1st midterm- Lecture material Flashcards
ATC classification stands for
Anatomic
Theraputic
Chemistry
What is the difference btw pharmacodynamics and pharmacokinetics?
Pharmacodynamics- How the drug effects the organ
Pharmacokinetics- How the body effects the drug
4 parts of Pharmacokinetics
Absorbtion
Distribution
Metabolism
Excretion
By alkalizing the urine, which type of drug will be increasingly excreted?
Weak acid
pH up will cause weak acid to go in/out to the CNS?
Out to the plasma
Increased excretion
ATP Binding Casett are for Infflux/Efflux?
Efflux
Solute carrier are for Infflux/Efflux?
Infflux
Which type will have gastric absorbtion?
Weak acid
Weak base
Weak acid
Which type will have Intestinal absorbtion?
Weak acid
Weak base
Weak base
Bioavailability=
Fraction of the drug that reach the systemic circulation
Volume of distribution=
Amount of drug in the body (mL) / Plasma conc. (mg/mL)
Example for a drug with low Volume of distribution
Where can we find it in the body?
Heparin
Plasma
Example for a drug with high Volume of distribution
Where can we find it in the body?
Digoxin
Total volume of the body
Biotransformation
Phase 1 reactions
Oxidation
Reduction
Hydrolysis
Biotransformation
Phase 2 reactions
Conjugation (Acetylation, Methylation, Glucoronidation…)
First order kinetics=
Increased plasma drug conc. -> Increased drug elimination
Zero order kinetics=
Rate of drug metabolism is constant
Rate of elimination becomes independant of drug conc.
In which case do we see this
Increased plasma drug conc. -> Increased drug elimination
First order kinetics
Plasma conc. of a certain drug is 200 mg
t1/2= 1 h
What will be the drug conc. after 1 hour?
100 mg
Clearance=
Volume of plasma cleared of drug per unit of time
Rate of elimination equation=
Clearance X Concentration
Nicotinic receptor MOA
How many Ach are required for activation?
Cation selective Na+ channels
2-5 Ach molecules
AchE mechanism
Ach binds active center
Enzyme cuts ester bond
Enzyme becomes acetylated, Choline leaves
Acetyl group leaves enzyme by spont. hydrolysis
Presynaptic stimulation by which receptors and which substances?
B2, M1, AT-1, PSG
4-Aminopyridine, a-Latroxine
Presynaptic inhibition by which receptors and which substances?
a2, M2, D2
Hemicholinium, Vasemicol, Botulinium
Muscarinic actions in the eye
Contraction of the iris sphincter and ciliary muscles
Reversible cholinesterase inhibitors
Competative
Edrophonium
Donepezil
What makes organophosphate irreversible drug?
Phosphorylation of AchE is irreversible
Phosphate cannot hydrolyze from the enzyme spontaneously
Aging happens after certain time- Final inactivation
Parasympatholytics
Tertiary tropeins
Atropine
Scopolamine
Benztropine
Parasympatholytics
Quaternary atropine
Butyl-Scopolamine Ipratropium Tiotropium (m3 selective) aclidinium (m3 selective) umeclinidium (m3 selective)
Parasympatholytics/antimuscurinic (non-selective tertiary) and( selective tertiary )
- non-selective teriary :
- Atropine
- Cyclopentolate
- scopolamine
- Procyclidine
- Oxybutinine
- modest selectivity for M3 selective tertiary
- Tolterodine
- Solifenacine
Centrally acting muscle relaxants
Drugs for spasticity only
Baclofen- GABA-B agonist
Centrally acting muscle relaxants
Drugs for both acute and chronic spasms
Diazepam
Tizanidine
Tolperisone
Carisoprodol
What is the nerutransmitter of the peripheral NS?
Ach
Nicotinic Ach-R two main types
Nn- Neuraonal (a,B subunits) - many varieties
Nm- Muscular ( (a1)2 Beta1. delta, epsilon) fixed, unique
What will happen when we give centrally acting muscle relaxants?
Decrease the tone of the skeletal muscles
What will happen when we give peripheral acting muscle relaxants?
Paralyze the skeletal muscles- total relaxation
Peripheral acting muscle relaxants
Postsynaptic acting
3 types
Curare derivatives
Depolarizing muscle relaxants
Ryanodine antagonists
Curare derivatives MOA
Competative antagonists at skeletal m Ach-R nicotinic receptor
Curare derivatives examples
D-tubocurarine
Doxacurium
Pancuronium
Vecuronium
Treatment of malignant hyperthermia
Dentrolene
yooo the dentis is not rolling
Epi activates which R?
All adrenergic
NE activates which R?
a, B1
Little effect on B2
Epi effects on MAP
Not changed dramatically
Isoprenaline Receptor preferance
B1=B2
Effect of Dopamine on renal D1-R
Vasodilation
Increased renal blood flow
Why is a-R agonist a good treatment for rhinitis?
Give a drug example
Local vasoconstriction
Oxymetalzoline
Phenylephrine
What a agonist is given in case of Glaucome?
Which a-R?
Brimonidine
a2
Where can we find Tyramine?
Cheese
Chicken liver
Red wine
Tyramine is metabolyzed by
MAO-A
Tyramine is an example of
Indirect acting sympathomymetics
Release NE from the nerve terminal
Amphetamine sructually related drug that is used to treat ADHD
Methylphenidate
Action of B blockers on the aqueous humor
Decreases
Non selective B Blockers
Propronalol
Timolol
Pindolol
Sotalol
Pls Tell People Sorry
B1 selective B blockers
Metoprolol
Atenolol
Esmolol
Nebivolol
B blocker+a1 blocker
Labetalol
Carvedilol
B blockers with intrinsic sympathomimetic activity
Pindolol
Acebutalol
B blocker with the highest lipid solubility
Propranolol
Nebivolol
B blocker with the lowest lipid solubility
Atenolol
Sotalol
Acebutalol
B blocker with NO mediated vasodilation
Nebivolol
What is the advantage of selective a1 blockers?
Less tachycardia
Non selective a blockers
Phentolamine
Phenoxybenzamine
Phenoxybenzamine indication
Pheochromocytoma
Ergotamine indication
Postpartum heorrhage
Migrane
a2-R agonists
Clonidine Guanfacine Moxonidine Methyl-dopa rilminidine Tizanidine brimonidine
Methytyrosine MOA
Blocks the NE synthesis
Local anasthetics effect
Reversible inhibition of neuronal activity by blocking the VDNC
No action potential formation
