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Pharm > 2.1 - Pharmacodynamics (cont.) > Flashcards

2.1 - Pharmacodynamics (cont.) Flashcards

1
Q

Types of receptor targets (4)

A
  1. Intracellular
  2. Transmembrane
  3. Ion Channels
  4. GPCR
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2
Q

Receptors for steroid or lipid soluble agents are found in ______

A

the cytoplasm/intracellular

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3
Q

Intracellular receptor signaling characteristically involves a

A

lag period

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4
Q

The effects of intracellular agents can persist after ____

A

the agonist concentration has been reduced to zero

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5
Q

Persistence of effects of intracellular agents is primarily due to _____

A

slow turnover of enzymes and proteins

(may also be from high affinity of receptors for the hormone)

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6
Q

Relationship between plasma levels of intracellular hormones and their effects

A

No simple temporal correlation

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7
Q

General examples of ligand-regulated transmembrane enzymes

A

Protein Tyr Kinases

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8
Q

Examples of receptor TK’s

A

Insulin

Epidermal Growth Factor (EGF)

Platelet-derived Growth Factor (PDGF)

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9
Q

Receptor that spans the membrane in a single pass

A

Protein Tyrosine Kinases

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10
Q

General 6 steps for RTK’s

A
  1. Hormone binds and induces conformational change
  2. Receptor molecules dimerize
  3. Kinase becomes capable of autophosphorylating (both cytoplasmic domains become phosphorylated)
  4. Downstream enzymes are activated
  5. Substrates become phosphorylated
  6. Signal is transduced
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11
Q

How does the cell limit RTK signal duration and intensity?

A

By downregulating the receptor

(ligand binding stimulates endocytosis of the receptor)

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12
Q

Drugs that act on Ion channels (ligand gated channels) act by…

A

blocking the actions of endogenous ligands that regulate ion flow through membrane channels

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13
Q

examples of ligand gated channels

A

Ach

GABA

excitatory aa. (glycine, aspartate, glutamate)

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14
Q

Main function of the ligand gated channel

A

after binding the agonist, it changes the electrical potential of the membrane to increase transmembrane conductance.

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15
Q

Time to effect of a ligand gated channel after binding of agonist

A

milliseconds

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16
Q

3 Examples of second messengers

A

Cyclic AMP

Calcium ion

Phosphoinositides (IP3)

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17
Q

Biggest advantage of GPCR signaling

A

amplification

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18
Q

Examples of GPCR systems

A

Adrenergic amines

serotonin

Ach (muscarinic effects)

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19
Q

Active form of G protein =

What is the function?

A

G-GTP

it can activate the Enzyme or Channel

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20
Q

Effector enzyme in a cAMP system

A

Adenylyl cyclase

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21
Q

cAMP exerts its effects by stimulating ________

A

cAMP dependent protein kinases (also EPAC)

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22
Q

cAMP system specificity is determined by

A

the distinct substrates of the kinases in different cells

23
Q

PLC results in release of ___ and___

A

IP3 and DAG

24
Q

DAG activates _________

A

protein kinase C

25
Q

cGMP activates _________

cGMP systems are characteristically __________

A

cGMP-dependent protein kinase

more specific than other messenger systems

26
Q

Quantal log-dose response relationship =

A

drugs may either show their effect or not at all

(can create a cumulative curve based on quantal data)

27
Q

“Normal frequency distribution”

A
  • The doses required to produce a specified quantal effect are log-normally distributed
  • Summating the responses results in a quantal dose-response curve
28
Q

“ED50”

A

Median effective dose

= the dose to get a response in HALF of the population

29
Q

LD50

A

(aka TD50)

The dose required to produce death or toxic symptom in half of the population

30
Q

The relative safety of a drug is expresed as…

A

LD50/ED50

(the larger ratio = greater safety)

31
Q

This drug was named in lecture as an example of a low therapeutic index

A

Theophylline

32
Q

Graded log-dose response is capable of showing…

A

progressively increasing effects with increased concentration of a drug

33
Q

Two mechanisms in development of tolerance

A
  1. Decrease the effective [] of the agonist at the site of action (ex. phenobarbital increases biotransformation of a number of drugs which are metabolized by liver enzymes)
  2. Decrease the normal reactivity of the receptor (ex. CNS drugs such as narcotics, depressants, and stimulants)
34
Q

Cross tolerance often affects drugs in ______

A

the same class

35
Q

What are beta arrestins?

A

Adapter proteins that form complexes with most G-protein-coupled receptors (GPCRs) following agonist binding and phosphorylation of receptors by G-protein-coupled receptor kinases (GRKs)

**Target the receptor for endocytosis

36
Q

Tachyphylaxis

A

The acute development of tolerance after giving a drug repeatedly in short time frame (the first gives the largest response)

**can NOT overcome by increasing dose**

37
Q

Example for tachyphylaxis

A

Ephedrine (releases NE)

in study, Reserpine depletes NE in vesicles. Used to simulate successive ephedrine doses.

**Epinephrine given directl still has effect after reserpine administration

38
Q

In allergic reaction, a drug acts as a __________ and combines with a protein to generate _______

A

hapten, antigen

39
Q

In drug allergy, there is no apparent ________

A

dose-response

(minute amounts still elicit response)

40
Q

Two other properties of allergic responses

A

Sensitiszing period is needed

Circulating antibodies can be found (skin test)

41
Q

Drug allergy effects are NOT related to…

A

pharmacologic activity

42
Q

Type 1 HS reaction

A
  1. Exposure –> IgE produced
  2. Fc part of IgE binds to mast cells/basophils
  3. Fab part binds to drug upon repeat exposure

*Rapid

**Local OR systemic

43
Q

T2HS is a ____ reaction

4 Steps?

Other stuff?

A

Antibody-dependent cytolytic reaction

  1. Drug binds to surgace component
  2. IgG and IgM are made
  3. Complement is activated
  4. Cell Lysis

Blood cells are primary target tissues, subsides within MONTHS of removal of drug

44
Q

Type 3 HS reaction forms ______

Three steps?

A

immune complexes

  1. Drug reacts with soluble IgG
  2. Immune complex deposited in vascular endothelium
  3. CMI cause local inflammation and complement activation
45
Q

T3HS examples

A

Serum sickness, hemolysis, allergic nephritis

46
Q

T3HS subsides…

A

within 1-2 weeks after drug is removed

47
Q

Type 4 HS =

A

Delayed type HS (cell mediated)

48
Q

T4HS time frame

A

hours or days after exposure

49
Q

T4HS is mediated by

A

Interaction between antigen and sensitized T cells or MQ

Causes release of lymphokines/cytokines

Subsequent influx of PMN and MQ

50
Q

Examples of T4HS

A

Contact dermatitis with topical drugs

51
Q

Idiosyncratic reaction =

Usually based on what?

Two examples?

A

genetically determined abnormal rxn to drug, either extreme sensitivity or insensitivity

usually a difference in METABOLIC enzymes

  1. (alteration in Vit. K epoxide reductase causes warfarin resistance)
  2. (Hemolytic anemia in G6PD if given primaquine)
52
Q

What is the basis behind pharmacogenetics

A

may be the result of SNPs in coding OR noncoding regions

(can affect target or metabolism, both intended and side effects,)

53
Q

Examples given for pharmacogenetics

A

Malignant hyperthermia (upon administration of inhaled anaesthetic from mutation in ryanodine receptor)

Cancers KRas, HER2, c-kit

Cystic fibrosis (CFTR variants)

Pharm (4 decks)

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