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61 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Name 3 naturally occuring catecholamines.
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Epi, Norepi, Dopamine
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give two examples of Synthetic catecholamines
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Isoproterenol, dobutamine
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Synthetic noncatecholamines evoke responses similar to what?
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To those produced by endogenous activity of the SNS.
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Name 4 examples of Synthetic noncatecholamines.
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Ephedrine, phenylephrine, amphetamine, metaraminol.
Direct or indirect acting. |
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Sympathomimetics
can occur as... |
Naturally occurring catecholamines
Synthetic catecholamines Synthetic noncatecholamines |
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What is the net effect sympathomimetic drugs on the cardiac function influence by?
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Baroreceptor-mediated reflex responses.
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List the Gross Pharmacologic Effects of Sympathomimetics.
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Vasoconstriction (Esp. in cutaneous & renal circulation)
Vasodilation. Bronchodilation. + chronotropic, + inotropic, vulnerable to cardiac dysrhythmias. Liberation of free fatty acids from adipose tissue. Hepatic glycogenolysis, modulation of insulin, renin, pituitary hormone secretion. CNS stimulation. |
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Describe the baroreflexor reflex
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Hypertension resulting in baroreceptor stimulation.
Initiated by stretch receptors located at specific points in the walls of several large systemic arteries Carotid baroreceptors send afferent response via Hering’s and glossopharyngeal nerves (IX) Aortic baroreceptors send afferent response via the vagus nerve |
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What is the body's physiologic response to the Stimulation of the
Baroreceptor Reflex? |
Result – ↓ heartrate
↓ contractility peripheral vasodilation |
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How is the baroreceptor stimulation initiation caused?
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streching of the stretch receptors located in the wall of several large systemic arteries
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Stimulation of the Carotid baroreceptors sends...
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afferent response via Hering’s and glossopharyngeal nerves (IX) to tractus solitarius of the medulla.
they respond at pressures greater then 60 mmHg Above these levels they respond progressively more rapidly and reach a maximum at 180 mmHg. |
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Stimulation of the Aortic baroreceptors sends.....
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afferent response via the vagus nerve to tractus solitarius of the medulla.
Responses are similar to carotid receptors except they operate in general at pressure levels about 30 mmHg higher then Carotid Baroreceptors (at 60 mmHg). |
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What is
Hering’s nerve and where is it located? |
Afferent nerve fibers leading from the carotid sinus by way of the glossopharyngeal nerve to the brain, innervating the baroreceptors in the wall of the carotid sinus and the chemoreceptors in the carotid body.
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In general how do baroreceptors respond?
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They respond to changes in blood pressure that reflexively control heart rate.
An increase in pressure diminishes heart rate. Rise in BP stretches the baroreceptors and causes them to transmit signals into the CNS. Feedback signals are then sent back through the ANS to the circulation to reduce BP. |
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What is the best known of the nervous mechanisms for arterial pressure control?
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Baroreceptor response
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How are Sympathomimetics
used clinically? |
Maintain BP
Asthma attacks Allergic reactions Prolong effects local anesthetics |
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What are some important concepts and causes of Hypotension requiring Sympathomimetics use?
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-Overdose of volatile agent
-Inaccurate assessment preload -Treatment of symptom vs underlying cause |
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Why is the treatment of hypotension with sympathomimetics not recommended for hypovolemia?
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Vasopressor should be used when BP must be increased promptly to prevent pressure-dependent decreases in blood flow that could result in tissue ischemia.
Disadvantages of using sympathomimetics that lack significant beta1 adrenergic effects to maintain BP include intense vasoconstriction and associated blood pressure increases that evoke reflex-mediated bradycardia, which leads to a decrease in cardiac output. |
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What type of Receptor Affinity do
Beta 1 receptors have for Epi & Norepi? |
Equal affinity for epi & norepi
E=N |
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What type of Receptor Affinity do
Beta 2 receptors have for Epi & Norepi? |
Greater affinity for epinephrine than for norepinephrine
E>N |
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Sympathomimetics exert their effects by activating either directly or indirectly on what receptors?
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alpha-adrenergic receptors
beta-adrenergic receptors dapaminergic receptors |
3
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Name 3 G protein-coupled receptors?
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alpha-adrenergic receptors
beta-adrenergic receptors dapaminergic receptors |
A
B D |
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What is the Beta 1 effect of cAMP?
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cAMP
Protein kinases Inward calcium ion influx Increased cytoplasmic calcium concentrations Enhanced activity of actin/myosin Increased inotropic effect |
Beta 1 response to epi vs norepi
E=N |
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What is the Beta 2 effect?
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Relaxation of bronchial, vascular and smooth muscles
Reflect hyperpolarization of the cell membranes and decreased inward calcium ion flux |
Beta2 receptors are more sensitive to epinephrine than norepinephrine
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What occurs Cellularly in response to and INCREASE in cAMP?
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Increase in cAMP increases the rate of inactivation of myosin light chain kinase, the enzyme responsible for triggering the interaction of actin with myosin in these cells. This appears to be the mechanism of vasodilation caused by B2 agonists.
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Alpha1 receptor stimulation causes an
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increases inward calcium ion flux and probably facilitates release of bound intracellular calcium
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What does Alpha2 receptor stimulation results in
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inhibits adenylate cyclase activity
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What influences the pharmacologic response evoked by sympathomimetics?
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Anatomic distribution of alpha- and beta-adrenergic receptors
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Why does Norepinephrine have minimal effects on airway resistance?
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adrenergic receptors in bronchial smooth muscle are not stimulated by this catecholomine
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Why are Epi and isoproterenol potent bronchodilators?
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As a result of their ability to activate beta2 receptors
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Explain the response of cutaneous blood vessels to epi or norepi.
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Cutaneous blood vessels possess alpha-adrenergic receptors resulting almost exclusively in vasoconstriction when activated by norepinephrine or epinephrine
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Explain the cause of the low and high dose response to epi that occurs in smooth muscles,
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Smooth muscles of blood vessels supplying skeletal muscles contain both beta2 and alpha1 receptors
-low doses of epi produce beta receptor-mediated vasodilation - -high doses produce apha receptor-mediated vasoconstriction which overrides evidence of beta stimulation |
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Epinephrine:
Where is it released? What is the lipid solubility of epi? How is it utilized by the body? |
1. Released from adrenal medulla
2. Poorly lipid soluble 3. Regulation of contractility, HR, vascular & bronchial sm. muscle tone, glycogenolysis (activation of heptaic phosphrylase enzyme), lipolysis (activation of triglyceride lipase - accel. breakdown of tyr to free fatty acids & glycerol) 4. Alpha1 receptor stimulation INHIBITS release of Insulin (hyperglycemia - common in preoperative period) |
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Epinephrine
what are the clinical uses ? what is the dose for it use? |
Combined with local anesthetics
to treat allergic reactions Anaphylaxis 0.3 – 0.5 mg IV 1:1000 solution CPR |
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Epinephrine causes ( )
because it is a ( ) inotrope describe epi's action on specific receptors. |
Positive inotrope, increase HR, systolic BP, decrease diastolic BP (Beta 2 effect), widened pulse press
Vasoconstriction cutaneous vessels, hepatorenal vasculature MICROgrams/min stimulate Alpha & Beta (with Alpha predominate) |
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Epinephrine dosing
single small moderate high |
Dosing
Single IV bolus dose 2–8 Mircog IV lasts ~ 1 – 5 min “small doses” 1-2 MICROg/min stimulates Beta2 ; “moderate doses” 4 MICROg/min stimulate Beta2 “high doses” 10 – 20 MICROg/min |
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Epinephrine is ( ) potent then norepi.
This causes what response in the body? (3) |
2-10 x’s more potent than norepi
1) causing increasing renal vascular resistance 2)Skeletal muscle vasodilation 3) Increased renin secretion (agonism of Beta receptors in the kidney) |
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What is Epinephrine effect on the
Smooth Muscles of the Airway? |
acts as a bronchodilator because it
is an Alpha Agonist however if an existing beta blockade is present it can result in bronchoconstriction |
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Norepinephrine
what is? where is it released? What does it cause? |
Endogenous neurotransmitter released from postganglionic sympathetic nerve endings
Produces intense arterial & venous vasoconstriction (alpha1 effect) in all vascular beds (liver, skeletal muscle, kidneys, skin) |
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Norephinephrine should not cause two clinical issues.
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Does not produce bronchodilation
Should not expect to see hyperglycemia |
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Norepinephrine
causes 2 effects clinically |
Increase in systolic & diastolic BP
medical Acidosis 2nd to intense vasoconstricition |
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Norepinephrine
dosing |
Dose
4 – 6 Microg/min continuous infusion for treatment of refractory hypotension If it Extravates, tissue necrosis Can tx with phentolamine 5 – 10 mg IV mixed in 10 ml NaCl 0.9% max dose 0.1 – 0.2 mg/kg |
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Dopamine is a precursor to?
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Epi and Norepi
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Dopaminie is relatively NONSPECIFIC for what receptors? (4)
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relatively nonspecific for
D1-2, alpha & beta receptors |
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Why must Dopamine be a continuous infusion?
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Metabolism is rapid
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D1 receptors located
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postsynaptically
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Agonism of D1 receptors-
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Agonism results in vasodilation
(renal, mesenteric, coronary, cerebral vessels) |
RMCC vasodilation
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D2 receptors are
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presynaptic
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Agonism of D2 receptors-
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Inhibits the release of Norepi
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What effect does Dopamine have on the heart?
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stimulates the release of endogenous norepi from the heart
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Dopamine has variability in plasma dopamine concentration of
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10 – 75 fold variablility in plasma dopamine conc despite identical infusion rates
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Dopamine may cause
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May observe drug-induced hyperglycemia
due to decrease insulin secretion |
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How do you treat tissue extravasation of dopamine?
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phentolamine prn
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How do DIRECT acting Sympathomimetics work?
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Activate adrenergic receptors directly,
potency of direct-acting synthetic noncatecholamines is LESS than that of catecholamines |
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Name Direct acting Sympathomimetics.
2 classes containing 5 drugs |
Synthetic noncatecholamines
phenylephrine, methoxamine Catecholamines Epi, norepi, dopamine |
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Most direct-acting sympathomimetics activate what?
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alpha- & beta-adrenergic receptors
(magnitude of alpha & beta activity varies from almost pure alpha-agonist activity (phenylephrine) to almost pure beta-agonist activity (isoproterenol) |
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Synthetic non-catecholamines that activate adrenergic receptors by evoking the release of what?
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the endogenous neurotransmitter norepinephrine from postganglionic sympathetic nerve endings
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Presumably, these drugs enter postganglionic sympathetic nerve endings & do what?
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they displace norepinephrine outward into the synaptic cleft
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Depletion of neurotransmitters, as with repeated doses of a sympathomimetic does what?
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blunts the pharmacologic responses normally evoked by the drug
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For some synthetic noncatecholamines (such as ephedrine) pharmacologic effects may reflect what?
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combinations of direct & indirect actions
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What is this characterized by mostly?
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alpha- & beta1 –adrenergic agonist effects b/c norepi is a weak beta2 adrenergic agonist
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