Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FTCM > L5, L7- Pharmacodynamics > Flashcards

L5, L7- Pharmacodynamics Flashcards

1
Q

(T/F) drugs can stimulate, inhibit, and add cellular functions

A

F- drugs cannot add functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

list the 7 major drug targets

A
  • ion channels
  • G-protein-linked receptors
  • enzyme-linked receptors
  • nuclear receptors
  • enzymes
  • transporters
  • structural proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

list the types of ion channels

A
  • voltage gated: regulated by change in membrane potential

- ligand gated- extracellular or intracellular mediator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

local anesthetics act by…

A
  • inhibiting V-gated Na channels on peripheral neurons that transmit pain to CNS => prevention of APs and pain perception
  • lipophilic, crosses plasma membrane and binds to intracellular side
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

GABA(a) receptors function as a (1) and is made up of the following subunits: (2). GABA binds to (3) subunit to stimulate receptor and benzodiazepines bind (4) subunit to (stimulate/inhibit) receptor function.

A 
1- Cl- channel (neuron inhibitor via hyperpolarization)
2- 2α, 2β, 1γ subunits
3- between α-β units
4- between α-γ units
5- stimulates (=> neuron inhibition)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

about 60% of prescription drugs act by binding _____

A

G-protein-linked receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

albuterol is a (1)-(agonist/antagonist) used for (3)

A

1/2- β2-agonist

3- asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

propanolol is a (1)-(agonist/antagonist) used for (3)

A

1/2- β-antagonist

3- HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

bethanechol is a (1)-(agonist/antagonist) used for (3)

A

1/2- muscarinic agonist

3- atonic bladder (to contract its SM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ipratropium is a (1)-(agonist/antagonist) used for (3)

A

1/2- muscarinic antagonist

3- asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe the make-up of G-protein and its general mechanism

A
  • α, β, γ subunits bound to receptor and membrane
  • α subunit is largest and binds GDP and hydrolyzes GTP

1) receptor activated, GDP is replaced by GTP
2) α subunit breaks off and binds effector
3) GTP hydrolyzed to GDP
4) α subunit returns to β, γ subunits on receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

list the 3 signals of the three G proteins

A
  • Gs: inc adenylyl cyclase => inc cAMP
  • Gi: dec adenylyl cyclase => dec cAMP
  • Gq: inc phospholipase C => IP3 and Ca2+ (+ DAG)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

define qiq qiss acronym

A

Muscarinic Receptors (qiq): M1-Gq, M2-Gi, M3-Gq

Adrenergic Receptors (qiss): α1-Gq, α2-Gi, β1-Gs, β2-Gs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

list some of the Ca2+ mediated response (hint- 5)

A

(usually via Gq)

  • SM contraction
  • inc force of cardiac muscle contraction
  • exocrine gland secretion
  • NT release from neurons
  • hormone release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

list the types of enzyme-linked receptors

A
  • ligand-regulated transmembrane enzymes

- cytokine receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe make-up of ligand-regulated transmembrane enzymes

A
  • polypeptides
  • extracellular hormone binding domain
  • cytoplasmic enzyme domain: tyrosine kinase (largest group), serine/threonine kinase, guanylyl cyclase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

list some classes of tyrosine kinase receptors

A

(most promote growth)

  • insulin receptor
  • epidermal GFR
  • platelet-derived GFR
  • nerve GFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe signalling of tyrosine kinase receptors

A
  • 2 ligands bind 2 receptors => dimerization and phosphorylate each other’s Tyr (2 each)
  • intracellular signalling proteins bind to phosphorylated Tyr
  • signalling cascade activated
  • regulation of transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

tyrosine kinase receptors play an important role in (1)

(2) mutations can lead to cancer

A

1- cell growth and differentiation

2- gain of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

the first tyrosine kinase inhibitor is (1) and functions to (2)

A

imatinib- for leukemia (discovered in 2001)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

list some of the types of cytokine receptors

A

(mostly peptides)

  • growth hormone
  • prolactin
  • EPO
  • interferons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

cytokine receptors lack (1) and therefore require (2)

A

1- intrinsic enzymatic activity

2- intracellular tyrosine kinase or Janus-kinase (JAK) family

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

describe signalling of cytokine kinase receptors

A
  • 2 ligands bind 2 receptors => dimerization and JAKs phosphorylate each other and the receptors (1 each, 4 total)
  • STATs bind to receptor and JAKs phosphorylated them
  • STATs dimerize, migrate to nucleus –> regulate transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

nuclear receptors are (1) and can bind (2) and (3)- they regulate gene expression usually involved in (4) and (5)

A 
1- ligand-activated transcription factors
2- ligands
3- DNA
4- metabolism
5- development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

list the type of nuclear receptor families

A
  • steroid hormones
  • thyroid hormone
  • vitD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

most enzyme binding drugs are (activators/inhibitors)

A

inhibitors

27
Q

describe mechanism of statins

A
  • competitive inhibitor for HMG-CoA reductase to stop cholesterol biosynthesis –> diminish intracellular cholesterol
  • upregulation of LDL receptors in hepatocytes => inc clearance of LDL from blood
28
Q

(1) drugs bind tubulin to prevent its polymerization into (2). As a result cells are usually in (3) state. (1) are effective drugs for (4).

A

1- vinca alkaloids
2- microtubules
3- arrested in metaphase (centrioles and mitotic spindles can’t pull chromosomes apart)
4- anticancer drugs

29
Q

antacid mechanism

A

neutralize gastric acid

30
Q

(1) binds (2) in the bladder [(2) is a metabolite of the anticancer drug cyclophosphamide] to prevent (3)

A

1- Mesna
2- acroleine
3- hemorrhagic cystitis

31
Q

mannitol mechanism

A
  • inc osmolarity of various bodily fluids

- promote diuresis or reduction of cerebral edema

32
Q

____ is used in hypercholesterolemia treatment to bind bile acids and prevent their reabsorption

A

cholestyramine, colestipol, colesevelam

33
Q

dimercaprol mechanism

A

cheleates heavy metal (mops them up for urinary excretion)

34
Q

what are structural analogs of pyrimidines and purines used for

A
  • incorporated in nucleic acids to alter their function

- used in cancer and antiviral chemotherapy

35
Q

define the two types of dose-response curve

A
  • Graded: effect (y-axis) v dose (x-axis)

- Quantal: % people where drug prevents event (y-axis) v dose (x-axis)

36
Q

(T/F) the effectiveness of a drug curve and the binding to receptor curve are always correlated and equal

A

F- due to signal amplification and spare receptors, maximum effectiveness (Emax) can be reached before 100% receptors are bound to drug (Bmax)

in other terms, EC50 < Kd

37
Q

why can Emax be reached at a lower concentration than for Bmax to be reached

A
  • Spare Receptors

- Signal Amplification

38
Q

define the x-axis in dose response curve for in vivo experiments and whole animal experiments

A

in vivo- log([drug])

whole animal- log(dose)

39
Q

define efficacy

A
  • the magnitude of response a drug produces
  • maximum efficacy = Emax, can also be used to define efficacy of the drug
  • way more important in determining clinical effectiveness then potency
40
Q

define potency

A
  • [drug] necessary to produce an effect at a given magnitude (efficacy)
  • the lower the EC50, the higher the potency
  • very little effect on the determining the usefulness of a drug (clinical effectiveness)
41
Q

list the types of anatagonism

A

Receptor Antagonism (binds receptor)- competitive, noncompetitive (allosteric site)

Nonreceptor Antagonism (doesn’t bind receptor)- functional (indirect or physiological), chemical

42
Q

define the types of competitive antagonism

A
  • antagonist binds the same binding site as the agonist
  • Reversible: weak bonds, effect can be surmountable by inc drug dose (equal efficacy, higher EC50)
  • Irreveresible: covalent bonds, effect is insurmountable (lowered efficacy)
43
Q

phenoxybenzamine mechanism of action and purpose of treatment

A
  • irreversible competitive antagonist for α-adrenoreceptors

- to Tx pheochromocytoma

44
Q

aspirin mechanism of action and purpose of treatment

A
  • irreversible competitive antagonist for COX enzyme

- to Tx pain, coagulation

45
Q

omeprazole mechanism of action and purpose of treatment

A
  • irreversible competitive antagonist for H+/K+ ATPase enzyme (PPI)
  • to Tx GERD
46
Q

define noncompetitive antagonism

A
  • antagonist binds to allosteric site (non-binding site of agonist) on receptor
  • lowers efficacy / Emax
  • insurmountable by inc [drug]
47
Q

ketamine mechanism of action and purpose of use

A
  • noncompetitive antagonist of NMDA receptor

- IV anesthetic

48
Q

define the types of functional antagonism

A

(a nonreceptor antagonism type)

  • Indirect: binds to macromolecule in downstream signaling pathway to reverse effects of agonist
  • Physiological: induces signaling cascade with opposing effects to agonist
49
Q

a molecule that inhibits PKA function and therefore blocks the effects of β-adrenoreceptor agonist is an example of what type of antagonism

A

indirect functional antagonism

50
Q

what is the best / common example of physiological functional antagonism

A

using epinephrine (–> inc BP, bronchodilation) to reverse the effects of histamine (–> dec BP, bronchoconstriction) in an allergic reaction

51
Q

define chemical antagonism

A

antagonist reacts chemically with agonist to form an inactive product (neutralizes the agonist)

52
Q

what is the best / common example of chemical antagonism

A

protamine is pos. charged protein and counteracts effects of neg. charged heparin, an anticoagulant

53
Q

define partial and full agonist- include what happens in the presence of both

A
  • Full => maximum response
  • Partial => submaximal response
  • if both are present, partial agonist acts as a competitive antagonist
  • Note- no effect on potency
54
Q

define Inverse Agonist

A
  • many receptors have constitutive activity

- inverse agonist reverse this baseline activity

55
Q

give some classic examples of inverse agonists

A
  • famotidine (Pepcid)

- metoprolol (β1 antagonist - HTN)

56
Q

define the criteria for a drug to be considered selective

A

drug binds its first target (=> therapeutic effects) with at least 10-fold difference in affinity than its second target (=> adverse effects)

57
Q

_____ is the term used to describe the event at which a drug’s effect diminishes in the course of a few minutes

A

desensitisation, tachyphylaxis

58
Q

define drug tolerance

A

gradual dec in responsiveness to a drug, taking days - weeks to develop

59
Q

define refractoriness

A

related to loss of therapeutic efficacy

60
Q

define drug resistance

A

loss of effectiveness of antimicrobial or antitumor drugs

61
Q

list the factors involved in desensitization and tolerance

A
  • change in receptors: activate ion channels (rapid desensitization), G-protein-coupled receptors (desensitization, via phosphorylation mechanism)
  • internalization of receptors (endocytosis of receptors upon repeated drug exposure)
  • exhaustion of mediators (tachyphylaxis due to depleted stores)
  • inc metabolic degradation (tolerance)
  • physiological adaptation (drug effect opposed by homeostatic response)
62
Q

define TD50 and LD50

A

TD50- dose required to produce toxic effect in 50% of animals (median toxic dose)

LD50- dose required to cause death in 50% of animals (median lethal dose)

63
Q

give equation for therapeutic index

A

TI = TD50 / ED50 (humans)

TI = LD50 / ED50 (animals)

64
Q

define therapeutic window

A

from minimum effective concentration to minimum toxic concentration

FTCM (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions