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Pharm exam 1 > Test 1 > Flashcards

Test 1 Flashcards

1
Q

What are receptors?

A

The component of a cell or organism that interacts with a drug and initiates the chain of events leading to the drug’s observed effects. Most receptors for clinically relevant drugs are proteins

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2
Q

Covalent bonds

A

Very strong bonds, in many cases, not reversible under biologic conditions.

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3
Q

Electrostatic bonds

A

Weaker than covalent bonds; tend to be much more common than the covalent bonding in drug-receptor interactions.

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4
Q

Receptors are responsible for ____

A

selectivity of drug action.

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5
Q

What size molecules diffuse more readily between compartments of the body?

A

Smaller molecules, less than 1,000 Da.

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6
Q

Lock & Key Phenomenon

A

Drug’s shape is complementary to that of the receptor site

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7
Q

Changes in a drug’s _________ can dramatically increase or decrease the molecule’s affinities for different receptors, altering its therapeutic and toxic effects

A

Chemical structure

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8
Q

What is chirality?

A

It is not super imposable to its mirror image

-Have the same physical & chemical properties like identical melting points

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9
Q

What kind of molecules cross biological barriers by passive diffusion?

A

Uncharged molecules.

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10
Q

What is a weak acid?

A

A neutral molecule that can reversibly dissociate into an anion (neg. charged molecule) and a proton (a hydrogen ion)

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11
Q

what is a weak base?

A

A neutral molecule that can form a cation by combining with a proton

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12
Q

What is pKa

A

The dissociation constant that governs the extent of dissociation when the substance is placed in solution
-an important determinant of how much drug is present in various body fluids.

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13
Q

What is a ligand?

A

A molecule that binds to a specific site on a protein or other larger molecules.

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14
Q

At least 2 functional domains within the receptor:

A
  • A ligand binding domain

- An effector domain

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15
Q

Receptors are:

A 
Regulatory proteins (mainly)
-enzymes, transport proteins, structural proteins, secreted glycoproteins, DNA
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16
Q

Receptors have at least 2 major functions:

A
  • Ligand binding

- Message propagation

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17
Q

Indirect effect-

A

Inhibition of metabolism of endogenous activator –> increased activator action on an effector molecule–> increased effect.

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18
Q

How many types of drug receptors are there??

A

five

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19
Q

Transmembrane receptor:

A

Regulates intracellular enzyme activity

-Binds & stimulates an intracellular protein kinase

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20
Q

Intracellular Receptors

A

Lipid soluble drugs can cross the cell membrane layer & attach to intracellular receptors
-receptor inside the nucleus

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21
Q

Glucocorticoid receptor

A

Glucocorticoid binding to its receptor relieves an inhibitory constraint on the transcription-stimulating activity of the protein.
-In the absence of hormone, the receptor is bound to hsp90, a protein that prevents normal folding into the active conformation of the receptor.

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22
Q

Nuclear hormone receptor-

A

Agonist and co-activator bind, the co-repressor is released and a conformational change occurs and gene transcription is stimulated. If corepressors are bound, activation does not occur.

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23
Q

How fast do gene-active hormones work?

A

lag period of 30 min-several hours.

-this is why you get a longer effect.

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24
Q

Ligand-Gated Ion Channels

A

Some drug mimic or block actions of endogenous ligands (e.g. acetylcholine, serotonin, GABA, glutamate) that regulate flow of ions through plasma membrane channels.
Receptor binding causes opening or closing of a channel to regulate the entrance or exit of a specific ion (e.g. Cl-) –
Receptor transmits signal across the plasma membrane by increasing transmembrane conductance of the relevant ion, thus altering the electrical potential across the membrane

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25
Q

Consequence of gated receptors:

A

Rapid onset and offset of effect
The time elapsed between ligand binding to a ligand-gated receptor and the cellular response can often be measured in milliseconds.

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26
Q

Transmembrane Receptors

A

Drug binds to receptor, triggering enzyme reactions – usually a 2nd messenger system (e.g., cAMP) or protein kinases – that result in a change in cell function.

ex- epinephrine, norepinephrine, insulin

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27
Q

Receptor tyrosine kinases (RTKs)

A

A family of (transmembrane) receptors
The active form of an RTK is phosphorylated at a tyrosine site.
Important cancer biomarkers; often important in certain types of human cancer

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28
Q

G-Protein Coupled Receptor (GPCR)

A
  • Largest receptor family - Humans express over 800 GPCRs

- Specialized regulatory protein that binds guanosine triphosphate (GTP) and guanosine diphosphate (GDP)

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29
Q

GPCRS Regulate-

A

Sensory perception

  • nerve activity
  • tension of smooth muscle
  • metabolism, rate and force of cardiac contraction
  • secretion of most glands
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30
Q

GPCRS Receptor activators:

A
  • Adrenergic amines
  • Serotonin
  • Acetylcholine
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31
Q

Drugs Acting at GPCRs

A
  • Drug binds to receptor that is coupled to an intracellular G-protein
  • Triggering G-protein activity results in activation or inhibition of 2nd messengers or the opening of channels
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32
Q

Agonist

A

Binding mimics effects of endogenous ligands

-some agonists work by inhibiting the mechanism responsible for terminating the action of the endogenous ligand

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33
Q

Primary agonist

A

A drug that binds to the same recognition site as the endogenous ligand

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34
Q

Allosteric agonist

A

A drug that binds to a different region on the receptor

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35
Q

Antagonist

A

Devoid of intrinsic receptor activity

  • Receptor binding prevents agonist binding, thus preventing the action of agonists and natural ligands
  • lose receptor function
36
Q

Partial agonists

A

Bind & activate a given receptor, but have only partial efficacy at the receptor compared to a full agonist, regardless of the concentration employed; they do not evoke as great a response as full agonists.
-can display both agonist & antagonist effects, depending on the presence of another agonist.

37
Q

Inverse agonists

A

binds to the same receptor binding-site as an agonist, but reduces constitutive activity of receptors, exerting the opposite pharmacological effect of a receptor agonist.

38
Q

Constitutive activity

A

Receptors are active even if nothing is bound to it.

39
Q

A receptor exists exactly 2 conformational states:

A
  • Active

- Inactive

40
Q

Agonists prefer to bind to ____

A

active receptors

41
Q

which way does an antagonist shift the equilibrium?

A
  • it does not shift the balance

- as long as its sitting there, the agonist can’t bind.

42
Q

A drug’s action is affected by:

A
  • The quantity of drug that reaches the receptor (pharmacokinetics)
  • The degree of attraction (affinity) between the drug and its receptor
43
Q

Affinity

A

The degree of attraction between the drug and its receptor

44
Q

Intrinsic efficacy

A

Once bound to their receptor, drugs vary in their ability to produce and effect.

45
Q

Both the affinity of a drug for its receptor and its intrinsic efficacy are determined by its __________

A

Chemical structure

46
Q

What kind of intrinsic efficacy does antagonists have?

A

-Doesn’t have much intrinsic efficacy because it doesn’t have an effect when bound to the receptor.

47
Q

What kind of intrinsic activity & affinity do agonists have?

A

Great affinity and intrinsic activity to bind effectively to their receptors and be capable of producing an effect.

48
Q

What are drug effects not produced through receptor interactions?

A
  • colligative effects
  • chemical interactions
  • Structural analogs of endogenous chemicals
49
Q

Colligative effect

A

An effect that depends on the number of solute particles dissolved in a given amount of solvent, not on the chemical natures of the solute or solvent.
ex- osmosis
-works simply because drug molecule is present

50
Q

neutralization

A

The reaction of an acid and a base to produce a salt and water

51
Q

Chelation

A

A method of removing heavy metals from the blood stream.

  • Chelating agent binds to the metal ion.
  • can be used for things like poisoning
52
Q

What is a structural analog

A

A compound having a structure similar to that of another one, but different from it in respect of a certain component.

  • Body cannot tell the difference
  • body will try and use it, but it won’t work
53
Q

Receptor occupancy theory

A

-How many receptors are actually bound by the drug at a particular time, the more receptors you bind, the more response you should get.

54
Q

The graded dose response

A

A little bit of a drug gives a little response, a lot of drug gives a large response.

55
Q

Potency

A
  • The concentration (EC50) or dose (ED50) of a drug required to produce 50% of that drug’s maximal effect.
56
Q

Allosteric Activator

A

Protein or enzyme that binds to its substrate/target, modulates the shape of it and positively influences its activity (or the activity of an agonist)

57
Q

Pharmacodynamic

A

Occur at the receptor

  • competitive binding interactions
  • Noncompetitive binding interactions
58
Q

Pharmacokinetic

A

result from one drug’s effects on the pharmacokinetics of another

59
Q

Pharmacologic

A

result from by drugs acting through different mechanisms

60
Q

Quantal dose response relationships

A
  • The all or none response
  • Threshold dose- the smallest dose that elicits a quantal response
  • ex- sleeping medication
61
Q

What determines how a drug affects you and how you respond?

A

Genetic variability

62
Q

Therapeutic index

A

LD50/ED50

  • you want dose to be high
  • ex of low therapeutic index- anesthesia
63
Q

Standard Safety Margin

A

LD1/ED99

  • ED99- effective dose in 1% of subjects
  • LD1- lethal dose in 99% of subjects
64
Q

Receptors are subject to many regulatory & homeostatic controls:

A
  • Regulation of receptor synthesis
  • Regulation of receptor degradation
  • receptor covalent modification
  • relocalization within the cell
65
Q

Receptor desensitization

A

Adaption, down-regulation

-continued or subsequent exposure to the same concentration of drug results in diminished response.

66
Q

Tachyphylaxis

A

Rapidly diminishing response to successive doses of a drug, rendering it less effective.

67
Q

Receptor down-regulation

A

A reduction of a cell’s response due to internalization and degrading of receptors

68
Q

Intrauterine

A

Conception to birth

69
Q

Neonate

A

Brith to 1 month

70
Q

premature neonate

A

Gestational age

71
Q

Full term neonate

A

Gestational age >37 weeks, post-natal age

72
Q

Infant

A

1 month to 2 years

73
Q

child

A

2 years to the onset of puberty

74
Q

Adolescent

A

Onset of puberty to adulthood

75
Q

Changes in GI absorption after birth

A
  • In full term infant, gastric pH ranges from 6-8 at birth, then declines to 1-3 within 24 hours
  • pH gradually returns to neutral agin by day 8
  • reaches adult values after 2 years
  • differences in the bioavailability of drugs in premature infants are poorly understood due to the lack of data
76
Q

77% higher busulifan glutathione conjugation rate in children aged 1-3 years compared to older children (9-17) leads to:

A

Leads to an enhanced first-pass intestinal metabolism and a reduced bioavailability

77
Q

L-amino acid transporter system

A

is immature in children and due to that, the oral clearance of drugs is higher, resulting in lower bioavailability

78
Q

P-gp expression in human intestinal tissue…

A

is relatively low levels in neonates

79
Q

Pgp pump

A

Drug gets absorbed, pop pump grabs it before going into circulation, and then pushes it back into the intestines …prevents things from getting absorbed.

  • Less pgp increases drug absorption
  • pgp does not affect all drugs
80
Q

Peds: Gastric Emptying and Intestinal Mobility

A
  • Gastric emptying time in neonates is prolonged relative to that of the adult
  • intestinal motility is irregular in neonates
81
Q

Where is the determinant of the rate of drug absorption from?

A

The small intestine

82
Q

Gastric Emptying & Intestinal Motility:clinical complications

A
  • Rate of drug absorption is slower in neonates, young infants
  • Delayed gastric emptying may partially account for delayed absorption for orally administered drugs
  • Time required to achieve Cmax may be prolonged
  • Overall bioavailability may be altered
  • drugs with limited absorption in adults may be absorbed efficiently in neonates because of prolonged contract time with GI mucosa
83
Q

Cmax

A

Peak concentration

84
Q

Intramuscular absorption may be altered in premature infants due to differences in:

A
  • Relative muscle mass
  • Poor perfusion to various muscles
  • Peripheral vasomotor instability
  • Insufficient muscular contractions compared to older children nd adults
  • intramuscular dosing is rarely used in neonates except in emergencies or when an intravenous site is inaccessible.
85
Q

Integumentary system in babies

A
  • Thickness in pre term babies is a lot thinner
  • Hydration of skin is reduced overtime in age
  • Body surface area:weight slow declines with age
86
Q

How would you expect the apparent Vd of water soluble drugs?

A

volume of distribution is lower later in life

87
Q

How would you expect the apparent Vd of lipid soluble drugs

A

volume of distribution is higher later in life, because there is less fat.

Pharm exam 1 (1 decks)

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