medication for Diabetes and Endocrine issues Flashcards
Sulfonylureas
Drug
* Glipizide
MOA
* insulin stimulator
Therapeutic use
* T2D
adverve effects
* hypoglycemia
* wt. gain
Drug interactions
* Beta blockers (can cause hypoglycemia)
* ETOH–> palpations, flushing, nausea
pt education
* Do not give sulfa allergy
* monitor and educate pt for s/s/ of hypoglycemia (tachycardica, palpations, sweating, tremor, nervousness)
* N/V/C
* give 30 min prior to breakfast
* if food is missed can increase risk of hypoglycemia
* no alcohol use
Biguanides
Drug
* Metformin
Therapeutic use
* T2DM
* PCOS, GI diabetes, prediabetes, metabolic syndrome
MOA
* DECREASES glucose production by the liver
* decreased glucose absorption from the gut
* increases the tissue response to insulin (increase uptake of glucose by the cells)
Adverse effects
* GI symptoms: decreased appetite, nausea, diarrhea, flatulence
* Do not use with renal disease or CHF
* Lactic Acidosis (rare)
* hyperventilation, myalgia, malaise, somnolence
Drug interactions:
* ETOH use increases lactic acidosis
* IV contrast that contains iodine increases risk of acute renal failure and exacerbate metformin induced lactic acidosis
- Additive effects:
- Least likely to cause hypoglycemia bc it does not promote insulin release
- Decreased LDL and increased HDL
- Weight loss
- no alcohol
- lacid acidosis education
- stop meds 1-2 days b4 recieving IV contrast
- Gliptins (DPP-4 Inhibitors)
Drug
* Sitagliptin
MOA
* increase insulin released by the pancreas
* reduces glucagon released by the liver
* dreases hepatic glucose production
adverse effects
* pancreatitis & hypersensitivity reactions
Nurse education
* edu. on pancreatitis
* severe and persistent abdominal pain with or without vomitting
* monitor for S/S of hypersensitivity reactions
* Anaphylaxis, angioedemia and stevens johnson syndrome
hydrocortisone
Therapeutic use
* addisons disease
* replacement therapy: prefered drug for all forms of adrenocorticoid
* perferred drug for all forms of adrenocorticoid insufficiency
* non endocrine applications: allergic reactions: inflammation and cancer
MOA
* pts with adrenocorticcal insuffciency require replacement therapy with a glucocortiocoid and some may need a mineralocorticoid
Adverse effects
* when taking chronically or in large doses it can be toxic
* adrenal suppression and promotion of cushings syndrome
* all glucocorticoids raise gluocse lvls
Adrenal drugs pt education
- Steroids should be used in low doses and short-term therapy
- Chronic high doses cause Adrenal suppression and potentiate Cushing’s syndrome
o Taper any high dose or long-term corticosteroids use - Can cause HTN, potassium loss, osteoporosis, infection, glucose intolerance, and PUD with long term use
- When give for replacement therapy must increase dosage during times of stress
- All glucocorticoids raise glucose levels
cortisone
Theapeutic use
* Addison’s Disease
* Cortisone is a prodrug that undergoes conversion to hydrocortisone (it’s active form) in the body
* Dexamethasone (glucocorticoid)
* Prednisone (glucocorticoid)
* perferred drug for adrenal insufficent
Adverse effects
* when taken chronically or in large doses can be toxic
* adrenal suppression and promotion of cushings syndrome
* raise glucose levels
Fludrocortisone
- used for adrenal insufficiency
- Congenital adrenal hyperplasia (CAH)
- Primary hypoaldosteronism
- only mineralocorticoid advailable and drug choice for chronic mineralocorticoid replacement
- potent mineralocorticoid that possesses significant glucocorticoid actvity
Adverse effects
* when doses are too high, salt and water are retained in excess amounts and potassium is lost
* can cause expansion of blood volume, hypertension, edema, cardiac enlargement and hypokalemia
Pt. Edu
* monitor pt for wt gain, elevation of blood pressure and hypokalemia
Levothyroxine
Theapeutic use
* synthetic prep of thyroxin (thyroid hormone) and is identical to that of the natural hormone
* indicated for all forms of hypothyrodism
MOA
* Acts as thyroid hormone and is converted to T3 in the body (active thyroid hormone)
* increases basal metabolic rate, enhances glycogenolysis and stimulates protein synthesis
Adverse effects
* Rarely causes adverse effects inappropriate dosage
* Acute overdose: thyrotoxicosis can occur
* S/S: Tachycardia, n/v, skin dryness
* Angina, tremor nervousness insomnia hyperemia (fever), heat and tolerance and sweating
* Chronic over dosage is associated with accelerated bone loss and increased risk of atrial fibrillation
Drug Interactions:
Drugs that reduce levothyroxine absorption:
* H2 receptor blockers
* Proton pump inhibitors
* Sucralfate
* Cholestyramine
* Colestipol
* Aluminum containing and acids
* Calcium and Iron supplements
* Magnesium salts
* Orlistat
Drugs that accelerate levothyroxine metabolism
* Phenytoin,
* carbamazepine
* Rifampin
* Sertraline
* warfarin
* phenytoin
pt. edu
* Patients should separate levothyroxine and any drugs by 4 hours
- Take in the AM om empty stomach and 30 minutes before a meal
- When therapy is successful clinical evaluation should reveal a reversal of the signs and symptoms of thyroid deficiency and no signs of thyroid excess
- Measurement of serum TSH
- For most patients’ replacement therapy must be continued for life
- Levothyroxine can increase requirements for insulin and digoxin
- Effects of warfarin are enhanced, monitor INR
propylthiouracil (PTU)
- suppresses synthesis of thyroid hormone
** therapeutic uses**
* graves disease
* other hyperthyroid states
* thyroid strom
MOA
* Suppresses synthesis of thyroid hormone
* different from methimazole
* PTU can cause liver injury, methimazole does not
* PTU has a shorter half-life: 2-3 DOSES DAILY are needed versus once daily for methimazole
* PTU crosses the placenta less readily vs. methimazole
* can be used in 1st trimester of pregnancy
* blocks conversion of T4 to T3 in the periphery, methimazole does not
Adverse effects
* uticartia, rash, pruritus
* can cause liver injury
* agranulocytosis is the most dangerous toxicity- fever
* hypothyroidism can occur if given in high doses
PT. EDU
* monitor liver enzymes
* monitor S/S of agranulocytosis–> serious condition characterized by a dramatic reduction in circulating granulocytes
* sore throat and fever= early indications
* take pulse daily
* monitor CBCs for WBCs
Methimazole
- first line drug for hyperthyroidism
- inhibits thyroid hormone systheis
- safter and more convenient than PTU except women who are pregnant or breastfeeding
Therapeutic use
* graves diseases
* adjunct to radiation therapy
* suppresses thyroid hormone prior to surgery
* thyrotoxic crisis
MOA
* BLOCKING synthesis of thyroid hormones
* prevents the oxidation of iodine
* prevents iodinated tyrosines from coupling
* does not destroy existing stores of thyroid hormone nad may take 3 to 12 weeks to produce a euthyoid state
ADVERSE EFFECTS
* Aoid in women who are pregnant or breastfeeding
* Can cause neonatal hypothyroidism goiter and congenital hypothyroidism
* considered safe for use in the 2nd and 3rd trimester
* agranulocytosus is the most dangerous toxicity
* hypothyrodism can occur
pt. teaching
* agranulocytosis
* watch for sore throat and fever
* monitor CBC for WBCs
insulin peak// duration// onset
rapid acting
* clear, can be taken with food and mixed with other insulins
(Lispro)
onset: 15-30 min
peaks within 30-90 min (0.5-2.5 hr)
duration: 3-6 hrs
(Aspart)
Onset: 10-20 min
peak: 1-3 hours
duration: 3-5 hours
(gluisine)
Oneset: 10-15 min
peak: 1-1.5 hours
duration: 3-5 hours
regular insulin
*clear, can be mixed with other insulins
* used with sliding scale and meals (30 min prior)
* only insulin that can be given IV
onset: 30 min- 1 hr
peak: 1-5 hours
duration: 6-10 hours
intermediate-acting (NPH)
* cloudy, can be given with short acting insulins
onset: 1-2 hours
peak: 4-12 hours
duration: 18-28 hours
long-acting ( Glargine, Detemir)
* cloudy should not be mixed
(Glargine)
onset: 1-2 hours
Duration: 18-24 hours
peak: none
(Detemir)
Oneset: 1-2 hours
Duration: 12-24 hours
peak: none
ultura duration
oneset: 360 min
peak: none
Duration: >24 (36) hr
