Pharmocology Exam 2

NMNC 3230

Emphysema

COPD

Risk factors: smoking, environment, inhaled irritants

cause: irritant is inhaled, the lung responds through Leukocytes releasing proteolytic enzymes into alveoli, and alveoli become inflamed

Alveoli stop being elastic, so gas exchange is decreased (air trapped in the bottom of the lungs)

Chronic Bronchilits

Continuous inflammation and low-grade infection of the bronchi

Excessive mucus secretion

does not really go away + do not breathe as well

Asthma

Recurrent and Reversible Shortness of Breath

Lung airway narrows

Alveolar ducts and alveoli remain open + Airflow is obstructed

Symptoms: Wheezing & Difficulty breathing

2 components:

• bronchoconstriction

• inflammation

Status Asthmaticus

Prolonged asthma attack that does not respond to typical drug therapy

May last several minutes to hours

medical emergency!

Beta Agonist Bronchodilators

Short-acting beta agonists (SABA)

• Rescue inhaler

• Albuterol

Long-acting beta agonists (LABA)

• For long term management

• Salmeterol

Albuterol (Proventil, Ventolin)

RESCUE INHALER

Class - Beta 2 Agonist Bronchodilator

SHORT ACTING

Indications

• Asthma

• COPD

Mechanism of Action - Dilates bronchioles by relaxing the bronchiole smooth muscle

Adverse effects

• Tremor

• Paradoxical bronchospasm

• Tachycardia

Nursing Implications

• Patient teaching: rescue inhaler

• Use of spacer

• Assess Lung sounds + CV status

• Worked = less wheezing

Ipratropium (Atrovent)

Class: Anticholinergic bronchodilator

Indication: COPD

Mechanism of action:

• Induces bronchodilation

• Blocks muscarinic receptor in airway smooth muscle.

Adverse effects:

• Increased IOP with angle closure glaucoma

• Paradoxical bronchospasm

Safety:

• Usual dose – 2 inhalations/ 4x day

• Pregnancy Category C

• Peds >12 years old

• Assess Lung sounds

•  Give second or in combo with albuterol

• Patient Teaching: How to administer

• Evaluate: Pulmonary status + ADR

Theophylline (Theo-Dur)

Class: Xanthine derivative bronchodilator

Indication: Asthma + COPD

Mechanism of action

• Cause bronchodilation by increasing cAMP which causes smooth muscle relaxation
Adverse effects

• Nausea, vomiting

• Tachycardia, palpitations

• Hyperglycemia

Safety

• Do not use with other stimulants-caffeine

• Do not smoke cigarettes or use tobacco

Nursing Implications

• Patient teaching: still keep rescue inhaler

• Oral

Fluticasone (Flovent)

Class: Corticosteroid (inhaled)

Indications: Asthma + COPD

Mechanism of action: Reduces inflammation in the airways

Adverse effects

• Oral candidiasis 31% (whenever inhaling steroids)

Safety

• Do not use for acute distress! Not a rescue inhaler.

• Pregnancy Category C

• Peds approved

Patient teaching

• Rinse mouth and spit out water after dose

• Oral care

Evaluation

• Not as strong as systemic corticosteroids

  • you cannot just switch

Prednisone

class: glucocorticoid

indication: Adrenocortical insufficiency, inflammatory diseases or conditions, allergies, organ transplantation, respiratory illness exacerbation

mechanism of action: inhibits inflammatory and immune responses

Adverse effects

• hypertension

• psychosis

• hyperglycemia

• abdominal obesity

Safety:

• DO NOT STOP TAKING IT ABRUPTLY

  • adrenocortical insufficiency

• may exacerbate or activate infections

• diminished response to vaccines

• Pregnancy category D

• peds: give every other day to avoid growth suppression

Montelukast (Singulair)

Class: Leukotriene antagonist

Indications: Asthma + Allergies

Mechanism of Action

• Blocks leukotriene receptors in airway

• Blocks inflammatory response responsible for asthma + allergies

Adverse effects:

• Headache

• Nausea + diarrhea

• Major personality changes

• Suicidal Thoughts

Safety

• March 2020 FDA warning about neuropsychiatric effects

Implementation

• Give in the evening

• Not used as a rescue medication

Histamine

A natural chemical in the body that causes inflammation

• Allergic rhinitis

• Anaphylaxis

• Angioedema

• Insect bite reactions

• Urticaria (hives) & pruritus (itching)

Antihistamines

end in -ine

H1 antagonists (a.k.a. “H1 blockers”, “antihistamines”) - allergy meds

• diphenhydramine (Benadryl)

H2 antagonists (a.k.a. “H2 blockers”): Reduces gastric acid in peptic ulcer

disease

Mechanism of action:

• Blocks action of histamine at H1 receptor sites

• Competes with histamine for binding at unoccupied receptors

• Limitations: Cannot push histamine off the receptor if already bound

• Prevents the actions of histamine rather than reversing them

• Give early in treatment before all the histamine binds to the receptors

Anticholinergic effects:

• Dry mouth

• Difficulty urinating

• Drowsiness

Diphenhydramine (Benadryl)

Class: Histamine 1 antagonist, 1st generation

Indications: Allergies, hives (urticaria), pruritis (itching), Sleep aid

Mechanism of Action

• Blocks H1 receptors in respiratory, GI tract, & blood vessels.

Adverse effects

• Anticholinergic side effects

• Sedation

Safety

• Can cause drowsiness, use caution when driving or operating machinery

• Elders – higher risk of sedation and confusion

• Pregnancy Category B

Nasal Decongestants

reduce congestion that occurs with allergic rhinitis, sinusitis, common cold

Pseudoephedrine: limits on quantities purchased due to potential to be altered to make meth

MOA: alpha 1 adrenergic activation

• vasoconstriction of blood vessels

• turbinates shrink, opening nasal passages

Phenylephrine (Neo-Synephrine)

Class: alpha 1 adrenergic agonist

ADR: anxiety, agitation, insomnia

• rebound congestion - avoid more than 3 days

• precautions: contraindicated in clients with narrow-angle glaucoma, uncontrolled heart disease, hypertension or dysrhythmia

Cough

Cough reflex:

• Initiated by irritation of the respiratory tract sensory receptors

Two Basic Cough Types:

• Productive (congested, removal of secretions)

• Non-productive: dry cough

Antitussives

Drugs used to stop or reduce coughing

Opioid and non-opioid

Used only for nonproductive coughs

Nursing Process:

• Avoid in very productive cough

• Track total dosage given

• See HCP for cough >7days

• NOT FOR LONG TERM USE

Codeine

Class: Opioid antitussive

Indications: Non-productive cough

Mechanism of Action

• Suppresses cough center in CNS

• decreases sensitivity of cough receptors

Adverse Effects:

• Dizziness

• Drowsiness

• Respiratory depression (especially in kids

Nursing Implications

• Not available OTC

• Has analgesic properties

• Restricted use in children

• Mix w/ sprite + jolly ranchers

Dextromethorphan “DM”

basically same as Codine

Class: Non-opioid antitussive

Indications: Non-productive cough

Mechanism of Action:

• Suppress the medullary cough reflex

• decreases sensitivity of the stretch receptors in the respiratory tract

Adverse effects:

• Dizziness

• Drowsiness

• Nausea

Safety

• Can be found in OTC combination cold medicine

• Drug of abuse (can cause hallucinations)

• Pregnancy Category C

• Peds - not for OTC use in children <4 years of age

Expectorants

Drugs which aid in mucus removal

Reduces secretion viscosity

Indications: Relief of productive coughs associated with:

Mechanism of Action:

• make mucus easier to cough up by stimulating secretory glands to put more water into mucus

Guaifenesin (Mucinex, Robitussin)

Class: Expectorant

Indications: Relief of productive cough

Mechanism of Action: Thins secretions + Increases efficiency of cough

Adverse effects: Nausea + Vomiting

Safety

• Pregnancy Category C

• Peds – Approved > 4 yr

Administer with plenty of water

Risk for overdose with other drugs

Blood Pressure

BP = CO x SVR

Blood Pressure = Cardiac Output x Systemic Vascular Resistance

CO = heart rate x stroke volume

SVR = the resistance to the blood flow

Renin-Angiotensin-Aldosterone System (RAAS)

regulates BP

ACE inhibitors = “-PRIL”

Angiotensin receptor blockers = “-SARTAN”

Captopril (Capoten)

Class: ACE inhibitor

Indication: HTN, HF, used alone or in combination with diuretics or other antihypertensives, renoprotective effects on kidneys

Mechanism of action: decrease SVR → vasodilation and cause diuresis

• inhibit ACE (AI → AII)

• inhibits vasoconstriction → decreases SVR

• inhibits aldosterone → water is not retained

Adverse Effects: Dry, non-productive cough, hypotension, hyperkalemia, ANGIOEDEMA

Losartan (Cozaar)

Class: Angiotensin Receptor Blocker (ARB)

Indication: hypertension, HF

Mechanism of action:

• block the binding of Angiotensin II to it’s receptor

  • blocking vasoconstriction (vasodilation)

  • blocking aldosterone secretion (decreased preload)

Adverse Effects:

• fatigue, chest pain

  • cough less likely than with ACE inhibitors

Calcium Channel Blockers

Mechanisms of action:

• relaxes coronary arteries and increases blood supply to the heart

• dilates peripheral arteries → decreases workload of the heart

• Decreases BP

• diltiazem also decreases heart rate and contractility

Diltiazem (Cardizem)

Class: calcium channel blocker

Indications: hypertension, angina, dysrhythmias, cerebral artery spasms, heart failure

Mechanism of action:

• causes relaxation of smooth muscle by blocking calcium binding

• decreases SVR

• decreases HR

Adverse effects

• hypotension, tachy or bradycardia, constipation or nausea, rash

alpha blockers

Mechanism of Action #1: arterial and venous dilation, reducing peripheral vascular resistance and blood pressure

• indication: hypertension

Mechanism of Action #2: effect on receptors on prostate gland and bladder decrease resistance to urinary outflow, thereby reducing urinary obstruction and relieving symptoms 

• indication: Benign prostatic hyperplasia

Common suffix: -osin

Doxazosin (Cardura)

Indication – hypertension, benign prostatic hyperplasia (BPH)

Mechanism of Action – alpha-1 receptor antagonist

Adverse Effects: orthostatic hypotension, tachycardia, vertigo, sexual dysfunction

Nursing Implications: First dose syncope

Beta blockers

Indications:

• Angina – decreases demand for myocardial oxygen

• Cardioprotection – inhibits stimulation from circulating catecholamines

• Dysrhythmias

• Hypertension – ability to reduce sympathetic stimulation of the heart, reducing heart rate and force of contraction

• Heart Failure

• Glaucoma (topical use)

• Migraine headache prophylaxis

Common suffix: -olol, -alol

Adverse Effects: Bradycardia, hypotension,

Contraindications: Asthma/COPD, heart block, pregnancy

Metoprolol (Lopressor, Toprol XL)

Class: Beta Blocker

Indication – angina, MI, cardiac dysrhythmias, hypertension, heart failure

Mechanism of Action – antagonist @ beta adrenergic receptors

Safety

• do not discontinue abruptly (black box warning): May precipitate MI, angina, cause rebound hypertension

• High alert drug

• pregnancy category C/not indicated

Direct Vasodilators

Indication: hypertension, angina

mechanism of action: directly cause peripheral vasodilation by causing smooth muscle relaxation,

decrease SVR

Patient Teaching for antihypertensives

Should not be stopped abruptly → rebound hypertensive crisis → stroke

Medication is only PART of therapy:

• diet, stress level, weight, and alcohol intake

• Avoid smoking and sodium, limit stress, and decrease caffeine intake

• Encourage supervised exercise

• AVOID Hot tubs, showers and baths, hot weather, or prolonged

  sitting, standing → hypotension → syncope

Report: HF symptoms

Impotence is an expected effect

Should not take any other medications w/out approval

Heart Failure (HF)

The heart cannot pump enough blood to supply the body’s demand for oxygenated blood

Failure of the ventricle to eject blood efficiently results in:

• fluid volume overload

• chamber dilation

• elevated intracardiac pressure

Symptoms:

• unusual shortness of breath or difficulty breathing

• Edema

• weight gain

• chest pain, palpitations

• excessive fatigue

Cause: anything that causes ischemia or high BP

Types of HF

Left-sided HF: blood backs up into the lungs

• fluid volume overload,

• chamber dilation

• increased intracardiac pressure.

Right-sided HF: blood backs up into the body

• venous congestion,

• pedal edema

• jugular venous distention,

• ascites,

• hepatic congestion

HF meds

Goals of treatment:

• increase cardiac output

• decrease workload of the heart

Positive inotropic drugs

drugs that increase force of contraction

Positive chronotropic drugs

drugs that increase heart rate

Positive dromotropic drugs

drugs that accelerate conduction

Digoxin (Lanoxin)

class: cardiac glycoside

Indications: systolic HF and atrial fibrillation

Mechanisms of action:

• positive inotropic effect: (stronger contraction)

• negative chronotropic effect: (slower HR)

• negative dromotropic effect: (decreased conduction)

Narrow therapeutic Index drug: normal = 0.5 – 2 ng/mL

TOXICITY greater w/ low potassium or magnesium

• digoxin binds to the K+ site of the Na+/K+-ATPase pump

  • low serum potassium levels increase the risk of digoxin toxicity

Adverse Effects:

• Toxicity → brady/tachycardia, nausea, yellow halos

  • Antidote: Digoxin Immune Fab (Digibind)

Nursing Implications:

• before giving dose, count apical pulse for 1 full minute

• HOLD DOSE & CONTACT PRESCRIBER IF:

  • apical pulse < 60 or > 100 bpm

  • S/S toxicity

Patient teaching:

• avoid giving with high fiber foods

• patients should IMMEDIATELY report a weight gain of:

  • 2 lb or more in 1 day or

  • 5 lb or more in a week

Kidney functions + processes

3 basic functions

• cleansing of extracellular fluid (ECF) and maintenance of ECF volume and composition

• maintenance of acid-base balance

• excretion of metabolic waste and foreign substances

3 basic renal processes

• filtration: occurs at the glomerulus

• reabsorption: 99% of H20, electrolytes and nutrients undergo reabsorption

• active tubular secretion: occurs at the proximal convoluted tubule

Diuretics

Act on the kidneys to INCREASE the production of urine → eliminating water

Na+ and H₂O play a major role in the regulation of: BV & BP

Decrease Preload

We use drugs that target kidneys to:

• decrease hypertension

• draw water off the body (decrease edema)

Loop Diuretics

End in “-nide” or “-mide”

Works in Loop of Henle

Drug effects:

• Reduces:

  • BP, PVR, SVR, Central Venous Pressure, left ventricular end diastolic pressure

STRONGEST + MOST POWERFUL DIURETIC

Furosemide (Lasix)

Class: loop diuretic, prototype

Indications: pulmonary edema, edematous states, hypertension, liver impairment (ascites)

Mechanism of Action: acts on ascending loop of henle to block reabsorption of water

Contraindications: hypersensitivity, hypersensitivity to sulfonamide antibiotics, anuria, hypovolemia, electrolyte depletion

Nursing Implications: rapid onset (PO 60 min, IV 5 min)

• Assess: renal function + K levels, hearing, lung sounds, urine output

• Take Potassium

Adverse Effects:

• Hypokalemia

• Hypotension

• Ototoxicity (give through IV slow or patient will lose hearing)

Thiazide and Thiazide-type Diuretics

Basically same as Loop Diuretics

DO NOT WORK FOR KIDNEY FAILURE

Hydrochlorthiazide (Hydrodiuril)

Class: Thiazide Diuretic

Indications: essential hypertension, HF, edema, diabetes insipidus

Mechanism of Action: inhibition of the resorption of Na, K, Cl, resulting in osmotic water loss @ the distal convoluted tubule

• result is increased Na+ in the filtrate, which causes less H2O resorption, which means more H2O is lost in the urine

Adverse Effect:

• HYPOKALEMIA

• HYPOnatremia

• photosensitivity

Nursing Process:

• Eat potatoes, bananas, leafy greens, etc.

Potassium-Sparing Diuretics

Mechanisms of action:

• Aldosterone antagonists – blocks aldosterone in the distal nephron,

promotes the excretion of Na+ and H2O, but the retention of K+

• Non-aldosterone antagonist K+ sparing diuretics

Spironolactone (Aldactone)

 class: Potassium-sparing diuretic

indications:

• hypertension

• to reverse K+ loss caused by thiazide

• edematous states

• HF

• primary hyperaldosteronism

• PMS

• PCOS

• acne in women

Adverse Effects:

• HYPERKALEMIA

• low BP

• Tumors

Drug-Drug Interactions:

• Thiazide and Loop diuretics

• any agent that raises

  potassium levels

• Lithium

• NSAIDS

Coronary Heart Disease Drugs

Antilipemics

• HMG-Co-A Reductase Inhibitors → atorvastatin (Lipitor)

Antianginals

• Nitrates → NTG (nitroglycerin)

How does Cholesterol relate to CHD?

The risk of CHD in patients with cholesterol levels of 300 mg/dL is 3-4x greater

Lipoproteins

Very-low-density lipoprotein(VLDL)

• From the liver

• Transports endogenous lipids to the cells

Low-density lipoprotein (LDL)

• deliver cholesterol to cells

  • used in membranes or for the synthesis of steroid hormones

High-density lipoprotein (HDL)

• Responsible for “recycling” of cholesterol

• “good cholesterol”

What lowers cholesterol?

Exercise increases HDL + lowers bad cholesterol

FOODS: fatty fish, olive oil, whole grains, fruits, vegetables, red wine, tea, etc.

There is a genetic predisposition to high cholesterol

Statins

end in -statin

Mechanism of Action: Lower blood cholesterol by decreasing the production of cholesterol.

• Inhibit HMG co-A reductase (enzyme necessary for liver to produce cholesterol)

Adverse Effects:

• Constipation

• Myalgias (muscle aches/pains)

• Rhabdomyolysis (damaged muscle gets into the bloodstream) - limit grapefruit juice

Contraindications: Pregnancy+ Liver Disease

Patient Teaching

• Report signs of myopathy immediately

• Caution with grapefruit juice

Evaluation

• Cholesterol, lipid profiles

• Liver enzymes

• Muscle pain, weakness

Anti-anginal Drugs

GOAL = BALANCE OXYGEN SUPPLY AND DEMAND IN THE MYOCARDIUM

Causes of Angina

 SUPPLY:

• when blood supply to the heart is inadequate → PAIN

• damaged cardiac cells/tissue resulting from inadequate O2 supply = ISCHEMIC HEART DISEASE

• primary cause: ATHEROSCLEROSIS

  • blood vessels become narrow with fatty deposits in the walls

DEMAND:

• the harder the heart works, the more oxygen it needs

• heart rate

• contractility

Types of Angina

CHRONIC STABLE ANGINA

• caused by atherosclerosis

• triggered by exertion, better w/ rest

UNSTABLE ANGINA

• caused by coronary artery disease

• precedes MI, gets progressively worse

VASOSPASTIC ANGINA

• spasms in smooth muscle vasculature of the heart

• occurs at rest

Goals of Antianginal Therapy

Mechanisms of Action

• decrease HR

• decrease contractility

• decrease preload (by venous dilation)

• decrease afterload (by decreasing diastolic bp)

Calcium Channel Blockers

• diltiazem(Cardizem)

Beta-Blockers

• metoprolol,atenolol

Nitrates

• nitroglycerin (NTG) (Nitrostat, Nitrobid)

Nitroglycerin (NTG)

class: antianginal, vasodilator

indication: all types of angina

mechanism(s) of action:

• dilates all blood vessels, including coronary arteries

• reduces preload and myocardial oxygen demand

adverse effects

• reflex tachycardia

• hypotension

• tolerance

Pharmacokinetics: large 1st pass

effect when given orally

• Sublingual tablets or spray: FAST

• IV: emergency

• Paste/Ointment: slow

• Transdermal patches: slow

Nitroglycerin (NTG) Patient Education

• IF ANGINA PAIN OCCURS:

  • STOP ACTIVITY & sit or lie down and take a SL tablet

  • IF there is no relief in 5 minutes, call 911 + take a 2nd SL tablet

  • if there is no relief in 5 minutes, take a 3rd SL tablet

  • DO NOT TRY TO DRIVE TO THE HOSPITAL

• burning/tingling sensation will be felt with sublingual dosage (still potent)

• keep a fresh supply of SL medication on hand

• Stored in an airtight, glass bottle with a metal cap and no cotton filler

• Do NOT use with phosphodiesterase 5 inhibitors (ex. Viagra, Levitra, etc.)

  • will cause profound hypotension

• Drug free 10-12 hours DAILY (tolerance)

• Encourage angina journal

Anticoagulants

Have no direct effect on a blood clot that is already formed

• Prevent intravascular thrombosis by decreasing blood coagulability

• Used prophylactically to prevent:

  • Clot formation (thrombus)

  • An embolus (dislodged clot)

Inhibit the action or formation of clotting factors, prevents clot formation

EX: Heparins, Vitamin K antagonists (warfarin), Direct Oral Anticoagulants

Indications:

• Used to prevent clot formation in certain settings in which clot formation is likely:

  • MI

  • Unstable angina

  • Atrial fibrillation

  • Indwelling devices, such as mechanical heart valves

  • Major orthopedic surgery- post op prevention of blood clots

Heparin

Classification – Anticoagulant

Mechanism of action – Inactivates clotting factors. Factor Xa/thrombin inhibitor. Does not lyse clots.

Adverse Effects:

• Bleeding

• Heparin induced thrombocytopenia (HIT)

Overdose or toxicity: protamine sulfate = reversal agent

Safety:

• High alert med

• Toxicity:

  • Symptoms: hematuria, melena (blood in the stool), petechiae, ecchymoses, and gum or mucous membrane bleeding

  • Stop drug immediately

  • IV protamine sulfate: 1 mg of protamine per 100 units of heparin.

Assessment

• Baseline coagulation labs, PT, PTT, INR

Implementation

• Double-check check dose with another nurse

• SubQ

• Patient Teaching – report bleeding, bleeding precautions

Evaluation

• Partial thromboplastin time (PTT) or Activated PTT (aPTT)

• Monitor for signs of hemorrhage

Enoxaparin (LMWH)

Classification - Anticoagulant

Indications: prevent blood clots

Mechanism of action: anti-Factor X and anti-thrombin activity. Does not lyse clots.

Black Box warning: Epidural or spinal hemorrhage, delay catheter placement until enoxaparin has lapsed, hold dose for 4+ hours after placement or removal of catheter

Warfarin (Coumadin)

Mechanism of action:

• Vitamin K antagonist: inhibits vitamin K synthesis by bacteria in the GI tract

• Inhibits production of vitamin K-dependent clotting factors II, VII, IX, and X

• Final effect prevention of clot formation

Pharmacokinetics: longer acting than heparin

Adverse Effects:

• Bleeding

• Toxicity

  • Discontinue the warfarin.

  • May take 36-42 hours before the liver can resynthesize enough clotting factors

  • Vitamin K1 can hasten the return to normal coagulation.

  • Severe bleeding

Safety

• Black Box warning – Major/fatal bleeding, monitor PT/INR, prevent bleeding risks

• Antidote: Vitamin K

• Pregnancy category X

Implementation

• High alert drug!

• Patient Teaching

  • Avoid activities the risk cuts, bruising, or injury. Soft toothbrush, etc

• Keep same diet

Evaluation

• INR

• Signs of bleeding

Antiplatelet drugs

Mechanism of Action: prevent platelet adhesion

Ex: aspirin (Ecotrin) + clopidogrel (Plavix)

Indications:

• Prevention of stroke or transient ischemic attack (TIA)

• Post MI prevention of thrombus

aspirin (acetylsalicylic acid, ASA)

Classification: Salicylate, NSAID, Antiplatelet agent

Mechanism of Action: inhibits the activation of Thromboxane A2→inhibits the enzyme cyclooxygenase in the platelet→ prevents formation of thromboxane

• leads to less platelet aggregation, less vasoconstriction

• makes it difficult to form platelet plug

Irreversible effect: antiplatelet effects last 7-10 days

Dosage: 81-325mg/day for antiplatelet effect

Safety:

• Narrow therapeutic index at high doses

• Don’t use with renal, hepatic failure, ulcers

Developmental concerns

• Don’t use in 3rd trimester

• Peds – don’t use without specific prescription

• Reye’s syndrome

Assessment

• Why are you giving it

• Contraindications: anticoagulants

Implementation

• Give with a full glass of water

• Patient Teaching

  • Max dosage in day: 3-4 g

  • Reduce amount with tinnitus

Evaluation

• Tinnitus

• Apply direct pressure longer for bleeding

Clopidogrel (Plavix)

Classification – Platelet Aggregation Inhibitor, ADP inhibitor

Mechanism of action – Irreversibly binds to platelet ADP receptor, prevents platelet aggregation. Platelet lifespan 7-10 days

Adverse Effects:

• Bleeding

• Flu-like symptoms

• GI symptoms

Safety

• herbal supplements may increase risk of bleeding

  • Ginkgo biloba, feverfew, evening primrose oil

• interactions: PPI’s reduce antiplatelet effects

• Black Box warning for CYP2C19 poor metabolizers – low dose or other treatments

• Stop one week before surgery

Evaluation

• CBC, Platelets

Thombolytic Drugs

Mechanism of action: breaks down existing clots by activating the conversion of plasminogen to plasmin (breaks down clots)

Ex: streptokinase (NMNEC), alteplase

Indications:

• Myocardial infarction

• Pulmonary embolism

• DVT or arterial thrombosis

• Catheter occlusion

• Acute ischemic stroke

T-PA Tissue plasminogen activator (Alteplase)

Classification - Thrombolytic

Pharmacodynamics – Binds to fibrin, activates plasminogen to plasmin, initiates fibrinolysis. Dissolves clot

Adverse effects:

• Internal, intracranial, or superficial bleeding

• Cardiac dysrhythmias

• Toxicity

Contraindications

• Active internal bleeding

• Recent major surgery, trauma, stroke

• Severe uncontrolled hypertension

• AV malformation

• Aneurysm

Implementation

• monitoring

• Time is critical

• IV sticks before administering

• Patient Teaching: report headache, stroke S/S

Evaluation

• Signs of reperfusion

  • Ventricular dysrhythmias

  • Resolution of S/S

• Bleeding

  • never give with drugs that enhance bleeding

Bleeding precautions

Epoetin alfa

Hematopoietic Drug

E for Erythrocyte

Mechanism of action: promote synthesis of blood components.

Beneficial during cancer treatment because it counteracts bone marrow suppression

• Synthetic erythropoietin

• Stimulates red blood cells in the bone marrow

Adverse Effects:

• Hypertension related to increased HCT

• heart failure

• malignancies

Patient Safety:

• report headache, sudden chest pain, unilateral weakness, numbness or paralysis, vision changes, N/V or seizure

Interventions: monitor - hemoglobin+ BP

Contraindications

• hypersensitivity

• uncontrolled HTN

• malignancies

Administration

• baseline BP, CBC, H & H, BUN

• do not shake vial or mix with other drugs