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64 Cards in this Set

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  • Back
Normal TSH
TSH: 0.35-5 (ideally 1-2?)
abnormal TSH with normal free T4 and free T3
Euthyroid Sick
Normal T3 and T4
Free T3: 2.3-4.2
Free T4: 0.7-1.5
TSH >5
Free T4 <0.7
Free T3 <2.3
Hypothyroid treatment
Armour Thyroid
Liothyronine (T3)
Levothyroxine (T4)
TSH approaches 0 (suppressed)
Free T4 >1.5
Free T3 >2.3
causes of hyperthyroidism
Graves disease
Toxic multinodular goiter
Autonomous nodule (hyper functioning)
Treatment of Hyperthyroidism
Beta blockers
Cholystyramine (Questran)
Methimazole (Tapazole)
Propylthiouricil (PTU)
Found in 1943 to inhibit thyroid hormone syntheses
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
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
side effects of PTU
*Agranulocytosis- biggest one
Abnormal liver function tests
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
Cholystyramine (Questran)
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
RAI (radioactive iodine)
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
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
Thyroid cancer TSH levels for papillary and medullary
Suppressive LT4 (TSH <0.5) for papillary, “normal” TSH for medullary
Can cause hypo or hyperthyroidism
Gold standard for bone mineral density testing
DEXA scan
normal BMD
BMD not > 1 SD below young adult mean
BMD for osteopenia
BMD 1-2.5 SD below young adult mean
osteoporosis BMD
BMD > 2.5 SD below young adult mean
compare to age-match population
compare to the norm, want to look at this
2ndry causes of osteoporosis
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
Primary hyperparathyroidism
COPD-rare (prob steroid)
Idiopathic hypercalciuria
Osteogenesis imperfecta
Osteomalacia -rare
what level does calcium absorption plataeu at
25(OH)D exceeds ~ 32 ng/ml (goal 30-40)
HRT treatment for osteoporosis
HRT does prevent bone loss and fractures but alternatives should be considered in view of WHI.
FDA approved - prevention and treatment (60 mg/d)
Increases BMD
Decreases vertebral fx
- Hot flashes
- ? Breast cancer
- ? Cardiovascular
FDA approved for treatment
Nasal or SQ
Modest BMD effects
Some vertebral fracture data (PROOF)
- Side effects (nasal, flushing, nausea) usually mild, allergy rare
- ? Analgesic effects
- ? Resistance due to antibody formation
Oral Bisphosphonates Alendronate/Risdronate/Ibandronate
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
1st Generation Oral Agents for Diabetes
2nd generation oral agents for diabetes
Glyburide (Micronase, Diabeta)
Glipizide (Glucotrol, Glucotrol XL)
Glimepiride (Amaryl)
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
Fecal: (extended release tablet), 10%
Renal: (extended release tablet), 80%, less than 10% unchanged
Dialyzable: no
Elimination Half Life
2 h to 4 h
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
Contradindication to metformin
CHF –contradindication
Thiazolidinedione (TZDs)
Actos (pioglitazone)
Avandia (rosiglitazone)
Nateglinide (Starlix)
Repaglinide (Prandin)
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.
diabetic ketoacidosis
hypersensitivity to nateglinide
type 1 diabetes
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.
Alpha-Glucosidase Inhibitor
Acarbose (Precose)
Miglitol (Glyset)
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.
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.
Basal Insulins
Intermediate acting
Long acting
Intermediate Acting (Basal)
Long Acting (Basal)
NPH Insulin onset, peak and duration
Onset: 1-4 hours
Peak: 4-12 hours
Duration: 14-24 hours
REgular insulin :onset, peak, duration
Onset: 30-60 minutes –downside b/c have to take 30 min before eat
Peak: 2-5 hours
Duration: 4-8 hours
Humalog (lispro) onset, peak, duration
Onset: 10-15 minutes
Peak: 30-90 minutes
Duration: 2-4 hours
Novolog (aspart)
Onset: 10-20 minutes
Peak: 40-50 minutes
Duration: 3-5 hours
Newer Insulins
Apidra (glulisine)
Lantus (glargine)
Levemir (detemir)
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)
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
Lantus (glargine)
advantages of lantus
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
disadvantages of lantus
Cannot be mixed with other insulins
Slower onset of action
If overdosed, prolonged risk of hypoglycemia
Available in pen form, but difficult to use
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)
advantages of Levemir
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)
disadvantages of Levemir
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)
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)
Effects of GLP-1 on Βeta Cells
Enhances glucose-dependent insulin secretion
Stimulates transcription of proinsulin and biosynthesis of insulin
Increases expressions of Glut-2 and glucokinase
Stimulates proliferation and neogenesis of beta cells from precursor ductal cells
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.
Symlin (pramlintide)
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).
Byetta (exenatide)
Newest oral agent for Type 2 DM
New class of drug: DPP-4 inhibitor
(dipeptidyl-peptidase 4 inhibitor)
Januvia (sitagliptin)