Term
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Definition
i. neurohormone that is released from the adrenal medulla (most circulating Epi is metabolized by MAO and COMT)
ii. Synthesis
1. TYR>>Dopa>>DA>>NE (DbetaH)>>Epi |
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Term
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Definition
a. increased automaticity
b. increased rate
c. increased conduction velocity
d. increased CO (beta-1 stimulated increase in contractility plus slight relaxation in blood vessels due to beta-2 stimulation at therapeutic dose
e. increased oxygen consumption
f. decreased efficiency |
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Term
| Epi BP effects (B2 and A1) |
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Definition
a. decreased at low doses via B2 dilation
b. increased as dose increases and A1 receptors – if both receptors occupied, A1 response predominates
c. at low doses MBP is often decreased, while at high doses MBP is increased |
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Term
| Epi respiratory (B2 and A1) |
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Definition
a. bronchioles are dilated via B2 receptors – effect is most prominent when bronchial muscle is constricted due to drugs or disease
b. secretions are decreased via A1 receptor |
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Term
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Definition
a. increased glycogen breakdown (B2)
b. decreased glycogen synthesis (A1)
c. decreased insulin secretion |
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Term
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Definition
1. anaphylactic shock (drug of choice)
a. B2 stimulation opens airways
b. B2 stimulation suppresses release of histamine and leukotrienes by inhibiting antigen – induced degranulation of mast cells
c. A1 stimulation can elevate blood pressure
2. Asthma: opens airways via B2
3. Hypersensitivity reaction: bee stings, food, drugs
a. B2 stimulation opens airways
b. B2 stimulation suppresses release of histamine and leukotrienes by inhibiting antigen – induced degranulation of mast cells
c. A1 stimulation can elevate blood pressure
4. Topical hemostasis
a. shrinks mucosa in nose, throat, larynx (A1) to improve visualization for surgical procedure
5. Cardiac arrest: resuscitate the heart via B1 stimulation
6. Support the blood pressure: not first line, try DA first |
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Term
| Epi side effects and contraindications |
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Definition
v. Side effects
1. arrhythmias, cerebral vascular accident, anxiety, fear, HA, palpitations, tremors
vi. Contraindication
1. if epi is administered in the presence of an alpha blocker, there is no pressor response: Epi Reversal (pure depressor) |
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Term
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Definition
i. transmitter of the postganglionic sympathetic neurons (can inhibit own release – alpha 2 synapses; PGE2 inhibits; ATII enhances; can be metabolized by MAO, catechol-o-methyl-transferase (COMT) – present in liver, kidney, and Gi with MAO presynaptically)
1. 90% is reaccumulated by the NET
2. if intracellular concentration of NE becomes elevated, NET exporst NE via facilitated diffusion
ii. Synthesis
1. TYR>>Dopa>>DA>>NE (DbetaH)>>Epi |
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Term
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Definition
1. Heart: Direct effects same as Epi (B1)
2. BP: increased systolic, diastolic and mean (A1)
3. CO: no change or slightly decreased due to A1-mediated constriction of blood vessels
4. Metabolism: decreased glycogen synthase activity via A1 |
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Term
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Definition
iv. Therapeutic uses
1. sometimes used in ER for shock – neurogenic shock associated with spinal anesthesia
v. Side effects
1. arrhythmias, cerebral vascular accident, anxiety, fear, HA, palpitations, tremors |
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Term
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Definition
| i. selective beta agonist that may be used to stimulate the heart |
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Term
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Definition
1. Heart
a. increased automaticity
b. increased rate
c. increased conduction velocity
d. increased CO (beta-1 stimulated increase in contractility plus slight relaxation in blood vessels due to beta-2 stimulation at therapeutic dose
e. increased oxygen consumption
f. decreased efficiency
2. Blood pressure: Decreased (B2)
3. Respiratory tract: relaxes bronchi (B2) |
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Term
| Isoproterenol uses and side effects |
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Definition
iii. Therapeutic uses
1. used in emergencies to stimulate heart in patients with heart block or to stimulate rate, especially to prepare for inserting a pacemaker – myocardial efficiency decreased
2. used to relax bronchi, but a B2 selective agonist preferred
iv. Toxicities and side effects
1. fatal arrhythmias, tachycardia, palpitation, anginal pain |
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Term
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Definition
i. transmitter in the CNS and the precursor for NE in postganglionic sympathetic nerve terminals
ii. Mechanism
1. agonist
iii. Uses
1. Cardiogenic shock
iv. Physiological effects
1. receptors activated (DA, B1, B2, A1 at high doses)
2. HR increased by B1 stimulation
3. BP decreased by DA receptor activation in renal and mesenteric beds, decreased by B2 receptor activation, increased at very high doses by A1 receptor activation
v. Toxicities and Side Effects
1. due to excessive sympathetic stimulation, tachycardia, angina pain, arrhythmias and DA receptor stimulation of the chemotrigger zone (CTZ), nausea and vomiting
2. does not cross the BBB |
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Term
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Definition
i. Mechanism
1. agonist
ii. Uses
1. Heart failure associated with open heart surgery or acute cardiac infarction
iii. Physiological effects
1. Heart: relatively selective for B1 receptors and has unique property of greater inotropic (contractility) than chronotropic (rate) effects – at high dose can also increase automaticity
2. BP: high does can increase via A1
iv. Toxicities and side effects
1. arrhythmias, does not cross BBB |
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Term
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Definition
i. Mechanism
1. agonist – activates alpha receptors
ii. Uses (limited sales of pseudoephedrine have increased its use)
1. Rhinitis
2. decongestant
3. pupillary dilator |
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Term
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Definition
i. Therapeutic uses
1. Bronchial asthma (B2 stimulation opens airways)
2. Anaphylactic shock (B2 stimulation inhibits release of mediator of the allergic response from mast cells)
3. relaxation of the pregnant uterus (B2)
ii. Toxicities and side effects
1. related to less than total selectivity for B2
2. high doses can activate B1 receptors on the heart
iii. a weak B (and alpha) agonist that also enhances the release of NE, also a CNS stimulant, can be used as a nasal decongestant and as pressor agent |
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Term
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Definition
i. Mechanism
1. agonist
ii. Uses:
1. Bronchial asthma
iii. Therapeutic uses
1. Bronchial asthma (B2 stimulation opens airways)
2. Anaphylactic shock (B2 stimulation inhibits release of mediator of the allergic response from mast cells)
3. relaxation of the pregnant uterus (B2)
iv. Toxicities and side effects
1. related to less than total selectivity for B2
2. high doses can activate B1 receptors on the heart
v. relative B2-selective agonist – more useful than the non-selective B-agonists for asthma |
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Term
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Definition
i. Therapeutic uses
1. Bronchial asthma (B2 stimulation opens airways)
2. Anaphylactic shock (B2 stimulation inhibits release of mediator of the allergic response from mast cells)
3. relaxation of the pregnant uterus (B2)
ii. Toxicities and side effects
1. related to less than total selectivity for B2
2. high doses can activate B1 receptors on the heart
iii. relative B2-selective agonist – more useful than the non-selective B-agonists for asthma |
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Term
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Definition
i. cause displacement of NE from the terminal – produces sympathomimetic effects
ii. Mechanism
1. substrate for NET and increases synaptic NE via facilitate diffusion = increases BP and HR
iii. Use:
1. Narcolepsy: release NE from nerve terminal by facilitated exchange diffusion
2. Wt. reduction: suppress appetite
iv. Toxicities and Side effects
1. Excessive CNS stimulation and peripheral CV effects can occur, risk of abuse |
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Term
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Definition
i. cause displacement of NE from the terminal – produces sympathomimetic effects
ii. Mechanism
1. substrate for NET and increases synaptic NE via facilitate diffusion = increases BP and HR
iii. Use:
1. Narcolepsy: release NE from nerve terminal by facilitated exchange diffusion
2. Wt. reduction: suppress appetite
iv. Toxicities and Side effects
1. Excessive CNS stimulation and peripheral CV effects can occur, risk of abuse |
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Term
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Definition
i. Use
1. Attention-Deficit/Hyperactivity disorder
ii. Toxicities and Side effects
1. Excessive CNS stimulation and peripheral CV effects can occur, risk of abuse |
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Term
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Definition
i. irreversible alpha blocker
ii. Block A1 receptors (somewhat selective over A2)
iii. duration of action about 24 hr – must synthesize new receptor to recover A1 effect
iv. Uses:
1. pheochromocytoma management (in combo with propranolol)
2. benign prostatic hypertrophy (relax smooth muscle in bladder, prostate capsule and prostatic urethra – improves urinary flow)
v. toxicity and side effects
1. postural hypotension is caused by A1 blockade
2. reflex tachycardia occurs – worse with non-selectives
3. nasal stuffiness
4. inhibition of ejaculation |
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Term
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Definition
i. non-selective alpha blocker
ii. the A1 blockage decreased BP
iii. A2 blockade prevents feedback inhibition by released NE causing more NE to be released onto B1 receptor in heartgreater tachycardia than with a selective blocker
iv. Uses: pheochromocytoma management (in combo with propranolol)
v. toxicity and side effects
1. postural hypotension is caused by A1 blockade
2. reflex tachycardia occurs – worse with non-selectives
3. nasal stuffiness
4. inhibition of ejaculation |
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Term
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Definition
| 1. antagonist – blocks beta receptor (B1 and B2 non-selective) |
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Term
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Definition
1. Cardiac
a. decreased HR due to B1 block, decreased CO (more pronounced during exercise)
b. decreased conduction velocity, myocardial oxygen demand, and spontaneous rate of depolarization
2. Vascular and blood pressure effects
a. B2 block may increase TPR, decrease in plasma renin due to B1 block, BP reduction: reduction in CO, reduction in plasma renin, decrease in sympathetic tone via effects in CNS
3. Metabolic
a. no effect on plasma glucose levels in normal persons (slows recovery from hypoglycemia in diabetics – less of a problem with B1 selectives)
b. increased plasma concentrations of TG (VLDL) and decreased concentrations of HDL
4. Respiratory tract
a. B2 block leading to increased airway resistance (can be life threatening to asthmatics |
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Term
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Definition
1. angina pectoris
2. supraventricular arrhythmias
3. HTN (usually with diuretics and vasodilators)
4. prophylaxis of migraine
5. Early in MI to reduce high sympathetic tone
6. Prophylaxis to decrease mortality after MI
7. Pheochromocytoma (with A blockers)
8. Performance anxiety |
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Term
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Definition
1. B1 block: decreased CO, heart block, Bradycardia
2. B2 block: bronchoconstriction
3. CNS: depression, lethargy |
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Term
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Definition
i. Selective B1 blocker
ii. Effects
1. Cardiac: like propanolol
2. Respiratory: less danger of respiratory side effects than propanolol (at high doses no B blocker is really selective) |
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Term
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Definition
| i. Selective B1 Blocker with 8 min half-life – emergency situations |
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Term
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Definition
i. Glaucoma
1. non-selective but used for B1 selective actions – decrease aqueous humor production |
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Term
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Definition
(block A1 receptor only)
i. adrenergic blocking agent (reversible)
ii. decreases BP, get reflex tachycardia
iii. Uses:
1. HTN
2. benign prostatic hypertrophy (relax smooth muscle in bladder, prostate capsule and prostatic urethra – improves urinary flow)
iv. toxicity and side effects
1. postural hypotension is caused by A1 blockade
2. reflex tachycardia occurs – worse with non-selectives
3. nasal stuffiness
4. inhibition of ejaculation |
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Term
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Definition
i. A2 antagonist: inhibits NE release, works directly at A2 receptor
ii. Uses
1. Essential HTN
2. reduction in side effects of opioid withdrawl
3. ADHD
4. Open angle glaucoma (apraclonidine)
iii. Toxicities and Side effects
1. dry mouth, sedation
2. HTN crisis may occur |
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Term
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Definition
i. A2 antagonist: inhibits NE release, must be metabolized to alpha-methyl-NE
ii. Uses
1. Essential HTN (safe in pregnancy)
iii. Toxicities and Side effects
1. dry mouth, sedation
2. autoimmune response (positive Coombs test) |
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Term
| Theophylline and Caffeine |
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Definition
1. antagonists at adenosine receptors – stimulates CNS
ii. Pharmacological actions
1. CNS
a. all cortical are sensitized – large doses sensitize the respiratory areas to CO2 and increase respiratory rate
2. CV
a. HR and contractility increases, systemic blood vessels dilated, TPR decreased (looks like B2 stimulation), cerebral blood vessels constricted
3. Respiratory tract: bronchi relaxed
iv. Therapeutic uses
1. bronchial asthma: intractable bronchial asthma is treated with theophylline in the form of animophylline
2. prophylactic management: can be use in combo with inhaled B2 agonists for management of chronic bronchial asthma |
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Term
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Definition
1. Mechanism
a. enter the NE terminal
b. blocks the VMAT (vesicular monoamine transporter) resulting in depletion of vesicular NE over time
2. Uses
a. HTN
3. Side effects
a. CNS depression
b. orthostatic hypoTN |
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Term
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Definition
neither agonist or antagonist)
1. Use: HTN
2. Mechanism
a. enters via the NET
b. uncouples the AP from calcium entry – concentrated in the vesicles and gradually depletes NE
3. Side effects: postural hypoTN, diarrhea, impaired sexual function – peripheral antiadrenergic actions |
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Term
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Definition
1. cause displacement of NE from the terminal – produces sympathomimetic effects
a. if MAO is intact, the displaced NE is metabolized
i. If MAOI is present, ingestion of tyramine can precipitate a HTN crisis
2. Dietary sources: aged cheeses, beers and lagers, wine, fava beans – MOA in the gut normally metabolizes |
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Term
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Definition
| 1. Blocks the NET and increases synaptic NE |
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Term
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Definition
| 1. Blocks the NET and increases synaptic NE |
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Term
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Definition
1. selective NE reuptake inhibitor is also used (ADHD)
2. Toxicities and Side effects
a. Excessive CNS stimulation and peripheral CV effects can occur, risk of abuse |
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Term
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Definition
1. urinary excretion of catecholamine metabolites
a. VMA: 2 – 4 mg
b. MOPEG: 1.2-1.8 mg
c. Normetanephrine 100-200 microg
d. Metanephrine: 100-200 microg
e. Epinephrine: 2-5 microg
f. NE: 25-50 microg |
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Term
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Definition
1. cAMP dependent PKA
a. activates hepatic glycogen phosphorylase – converts glycogen to G-1-P
b. inhibits hepatic glycogen synthase
c. in heart, phosphorylates phospholamban and troponin
2. PKC
a. phosphorylates glycogen synthase (decreases activity)
b. phosphorylates many ion channels, pumps and ion exchangers |
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Term
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Definition
1. Increasing size of amino group substitution increases beta receptor affinity
2. Maximum alpha and beta activity conferred by 3 and 4 position hydroxyl group
3. removal of a hydroxyl group from the ring increases CNS penetration
4. Non catecholamines are not metabolized by COMT – substitution of the alpha carbon blocks MAO metabolism |
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Term
| Non-catecholamine alpha stimulators |
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Definition
relatively selective for A1 (exceptions covered under antiadrenergics)
1. Therapeutic uses
a. decongestion of mucous membranes
b. raise blood pressure (pressor)
c. dilate pupil – eye drops
2. Toxicities and side effects
a. excessive A1 stimulation can elevate the blood pressure
3. Examples: phenylephrine, phenylpropanolamine, ephedrine |
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Term
| Non-chatecholamine beta-stimulators |
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Definition
1. Therapeutic uses
a. Bronchial asthma (B2 stimulation opens airways)
b. Anaphylactic shock (B2 stimulation inhibits release of mediator of the allergic response from mast cells)
c. relaxation of the pregnant uterus (B2)
2. Toxicities and side effects
a. related to less than total selectivity for B2
b. high doses can activate B1 receptors on the heart |
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Term
| Non-catecholamine CNS stimulants |
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Definition
1. Therapeutic uses
a. Narcolepsy
i. Release NE from nerve terminal by facilitated exchange diffusion
b. Wt. reduction
i. suppress appetite
c. Attention-deficit disorder
2. Toxicities and Side effects
a. Excessive CNS stimulation and peripheral CV effects can occur, risk of abuse |
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