Exam #2 Flashcards
(39 cards)
chronotropy
positive chronotropy is increased heart rate (SA node)
inotropy
positive inotropy is increased force of contraction (atrial and ventricular cardiac muscle)
pharmacologic antagonist
bind to the same receptor as the agonist
competitive reversible:
- curve shifts right
- surmountable
- Emax stays same, EC50 inc., potency dec.
non-competitive (irreversible)”
- curve shifts down
- non-surmountable
- Emax dec, EC50 and potency stay same
physiologic antagonist
bind to a different receptor that mediates a physiologic response that is opposite to that of activation of the receptor for the agonist
G proteins for specific muscarine receptors
M3 (and M1): Gq = inc. contraction via IP3 and phospholipase C (GI)
M2 (and M2): Gi = dec. contraction via dec. cAMP (Heart)
sweat glands - part of ANS, NT released, and receptor type
part of SNS, but Ach is released to muscarinic receptors - exception
- not important in pharmacotherapy
G proteins for specific adrenergic receptors
a1: Gq = inc. contraction via IP3 and phospholipase C (vascular SM)
a2: Gi = dec. contraction via dec. cAMP (dec. SNS)
b1 and b2: Gs = inc. contraction via inc. cAMP (inc. HR and bronchodilation)
relationship between agonist and antagonist effect and tone
antagonist = effect is proportional to level of tone
- depends on receptor type and quantity
agonist = can overcome tone when use enough
- depends on dose
epinephrine reversal
when epi causes hypotension since patient on an a1 blocker (antagonist) –> excess b2 vasodilation
- treat with an a1 agonist (phenylephrine - Sedated PE)
sensitization to epi-induced hypertension
see excess inc. in HTN since patient is on a non-selective beta blocker –> unopposed epi a1 vasoconstriction
clonidine
activates a2 receptors
- dec. SNS outflow
- dec. release of Ach from cholinergic (muscarinic) neurons innervating the salivary glands
Treatment: HTN and opioid/alcohol withdrawal sxs
SE: dry mouth
- activates a2 receptors on cholinergic neurons in GI tract
- dec. Ach release from cholinergic neurons innervating salivary glands
beta-1 antagonists
beta-1 selectivity seen at low doses only - push dose can spill over to beta 2 (bad for asthmatic - bronchospasm)
metoprolol
atenolol
if there is no PNS innervation of the vasculature, how does muscarinic activation (Ach) on muscarinic receptors result in vasodilation?
indirect effect mediated via generation of nitric oxide –> cGMP –> dec. BP
side effects of muscarinic blocking agent (most sensitive to least sensitive)
Exocrine glands: reduced salivary and bronchial secretions → dry mouth
Sweat glands: impaired sweating and direct vasodilation → increased body temperature (“atropine flush” at high doses); most life-threatening result of overdose
• Children are especially susceptible (OD toxicity)
Heart: block of cholinergic slowing of heart rate → tachycardia
Eye: mydriasis and paralysis of accommodation (cycloplegia) → blurred vision, ↑ IOP (block aqueous humor drainage)
Lungs: relaxation of bronchiolar smooth muscle → bronchodilation
Genitourinary tract: relaxation of ureters and bladder wall muscle (detrusor) → urinary retention
Gastrointestinal tract: reduced gastrointestinal motility → constipation; gastric secretions (HCl, pepsin) blocked less effectively than salivary secretions
CNS effects: restlessness, delirium; sedation with scopolamine
lethal injection
Sodium thiopental: IV general anesthetic = unconscious
• Now unavailable in US – benzodiazepines* used
Pancuronium*: neuromuscular blocker = blocks respiration and involuntary muscle movements
Potassium chloride*: Produces complete heart block
• * 2016 – restricted from use in executions by Pfizer
baroreceptor reflex
Activation of baroreceptor (increased arterial pressure increases vessels tension and activates)
• Inhibits sympathetic discharge from medulla: vasodilation, dec. HR (reflex bradycardia)
• Vagus nerve activity increases (PNS) → dec. HR
• Overall: decrease blood pressure
Relaxation of baroreceptor (decreased arterial pressure)
• Disinhibits tonic sympathetic discharge, resulting in SNS-mediated release of NE
o Heart: B1 receptors → reflex tachycardia (inc. HR)
o Blood vessels: α1 receptors → vasoconstriction
• Overall: increase in arterial blood pressure
indirect acting sympathomimetics (adrenergic agonists) vs. indirect acting parasympathomimetics (cholinergic agonists)
Indirect-acting sympathomimetics (adrenergic agonists) act like NE by being uptaken by NET, transported to storage vesicle (VMAT), and displaces endogenous NE which is released into synapse
Indirect acting parasympathominetics (cholinergic agonists) inhibit the enzyme (AchE) the breaks down Ach; thus, prolonging the time Ach is in synapse
substance most associated with the acute bronchospastic response seen in patients with asthma
- target pharmacotherapy
leukotrienes
why should NSAIDs be used cautiously in patients with asthma
b/c they inc release of leukotrienes and can cause bronchospastic response
effects of endogenous histamines
vasodilation of arterioles via NO (hypotention / reflex tachycardia)
inc. capillary permeability (edema, urticaria, hives)
contraction of GI smooth muscle and inc. secretions
bronchoconstriction
stimulation of nerve endings (pain, itching)
triple response: wheal and flare
anaphylactic reaction
most effective physiologic antagonist of histamine in smooth muscle
epinephrine and albuterol
Note: antihistamines are pharmacologic antagonists
treatment of acute cough due to the common cold
1st generation antihistamine/decongestant (e.g., diphenhydramine/pseudoephedrine)
Naproxen (tid x 5 days): blocks inflammation that stimulates cough afferents (for pain)
Comments: antitussives mixed results; zinc not recommended; 2nd generation antihistamines ineffective
treatment of cough due to upper airway cough syndrome (postnasal drip)
1st generation antihistamine/decongestant (e.g., diphenhydramine/pseudoephedrine
treatment of dry, non-productive coughs that keep you up at night
anti-tussives (opioids or opioid agonists work at level of cough center
