©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
 Baroreceptor
- aorta and carotid sinus
- pressure receptor
- vasomotor center in the medulla
- hormones: antidiuretic (produced by the
hypothalamus and is stored and release by the
posterior pituitary gland) , atrial natriuretic
peptide, brain natriueretic peptide
HYPERTENSION
-an increase in blood pressure such that the systolic
pressure is greater than 140 mmHg and the diastolic
pressure is greater than 90 mmHg
SAMPLE
-Hydrochlorothiazide (hydroDIURIL)
CI and CAUTION
-Thiazide: renal insufficiency (creatinine clearance > 30
ml/min)
SYMPATHOLITICS (sympathetic Depressants)
1. Beta- adrenergic blockers
2. Centrally acting alpha2- agonists
3. Alpha- adrenergic blockers
4. Adrenergic neuron blockers (peripherally acting
sympatholytics
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
the venous circulation
-cause generalized vascular and coronary
vasodilation thus increasing blood flow through
the coronary arteries to the myocardial cells
-reduces myocardial ischemia but can cause
hypotension
MOA: cause vasodilation due to relaxation of
smooth muscles
Potent dilating effect on coronary
arteries
INDICATION: used for prophylaxis and
treatment of angina
CONTRAINDICATION: severe anemia,
head trauma or cerebral hemmorhage
EXAMPLES:
1. NITROGLYCERIN (NITROBID, NITROSTAT)
-AVERAGE DOSE PRESCRIBED FOR
SUBLINGUAL NITROGLYCERIN TABLET: 0.4
mg or gr 1/150 – repeated every 5 minutes for a
total of 3 doses
-SL TABLETS: decompose when exposed to
heat and light – should be kept in their original
AIRTIGHT GLASS CONTAINERS
- not swallowed because it undergoes first-
pass metabolism by the liver which decreases
its effectiveness
2. ISOSORBIDE DINITRATE ( ISORDIL,
SORBITRATE)
3. ISOSORBIDE MONONITRATE ( MONOKET,
IMDUR)
SIDE EFFECTS: Headache – most common
but may become
less frequent with
continued use
Hypotension, dizziness, weakness and
faintness
When nitroglycerin is discontinued, the dose
should be tapered over several weeks to
prevent the rebound effect of severe pain
caused by myocardial ischemia.
Reflex Tachycardia- occur if nitrate is given too
rapidly; heart rate increases greatly because of
overcompensation of the cardiovascular
system.
DRUG INTERACTIONS: increase effect with
alcohol, beta-blockers, calcium channel
blockers, antihypertensiveness; decrease
effects of heparin
NURSING INTERVENTION: NITROGLYCERIN
1. Monitor VS
2. Instruct to rise slowly to standing position
3. Sip water before sublingual nitrates
4. Apply ointments- use gloves
5. Do not apply nitrates with defibrillation-
cardioverter
6. Instruct patient to take PRN nitrates at the
first hint of angina pain.
- If pain persists, repeat in 5 mins
- DO NOT GIVE MORE THAN 3 TABLETS
- if chest pain persists longer than 15 mins,
immediate medical help is necessary
7. Never chew or swallow
8. burning sensation-normal
9. Lying down or sit to prevent dizziness
10 .Blood level monitor
11. Take before meals
12. Limit caffeine intake
13. To avoid hypotension, weakness and
faintness, instruct client not to ingest alcohol
while taking nitroglycerin
14. Tolerance can occur.
15. Instruct client about the Transderm-Nitro
patch. Apply once a day, usually in the morning.
Rotation of skin sites is necessary. The patch is
usually applied to the chest wall, but thighs and
arms may also be used. Avoid hairy areas.
15. Headaches commonly occur when first
taking nitroglycerin products and last about 30
mins. Acetaminophen is suggested for relief.
16. If hypotension results from SL nitroglycerin,
place in supine position with legs elevated.
• BETA-BLOCKERS
-decrease the workload of the heart and
decrease oxygen demands
-effective with stable angina
-decrease the effects of the sympathetic
nervous system by blocking the action of the
catecholamines epinephrine and
norepinephrine thereby decreasing the heart
rate and blood pressure
-used as antianginal, antidysrhythmic and
antihypertensive
-effective as antianginal because by decreasing
the heart rate and myocardial contractility, they
reduce the need for oxygen consumption and
consequently reduce anginal pain
-most useful for classic angina
-should not be abruptly discontinued; dose
should be tapered over a specified no. of days
to avoid reflex tachycardia and recurrence
angina pain
-clients with decreased heart rate and blood
pressure usually cannot take beta blockers
-clients with second or third degree AV block
should not take beta-blockers
EXAMPLES OF NONSELECTIVE BETA-
BLOCKERS:
 Propanolol ( Inderal)
 Nadolol ( Corgard)
 Pindolol ( Visken)
- Decrease heart rate and can cause
bronchoconstriction
- Cardioselective beta-blockers act more
strongly on the beta1 receptor thus
decreasing the heart rate but avoiding
 bronchoconstriction because of their
relative lack of activity at the beta2
receptor
EXAMPLES OF SELECTIVE BETA-
BLOCKERS:
 Atenolol ( Tenormin)
 Metoprolol ( Lopressor, Toprol-XL)
- grp of choice for controlling angina
pectoris
SIDE EFFECTS AND ADVERSE REACTIONS:
decrease in heart rate and blood pressure –
both selective and non selective drugs
bronchospasm, behavioural or psychotic
response and impotence – potential adverse
reactions for non-selective beta-blockers
NURSING INTERVENTION:
Vital signs need to be closely monitored in the ischemic attacks (TIAs)
early stages of beta blocker therapy
When discontinuing, dosage should be tapered
for 1-2 wks to prevent rebound effect like reflex
tachycardia or life-threatening cardiac
dysrhythmias
Monitor PR
Inform patient it is a long term med
• CALCIUM CHANNEL BLOCKERS
- decrease the workload of the heart and
decrease oxygen demands
- effective in treating variant angina pectoris
-treatment of stable and variant angina pectoris,
certain dysrhythmias and hypertension
-relax coronary artery spasm and relax
peripheral arterioles decreasing cardiac oxygen
demand
-decrease cardiac contractility, decrease
afterload, decrease peripheral resistance and
reduce the workload of the heart thus
decreasing the need for oxygen
-achieve their effect in controlling variant angina
by relaxing coronary arteries and in controlling
classic angina by decreasing oxygen demand
CALCIUM- activates myocardial contraction,
increasing the workload of the heart and the
need for more oxygen
EXAMPLES:
Verapamil (Calan)- first calcium blocker
- Bradycardia is a common
problem
Nifedipine ( Procardia) – most potent of the calcium
blockers, promotes vasodilation of the coronary and
peripheral vessels
-hypotension can result
Diltiazem (Cardizem)
SIDE EFFECTS AND ADVERSE REACTIONS
- Headache
- Hypotension ( more common with Nifedipine
and less common with Diltiazem)
- Dizziness
- Flushing of the skin
- Reflex Tachycardia – can occur as a result of
hypotension
- Can cause changes in the liver and kidney
function – serum liver enzymes should be
checked periodically
Anti-platelet
• Used to prevent thrombosis in the arteries by
suppressing platelet aggregation
• Mainly for prophylactic use in:
o Prevention of myocardial infarction or stroke
for client w/ familial hx
o Prevention of repeat MI or stroke
o Prevention of a stroke for clients having transient
xamples:
• ASPIRIN
o Long-term & low dose aspirin therapy
 Effective & inexpensive tx for
suppressing platelet aggregation
o MOA: inhibits cyclooxygenase (enzyme
needed by platelet to synthesize
thromboxane A2 (TxA2)
o Indications:
 Prevention of thrombosis before or after
CVA or MI
 Familial hx of MI or stroke
o Dose: 81, 162, or 325 md/day
 Should be discontinued at least 7 days
before surgery
• CLOPIDOGREL (Plavix)
o MOA:
 inhibits platelet aggregation
 prevents ADP from binding w/ the ADP
platelet recptor
o May be prescribed singly or w/ aspirin
(more effective)
o CI: peptic ulcer, active bleeding, intracranial
hemorrhage
o SE: upper RTI, flulike symptoms, dizziness,
HA, fatigue, chest pain, diarrhea, may
cause HTN & bronchitis
Drug interaction: NSAIDs – may  bleeding
o Lab: prolongs bleeding time
o Herb: ginger, garlic, gingko, feverfew – may
 bleeding
• GP IIb/IIIa inhibitors
o MOA: blocks the binding of fibrinogen to the
glycoprotein IIb/IIIa receptor on the platelet
surface
o Used primarily for acute coronary
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.

-(Contraindications and cautions)
→ prescribed cautiously for clients with and (↑) salivation.
low BP and HR
(2) Metoclopramide HCl (Reglan)
-usually prescribed to treat gastroesophageal
reflux disease (GERD)
- (↑) gastric emptying time
► DIRECT-ACTING CHOLINERGIC: EYE
-♥Pilocarpine
→ constricts pupils of the eyes thus
opening the canal of Schlemm to promote
drainage of aqueous humor (fluid) .
→Used to treat glaucoma by relieving -Drugs used to (↑) muscular strength in myasthenia
fluid (intraocular) pressure in the eye.
-♥NURSING INTERVENTIONS: (Direct Acting)
-Monitor VS→ HR and BP (↓) when large doses of
cholinergics are given.
-Record I&O→ (↓) urinary output should be reported acting
because it may be r/t urinary obstruction.
-Give 1 hr. before or 2 hrs. after meals.
-Auscultate for bowel sounds→ report (↓) or
hyperactive bowel sounds.
-Auscultate breath sounds for rales or rhonchi→
cholinergic drugs can (↑) bronchial secretions.
-Have IV atropine sulfate (0.6 mg) available as an
antidote for cholinergic overdose.
**Early signs of overdose include salivation,
sweating, abdominal cramps, and flushing.
-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.
-Encourage client to maintain effective oral hygiene if however, this bond can be broken with the use of the
excess salivation occurs.
► 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.
**Cholinesterase- break down into choline and
acetic acid.
- may destroy acetylcholine before it reaches
the receptor or after it has attached to the site.
-drugs that inhibit cholinesterase are called
cholinesterase inhibitors, acetylcholinesterase (AChE)
inhibitors, or anticholinesterases.
**By inhibiting cholinesterase, more
acetylcholine is available to stimulate receptor
and remain in contact with it longer.
-Primary use of cholinesterase inhibitors is to treat
myasthenia gravis (a neuromuscular disorder)
because cholinesterase inhibitors are useful to ↑ muscle
tone.
-♥ NURSING INTERVENTIONS: (Indirect- Acting)
-Beware of the possibility of cholinergic crisis
(overdose); symptoms include muscular weakness
-Instruct client to take the drug on time to avoid
respiratory muscle weakness.
-Instruct client to assess changes in muscle
strength→ cholinesterase inhibitors (↑) muscle
strength.
- cholinesterase inhibitors can be separated into
reversible inhibitors and irreversible inhibitors.
► REVERSIBLE CHOLINESTERASE INHIBITORS
-Use to: (1) produce pupillary constriction in the
treatment of glaucoma.
(2) (↑) muscle strength in myasthenia gravis.
gravis include:
(1) Neostigmine (Prostigmin) → short- acting
(2) Pyridostigmine bromide (Mestinon)
→moderate-acting
(3) Ambenonium chloride (Mytelase) →long-
(4) Edrophonium chloride (Tensilon) → short-
acting for diagnostic purposes
-(Caution) →clients with bradycardia, asthma, peptic
ulcers, or hyperthyroidism.
-(Contraindications) →clients with intestinal or urinary
obstruction.
► IRREVERSIBLE CHOLINESTERASE INHIBITORS
-potent agents because of their long-lasting effect.
-these drugs are used to produce pupillary constriction
inhibitor and cholinesterase is considered permanent;
drug Pralidoxime (Protopam)→ an antidote to reverse
the irreversible organophosphate.
Cholinergic Blocking Agents
-are drugs that inhibit the actions of
acetylcholine by occupying the acetylcholine
receptors.
-also known as parasympatholytics, adrenergic
blocking agents, cholinergic or muscarinic
antagonists, and antiparasympatethics.
-Major body tissues and organs affected by the
anticholinergic group of drugs are the heart,
respiratory tract, GI tract, urinary bladder, eyes,
and exocrine glands.
*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
- Check for history to hypersensitivity to
Atropine; anticholinergics.
- Ensure adequate hydration; provide
environmental control to prevent
hyperpyrexia (temperature).
- Have patient void before taking
medication if urinary retention is a
problem.
- Advise patient to finish course of
medicine.
- Take the medicine as prescribed, 30
min. before meals; avoid excessive
dosage.
- Avoid hot environments; for the patient EXCRETION: Urine
will be heat intolerant, the dangerous
reaction may occur.
- Teaching the patient that there are
various side effects and to take
precautions before any actions.
- Advise the patient not to involve self
into extreme activities e.g. driving.
- Tell patient to report rash, eye pain,
difficulty breathing, irregular heartbeats,
loss of coordination, abdominal
distention, difficulty swallowing,
sensitivity to light and, constipation.
GLYCOPYRROLATE
(Robinul)
DRUG CLASS:
Anticholinergic,antimuscarinic, parasympatholytic,
antispasmodic
MODE OD ACTION
-competitively blocks the effects of acetylcholine at
receptors that mediate the effects of parasympathetic
postganglionic impulses; depresses salivary and
bronchial secretion; dilates the bronchi, inhibits vagal
influences to the heart, relaxes the GI and GU tracts,
inhibits gastric secretions.
INDICATIONS
• As a preoperative medication to decrease
salivary secretions.
• As an antispasmodic drug to treat peptic ulcers,
because it relaxes the smooth muscles of the
GI tract and decrease peristalsis.
• As an agent to increase heart rate when
bradycardia is present.
CONTRAINDICATIONS
-contraindicated with glaucoma, adhesions between iris
and lens, stenosing peptic ulcer, toxic megacolon,
cardiac arrhythmias, MI, COPD, impaired liver or kidney
functions. Use cautiously with elderly with Down
syndrome, brain damage, spasticity, HPN,
hyperthyroidism, pregnancy.
PHARMACOKINETICS
ROUT ONSET PEAK DURATION
E
ORAL 60min 60min 8-12 hr
IM, SC 15- 30-45 2-7 hr
30min min
IV 1 min End of
infusion
METABOLISM: Hepatic: T ½: 2.5 hr
DISTRIBUTION: crosses placenta; enters breast milk
ADVERSE EFFECCTS
 Headache, flushing, nervousness,
drowsiness, mental confusion, fever.
 Tachycardia
 Dry mouth, altered taste perceptions,
nausea, vomiting, dyphagia,
heartburn, constipation, bloated feeling,
paralytic ileus.
 Urinary hesitancy and retention;
impotence.
 Irritation at the site of IM injection.
 Blurred vision, mydriasis, cycloplegia,
photophobia, increased IOP.
DRUG-DRUG INTERACTION
-decreased antipsychotic effectiveness of
haloperidol with anticholinergic drugs, increased
anticholinergic side effects with amantadines, TCAs,
decreased antipsychotic effects and increased
anticholinergic effects with phenothiazines.
NURSING RESPONSIBILITIES
• Assess for glaucoma, adhesions between iris
and lens, stenosing peptic ulcer.
- Ensure adequate hydration; provide
environmental control to prevent
hyperpyrexia (temperature).
- Have patient void before taking
medication if urinary retention is a
problem.
- Advise patient to finish course of
medicine.
• Take the medicine as prescribed.
• Teach patient to have proper diet.
• Tell patient to report rash, eye pain, difficulty
breathing, irregular heartbeats, loss of
coordination, abdominal distention, difficulty
swallowing, sensitivity to light and, constipation.
Anxiolytic and Hypnotic agents

An anxiolytic or anti-anxiety agent is a drug prescribed
Anxiety disorders as recognized clinically include:
• Generalized anxiety disorder (excessive anxiety
lacking any clear reason)
• Panic disorder (sudden attack of overwhelming
fear occur in association with marked somatic
symptoms, such as sweating, tachycardia,
chest pains, trembling and choking.)
• Phobias (strong fears of specific objects or
situations e.g. snakes, open spaces, flying,
social interactions)
Classification of Anxiolytic and Hypnotic Drugs
• Benzodiazepines
• Buspirone
• Barbiturates
• B-blockers
• Sedative antihistamines
• Antidepressant
• Antiepileptic drugs
• Zolpidem. (for insomnia)
Benzodiazepines
Act by binding to GABA receptor, thus enhancing the
inhibitory effect of GABA.
ANXIOLYTIC effects are mediated by GABA receptor
containing the A2 subunit, while sedation occurs
through those with the a1 subunit.
Effects of Benzodiazepines
Benzodiazepines cause:
- Reduction of anxiety and aggression.
- Sedation, leading to improvement of insomnia.
- 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
coordination (clonazepam)
Side effects of benzodiazepines
-drowsiness and confusion
-amnesia
-Impaired coordination, which considerably affects
manual skill such as driving performance.
BUSPIRONE
Buspirone is a partial agonist at 5-HT1a
receptors is used to treat various anxiety
disorders. It alsobinds to dopamine receptors
(e.g. ipsapirone)
Side Effect of Buspirone
- Nausea
for the treatment of symptoms of anxiety.
- Dizziness
- Headache and restlessness
BARBITURATES
Barbiturates are Non-selective CNS depressants
(act partly by enhancing action of GABA) that
produce effect ranging from sedation and reduction
of anxiety and death from respiratory and
cardiovascular failure-therefore dangerous in
overdose.
Barbiturates Drug
- Phenobarbital, to treat epilepsy
- Thiopental, used as an intravenous
anaesthetic agent.
Antidepressants as Selective serotonin reuptake
inhibitors such as fluoxetine and sertraline are used
to treat certain anxiety disorders.
Drug interaction with anxiolytic or hypnotic Drugs
- Cimetidine metabolism of benzodiazepines
inhibited by cimetidine
- Rifampicin metabolism of benzodiazepines
possibly accelerated by rifampicin.
- Theophylline effects of benzodiazepines
possibly reduced by theophylline.
- Digoxin/ alprazolam increases plasma
concentration of digoxin (inc. Risk of toxicity)
- Valproate/ clobazam possibly inc. Plama
concentration of valproate.
- Omeprazole/ metabolism of diazepam
possibly inhibited by omeprazole.
 Tricyclic antidepressants (TCAs) or
Tricycles
Action: block reuptake of serotonin and
norepinephrine by synaptic neurons
CI: - with MAOIs or within 14days of use, during
acute MI recovery.
- ↓ effects with carbamazepine,
Phenobarbital, rifampin,
cholestyraminemcolestipol, tobacco
- ↑ effects with cimetidine, quinidine,
indinavir, retonavir, CNS depressants,
SSRIs, haloperidol
- ↑ effect of amphetamines,
anticholinergics, epinephrine,
hypoglycemics, phenylephrine
Labs: ↑ glucose, false ↑ carbamasepinen levels
S/E: agranulocytosis, orthostatic hypotension
 Nx Intervention: monitor CBC, advice client to
stand-up slowly
 Fluxetine or Floxetine (Prozac)
Action: Selective Serotonin Reuptake Inhibitors
(SSRIs)
CI: - MAOI or thioridazine (wait for 5 weeks after
discontinuation before MAOI)
- ↑ effect with CNS depressants, MAOIs,
st. John’s wort
- ↑ effects of alparazolam,
carbamazepine, clozapine, cardiac
glycosides, diazepam,
dextromethorpan, loop diuretics,
haloperidol, phenytoin, ritonavir, warfin,
sympathomimetic drugs.
- ↓ effects of buspirone
Labs: BUN, Cr, urine albumine
S/E: dry mouth, blurred vision, insomnia, HA,
nervousness, anorexia, nausea, diarrhea, suicidal
ideation. Some may experience sexual dysfunction.
SE may decrease or cease over 2-4 wks
Nx Intervention: monitor kidney output, ↑ fluid and
fiber intake
 monoamine oxidase inhibitors
(MAOIs)
Action: ↑CNS synaptic serotonin or norepinephrine
CI: acute recovery from MI, CHF, angina, arrythmias
S/E: risk of hypertensive crisis –they are particularly
effective in treating atypical depression and have
also shown efficacy in smoking cessation.
Nx Intervention: avoid dairy products or food
(cheese, chocolates, cake) , avoid foods with ↑
tyramine content.
 atypical antidepressants / second-
generation antidepressants
CI: Should not be taken with MAOIs, should not be
used within 14 days after discontinuing MAOIs.
S/E: drowsiness, dizziness, EPS, postural
hypotension, increased apetite, urinary retention,
light-headedness, orthostatic hypotension, dry
mouth,
Nx intervention: take it with food to decrease GI
distress
ito lang nakuha ko sa book e :|
NURSING PROCESS:
Assessment:
 Record client’s baseline VS and weight for
future comparison
 Check clients liver and renal function by
assessing urine output (>600ml/d), blood urea
nitrogen (BUN), and serum creatinine and liver
enzyme levels
 Obtain health hx of episodes of depression,
assess mental status and assess for suicidal
tendencies.
 Secure a drug hx of the current drugs, alcohol Antiepileptic
and herbs client is taking. CNS depressants can
cause an additive effect. Antidepressants that
cause anticholingeric-like symptoms are
contraindicated if client has glaucoma
 Assess for tardive dyskinesia and neuroleptic
malignant syndrome (NMS), including
hyperpyrexia, muscle rigidity, tachycardia and
cardiac dysrhythmias.
Nursing diagnosis:
 Risk for self-directed violence and injury related
to feelings of despair.
 Anxiety related to situational crisis
 Social isolation related to feelings of sadness
 Ineffective coping related to negative thought
patterns
 Hopelessness related to feelings of despair
 Deficient knowledge related to inexperience
with escitalopram (Lexapro)
 Ineffective health maintenance related to lack of
interest
Planning
Nx Interventions:
 Observe for s/sx of depression: mood
changes, insomnia, apathy or lack of
interest in activities
 Check clients VS. Orthostatic
hypotension is common. Check for
anticholinergic-like symptoms; dry
mouth, ↑ heart rate, urinary retention,
constipation. Check weight 2-3xweek
 Monitor client for suicidal tendencies
when marked depression is present.
 Observe client for seizures when client
is taking an anticonvulsant;
antidepressants lower seizure
threshold. The anticonvulsant dose
might need to be increased.
 Monitor drug-drug and food-drug
interactions. Provide client with a list of
food to avoid when taking MAOIs.
These include cheese, red wine, beer,
liver, bananas, yogurt, and sausage.
 Check client for extremely ↑BP when
taking MAOIs. Sympathomimetic-like
drugs and foods containing tyramine
may cause a hypertensive crisis if taken
with MAOIs
Side Effects:
 Advise client that antidepressants may
be taken at bedtime to decrease
dangers from the sedative effect. Have
client check with health care provider.
Transient side effects include nausea,
drowsiness, HA, and nervousness.

 Drugs used for epileptic seizures
 It suppresses the abdominal electric
impulses from the seizures
 It is also classified as CNS
depressants.
ANTICONVULSANTS ACTS IN THREE WAYS
 By suppressing sodium influx through the drug
binding to the sodium channel
 By suppressing the calcium influx, preventing
the electric current generated by the calcium
oins
 By increasing the action of gamma-aminobutyic
acid, which inhibits neurotransmitter throughout
the brain.
INTERNATIONAL CLASSIFICATIONS OF SEIZURES
• Grand mal (tonic-clonic)
- most common form of seizure.
- In the TONIC PHASE; the skeletal muscle
contract/ tighten in a spasm,usully last 3-5
seconds.
- In the CLONIC PHASE; there is dysrhytmic
muscular contraction, or jerkiness of legs and
arms lasting for 2-4 minutes.
• Petit mal ( absence)
- breif loss of consciousness lasting less than
10 seconds; fewer than 3 spike waves on the
electroencephalogram (EEG) printout
- It usually occurs in children.
• Psychomotor
- Complex symptoms; automatisms(repetitive
behavior such as chewing or swallowing
motions), behavioral changes, and motor
seizures.
A. HYDANTOINS
-It acts by inhibiting sodium influx, stabilizing
cell membrane, redcing repetitive neuronal
firing, and limiting seizures.
-Should no tbe used during pregnancy, because
it can have a TERATOGENIC effect on the
fetus.
-THERAPEUTIC RANGE: 10-20mcg/ml.
*CONTRAINDIATION:
- hypersensitivity, heart block, psychiatric
disorders, during pregnancy.
*SIDE EFFECTS:
- headache, confusion, dizziness, decreased
coordination, slurred speech, rash, anorexia,
nausea and vomiting, hypotension(IV), pink-
red/brown discoloration of urine.
*NURSING RESPONSIBILITIES:
- Give alower dose for newborns, persons with D.OXAZOLIDONES/ OXAZOLIDINEDIONE
liver disease, and older adults: DECREASE IN
METABOLISM RESULTING IN MORE
AVAILABLE DRUGS.
- Watch out for drug toxicity.
- Monitor the therapeutic serum drug range: TO
ENSURE DRUG EFFECTIVENESS.
B. BARBITUATES
 Prescribed to treat partial seizure,
grand mal seizures and episodes of
status epileptic siezures, meningitis ,
toxic reactions and eclampsia.
 May also be used to manage delirium
treatment.
 Drugs that act as CNS depressants and
by the virtue of this they produced a
wide spectrum of effect from mild
sedation to total anesthesia.
*SIDE EFFECTS:
- Agitated mood; clumsiness; confusion;
dizziness; excessive daytime drowsiness;
headache; injection site reactions;
lightheadedness; low blood pressure; nausea;
slow heartbeat; slowed breathing; vomiting.
*NURSING INTERVETION:
- use only for few days at the most
- advice patient not to drive.
- do not discontinue abruptly.
C. SUCCUNIMIDES
 Used to treat absence or petit mal
siezures
 It acts by decreasing the calcium influx
through the T-type calcium cahnnels.
 THERAPEUTIC RANGE: 40-
100mcg/ml.
 Drug of choice:
ETHOSUXIMIDE(ZARONTIN)
*ADVERSE EFFECTS:
- blood dyscrasias, renal and liver impairment,
and systemic lupus erythematosus.
*SIDE EFFECTS:
- drowsiness, dizziness, confusion, blurred
vision.
*NURSING RESPONSIBILITIES:
- may cause gastric irritation; must be taken
with food.
-advice patient to increase fluid intake.
-Monitor CBC and differential before and
frequently during therapy.
-Take drug as prescribed, and do not
discontinue drug abruptly.
-advice patient no to drink alcohol.
 Prescribed to treat petite mal seizures.
 DRUGS: Trimethadione and
Paramethadione.

A. Trimethadione
*SIDE EFFECTS:
- Mild dizziness, poor coordination, or
drowsiness;blurred or double vision, or irregular
back-and-forth movements of the
eyes;decreased appetite, nausea, or vomiting;
or increased sensitivity of the skin to sunlight.
*NURSING RESPONSIBILITIES:
-Drugs should be gradually withdrawn.
- Take trimethadione exactly as directed by your
doctor.
- Advice the patinet to take each dose of
trimethadione with a full glass of water.
Trimethadione can be taken on an empty
stomach or with food to decrease stomach
upset.
- Advice the patient to chew the chewable
tablets before swallowing them.
B. Paramethadione
*SIDE EFFECTS:
-mild dizziness, poor coordination, or
drowsiness;blurred or double vision, or irregular
back-and-forth movements of the
eyes;decreased appetite, nausea, or vomiting;
or increased sensitivity of your skin to sunlight.
*NURSING RESPONSIBILITIES:
-Do not discontinue drug abruptly.
- Carry or wear a medical identification tag to let
others know that you are taking this medicine in
the case of an emergency.
-Take paramethadione exactly as directed by
your doctor.
-Take each dose of paramethadione with a full
glass of water. Paramethadione can be taken
with food if it upsets your stomach.
E.BENZODIAZEPINES
 CLONAZEPAM
 Effective in controlling petit mal
(absence) seizures
 Tolerance may occur 6 months after
drug therapy starts
 Consequently dosage has to be
adjusted.
 THERAPEUTIS RANGE: 20-80 ng/ml.
*SIDE EFFECTS: F.IMINOSTILBENES
- drowsiness, dizziness, GI upset, fatigue,
nervousness, depression, emotional changes,
bedwetting, urinary incontinence.
* NURSING RESPONSIBILITIES:
-Monitor addiction-prone patients carefully
because of thier predipositon to habituation to
habituation and drug dependence.
- Monitor for liver function and blood counts.
-Advice patient to take drug on time.
- Avoid alcohol.
- Avoid pregnancy. Using barrier contraceptives
is adviced while taking this drug.
-Always take drug with food.
- Avoid driving and other dangerous activities.
 CLORAZEPATE DIPOTASSIUM
 Frequently administered in adjunctive
therapy for trearting partial seizures.
*SIDE EFFECTS:
- drowsiness, dizziness, GI upset, fatigue,
nervousness, depression, emotional changes,
bedwetting, urinary incontinence.
*NURSING RESPONSIBILITIES:
- Advice patient to take drug on time.
- Avoid alcohol
- Avoid pregnancy. Using barrier contraceptives
is adviced while taking this drug.
-Always take drug with food.
- Avoid driving and other dangerous activities.
 DIAZEPAM
 Primarily prescribed for treating acute
status epilepticus
 Must be administed IV to achive the
desired response.
 Drug has a short-term effect; other
drugs such as phentoin and
phenobarbital need to be given during
or immediately after administration of
diazepam.
*SIDE EFFECTS:
- drowsiness, dizziness, GI upset, fatigue,
nervousness, difficulty concentrating.
*NURSING RESPONSIBILITIES:
- advice patient to take this drug on time. Do not
attempt to discontinue drug without consulting
the health care provider.
- Caregiver should learn to assess seizures,
administer rectal form, and monitor patient.
- Use of barrier contraceptives is adviced while
on this drug.
 Prescribed to treat grand mal seizures,
complex partial seizures and status
epilepticus.
 Effective in treating refractory seizures
disorders that have not responded to
other anticonvulsant therapies.
 Most common drug: CARBAMAZEPINE
  Used for psychiatric disorders,
trigeminal neuralgia, and alcohol
withdrawal.
 THERAPEUTIC RANGE: 5-12 mcg/ml.
*SIDE EFFECTS:
- Drowsiness, dizziness, blurred vision, GI
upset.
*NURSING RESPONSIBILITIES:
- Take drug as prescribed. Swallow the tablets
in whole; do not crush, cut or chew the tablet.
- Do not discontinue drug abruptly.
- Avoid alcohol, sleep-inducing, or over-the-
counter drugs ; these could dangerous effects.
- Arrange for frequent check-ups, including
blood tests, to monitor response to drug.
- Use of contraceptives at all times, is advised.
-advise patient not to drive or do dangerous
activities.
- Take drug with meals.
G.VALPROATE
 Is prescribed for petite mal, grand mal,
and mixed type of seizures.
 HEPATOTOXICITY is one of the
possible adverse reactions.
 THERAPEUTIC RANGE: 40-100
mcg/ml.
 Drug: DIVALPROEX
SODIUM(Depakote)
- for treatment of manic episodes associated
with bipolar disorder.
* SIDE EFFECTS:
- mild stomach cramps, change in menstrual
cycle, diarrhea, loss of hair, indigestion,
decreased appetite, nausea and vomiting,
trembling in the hands and arms, and weight
loss or weight gain.
Less common side effects include severe
stomach cramps or continued nausea and
vomiting, changes in mood, behavior, or
thinking, double vision or seeing spots, severe
fatigue ,easy bruising or unusual bleeding,
yellow cast to the skin or the whites of the eyes
(jaundice), odd eye movements, and increased
seizures.
*NURSING RESPONSIBILITIES:
- Take this medication exactly as it was
prescribed for you. Do not take the medication
in larger amounts, or take it for longer than
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.
Antiparkinsonism
Panrkinsonism -is a chronic neurologic disorder that
affects the extrapyramidal motor tract (which controls
posture, balance, and locomotion).
Symptoms: (1)involuntary tremors of the limbs,
(2)rigidity of muscles, and (3) slowness of movement
Levodopa + Carbidopa :
MOA: ↑ CNS dopamine levels
CI: suspicious skin lesion (may activate melanoma),
helanoma, MAOI use
SE: Psych disturbances, orthostatic, ↓ BP, dyskinesias
Drug-Drug Interaction: ↑ Risk of hypotension with
antihypersives, ↑ risk of HTN with MAOIs, ↑ effect with
antacids, ↓ effect with anticholinergics and
anticonvulsants
Drug-Lab: ↑ Alk phos, aspartate aminotransferase,
bilirubin, BUN, uric acid, ↓ HMG
Nursing Intervention: Darkened urine, Sweat may
result, N crush/chew S tabs, take with food,
muscle/eyelid twitching may suggest toxicity
Benztropine:
MOA: blocks striatal cholinergic receptors
SE: Anticholinergic (tachycardia, ileus, nausea and
vomiting, etc) anlydrosis, heat stroke
Drug-Drug Interaction: ↑ sedation and depressant
effects with CNS depressants, ↑ anticholinergic effect
with antihistamine, phenothiazine, quinidine, ↑ effect of
digoxin, ↓ effect of levodopa, ↓ effect with antacids and
antidiarrheal drugs
Nursing Interaction: ↑ susceptibility to heat stroke,
take with meals to avoid GI upset
Muscle Relaxant
 relieve muscular spasms and pain
associated with traumatic injuries and
spasticity from chronic debilitating
disorders.
 Depress neuron activity in the spinal
cord or brain act directly on the skeletal
muscles.
A. Spasticity – results from increased muscle tone from
hyper-excitable neurons or lack of inhibition in the spinal
cord or skeletal muscles. Ex: baclofen（Lioresal）,
Dantroline(Dantrium) , Tizanidine (Zanaflex).
B. Muscle spasm – to decrease pain and increase
range of motion. Ex: Carisoprodol(Soma),
Chlorzoxazone(Paraflex), cyclobenzaprine(Flexeril),
metaxalone(Skelaxin), methocarbamol(Robaxin) and
Orphenedrine citrate(Norflex)
SE : N/V, dizziness, weakness, insomnia, drowsiness,
HA, light-headedness, GI sensitivity, diarrhea and
abhdominal distress.
Stages of General Anesthesia
AE: Asamthic attack, tachycardia, hypotension and
diplopia.
Drug-drug interaction: increase CNS depression w/
alcohol, narcotics, sedative-hypnotics, antihistamines
,tricyclic anti-depressants. May increase risk of
ventricular fibrillation w/ calcium channel blockers.
Nsg Intervention:
 monitor VS, serum liver enzymes levels
 observe for CNS side Effects
 it should not abruptly stop. Tapered
over 1week.
 Advise Px not to drive or use dangerous
machinery.
 Inmform px that muscle relaxant usually
taken not longer than 3weeks.
 Tae meds with meals.
 Avoid with alcohol and CNS
depressants
 Warn px that this medication are
contraindicated with pregnant and
nursing mothers.
General and local Anesthetics
-↓ pain
 ANALGESIA (Induction Stage)
- begins w/ consciousness & ends w/ loss of
consciousness
- SPEECH is difficult; sensations of SMELL &
PAIN are lost
- DREAMS, AUDITORY & VISUAL
HALLUCINATIONS may occur
 Excitement or Delirium
- produces loss of consciousness caused by
DEPRESSION of the cerebral cortex
- confusion, excitement or delirium occur
-SHORT induction time
 Surgical
- surgery is performed usu at phase 2 & upper
phase 3
*as anesthesia deepens, respirations become
SHALLOW and RR is ↑
 Medullary Paralysis
- TOXIC
- respirations are lost, circulatory collapse occur
- ventilator assistance is necessary

GENERAL ANESTHETICS ASSESSMENT: (before surgery)

-depress the CNS
-alleviate pain
-cause a loss of consciousness
NITROUS OXIDE
-“laughing gas”; first anesthetic
-effective and is frequently used in dental surgeries
Balanced Anesthesia
-a combination of drugs; frequently used in general
anesthesia
It includes:
• Hypnotic (at night)
• Premed w/ a narcotic analgesic/
benzodiazepine plus an anticholinergic (given
about 1hr before surgery to ↓ secretions)
• Short-acting barbiturate
• Inhaled gas (often nitrous oxide & O2)
• Muscle relaxant as needed
MOA:
-minimizes CV problems
-↓ amt of general anesthetic needed
-reduces possible postanesthetic N/V
-minimizes the disturbance of organ function
The response may differ accdg to variables r/t the health
status of the individual.
 Age (young and elderly)
 Current health disorder
 Pregnancy
 Hx of heavy smoking
 Obesity
 Freq use of alcohol and drugs
Inhalation Anesthetics
-used to deliver general anesthesia dur the 3rd stage of
anesthesia
- provide smooth induction
-usu combined w/ a barbiturate (ex. Thiopental), a
strong analgesic (ex. Morphine) & a muscle relaxant
(ex. Pancuronium) for SURGICAL PROCED.
∆ NITROUS OXIDE & CYCLOPROPANE- absorbed
quickly, have rapid action, eliminated rapidly
- CYCLOPROPANE is no longer used bec of its highly
flammable state as ether
∆ Halothane, isoflurane, enflurane- 1hr for recovery of
consciousness
∆ Desulfrane, sevoflurane- minutes for recovery
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
3. chronic progressive- progressive MS
symptoms (wheelchair bound)
* goals for treatment strategies are to
decrease inflammation process of nerve
fibers and improve conduction of
demyelinating axons
Skeletal Muscle Relaxants
1. relieve symptoms of spasticity w/c results during preg. And menopause
from increased muscle tone from
hyperexcitable neurons caused by increased
stimulation from cerebral neurons or lack of -Two types of Migraine: Classic migraines
inhibition in the spinal cord
Centrally acting Muscle relaxants
2. suppress hyperactive reflex and muscle
spasms that do not respond to anti-
inflammatory agents or physical therapy
3. for spasticity: baclofen (Lioresal),
dantrolene (Dantrium), tizanidine (Zanaflex) -NOT associated with an aura
and Diazepam a benzodiazepine
4. agents for muscle spasms are used to
decrease pain and increase range of
motion, ex. Carisoprodol (Soma),
chlorpleresin carbamate (Maolate),
chlorzoxazon (Paraflex) etc…
Side effects:
1. dizziness
2. drowsiness
Anti Migraine drugs
♥ Migraine HA
-unilateral throbbing head pain
accompanied by N/V and photophobia
-Sx frequently persist foo4-24 hrs and for
several days in some cases
-2/3 are experienced by women in their
20s and 30s s
-Sx usually decrease or are absent
-disrupts daily activities
and Common Migraines
Classic migraines
-associated with an AURA that occurs
minutes to 1 hour before onset
Common migraines
♥ Cluster HA
-severe unilateral non throbbing pain
usually located around the eye
-occur in a series of cluster attacks---one
or more attacks every day for several
weeks
-NOT associated with an aura, do not
cause N/V
-men are more commonly affected
Preventive treatment of migraine
HA
1. Beta adrenergic blockers:
Propanolol (Inderal), atenolol
(Tenormin)
2. Anti convulsants: valproic acid
(depakote), gabapentin (neurontin)
- Dihydroergotamine (an ergot
alkaloid) can be SQ, IM, IV or nasal
spray
→Triptans (5-HT receptor agonist)
-Sumatriptan(Imitrex): short duration of
action, 1st triptan drug, considered more
effevtive than ergotamine in treating
acute migraine attacks

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 