drugs that decrease/delay drug metabolism result in accumulation of drug and prolongation of the effects of the drug; may lead to drug toxicity

Drug absorbed into the systemic circulation thru the mucosa of the stomach and/or small or large intestine.  Orally administered

a.       time required for a drug to elicit a therapeutic response after dosing

a.       time required for a drug to reach its maximum therapeutic response in the body

a.       length of time the concentration of a drug in the blood or tissues is sufficient to elicit a response

use of many different drugs concurrently in treating a patient, who often has several health problems

135 – 145 mEq/L      

3.5 – 5.0mEq/L

10 – 20 mg/dL          

1.3 – 2.1 mEq/L

Understanding specific impact of cultural factors on patient drug response (hampered by lack of clarity of race, ethnicity, culture)

effects of specific patient characteristics on the pharmacokinetics of specific drugs characteristics: diet/cultural/genetic

getting all information on a patient’s medications

integration of knowledge and physical skills.  Ex – giving an insulin injection

 relieves pain without loss of consciousness

drugs from other chemical categories to aid in pain management

Morphine drug class

Opioid agonists

Morphine MOA

CNS depression. Can irritate the GI tract/chemoreceptor trigger zone in CNS/causing nausea and vomiting/slow peristalsis & increase absorption of water. Urinary retention

alcohol/antihistamines/benzos/CNS depressants; additive respiratory depression

used commonly in transdermal patches (pp. 148) long-term control of malignant; non-malignant chronic pain

ü  Severe asthma (suppresses respiratory system)

ü  Drug allergy (discuss true vs. expected allergy)

•       Itching is expected due to opioid histamine release, not a true allergy

•       Nausea is expected due to GI suppression, not a true allergy

ü  Most serious is CNS depression (respiratory suppression)

•       Cardiovascular – hypotension, flushing, bradycardia

•       CNS – sedation (mental clouding), disorientation, euphoria, lightheadedness, dysphoria

•       GI – nausea, vomiting, constipation, spasms,

•       Genito-urinary- urinary retention

•       Integumentary –itching, rash, wheal formation

•       Respiratory – depression and aggravation of asthma

Narcan (naloxone) must be given in severe respiratory distress from opioid overdose, regardless of withdrawal syndrome

 Acetaminophen (Tylenol) drug class

Non-opioid Analgesics

   Acetaminophen (Tylenol)  Mechanism of action

ü  Blocks pain by inhibition of prostaglandin synthesis; acts on hypothalamus to lower body temperature; vasodilation/increased peripheral blood flow. Lacks anti-inflammatory effects as opposed to NSAID’s

      Acetaminophen (Tylenol)      Indications

ü  Mild to moderate pain and fever

ü  Used for contraindications of aspirin

•       Acetaminophen (Tylenol) Contraindications

ü  liver disease/drug allergy (can cause liver damage)

•       Acetaminophen (Tylenol) Adverse effects

ü  Normally well tolerated

ü  Rash, nausea, vomiting

•       Acetaminophen (Tylenol)

ü  Potentially lethal

ü  7-10 grams to cause hepatic necrosis

ü  Acetylcysteine (acetadote) is the antidote for Tylenol toxicity

ü  Max dose: 4g average person/2g those elderly patients and patients with liver dysfunction and chronic heavy alcohol abusers

ü  Acetadote: IV is available

Opioid analgesic  Nursing Diagnoses 

ü  Impaired gas exchange related to opioid induced CNS/respiratory depression

ü  Acute pain related to disease process

ü  Chronic pain related to disease process

ü  Constipation related to CNS depressant effects on GI

ü  Deficient knowledge related to lack of familiarity with opioids

ü  Stimulate the sympathetic nervous system

ü  Mimic the effects of the neurotransmitters (epinephrine/norepinephrine/dopamine)

ü  These neurotransmitters are also known as catecholamine.

Alpha-Adrenergic Receptors response

ü  Vasoconstriction & CNS stimulation

• A₁ Receptors effects on blood vessels, liver, GI, bladder, penis, uterus

§  Blood vessels   (A1): vasoconstriction (increase BP)

§  Liver               (A1): glycogenolysis (more sugar)

§  GI Tract         (A1): Decreased motility

§  Bladder           (A1): constriction

§  Penis                (A1): ejaculation

§  Uterus                         (A1): contraction

• A₂ Receptors

ü  Control release of neurotransmitters

ü  Bronchial/GI/Uterine relaxation

ü  Cardiac stimulation

• B₁ Receptors (One Heart)

ü  In the heart

ü  Cardiac muscle: increased contractility

ü  Sinoatrial/Atrioventricular node: increased heart rate

• B₂ Receptors (Two Lungs)

ü  In smooth muscle of bronchioles, arterioles and visceral organs

§  Lungs              (B2): Relaxation of bronchial smooth muscles (dilation)

§  Uterus             (B2): relaxation

§  GI Tract         (B2): relaxation of smooth muscle

Dopaminergic Receptors

Dilation of arteries

ü  Kidney

ü  Heart

ü  Brain

Increases blood flow

When stimulated by dopamine

• binds directly to the receptor causing a physiologic response

• stimulates the receptor by binding to it and indirectly stimulates the receptor causing the release of the neurotransmitter

Dobutamine (dobutrex) MOA

B₁ Adrenergic
ü  Stimulates the heart muscle
What does it do?
ü  Increases cardiac output by increasing contractility which increases stroke volume (increase BP/HR)
ü  Used for patients with heart failure/weight based drug…..mcg/kg/min (weight based)
ü  IV only
 

• Alpha and Beta receptors (can activate both depending on route)
• What does it do?

ü  Alpha-1 receptors: continuous IV infusion: for vasoconstriction to elevate BP

ü  Beta-1 receptors: used for cardiac arrest: 1 milligram IV push every 3 minutes

ü  Beta-2 receptors: subcutaneous injection to treat anaphylactic shock (epi-pen)

• A₁ Adrenergic

ü  Vasoconstrictor

§  Constriction of both arterioles and veins = peripheral vasoconstriction

§  Used for treatment of symptomatic orthostatic hypotension

§  10 mg PO three times a day (TID).

§  Maximum daily dose is 40 mg

§  PO Only

ü  Heart problems – (hyper/hypo tension; tachycardia; heart failure; heart attack

ü  Renal function – Alpha adrenergics (epinephrine/continuous IV infusion) can cause decreased renal function/renal damage

ü  Vital signs

ü  IV Site (Central line)

§  As soon as possible get a central line for your patient. Using these drugs through a peripheral line can cause vasoconstriction around site and eventual tissue necrosis.

ü  Cardiac monitoring

ü  Patient teaching

§  Observe for adverse effects: chest pain, palpitations, blurred vision, headache

§  Carvedilol (Coreg) MOA

§Alpha-1/Non-selective beta blocker

§Decreases cardiac output, exercise induced tachycardia

§Heart failure primarily (can be used for hypertension/angina)

Carvedilol (Coreg) indications

·         used primarily for treatment of heart failure but also beneficial for hypertension and angina. 

Carvedilol (Coreg) MOA

Carvedilol (Coreg) assessment

·         obtain baseline vital signs from patient or family members and ask for BP/pulse parameters

·         Beta₁ blocker

Metoprolol (Lopressor, Toprol XL) Indications

§  Tamsulosin (Flomax) MOA 

§Alpha blocker

§  Tamsulosin (Flomax) Indications 

§Symptoms of Benign Prostatic Hyperplasia (BPH)

§Increase Urine output

§Hypersensivity, prostate cancer

o   circulates catecholamines and prevents them from stimulating the heart. Catecholamines are released after a heart attack; unopposed stimulation would further increase oxygen demand/force of contraction

o   slow down conduction in SA/AV node with decreases heart rate. Heart failure

[image]GI: nausea, vomiting, diarrhea

·         GI: increase gastric secretions, increase GI motility

·         GU: urinary frequency

·         Cardio: reduces heart rate

·         Alzheimer’s: increases amount of acetylcholine in the brain; helps to maintain memory and learning capabilities

[image]GI: abdominal cramps, nausea, vomiting

Bethanechol (urecholine) MOA

·         causes increased bladder and GI tract tone and motility, which increases the movement of contents through these areas. It also causes the sphincter in the bladder and GI tract to relax, allowing them to empty

Bethanechol (urecholine) indications

Bethanechol (urecholine) adverse effects

Donepezil (Aricept) MOA

·         Mild-moderate Alzheimer’s  

·         Increases levels of acetylcholine in the brain increasing memory function

Donepezil (Aricept) adverse effects

Donepezil (Aricept) teaching

·         May take up to 6 weeks for therapeutic effects

Not a cure for Alzheimer’s disease

•       Parasympathomimetics 

–      Parasympathetic Nervous System (PSNS) theme is ‘rest and digest’

–      Mimic the effects of the neurotransmitter; Acetylcholine. 

–      Receptors are located throughout the body.

–      Receptors are called nicotinic and muscarinic 

•       Rest & Digest

–      GI: Increased gastric secretions/increased GI motility

–      GU: urinary frequency

–      Cardiovascular: reduced heart rate

–      Alzheimer's: : increase the amount of acetylcholine in brain; helps to maintain memory and learning capabilities

–      Cholinergic Drugs 

Atropine indications

§  For symptomatic bradycardia

§  GI: decrease in motility/peristalsis and smooth muscle relaxation

§  GU: decreased bladder contraction resulting in urinary retention

§  Cardiovascular: : increase in heart rate 

Atropine nursing implications 

§  Telemetry/vital sign monitoring; notify physician

Dicyclomine (bentyl) indications 

§  Treatment for Irritable Bowel Syndrome (IBS)

Dicyclomine (bentyl) nursing implications

§  Use caution in patients that have? (Obstruction/Ileus)

Tolterodine (detrol) indications

§  Used for Bladder leakage caused by overactive bladder

Tolterodine (detrol) adverse effects

§  Headache, dizziness, dry mouth

§  Diphenhydramine (Benadryl) drug class

§Nonselective antihistamine

§  Diphenhydramine (Benadryl) indications

§Allergy symptoms, rhinitis, motion sickness, night time sedation, nonproductive cough

§Peripherally/centrally acting; often used as a hypnotic

§  Loratidine (Claritin) MOA

§  Benzonatate (Tessalon Pearles) drug class

§Non-opioid antitussive

§  Benzonatate (Tessalon Pearles) MOA

§Benzonatate is thought to act as a local anesthetic, numbing stretch receptors in the lower airway and lungs, thereby reducing the drive to cough after taking a deep breath.

§  Benzonatate (Tessalon Pearles) indications

§Used for non-productive cough

§  Dextromethorphan (Robitussin DM) drug class

§Non-opioid antitussive

§  Dextromethorphan (Robitussin DM) MOA

§Depresses cough center in CNS by direct effect on the medulla

§  Dextromethorphan (Robitussin DM) Indications

§Nonproductive cough caused by colds or inhaled irritants

§  Dextromethorphan (Robitussin DM) toxicity

§Robo-tripping (CNS depressant)

§  Guaifenesin (Mucinex) drug class

§Expectorant

§  Guaifenesin (Mucinex) MOA

§Reflex stimulation(loosing/thinning secretions)

§Increases the volume & reduces the viscosity of secretions in the trachea and bronchi to facilitate secretion removal

§  Guaifenesin (Mucinex) indications

§Beneficial to productive cough

§  Albuterol drug class

Bronchodilator

Selective or non-selective adrenergic agonist

§  Atrovent (Ipratropium) drug class

§Anticholinergic blocking acetylcholine; bronchodilator

§  Atrovent (Ipratropium) MOA

§Inhibits action of acetylcholine at receptor sites on the bronchial smooth muscle resulting in bronchodilation

§  Atrovent (Ipratropium) indications

§NOT for acute use because actions are prolonged

§To manage chronic bronchitis, emphysema or COPD

§  Atrovent (Ipratropium) conraindications

§Hypersensitivity to atropine, bromine, soybean or peanut products

§  Atrovent (Ipratropium) adverse effects

§  Theophylline (elixophyllin) drug class

§Xanthine derivatives (bronchodilator)

§  Theophylline (elixophyllin) indications

§For chronic issues, NOT acute symptoms

§Bronchial asthma, bronchospasm of COPD, chronic bronchitis, emphysema

§  Theophylline (elixophyllin) MOA

§Relaxes smooth muscle of respiratory system by blocking phosphodiesterase which increases cAMP

§  Theophylline (elixophyllin) teaching

§For chronic issues, NOT acute symptoms

§Hard to “come off” of this drug

§  Methylprednisolone (Solu-Medrol) indications

§  Methylprednisolone (Solu-Medrol)

§  Methylprednisolone (Solu-Medrol) drug class

Corticosteroids (Anti-inflammatory)

Corticosteroids (Anti-inflammatory)

§  Prednisone cautions

§Taper drug DO NOT just stop (can cause adrenal gland failure or death)

§Px on Pred. can have paper thin skin

§  Prednisone indications

§Oral corticosteroid after tapering Solu-medrol

§  Flonase (Fluticasone) drug class

Corticosteroids (Anti-inflammatory)

§  Flonase (Fluticasone) indications

§Asthma (prophylaxis/maintenance)

§Prevention of chronic asthma, nasal symptoms of seasonal allergies/nonallergenic rhinitis

Corticosteroids (Anti-inflammatory) assessment

ü  Assess for bradycardia, hypotension, dizziness

Digoxin (lanoxin) drug class

•       Cardiac glycoside

Digoxin (lanoxin) indications

Digoxin (lanoxin) inotrope, chronotrope, dromotrope effects

•       Positive inotropic/Negative chronotropic/Negative dromotropic

Digoxin (lanoxin)  adverse effects

•       Augments PSNS (cholinergic) stimulation via the vagus nerve

•       Increased diastolic filling

•       Check apical pulse rate for one full minute. If pulse is less than 60/HOLD

•       Can be given PO/IV. PO dose is usually written in micrograms                          (250 micrograms = 0.25 milligrams)

•       If given IV; dose needs to be given over at least five minutes.

•       Note baseline assessment of patient.

Digoxin (lanoxin) toxicity causes

•       Low therapeutic index

•       Therapeutic dose and toxic dose is SMALL. Normal ranges are 0.5-2.0 mg/mL

•       Hypokalemia/Decreased renal function

•       Hypokalemia/low magnesium levels/decreased renal function: can increase potential for digoxin toxicity

Digoxin toxicity s/s

•       confusion, fatigue, blurred vision, perception of green/yellow halos

Digoxin toxicity treatment

•       Digibind is the treatment for digoxin toxicity. It is only available in 40 milligram vial; dosed on digoxin level and weight of patient; given IV over thirty minutes

Milrinone (primacor) drug class

•       Phosphodiesterase inhibitor (PDI)

Milrinone (primacor) indications

•       Vasodilator - reduces reduction force against which the heart must pump to eject blood

•       Positive inotropic - more calcium available to for heart contraction

Milrinone (primacor)  MOA

•       Intracellular release of cAMP

ü  Block sodium channel; decrease action potential

ü  Can cause seizures, confusion, bradycardia, hypotension (Assess for)

ü  Depresses SNS stimulation (beta blocker/antagonist)

ü  Catecholamine protector: Cates released after MI can make heart more irritable

ü  Assess for hypotension, bradycardia

 ü  IV/PO

ü  Increases action potential duration

ü  Increases the effect of Coumadin/Digoxin; grapefruit juice can inhibit

ü  Assess for bradycardia, dizziness, photosensitivity, hypo/hyper thyroidism (75%) and pulmonary toxicity (dyspnea, cough, fibrosis)

ü  May upset GI, take with food; wear sunglasses

ü  Oral for maintenance

ü  Give IV for Tachycardia

•       Chronic stable angina

•       Atherosclerosis is primary cause.

ü  Triggers: exercise, emotions, nicotine, alcohol, caffeine, cocaine.

ü  Pain can be intense and is gone with patient rest or medications (nitroglycerine ER capsules/TD patch) 

•       Unstable angina

•       Pain increases in severity and frequency of attacks increase.

•       End result of unstable angina is heart attack.

•       Pain can occur at rest.

•       Early progressive of coronary artery disease (not getting better/gets worse)

•       Vasospastic angina

•       Spasms in smooth muscle that surrounds plaque-filled arteries.

•       Occurs at rest without any precipitating cause. 

•       Acute attacks (IV, sublingual)

•       Nitrates dilate all blood vessels (arteries/veins)

•       Dilate large and small coronary arteries;

•       Redistribute blood and oxygen to previously ischemic tissue.

•       Atherosclerotic arteries can benefit from nitrates 

•       Monitoring blood pressure/heart rate (systolic less than 90/pulse less than 60). Assess pain (level, location, duration)

•       Patients should avoid alcohol, hot tubs, hot showers, hot environment

•       Heat can exacerbate vasodilation; this leads to dizziness, syncope, orthostatic hypotension

•       Negative, Negative, Negative

§  Reduces myocardial oxygen demand; aides in treatment of angina by reducing workload of heart, increases oxygen supply

§  Slows heart rate; coronary arteries have more diastolic time to fill with oxygen/nutrient-rich blood

•       Bradycardia/hypotension, dizziness, drowsiness. Non-selective beta blockers and asthma.

•       Do not stop abruptly; daily weight; reduce orthostatic hypotension

§  Blocking calcium prevents muscle contraction, promotes myocardial relaxation, coronary arteries dilate; blood flow increases, oxygen supply increases. Dilation of systemic arteries occur as well; decrease in force (resistance); decreases workload of heart and subsequent oxygen demand

•       hypotension

o   Doxasozin (Cardura) drug class

o   Doxasozin (Cardura) MOA

§  Dilate arteries and veins, reduces peripheral vascular resistance, decreases blood pressure

o   Clonidine (catapres) drug class

[image]Centrally acting adrenergic drugs

o   Clonidine (catapres) MOA

§  Stimulating alpha 2 receptors in the brain; receptor stimulation actually reduces sympathetic outflow; results in lack of norepinephrine production; reduces blood pressure

o   Doxasozin (Cardura) indications

o   Clonidine (catapres) indications

o   Clonidine (catapres) contraindicaitons

§  Those with asthma need to be careful with nonselective beta blocker can cause airway constriction

o   Clonidine (catapres) adverse effects

[image]Orthostatic hypotension (tell patients to change positions slowly), drowsiness, dizziness. Also rebound hypertension if discontinued abruptly

·         Angiotensin-converting enzyme (ACE) inhibitor

o   First line treatment for heart failure and hypertension 

·         Angiotensin-converting enzyme (ACE) inhibitor patient adherence

§  Is more likely because most ACE inhibitors can be given just once a day (longer half-life/duration of action)

·         Angiotensin-converting enzyme (ACE) inhibitor MOA

§  Inhibit conversion of angiotensin I to angiotensin II. Angiotensin II is potent vasoconstrictor, includes aldosterone, stimulates sodium/water resorption, raise blood pressure. Also prevents breakdown of vasodilator bradykinin

·         Angiotensin-converting enzyme (ACE) inhibitor protective effect on kidneys

§  Reduced filtration pressure

·         Angiotensin-converting enzyme (ACE) inhibitor contraindications

§  Baseline potassium level of 5 or higher

§  Chronic kidney disease

·         Angiotensin-converting enzyme (ACE) inhibitor adverse effects

§  Dry, non-productive cough; hyperkalemia (ACE inhibitors promote potassium resorption in the kidney), angioedema (acute)

·         Angiotensin-converting enzyme (ACE) inhibitor interactions

·         Angiotensin II Receptor blockers (ARB’s)

o   The ‘Tan’s

·         Angiotensin II Receptor blockers (ARB’s) MOA

§  Block binding of angiontensin II to type I angiotensin II receptors (these receptors are located in primarily vascular smooth muscle and adrenal gland. They block vasoconstriction/aldosterone secretion also). ARBS do not cause a cough

·         Angiotensin II Receptor blockers (ARB’s) adverse effects

§  Upper respiratory infections, headache, occasional dizziness

o   Amlodipine (Norvasc) drug class 

[image]Calcium-channel blockers

·         Angiotensin II Receptor blockers (ARB’s) indications

o   Amlodipine (Norvasc) MOA 

§  Smooth muscle relaxation, preventing contraction from occurring

o   Amlodipine (Norvasc) indications

o   Hydralazine hydrochloride drug class

o   Hydralazine hydrochloride MOA

§  Directly elicit peripheral vasodilation; reduces systemic vascular resistance, lowers blood pressure. They do not work on adrenergic  receptors, there are not adrenergic-receptor blockers

o   Hydralazine hydrochloride adverse effects

§  Dizziness, headache, nasal congestion

o   Hydralazine hydrochloride indications

vital signs, lab tests: sodium, potassium, calcium, magnesium, BUN, creatinine. Also try to find underlying cause for hypertension

o   Assess patient for dizziness, fatigue, orthostatic hypotension

·         Rebound hypertension:

o   When patient stops taking medications abruptly; can put patient at risk for stroke

·         Patient teaching:

o   Daily weight, journaling of blood pressures; monitoring medication side effects, diet, exercise, stress, not smoking

·         Loop diuretics MOA

o   Block Na/Cl resorption

o   Dilation of numerous blood vessels (kidney, lung, peripheral)

o   Furosemide (Lasix) drug class 

·         Loop diuretic

o   Furosemide (Lasix) indications 

·         Edema associated with heart failure; hypertension

o   Furosemide (Lasix) adverse effects 

·         Dizziness, tinnitus, hypokalemia

o   Furosemide (Lasix) administration 

·         10 mg/minute IV

·         If given too fast, patient can lose hearing

·         Osmotic Diuretics MOA

§  Works along entire nephron

o   Mannitol (osmitrol) drug class

·         Osmotic Diuretics

o   Mannitol (osmitrol) indications

o   Spironolactone (aldactone) drug class 

·         Potassium-sparing Diuretics

o   Spironolactone (aldactone) indications 

§  Hypertension, cardio-protective; prevents remodeling of ventricle walls

o   Spironolactone (aldactone) adverse effects 

[image]Hyperkalemia

o   Spironolactone (aldactone) contraindications 

§  Kidney failure

o   Hydrochlorothiazide (Hydrodiuril) drug class

·         Thiazide Diuretics

o   Hydrochlorothiazide (Hydrodiuril) MOA

§  Reduces peripheral vascular resistance; decreased systemic vascular resistance;

§  As renal function decreases, thiazide diuretic lose their efficiencydecreased blood pressure

o   Hydrochlorothiazide (Hydrodiuril) indications

§  Hypertension, edema

o   Hydrochlorothiazide (Hydrodiuril) adverse effects

o   Obtain baseline electrolyte levels, baseline renal function, vital signs

o   Evaluate for orthostatic hypotension

·         Dietary teaching

o   Foods high in potassium: bananas, oranges, potatoes, broccoli

·         Daily weight, journaling of blood pressures, change positions slowly

o   Hyperkalemia causes

·         ACE inhibitors, burns, infections, potassium supplementation, potassium-sparing diuretics, renal failure

o   Hyperkalemia symptoms

·         Muscle weakness, paralysis, cardiac dysrhythmias, cardiac arrest

·         Sodium polystyrene sulfonate (Kayexelate)

o   Can give PO and rectally

o   Potassium excreted through feces

·         IV administration of D50 with insulin (causes rapid intracellular shift of potassium)

·         Sodium bicarbonate

·         Calcium gluconate/chloride

o   Hypokalemia causes

·         Vomiting, diarrhea, crash diets, loop diuretic use, thiazide diuretic use, malabsorption

o   Hypokalemia early symptoms

o   Anorexia, hypotension, lethargy, mental confusion, muscle weakness, nausea

o   Cardiac dysrhythmias, neuropathy, paralytic ileus, secondary alkalosis

·         Potassium chloride (Klor-Con)

o   IV and PO

o   Hypernatremia causes

·         Poor renal excretion

·         Dry mucous membranes, weakness, confusion increased thirst, fever, low urine output

o   Hypernatremia treatment

·         IV fluids (5% or 10% Dextrose in water; producing intravascular sodium dilution and enhanced urine output); diuretics (used to enhance sodium excretion)

o   Hyponatremia causes

·         Prolonged vomiting, diarrhea, excessive perspiration

·         Lethargy, confusion, muscle weakness

o   Hyponatremia treatment

·         Fluid restriction, salt tablets, hypertonic saline (3% or 5%) 

Never give potassium replacement in a push or bolus infusion (can cause cardiac arrest)

must be diluted

10 mEq/ hour

o   Any process that stops bleeding

·         Coagulation

o   Hemostasis that occurs by physiologic clotting of blood

·         Thrombus

o   Technical term for blood clot

·         Embolus

o   Thrombus that moves from point of origin (can end up anywhere; but if they get in heart, lung, brain)

·         Anticoagulants MOA

o   Inhibit action & formation of clotting factors; prevent clots from forming

o   Prevent platelet plugs; inhibiting platelet aggregation

o   Break down clots, or thrombi that have already formed

o   Heparin drug class

·         Anticoagulant

o   These drugs have no effect on a blood clot that is already formed. By thinning blood; prevent intravascular thrombosis; preventing extension of an established clot or a thrombus

o   Heparin dosing

·         Prophylaxis for patients at risk for DVT: for treatment in patients who already have DVT/PE dosing is Continuous IV infusion.

·         Weight based

·         Need to check PTT every 6 hours

o   Heparin adverse effects

·         heparin induced thrombocytopenia

o   acute fall in the number of platelets more that 50% from baseline

·         signs and symptoms

o   hematuria, blood in stool, eccymoses, bleeding from gums)

·         protamine sulfate is antidote for heparin

o   Warfarin (Coumadin) MOA

·         Inhibits vitamin K synthesis in GI tract

o   Warfarin (Coumadin) drug class

o   Warfarin (Coumadin) interactions

·         Warfarin and amiodarone; 50% increase in INR

o   Warfarin (Coumadin) administration teaching

§  Long-acting

·         It takes many days to get Coumadin level therapeutic

·         INR is lab value that evaluated Coumadin level

o   Warfarin (Coumadin) toxicity

·         Stop medication

·         May take 36-42 hours for liver to regenerate clotting factors

·         Vitamin K reverses effects of Warfarin , once given, warfarin resistance will occur for up to 7 days

·         Fresh frozen plasma works faster

o   Enoxaparin (lovenox) drug class

o   Enoxaparin (lovenox) indications

§  Bridge therapy

·         Given in conjunction with Coumadin until INR is therapeutic; once INR is therapeutic, lovenox is discontinued

o   Enoxaparin (lovenox) toxicity

·         Protamine sulfate can also be given to reverse effects

·         Antiplatelet drugs MOA

§  Inhibit platelet aggregation(platelets run to site of injection; recruit other platelets to come to site of injury) disruption of blood flow, trauma, rupture of plaque from vessel wall; they vasoconstrict; limit blood flow to the damaged blood vessel

·         Antiplatelet drugs indications

§  Stroke, MI prevention; thrombosis

·         Antiplatelet drugs adverse effects

o   Aspirin indications 

o   Clopidogrel (Plavix) indications

§  Stroke prevention/post MI-prevention of thrombosis

§  Lyse thrombin in the blood vessels in heart/brain. Before stent and coronary intervention; this was the treatment of choice. Natural thrombolytic system takes several days to break down a clot

·         Thrombolytic drugs indications

§  Acute MI, acute ischemic stroke

·         Thrombolytic drugs adverse effects

[image]Bleeding

o   Alteplase (t-PA) assessment

o   Alteplase (t-PA) drug class

·         Thrombolytic

o   Alteplase (t-PA) implementation

o   Double or triple check dosing of any coagulation modifier drug

o   Alteplase (t-PA) injections

o   No injections two inches from umbilicus

·         First line of therapy

o   Reduce LDL by 30-40%

o   Reduce triglycerides

o   Increase HDL

§  HMG-CoA reductase inhibitors The “statins” teaching

·         6-8 weeks

o   Before therapeutic effect is seen