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1st midterm- Lecture material Flashcards

1
Q

ATC classification stands for

A

Anatomic
Theraputic
Chemistry

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2
Q

What is the difference btw pharmacodynamics and pharmacokinetics?

A

Pharmacodynamics- How the drug effects the organ

Pharmacokinetics- How the body effects the drug

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3
Q

4 parts of Pharmacokinetics

A

Absorbtion
Distribution
Metabolism
Excretion

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4
Q

By alkalizing the urine, which type of drug will be increasingly excreted?

A

Weak acid

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5
Q

pH up will cause weak acid to go in/out to the CNS?

A

Out to the plasma

Increased excretion

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6
Q

ATP Binding Casett are for Infflux/Efflux?

A

Efflux

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7
Q

Solute carrier are for Infflux/Efflux?

A

Infflux

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8
Q

Which type will have gastric absorbtion?

Weak acid
Weak base

A

Weak acid

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9
Q

Which type will have Intestinal absorbtion?

Weak acid
Weak base

A

Weak base

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10
Q

Bioavailability=

A

Fraction of the drug that reach the systemic circulation

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11
Q

Volume of distribution=

A

Amount of drug in the body (mL) / Plasma conc. (mg/mL)

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12
Q

Example for a drug with low Volume of distribution

Where can we find it in the body?

A

Heparin

Plasma

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13
Q

Example for a drug with high Volume of distribution

Where can we find it in the body?

A

Digoxin

Total volume of the body

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14
Q

Biotransformation

Phase 1 reactions

A

Oxidation
Reduction
Hydrolysis

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15
Q

Biotransformation

Phase 2 reactions

A

Conjugation (Acetylation, Methylation, Glucoronidation…)

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16
Q

First order kinetics=

A

Increased plasma drug conc. -> Increased drug elimination

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17
Q

Zero order kinetics=

A

Rate of drug metabolism is constant

Rate of elimination becomes independant of drug conc.

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18
Q

In which case do we see this

Increased plasma drug conc. -> Increased drug elimination

A

First order kinetics

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19
Q

Plasma conc. of a certain drug is 200 mg
t1/2= 1 h
What will be the drug conc. after 1 hour?

A

100 mg

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20
Q

Clearance=

A

Volume of plasma cleared of drug per unit of time

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21
Q

Rate of elimination equation=

A

Clearance X Concentration

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22
Q

Nicotinic receptor MOA

How many Ach are required for activation?

A

Cation selective Na+ channels

2-5 Ach molecules

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23
Q

AchE mechanism

A

Ach binds active center
Enzyme cuts ester bond
Enzyme becomes acetylated, Choline leaves
Acetyl group leaves enzyme by spont. hydrolysis

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24
Q

Presynaptic stimulation by which receptors and which substances?

A

B2, M1, AT-1, PSG

4-Aminopyridine, a-Latroxine

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25
Presynaptic inhibition by which receptors and which substances?
a2, M2, D2 | Hemicholinium, Vasemicol, Botulinium
26
Muscarinic actions in the eye
Contraction of the iris sphincter and ciliary muscles
27
Reversible cholinesterase inhibitors | Competative
Edrophonium | Donepezil
28
What makes organophosphate irreversible drug?
Phosphorylation of AchE is irreversible Phosphate cannot hydrolyze from the enzyme spontaneously Aging happens after certain time- Final inactivation
29
Parasympatholytics | Tertiary tropeins
Atropine Scopolamine Benztropine
30
Parasympatholytics | Quaternary atropine
Butyl-Scopolamine Ipratropium Tiotropium
31
Parasympatholytics | Tertiary N
``` Procyclidine Cyclopentolate Oxybutinine Tolterodine Solifenacine ```
32
Centrally acting muscle relaxants | Drugs for spasticity only
Baclofen- GABA-B agonist
33
Centrally acting muscle relaxants | Drugs for both acute and chronic spasms
Diazepam Tizanidine Tolperisone Carisoprodol
34
What is the nerutransmitter of the peripheral NS?
Ach
35
Nicotinic Ach-R two main types
Nn- Neuraonal (a,B subunits) | Nm- Muscular (a2Bgd)
36
What will happen when we give centrally acting muscle relaxants?
Decrease the tone of the skeletal muscles
37
What will happen when we give peripheral acting muscle relaxants?
Paralyze the skeletal muscles- total relaxation
38
Peripheral acting muscle relaxants Postsynaptic acting 3 types
Curare derivatives Depolarizing muscle relaxants Ryanodine antagonists
39
Curare derivatives MOA
Competative antagonists of the Nm Ach-R
40
Curare derivatives examples
D-tubocurarine Doxacurium Pancuronium Vecuronium
41
Treatment of malignant hyperthermia
Dentrolene yooo the dentis is not rolling
42
Epi activates which R?
All adrenergic
43
NE activates which R?
a, B1 | Little effect on B2
44
Epi effects on MAP
Not changed dramatically
45
Isoprenaline Receptor preferance
B1=B2
46
Effect of Dopamine on renal D1-R
Vasodilation | Increased renal blood flow
47
Why is a-R agonist a good treatment for rhinitis? | Give a drug example
Local vasoconstriction Oxymetalzoline Phenylephrine
48
What a agonist is given in case of Glaucome? | Which a-R?
Brimonidine | a2
49
Where can we find Tyramine?
Cheese Chicken liver Red wine
50
Tyramine is metabolyzed by
MAO-A
51
Tyramine is an example of
Indirect acting sympathomymetics | Release NE from the nerve terminal
52
Amphetamine sructually related drug that is used to treat ADHD
Methylphenidate
53
Action of B blockers on the aqueous humor
Decreases
54
Non selective B Blockers
Propronalol Timolol Pindolol Sotalol Pls Tell People Sorry
55
B1 selective B blockers
Metoprolol Atenolol Esmolol Nebivolol
56
B blocker+a1 blocker
Labetalol | Carvedilol
57
B blockers with intrinsic sympathomimetic activity
Pindolol | Acebutalol
58
B blocker with the highest lipid solubility
Propranolol | Nebivolol
59
B blocker with the lowest lipid solubility
Atenolol Sotalol Acebutalol
60
B blocker with NO mediated vasodilation
Nebivolol
61
What is the advantage of selective a1 blockers?
Less tachycardia
62
Non selective a blockers
Phentolamine | Phenoxybenzamine
63
Phenoxybenzamine indication
Pheochromocytoma
64
Ergotamine indication
Postpartum heorrhage | Migrane
65
a2-R agonists
``` Clonidine Guanfacine Moxonidine Methyl-dopa Tizanidine ```
66
Methytyrosine MOA
Blocks the NE synthesis
67
Local anasthetics effect
Reversible inhibition of neuronal activity by blocking the VDNC No action potential formation

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