The flashcards below were created by user
Anonymous
on FreezingBlue Flashcards.
-
Mechanisms of Adrenergic Receptor
Activation by Agonist Drugs (4)
- Direct Receptor Binding
- Promotion of Norepinephrine (NE) Release
- Inhibition of NE Reuptake
- Inhibition of NE Inactivation-
-
Mechanisms of Adrenergic Receptor Activation by Agonist Drugs:
Direct Receptor Binding
- Most common mechanism,activate peripheral adrenergic receptors.
- Drugs mimic the actions of natural transmitters
-
Mechanisms of Adrenergic Receptor Activation by Agonist Drugs
Promotion of Norepinephrine (NE) Release-
Acts on terminals of sympathetic nerves to cause NE release
Example: amphetamines and ephedrine
-
Mechanisms of Adrenergic ReceptorActivation by Agonist Drugs
Inhibition of NE Reuptake
- Blocks NE reuptake, NEaccumulates in the synaptic space, increases receptoractivation
- i.e. tricyclic antidepressants .
-
Mechanisms of Adrenergic ReceptorActivation by Agonist Drugs
Inhibition of NE Inactivation
NE terminals can be inactivated by monoamine oxidase (MAO). Thereforedrugs that inhibit MAO can increase the amount of NEavailable i.e. MAOI’s
-
Catecholamines and noncatecholamines differ in three respects:
- Oral usability
- Duration of action
- Ability to act in the CNS
-
Catecholamine's: (Epineherine, Norepinepherine)
3 properties in common
- Cannot be used orally
- Brief duration of action
- Cannot cross the blood-brain barrier
-
Norepinephrine, dopamine, & dobutamine only work if
given by continuous infusion
-
Catecholamine’s are ____ _____, cannot cross the blood-brain barrier
polar molecules
-
Catecholamine's: IV solutions can turn pink or brown over time;
Discard if discolored
-
Adrenergic Agonists affect: (4)
- alpha 1,
- alpha 2,
- beta 1 &
- beta 2 adrenergic receptors
-
Noncatecholamines (4)
- can be given orally &
- have longer half-lives
- less polar,
- can cross the blood brain barrier
-
Alpha 1 Receptors :cause two responses
- vasoconstriction (in blood vessels of skin, viscera, and mucous membranes) &
- mydriasis (dilation of the pupil)
-
Alpha 1 Activation
Hemostasis
Stop bleeding primarily in skin & mucous membranes (Epinephrine)
-
Alpha 1 Activation
Nasal Decongestion
Relieve congestion by vasoconstriction of mucous membranes (phenylephrine & pseudoephedrine)
-
Alpha 1 Activation
Adjunct to Local Anesthesia-
Combined with anesthetics to delay anesthetic absorption, vasoconstriction at the site.(Epinephrine)
-
Alpha 1 Activation
Elevation of BP-
Vasoconstriction can elevate BP, ONLY usedwhen other therapies have failed
-
Alpha 1 Activation
Mydriasis-
facilitates eye exams & ocular surgery
-
Alpha 1 Adverse Effects (3)
- Hypertension
- Necrosis
- Bradycardia
-
Alpha 1 Adverse Effects
Hypertension
- Widespread vasoconstriction can cause HTN, particularly parenteral administration IV:
- Must monitor CV status continuously
-
Alpha 1 Adverse Effects
Necrosis
Extravasation & necrosis with IV infiltrate,(intense vasoconstriction), alpha 1 blocker (antagonist) to minimize damage (phentolamine)
-
Alpha 1 Adverse Effects
Bradycardia
Reflex response to increase in BP, cancause cardiac collapse & impaired tissue perfusion
-
Alpha 2 Activation
Peripherally inhibit NE release (but little clinical relevance)
-
Alpha 2 Activation
In CNS receptors cause
- Reduction of sympathetic outflow to heart & blood vessels
- Relief of severe pain
-
Beta 1 Activation
- Heart Failure
- Shock
- Atrioventricular (AV) Heart Block
- Cardiac Arrest from Asystole
-
Beta 1 Activation
Heart Failure-
Beta 1 receptors increase force of contraction (inotropic effect),improves cardiac Fxn
-
Beta 1 Activation
Shock
- (Shock=profound hypotension) Beta 1’s increase heart rate (HR), force of contraction=increased cardiac output (CO), & improves tissue perfusion
-
Beta 1 Activation
Atrioventricular (AV) Heart Block-
Beta 1’s enhance conduction through AV node (temporarily, until pacemaker )
-
Beta 1 Activation
Cardiac Arrest from Asystole-
Beta 1’s can initiate acontraction in a heart that has stopped, (CPR & TXrequired, Epinephrine)
-
Beta 1 Adverse Effects (2)
- Altered Heart Rate or Rhythm
- Angina Pectoris
-
Beta 1 Adverse Effects
Altered Heart Rate or Rhythm
Overstimulation of beta 1’s can produce tachycardia & dysrhythmias
-
Beta 1 Adverse Effects
Angina Pectoris-
Angina Pectoris- Beta 1’s increase cardiac oxygen demand, which can cause angina in pts with impaired coronary circulation
-
Beta 2 Activation (3)
- Limited to lungs and uterus
- Asthma- Beta 2 receptors promote bronchodilation, Selective beta 2 receptors(albuterol) preferred, (Drugs that activate beta 1 receptors can stimulate tachycardia & angina).Most via inhalation to minimize adverse systemic effects, systemic toxicity with overdosing
- Can Delay Preterm Labor- Relaxes uterine smoothmuscles
-
Beta 2 Adverse Effects (2)
-
Beta 2 Adverse Effects Hyperglycemia
- (highest risk: diabetic pts)
- beta 2 receptors stimulate breakdown of glycogen into glucose
-
Beta 2 Adverse Effects
Tremor
Most common, beta 2;s in muscles cause enhanced contractions, fades over time, minimized by starting at low dose
-
Dopamine Receptor
- Activation of peripheral dopamine receptor causes dilation of renal vasculature
- *Dopamine (the drug) used in shock to dilaterenal blood vessels & reduce risk of renal failure
- Dopamine also enhances cardiac performance
Assess Urinary output (UOP), increases when kidneys are functioning, shock=no/low perfusion to kidenya and low UOP
-
Epinephrine
Receptor specificity:
alpha 1, alpha 2, beta 1 and beta 2
-
Epinephrine
Therapeutic Uses:
- Alpha 1-mediated vasoconstriction
- Beta 1’s - to overcome AV heart block,
- Beta 2’s: promotes bronchodilation
- **Epinephrine is the Tx of choice for anaphylactic shock*
-
Epinephrine Therapeutic Uses: Alpha 1-mediated
vasoconstriction, used to delayabsorption of anesthetics, control superficial bleeding, &elevate BP. (Was used for nasal decongestion) Alsomydriasis.
-
Epinephrine Therapeutic Uses: Beta 1’s -
to overcome AV heart block, & restore cardiac function in pts experiencing cardiac arrest.
-
Epinephrine Therapeutic Uses:Beta 2’s:
promotes bronchodilation
-
Epinephrine ROUTE:
Topical, injection or IV administration only.
-
Epinephrine half-life
Short (due to MAO and COMT)
-
Epinephrine Adverse Effects:
- Can cause Hypertensive Crisis-
- Can cause Dysrhythmias-
- Angina Pectoris-
- Necrosis Following IV Extravasation-
- Hyperglycemia
-
Epinephrine Adverse Effects:Hypertensive Crisis
Can cause Hypertensive Crisis- Alpha 1 stimulation,vasoconstriction, dramatic increase in BP (IV infusion)
-
Epinephrine Adverse Effects: Dysrhythmias
Can cause Dysrhythmias- Beta 1 stimulation
-
Epinephrine Adverse Effects: Angina Pectoris
Angina Pectoris- Beta 1 increases cardiac work & oxygendemand
-
Epinephrine Adverse Effects: Necrosis
Necrosis Following IV Extravasation-alpha-adrenergic antagonist can minimize (phentolamine)
-
Epinephrine Adverse Effects:Hyperglycemia
Hyperglycemia- beta 2’s, typically in diabetic pts only
-
Epinephrine Drug Interactions: (5)
- MAO Inhibitors
- Tricyclic Antidepressants-
- General Anesthetics-
- Alpha-adrenergic Blocking Agents
- Beta-adrenergic Blocking Agents-
-
Epinephrine Drug Interactions:MAO Inhibitors-
Prolong and intensify the effects ofepinephrine & other catecholamines
-
Epinephrine Drug Interactions: Tricyclic Antidepressants-
Block the uptake ofcatecholamines, so can intensify & prolong epinephrineeffects.
-
Epinephrine Drug Interactions: General Anesthetics-
Can cause tachydysrhythmias when used together
-
Epinephrine Drug Interactions:
Alpha-adrenergic Blocking Agents
(antagonists) Can prevent receptor activation by epinephrine(*Phentolamine: antidote used to treat toxicity)
-
Epinephrine Drug Interactions: Beta-adrenergic Blocking Agents-
Can prevent receptoractivation by epinephrine, reduce adverse effectscaused by epinephrine
-
Epinephrine
Catecholamine or Noncatecholamine
Catecholamine
-
Norepinephrine (6)
- Receptor specificity: Alpha 1, Alpha 2, Beta 1
- Catecholamine
- *Same as Epi, except no Beta 2 stimulation
- Does not promote hyperglycemia
- Typically only used in hypotensive states & cardiacarrest
- IV infusion only
-
Isoproterenol (3)
- Receptor Specificity: Beta 1 and Beta 2
- Catecholamine
- *First beta selective medication
-
Isoproterenol Therapeutic Uses:
- Cardiovascular-overcome AV heart block, restart heart following cardiac arrest, increase cardiac output in shock
- Bronchospasm- Not used to treat asthma ONLY bronchospasm, (more selective medications treat asthma)
-
Isoproterenol
Adverse Effects:
- Beta 1 activation- tachy-dysrhythmias & angina
- Beta 2 activation- hyperglycemia
-
Isoproterenol Drug Interactions:
- Effects are enhanced by MAO Inhibitors andtricyclic antidepressants; Reduced by beta-blockers
- Can cause dysrhythmias when given with inhaled anesthetics
-
Inotropic drugs influence the
- strength or contractilty of muscle tissue.
- Increase the force of the heart's contractions
-
Two types of Inotropic drugs
Cardiac Gylcosides and phophodiesterase (PDE) inhibitors
-
-Slow heart rate and slow electrical impulse conduction through the AV node.
-Useful for pts who have artrial fibrillations.
-Can help control HR and prevent it from becoming too fast
- Incrs. perfusion of tissues improves function/help decrease edema (interstitial fld)
Cardiac Glycosides
-
Cardiac Glycosides Prototype
Digoxin
-
Digoxin Actions
- Inhibits sodium-potassium- activated adenosine triphosphas: reg. amt. of Na and K+ inside the cell resulting in increased intracellular levels of Na and K.
- Promotes the movement of Ca from extra cellular to intracellular cytoplasm and strengthens myocardial contraction
- Acts on the CNS to enhance vagal tone, slowing contractions through the SA and AV nodes- provides an antiarrhythmic effect.
-
Digoxin Indications (3)
- heart failure
- Atrial Fib. and flutter
- Supraventricular tachycardia
-
Digoxin Nursing Considerations
- Monitor pt for adverse effects
- W/hold if apical pulse is less than 60 bpm and notify prescriber
- monitor serum K and digoxin levels
- assess renal function
-
Digoxin Pharmacokinetics
- intestinal asbsorption varies greatly
- cap. most efficent, then elixr then tabs
- absorp. hightest concen. in heart musc., liver, and kideny
- poorly bound to plasma protiens
- Most is excrete from kid. unchanged
-
Digoxin Pharmacodynamics
- boost intracellular Ca at the cell membrane
- enable stronger heart contractions
- may enhance movement of Ca into myocardial cells and stimulate the release for block re-uptake of noreponephrine at the adrenergic nerve terminal
- Works on CNS to slow HR
- Increases refractory period
-
-
Digoxin ______ Cardiac Output:
- Increased:
- -Increases contractilityby restoring cardiac muscle fibers to near health,increases the stroke volume of failing heart =cardiac output rises
-
Digoxin Three major secondary responses due to increased cardiac output:
- – Decreased sympathetic tone
- – Urine production increases
- – Renin release declines
- – These responses can reverse virtually all signs and symptoms of heart failure.
-
Digoxin (Cardiac Glycoside)Adverse Effects 1:
Cardiac Dysrhythmias
-
Digoxin (Cardiac Glycoside) Adverse Effects 1: Cardiac Dysrhythmias:
Digoxin: used in therapeutic doses to slow fastheart rates, but causes dysrhythmias if given inhigh doses or in the presence of hypokalemia
-
Elevated digoxin levels- Narrow therapeutic window/Range:
(0.5-0.8 ng/mL; variance among range, most state no higher than 1.5 ng/ml) levels slightly higher than therapeutic produce toxicity
-
Managing Digoxin-Induced Dysrhythmias:–
- Withdraw digoxin & potassium-wasting diuretics
- – Monitor serum potassium
- – Anti-dysrhythmic drug is sometimes needed (Lidocaine & phenytoin most effective for ventricular dysrhythmias, atropine for bradycardias)
- – Can give reversal agent: Digibind or Digifab, Cost$2,000-$3,000, only use when severe (also can cause arrhythmias as it binds digoxin)
-
Digoxin (Cardiac Glycoside) Adverse Effects 2: Non-cardiac Adverse Effects
- **GI- anorexia, nausea, and vomiting
- **CNS- Fatigue & visual disturbances (blurred vision, yellow tinge to vision, halos around dark objects)
-
Digoxin (Cardiac Glycoside) Drug Interactions:
- *Diuretics- Thiazide and Loop Diuretics promoteloss of potassium (increases risk of dysrhythmias)
- ACE Inhibitors and ARBs- Can increase potassiumlevels (decreases digoxin levels)
- Sympathomimetics- Can add to the inotropiceffects of digoxin
-
Plasma Digoxin Levels:
- Therapeutic Range: 0.5-0.8 ng/mL.
- Anything over 1 ng/mL offers no additional benefit and increases the risk of toxicity.
-
Herbs and Digoxin
St. John's wort and ginseng can ^ levels of digoxin and ^ risk of toxicity
-
S/S of Digoxin toxicity:
- slow to rapid ventricular rhythms
- nausea and vomiting
- blurred vision
- anorexia
- abdomin. discomfort
- mental changes
|
|