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phrm > 1st midterm- Lecture material > Flashcards

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
Q

Presynaptic inhibition by which receptors and which substances?

A

a2, M2, D2

Hemicholinium, Vasemicol, Botulinium

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26
Q

Muscarinic actions in the eye

A

Contraction of the iris sphincter and ciliary muscles

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27
Q

Reversible cholinesterase inhibitors

Competative

A

Edrophonium

Donepezil

28
Q

What makes organophosphate irreversible drug?

A

Phosphorylation of AchE is irreversible
Phosphate cannot hydrolyze from the enzyme spontaneously
Aging happens after certain time- Final inactivation

29
Q

Parasympatholytics

Tertiary tropeins

A

Atropine
Scopolamine
Benztropine

30
Q

Parasympatholytics

Quaternary atropine

A

Butyl-Scopolamine
Ipratropium
Tiotropium

31
Q

Parasympatholytics

Tertiary N

A 
Procyclidine
Cyclopentolate
Oxybutinine
Tolterodine
Solifenacine
32
Q

Centrally acting muscle relaxants

Drugs for spasticity only

A

Baclofen- GABA-B agonist

33
Q

Centrally acting muscle relaxants

Drugs for both acute and chronic spasms

A

Diazepam
Tizanidine
Tolperisone
Carisoprodol

34
Q

What is the nerutransmitter of the peripheral NS?

A

Ach

35
Q

Nicotinic Ach-R two main types

A

Nn- Neuraonal (a,B subunits)

Nm- Muscular (a2Bgd)

36
Q

What will happen when we give centrally acting muscle relaxants?

A

Decrease the tone of the skeletal muscles

37
Q

What will happen when we give peripheral acting muscle relaxants?

A

Paralyze the skeletal muscles- total relaxation

38
Q

Peripheral acting muscle relaxants
Postsynaptic acting
3 types

A

Curare derivatives
Depolarizing muscle relaxants
Ryanodine antagonists

39
Q

Curare derivatives MOA

A

Competative antagonists of the Nm Ach-R

40
Q

Curare derivatives examples

A

D-tubocurarine
Doxacurium
Pancuronium
Vecuronium

41
Q

Treatment of malignant hyperthermia

A

Dentrolene

yooo the dentis is not rolling

42
Q

Epi activates which R?

A

All adrenergic

43
Q

NE activates which R?

A

a, B1

Little effect on B2

44
Q

Epi effects on MAP

A

Not changed dramatically

45
Q

Isoprenaline Receptor preferance

A

B1=B2

46
Q

Effect of Dopamine on renal D1-R

A

Vasodilation

Increased renal blood flow

47
Q

Why is a-R agonist a good treatment for rhinitis?

Give a drug example

A

Local vasoconstriction
Oxymetalzoline
Phenylephrine

48
Q

What a agonist is given in case of Glaucome?

Which a-R?

A

Brimonidine

a2

49
Q

Where can we find Tyramine?

A

Cheese
Chicken liver
Red wine

50
Q

Tyramine is metabolyzed by

A

MAO-A

51
Q

Tyramine is an example of

A

Indirect acting sympathomymetics

Release NE from the nerve terminal

52
Q

Amphetamine sructually related drug that is used to treat ADHD

A

Methylphenidate

53
Q

Action of B blockers on the aqueous humor

A

Decreases

54
Q

Non selective B Blockers

A

Propronalol
Timolol
Pindolol
Sotalol

Pls Tell People Sorry

55
Q

B1 selective B blockers

A

Metoprolol
Atenolol
Esmolol
Nebivolol

56
Q

B blocker+a1 blocker

A

Labetalol

Carvedilol

57
Q

B blockers with intrinsic sympathomimetic activity

A

Pindolol

Acebutalol

58
Q

B blocker with the highest lipid solubility

A

Propranolol

Nebivolol

59
Q

B blocker with the lowest lipid solubility

A

Atenolol
Sotalol
Acebutalol

60
Q

B blocker with NO mediated vasodilation

A

Nebivolol

61
Q

What is the advantage of selective a1 blockers?

A

Less tachycardia

62
Q

Non selective a blockers

A

Phentolamine

Phenoxybenzamine

63
Q

Phenoxybenzamine indication

A

Pheochromocytoma

64
Q

Ergotamine indication

A

Postpartum heorrhage

Migrane

65
Q

a2-R agonists

A 
Clonidine
Guanfacine
Moxonidine
Methyl-dopa
Tizanidine
66
Q

Methytyrosine MOA

A

Blocks the NE synthesis

67
Q

Local anasthetics effect

A

Reversible inhibition of neuronal activity by blocking the VDNC
No action potential formation

phrm (11 decks)

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