of angiotension I to angiotensin II<\/li>\n\n\n\n
blocking the enzyme kininase II<\/li>\n<\/ol>\n\n\n\n
\uf0b7 Mechanism of action of Digoxin
Correct Answer:
inhibition of Na\/K ATPase in the plasma membrane
=increased calcium in sarcoplasmic reticulum
= excitation coupling occurs
= increased cardiac contractibility (intropy)<\/p>\n\n\n\n
- \n
- SA node is depressed by stimulating vagal activity<\/li>\n\n\n\n
- prolonged AV node conduction via vagal stimulation
*decreases activation of sympathetic nervous system<\/li>\n\n\n\n - increases CO and cause diuresis<\/li>\n\n\n\n
- not as effective in high output failure
*improved quality of life but no decrease in mortality<\/li>\n<\/ul>\n\n\n\n\uf0b7 Antihypertensive medication classes contraindicated in asthma.
Correct Answer:
Beta blockers- increased bronchial obstruction and airway reactivity, may
exacerbate COPD\/asthma
ACEs- can cause cough (then use ARB)
***Ca++ channel blockers are preferred with asthma & COPD
\uf0b7 Mechanism of action of Penicillin.
Correct Answer:
Inhibition of forming bacterial cell wall by interfering with the final stage of
peptidoglycan synthesis.<\/p>\n\n\n\n- \n
- bind to the active site of PBPs(Penicillin Binding Proteins). This prevents
cross-linking peptides from binding to the tetrapeptide side chains.<\/li>\n\n\n\n - activates autolytic enzymes
\uf0b7 Uses of PCN
Correct Answer:
mild to moderately severe infections such as pneumococcus, staphyloccus,
group A strep, T.Pallidum (syphillus and diptheria), h influenza, shigella,
gonorrhea and e-coli.<\/li>\n<\/ul>\n\n\n\n\uf0b7 Uses of beta-blockers
Correct Answer:
HTN, Angina, Secondary prevention post-MI, Chronic HF, Arrhythmias. Other
uses for nonselective BB include prophylactic treatment of migraines, graves’
disease, glaucoma, hypertrophic subaortic stenosis, and essential tremors.
Powered by https:\/\/learnexams.com\/search\/study?query=<\/a><\/p>\n\n\n\nfirst-line treatment for Heart failure<\/a><\/p>\n\n\n\n
Diuretics (if fluid retention is present), ACE inhibitors, Beta-Blockers, and digoxin (if systolic heart failure, a-fib, or diuretic failure) *use ARB’s if ACEI’s are contraindicate)<\/a><\/p>\n\n\n\n
Beta-blocker meds<\/a><\/p>\n\n\n\n
Bisoprolol, carvediol, and metoprolol (common)
Others:
atenolol (Tenormin)
bisoprolol fumarate (Zebeta)
carteolol (Cartrol, discontinued)
carvedilol (Coreg)
labetalol (Trandate [Normodyne – discontinued])
metoprolol (Lopressor, Toprol XL)
nadolol (Corgard)
penbutolol (Levatol)
propranolol (Hemangeol, Inderal LA)
timolol ophthalmic solution (Timoptic, Betimol, Istalol)<\/a><\/p>\n\n\n\nthiazide diuretics meds<\/a><\/p>\n\n\n\n
chlorothiazide [(Diuril) (oral or sodium injection)]
chlorthalidone (Hygroton)
indapamide (Lozol)
hydrochlorothiazide (Hydrodiuril)
methyclothiazide (Enduron)
metolazone (Zaroxolyn, Diulo, Mykrox)<\/a><\/p>\n\n\n\nloop diuretic meds<\/a><\/p>\n\n\n\n
Bumetanide (Bumex)
Ethacrynic acid (Edecrin)
Furosemide (Lasix)
Torsemide (Demadex)<\/a><\/p>\n\n\n\nk-sparing diuretic meds<\/a><\/p>\n\n\n\n
Amiloride.
Eplerenone (Inspra)
Spironolactone (Aldactone)
Triamterene (Dyrenium)<\/a><\/p>\n\n\n\nAce-Inhibitor meds<\/a><\/p>\n\n\n\n
Lisinopril (Prinivil, Zestril)
Benazepril (Lotensin)
Captopril
Enalapril (Vasotec)
Fosinopril
Moexipril
Perindopril (Aceon)
Quinapril (Accupril)
Ramipril (Altace)
Trandolapril (Mavik)<\/a><\/p>\n\n\n\nangiotensin II receptor blockers<\/a><\/p>\n\n\n\n
Azilsartan (Edarbi)
Candesartan (Atacand)
Eprosartan.
Irbesartan (Avapro)
Losartan (Cozaar)
Olmesartan (Benicar)
Telmisartan (Micardis)
Valsartan (Diovan)<\/a><\/p>\n\n\n\nOther medications to control heart failure (after first line not sufficient)<\/a><\/p>\n\n\n\n
Spironolactone
Nitrates and hydralazine (lower mortality in class 3&4 for African American)
Calcium channel blockers
(Can worsen hf use caution **BUT NEVER IN SYSTOLIC DYSFUNCTION)<\/a><\/p>\n\n\n\ntreatment of Acute (decomponsated) heart failure<\/a><\/p>\n\n\n\n
L – loop
M – morphine
N -nitrates\/nitroprusside\/nesiritride
O – oxygen
P – positioning
Nitroprusside- vasodilator
Nesiritride- atrial peptide , vasodilator and diuretic
IV loop diuretics
– Cause venodilation and diuresis – Reduces pre-load
IV opiates (e.g. morphine)
– Reduce anxiety
– Vasodilates, reducing preload
– Reduces sympathetic drive
– Not routinely offered
IV, buccal or sublingual nitrates (Glyceryl trinitrates “GTN”)
– Reduce preload and afterload
– vasodilates
Oxygen >> maintains O2 sats
(Positioning – keep patient upright)<\/p>\n\n\n\nTreatment of pulmonary edema<\/a><\/p>\n\n\n\n
Furosemide
-40 mg
-IV PUSH
slowly over 1 to 2 minutes
2) Bumentadine
-diruetic
3) Nitroglycerine
-decrease afterload
-increase CO
4) Morphine
-vasodilation
5) Nesirtide
-dont give for more than 48 hrs
-turn off 2 hours b4 drawing BNP
-vasodilates veins and arteries<\/a><\/p>\n\n\n\nside effects of Ace inhibitors<\/a><\/p>\n\n\n\n
CATCHH
Cough
Angioedema\/abdominal pain
Teratogen (fetal renal malformations)
Creatinine increased
Hyperkalemia
Hypotension
Others * leukopenia, myalgia, headache, renal insufficiency.<\/a><\/p>\n\n\n\nMethod of action of ace inhibitors<\/a><\/p>\n\n\n\n
1. inhibits angiotensin converting enzyme (ACE), interfering with conversion of angiotension I to angiotensin II
2. inhibit the breakdown of bradykinin to potent\/natural vasodilator by blocking the enzyme kininase II<\/a><\/p>\n\n\n\nantihypertensive medication classes contraindicated in asthma.<\/a><\/p>\n\n\n\n
Beta blockers- increased bronchial obstruction and airway reactivity, may exacerbate COPD\/asthma
ACEs- can cause cough (then use ARB)
***Ca++ channel blockers are preferred with asthma & COPD<\/a><\/p>\n\n\n\nmechanism of action of Digoxin<\/a><\/p>\n\n\n\n
inhibition of Na\/K ATPase in the plasma membrane
=increased calcium in sarcoplasmic reticulum
= excitation coupling occurs
= increased cardiac contractibility (intropy)
* SA node is depressed by stimulating vagal activity
* prolonged AV node conduction via vagal stimulation
*decreases activation of sympathetic nervous system
* increases CO and cause diuresis
* not as effective in high output failure
*improved quality of life but no decrease in mortality<\/p>\n\n\n\n![\"Image:](\"https:\/\/quizlet.com\/cdn-cgi\/image\/f=auto,fit=cover,h=100,onerror=redirect,w=120\/https:\/\/o.quizlet.com\/zvNC.O0dZkmQ.XinZv2R9A.png\")
<\/figure>\n\n\n\nmechanism of action of Penicillin.<\/a><\/p>\n\n\n\n
Inhibition of forming bacterial cell wall by interfering with the final stage of peptidoglycan synthesis.
– bind to the active site of PBPs(Penicillin Binding Proteins). This prevents cross-linking peptides from binding to the tetrapeptide side chains.
– activates autolytic enzymes<\/a><\/p>\n\n\n\nuses of PCN<\/a><\/p>\n\n\n\n
mild to moderately severe infections such as pneumococcus, staphyloccus, group A strep, T.Pallidum (syphillus and diptheria), h influenza, shigella, gonorrhea and e-coli.<\/a><\/p>\n\n\n\n
Uses of beta-blockers<\/a><\/p>\n\n\n\n
HTN, Angina, Secondary prevention post-MI, Chronic HF, Arrhythmias. Other uses for nonselective BB include prophylactic treatment of migraines, graves’ disease, glaucoma, hypertrophic subaortic stenosis, and essential tremors.<\/a><\/p>\n\n\n\n
![\"Image:](\"https:\/\/quizlet.com\/cdn-cgi\/image\/f=auto,fit=cover,h=200,onerror=redirect,w=240\/https:\/\/o.quizlet.com\/i\/paIegSrgXHz_DMm6nRDKMw.jpg\")
<\/figure>\n\n\n\nAction of Beta blockers<\/a><\/p>\n\n\n\n
Competitive blockade of the beta adrenergic receptor.
= decreased HR, contractility, bp, & oxygen demand
* Decreased HR and contractility r\/t slower AV conduction system & prolonged the refractory period
*Decreased BP r\/t decreased cardiac output
*Slows renin release due to decreased sympathetic peripheral outflow (carteolol, labetolol, and pindolol do not consistently inhibit renin release)
Beta receptors (found in heart and stimulation from catecholamines causes an increased HR, BP, contractility & av conduction and decrease av node refractory period)<\/p>\n\n\n\n![\"Image:](\"https:\/\/quizlet.com\/cdn-cgi\/image\/f=auto,fit=cover,h=200,onerror=redirect,w=240\/https:\/\/o.quizlet.com\/rfJksgLqqIVRpt7O0ag6bA.jpg\")
<\/figure>\n\n\n\nSide Effects of Beta Blockers<\/a><\/p>\n\n\n\n
weight gain, bradycardia, flatulence, gastritis, nausea, constipation, sexual dysfunction, impotence, decreased libido, pharyngitis, joint pain, dizziness, vertigo, cough, nasal stuffiness, rash, and visual disturbances.
(sleepy heart is sick in bed)
1. Sleepy Heart = bradycardia
2. Sick = gastritis, dizzy, cough, nasal stuffiness, rash, constipated, nausea, pharyngitis, joint pain, vertigo, visual disturbances
3. Bed = impotence and decreased libido<\/p>\n\n\n\nCautions for Beta blockers<\/a><\/p>\n\n\n\n
CAUTION
Heart Conditions: heart block, sinus bradycardia, cardiogenic shock, or acute heart failure.
Diabetics: may intensify hypoglycemia and prolong gluconeogenesis through inhibited release of insulin.
Not first line therapy for Hypertension r\/t risk for developing DM<\/a><\/p>\n\n\n\nWhen to start beta-blockers for heart failure<\/a><\/p>\n\n\n\n
Per lecture slide: Beta blockers decrease mortality BUT CAN worsen heart failure if started during Acute Heart Failue
ADD when stable: AFTER diuresis & other meds are started<\/a><\/p>\n\n\n\nUses for tetracyclines<\/a><\/p>\n\n\n\n
aerobic and gram positive and gram negative bacteria. Examples.are rickettsia, mycoplasma, protozoa, chlamydia, malaria and bacteria exacacerbation of COPD. Ineffective against fungus\/viruses<\/a><\/p>\n\n\n\n
mechanism of action of Tetracyclines.<\/a><\/p>\n\n\n\n
inhibit protein synthesis on the susceptible organism by binding to the 30S ribosome subunit which impedes the binding of aminoacyl tRNA to the receptor site on the messenger RNA ribosome complex.<\/a><\/p>\n\n\n\n
Side effects of tetracyclines<\/a><\/p>\n\n\n\n
loss of appetite, jaundice, abdominal pain which could be possible hepatotoxicity. Change of mental status may be due to intercranial pressure. May also have anaphylaxis, periorbital edema, rashes or systemic lupus erythematous-like syndrome. May increase AST, ALT, BUN, amylase, bilirubin and serum alkaline phosphatase.<\/p>\n\n\n\n
usage of Antiarrhythmic’s<\/a><\/p>\n\n\n\n
-paroxysmal SVT, a-fib, PVC’s<\/a><\/p>\n\n\n\n
mechanism of action of Antiarrhythmic Agents.<\/a><\/p>\n\n\n\n
educe electrical irregularity of the heart by altering the action potential of cardiac cells.
-Class IA drugs (quinidine, disopyramide, procainamide) depress rapid depolarization of the action potential.
-Class IB drugs (lidocaine, mexiletine, tocainide) exert less effect on sodium channels at rest but are more prominent during depolarization.
-Class IC drugs (flecainide, propafenone) depress phase 0 markedly and profoundly slow conduction.
-Class II (beta-blockers) work by inhibiting sympathetic stimulation.
-Class III (amiodarone, dronedarone, ibutilide, dofetilide, sotalol) prolong phase 3 repolarization by blocking potassium channels.
-Class IV (verapimil, diltiazem) inhibit calcium ion influx through slow channels into conductile and contractile myocardial cells & vascular smooth muscle cells; also slow AV conduction & prolong effective refractory period w\/in AV node.<\/p>\n\n\n\nSide effects of Antiarrhythmic Agents.<\/a><\/p>\n\n\n\n
(N\/V\/D, abd pain, light-headedness, headache, palpitations)
-amiodarone (photosensitivity, skin discoloration)
-digoxin (yellow halo around objects, nausea, decreased appetite, fatigue)
-esmolol (bradycardia, reduced exercise capacity, HF, hypertension, AV block, bronchoconstriction, fatigue)
-procainamide (nausea, prolonged use may lead to lupus-like syndrome)
-disopyramide (dry mouth, blurred vision, constipation, urinary retention, acute angle-closure glaucoma (rare), may cause or worsen CHF, hypotension.<\/a><\/p>\n\n\n\ntreatment of Parkinson’s disease<\/a><\/p>\n\n\n\n
First line drugs….. Levodopa, dopamine agonists, Radagiline.
Nonpharmacologic trx…optimize the pt’s general health, nutrition, emotional and neuromuscular status, group support, exercise, and education
carbidopa goes with levodopa to avoid levodopa being broken down in the periphery<\/a><\/p>\n\n\n\nfirst line treatment of depression.<\/a><\/p>\n\n\n\n
First line is generally NON-Pharmacologial – such as counseling, therapy, life-style changes, cognitive behavioral therapy
But……
First line pharmacological: SSRIs, except fluvoxamine, SNRIs (Venlafaxine), NDRIs (buporopion)
– Second line: SNRis, NDRIs, TCAs
-Third line: SARIs, MAOIs
– SSRIs are frequently chosen as a first-line agent because of their side effect profile and the relative lack of danger associated with overdose.
-Venlafaxine has a higher incidence of nausea and vomiting than the SSRIs. May be associated with an increased risk of cardiovascular events
– Paroxetine and mirtazapine result in higher weight gain. Most antidepressants studied beyond 3-6 months are associated with significant weight gain unrelated to response.
-Bupropion has a significantly lower rate of sexual adverse events than the SSRI.
– Paroxetine has the highest rate of sexual dysfunction than other SSRIs
– SSRIs are associated with an increase risk for nonfatal suicide attempts and may be associated with higher risk of side effects in older patients than older antidepressants.
– Bupropion may be associated with an increased risk of seizures
– Trazadone is associated with higher incidence of somnolence
Treatment
\u2022 Establish diagnosis
\u2022 Assess suicide risk
\u2022 Institute counseling or psychotherapy (this is often ignored or ineffectively communicated)
\u2022 Enlist patient participation in nonpharmacologic treatment such as exercise
\u2022 Begin drug therapy as needed. Choose based on adverse effect profile, cost, and patient preference
\u2022 Assess patient status, therapeutic response, and adverse effects of therapy on a regular basis; monitor for increased suicidal thoughts and behaviors.
Pg. 523
*Just some extra info<\/p>\n\n\n\npreferred antidepressants used in the elderly (less anticholgenic effects)<\/a><\/p>\n\n\n\n
SSRI’s- Fluoxetine (Prozac), Praoxetine ( paxil), citalopram (celexa), escitalopram (lexapro)
MAOI’S- phenelzine ( nardil), tranylcypromine (parnate)
Bupropion- is an SSNRI- (other name Wellbutrin)
Nefazodone- is an SARI & SSRI (serotonin 2 agonists\/blockers\/serotonin reuptake inhibitor
SSNRI’s- venlafaxine (Effexor)
Mirtazapine- (remeron)- \u03b12- non adrenergic antagonist
** note Citalopram, fluoxetine, and fluvoxamine have weak cholinergic inhibition
Elderly need lower dosages due to renal and hepatic dysfunction that will.slow drug metabolism and excretion. SSRSs produces more anticholinergic side effects, and is less tolerated. NonSSRIs antidepressants such as bupropion or venlafaxine has increased risks of falls. TCAs causes anticholinergic effects such as orthostasis, sedation and urinary retention. Avoid amitriptyline
SSRIs considered to have the best safety profile in the elderly are citalopram, escitalopram, and sertraline. Of the SSRIs, fluoxetine is generally not recommended for use in the elderly because of its long half-life and prolonged side effects. Paroxetine is also typically not recommended for use in the elderly as it has the greatest anticholinergic effects<\/p>\n\n\n\n6 common SSRIs<\/a><\/p>\n\n\n\n
FLU FLU PECS
Fluoxetine
Fluvoxamine
Paroxetine
Escitalopram
Citalopram
Sertraline
OR FLashbacks PARalyze SEnior CITizens
Fluoxetine\/Fluvoamine Paroxetine Sertraline Citalopram (Escitalopram)<\/a><\/p>\n\n\n\nadverse effects associated with SSRIs<\/a><\/p>\n\n\n\n
anxiety, agitation, anorexia, GI distress, headache, hypotension, sexual dysfunction
Nausea, decreased sexual function, weight gain
Serotonin syndrome: hyperacticity, tachycardia, hypertension, tremors, GI upset, sweating, AMS, fever agitation, myoclonus, hyperthermia (will occur within 24hrs, treated with supportive care)
Hyperthermia is hallmark sign according to ppt
Headache
*Sweating
*Anxiety and Agitation
*GI effects (n\/v\/d)
*Changes in weight
*Weakness and fatigue
*Sleep disturbances (insomnia or somnolence)
*Sexual dysfunction
*Serotonin Syndrome
*SIADH
*Bruxism (grinding, clenching, or gnashing of teeth)<\/p>\n\n\n\nAnti-depressant actions SSRI’s and SNRI’s<\/a><\/p>\n\n\n\n
All current antidepressants act on neurotransmitter systems by affecting three distinct processes: neurotransmitter degradation, neurotransmitter reuptake, and neurotransmitter binding.
\u2022 Degradation of all three neurotransmitter is accomplished by monoamine oxidase (MAO) enzyme. The catechol-O-methyltransferase (COMT) enzyme degrades norepinephrine and dopamine
\u2022 Another mechanism of action of antidepressants involves inhibiting the reuptake of neurotransmitters in the synapse. Neurotransmitters are removed from the synapse by reuptake pump on the presynaptic neuron. Inhibiting this reuptake enhances the amount of transmitter in the synapse.
\u2022 The third mechanism of action of antidepressants involves neurotransmitter receptor binding sensitization. This is a delayed effect.
\u2022 SSRIs: work by increasing the amount of serotonin by blocking the presynaptic serotonin reuptake pump. There are at least 14 different postsynaptic serotonin receptors present in humans. Each one controls a different physiological and\/or psychiatric function. The action of SSRIs depends on which postsynaptic receptor is stimulated. It is believed that receptor 5-HT1A is primarily responsible for antidepressant effects and the other receptor subtype may be responsible for the side effects of SSRIs
\u2022 SNRI: Venlafaxine (Effexor) and desvenlafaxine are non-tricyclic antidepressants with dual serotonin and norepinephrine reuptake inhibition and weak reuptake inhibition of dopamine, that demonstrates efficacy for depression and produces less side effects than tricyclics. They do act on all three of the monoamine neurotransmitters, as do the TCAs. Different from TCA but like SSRIs, venlafaxine has virtually no affinity for muscarinic, histaminergic, or \u03b11-adrenergic receptors. The side effects are closer to SSRI than TCA. At high doses there’s a risk for high blood pressure. Another SNRIs is duloxetine hydrochloride (Cymbalta) which is approved for major depressive disorder. Milnacipran is a non-FDA-approved antidepressant.
all antidepressants act on neurotransmitter systems by affecting three distinct processes: neurotransmitter degradation, neurotransmitter reuptake, and neurotransmitter binding.
SSRI’s (Selective Serotonin reuptake inhibitors): first line meds<\/strong> increase the amount of serotonin by blocking the presynaptic serotonin reuptake pump.
-Fluoxetine (Prozac)
-Paroxetine (Paxil)
-Citalopram (Celexa)
-Escitalopram (Lexapro)
SNRI’s (Serotonin\/Norepinephrine reuptake inhibitors): increase the amount of serotonin\/norepinephrine by blocking the presynaptic serotonin\/norepinephrine reuptake pump.
-Venlafaxine (Effexor)
-Duloxetine (Cymbalta)
SARI’s (Serotonin 2 Agonist\/serotonin reuptake inhibitors): similar to SSRI’s; but block re-uptake both pre & post synaptically; block 5-HT receptors.
-Trazadone (Desyrel)
-Nefazodone (Serzone)
NDRI’s (Norepinephrine & Dopamine reuptake inhibitors): increase the amount of dopamine\/norepinephrine by blocking the presynaptic dopamine\/norepinephrine reuptake pump.
-Buproprion (Wellbutrin)
TCA’s (Tricyclinc antidepressants): block reuptake of norepinephrine & serotonin at the presynaptic neurons. Also block sodium channels in the heart & brain, which can cause arrhythmia’s and seizures.
-Nortriptyline
-Amitriptyline
Nonadrenergic antagonists: block negative feedback loop; raises serotonin levels.
-Mirtazapine (Remeron)
MOI’s (Monoamine Oxidase inhibitors): last line agents; many drug interactions<\/strong> inhibit the breakdown of neurotransmitters.
-Phenelzine (Nardil)
-Tranylcypromine (Parnate)<\/p>\n\n\n\nSSRI for kids?<\/a><\/p>\n\n\n\n
SSRI’s use in pt older than 18 years use Fluoxetine in those 8 years or older.
Fluoxetine is the only SSRI approved for depression in children<\/a><\/p>\n\n\n\ntreatment of Alzheimer’s Disease<\/a><\/p>\n\n\n\n
donepezil, galantamine RT, or rivastigmine patch first line therapy once a day dosing, switching between meds should be considered after a minimum of 6 months. Moderate to severe dementia may be started on Memantine. If anticholinergic drugs are not tolerated, pt may be started on an NMDA.
donepezil ( Aricept) cholinesterase inhibitors class * the best tolerated <\/strong>*
glantamine ER ( Razadyne ER) cholinesterase inhibitors class
Rivastigmine ( exelon) cholinesterase inhibitors class
Non pharmocological treatment: behavioral and environmental management, caregivers support groups, respite care.
book stated to start these meds at 5mg\/day, if tolerated after 4 weeks increase to 10mg\/day. Dose can be as high as 23mg\/day<\/p>\n\n\n\nfirst-line treatment for generalized seizure management<\/a><\/p>\n\n\n\n
Pedi- first line is phenobarbital
Generalized seizure management
o Carbamazepine ( tegretol) miscellaneous class
o Phenobarbital ( luminal) Barbiturates class
o Phenytoin ( Dilantin) Hydantoins class
o valproate ( depakene) GABA analogs ( new drug)<\/a><\/p>\n\n\n\nlab monitoring of carbamazepine<\/a><\/p>\n\n\n\n
Baseline and periodic liver function tests should be performed. Carbamazepine should be discontinued immediately if liver dysfunction occurs or acute liver disease is suspected.
CBC prior to starting and every 3 months during first year to watch for wbc decline below 2500\/mm
Baseline and periodic liver function check- possible acute liver disease
Baseline and periodic urinalysis and kidney function tests can causes SIADH and hyponatremia
Baseline and periodic eye exams- lense opacities have occured<\/p>\n\n\n\nside effects of Carbamazepine<\/a><\/p>\n\n\n\n
Dizziness, drowsiness, ataxia, nausea and vomiting, rashes, photosensitivity reactions, toxic epidermal necrolysis, Stevens-Johnson syndrome, hypersensitivity (e.g., fever, rash, eosinophilia), pulmonary hypersensitivity (e.g., fever, dyspnea, pneumonitis)
aplastic anemia and agranulocytosis. Mild anticholingeric. GI symptoms, dizziness and drowsiness<\/a><\/p>\n\n\n\ncommon drugs that require serum level monitoring<\/a><\/p>\n\n\n\n
Coumadin 2.0 to 3.0
K 3.5 to 5.0
Gentamycin 5-12 ug\/ml
Lithium 1-1.5mEq\/L
Theophylline 5-15 mch\/ml
Phenytoin 10-20 ug\/ml
Carbamazine 4-12mg\/L
theophylline, anti-epileptics, phenytoin (dilantin), carbamazepine (Tegretol, Carbatrol, Epitol), digoxin, and aminoglycoside antibiotics (gentamicin, tobramycin, amikacin, neomycin, streptomycin), lithium
Amikacin: 15 to 25 mcg\/mL (25.62 to 42.70 micromol\/L)
Aminophylline: 10 to 20 mcg\/mL (55.50 to 111.00 micromol\/L)
Amitriptyline: 120 to 150 ng\/mL (432.60 to 540.75 nmol\/L)
Carbamazepine: 5 to 12 mcg\/mL (21.16 to 50.80 micromol\/L)
Cyclosporine: 100 to 400 ng\/mL (83.20 to 332.80 nmol\/L) (12 hours after dose)
Desipramine: 150 to 300 ng\/mL (563.10 to 1126.20 nmol\/L)
Digoxin: 0.8 to 2.0 ng\/mL (1.02 to 2.56 nanomol\/L)
Disopyramide: 2 to 5 mcg\/mL (5.89 to 14.73 micromol\/L)
Ethosuximide: 40 to 100 mcg\/mL (283.36 to 708.40 micromol\/L)
Flecainide: 0.2 to 1.0 mcg\/mL (0.5 to 2.4 micromol\/L)
Gentamicin: 5 to 10 mcg\/mL (10.45 to 20.90 micromol\/L)
Imipramine: 150 to 300 ng\/mL (534.90 to 1069.80 nmol\/L)
Kanamycin: 20 to 25 mcg\/mL (41.60 to 52.00 micromol\/L)
Lidocaine: 1.5 to 5.0 mcg\/mL (6.40 to 21.34 micromol\/L)
Lithium: 0.8 to 1.2 mEq\/L (0.8 to 1.2 mmol\/L)
Methotrexate: varies with use
Nortriptyline: 50 to 150 ng\/mL (189.85 to 569.55 nmol\/L)
Phenobarbital: 10 to 30 mcg\/mL (43.10 to 129.30 micromol\/L)
Phenytoin: 10 to 20 mcg\/mL (39.68 to 79.36 micromol\/L)
Primidone: 5 to 12 mcg\/mL (22.91 to 54.98 micromol\/L)
Procainamide: 4 to 10 mcg\/mL (17.00 to 42.50 micomol\/L)
Quinidine: 2 to 5 mcg\/mL (6.16 to 15.41 micromol\/L)
Salicylate: varies with use
Sirolimus: 4 to 20 ng\/mL (4 to 22 nmol\/L) (12 hours after dose; varies with use)
Tacrolimus: 5 to 15 ng\/mL (4 to 25 nmol\/L) (12 hours after dose)
Theophylline: 10 to 20 mcg\/mL (55.50 to 111.00 micromol\/L)
Tobramycin: 5 to 10 mcg\/mL (10.69 to 21.39 micromol\/L)
Valproic acid: 50 to 100 mcg\/mL (346.70 to 693.40 micromol\/L)
Dig tox (pg 288)- Report any occurrence of yellow halo around objects, nausea, decreased appetite, or episodes of extreme fatigue; these symptoms may indicate early toxicity. Dig tox at >2 ng\/ml, therapeutic is 0.5-2 ng\/ml drawn q6-8 hrs prior to next dose<\/p>\n\n\n\nroll of the NP in practice and what guides NP practice.<\/a><\/p>\n\n\n\n
“There is an increased need for professionals who can provide cost-effective healthcare. Healthcare needs to be accessible and available. Advanced practice nurses are fulfilling this role.” – week 1 lesson
Based on the definition given by the American Association of Colleges of Nursing (AACN) and other widely accepted usages, the term advanced practice registered nurse (APRN) has been used to indicate master’s-prepared nurses who provide direct clinical care. This term encompasses the roles of nurse practitioner (NP), certified nurse-midwife (CNM), certified registered nurse anesthetist (CRNA), and clinical nurse specialist (CNS). The first three roles require a license beyond the basic registered nurse (RN) license. The role of the clinical nurse specialist requires a master’s degree but does not require separate licensing unless the CNS is applying for prescriptive authority. (DeNisco 5)
DeNisco, Susan M. Advanced Practice Nursing, 3rd Edition. Jones & Bartlett Learning, 20150306. VitalBook file. (p. 5).
All professional disciplines are based on their unique knowledge, which is expressed in models and theories that are applied in practice. The focus of nursing knowledge is on humans’ health experiences within the context of their environment and the nurse-client relationship. Theory-based nursing practice is the application of various models, theories, and principles from nursing science and the biological, behavioral, medical, and sociocultural disciplines to clinical nursing practice. Conceptual models and theories provide a broad knowledge base to assist nurses in understanding and interpreting the client’s complex health situation and in planning nursing actions to achieve desired client outcomes. “Explicit use of conceptual models of nursing and nursing theories to guide nursing practice is the hallmark of professional nursing”; it distinguishes nursing as an autonomous health profession (Fawcett, 1997, p. 212). (DeNisco 427)
DeNisco, Susan M. Advanced Practice Nursing, 3rd Edition. Jones & Bartlett Learning, 20150306. VitalBook file (p. 427).<\/p>\n\n\n\nmechanism of action for oral contraceptives pills<\/a><\/p>\n\n\n\n
inhibition of follicular development, ovulation and alteration in cervical mucous
Estrogen mechanism-
\u2022 Suppress LH\/FSH- inhibiting ovulation
\u2022 Alters endometrium- inhibiting implantation
\u2022 Ovum transport is accelerated
\u2022 Luteolysis may occur as estrogen causes progesterone levels to fall
Progesterone mechanism-
\u2022 Thicken cervical mucus- decrease sperm transport
\u2022 Suppression of endometrium- inhibits implantation
\u2022 Slowed ovum transport
\u2022 HPO axis alteration- inhibits ovulation<\/p>\n\n\n\ncontraindications for oral contraceptives<\/a><\/p>\n\n\n\n
Smoking over age 35, Migraines, DVTS, cerebrovasicular diease, CAD, MI, Breast cancer, endometrium CA, liver disease or cancer, pregnenacy
\u2022 history of thromboembolic events
\u2022 hypersensitivity
\u2022 endometrial cancer
\u2022 Coranary artery disease
\u2022 Breast cancer
\u2022 Pregnancy
\u2022 Liver tumor
\u2022 Undiagnosed abnormal uterine bleeding
Who should get progestin only pills-
\u2022 Breastfeeding
\u2022 History of migraine
\u2022 Contraindications of estrogen
Oral contraceptives may cause fluid retention
Serum folate levels may be decerased by oral contraceptives, women who become pregnant shortly after stopping therapy may have a greater chance of birth defects
May precipitate attacks of acute intermittent porphyria<\/p>\n\n\n\nmechanism of action of Antiprotozoal agents<\/a><\/p>\n\n\n\n
Metronidazole
Metronidazole is considered a cytotoxic agent, but its exact mechanism of action is not well understood. Metronidazole damages DNA synthesis, resulting in cell death. Most probably, metronidazole initially enters cells by passive diffusion and then is activated by an enzymatic system that is present only in certain cells, such as anaerobic cells and protozoa. A reaction occurs, and a nitrogen group is reduced. The metabolites are toxic substances that bind to DNA and RNA and interrupt synthesis.
Chloroquine
The exact mechanism of action is unknown. Chloroquine raises the internal pH of parasites. It also may influence hemoglobin digestion or interfere with parasite\/nucleoprotein synthesis.<\/p>\n\n\n\nantifungal medications and which antifungal’s treat different diseases and fungal infections<\/a><\/p>\n\n\n\n
Ketoconazole- candidiasis, histoplasmosis, severe tinea, onychomycosis (funal infection of the nail)
Fluconazole- candidiasis- first line treatment
Itraconazole- onychomycosis, blastomycosis\/histoplasmosis, aspergillosis
Terbinafine- onychomycosis first line treatmrnt- finernails and toes
Griseofulvin- (fungal) tinea corporis, tinea cruris, tinea capitis, tinea pedis, tinea unguium<\/p>\n\n\n\ncontraindications when prescribing contraceptive management<\/a><\/p>\n\n\n\n
hypercoagulation disorders – (Estrogen increases coagulability) COCP’s, transdermal & vaginal ring are contraindicated (safe if treated with anticoagulants) – page 619
IMPLANTS – contraindicated for thrombophlebitis, undiagnosed genital bleeding, acute liver disease, liver tumors, breast cancer – page 622
Depo shot is preferred for Seizure disorders COCP are CONTRAINDICATED DUE TO anti-convulsive interactions – page 619
COCP – smokers >35 yrs, diabetes mellitus with vascular disease, hypertriglyceridemia, hx of stroke, MI, or DVT, gallbladder disease, vascular headache\/migraine with neurologic symptoms (like aura’s), endometrial carcinoma, hepatic adenoma\/carcinoma, acute liver disease, known\/suspected pregnancy, cholestatic jaundice, hypersensitivities, lupus, sickle cell, valvular heart disease, coronary artery disease, major surgery with prolonged immobilization – page 619-624
IUD’s – Contraindicated for uterine fibroids, Pelvic inflammatory disease, postpartum endometriosis, infected abortion within 3 months, cervical neoplasia, untreated cervicitis\/vaginitis, high STD risk woman, small\/large uterus (<6 cm or >9 cm) – Paraguard contraindicated for anticogulants, bleeding disorders, copper allergy, or wilson’s disease – page 622
Yaz (ethinyl estrodiol and drospirenone) – CHECK POTASSIUM LEVEL caution with ACEI, ARB’s, aldosterone antagonists, k-sparing diuretics, heparin, long-term NSAID’s – Contrindicated with renal insufficiency, hepatic dysfunction, adrenal insufficiency, smoking over 35, thrombohemolytic disease, breast cancer, ovarian cancer, uterine bleeding – WARNING FOR HYPERKALEMIA
transdermal patch and vaginal ring are HIGHER RISK FOR BLOOD CLOT than the COCP
Progestrin only emergency contraception has few side effects and NO contraindications – page 621
Progestin-only pills (mini pills), implants, depo shot, and IUD’s – are SAFE for pts with breastfeeding and with contraindication to estrogen – page 621<\/p>\n\n\n\ntreatment for Generalized Anxiety disorder<\/a><\/p>\n\n\n\n
lorazepam (Ativan) oxazepam (Serax) specific to GAD. Also some SSRI’s… pg 517… Some SSRIS are indicated for the treatment of some anxiety disorders (GAD or social anxiety disorder) .escitalopram, paroxetine, venlofaxine, duloxetine
Acute-benzodiazepines; long term -SSRI, venlafaxine, buspirone pg. 542
TCAs and Benzos were once 1st line agents but less is being prescribed due to side effects, abuse potential and tolerance. 1st line druv is now SSRIs due to less side effects. Starting dose is 50% less than dose used to treat depression due to side effects of insomnia and restlessness. Benzos can be used for short time agents with antidepressants. Prefer lorazepam or clonazepam due to longer acting. Pg 542-543<\/p>\n\n\n\ntreatment for ADHD and monitoring<\/a><\/p>\n\n\n\n
Treatments
\u2022 For children stimulants are not the initial treatment. Nonpharmacological treatments are attempted first, which include classes and counseling for parents in behavior modification (such as point systems that allow children to earn rewards), social skill training, cognitive-behavioral therapy, support groups, biofeedback, and mediation all go into a comprehensive, multidisciplinary management program. Guidelines recommend parents and teachers working together to assess efficacy of treatment plan.
\u2022 All available stimulants appear to be equally effective. Methylphenidate (Ritalin, Ritalin SR, Metadate SR, Concerta, Metadate CD, Ritalin LA, Methylin, Daytrana Transdermal System) is usually first-line drug of choice for AD-HD
\u2022 When giving medication to children parents must give permission first.
\u2022 Although some parents chose not to tell the childrens teachers about placing their child on medication, teachers may be very helpful in evaluation response from therapy. The Connors Teacher’s Rating Scale, should be completed prior to initiation of therapy and 1 to 2 weeks after initiation.
\u2022 A once a day methylphenidate (Concerta) may be used to help children for whom multiple doses per day are difficult.
\u2022 If paradoxical aggravation of symptoms or other adverse effects occur, reduce dosage or, if necessary discontinue drug.
\u2022 If patients do not respond to methylphenidate, other medications from another class. Amphetamines are usually used such as Adderall, Vyvanse, Kapvay, Dexedrine.
\u2022 TCA antidepressants have been used as both primary and adjunctive therapy in children who fail to achieve positive response to stimulants. The specific agents used are desipramine and nortriptyline, primary because of their effects on norepinephrine reuptake. They should be avoided in patients with cardiac disease, specifically conduction abnormalities
Monitor
\u2022 The American Heart Association recommends careful screening of all children and adolescents prior to initiating pharmacological therapy for ADHD, including a detailed patient and family history and physical examination. Ideally, a baseline electrocardiogram should be obtained and careful follow-up monitoring instituted.
\u2022 FDA recommends that clinicians periodically monitor heart rate or blood pressure on patients
\u2022 Monitor for exacerbation of preexisting psychiatric conditions, or new-onset episodes of psychosis, aggression, or mania
\u2022 Patients should be seen more frequently during dosage adjustment period. Once stable, they should be followed about once every 6-12 months. Blood pressure and weight should be monitored.
Patient Variables
\u2022 Geriatrics: Methylphenidate has an unlabeled use in the elderly population. It may increase mental alertness and stimulate appetite.
\u2022 Pediatrics: Us in children younger than 6 years of age is off-label
\u2022 Pregnancy and Lactation: studies have not been adequate to determine safety; they are not recommended for women of childbearing age
\u2022 Gender: women who use modafinil (Brand name: Provigil. Short-acting psychostimulant) and oral contraceptives should take precaution to avoid pregnancy
\u2022 Use and Abuse: use with caution in emotionally unstable patients and in those with history of alcoholism or other drug dependence. Chronic abuse can lead to marked tolerance and psychologic dependence with varying degree of abnormal behaviors. Frank psychotic episodes can occur.
Information found on pg. 447-452. Quick reference table on pg. 456 table 41-2<\/p>\n\n\n\nthe role of the Drug Enforcement Administration<\/a><\/p>\n\n\n\n
DEA will register individuals who may prescribe narcotics and other controlled substances. However registration depends on state authority to prescribe controlled substances. The DEA classifies narcotics and Other Drugs such as depressants and stimulants by their abuse potential with differing levels of control assigned to each class
DEA MISSION STATEMENT
The mission of the Drug Enforcement Administration (DEA) is to enforce the controlled substances laws and regulations of the United States and bring to the criminal and civil justice system of the United States, or any other competent jurisdiction, those organizations and principal members of organizations, involved in the growing, manufacture, or distribution of controlled substances appearing in or destined for illicit traffic in the United States; and to recommend and support non-enforcement programs aimed at reducing the availability of illicit controlled substances on the domestic and international markets.
In carrying out its mission as the agency responsible for enforcing the controlled substances laws and regulations of the United States, the DEA’s primary responsibilities include:
Investigation and preparation for the prosecution of major violators of controlled substance laws operating at interstate and international levels.
Investigation and preparation for prosecution of criminals and drug gangs who perpetrate violence in our communities and terrorize citizens through fear and intimidation.
Management of a national drug intelligence program in cooperation with federal, state, local, and foreign officials to collect, analyze, and disseminate strategic and operational drug intelligence information.
Seizure and forfeiture of assets derived from, traceable to, or intended to be used for illicit drug trafficking.
Enforcement of the provisions of the Controlled Substances Act as they pertain to the manufacture, distribution, and dispensing of legally produced controlled substances.
Coordination and cooperation with federal, state and local law enforcement officials on mutual drug enforcement efforts and enhancement of such efforts through exploitation of potential interstate and international investigations beyond local or limited federal jurisdictions and resources.
Coordination and cooperation with federal, state, and local agencies, and with foreign governments, in programs designed to reduce the availability of illicit abuse-type drugs on the United States market through nonenforcement methods such as crop eradication, crop substitution, and training of foreign officials.
Responsibility, under the policy guidance of the Secretary of State and U.S. Ambassadors, for all programs associated with drug law enforcement counterparts in foreign countries.
Liaison with the United Nations, Interpol, and other organizations on matters relating to international drug control programs.<\/p>\n\n\n\n
- bind to the active site of PBPs(Penicillin Binding Proteins). This prevents