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76 Cards in this Set

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Which drug has anabolic effects in muscle and catabolic effects in lipid cells to shift balance of body mass to muscle mass and reduce central adiposity?
Growth hormone
Primary effects of GH (somatotropin) are mediated by what?
Insulin-like growth factor 1 (IGF-1) and IGF-2
Adverse effects of GH
intracranial HTN, scoliosis, hypothyroidism, pancreatitis, gynecomastia, peripheral edema, mylagias, arthragias, carpal tunnel syndrome
Clinical uses of GH
1) Peds pts with short stature
2) GH deficiency in adults
3) Wasting in AIDS pts
4) Short bowel syndrome (improves GI function)
What are uses for Dopamine agonists?
(Bromocriptine, Cabergoline, Pergolide)
1) suppress prolactin release
2) Parkinson's - reduce levodopa requirements
3) Tx of hyperprolactinemia and acromegaly
SE of dopamine agonists
Light headedness
orthostatic hypotension
psychiatric manifestations
How much more potent is T3 than T4?
3-4 times
What happens to T4 and T3 in hyperthyroidism?
Production T4/T3 increased;
half-lives decreased
What happens to T4 and T3 in hypothyroidism?
Production T4/T3 decreased;
Half-lives increased
What are the S/S of toxicity of thyroxine in both childrena and adults?
Children: restlessness, insomnia, accelerated bone maturation and growth
Adults: Increased nervousness, heat intolerance, episodes of palpitation and tachycardia, unexplained wt. loss.
What do you do if you see S/S of toxicity with thyroxine?
Monitor TSH
What does chronic overtreatment of thyroxine increase the risk of?
A fib
accelerated osteoporosis
What drugs can induce hypothyroidism?
Cytokines (interferons/Interleukins)
Which are short-medium acting corticosteroids?
Which are medium acting corticosteroids?
Which are the long acting corticosteroids?
Which are the mineralcorticoids?

There are the same potency ratios of glucocorticoids to mineralcorticoids?
What developments do you monitor for with adrenocortical agents?
Na retention with edema or HTN
Peptic ulcer
Hidden infections
When would you use great caution when prescribing adrenocortical agents?
Peptic ulcer
heart disease
HTN with HF
What are the properties of mineralcorticoids?
Promotes reabsorption of Na from distal convoluted tubule, cortical collecting renal tubules, and coupled to K and hydrogen ion excretion
Where is aldosterone synthesized?
zona glomerulosa of the adrenal cortex
ACTH produces moderate stimulation of release of aldosterone, but in the abscence of ACTH 50% is produced (by RAAS or other factors)
What is a steroid hormone produced by adrenal gland, which is a precursor of aldosterone? It's secretion is under control of ACTH.
Which drug is a synthetic steroid used for treatment of adrenal insufficiency and orthostatic hypotension?
Fludrocortisone (florinef)
Name 3 rapidly acting insulin preparations
Name 3 benefits of rapid-acting insulins

1) more closely mimics normal endogenous prandial insulin secretion (than regular)
2) can use immediately before meals
3) perfered insulin for pumps
What are the onset, peak and duration of rapid-acting insulins?
Onset: 5-15 min
Peak: 1-2 hrs
Duration: 3-5 hrs
Name the 3 short acting insulins
Regular Novolin R
Regular Hunulin R
Regular Exubra
Which insulin is taken 30-45 minutes before meals to avoid mismatch?
Regular Novolin R and Humulin R
What drug is inhaled (1-4mg) powder premeal; determined by body weight?
What is the conversion from mg to units for exubera?
1mg=3units regular insulin
3mg=8units regular insulin
What other med besides exubera is given to type 1 diabetics?
longer acting insulin
Can type 2 diabetics use exubera as monotherapy?
(or with oral agents or with longer acting insulin)
What are the pharmacokinetics of short-acting insulins?
onset: within 30 min
peak: 2-3 hrs
duration: 4-12 hrs
Regular Novolin R
Regular Hunulin R
Regular Exubra
What has absorption and onset which are delayed by combining appropriate amounts of insulin and protamine?
Intermediate-acting insulins
NPH Humulin N
NPH Novolin N
(they are mixed with rapid or short-acting insulins)
Intermediate-acting insulins
What are premixed insulins made of?
Rapid or short-acting mixed with NPH
What does Novolin 70/30 or Humulin 70/30 mean?
70% NPH
30% regular insulin
what % NPH/Regular
What does 75/25 NPL, lispro mean?
75% Neutral protamine lispro/
25% insulin lispro
What does 70/30 NPA, Aspart mean?
70% Neutral protamine aspart/
30% insulin aspart

Insulin glargine and detemir are given separately.
What kind of insulins are detemir (Levemir) and glargine (Lantus)?
long-acting insulins
How does insulin detemir (Levemir) work?
Availablility is prolonged by increasing self-aggregaion in SQ tissue and reversible albumin binding.
(less hypoglycemia than NPH)
[given 2 x a day]
How does insulin glargine (Lantus) work?
Insulin molecules slowly dissolve away from the crystalline depot and provide slow, continuous level of circulating insulin.
[given once daily, 2 times if necessary]
What are the pharmacokinetics of long-acting insulins?
Onset: 1-3 hrs
Peak: none, max effect 4-6 hrs
Duration: 24+ hrs
What are the S/S of hypoglycemia?
Tachycardia, palpitations, sweating, tremulousness, nausea, hunger, convulsions, coma
What are the causes of hypoglycemia?
Meal delay, inadequate carbo intake, unusual physical exertion, larger dose than immediate need
What is the treatment for hypoglycemia?
1) Oral glucose tabs, sugar containing beverage or food.
2) 20-50 mL D50 IV over 2-3 min
3) Glucagon 1 mg SQ or IM
Name 3 second generation oral diabetic agents
Which oral diabetic agent is contraindicated in hepatic and renal impairment?
Glyburide (diabeta, micronase, glynase)
Which oral diabetic agent makes you hypoglycemic and flush if you drink ETOH with it?
Glyburide (diabeta, micronase, glynase)
What is the dose of Glyburide (diabeta, micronase, glynase)?
2.5-10 mg QD in am
What is the dose of Glipizide (Glucotrol, Glucotrol XL)?
5-15 mg 30 min prior to breakfast
Max 40mg, divide doses
XL provides 24hr action
Which oral diabetic agent causes less hypoglycemia per lecture?
Glipizide (Glucotrol, Glucotrol XL)

shorter half-life
Which oral diabetic agent is 90% metabolized in liver and 10% in urine, and is contraindicated in hepatic impairment?
Glipizide (Glucotrol, Glucotrol XL)
Which oral diabetic agent is completely metabolized by the liver, has the lowest dose and the longest 1/2 life?
Glimepiride (Amaryl)
dose=1-8mg QD
What is a caution to administration of oral diabetic agents?
Elderly and CV disease
What are meglitinides?
Oral diabetic agents that modulate beta-cell insulin release by regulating K efflux through K channels. They have 2 common binding sites to sulfonylureas and 1 unique binding site.
What is the dose of Repaglinide (prandin) and cautions?
0.25-4mg 15-30 min before meals
caution with renal or hepatic disfunction - CYP3A4
What are the adverse effects of Repaglinide (Prandin)?
Hypoglycemia - if meal skipped/delayed
Which oral diabetic agent has no sulfur structure?
Repaglinide (Prandin)
What is Sitagliptin (januvia)?
-Inhibitor of DPP4
-enzyme that degrades incretin and other GLP1 like molecules
-increases insulin release and decreases hepatic glucose production
What is the dose for Sitagliptin (januvia)?
100mg PO QD, with diet and exercise
Does Sitagliptin (januvia) require a renal adjustment?
Can Sitagliptin (januvia) be used for Type I diabetics?
nope, only for type 2

monotherapy or combo with other oral agents
What drug can be used for severe hypoglycemia, endocrine diagnosis, beta-blocker poisioning, or radiology of the bowel?
What are the pharmacologic effects of glucagon?
1) producton of cAMP, facilitating catabolism of stored glycogen and increased gluconeogeneis and ketogenesis.
2) potent inotropic and chronotropic effect on heart
3) large doses cause relaxation of the intestine
What is a peptide produced in the parathyroid gland that has rapid clearance in liver and kidney and regulates Ca and Phos flux across the membranes in bone and kidney?
Parathyroid hormone (PTH)
What is a steroid produced in the skin and found in food; hydroxylated in the liver and further converted in the kidney; cleared in the liver - determined by binding affinity?
Vitamin D
What is the net effect on serum levels of PTH?
Increased serum Ca
Decreased serum Phos
What is the net effect on serum levels of Vitamin D?
Increased serum Ca
Increased serum Phos
What are the major causes of hypocalcemia?
Hypoparathyroidism, Vitamin D deficiency, kidney disease, and malabsorption.
What are the major causes of hypercalcemia?
Hyperparathyroidism, cancer, thiazide therapy
What are the major causes of hyperphosphatemia?
renal failure, hypoparathyroidism, vit D intoxication, tumoral calcinosis
What is the clinical presentation of hyperphospatemia?
due to the effects of hypocalcemia
(neuromuscular - tetany, muscle cramps, etc)
What are the major causes of hypophosphatemia?
Primary hyperparathyroidism, vit D deficiency, idiopathic hypercalciuria, vit D resistant rickets, other renal phos. wasting, overuse of binders, TPN without proper Phos.
What is the clinical presentation of hypophospatemia?
Muscle weakness, rhabdo, osteomalacia