• 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
Reading...
Front

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

image

Play button

image

Play button

image

Progress

1/91

Click to flip

91 Cards in this Set

  • Front
  • Back
Pilocarpine
Muscarinic Agonist
Tx of glaucoma and xerostomia
Miotic; works on ciliary muscle
Neostigmine
Acetylcholine Esterase Inhibitor
Quat. Amine = No CNS
Tx Myasthenia Gravis
Atropine
Competitive muscarinic antagonist
*Blocks Ach but can ↑Ach to overcome
Tertiary amine – into CNS
Effects depend on ‘tone’ -↑ HR if PNS
Overdose – treat with AChEI (↑ Ach)
Scopolamine
Muscarinic antagonist
Tertiary amine – in CNS
Duration can be days
- tx motion sickness due to CNS depressant effects
- ↑ doses = excitation
Tolterodine
Muscarinic antagonist
- tx incontinence & overactive bladder
*Functional selectivity for urinary bladder
Mecamylamine
Nicotinic Antagonist/Ganglionic Blocking Agent
Tertiary amine – into CNS
Competative inhibitor with nicotine
Blocks Nn – affects CNS and periphery
**Orthostatic Hypotension → tone will not allow a change in BP
Succinylcholine
Nicotinic Agonist/Skeletal Muscle Relaxant
Safe from AChE
Causes hyperkalemia, increased IOP, releases histamine, and malignant hyperthermia
Tubocurarine
NMJ Blocking Agent
Non-depolarizing
Skeletal Muscle Relaxants
Binds Nm reversibly for Ach @ NMJ end-plate
Flaccid paralysis w/out preliminary contractions (no twitch)
Doesn’t gain access to brain
Cyclobenzaprine
Skeletal Muscle Relaxants
Spasmolytic
(Analogue Tricyclic Antidepressants)
Decrease NE reuptake (atropine like)
- tx (acute, short-term) muscle spasm associated w/ muscoskeletal injury
Works with Internuncial neuron
Tizanidine
CNS-active muscle relaxant
Sympathomimetic
Clonidine-like compound
α2 agonist
- tx muscle spasticity
Sildenafil
Inhibits cGMP degredation
Inhibits phosphodiesterase
↑ cGMP relaxes smooth muscle → increase in blood flow = erection
Arginine → NO (via NOS-regulated by Calcium/calmodulin) → Guanylyl Cyclase → cGMP
Ryanodine
Mediates release of calcium from SR
Receptor on T-tubules
↑ calcium → Muscle contraction
Glucagon
Antidote for β-blockers - ↑ cAMP
Released from pancreas when blood glucose levels are low
Binds glucagon receptors on liver cells → release of glucose or synthesis
MAO Inhibitor
Sympathomimetic
Drug interactions
Tyramine in foods → dangerous increase in BP if w/ MAOI
↑ NE due to stopping metabolism

**meperidine + MAOI → fever & convulsions
Bretylium
Anti-Release of NE
Prevents NAP-induced NE release
Used to terminate ventricular fibrillation
Use IV only in emergency to raise BP
Possible calcium interference
Local anesthetic activity
Guanethidine/Guanadrel
Anti-Release then Depletion of NE
Prevent NAP-induced NE release
Chronic use → depletion
Initial sympathomimetic effects – initial release of NE due to drug uptake into nerve (co-transporter)
Peripheral effect
Reserpine
Depletion of NE
Blocks vesicular NE and DA uptake → NE depletion
Blocks VMAT (Vesicular Monoamine Transporter)
Causes smooth ↓ in BP
CNS effects: ↑ vagal outflow-bradycardia (↓ HR/CO/PR); psychic depression; sedation
No initial sympathomimetic effects
Phentolamine
Competitive Antagonist
Blocks α1 & 2 – nonselective α blocker
Short half-life and fact acting
Used to tx/diagnose catecholamine-secreting tumor
Phenoxybenzamine
Covalent binding to α receptors
Blocks α1 & 2 – unselective α blocker
Irreversible – alkylate
Long acting
tx shock
Prazosin
Selective α1 antagonist
Prototype
First dose – syncope (wait till PM for first dose due to orthostatic hypotension)
- tx high BP
Tamsulosin
Selective α1 antagonist
Selective for α1A (Subtype prominent in bladder sphincter smooth muscle)
Blood vessels have tons of α1A
When pts age - ↑ α1B which means less vessel wall effects (Younger pts have more vessel wall effects)
- tx BPH (Benine Prostetic Hyperplasia)
Yohimbine
α2 antagonist – can get into CNS
↑ SNS outflow from CNS →↑ BP
- tx orthostatic hypotension
Carvedilol
Mixed α & β blockers
- tx CHF
Can cause orthostatic hypotension
Labetalol
Mixed α & β blockers w/ some β2 agonist activity
- tx for high BP
Can cause orthostatic hypotension
Propranolol
Non-selective β blocker
Prototype
Potentiates pressor effect of epinephrine by blocking β2 vasodilator activity
Prevents hypokalemia
“Local Anesthetic” effect (blocks Na+ channels)
- tx angina, HTN, dysrhythmias, glaucoma
Esmolol
Β1 selective blocker
IV – short half-life
High doses can affect β2 activity (bronchioles effects – constriction)
- tx acute arrhythmias
Metoprolol
Β1 selective blocker
“Cardio selective”
Used chronically in heart failure
High doses – affect β2 (bronchioles effects – constriction)
Nebivolol
Β1 selective blocker
Direct vasodilator effect by ↑ NO release
- tx HTN
Metyrosine
Tyrosine hydroxylase inhibitor
Decreases NE concentration
Tx pheochromocytoma before surgery
Nadolol
Nonselective beta blocker
Tx HTN
Least lipophilic
Pindolol
Nonselective beta blocker
Don’t use with asthma
Tx HTN
Less bradycardia b/c partial agonist activity
Less lipophilic
Norepinephrine
Endogenous catecholamine
sympathomimetic
α1, α2, β1, β3 (no β2)
vasoconstriction (↑PR ↓HR, ↓CO)
made from tyrosine
reuptake via Uptake I/NET (90%)
metabolized by MAO and COMT
Dopamine
Endogenous catecholamine
sympathomimetic
D1, D2, α1, β1
Low doses = D1, β1 = vasodilatation
No change PR, ↑HR, ↑CO
High doses = α = vasoconstriction
↑PR, ↓HR, ↓CO (like NE)
D1 receptors in kidney
Epinephrine
Endogenous catecholamine sympathomimetic; ↓HIS release
α1, α2, β1, β2, β3
Low doses = β2 = vasodilatation
↓PR, ↑HR, ↑CO
High doses = α = vasoconstriction
↑PR, ↓HR, ↓CO (like NE)

Circulating NT
Isoproterenol
Sympathomimetic
only β (no α)
vasodilatation (↓PR ↑↑HR ↑↑CO)
Phenylephrine
direct acting sympathomimetic at α1
nasal decongestant…local administration
Albuterol
direct acting sympathomimetic at β2 dilate; tx acute asthma
Amphetamine
indirect acting sympathomimetic
facilitate NE release (displace NE via NET)
Cocaine
indirect acting sympathomimetic
prevents uptake of NE (blocks NET)
potent local anesthetic & vasoconstrictor b/c ↑[NE] in synapse
α1 SE = ↓IOP, mydriasis
Prazosin
Sympatholytic
α blocker (affinity but no efficacy)
Propranolol
Sympatholytic
β blocker (affinity but no efficacy)
Metaraminol
false transmitter of NE (α1 agonist)
less potent than NE
depletes neuronal NE
pressor
some β1 effects initially (from NE)
stopping infusion = huge ↓bp
Tyramine
indirect acting sympathomimetic
facilitate NE release
displace NE from cell via NET (↑[NE] in synapse)…longer t1/2
in cheese and wine
Ephedrine
mixed sympathomimetic
direct activity on β2
displace NE
can dilate bronchioles
Oxymetazolone
sympathomimetic at α2 and α1
nasal decongestant
α-methyl DOPA
levonordefrin
prodrug (cross BBB)
false transmitter (???effectiveness)
α-methyl DOPA → α-methyl DA →α-methyl NE
in CNS α2 causes ↓bp (more vagal)
Pseudoephedrine
α1 agonist
tx incontinence (α1) constrict sphincter
caution with BPH
NOT α1 selective
Clonidine
α2 agonist sympathomimetic in CNS
↓bp b/c enhance vagal and ↓SNS
Tx pain (CNS) b/c enhance PNS
Salmeterol
Sympathomimetic at β2 (dilate)
Long acting (not for acute attack)
Ritodrine
Terbutaline
Sympathomimetic at β2
Relax to delay labor
Systemic admin = relax bronch sm muscle; Also, ↓bp so ↑SNS which ↑renin…↑CO, tachycardia
Moxonidine
I1 agonist
Tx HTN
Not in USA
Fenoldopam
sympathomimetic at D1
↓bp, retain renal blood flow
Dobutamine
Sympathomimetic at β1
Pressor
Functionally cardioselective
↑CO with little effect on TPR
Chronotropic
changes HR
Inotropic
Changes force of contraction
Tocolytic
relaxes uterine smooth muscle to prevent premature labor
Lusitropic
myocardial relaxation
Which organs ONLY receives SNS innervation?
Most blood vessels
Sweat glands
Spleen
Piloerector Muscles
Which receive ONLY PNS innervation?
ciliary muscle in eye
Location of Nicotinic Receptors
all ganglia
adrenal medullary cells
skeletal muscle NMJ
CNS
What happens when ACh is injected?
Will bind to endothelial cell receptors, increasing Nitric Oxide and causing vasodilation
Mimetic Effect at Nm receptors
(name drugs)
ACh
Nicotine
Succinylcholine
Mimetic Effects at Nn receptors
ACh
Nicotine
Location, Signaling and Use of M1 receptors
CNS neurons
ganglion cells near parietal cells of stomach
Signalled via activation of PLC, increases IP3 and increases Ca2+
Used for Alzheimers, M1 block for ulcers
Location, Signaling and Use of M2 receptors
Heart
Autoreceptors
Soem smooth muscle
Signalled via K+ channel activation, which inhibits adenylyl cyclase and decreases Ca2+
Used for cardiac slowing
Location, Signaling and Use of M3 receptors
In exocrine glands,smooth muscle, and endothelium
Signalled via activation of PLC, increases IP3 which increases Ca2+
Can vasodilate via NO, secretion, smooth muscle contraction
What acts on radial muscle?

What acts on ciliary muscle?
NE = radial muscle of eye

Pilocarpine = ciliary muscle
DUMBBELSS
Diarrhea
Urination
Miosis
Bradycardia
Bronchoconstriction
Excitation of skeletal muscle and the CNS
Lacrimation
Salivation
Sweating
Antidotes for AChEIs
2-PAM

Atropine
Uses for Sympathomimetics
Alleviate symptoms (decongestant)
Delay Labor
Tx incontinence
Tx Asthma
Life Support by treating anaphylaxis
Delay absorption of drugs at injection site
Vasoconstriction to decrease bleeding
Pressor
B1 Agonists
(via activation of AC)
increase cardiac excitation
increase renin release from renal JG cells
B2 Agonists
(via activation of AC)
Increase plasma glucose levels
Relaxes smooth muscle
Also some receptor in heart (increases in heart failure)
B3 agonists
(via activation of AC)
Increase plasma free fatty acids
MOA of Sympathomimetics
Act on GPCR to change activity of adenylyl cylase and PLC, as well as Calcium and Potassium channels
D Agonists
(via activation of AC)
vasodilatation
cardiac stimulation
increases kidney blood flow
Alpha 2 agonists
(via inhibition of AC)
inhibit NE release via autoreceptors
Alpha 1 Agonists
(via activation of PLC)
Contraction of smooth muscle of the radial muscle of the iris and bladder sphincter
Alpha 2 agonists
(via activation of K+ channels, also inhibit Ca channel opening)
Muscles relax (since decrease in Ca, harder to get action potential)
B Agonists
(via activation of Ca channels)
PKA, acts directly to open cardiac L type Ca channels
Cardiovascular Alpha 1 & 2 Receptors
(What is the effect?)
Vasoconstriction
Cardiovascular B2 receptor
(What is the effect?)
Vasodilatation of skeletal muscle
Cardiovascular D1 Receptor
(What is the effect?)
Vasodilation of vessels supplying kidney
Cardiovascular B1 Receptor
(What is the effect?)
Increase cardiac excitation
dysrhythmogenic
increase renin secretion
Norepinephrine effects on Arterial Pressure
Increase PR
Decrease HR (reflex)
Decrease CO
Epinephrine effects on Arterial Pressure
Decrease PR at low dose, Increase at high dose
Increase HR at low dose, decrease HR at high dose
Increase CO at low dose, Decrease CO at high dose
Isoproteronol effects on Arterial Pressure
Decrease PR
Increase HR x 2
Increase CO x 2
Dopamine effects on Arterial Pressure
no change in PR(no B2), increase PR at high dose
Increase HR at low dose, Decrease HR at high dose
Increase CO at low dose, Decrease CO at high dose
-olol
Beta blocker
-ol
Sympathomimetic
-ilol
-alol
Mixed alpha and beta blocker
-osin
Alpha 1 antagonists