This is accomplished by a selective ion channel mechanism. Repaglinide inhibits adenosine triphosphate (ATP)-potassium channels on the beta cell membrane and potassium efflux. The resulting depolarization and calcium influx induces insulin secretion.
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Repaglinide-MOA
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Alpha-Glucosidase Inhibitor
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Acarbose (Precose)
Miglitol (Glyset) |
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lowers postprandial blood glucose concentrations in patients with diabetes by competitive, reversible inhibition of pancreatic alpha-amylase and membrane-bound intestinal alpha-glucoside hydrolases. These enzymes inhibit hydrolysis of complex starches to oligosaccharides in the lumen of the small intestine and hydrolysis of oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the brush border of the small intestine. Acarbose does not enhance insulin secretion and, when used as monotherapy, should not cause hypoglycemia.
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Acarbose
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By reversibly inhibiting α-glucoside hydrolase enzymes which are located in the brush border of the small intestine, miglitol delays the hydrolysis of ingested complex sugars. By slowing the breakdown of oligosaccharides and disaccharides into monosaccharides, this action slows the absorption of glucose into the bloodstream and thus reduces postprandial hyperglycemia. Unlike other antihyperglycemic agents such as sulfonylureas, miglitol does not enhance insulin secretion.
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Miglitol
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Basal Insulins
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Intermediate acting
Long acting |
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Intermediate Acting (Basal)
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NPH
Lente |
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Long Acting (Basal)
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Ultralente
Lantus Levemir |
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NPH Insulin onset, peak and duration
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Onset: 1-4 hours
Peak: 4-12 hours Duration: 14-24 hours |
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REgular insulin :onset, peak, duration
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Onset: 30-60 minutes –downside b/c have to take 30 min before eat
Peak: 2-5 hours Duration: 4-8 hours |
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Humalog (lispro) onset, peak, duration
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Onset: 10-15 minutes
Peak: 30-90 minutes Duration: 2-4 hours |
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Novolog (aspart)
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Onset: 10-20 minutes
Peak: 40-50 minutes Duration: 3-5 hours |
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Newer Insulins
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Apidra (glulisine)
Lantus (glargine) Levemir (detemir) |
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Newer long acting basal insulin
Usually given every 24 hours (occasionally twice daily dosing) Onset: 90-120 minute post injection Duration: 22-24 hours |
Lantus (glargine)
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MECHANISM OF ACTION 1) This compound is less soluble than native human insulin at physiological pH, and precipitates in skin following subcutaneous injection, resulting in delayed absorption
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Lantus (glargine)
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advantages of lantus
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Long duration of action
Once daily injection for most patients Clinically is used in combination with oral agents and short acting insulin Patients who are fasting should receive between 75% and 100% of dose No peak like NPH |
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disadvantages of lantus
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Cannot be mixed with other insulins
Slower onset of action If overdosed, prolonged risk of hypoglycemia Available in pen form, but difficult to use |
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Newest insulin
Lasts 12-24 hours depending on dose Onset: 3-4 hours Duration: 5.7 hours at lowest doses, 23.2 hours at highest doses |
Levemir (detemir)
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advantages of Levemir
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Flatter peak than NPH, but not as flat as Lantus
Less intrapatient variablilty Less weight gain Depending on dose, may be given once daily Fasting patients should receive 75%-90% of dose Nice pen (flexpen design) |
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disadvantages of Levemir
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Cannot be mixed with other insulins
Risk of prolonged hypoglycmia Dose dependant duration of action ¼ as potent as NPH, possibly requiring larger doses (clinically, not an issue) |
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Insulin option for patients who cannot or will not inject insulin
May be used with basal insulins or oral agents Usually given with each meal Onset: 10-20 minutes Duration: 6 hours May be used in Type 1 and Type 2 |
Exubera (inhaled insulin)
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Effects of GLP-1 on Βeta Cells
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Acute
Enhances glucose-dependent insulin secretion Subacute* Stimulates transcription of proinsulin and biosynthesis of insulin Increases expressions of Glut-2 and glucokinase Chronic* Stimulates proliferation and neogenesis of beta cells from precursor ductal cells |
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MECHANISM OF ACTION a) Stable, non-aggregating analogue of endogenous amylin (peptide cosecreted with insulin by pancreatic beta cells); mimics amylin effects. Primary: delays gastric emptying. May also regulate glucagon release.
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Symlin (pramlintide)
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enhancement of insulin secretion (glucose-dependent), glucose-dependent suppression of inappropriately high glucagon secretion, slowing of gastric emptying, reduction of food intake, promotion of beta-cell proliferation and neogenesis, reduction in adiposity, and insulin-sensitizing effects (animal models).
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Byetta (exenatide)
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Newest oral agent for Type 2 DM
New class of drug: DPP-4 inhibitor (dipeptidyl-peptidase 4 inhibitor) |
Januvia (sitagliptin)
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