Pharm II Flashcards
Epinephrine
Β>α,
low dose ↑ systolic ↓diastolic ↑CO
High dose α ↑BP vasoconstriction, ↑HR
-Bronchospasm β2 dilate, α1 ↓secretions
Use: Anaphylaxis, Cardiac arrest, bronchospasm
Toxicity: Arrhythmia
Contraindication: Late term pregnancy
Norepinephrine
α1, α2, β1:
vasoconstriction, ↑TPR ↑HR
β1↑systolic, α↑diastolic
*Baroreceptor reflex ↓HR from ↑↑BP
Use: Vasodilatory shock
Toxicity:
Ischemia
Arrhythmia
hypertension
Contraindication: Pre-existing vasoconstriction/ischemia,
late term pregnancy
Dopamine
D>β>α
Low dose D ↓TPR (at splanchnic vessels*)
Medium β1 ↑HR
Higher α ↑BP ↑TPR, vasoconstriction
Use: Hypotension due to low CO secondary to cardiogenic shock
Toxicity:
Low dose-hypotension
High dose-ischemia
Contraindication:
Uncorrected tachyarrhythmia or Ventricular Fibrillation
indirect sympathomimetics
Amphetamine Methamphetamine Methylphenidate Ephedrine Pseudophedrine Thyramine
Amphetamine Methamphetamine Methylphenidate Ephedrine Pseudophedrine Thyramine **A man mainly eats pizza toppings*
reverse reuptake channel- ↑ Ca independent release
Cardio: α vasocronstriction, ↑ diastolic; β ↑HR, contraction, ↑systolic ((May get baro ↓HR) balanced)
CNS: stimulant, anorexia agent
Toxicity: tachycardia
Use: ADD, narcolepsy, nasal congestion
Contraindication:Rx with MAO inhibitor 2wk, HTN
phenylephrine
α1 agonist-turns on α1
↑TPR ↑MAP ↓HR (baro reflex) Pupillary dilation
↓Broncho/sinus secretions
NOT at catecholamine
Use: SV tachycardia, Mydriatic, Nasal decongestant
Toxicity: Hypertension
Contra: Hypertension, Ventricular tachycardia
Clonidine
α2 agonist (recall α2 paired to Gαi- inhibit)
acute: ↑BP=periph, chronic: ↓BP=central
cross BBB, reduces sympathetic stimulation from pre-motor neuron: ↓constriction ↓BP by ↓SNS
periphery= minor vasoconstriction
Use: Hypertension due to SNS drive
Toxicity:
Dry mouth (↓secrete)
Bradycardia
Sedation
WITHDRAWL can be life-threatening hypertensive crisis
Non-selective β blocker
Propranolol
Nadolol
timolol
Propranolol Nadolol timolol ↓HR ↓contractiity ↓renin release (BP) ↓SNS activation ↓aqueous humor (↓β)
Use: Hypertension, angina, glaucoma, early HF, arrhythmia
Contraindication: Bronchospasm=asthma Sinus bradycardia 2nd & 3rd Heart Block Cardiogenic shock
Cardioselective
Atenolol
Metoprolol
Esmolol= Emergent
Atenolol
Metoprolol
Esmolol= Emergent (IV, small t1/2)
↓HR ↓contractiity ↓renin release (BP)
↓SNS activation
Use: Hypertension, angina, arrythmia Hypotension
Toxicity: Bradycardia
Dizzy, depressed, insomnia
Contraindication: Sinus bradycardia
2nd & 3rd Heart Block
Cardiogenic shock
Partial Agonist both B1 and B2
Pindolol
↓BP ↓contractiity ↓renin release (BP)
↓SNS activation
Use: Hypertension when other BB not tolerated
Toxicity: Bradycardia
Dizzy, depressed, insomnia
Contraindication: Sinus bradycardia
2nd & 3rd Heart Block
Cardiogenic shock
Phenoxybenzamine
Irreversible α antagonist-covalently binds
↓BP (block α allows β)
↑chronotrpy/ionotrpy
Use: Hypertension with pheochromocytoma (adrenal tumor),
Vasoconstrictor induced extravasation (iv)
Toxicity:
Prolonged hypotension
Reflex Tachycardia
Nasal congestion
Contraindication:
Coronary artery disease
Phentolamine
Irreversible α antagonist-covalently binds
↓BP (block α allows β)
↑chronotrpy/ionotrpy
Use: Hypertension with pheochromocytoma (adrenal tumor),
Vasoconstrictor induced extravasation (iv)
Toxicity:
Prolonged hypotension
Reflex Tachycardia
Nasal congestion
Contraindication:
Coronary artery disease
Selective α1 antagonist
Prazosin
Doxazosin
Terazosin
Please Don’t Touch
Inhinits vasoconstriction
Relax prostate sm
Use: Hypertension
Benign prostatic hyperplasia (BPH)
Toxicity:
Syncopy
Orthostatic Hypertension
Nicotine
Stimulate Nn in CNS,
Used in smoking cessation
Succinylcholine
Block Nm- nicotinic receptors @nm junction
Use: Blocks depolarization, blocks muscle contraction
Used as muscle relaxant for intubation/CST
Contraindication: FAMILIAL HYPERTHERMIA or skeletal muscle myopathy, recent crush injury
Quaternary Nitrogen Analog
Acetylcholine
Methacholine
Carbachol
Betanechol
Acetylcholine
Binds nicotinic and muscarinic, rapidly hydrolyzed by cholinesterase
No therapeutic use
Methacholine
Bind muscarinic on sm and heart
Hydrolyze more slowly, longer t1/2
Used to Dx bronchial hyperactivity (asthma) Bronchilar constriction
Contraindication: Pt on β-blocker, antidote is β- agonist (dilate bronchiole)
Carbachol
Muscarinic and nicotinic, resistant to acetylcholinesterase
Use: Opthalmo miotic (constrict) to ↓pressure in glaucoma or post Sx
Toxicity: Excessive muscarinic and nicotinic activation, only for topical use
Bethenchol
Muscarinic only, resistant to hydrolysis
GI tract and bladder ↑Nm input (M3)
Less M2 (heart activation)
Use: NON-Obstructive urinary retention (post partum/post-op)
Contraindication: Bradycardia Peptic ulcer, asthma, bradycardia
Naturally occurring tertiary ammines
Muscarine
No therapeutic use, resist hydrolysis
Pilocarpine
Pure muscarinic activity, CROSS BBB, on eye it contracts ciliary muscle & sphincter, flattening iris and allowing drainage of Aq. H.
Use:Dry mouth (radiation and Sjogrens Syn),
Treat glaucoma,
Contraindication: Careful with pt on β-blocker may slow HR (conduction)
Cholinesterases
Acetylcholinesterase- synaptic cleft
Butyrylcholinesterase- plasma
Neostigmine
Reversible cholinesterase inhibitor, skeletal muscle endplate
Tx myasthenia gravis, the loss of Nm receptor Reverse neuromuscular blockade
Toxicity: excess Ach action at peripheral Muscarinic and nicotinic receptors
Contraindication: Intestinal obstruction (M1)
Endophonium
Inhibits cholinesterase reversibly, stimulates nicotinic receptors
(act fast and short)
Improve myasthenia gravis (not enough receptors, need more Ach), OR, worsen cholinergic crisis (too much Ach)
Use: Dx btwn Myasthenia gravis & Cholinergic crisis Toxicity: Bradycardia
Contraindication: Blocked intestinal or urinary tract
Physostigmine
Cross BBB, slow hydrolysis by cholinesterase Use: Counteract delirium
Toxicity: Convulsions,
Contraindications: Asthma, cardiac insufficiency, GI blockage
Donepezil
Treat Alzheimer’s, inhibits cholinesterase in CNS, long t1/2
Organophosphate poisoning
Irreversible inhibitor cholinesterase
Diarrhea Urination Miosis Bradycardia Bronchorrea (secretions & constriction) Emesis Lacrimation Salivation/Sweating Gastrointestinal distress Weakness/paralysis
Bumbbelss SLUDGE
Tx is atropine
Ventilation, suction, 2-PAM
Echothiophate
Organophosphate, long-term miosis in glaucoma (topical)
Use: Glaucoma
Toxicity: Blurred vision, brow ache
Muscarinic Antagonist
Atropine
Scopolamine
Glucopyrrolate
Atropine
Uses: ↓urgency urination ↓GI hypermobility Tx cholinesterase inhibitor poisoning Cause mydriasis/cycloplegia (optho) Reverse bradycardia from vagal origin
Atropine Poisoning: Blind, Mad, Red, Hot, Dry, dilated, loss bowel and bladder tone, ↑HR and ↑BP
Tx toxicity with supportive measure, lower temp, catheter, kept in dark room, sedated
Scopolamine
Sedative effect,
Use: Prepare for anesthesia and ↓secretions,
↓nausea and vomiting from chemo/motion sickness
Contraindication: Narrow angle glaucoma
Glucopyrrolate
Used post-op, anti-muscarinic protects gut
Curare drugs:
-non-depolarizing blocking drugs
Pancuronium Tubocurarine Vecuronium Mivacurium Rocuronium
Pancuronium :75 min
Tubocurarine 100 min- muscarinic block ↑HR↑CO
Vecuronium: 60 min
Mivacurium: 5 min** histamine release ↓BP
Rocuronium: 60 min- muscarinic block ↑HR↑CO
Note duration of action< t1/2
-Receptor Reserve: resp>course>fine>eye
NOT analgesic
Apnea (pt wont breathe)
-Inhaled anesthetic and antibiotics enhance effect
Antidote: cholinesterase inhibitors = neostigmine
Glucopyrrolate relieves effect on GI
Succinylcholine
Depolarizing block, muscle depolarizes then gets stuck Fasciculation’s
- Phase I is depolarized membrane (no antidote)
- Phase II membrane repolarized but insensitive to Ach, Tx with cholinesterase inhibitor to ↑↑Ach
Rapid onset and metabolized in plasma, termination by diffusion away
Flaccid paralysis,
Intubation, ECT Cholinesterase inhibitors augment block (↑Ach↑depolarization)
Note:
non-analgesic, apnea, pt has pain from fascination, (arrhythmia, hypertension, bradycardia)
Hyper K+
Contraindication:
Malignant Hyperthermia and Muscle myopathy, recent trauma
Spasmolytic: skeletal muscle relaxant
Baclofen Tizanidine Dantrolene Benzodiazepines: -diazepam, clonazepam General idea
- decease Ia fibers that excite the motor neuron
- increase activity of inhibitory (GABA) internuncial neurons
net effect is decrease in motor neuron excitement
Tx for ↑sk. muscle tone
- loss of supraspinal control
- increase activation
- increased α/γ motor stretch reflex
Baclofen
GABA receptor agonist
-reduces Ca influx, reduces release excitate nt
*Cross BBB
Note- given orally or intrathecal catheter on spinal cord where needed
Tx: Spinal spasticity, MS Toxicity: Drowsiness
Benzodiazepine
-diazepam, clonazepam
Facilitate GABA inhibition- allosteric on GABA receptor
↑likelihood of GABA binding its receptor, hyperpolarize membrane with Cl- (less likely to have an excitatory AP)
Use: Spinal spasticity, MS Toxicity: Drowsiness, sedation
Tizanidine
α2 agonist (recall Gαi), less likely to have AP
- ↓PKA↓Pi on Ca channel, ↓AP thus opposes excitatory nt release
Use: Spinal spasticity, MS Toxicity: Drowsiness
Hypotension
Dantrolene
Blocks Ca++ release from SR in skeletal muscle, “promotes weakness”
↓Ca↓ strength
Use: Spasticity, Malignant Hyperthermia
Toxicity: Muscle weakness, Sedation
Metyrosine
Competitive inhibition of tyrosine hydroxylase (RL enzyme Tyr→ DOPA) Hypertension
Reserpine
Blocks VMAT, dopamine does not get into vesicle Hypertension
Bretylium
Hyperpolarizes membrane, stops AP and nt release Ventricular Arrhythmia
Cocaine
Inhibits nt reuptake (dopamine, NE, SR) Analgesia in Sx (also a bad decision)
Amphetamine
Ephedrine
Enters cell through monoamine reuptake (NE, Sr, Dopamine),
phosphorylates vesicular transporter & reuptake channel;↑cytosolic nt, and reverses channel ↑↑nt release non-ca dependent
Use: Narcolepsy, ADHD
Naloxone
Naltrexone
Non-protein, cross BBB and block opioid receptor
Used in opioid overdose/dependence
SSRIs
Does not allow SR reuptake from synapse Depression, anxiety
ACE inhibitors, Lisinopril
Hypertension Inhibition of peptide cleavage Angio I to II (keeps it inactive)
MAO inhibitors
MAO digests nt in cytosol from uptake, inhibition will ↑↑cytosolic nt, ↑nt released and may reverse reuptake channel direction allowing non Ca dependent nt release
Release WAY MORE nt
Use: depression
Toxic when taken with tyramine foods (rich, fermented)- competes with NE to get into vesicle
L-DOPA
Precursor loading, ↑dopamine production
Use: Parkinson’s Disease
Carbidopa
“eats up” dopamine in the periphery (does not cross BBB), allowing it to function in the CNS
Use: Parkinson’s Disease
