Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

60 Cards in this Set

  • Front
  • Back
1. NE
2. q
3. Inc IP3, Inc Ca,Inc DAG Inc PKC
4. Inc vascular smooth muscle contraction
1. ACh
2. q
3. Inc IP3, Inc Ca,Inc DAG Inc PKC
4. Inc exocrine gland secreations and smooth muscle motility
1. His
2. s
3. Inc cAMP, Inc PKA
4. Inc gastric acid secretion
Beta 2
1. NE
2. s
3. Inc cAMP, Inc PKA
4. Vasodilation, bronchodilation Inc glucagon release
Alpha 2
1. NE
2. i
3. Dec cAMP, Dec PKA
4. dec sympathetic outflow, dec insulin release
1. ACh
2. i
3. Dec cAMP, Dec PKA
4. dec heart rate
Beta 1
1. NE
2. s
3. Inc cAMP, Inc PKA
4. Inc HR, contractility, renin release, lipolysis, aqueous humor formation
1. ACh
2. q
3. Inc IP3, Inc Ca,Inc DAG Inc PKC
4. CNS stimulation
What do Alpha 1 agonists do to the following
Vascular smooth muscle
Mydriasis (dilation)
Genitourinary smooth muscle
Inc sphincter tone
Glycogenolysis, gluconeogesesis
What do B1 agonist do to the following
Heart rate
Inc renin
What do B2 agonists do to the following
Bronchial smooth muscle
Vascular smooth muscle
uterine smooth muscle
glycogenelisis and gluconeogenesis
Are there any drugs that are seletive to a given muscarinic receptor
no, but potency at each can vary
What do cholinergic agonists do at the following places and via what receptor
stimulation- M1
Heart Rate
Decrease M2
pupillary constriction (miosis), ciliary contraction (glaucoma treatment) M3
GI, GU tract
Inc motility, secretions, bladder constriction, sphincter relaxation M3
Bronchoconstriction and Inc secreations- M3
Where are nicotinic receptors located
autonomic ganglia of sympathetic and parasympathtic systems, as well as at the adrenal medulla
What is the neurotrasmitter
What drug blocs nicotinic receptor
What does botulinum toxin do
Block ACh relases for pre-synaptic neuron
What do AChesterase do
breaks ACh into choline and acetate so that choline can be reuptaken by presynaptic neuron
What does cocaine do
Blocks reuptake of NE into presynaptic neuron
amount of drug in body/_______ = Vd
plasma drug concentration (note: Vd is Volume of Distribution)
rate of elimination of drug/[plasma drug] = ?
CL (Clearance)
(.7)(Vd)/CL = ?
T 1/2
A drug infused at a constant rate reaches about 94% of steady state after _______ t 1/2s.
A loading dose is calculated using this formula.
(Cp)(Vd)/F (note: Cp = target plasma concentration, and F = bioavailability)
A maintenance dose is calculated using this formula.
Rate of elimination is proportional to _______ ______ in 1st order elimination.
drug concentration
In the case of EtOH, which is elimated by _____ order elimination, a constant amount of drug is eliminated per unit time.
Phase ____ (I or II) reactions yield slightly polar metabolites that are often _____ (active or inactive)
I, active
Phase ____ (I or II) reactions yield very polar metabolites that are often _____ (active or inactive) and are excreted by the _______.
II, inactive, kidney
Phase II reactions are often of this type.
Cytochrome P-450 is involved in _____ phase (I or II) reactions.
A patent lasts for _____ years after filing for application.
How many phases are there in drug development?
Drugs are first tested in patients in phase _____ of clinical testing, pharmacokinetic safety is determined in phase ______ of clinical testing, double blind tests are done in phase ____ and post-market surveillance is done in phase _____.
In a dose response curve, a competitive antagonist shifts the curve _____, while a non-competitive antagonist shifts the curve ______.
right, down
What pharmacologic relationship would determine the existence of spare receptors?
EC50 < Kd
What does it mean if EC50 and Kd are equal?
The system does not have spare receptors
A partial agonist acts on the same receptor system as a full agonist? T/F
What's the main difference between a partial agonist and a full agonist?
A partial agonist has a lower maximal efficacy.
Is a partial agonist less potent than a full agonist?
Not necessarily. It can be less, more or equally potent as a full agonist.
Parasympathetic preganglionic neurons release the neurotransmitter -------- which act on -------- receptors.
Ach, nicotinic.
Sympathetic preganglionic neurons to sweat glands release the neurotransmitter ------- which act on ------- receptors.
Ach, nicotinic.
Ach is synthesized from acetyl-CoA and choline by the enzyme ---------.
Choline acetyltransferase.
In the noradrenergic nerve terminal, tyrosine is hydroxylated to -------, which is decarboxylated to --------, which is finally hydroxylated to NE.
DOPA, dopamine.
The action of NE and DA is terminated by --------- and ----------.
Reuptake, diffusion (different than for Ach).
The drugs --------- and ---------- inhibit the reuptake of NE.
Cocaine, TCA.
Ach inhibits the release of NE from the noradrenergic nerve terminal by binding to --------- receptors.