NR508 Week 4-Midterm
Roles and Responsibilities of APRN
1. All states have title protection for NP
2. All but 5 states stat's board of nursing control practice and licensure.
3. Scope of practice determined by individual NP license of licensing jurisdiction.New prescribers must know
the rules
4. in 17 states, NPs have independent scope of practice and prescriptive authority.
5.6 states have full autonomous practice and prescriptive authority.
Clinical Judgement in prescribing
1. Best therapy
2. Least expensive
3. Least likely to cause ADR
4. Clear indication for drug?
5. Are drugs effective in treating disorder?
6. What is goal of therapy?
7. Under what conditions is it determined that drug is not meeting goal and change should be made?
8. Unnecessary duplications?
9. OTC be just as useful?
10. Cost?
Collaboration with other prescribers
1. Physician: can offer insight
2. Pharmacists: pharm knowledge
3. Other APRNs: clinical experience shared and collaboration
4. PAs
5. RNs.
Autonomy and prescriptive authority
1. More states are broadening and expanding legal, reimbursement, and prescriptive authority.
2. Gains can be reversed, so address concerns.
3. Some push for physician control.
Alpha2Agonists: MOA
1. Activation of central alpha 2 receptors results in inhibition of cardioacceleration and vasoconstriction
centers in brain.
,2. Lead to decrease in peripheral outflow of norepinephrine which leads to decrease in:
a. peripheral resistance
b. renal vascular resistance
c. heart rate
d. blood pressure
3. Decrease in BP is due to sympathetic function therefore sodium retention and increased blood volume may
occur: give with diuretic.
4. Second or third line HTN drug treatment.
Alpha2Agonists: Drugs in class
1. Clonidine
2. guanabenz
3. guanfacine
4. methyldopa.
Alpha2Agonists: Clonidine, off-label use
Tx of withdrawal d/t ability to lower adrenergic stimulation associated with withdrawal.
Alpha2Agonists: ADRs
Oral and transdermal doses:
bradycardia, AV block, palpitations, tachycardia, hallucinations, sleep disorders, contact dermatitis, dry
mouth, orthostatic hypotension, constipation, nausea, urinary retention, decreased sexual activity, weight
gain, leg gramps, and thrombocytopenia.
MOST COMMON: dry mouth
Alpha2Agonists: Discontinue instructions
Do not stop abruptly d/t lack of alpha 2 receptors impair homeostatic balance that regulates SNS:
Gradual taper over 4 days.
Alpha2Agonists: Guanabenz and guanfacine
1. Used to treat HTN.
2. EXR guanfacine: ADHD
Alpha2Agonists: Methyldopa
1. Parallels synthesis of norepinephrine (NE)
2. Stimulation by this metabolite: decrease in sympathetic outflow to the heart, kidneys, and blood vessels.
3. End result: decreased in BP, peripheral resistance, HR, sl. decrease in CO. Produces renal vascular
resistance.
4. Positive coombs test
5. Rarely hemolytic anemia.
, Beta-adrenergic antagonists: affects on body systems
1. Heart: Highest # of receptors are in heart: decreased HR in rapid rhythms, angina, BP, reflex orthostatic
tachycardia.
2. Renal: Receptors in juxtaglomerular apparatus of kidney reduces release of renin. Decrease in BP.
3. Respiratory: Receptors interfere with endogenous adrenergic bronchodilator activity therefore increase
airway restriction which is problem in pt with reactive airway diseases like asthma.
4. Ocular: Decrease intraocular pressure.
5. Metabolic and endocrine: Inhibit lipolysis resulting in increased TG and Cholesterol and decreased HDL.
Also increased glucose production and inhibits insulin secretion.
Beta-adrenergic antagonists: ADRs
Usually mild and transient and rarely require d/c of drug.
1. Cardiovascular: Bradycardia, CHF with pulm edema, hypotension
2. CNS: Decreased O2 to brain d/t hypotension, anxiety, depression, drowsiness, insomnia, nightmares,
mental status changes. Esp seen in older adults.
3. Endocrine: Hyper/hypoglycemia, unstable DM.
4. Gastrointestinal: Dry mouth uncommon but maybe. Changes in GI motility: anorexia, n/v, flatulence,
constipation.
5. GU: Impotence or decreased libido.
6. Resp: Bronchospasm and dyspnea. Nasal stuffiness.
7. Less common: muscle and joint pain, rashes, facial swelling.
Beta-adrenergic antagonists: Abrupt withdrawal
1. May precipitate life-threatening arrhythmias, hypertension, MI, severe angina, and death.
2. Taper by one-half every 4 days.
Beta-adrenergic antagonists: Absorption and distribution
1. Well absorbed and distributed
2. Crosses: placenta and breast milk
3. Lipid solubility determines CNS penetration.
Beta-adrenergic antagonists: metabolism and excretion
1. Metab extensively by liver and eliminated by bile and feces.
2. Dosage adj in hepatic impair.
3. Nebivolol: larger percent of pop: extensive metabolizers-half life 12 hours. Sm. percent of pop: poor
metabolizers-half life 19 hrs.
4. Some require dose adjust in renal (atenolol, nadolol, nebivolol, acebutolol).
Beta-adrenergic antagonists: precautions and contraindications
Roles and Responsibilities of APRN
1. All states have title protection for NP
2. All but 5 states stat's board of nursing control practice and licensure.
3. Scope of practice determined by individual NP license of licensing jurisdiction.New prescribers must know
the rules
4. in 17 states, NPs have independent scope of practice and prescriptive authority.
5.6 states have full autonomous practice and prescriptive authority.
Clinical Judgement in prescribing
1. Best therapy
2. Least expensive
3. Least likely to cause ADR
4. Clear indication for drug?
5. Are drugs effective in treating disorder?
6. What is goal of therapy?
7. Under what conditions is it determined that drug is not meeting goal and change should be made?
8. Unnecessary duplications?
9. OTC be just as useful?
10. Cost?
Collaboration with other prescribers
1. Physician: can offer insight
2. Pharmacists: pharm knowledge
3. Other APRNs: clinical experience shared and collaboration
4. PAs
5. RNs.
Autonomy and prescriptive authority
1. More states are broadening and expanding legal, reimbursement, and prescriptive authority.
2. Gains can be reversed, so address concerns.
3. Some push for physician control.
Alpha2Agonists: MOA
1. Activation of central alpha 2 receptors results in inhibition of cardioacceleration and vasoconstriction
centers in brain.
,2. Lead to decrease in peripheral outflow of norepinephrine which leads to decrease in:
a. peripheral resistance
b. renal vascular resistance
c. heart rate
d. blood pressure
3. Decrease in BP is due to sympathetic function therefore sodium retention and increased blood volume may
occur: give with diuretic.
4. Second or third line HTN drug treatment.
Alpha2Agonists: Drugs in class
1. Clonidine
2. guanabenz
3. guanfacine
4. methyldopa.
Alpha2Agonists: Clonidine, off-label use
Tx of withdrawal d/t ability to lower adrenergic stimulation associated with withdrawal.
Alpha2Agonists: ADRs
Oral and transdermal doses:
bradycardia, AV block, palpitations, tachycardia, hallucinations, sleep disorders, contact dermatitis, dry
mouth, orthostatic hypotension, constipation, nausea, urinary retention, decreased sexual activity, weight
gain, leg gramps, and thrombocytopenia.
MOST COMMON: dry mouth
Alpha2Agonists: Discontinue instructions
Do not stop abruptly d/t lack of alpha 2 receptors impair homeostatic balance that regulates SNS:
Gradual taper over 4 days.
Alpha2Agonists: Guanabenz and guanfacine
1. Used to treat HTN.
2. EXR guanfacine: ADHD
Alpha2Agonists: Methyldopa
1. Parallels synthesis of norepinephrine (NE)
2. Stimulation by this metabolite: decrease in sympathetic outflow to the heart, kidneys, and blood vessels.
3. End result: decreased in BP, peripheral resistance, HR, sl. decrease in CO. Produces renal vascular
resistance.
4. Positive coombs test
5. Rarely hemolytic anemia.
, Beta-adrenergic antagonists: affects on body systems
1. Heart: Highest # of receptors are in heart: decreased HR in rapid rhythms, angina, BP, reflex orthostatic
tachycardia.
2. Renal: Receptors in juxtaglomerular apparatus of kidney reduces release of renin. Decrease in BP.
3. Respiratory: Receptors interfere with endogenous adrenergic bronchodilator activity therefore increase
airway restriction which is problem in pt with reactive airway diseases like asthma.
4. Ocular: Decrease intraocular pressure.
5. Metabolic and endocrine: Inhibit lipolysis resulting in increased TG and Cholesterol and decreased HDL.
Also increased glucose production and inhibits insulin secretion.
Beta-adrenergic antagonists: ADRs
Usually mild and transient and rarely require d/c of drug.
1. Cardiovascular: Bradycardia, CHF with pulm edema, hypotension
2. CNS: Decreased O2 to brain d/t hypotension, anxiety, depression, drowsiness, insomnia, nightmares,
mental status changes. Esp seen in older adults.
3. Endocrine: Hyper/hypoglycemia, unstable DM.
4. Gastrointestinal: Dry mouth uncommon but maybe. Changes in GI motility: anorexia, n/v, flatulence,
constipation.
5. GU: Impotence or decreased libido.
6. Resp: Bronchospasm and dyspnea. Nasal stuffiness.
7. Less common: muscle and joint pain, rashes, facial swelling.
Beta-adrenergic antagonists: Abrupt withdrawal
1. May precipitate life-threatening arrhythmias, hypertension, MI, severe angina, and death.
2. Taper by one-half every 4 days.
Beta-adrenergic antagonists: Absorption and distribution
1. Well absorbed and distributed
2. Crosses: placenta and breast milk
3. Lipid solubility determines CNS penetration.
Beta-adrenergic antagonists: metabolism and excretion
1. Metab extensively by liver and eliminated by bile and feces.
2. Dosage adj in hepatic impair.
3. Nebivolol: larger percent of pop: extensive metabolizers-half life 12 hours. Sm. percent of pop: poor
metabolizers-half life 19 hrs.
4. Some require dose adjust in renal (atenolol, nadolol, nebivolol, acebutolol).
Beta-adrenergic antagonists: precautions and contraindications
