For midterm- PD&PK Flashcards

1
Q

Racemic mixture

A

50:50 mixture of both enantiomers

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2
Q

True or false: Local anesthetics bind to voltage activated (gated) sodium (Na+) channels to shorten the refractory period

A

False

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3
Q

Which form of transfer of drugs across membranes dominates for most drugs
A. Active transport
B.Paracellular transport
C. Facilitated transport
D.Passive diffusion

A

Passive diffusion

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4
Q

Decreased clearance of a drug could ______ the elimination half life

A
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5
Q

Decreased distribution of a drug could _____ the elimination half life

A

decrease

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6
Q

Secondary structure results from

A

Protein a.a interacting with other nearby a.a’s on same protein

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7
Q

Tertiary structure results from

A

Interaction of more distant a.a’s along a.a

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8
Q

Quaternary structure

A

Multiple polypeptides interact

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9
Q

Order of bond strength

A

Covalent > ionic > hydrogen > van der waals

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10
Q

Enantiomers

A

S: left handed
R: right randed
(based on organization around chiral centre)

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11
Q

Racemic mixture

A

50:50 mix of both enantiomers

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12
Q

Ranitidine: what is it and what is interesting about it

A

H2 (histamine receptor) antagonist or blocker
* Reduce Hcl production
* Limited effects in body due to restriction of H2 receptors in the
stomach

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13
Q

Nicotinic acetylcholine receptor: what type of channel, how does it open and where is it found?

A

Ligand-gated channel

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14
Q

Most important receptor type for drugs

A

Proteins

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15
Q

Ion channels have key role in

A

-neurotransmission
-sm. & sk. muscle contraction
-cardiac contraction
-secretion

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16
Q

Excitatory NTs

A

ACh or glutamate

17
Q

Inhibitory NTs

A

Glycine or GABA

18
Q

What binds to channel to prolong refractory period

A

Local anesthetics

19
Q

G-protein activated by

A

NTs, eicosanoids, peptides, opioids

20
Q

G-proteins work where

A

Over 50% - sensory perception

Remainder - nerve regulation, sm muscle tension, force/rate of cardiac contraction, secretion

21
Q

Major role of G proteins

A

Activate effector molecules, produce second messengers

22
Q

Hormones of a tyrosine-kinase associated receptor

A

Growth hormone, prolactin

23
Q

Nuclear hormone receptor (intracell.)

A

Circulating steroid hormone (lipophilic) –> diffuse thru PM –> bind TF –> modify nuclear events

24
Q

NO affect on cGMP

A

NO binds N-term coluble cGMP –> enhance cGMP amp

25
Q

2 major types of D-R relationships

A

Graded: D-R of an individual
Quantal: D-R of a population of individuals

26
Q

Fraction of all available receptors that are ligand bound

A

[LR]/Ro

27
Q

Affinity of a drug is most influenced by changes in the _______ rate

A

Off

28
Q

Efficacy (Emax)

A

Maximal response produced by the drug at that receptor

29
Q

Potency (EC50)

A

Drug concentration which elicits 50% of the maximal response
(Emax); function of affinity and efficacy

30
Q

Therapeutic index (TD50/ED50)

A

Estimate of relative safety margin of drug

31
Q

More potent drugs have a ______ affinity (______ Kd ) for their receptors

A

Greater affinity, lower Kd

32
Q

More efficacious drugs (larger Emax ) usually cause a _________ proportion of their receptors to be activated

A

Greater

33
Q

Partial agonist

A

Not able to achieve the same maximal response at a given receptor compared to a full agonist; even with increasing [agonist] BUT MAY SHOW GREATER POTENCY

34
Q

Types of receptor agonists

A

Reversible (competitive)
Irreversible (non-competitive)

35
Q

Nonreceptor antagonists

A

Chemical antagonist
Physiologic antagonist

36
Q

Increase in Kd does what to potency

A

Decrease

37
Q

What do noncompetitive antagonists do

A

Depress the maximal response or efficacy (Emax ), can also decrease potency

38
Q
A