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130 Cards in this Set

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  • Back
What proportion of insulin is released as a basal amount and as a bolus amount?
How long does an insulin bolus typically last?
2 hours
What is the amount of basal insulin released?
1 unit of insulin/hr regardless of food intake
How does bolus insulin act?
Limits postprandial hyperglycemia by stimulating glucose uptake by peripheral tissue; released in response to food
How is insulin secreted?
1. Glucose enters beta cells via Glut-2
2. K+ channels are blocked, causing membrane depolarization and opens Ca2+ channels
3. Ca2+ signal induces insulin secretion
What is diabetes mellitus?
Syndrome that develops when insulin secretion or activity are not sufficient to maintain normal blood glucose levels
How do Type 1 and Type 2 DM compare?
Type 1 results from beta cell destruction --> ABSOLUTE lack of insulin

Type 2 results from progressive insulin secretory defect and insulin resistance --> RELATIVE lack of insulin
What are some acute complications of DM?
Hypoglycemia; diabetic ketoacidosis (DKA); HHONK
What are some chronic complications of DM?
1. Microvascular -- retinopathy, nephropathy, neuropathy
2. Macrovascular -- CV, cerebrovascular, peripheral vascular disease
What are the goals for glycemic control?
Hgb A1c of <7.0% (or </= 6.5% with other sources)
How often should Hgb A1c levels be obtained?
Every 6 months for patients at goal

Quarterly for uncontrolled patients
What are non-glycemic goals for patients with DM?
1. BP < 130/80
2. LDL < 100 (<70 in CV patients)
3. Triglycerides < 150
What is the goal for peak postprandial glucose (1-2 hrs after meal)?
< 180
Why can insulin not be administered orally?
Peptide hormone -- would be denatured by stomach acid before it could take effect
In which Type 2 DM patients would insulin be appropriate?
1. Patients who cannot control their condition with diet, exercise, and oral meds
2. Newly diagnosed Type 2 presenting with severe, symptomatic hyperglycemia
What are the rapid-acting insulins?
insulin lispro, insulin aspart, insulin glulisine
When should rapid-acting insulin be administered?
Immediately before meal (onset: 15-30 min)
What routes can rapid-acting insulin be administered?
subQ and IV
How does rapid-acting insulin appear?
What are the short-acting insulins?
Regular novolin R, regular humulin R
When should short-acting insulin be administered?
30-45 min before meals (onset: 30 min)
What routes are possible for short-acting insulin?
subQ and IV (shorter duration of action)
What is the appearance of short-acting insulin?
What are the intermediate-acting insulins?
NPH humulin N, NPH novolin N
When is intermediate-acting insulin administered?
Usually administered once or twice daily (onset: 2-4 hrs); can be used as basal insulin
What is the appearance of intermediate-acting insulin?
How is intermediate-acting insulin administered?
subQ only
What are the long-acting insulins?
Insulin glargine, insulin detemir
Of the long-acting insulins, which does not have a peak?
Insuline glargine (Lantus)
When should long-acting insulin be administered?
Any time of day (depending on patient's eating habits) as long as it is consistently administered
What is the appearance of long-acting insulins?
What is the route of administration for long-acting insulins?
SubQ only
How does hepatic or renal failure affect insulin duration of action?
Liver disease -- glucose is not produced by liver so a little insulin goes a long way

Renal disease -- excretion is very slow so less insulin is required
How do insulin combination products work?
~30% is rapid/short-acting to cover meals
~70% is intermediate/long-acting to provide basal insulin
What are some guidelines for dosing insulin?
1. 1 unit of insulin will lower BG by 50-100
2. Start with low dose and titrate up
3. Wait 24 hrs before adjusting dose
How long are vials/pens of insulin valid for at room temperature?
28 days
What are the s/s of hypoglycemia?
Sympathetic: tachycardia, palpitations, sweating, and tremulousness
Parasympathetic: nausea and hunger
What is a possible consequence of not rotating injection sites?
How is hypoglycemia treated?
Mild (pt. conscious) -- simple sugar should be administered

Severe (unconscious) -- 20-50 ml of 50% dextrose IV; 1 mg glucagon subQ or IM
What is the MOA of sulfonylureas?
Increase secretion of pre-formed insulin by closing K+ channels (cause insulin release whether or not glucose is present)
What is the secondary effect of sulfonylureas?
Increase insulin receptor sensitivity and decrease hepatic glucose output
What is the #1 complication of sulfonylureas?
Which second gen. sulfonylureas are good for patients with renal dysfunction?
1. Glipizide (90% hepatic elimination)
2. glimepiride (100% hepatic elimination)
Why are first gen. sulfonylureas not favorable?
High frequency of hypoglycemia and lower potency
In which patients are sulfonylureas contraindicated?
Patients with sulfa allergies
What are some adverse effects of sulfonylureas?
Photosensitivity (wear sunscreen); Abnl liver fxn tests; weight gain
What is the MOA of meglitinides?
Same as sulfonylureas (increase secretion of pre-formed insulin by closing K+ channels)
How are meglitinides r/t sulfonylureas?
structurally similar but w/o sulfa moiety (okay for pts with sulfa allergies)
What drugs are meglitinides?
repaglinide; nateglinide
What are the potential advantages of meglitinides?
1. Rapid onset and short duration of action
2. Okay with renal insufficiency
3. May be okay with pts who skip meals
What are the adverse effects of meglitinides?
Hypoglycemia; weight gain
How are meglitinides metabolized?
Liver -- CYP 3A4; caution with drug-drug interactions
What is the MOA for biguanides?
Decrease hepatic glucose output
What are the secondary effects of biguanides?
Increase peripheral glucose uptake and utilization
What is the name of the medication in the biguanide class?
Metformin (glucophage)
What is the #1 reason for patients d/c biguanides (metformin)
GI intolerance (GI upset, lactic acidosis)
How are biguanides excreted?
100% renal
In which patients are biguandies contraindicated?
1. Renal impairment -- M creat >= 1.5; F creat >= 1.4
2. Hepatic impairment -- lactic acid elimination problem
3. Hypoxic states, acute/chronic alcohol abuse, elderly, CHF (on drug therapy)
What are some special considerations for patients using metformin?
Patient needs to be well-hydrated when undergoing diagnostic tests with iodinated contrast materials --> kidney dysfxn if dehydrated => metformin not excreted, leading to lactic acidosis
What are the alpha-glucosidase inhibitors?
acarbose; miglitol
What is the MOA for alpha-glucosidase inhibitors?
Potent competitive inhibitor of brush border alpha-glucosidases necessary for the breakdown of complex carbs
What are the adverse effects of alpha-glucosidase inhibitors?
Abdominal pain, flatulence, diarrhea

Acarbose -- increase LFTs at very high doses
In what patients is alpha-glucosidase inhibitor use contraindicated?
Significant GI disorders
What is the therapeutic effect of alpha-glucosidase inhibitors?
Delayed breakdown of carbs allows insulin time to be released --> insulin needed (Type 2 DM only)
What are the thiazolidinediones?
Rosiglitazone, pioglitazone
What is the MOA of thiazolidinediones?
Bind to the nuclear steroid hormone receptor and promote glucose uptake into skeletal and muscle/adipose tissue
What are the effects of thiazolidinediones?
1. Decrease insulin resistance
2. Increase insulin sensitivity
3. Do not effect insulin secretion
What are the adverse effects of thiazolidinediones?
Hepatotoxicity (LFT q6 mos.); edema (worse when combined with insulin)
What are the cautions/contraindications of thiazolidinediones?
May cause or exacerbate CHF

Contraindicated in patients with Class 3 or 4 heart failure
What are incretins?
GI hormones released in response to glucose (GLP-1, GIP); incretins are broken down by DPP-4
How does GLP-1 act?
1. Enhances glucose-dependent insulin secretion
2. Suppression of glucagon secretion
3. Slows the rate of gastric emptying
4. Reduces appetite
Which incretin mimetic functions as a GLP-1 agonist?
exenatide (Byetta)
What are some cautions for exenatide (Byetta)?
Not recommended in patietns with CrCl < 30

Use caution when starting or titrating up dose in patients with CrCl of 30-50

Contraindicated in patients with severe GI disorders
What are the adverse effects of exenatide (Byetta)?
Hypoglycemia (esp. in combo with sulfonylureas); nausea/diarrhea; headache, pancreatitis
Which incretin mimetics are DPP-4 inhibitors?
sitagliptin, saxagliptin
What is the therapeutic effect of DPP-4 inhibitors?
GLP-1 lasts longer (increased insulin secretion, glucagon suppression, etc.)
How is exenatide (Byetta) administered?
How are DPP-4 inhibitors (incretin mimetics) administered?
What are the adverse effects of DPP-4 inhibitors (incretin mimetics)?
1. No evidence of hypoglycemia to date
2. Recent cases of pancreatitis with sitagliptin
What drug is an amylin analogue?
pramlintide (Symlin)
What is the MOA of the amylin analogue?
1. Slows gastric emptying
2. Suppresses glucagon secretion
3. Decreases glucose output by liver
What is the therapeutic use of amylin analogues?
1. Adjunctive therapy with insulin for type 1 DM
2. Type 2 DM
How is the amylin analogue administered?
subQ only
What considerations should be given to amylin analogues?
1. Empiric insulin dose reduction necessary
2. Administer prior to meals
What are the adverse effects of amylin analogues?
Severe hypoglycemia (perhaps because of combo with insulin therapy); GI disturbances
In what cases should insulin be used early in Type 2 DM patients?
1. Hgb A1c > 10%
2. Random glucose > 300 or fasting glucose > 250
3. Hyperglycemic symptoms
4. Presence of urine ketones
What are the possible causes of HYPERthyroidism?
1. Graves disease
2. Thyroid-stimulating antibodies
3. Meds (amiodarone)
What occurs in HYPERthyroidism?
1. Elevated total T4 and free T4 serum concentrations
2. Suppressed TSH concentrations (except in TSH-secreting adenomas)
What is the purpose of surgery for HYPERthyroidism?
Removal of the thyroid gland once the patient is pharmacologically euthyroid
What are the most common complications of surgery for HYPERthyroidism?
1. Hypothyroidism
2. Hypoparathyroidism
3. Vocal cord abnormalities
What is the MOA of thioureas?
Inhibit iodination of tyrosine and the coupling of iodotyrosines

Does not affect release of preformed T4 and T3 (body still has to utilize pre-made TH)
What meds fall into the thioureas?
Propylthiouracil (PTU), methimazole
What additional MOA does PTU have?
Inhibits the peripheral conversion of T4 to T3
How long does it take for thioureas to act?
They have short half-lives but accumulate in the thyroid gland to exert longer effects --> patient becomes euthyroid in 1-2 months
What are the adverse effects of thioureas?
Rash; fluid retention; decreased WBC count

If decreased WBC count is not caught and treated early, can lead to long-term immunocompromise
What are the indications for iodine-containing compounds?
Used for pre-surgery to prevent active secretion of TH during surgery (MOA is the immediate inhibition of the release of T4 and T3)

Not used for routine tx
What are the names of common iodine-containing compounds?
Lugol's solutio, potassium iodide solutions (SSKI)
What are some adverse effects of iodine-containing compounds?
Rash, metallic taste, sore gums, GI discomfort, HYPOthyroidism
What is the MOA of beta-adrenergic antagonists?
1. Decrease symptoms of adrenergic stimulation caused by increased T4 concentrations
2. Inhibit peripheral conversion of T4 to T3
What is the most commonly used beta-adrenergic antagonist for HYPERthyroidism?
Propranolol (non-selective beta blocker)

Any beta blocker will have safe effect though
What are the adverse effects of a beta-adrenergic antagonist?
Decreased BP, bradycardia, cardiac arrest, CHF; asthma
What is the MOA of corticosteroids for HYPERthyroidism?
1. Decrease thyroid action
2. Decrease immune response in Grave's disease
How does radioactive iodine work?
Concentrates in the thyroid and destroys thyroid tissue
What may be used as adjunctive therapy until radioactive therapy takes effect?
Beta-adrenergic antagonists can be used to control symptoms
What is an absolute contraindication for radioactive iodine?
Pregnancy -- will destroy baby's thyroid gland too
What are the possible causes of HYPOthyroidism?
1. Hashimoto's thyroiditis
2. Surgery
3. Meds (radioactive iodine, lithium, amiodarone)
What are the diagnostic criteria for HYPOthyroidism?
1. Decreased total T4 and free serum T4
2. Elevated TSH concentrations
3. Thyroid antibodies
What are the goals of therapy for HYPOthyroidism?
1. Restore normal thyroid concentrations in tissue
2. Provide symptomatic relief
What are the natural thyroid hormones?
Thyroid -- made from desiccated hog, beef, or sheep thyroid

Thyroglobulin -- purified hog gland extract
Why are natural thyroid hormones less favorable?
1. Bioavailability is unpredictable
2. Allergies (animal products)
What synthetic thyroid hormones are available?
Levothyroxine, liothyronine, liotrix
Which synthetic thyroid hormone is the drug of choice and why?

Advantages: chemically stable, inexpensive, free of antigenicity
Which synthetic thyroid hormone has a higher incidence of cardiac events?
Liothyronine -- dysrhythmias
What special consideration must be paid to levothyroxine?
It is a pro-drug so it must be activated in body
--> takes 2-3 weeks to get to steady state of T4 to T3 conversion
What are the adverse effects of levothyroxine?
Heart failure, angina, MI; HYPERthyroidism
What dose adjustments should be made for elderly patients or patients with hx of heart disease taking levothyroxine?
Half the dose
What is the primary action of the hypothalamus-pituitary-adrenal system?
Regulate the production of cortisol
Whats is the peak secretion time of cortisol?
When do MI's often occur?
Morning hours because that is when cortisol levels are the highest
How does negative feedback affect cortisol?
Occurs when cortisol blood levels exceed those produced by usual physiological amounts (cortisol production decreases)
What is stress feedback in r/t cortisol?
When the body is stressed this results in an increase in cortisol production
What are the indications for corticosteroids in patients experiencing adrenal insufficiency?
1. Adrenal crisis
2. Addisonian crisis

--> replacement of corticosteroids
What formulations are corticosteroids available as?
1. Oral (100% absorption)
2. IV (succinate)
3. IM (acetate)
Which form of corticosteroids should NOT be used for patients in crisis?
IM (acetate) -- formulated to work over time
Which corticosteroid has no mineralcorticoid effect?
What is the MOA of mitotane (Lysodren)?
1. Blocks cortisol synthesis through inhibition of 11-beta-hydroxylation
2. Destroys functional adrenal tissue
What are the adverse effects of mitotane?
Abdominal discomfort; lethargy
What is the MOA of ketoconazole and etomidate?
Inhibits enzymes that produce cortisol
What is the therapeutic effect of ketoconazole and etomidate?
Controls cortisol production -- steroid replacement is not necessary (adrenal tissue remains functional)
What are the adverse effects of ketoconazole?
Gynecomastia; abdominal discomfort; reversible hepatic transaminase elevations