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©BSN-2H NOTES

CONDITIONS R/T UNTREATED HYPERTENSION


Cardio: -CAD and cardiac death
-Stroke
Anti-hypertensive drugs -Renal failure
-Loss of vision
Periods of Cardiac Cycle
1. Diastole STEP CARE APPROACH IN TREATING
- Peroid of rest HYPERTENSION
- Blood is returned to the heart Step 1: Lifestyle Modification
2. Systole Step 2: Drug therapy (diuretics, ace inhibitors)
- Period of contraction Step 3: Drug therapy- switching of meds
- -Blood is pumped out of the heart Step 4: Adding more drugs

5 Phases NON-PHARMACOLOGIC CONTROL OF


1. HYPERTENSION
2. Depolarization  Stress-reduction techniques
3. Repolarization  exercise
4. Hyperpolarization  salt restriction
5.  decreased alcohol ingestion
 weight reduction
BLOOD PRESSURE
Element Determining BP PHARMACOLOGIC CONTROL OF HYPERTENSION
• HR
• PR DIURETICS
- Amount of blood that is pumped out of the-first line drugs for treating mild hypertension
ventricle with each heart beat
 Total peripheral resistance MOA
- resistance of the muscular arteries to the blood-promotes sodium depletion
being pumped through -decreases extracellular fluid volume

REGULATORS OF BP SAMPLE
 Baroreceptor -Hydrochlorothiazide (hydroDIURIL)
- aorta and carotid sinus
- pressure receptor CI and CAUTION
- vasomotor center in the medulla -Thiazide: renal insufficiency (creatinine clearance > 30
- hormones: antidiuretic (produced by the ml/min)
hypothalamus and is stored and release by the
posterior pituitary gland) , atrial natriuretic SYMPATHOLITICS (sympathetic Depressants)
peptide, brain natriueretic peptide 1. Beta- adrenergic blockers
2. Centrally acting alpha2- agonists
HYPERTENSION 3. Alpha- adrenergic blockers
-an increase in blood pressure such that the systolic 4. Adrenergic neuron blockers (peripherally acting
pressure is greater than 140 mmHg and the diastolic sympatholytics
pressure is greater than 90 mmHg 5. Alpha1 and Beta1 adrenergic blockers

ESSENTIAL HYPERTENSION 1. BETA-ADRENBERGIC BLOCKERS


- most common type, affecting 90% of persons -beta blockers
with high blood -used as anti-hypertensive drug in combination with
- exact origin is unknown loop diuretic
- contributing factors: family hx of hypertension,
hyperlipidemia, African American background, MOA
diabetes, obesity, aging, stress, excessive Beta (B1 and B2)- adrenergic blockers reduce CO by
smoking and alcohol ingestion diminishing the sympathetic nervous system response
to decrease basal sympathetic tone
SECONDARY HYPERTENSION
- 10 % SAMPLE:
- related to renal and endocrine disorders *propanOLOL (inderal)
- inhibit beta1 (heart) and beta2 (bronchia)l receptors -blocks alpha- adrenergic receptor resulting in
vasodilation and decreased BP
CI and CAUTION -decrease very low density lipoproteins (VLDL) and low
-2nd or 3rd degree AV block or sinus bradycardia density lipoproteins (LDL)
-Propanolol: not be given to clients with COPD -Increase High density lipoprotein levels (HDL)

SE SAMPLE
-decreased PR -Selective alpha1(ZOSIN)= prazosin, terazosin,
-markedly decreased BP doxazosin ------- reduce BP and used to treaty benign
-bronchospasm prostatic hypertension
-insomnia -Phentolamine, phenoxybenzamine and tolazolin----for
-depression hypertensive crisis and severe hypertension
-nightmares
-sexual dysfunction SE and AE
NSG INT. -ZOSIN: orthostatic hypotension, dizziness, faintness,
-Monitor VS especially BP light headedness, increased HR, nausea, drowsiness,
-Monitor laboratory results, especially BUN, serum nasal congestion, vasodilation, edema, wt gain
creatinine, AST and LDH -PHENTOLAMIN: hypotension, reflex tachycardia,nasal
-Instruct client to do not discontinue meds abruptly congestion, GI disturbances
because rebound hypertension may occur
-Inform client that herbs can interfere with beta blockers D-D
- prazosin + anti inflammatory = peripheral edema
2. CENTRALLY ACTING ALPHA2-AGONISTS - prazosin + mitroglycerin= faintness (syncope caused
USE by decrease BP)
MOA
-stimulate the alpha2 receptors NSG INT
-increase vagus activity -Monitor VS especially BP
-decrease CO -Check daily for fluid retention in the extremities
-decrease serum epinephrine, norepinephrine and -Encourage client to decrease salt intake
rennin release -instruct client to report edema if present

*which results to: decrease the sympathetic response 4.ADRENERGIC NEURON BLOCKERS
from the brainstem to the peripheral vessels -potent antihypertensive drugs
-last choice for treatment of chronic hypertension
SAMPLE:
-Methyldopa (Aldomet) = one of the 1st drugs widely MOA
used to control hypertension -block norepinephrine release from sympathetic nerve
-Clonidine- transdermal, 7 day duration of action endings causes decrease in norepinephrine which
-Guanfacine, guanabenz results to decrease BP

CI and CAUTION *decrease in CO and peripheral vascular resistance


-Methydopa: impaired liver function, PAL
SAMPLE
SE and AE -Reserpine, guanethidine,and guanadrel
-dry mouth, dizziness, slow HR (bradycardia)
-Na and water retention resulting in peripheral edema SE
-orthostatic hypotension
NSG INT -Na and water retention
-Serum liver enzymes should be monitored periodically -may cause vivid dreams, nightmares and suicidal
-must not be abruptly discontinued because of rebound intention
hypertension crisis
-Diuretic may be ordered with methyldopa or clonidine NSG INT
to decrease edema -advise client to rise slowly from sitting position

3.ALPHA ADRENERGIC BLOCKERS 5.ALPHA1 AND BETA1 ADRENERGIC BLOCKERS


-useful in treating hypertension in client with lipid MOA
abnormalities -blocks both the alpha1 and beta1 receptor
- large doses could block beta2 adrenergic receptors
MOA and may cause AV block
spironolactone
*causes vasodilation, decreasing resistance to blood
flow SE
-constant irritated cough
SAMPLE
-Labetalol (Normodyne) NSG INT
-Carteolol (Cartrol) -Monitor lab test (BUN, creatinine, protein) and blood
glucose levels
CI -Wastch for hypoglycaemic reactions in clients with
-clients who have sever asthma diabetes mellitus
-Instruct client to administer with food
SE -Instruct client not to abruptly discontinue meds
-orthostatic (postural) hypotension -Teach client to record BP
-GI disturbances -Instruct client to take captopril 20 minutes to 1 hour
-Nervousness before meal.
-dry mouth -Inform patient that taste of food may be diminished
-fatigue during 1st month of drug therapy

DIRECT ACTING ARTERIOLAR VASODILATOR ANGIOTENSIN II RECEPTOR BLOCKERS


-very potent antihypertensive drugs -similar to ACE inhibitors

MOA MOA
-relaxes the smooth muscles of the vessels, mainly the -prevent release of aldosterone
arteries causing vasodilation -blocks angiotensin ii from the AT1 receptors
-promotes an increase blood flow to the brain and
kidneys *causes vasodilation and decrease peripherak
resistance
*BP decreases, Na and water are retained causing
peripheral edema CI
-pregnancy
SAMPLE
-hydralazine SAMPLE (SARTANS)
-menoxidil -Losartan (Cozaar)
-Nitroprusside and diazoxide (acute HPN) -Valsartan (Diovan)
-Irbesartan (Avapro)
SE -Olmesartan medoxomil (Benicar)
-hydralazine: tachycardia, palpitaitons, edema, nasal -Telmisartan (Micardis)
congestion, HA, dizziness, bleeding, lupus like
syndrome, tingling, numbness SE
-Nitroprusside and diazoxide: reflex tachycardia, -URI
palpitaions, agitation, nausea,and confusion, -HA
hyperglycemia -Dizziness

ANGIOTENSIN CONVERTING ENZYME (ACE) DIRECT RENIN INHIBITOR


INHIBITORS
-promotes sodium retention and K excretion MOA
-treats HPN and HF -reduces angiotensin I and II, aldosterone levels

MOA SAMPLE
-Inhibits the formation of angiotensin II -aliskiren (Tekturna)
-blocks the release of aldosterone
CALCIUM CHANNEL BLOCKERS
SAMPLE -calcium agonists and calcium blockers
-Captopril (Capoten) -highly protein bound but have short half life
-Enalapril (Vasotec)= only ACE available on oral form
MOA
CI -block the binding of Ca to its receptor
-Pregnant women
-shoukd not be taken with K sparring diuretics such as *results: preventing muscle contraction, smooth muscle
relaxation, decrease peripheral smooth muscle tone S.E.:HA,weakness, drowsiness, vision changes, GI
upset, digitalis toxicity.
SAMPLE Digitalis toxicity
-dihydropyridine (amlodipine) – common s/sx: anorexia, diarrhea, bradycardia, PVC, N/V, cardiac
=largest group of calcium channel blockers dysrhythmias, blurred vision, visual illusions, HA,
= used to control HPN malaise, confusions, delirium.
= Nimodipine- prevent ischemic brain injury due Digoxin
to vasospasm -antidote for digitalis toxicity
-diphenylalkalamine (verampil) -digoxin immune tab(orine, digiland)
=used to treat chronic hypertension, angina pectoris Assessment:
and cardiac dysrhytmias -drug and herbal history
-benzodiazepines (diltiazem) -VS, PR
-ECG
SE/AE -renal function
-flush -serum electrolytes
-headache -s/sx of digitalis toxicity
-dizziness Intervention:
-ankle edema -monitor PR,don’t administer if PR below 60
-bradycardia -eat foods high in potassium
-AV block -drug compliance
-avoid OTC drugs
CI -weigh daily
-heart block

NSG INT Cardiac dysrhythmia (arrhythymia)


-do not prescribe with beta blockers -any deviation from the normal rate or pattern of
the hearbeat
Cardiotonic agents -bradycardia; tachycardia
ECG- identifies the type of dysrhythmia
Cardiac Glycosides
-heart failure P wave – indicates atrial activation
-positive inotropic action QRS complex – ventricular depolarization
-negative chronotropic action T wave – ventricular depolarization
-increase stroke volume
Ex. PR interval – AV conduction time
Digoxin(lanoxin, lanixocaps) QT interval – ventricular action potential
-doesn’t need liver to metabolize Atrial Dysrhythmias – prevent proper filling of the
-more dosage ventricles and decrease cardiac output by 1/3
Digitoxin(crystodigin) Ventricular dysrhythmias – life threatening because
-needs liver ineffective filling of the ventricles results in decreased /
-less dosage absence of cardiac output
I:CHF, Atrial flutter, atrial fibrillation, paroxysmal atrial
tachycardia. Cardiac Action Potentials
CI: -ventricular tachycardia/fibrillation Phase 0 – rapid depolarization caused by an influx of
-heart block sodium ions
-acute MI(heart attack/myocardial infarction) Phase 1 – initial repolarization; termination of sodium
-renal insufficiency ions
-electrolyte abnormalities Phase 2 – is the plateau; characterized by the influx of
ex. Hypokalemia(increase effect of digoxin toxicity) ions
Drug interactions Phase 3 – rapid repolarization
-diuretics(potassium losing) Phase 4 – resting membrane potential between
-glucocorticoids hearbeats
-antacids
-herbal interaction Type of Antidysrhythmic drugs
-thyroid hormones Class I (sodium channel blockers)
-verapamil, amiodarone, quinidine, quinine,  Slow conduction and prolong repolarization
erythromycin, tetracycline or cyclosporine.  Quinidine, Procainamide, Disopyramide
NORMAL THERAPEUTIC LEVEL OF DIGOXIN
-0.5-2ng/ml
Class II (beta blockers) Evaluate the effectiveness of the prescribed
 Reduce calcium entry antydysrhythmic by comparing heart rates with
 Decrease conduction velocity, automaticity and baseline hear rate and assessing client’s
recovery time response to drugs
 Propanolol (inderal)
Antianginal agents:
 Acebutolol (sectral)
 Esmolol (brevibloc) ANTI ANGINAL DRUGS - used to treat angina pectoris
 Sotalol (betapace)
Class III (drugs that prolong repolarization) ANGINA PECTORIS - condition of acute cardiac pain
 Prolong repolarization during ventricular caused by inadequate blood flow to the myocardium
dysrhythmias due to either plaque occlusions within or spasms of the
 Prolong action potential duration coronary arteries, with decreased blood flow, there is a
 Bretylium (bretylol) decrease in O2 to the myocardium which results in pain
 Amiodarone (cordarone) ANGINAL PAIN - tightness, pressure in the center of
the chest and pain radiating down the
Class IV (calcium channel blockers) left arm
 Block calcium influx -usually lasts for only a few
 Slow conduction velocity minutes
 Decrease myocardial contractility REFERRED PAIN: felt in the neck and left arm- severe
angina pectoris
 Increase refraction in the AV node
ANGINAL ATTACKS may lead to MYOCARDIAL
 Verapamil (Calan, Isoptin) INFARCTION or HEART ATTACK.
 Diltiazem (cardizem) STRESS TESTS, ECHOCARDIOGRAM, CARDIAC
PROFILE LABORATORY TESTS AND CARDIAC
Nursing process CATHETERIZATION – determine the degree of
• Obtain health and drug histories blockage in the coronary arteries
• Obtain baseline VS and ECG for future
comparisons TYPES OF ANGINA PECTORIS
1.CLASSIC (STABLE) - occurs with stress or exertion
Diagnosis 2.UNSTABLE (PREINFARCTION)
• Decreased cardiac output related to cardiac - occurs frequently over the course of a day with
dysrhythmia progressive severity
• Anxiety related to irregular heartbeat -often indicates an impending MI
• Risk for activity intolerance related to lack of -emergency that needs immediate medical intervention
oxygen because of irregular heart rate 3.VARIANT (PRINZMETAL, VASOSPASTIC) - occurs
during rest
Nursing intervention -caused by vessel spasm (vasospasm)
 Monitor VS signs. Hypotension can
occur FIRST TWO TYPES: caused by a narrowing or partial
 Administer drug by IV push or bolus occlusion of the coronary arteries
over a period of 2-3 mins, or as
prescribed NONPHARMACOLOGIC WAYS OF DECREASING
 Monitor ECG for abnormal patterns and ANGINAL ATTACKS:
report findings - Avoid heavy meals, smoking, extremes in
Client teaching weather changes, strenuous exercise and
 Instruct client to take prescribed drug as emotional upset
ordered - Promote nutrition, moderate exercise, adequate
 Provide specific instructions for each rest and relaxation techniques
drug ANTIANGINAL DRUGS- increase blood flow either by
Side effects: increasing oxygen supply or by decreasing oxygen
demand by the myocardium
 Instruct client to report side effects and
TYPES OF ANTIANGINAL DRUGS
adverse reactions to the health care
provider. These can include dizziness, • NITRATES- fast effect
faintness, N/V. -MAJOR SYSTEMIC EFFECT: reduction of
 Advise client to avoid alcohol, caffeine, venous tone which decreases the workload of
and tobacco. the heart and promotes vasodilation
Evaluation: -effective in treating variant angina pectoris
-first agents used to relieve angina
-affect coronary arteries and blood vessels in - DO NOT GIVE MORE THAN 3 TABLETS
the venous circulation - if chest pain persists longer than 15 mins,
-cause generalized vascular and coronary immediate medical help is necessary
vasodilation thus increasing blood flow through 7. Never chew or swallow
the coronary arteries to the myocardial cells 8. burning sensation-normal
-reduces myocardial ischemia but can cause 9. Lying down or sit to prevent dizziness
hypotension 10 .Blood level monitor
MOA: cause vasodilation due to relaxation of 11. Take before meals
smooth muscles 12. Limit caffeine intake
Potent dilating effect on coronary 13. To avoid hypotension, weakness and
arteries faintness, instruct client not to ingest alcohol
INDICATION: used for prophylaxis and while taking nitroglycerin
treatment of angina 14. Tolerance can occur.
CONTRAINDICATION: severe anemia, 15. Instruct client about the Transderm-Nitro
head trauma or cerebral hemmorhage patch. Apply once a day, usually in the morning.
EXAMPLES: Rotation of skin sites is necessary. The patch is
1. NITROGLYCERIN (NITROBID, NITROSTAT) usually applied to the chest wall, but thighs and
-AVERAGE DOSE PRESCRIBED FOR arms may also be used. Avoid hairy areas.
SUBLINGUAL NITROGLYCERIN TABLET: 0.4 15. Headaches commonly occur when first
mg or gr 1/150 – repeated every 5 minutes for a taking nitroglycerin products and last about 30
total of 3 doses mins. Acetaminophen is suggested for relief.
-SL TABLETS: decompose when exposed to 16. If hypotension results from SL nitroglycerin,
heat and light – should be kept in their original place in supine position with legs elevated.
AIRTIGHT GLASS CONTAINERS
- not swallowed because it undergoes first- • BETA-BLOCKERS
pass metabolism by the liver which decreases -decrease the workload of the heart and
its effectiveness decrease oxygen demands
2. ISOSORBIDE DINITRATE ( ISORDIL, -effective with stable angina
SORBITRATE) -decrease the effects of the sympathetic
3. ISOSORBIDE MONONITRATE ( MONOKET, nervous system by blocking the action of the
IMDUR) catecholamines epinephrine and
SIDE EFFECTS: Headache – most common norepinephrine thereby decreasing the heart
but may become rate and blood pressure
less frequent with -used as antianginal, antidysrhythmic and
continued use antihypertensive
Hypotension, dizziness, weakness and -effective as antianginal because by decreasing
faintness the heart rate and myocardial contractility, they
When nitroglycerin is discontinued, the dose reduce the need for oxygen consumption and
should be tapered over several weeks to consequently reduce anginal pain
prevent the rebound effect of severe pain -most useful for classic angina
caused by myocardial ischemia. -should not be abruptly discontinued; dose
Reflex Tachycardia- occur if nitrate is given too should be tapered over a specified no. of days
rapidly; heart rate increases greatly because of to avoid reflex tachycardia and recurrence
overcompensation of the cardiovascular angina pain
system. -clients with decreased heart rate and blood
DRUG INTERACTIONS: increase effect with pressure usually cannot take beta blockers
alcohol, beta-blockers, calcium channel -clients with second or third degree AV block
blockers, antihypertensiveness; decrease should not take beta-blockers
effects of heparin EXAMPLES OF NONSELECTIVE BETA-
NURSING INTERVENTION: NITROGLYCERIN BLOCKERS:
1. Monitor VS  Propanolol ( Inderal)
2. Instruct to rise slowly to standing position  Nadolol ( Corgard)
3. Sip water before sublingual nitrates  Pindolol ( Visken)
4. Apply ointments- use gloves - Decrease heart rate and can cause
5. Do not apply nitrates with defibrillation- bronchoconstriction
cardioverter
6. Instruct patient to take PRN nitrates at the
- Cardioselective beta-blockers act more
strongly on the beta1 receptor thus
first hint of angina pain.
decreasing the heart rate but avoiding
- If pain persists, repeat in 5 mins
bronchoconstriction because of their - Dizziness
relative lack of activity at the beta2 - Flushing of the skin
receptor - Reflex Tachycardia – can occur as a result of
EXAMPLES OF SELECTIVE BETA- hypotension
BLOCKERS: - Can cause changes in the liver and kidney
 Atenolol ( Tenormin) function – serum liver enzymes should be
 Metoprolol ( Lopressor, Toprol-XL) checked periodically
- grp of choice for controlling angina
pectoris Anti-platelet

SIDE EFFECTS AND ADVERSE REACTIONS: • Used to prevent thrombosis in the arteries by
decrease in heart rate and blood pressure – suppressing platelet aggregation
both selective and non selective drugs • Mainly for prophylactic use in:
bronchospasm, behavioural or psychotic o Prevention of myocardial infarction or stroke
response and impotence – potential adverse for client w/ familial hx
reactions for non-selective beta-blockers o Prevention of repeat MI or stroke
NURSING INTERVENTION: o Prevention of a stroke for clients having transient
Vital signs need to be closely monitored in the ischemic attacks (TIAs)
early stages of beta blocker therapy xamples:
When discontinuing, dosage should be tapered • ASPIRIN
for 1-2 wks to prevent rebound effect like reflex o Long-term & low dose aspirin therapy
tachycardia or life-threatening cardiac  Effective & inexpensive tx for
dysrhythmias suppressing platelet aggregation
Monitor PR o MOA: inhibits cyclooxygenase (enzyme
Inform patient it is a long term med
needed by platelet to synthesize
thromboxane A2 (TxA2)
• CALCIUM CHANNEL BLOCKERS o Indications:
- decrease the workload of the heart and
 Prevention of thrombosis before or after
decrease oxygen demands
CVA or MI
- effective in treating variant angina pectoris
-treatment of stable and variant angina pectoris,  Familial hx of MI or stroke
certain dysrhythmias and hypertension o Dose: 81, 162, or 325 md/day
-relax coronary artery spasm and relax  Should be discontinued at least 7 days
peripheral arterioles decreasing cardiac oxygen before surgery
demand • CLOPIDOGREL (Plavix)
-decrease cardiac contractility, decrease o MOA:
afterload, decrease peripheral resistance and  inhibits platelet aggregation
reduce the workload of the heart thus  prevents ADP from binding w/ the ADP
decreasing the need for oxygen platelet recptor
-achieve their effect in controlling variant angina o May be prescribed singly or w/ aspirin
by relaxing coronary arteries and in controlling (more effective)
classic angina by decreasing oxygen demand o CI: peptic ulcer, active bleeding, intracranial
CALCIUM- activates myocardial contraction,
hemorrhage
increasing the workload of the heart and the
need for more oxygen
o SE: upper RTI, flulike symptoms, dizziness,
EXAMPLES: HA, fatigue, chest pain, diarrhea, may
Verapamil (Calan)- first calcium blocker cause HTN & bronchitis
- Bradycardia is a common Drug interaction: NSAIDs – may  bleeding
problem
Nifedipine ( Procardia) – most potent of the calcium o Lab: prolongs bleeding time
blockers, promotes vasodilation of the coronary and o Herb: ginger, garlic, gingko, feverfew – may
peripheral vessels  bleeding
-hypotension can result • GP IIb/IIIa inhibitors
Diltiazem (Cardizem) o MOA: blocks the binding of fibrinogen to the
SIDE EFFECTS AND ADVERSE REACTIONS glycoprotein IIb/IIIa receptor on the platelet
- Headache surface
- Hypotension ( more common with Nifedipine o Used primarily for acute coronary
and less common with Diltiazem) syndromes (unstable angina or non-Q-wave
MI) conversion of pro thrombin to thrombin and
o Prevents reocclusion of coronary arteries fibrinogen to fibrin.
flowing percutaneous transuminal coronary
angioplasty (PTCA) – given before & after Indications:
PTCA - prevents and treats venous vessel
o Example: abciximab (ReoPro) – drug of disorders such as DVT, pulmonary
choice for angioplasty embolism and emboli in arterial fibrillation,
• CILOSTAZOL (Pletal) diagnoses and treats disseminated
o Also a vasodilator that may be used for intravascular coagulation; preferred
intermittent claudication anticoagulant during pregnancy.
Nursing Considerations:
• Monitor BP Contraindications:
Bleeding tendencies
• Provide safety precautions
Thrombocytopenia
• Monitor INR regularly
Post operative clients
• Advise client not to smoke. Nicotine causes
vasoconstriction, which alters the effectiveness Side Effect:
of antiplatelet agents bleeding
• Monitoring for abnormal bleeding
Tests:
Anticoagulant PTT and aPTT
Pathophysiology
• Thrombus is the formation of a clot in an arterial Drug-Drug interactions:
or venous vessel. - any drugs that will cause bleeding
• Arterial clots are usually made up of WBC and -
RBC initiating the process, followed by fibrin Antidote:
formation and trapping of RBC in fibrin mesh. Protamine Sulfate (1mg of protamine for every
• Embolus – blood clot moving through the 1mg of LMWH)
bloodstream.
• Thromboxane A2 – product of prostaglandin and *Low-molecular-weight heparins (no need for PTT/aPTT
a potent stimulus for platelet aggregation. monitoring)
• Glycoprotein IIb/IIIa or GP IIb/IIIa – platelet - + ½ : 2-4 times longer than heparin
receptor protein that binds fibrinogen. - administered subQ once or twice per
day.
Anticoagulants - usually injected at abdomen.
- inhibits clot formation. - preferable when client is at home
- act prophylactically to prevent new clots because a family member can be taught how
from forming. to administer.
- Used in clients with arterial and venous
vessel disorder.
Examples:
Venous Problems Arterial Problems Dalteparin sodium (Fragmin)
Deep Vein Coronary Thrombosis Enoxaparin sodium (Lovenox)
Thrombosis (DVT) (myocardial infarction) Tinzaparin sodium (Innohep)
Pulmonary Presence of artificial
Embolism heart valves
Cerebrovascular Accident ORAL
(CVA)
Warfarin
MAO:
PARENTERAL (IV/SubQ) - antagonist of vit. K, which is necessary
for the synthesis of clotting factors VII, IX, X
Heparin and pro thrombin; as a result, it disrupts the
MOA: coagulation cascade.
- prevent new fibrin/clot formation by
enhancing inhibitory actions of antithrombinIndications:
III on several factors essential to normal - prevent venous thrombosis and
blood clotting, thereby blocking the thromboembolism associated with atrial
fibrillation and prosthetic heart valves; risk of promote the conversion of plasminogen to
recurrent transient ischemic attack, CVA and plasma.
MI.
3. Alteplase a.k.a Tissue Plasminogen Activator (TPA)
Contraindications:
bleeding  MOA: promotes conversion of plasminogen to
vit. K deficiency plasmin and initiates fibrinolysis
pregnancy – category x  Use: to dissolve clot following an acute MI,
breastfeeding – crosses into breast milk pulmonary embolism, acute ischemic stroke.
Side Effect:  Contraindication: internal bleeding, bleeding
red-orange discoloration of urine disorders, recent CVA, surgery or trauma,
weakening of bones bacterial endocarditis, severe liver dysfunction,
(long-term use) severe uncontrolled hypertension
Tests:  Side Effects: bleeding
PT and INR  Adverse Reaction: Life-threatening:
intracerebral hemorrhage, stroke, atrial or
Antidote: ventricular dysrhythmias.
Vitamin K  Drug-Drug Interaction: increase bleeding when
taken with oral anticoagulants, NSAIDs,
NSG RESPONSIBILITY cefotetan, plicamycin
 check VS - PR, BP (bleeding)
 control and prevent bleeding 4. Reteplase (Retavase)
 if bleeding occurs, apply pressure for at least 5-  Use: to treat coronary thrombosis by
10 minutes causing lysis of thrombi; inhibits fibrin
 heparin: PTT and aPTT aspect of the thrombus
warfarin: PT and INR  Pregnancy Category C
 heparin: IV/subQ  More effective than TPA with less risk of
warfarin: oral hemorrhage
 instruct client to decrease intake of green, leafy 5. Tenecteplase (TNKase)
vegetables when taking warfarin.  Use: to reduce mortality associated with
 Check for bleeding, tarry stools AMI
 Soft toothbrush to prevent gums from bleeding  A “clot buster” that can be administered
 Caution with use of electric razor in 5 seconds in one dose
 Do not smoke – increases drug metabolism  Pregnancy Category C
 Use acetaminophen for pain instead of aspirin  Dose is based on body weight
(bleeding)
 Avoid coffee, tea, cola (caffeine), excessive Nursing Responsibilities:
alcohol. - Monitor VS
- Observe for s/sx of active bleeding from
Thrombolytics the mouth to the rectum.
Used since the early 1980s to promote the AMINOCAPROIC ACID – can be given as an
fibrinolytic mechanism (converting plasminogen intervention to stop bleeding.
to plasma, which destroys the fibrin in the blood - Check for active bleeding for 24hrs after
clot). thrombolytic therapy has been
Should be administered within 3 hours of a discontinued.
thrombolic stroke. - Observe for signs of allergic reaction to
streptokinase : itching, hives, flush,
Five commonly used thrombolytics are: fever, dyspnea, bronchospasm,
hypotension, and/or cardiovascular
1. Streptokinase (Streptase, Kibikinase) collapse.
Use: act systematically to promote the conversion - Avoid administering aspirin and
of plasminogen to plasma. NSAIDs. Acetaminophen can be
: dissolve blood clots caused by coronary substituted.
artery thrombi - Monitor ECG
 Pregnancy Category C - Instruct the client to report any side
effects, such as lightheadedness,
2. Urokinase dizziness, palpitations, nausea,
 Use: enzymes that act systematically to pruritus or urticaria.
►Table V-I (Autonomic nervous systems: sympathetic
NEURO: and parasympathetic ) p. 265

Adrenergic agents ► CHOLINERGICS or PARASYMPATHOMIMETICS


Adrenergic agents -Drugs that stimulate the nervous system.
- release norepinephrine at the neurotransmitter -They mimic the parasympathetic neurotransmitter
for sympathetic nervous system acetylcholine(ACh).
- activates preparatory body from vigorous body -Cholinergic drugs are also called cholinomimetics,
activity cholinergic stimulants, or cholinergic agonists.
- stimulate adrenergic nerves mimicking the -♥Two types of cholinergic receptors:
action of nor. E or indirectly releasing nor. E. (1)Muscarinic receptors- stimulate smooth muscle and
- combat life threatening disorders w/c include slow the heart rate.
acute attacks of bronchial asthma, shock, (2)Nicotinic receptors (neuromuscular)- affect skeletal
cardiac arrest and allergic reactions muscles.
Receptor sites -♥Major responses of cholinergic drugs are:
alpha ♠stimulate bladder and GI tone
vasoconstriction,iris dilatation, intestinal relaxation, ♠constrict pupils
intestinal sphinter contraction, bladder sphinter ♠(↑) neuromuscular transmission
contraction. -♥Other effects of cholinergic drugs:
beta ♠(↓) HR and BP
vasodilation, carsio acceleration, intestinal relaxation, ♠(↑)salivary, GI, and bronchial glandular
uterus relaxation, bronchodilation secretions
SE:
nervousness, agitation, wakefulness ►DIRECT-ACTING CHOLINERGICS
nsg responsibility -act on receptors to activate a tissue response
divert attention -primarily selective to the muscarinic receptors but are
drug-drug nonspecific because the muscarinic receptors are
furazolidone ( furoxone ) located in the smooth muscles of the GI and
trycyclic ( antidepressants ) genitourinary tracts, glands, and heart.
adapin, asendin, arentyl -♥Example: (1) Bethanechol chloride(Urecholine)
elavil , endep , norpramin -acts on muscarinic (cholinergic) receptor
pomelor , sinequan -used primarily to ↑ urination
summontil ,tofranil , vivactil -(Pharmacokinetics) → poorly absorbed from
gunathedine. the GI tract
→ excreted in the urine
Cholinergic Agents
-(Pharmacodynamics) → use to promote
Peripheral Nervous System micturition(urination) by stimulating the
System muscarinic cholinergic receptors.
→client voids approximately 30 mins. to
1.5 hrs. after taking an oral dose of this drug.
→ (↑)peristalsis in the GI tract.
Autonomic NS Somatic NS → NO: IM or IV route
YES: SubQ route
** micturition usually occurs within 15
mins. via subQ route.
Sympathetic NS Parasympathetic NS
NS NS →duration of acton is 4-6 hrs. for oral
route and 2 hrs. for subQ route.

-(Side effects and adverse reactions):


►Parasympathetic Nervous System → hypotension
-also called the cholinergic system, because the → bradycardia
neurotransmitter at the end of the neuron that → excessive salivation
innervates the muscle is acetylcholine. → (↑) gastric acid secretion
→ abdominal cramps
►See figure V-2 (Sympathetic ad parasympathetic → diarrhea
effects in the body), p. 264 → bronchoconstriction
→ (in some cases) cardiac dysrythmias.
-♥ NURSING INTERVENTIONS: (Indirect- Acting)
-Beware of the possibility of cholinergic crisis
-(Contraindications and cautions) (overdose); symptoms include muscular weakness
→ prescribed cautiously for clients with and (↑) salivation.
low BP and HR -Instruct client to take the drug on time to avoid
respiratory muscle weakness.
-Instruct client to assess changes in muscle
(2) Metoclopramide HCl (Reglan) strength→ cholinesterase inhibitors (↑) muscle
-usually prescribed to treat gastroesophageal strength.
reflux disease (GERD)
- (↑) gastric emptying time - cholinesterase inhibitors can be separated into
reversible inhibitors and irreversible inhibitors.
► DIRECT-ACTING CHOLINERGIC: EYE
-♥Pilocarpine ► REVERSIBLE CHOLINESTERASE INHIBITORS
→ constricts pupils of the eyes thus -Use to: (1) produce pupillary constriction in the
opening the canal of Schlemm to promote treatment of glaucoma.
drainage of aqueous humor (fluid) . (2) (↑) muscle strength in myasthenia gravis.
→Used to treat glaucoma by relieving -Drugs used to (↑) muscular strength in myasthenia
fluid (intraocular) pressure in the eye. gravis include:
(1) Neostigmine (Prostigmin) → short- acting
-♥NURSING INTERVENTIONS: (Direct Acting) (2) Pyridostigmine bromide (Mestinon)
-Monitor VS→ HR and BP (↓) when large doses of →moderate-acting
cholinergics are given. (3) Ambenonium chloride (Mytelase) →long-
-Record I&O→ (↓) urinary output should be reported acting
because it may be r/t urinary obstruction. (4) Edrophonium chloride (Tensilon) → short-
-Give 1 hr. before or 2 hrs. after meals. acting for diagnostic purposes
-Auscultate for bowel sounds→ report (↓) or -(Caution) →clients with bradycardia, asthma, peptic
hyperactive bowel sounds. ulcers, or hyperthyroidism.
-Auscultate breath sounds for rales or rhonchi→ -(Contraindications) →clients with intestinal or urinary
cholinergic drugs can (↑) bronchial secretions. obstruction.
-Have IV atropine sulfate (0.6 mg) available as an
antidote for cholinergic overdose. ► IRREVERSIBLE CHOLINESTERASE INHIBITORS
**Early signs of overdose include salivation, -potent agents because of their long-lasting effect.
sweating, abdominal cramps, and flushing. -these drugs are used to produce pupillary constriction
-Report severe dizziness or a (↓) in HR below 60 bpm. and to manufacture organophosphate insecticides.
-Instruct client arise slowly from lying position slowly to -the bond between the irreversible cholinesterase
avoid dizziness or orthostatic hypotension. inhibitor and cholinesterase is considered permanent;
-Encourage client to maintain effective oral hygiene if however, this bond can be broken with the use of the
excess salivation occurs. drug Pralidoxime (Protopam)→ an antidote to reverse
the irreversible organophosphate.
► INDIRECT-ACTING CHOLINERGICS
-do not act on receptors
-inhibit cholinesterase by forming a chemical complex,
thus permitting acetylcholine to persist and attach to the
receptor. Cholinergic Blocking Agents
**Cholinesterase- break down into choline and
acetic acid. -are drugs that inhibit the actions of
- may destroy acetylcholine before it reaches acetylcholine by occupying the acetylcholine
the receptor or after it has attached to the site. receptors.
-drugs that inhibit cholinesterase are called
cholinesterase inhibitors, acetylcholinesterase (AChE) -also known as parasympatholytics, adrenergic
inhibitors, or anticholinesterases. blocking agents, cholinergic or muscarinic
**By inhibiting cholinesterase, more antagonists, and antiparasympatethics.
acetylcholine is available to stimulate receptor
and remain in contact with it longer. -Major body tissues and organs affected by the
-Primary use of cholinesterase inhibitors is to treat anticholinergic group of drugs are the heart,
myasthenia gravis (a neuromuscular disorder) respiratory tract, GI tract, urinary bladder, eyes,
because cholinesterase inhibitors are useful to ↑ muscle and exocrine glands.
tone.
*Anticholinergics and cholinergic drugs have opposite muscarinic receptor. It increases the heart rate by
effects. The major responses to anticholinergics are blocking vagus stimulation and promotes dilation of the
decreased in GI motility, a decrease salivation, dilation pupils by paralyzing the iris sphincter.
of pupils, and an increase in pulse. Other effects include
decreased bladder contraction, which can result to ROUTE:
urinary retention, and decreased rigidity and tremors - Oral, IM, IV, Opthalmic
related to neuromuscular excitement.
CONTRAINDICATIONS
-narrow angle glaucoma, obstructive GI disorders,
EFFECTS OF ANTICHOLINERGICS paralytic ileus, ulcerative coditis, tachycardia, benign
prostatic hypertrophy, myasthenia gravis, and
Cardiovascular- increases heart rate with large doses. myocardial ischemia.
Small doses can decrease heart rate. *use caution with renal or hepatic disorders, COPD,
heart failure
Gastrointestinal- relaxes smooth muscle tone of GI
tract, decreasing GI motility and peristalsis. Decrease DOSAGE
gastric and intestinal secretions. A: PO/IM/IV: 0.4-0.6mg PRN
C: PO/IM/IV: 0.01 mg/kg/dose: max: 0.4mg/dose, q4-
Urinary Tract- relaxes the bladder detrusor muscle and Eh, PRN
increases constriction of the internal sphincter. Urinary
retention can result. PHARMACOKINETICS
ROUTE ONSET PEAK DURATION
Ocular- dilates pupils (mydriasis) and paralyzes ciliary IM 10-15min 30 min 4hr
muscle (cycloplegia), causing a decrease in IV Immediate 2-4min 4hr
accommodation. SC Varies 1-2 hr 4hr
TOPICAL 5-10min 30-40 7-14 days
Glandular- decrease salivation, perspiration, and min
bronchial secretions. METABOLISM: Hepatic; T ½: 2.5hr
DISTRIBUTION: crosses placenta; enters breast milk
Bronchial- dilates the bronchi and decreases bronchial EXCRETION: Urine
secretions.
ADVERSE EFFECTS
Central nervous system- decreases tremors and  Blurred vision, mydriasis, cycloplegia,
rigidity of muscles. Drowsiness, hallucinations, and photophobia, flushing, nervousness,
disorientation can result from large doses. weakness, dizziniess, insomnia, mental
confusion or excitement.
ATROPINE
-is a classic anticholinergic or muscarinic antagonist  Palpitations, bradycardia (low
drug. SCOPALAMINE was the second belladonna dosage), tachycardia(high dosage).
alkaloid produced. Atropine and scopolamine act on the  Dry mouth, altered taste perception,
muscarinic but they have a little effect on nicotinic nausea, vomiting, dyphagia, heartburn,
receptor. paralytic ileus.
-atropine is useful ;( INDICATIONS)  Urinary hesitancy and retention;
 As a preoperative medication to decrease impotence.
salivary secretions.  Ophthalmic: transient stinging, systemic
 As an antispasmodic drug to treat peptic ulcers, adverse effects depending on amount
because it relaxes the smooth muscles of the absorbed.
GI tract and decrease peristalsis.
 As an agent to increase heart rate when DRUG-TO-DRUG INTERACTIONS
bradycadia is present. - Increased anticholinergic effects with other drugs that
have anticholinergic activity-certain antihistamines,
*atropine can also be used as an antidote for muscarinic certain antiparkinsonians. TCAs, MAOI’s. Decreased
agonist poisoning caused by an overdose of antipsychotic effectiveness of haloperidol with atropine.
cholinesterase inhibitor or a muscarinic drug such as Decreased effectiveness of phenothiazines, but
bethanechol. increased incidence of paralytic ileus. If cholinesterase
and atropine are given together, opposing effects will
MODE OF ACTION: render both drugs ineffective.
-Atropine sulfate blocks acetylcholine by occupying the
NURSING REPONSIBILITIES hyperthyroidism, pregnancy.
- Check for history to hypersensitivity to
Atropine; anticholinergics. PHARMACOKINETICS
- Ensure adequate hydration; provide ROUT ONSET PEAK DURATION
environmental control to prevent E
hyperpyrexia (temperature). ORAL 60min 60min 8-12 hr
- Have patient void before taking IM, SC 15- 30-45 2-7 hr
medication if urinary retention is a 30min min
problem. IV 1 min End of
- Advise patient to finish course of infusion
medicine.
- Take the medicine as prescribed, 30
min. before meals; avoid excessive METABOLISM: Hepatic: T ½: 2.5 hr
dosage. DISTRIBUTION: crosses placenta; enters breast milk
- Avoid hot environments; for the patient EXCRETION: Urine
will be heat intolerant, the dangerous
reaction may occur. ADVERSE EFFECCTS
- Teaching the patient that there are  Headache, flushing, nervousness,
various side effects and to take drowsiness, mental confusion, fever.
precautions before any actions.  Tachycardia
- Advise the patient not to involve self
 Dry mouth, altered taste perceptions,
into extreme activities e.g. driving.
nausea, vomiting, dyphagia,
- Tell patient to report rash, eye pain,
heartburn, constipation, bloated feeling,
difficulty breathing, irregular heartbeats,
paralytic ileus.
loss of coordination, abdominal
 Urinary hesitancy and retention;
distention, difficulty swallowing,
impotence.
sensitivity to light and, constipation.
 Irritation at the site of IM injection.
GLYCOPYRROLATE  Blurred vision, mydriasis, cycloplegia,
(Robinul) photophobia, increased IOP.

DRUG CLASS:
Anticholinergic,antimuscarinic, parasympatholytic, DRUG-DRUG INTERACTION
antispasmodic -decreased antipsychotic effectiveness of
haloperidol with anticholinergic drugs, increased
MODE OD ACTION anticholinergic side effects with amantadines, TCAs,
-competitively blocks the effects of acetylcholine at decreased antipsychotic effects and increased
receptors that mediate the effects of parasympathetic anticholinergic effects with phenothiazines.
postganglionic impulses; depresses salivary and
bronchial secretion; dilates the bronchi, inhibits vagal NURSING RESPONSIBILITIES
influences to the heart, relaxes the GI and GU tracts, • Assess for glaucoma, adhesions between iris
inhibits gastric secretions. and lens, stenosing peptic ulcer.
- Ensure adequate hydration; provide
INDICATIONS environmental control to prevent
• As a preoperative medication to decrease hyperpyrexia (temperature).
salivary secretions. - Have patient void before taking
• As an antispasmodic drug to treat peptic ulcers, medication if urinary retention is a
because it relaxes the smooth muscles of the problem.
GI tract and decrease peristalsis. - Advise patient to finish course of
• As an agent to increase heart rate when medicine.
bradycardia is present. • Take the medicine as prescribed.
• Teach patient to have proper diet.
CONTRAINDICATIONS • Tell patient to report rash, eye pain, difficulty
-contraindicated with glaucoma, adhesions between iris breathing, irregular heartbeats, loss of
and lens, stenosing peptic ulcer, toxic megacolon, coordination, abdominal distention, difficulty
cardiac arrhythmias, MI, COPD, impaired liver or kidney swallowing, sensitivity to light and, constipation.
functions. Use cautiously with elderly with Down
syndrome, brain damage, spasticity, HPN, Anxiolytic and Hypnotic agents
for the treatment of symptoms of anxiety.
An anxiolytic or anti-anxiety agent is a drug prescribed

Anxiety disorders as recognized clinically include: - Dizziness


• Generalized anxiety disorder (excessive anxiety - Headache and restlessness
lacking any clear reason)
BARBITURATES
• Panic disorder (sudden attack of overwhelming Barbiturates are Non-selective CNS depressants
fear occur in association with marked somatic
(act partly by enhancing action of GABA) that
symptoms, such as sweating, tachycardia,
produce effect ranging from sedation and reduction
chest pains, trembling and choking.)
of anxiety and death from respiratory and
• Phobias (strong fears of specific objects or cardiovascular failure-therefore dangerous in
situations e.g. snakes, open spaces, flying, overdose.
social interactions)
Barbiturates Drug
Classification of Anxiolytic and Hypnotic Drugs - Phenobarbital, to treat epilepsy
• Benzodiazepines
- Thiopental, used as an intravenous
• Buspirone anaesthetic agent.
• Barbiturates
• B-blockers Antidepressants as Selective serotonin reuptake
• Sedative antihistamines inhibitors such as fluoxetine and sertraline are used
• Antidepressant to treat certain anxiety disorders.
• Antiepileptic drugs
• Zolpidem. (for insomnia) Drug interaction with anxiolytic or hypnotic Drugs

Benzodiazepines - Cimetidine metabolism of benzodiazepines


Act by binding to GABA receptor, thus enhancing the inhibited by cimetidine
inhibitory effect of GABA. - Rifampicin metabolism of benzodiazepines
ANXIOLYTIC effects are mediated by GABA receptor possibly accelerated by rifampicin.
containing the A2 subunit, while sedation occurs - Theophylline effects of benzodiazepines
through those with the a1 subunit. possibly reduced by theophylline.
- Digoxin/ alprazolam increases plasma
Effects of Benzodiazepines concentration of digoxin (inc. Risk of toxicity)
- Valproate/ clobazam possibly inc. Plama
Benzodiazepines cause: concentration of valproate.
- Reduction of anxiety and aggression. - Omeprazole/ metabolism of diazepam
- Sedation, leading to improvement of insomnia. possibly inhibited by omeprazole.
- Benzodiazepines decrease the time taken to
get to sleep, and increase the total duration of Anti-depressant
sleep, and increase the total duration of sleep.
- Muscle relaxation and loss of motor  Tricyclic antidepressants (TCAs) or
coordination (clonazepam) Tricycles
Action: block reuptake of serotonin and
Side effects of benzodiazepines norepinephrine by synaptic neurons
-drowsiness and confusion CI: - with MAOIs or within 14days of use, during
-amnesia acute MI recovery.
-Impaired coordination, which considerably affects - ↓ effects with carbamazepine,
manual skill such as driving performance. Phenobarbital, rifampin,
cholestyraminemcolestipol, tobacco
BUSPIRONE - ↑ effects with cimetidine, quinidine,
indinavir, retonavir, CNS depressants,
Buspirone is a partial agonist at 5-HT1a SSRIs, haloperidol
receptors is used to treat various anxiety - ↑ effect of amphetamines,
disorders. It alsobinds to dopamine receptors
anticholinergics, epinephrine,
(e.g. ipsapirone)
hypoglycemics, phenylephrine
Side Effect of Buspirone
Labs: ↑ glucose, false ↑ carbamasepinen levels
- Nausea
S/E: agranulocytosis, orthostatic hypotension
Nx Intervention: monitor CBC, advice client to and herbs client is taking. CNS depressants can
stand-up slowly cause an additive effect. Antidepressants that
cause anticholingeric-like symptoms are
 Fluxetine or Floxetine (Prozac) contraindicated if client has glaucoma
Action: Selective Serotonin Reuptake Inhibitors  Assess for tardive dyskinesia and neuroleptic
(SSRIs) malignant syndrome (NMS), including
CI: - MAOI or thioridazine (wait for 5 weeks after hyperpyrexia, muscle rigidity, tachycardia and
discontinuation before MAOI) cardiac dysrhythmias.
- ↑ effect with CNS depressants, MAOIs,
st. John’s wort Nursing diagnosis:
- ↑ effects of alparazolam,  Risk for self-directed violence and injury related
carbamazepine, clozapine, cardiac to feelings of despair.
glycosides, diazepam,  Anxiety related to situational crisis
dextromethorpan, loop diuretics,  Social isolation related to feelings of sadness
haloperidol, phenytoin, ritonavir, warfin,  Ineffective coping related to negative thought
sympathomimetic drugs. patterns
- ↓ effects of buspirone  Hopelessness related to feelings of despair
Labs: BUN, Cr, urine albumine  Deficient knowledge related to inexperience
S/E: dry mouth, blurred vision, insomnia, HA, with escitalopram (Lexapro)
nervousness, anorexia, nausea, diarrhea, suicidal  Ineffective health maintenance related to lack of
ideation. Some may experience sexual dysfunction. interest
SE may decrease or cease over 2-4 wks Planning
Nx Intervention: monitor kidney output, ↑ fluid and Nx Interventions:
fiber intake  Observe for s/sx of depression: mood
 monoamine oxidase inhibitors changes, insomnia, apathy or lack of
(MAOIs) interest in activities
Action: ↑CNS synaptic serotonin or norepinephrine  Check clients VS. Orthostatic
CI: acute recovery from MI, CHF, angina, arrythmias hypotension is common. Check for
S/E: risk of hypertensive crisis –they are particularly anticholinergic-like symptoms; dry
effective in treating atypical depression and have mouth, ↑ heart rate, urinary retention,
also shown efficacy in smoking cessation. constipation. Check weight 2-3xweek
Nx Intervention: avoid dairy products or food
 Monitor client for suicidal tendencies
(cheese, chocolates, cake) , avoid foods with ↑
when marked depression is present.
tyramine content.
 atypical antidepressants / second-  Observe client for seizures when client
generation antidepressants is taking an anticonvulsant;
CI: Should not be taken with MAOIs, should not be antidepressants lower seizure
used within 14 days after discontinuing MAOIs. threshold. The anticonvulsant dose
S/E: drowsiness, dizziness, EPS, postural might need to be increased.
hypotension, increased apetite, urinary retention,  Monitor drug-drug and food-drug
light-headedness, orthostatic hypotension, dry interactions. Provide client with a list of
mouth, food to avoid when taking MAOIs.
Nx intervention: take it with food to decrease GI These include cheese, red wine, beer,
distress liver, bananas, yogurt, and sausage.
ito lang nakuha ko sa book e :|  Check client for extremely ↑BP when
taking MAOIs. Sympathomimetic-like
NURSING PROCESS: drugs and foods containing tyramine
Assessment: may cause a hypertensive crisis if taken
 Record client’s baseline VS and weight for with MAOIs
future comparison Side Effects:
 Check clients liver and renal function by  Advise client that antidepressants may
assessing urine output (>600ml/d), blood urea be taken at bedtime to decrease
nitrogen (BUN), and serum creatinine and liver dangers from the sedative effect. Have
enzyme levels client check with health care provider.
 Obtain health hx of episodes of depression, Transient side effects include nausea,
assess mental status and assess for suicidal drowsiness, HA, and nervousness.
tendencies.
 Secure a drug hx of the current drugs, alcohol Antiepileptic
- Watch out for drug toxicity.
 Drugs used for epileptic seizures - Monitor the therapeutic serum drug range: TO
 It suppresses the abdominal electric ENSURE DRUG EFFECTIVENESS.
impulses from the seizures
 It is also classified as CNS B. BARBITUATES
depressants.  Prescribed to treat partial seizure,
ANTICONVULSANTS ACTS IN THREE WAYS grand mal seizures and episodes of
 By suppressing sodium influx through the drug status epileptic siezures, meningitis ,
binding to the sodium channel toxic reactions and eclampsia.
 By suppressing the calcium influx, preventing  May also be used to manage delirium
the electric current generated by the calcium treatment.
oins  Drugs that act as CNS depressants and
 By increasing the action of gamma-aminobutyic by the virtue of this they produced a
acid, which inhibits neurotransmitter throughout wide spectrum of effect from mild
the brain. sedation to total anesthesia.
INTERNATIONAL CLASSIFICATIONS OF SEIZURES
• Grand mal (tonic-clonic) *SIDE EFFECTS:
- most common form of seizure. - Agitated mood; clumsiness; confusion;
- In the TONIC PHASE; the skeletal muscle dizziness; excessive daytime drowsiness;
contract/ tighten in a spasm,usully last 3-5 headache; injection site reactions;
seconds. lightheadedness; low blood pressure; nausea;
- In the CLONIC PHASE; there is dysrhytmic slow heartbeat; slowed breathing; vomiting.
muscular contraction, or jerkiness of legs and
arms lasting for 2-4 minutes. *NURSING INTERVETION:
- use only for few days at the most
• Petit mal ( absence) - advice patient not to drive.
- breif loss of consciousness lasting less than - do not discontinue abruptly.
10 seconds; fewer than 3 spike waves on the C. SUCCUNIMIDES
electroencephalogram (EEG) printout  Used to treat absence or petit mal
- It usually occurs in children. siezures
 It acts by decreasing the calcium influx
• Psychomotor through the T-type calcium cahnnels.
- Complex symptoms; automatisms(repetitive  THERAPEUTIC RANGE: 40-
behavior such as chewing or swallowing 100mcg/ml.
motions), behavioral changes, and motor  Drug of choice:
seizures. ETHOSUXIMIDE(ZARONTIN)

A. HYDANTOINS *ADVERSE EFFECTS:


-It acts by inhibiting sodium influx, stabilizing - blood dyscrasias, renal and liver impairment,
cell membrane, redcing repetitive neuronal and systemic lupus erythematosus.
firing, and limiting seizures.
-Should no tbe used during pregnancy, because *SIDE EFFECTS:
it can have a TERATOGENIC effect on the - drowsiness, dizziness, confusion, blurred
fetus. vision.
-THERAPEUTIC RANGE: 10-20mcg/ml.
*CONTRAINDIATION: *NURSING RESPONSIBILITIES:
- hypersensitivity, heart block, psychiatric - may cause gastric irritation; must be taken
disorders, during pregnancy. with food.
*SIDE EFFECTS: -advice patient to increase fluid intake.
- headache, confusion, dizziness, decreased -Monitor CBC and differential before and
coordination, slurred speech, rash, anorexia, frequently during therapy.
nausea and vomiting, hypotension(IV), pink- -Take drug as prescribed, and do not
red/brown discoloration of urine. discontinue drug abruptly.
*NURSING RESPONSIBILITIES: -advice patient no to drink alcohol.
- Give alower dose for newborns, persons with D.OXAZOLIDONES/ OXAZOLIDINEDIONE
liver disease, and older adults: DECREASE IN  Prescribed to treat petite mal seizures.
METABOLISM RESULTING IN MORE  DRUGS: Trimethadione and
AVAILABLE DRUGS. Paramethadione.
habituation and drug dependence.
A. Trimethadione - Monitor for liver function and blood counts.
*SIDE EFFECTS: -Advice patient to take drug on time.
- Mild dizziness, poor coordination, or - Avoid alcohol.
drowsiness;blurred or double vision, or irregular - Avoid pregnancy. Using barrier contraceptives
back-and-forth movements of the is adviced while taking this drug.
eyes;decreased appetite, nausea, or vomiting; -Always take drug with food.
or increased sensitivity of the skin to sunlight. - Avoid driving and other dangerous activities.

*NURSING RESPONSIBILITIES:  CLORAZEPATE DIPOTASSIUM


-Drugs should be gradually withdrawn.  Frequently administered in adjunctive
- Take trimethadione exactly as directed by your therapy for trearting partial seizures.
doctor.
- Advice the patinet to take each dose of *SIDE EFFECTS:
trimethadione with a full glass of water. - drowsiness, dizziness, GI upset, fatigue,
Trimethadione can be taken on an empty nervousness, depression, emotional changes,
stomach or with food to decrease stomach bedwetting, urinary incontinence.
upset.
- Advice the patient to chew the chewable *NURSING RESPONSIBILITIES:
tablets before swallowing them. - Advice patient to take drug on time.
- Avoid alcohol
B. Paramethadione - Avoid pregnancy. Using barrier contraceptives
*SIDE EFFECTS: is adviced while taking this drug.
-mild dizziness, poor coordination, or -Always take drug with food.
drowsiness;blurred or double vision, or irregular - Avoid driving and other dangerous activities.
back-and-forth movements of the
eyes;decreased appetite, nausea, or vomiting;  DIAZEPAM
or increased sensitivity of your skin to sunlight.  Primarily prescribed for treating acute
status epilepticus
*NURSING RESPONSIBILITIES:  Must be administed IV to achive the
-Do not discontinue drug abruptly. desired response.
- Carry or wear a medical identification tag to let
 Drug has a short-term effect; other
others know that you are taking this medicine in
drugs such as phentoin and
the case of an emergency.
phenobarbital need to be given during
-Take paramethadione exactly as directed by
or immediately after administration of
your doctor.
diazepam.
-Take each dose of paramethadione with a full
glass of water. Paramethadione can be taken
*SIDE EFFECTS:
with food if it upsets your stomach.
- drowsiness, dizziness, GI upset, fatigue,
nervousness, difficulty concentrating.
E.BENZODIAZEPINES
 CLONAZEPAM *NURSING RESPONSIBILITIES:
 Effective in controlling petit mal - advice patient to take this drug on time. Do not
(absence) seizures attempt to discontinue drug without consulting
 Tolerance may occur 6 months after the health care provider.
drug therapy starts - Caregiver should learn to assess seizures,
 Consequently dosage has to be administer rectal form, and monitor patient.
adjusted. - Use of barrier contraceptives is adviced while
 THERAPEUTIS RANGE: 20-80 ng/ml. on this drug.

*SIDE EFFECTS: F.IMINOSTILBENES


- drowsiness, dizziness, GI upset, fatigue,  Prescribed to treat grand mal seizures,
nervousness, depression, emotional changes, complex partial seizures and status
bedwetting, urinary incontinence. epilepticus.
 Effective in treating refractory seizures
* NURSING RESPONSIBILITIES: disorders that have not responded to
-Monitor addiction-prone patients carefully other anticonvulsant therapies.
because of thier predipositon to habituation to  Most common drug: CARBAMAZEPINE
 Used for psychiatric disorders, Antiparkinsonism
trigeminal neuralgia, and alcohol
withdrawal. Panrkinsonism -is a chronic neurologic disorder that
 THERAPEUTIC RANGE: 5-12 mcg/ml. affects the extrapyramidal motor tract (which controls
*SIDE EFFECTS: posture, balance, and locomotion).
- Drowsiness, dizziness, blurred vision, GI Symptoms: (1)involuntary tremors of the limbs,
upset. (2)rigidity of muscles, and (3) slowness of movement

*NURSING RESPONSIBILITIES: Levodopa + Carbidopa :


- Take drug as prescribed. Swallow the tablets MOA: ↑ CNS dopamine levels
in whole; do not crush, cut or chew the tablet. CI: suspicious skin lesion (may activate melanoma),
- Do not discontinue drug abruptly. helanoma, MAOI use
- Avoid alcohol, sleep-inducing, or over-the- SE: Psych disturbances, orthostatic, ↓ BP, dyskinesias
counter drugs ; these could dangerous effects. Drug-Drug Interaction: ↑ Risk of hypotension with
- Arrange for frequent check-ups, including antihypersives, ↑ risk of HTN with MAOIs, ↑ effect with
blood tests, to monitor response to drug. antacids, ↓ effect with anticholinergics and
- Use of contraceptives at all times, is advised. anticonvulsants
-advise patient not to drive or do dangerous Drug-Lab: ↑ Alk phos, aspartate aminotransferase,
activities. bilirubin, BUN, uric acid, ↓ HMG
- Take drug with meals. Nursing Intervention: Darkened urine, Sweat may
result, N crush/chew S tabs, take with food,
G.VALPROATE muscle/eyelid twitching may suggest toxicity
 Is prescribed for petite mal, grand mal,
and mixed type of seizures. Benztropine:
 HEPATOTOXICITY is one of the MOA: blocks striatal cholinergic receptors
possible adverse reactions. SE: Anticholinergic (tachycardia, ileus, nausea and
 THERAPEUTIC RANGE: 40-100 vomiting, etc) anlydrosis, heat stroke
mcg/ml. Drug-Drug Interaction: ↑ sedation and depressant
effects with CNS depressants, ↑ anticholinergic effect
 Drug: DIVALPROEX
with antihistamine, phenothiazine, quinidine, ↑ effect of
SODIUM(Depakote)
digoxin, ↓ effect of levodopa, ↓ effect with antacids and
- for treatment of manic episodes associated
antidiarrheal drugs
with bipolar disorder.
Nursing Interaction: ↑ susceptibility to heat stroke,
take with meals to avoid GI upset
* SIDE EFFECTS:
- mild stomach cramps, change in menstrual
Muscle Relaxant
cycle, diarrhea, loss of hair, indigestion,
decreased appetite, nausea and vomiting,
trembling in the hands and arms, and weight  relieve muscular spasms and pain
loss or weight gain. associated with traumatic injuries and
spasticity from chronic debilitating
Less common side effects include severe disorders.
stomach cramps or continued nausea and  Depress neuron activity in the spinal
vomiting, changes in mood, behavior, or cord or brain act directly on the skeletal
thinking, double vision or seeing spots, severe muscles.
fatigue ,easy bruising or unusual bleeding, A. Spasticity – results from increased muscle tone from
yellow cast to the skin or the whites of the eyes hyper-excitable neurons or lack of inhibition in the spinal
(jaundice), odd eye movements, and increased cord or skeletal muscles. Ex: baclofen(Lioresal),
seizures. Dantroline(Dantrium) , Tizanidine (Zanaflex).
B. Muscle spasm – to decrease pain and increase
*NURSING RESPONSIBILITIES: range of motion. Ex: Carisoprodol(Soma),
- Take this medication exactly as it was Chlorzoxazone(Paraflex), cyclobenzaprine(Flexeril),
prescribed for you. Do not take the medication metaxalone(Skelaxin), methocarbamol(Robaxin) and
in larger amounts, or take it for longer than Orphenedrine citrate(Norflex)
recommended by your doctor. Follow the
instructions on your prescription label. MOA: blocks interneural activity.
- Advice patient to increase fluid intake.
- Do not discontinue abruptly. CI: severe liver or renal disease.
SE : N/V, dizziness, weakness, insomnia, drowsiness, -↓ pain
HA, light-headedness, GI sensitivity, diarrhea and
abhdominal distress.
Stages of General Anesthesia
AE: Asamthic attack, tachycardia, hypotension and
diplopia.  ANALGESIA (Induction Stage)
- begins w/ consciousness & ends w/ loss of
Drug-drug interaction: increase CNS depression w/ consciousness
alcohol, narcotics, sedative-hypnotics, antihistamines - SPEECH is difficult; sensations of SMELL &
,tricyclic anti-depressants. May increase risk of PAIN are lost
ventricular fibrillation w/ calcium channel blockers. - DREAMS, AUDITORY & VISUAL
HALLUCINATIONS may occur
Nsg Intervention:
 monitor VS, serum liver enzymes levels  Excitement or Delirium
 observe for CNS side Effects - produces loss of consciousness caused by
 it should not abruptly stop. Tapered DEPRESSION of the cerebral cortex
over 1week. - confusion, excitement or delirium occur
 Advise Px not to drive or use dangerous -SHORT induction time
machinery.
 Inmform px that muscle relaxant usually  Surgical
taken not longer than 3weeks. - surgery is performed usu at phase 2 & upper
 Tae meds with meals. phase 3
 Avoid with alcohol and CNS *as anesthesia deepens, respirations become
depressants SHALLOW and RR is ↑
 Warn px that this medication are
contraindicated with pregnant and  Medullary Paralysis
nursing mothers. - TOXIC
- respirations are lost, circulatory collapse occur
General and local Anesthetics - ventilator assistance is necessary

GENERAL ANESTHETICS ASSESSMENT: (before surgery)


-depress the CNS
-alleviate pain The response may differ accdg to variables r/t the health
-cause a loss of consciousness status of the individual.
 Age (young and elderly)
NITROUS OXIDE  Current health disorder
-“laughing gas”; first anesthetic  Pregnancy
-effective and is frequently used in dental surgeries  Hx of heavy smoking
 Obesity
Balanced Anesthesia  Freq use of alcohol and drugs
-a combination of drugs; frequently used in general
anesthesia Inhalation Anesthetics
-used to deliver general anesthesia dur the 3rd stage of
It includes: anesthesia
• Hypnotic (at night) - provide smooth induction
• Premed w/ a narcotic analgesic/ -usu combined w/ a barbiturate (ex. Thiopental), a
benzodiazepine plus an anticholinergic (given strong analgesic (ex. Morphine) & a muscle relaxant
about 1hr before surgery to ↓ secretions) (ex. Pancuronium) for SURGICAL PROCED.
• Short-acting barbiturate
• Inhaled gas (often nitrous oxide & O2) ∆ NITROUS OXIDE & CYCLOPROPANE- absorbed
quickly, have rapid action, eliminated rapidly
• Muscle relaxant as needed
- CYCLOPROPANE is no longer used bec of its highly
flammable state as ether
MOA:
-minimizes CV problems
∆ Halothane, isoflurane, enflurane- 1hr for recovery of
-↓ amt of general anesthetic needed
consciousness
-reduces possible postanesthetic N/V
∆ Desulfrane, sevoflurane- minutes for recovery
-minimizes the disturbance of organ function
AE: respiratory depression, hypotension, dysrhythmias, anaesthesias
hepatic dysfunction - may be used in dentistry
*clients @ risk- malignant hyperthermia ♥Prilocaine HCl (amide)
- for peri nerve block, infiltration, caudal and epidural
Intravenous Anesthetics anesthetics
-used for general anesthesia/ for the induction stage - may be used in dentistry
-short term surgery
∆ THIOPENTAL SODIUM- ultrashort acting barbiturate Long Acting
used for short term surgery; still used for rapid induction ♥Bupivacaine (amide)
stage and dental procedures - for peri nerve block, infiltration, caudal and epidural
anesthesia
IV anesthetics have rapid onsets & short durations of ♥Dibucaine (amide)
action. - for topical use to affected area (creams, ointments)
∆ Droperidol, etomidate, ketamine hydrochloride ♥Etidocaine (amide)
- for peri nerve block, infiltration, caudal and epidural
∆ MIDAZOLAM and PROPOFOL anesthesia
-for induction & maintenance of anesthesia ♥Tetracaine (ester)
-conscious sedation for minor surgery/ procedures like - for spinal anesthesia, topical use to affected areas
mech ventilation/ intubation such as the eye (to anesthesize cornea), to nose and
*Clients are sedated and relaxed but is RESPONSIVE throat (for bronchoscopy), to skin (for relief of pain and
TO COMMANDS pruritus)

AE (IV anesthetics): respi & cardio depression; ↑ risk for Spinal Anesthesia
bacterial infection (propofol) - a local anesthetic injected in the SUBARACHNOID
SPACE @ the 3rd or 4th LUMBAR SPACE
Topical Anesthetics - may result to HEADACHE possibly bec of a ↓ in CSF
-limited to mucous mem, broken/ unbroken skin pressure caused by a leak of fluid @ the needle
surfaces and burns insertion point
-solution, liquid spray, ointment, cream, gel, powder ** Encourage client to remain FLAT in bed ff surgery &
- ↓ sensitive nerve endings of the affected area to take ↑ fluids. (↓ likelihood of leaking spinal fluid)

SPINAL BLOCK- penetration of the anesthetic into the


LOCAL ANESTHETICS subarachnoid mem, the 2nd layer of the local anesthetic
- block pain @ the site where the drug is administered
-allow consciousness to be maintained EPIDURAL BLOCK- placement of the local anesthetic
- useful in dental procedures, suturing skin lacerations, in the outer covering of the spinal cord/ dura matter
short term/minor surgery @ a localized area, blocking
nerve impulses (nerve block) below the insertion of a CAUDAL BLOCK- placed near the sacrum
spinal anesthetic, dx procedures (lumbar puncture and
thoracentesis) SADDLE BLOCK- given @ the lower end of the spinal
-ESTERS & AMIDES; amides have a very low incidence column to block the perineal area
of allergic rxn -usu used for women in labor dur child birth

Short Acting: Nursing Process


♥Chloroprocaine (ester) ASSESSMENT
- for infiltration, caudal and epidural anesthesia -VS
♥Procaine HCl (ester) -drug hx (particularly those that affect cardiopulmonary
- for nerve block, infiltration, epidural and spinal systems)
anesthesia
**CAUTION to clients allergic to ester-type anesthetics. DIAGNOSIS
-Pain r/t injury
Moderate Acting: - Ineffective breathing pattern r/t CNS depression
♥Lidocaine (amide)
-for nerve block, infiltration, epidural and spinal PLANNING
anesthesia - participate in pre-op preparation & understand post-op
- used to treat cardiac dysrhythmias care
♥Mepivacaine (amide) - VS will remain stable ff surgery
- for nerve block, infiltration, caudal and epidural
INTERVENTION MOA:
-Prepare client for surgery by explaining preparations Prevents destruction of acetylcholine thus,
and completing the pre-op orders inclu premeds permits transmission of neuromuscular
(enhance safety and effectiveness of anesthesia and impulses
surgery)
-Monitor post-op state of sensorium. Report if still neostigmine (Prostigmin)
unresponsive/ confused for a time 5. fast-acting but has a short duration with a
-Check pre-op and post-op urine output half-life of 0.5-1hr. Given q2-q4
-Monitor VS (hypotension and respi distress may occur) pyridostigmine bromide (Mestinon)
-Administer analgesic/ a narcotic analgesic w/ caution 6. has intermediate action; given q3-q6
until client fully recovers from anesthetic ambenonium chloride (Mylelase)
-Doses may need to be adjusted to prevent adverse 7. given when client does not repond to
reactions neostigmine and ambenonium chloride
endrophonium (Tensilon)
EVALUATION 8. short-acting drug used to distinguish
-client’s response to anesthetics between Myasthenia crisis and cholinergic
crisis(both have similar symptoms)
9. after administration, if symptoms are
alleviated because of increase in Ach, the
Neuromuscular cause is myasthenia crisis and if symptoms
become severe, the cause is cholinergic
Neuromuscular Disorders crisis.
 Myasthenia gravis
1. lack of nerve impulses and muscle
responses at the myoneural(nerves in
muscle endings) junction
2. causes fatigue and muscular weakness of
the respiratory system, facial muscles and
extremities
3. includes ptosis (drooping eyelid) and
difficulty in chewing and swallowing due to Symptoms of Symptoms of
cranial nerve involvement Underdosing Overdosing
4. caused by inadequate or low secretion of
acetylcholine because of an increase in
enzyme acetylcholinesterase which breaks Muscle weakness Muscle weakness
down acetylcholine at the myoneural Dyspnea Dyspnea
junction Dysphagia Dysphagia
Increased salivation
Pathophysiology: bradycardia
Abdominal cramping
↓ amts. Of Ach Increased tearing
↓ &sweating
Antibody response against alpha subunit of Myasthenia crisis Cholinergic crisis
Acetylcholine receptor sites (AChR) in the
skeletal muscle
↓ Side effects:
Antibodies attack AChR sites  GI disturbances
↓ N/V
Antibodies accumulate at neuromuscular Diarrhea
transmission Abdominal cramps

 Increase salivation
Inhibition of normal neuromuscular transmission
↓  Tearing
Ineffective muscle contraction  Miosis (constricted pupil)

Nursing Interventions:
Acetylcholinesterase inhibitors/  Assess for respirations (depth and rate) and
cholinesterase inhibitors muscle strength
 Check for liver and kidney function
 Make sure that Acetylcholinesterase inhibitors/ 3. light headedness
cholinesterase inhibitors are administered on 4. Headache
time bec. Late administration results to muscle 5. N/V
weakness 6. Diarrhea
 Avoid taking muscle relaxants 7. GI upset
 Administer drug with food to avoid GI
disturbances Nursing Interventions:
 Check for availability and prepare atropine  Avoid drugs such as histamine (H2)
sulfate(antidote) in case of overdosing blocker, indomethacin, beta-blockers
 Multiple sclerosis  Avoid CNS depressants(barbiturates,
-autoimmune disorder that attacks the myelin narcotics, alcohol) while taking muscle
sheath of the nerve fibers of the brain and relaxants
spinal cord which causes plaques (lesions)  Discourage driving and operating
- symptoms include diplopia, weakness in machines
extremities and spasticity (for carisoprodol)
- Lab tests mau suggest MS • Monitor serum liver and
 Increase immunoglobulin G in cerebrospinal enzyme levels. Report elevated levels
fluid of ALT,ALP,GGT
 Increase IgG/albumin ratio • Tapered over 1wk. to
 Multiple lesions observed through MRI avoid rebound spasms
• Usually taken for no
3 Phases longer than 3wks.
1. Acute Attack- characterized by fatigue, • Take with food to
motor weakness, optic neuritis decrease GI upset

2. remission exacerbation- recurrence of Anti-Migraine drugs


clinical symptoms, spasticity
Anti Migraine drugs
3. chronic progressive- progressive MS ♥ Migraine HA
symptoms (wheelchair bound)
-unilateral throbbing head pain
accompanied by N/V and photophobia
* goals for treatment strategies are to -Sx frequently persist foo4-24 hrs and for
decrease inflammation process of nerve several days in some cases
fibers and improve conduction of
demyelinating axons
-2/3 are experienced by women in their
20s and 30s s
Skeletal Muscle Relaxants -Sx usually decrease or are absent
1. relieve symptoms of spasticity w/c results during preg. And menopause
from increased muscle tone from -disrupts daily activities
hyperexcitable neurons caused by increased
stimulation from cerebral neurons or lack of -Two types of Migraine: Classic migraines
inhibition in the spinal cord and Common Migraines
Centrally acting Muscle relaxants Classic migraines
2. suppress hyperactive reflex and muscle -associated with an AURA that occurs
spasms that do not respond to anti-
minutes to 1 hour before onset
inflammatory agents or physical therapy
3. for spasticity: baclofen (Lioresal), Common migraines
dantrolene (Dantrium), tizanidine (Zanaflex) -NOT associated with an aura
and Diazepam a benzodiazepine ♥ Cluster HA
4. agents for muscle spasms are used to -severe unilateral non throbbing pain
decrease pain and increase range of
motion, ex. Carisoprodol (Soma), usually located around the eye
chlorpleresin carbamate (Maolate), -occur in a series of cluster attacks---one
chlorzoxazon (Paraflex) etc… or more attacks every day for several
Side effects: weeks
1. dizziness
2. drowsiness
-NOT associated with an aura, do not
cause N/V - Dihydroergotamine (an ergot
-men are more commonly affected alkaloid) can be SQ, IM, IV or nasal
Preventive treatment of migraine spray
HA
1. Beta adrenergic blockers: →Triptans (5-HT receptor agonist)
Propanolol (Inderal), atenolol -Sumatriptan(Imitrex): short duration of
(Tenormin) action, 1st triptan drug, considered more
effevtive than ergotamine in treating
2. Anti convulsants: valproic acid acute migraine attacks
(depakote), gabapentin (neurontin)

3. Tri cyclic antidepressants:


amitriptyline (elavil), imipramine
(tofranil)

→Tx or cessation of a migraine attack


depends on the intensity of pain
→drugs used to treat migraines include:
Analgesics, opoid analgesics, ergot
alkaloids, selective serotonin (5-HT)
receptor agonists, also known as
triptans
→for mild migraine attacks: aspirin (may
be used w/ caffeine), NSAIDS s/a
ibuprofen or naproxen (Aleve)
→Opoid analgesics: Meperidine
(Demerol) and butorphanol nasal spray
(Stadol NS)
→Ergotamine tartrate
- nonspecific serotonin agonist and
vasoconstrictor

- used to treat moderate to severe


migraine attacks

- should be taken early during the


attack

- N/V might occur (antiemetics


decrease these sx)

- available in sublingual tablets or


with caffeine in oral tablets and
suppositories
BSN-2H NOTES 

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