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Pharmacology -- Test #1 > Pharmacodynamics II > Flashcards

Pharmacodynamics II Flashcards

1
Q

Give examples of intracellular receptors

A 
Corticosteroids
Mineralocorticoids
Sex  steroids
Vitamin D
Thyroid Hormone
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2
Q

How do intracellular receptors work?

A

Binding specific DNA sequences near the gene whose expression is to be regulated. This causes changes in protein transcription.

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3
Q

Course of action for steroid drugs?

A

Characteristic Lag Period

Effects persist after the concentration has been reduced to zero due to slow turnover of most enzymes and proteins

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4
Q

Examples of protein tyrosine kinases.

A

Insulin
EGF
PDGF

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5
Q

Protein tyrosine kinases span the lipid bilayer ____ times

A

one

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6
Q

What is the mechanism for protein tyrosine kinase activity

A

Hormone binds EC domain and change conformation
Receptor molecules bind, brining together kinase domains
Kinase phosphorylates itself
Tyrosine residues in both cytoplasmic domains become phosphorylated
Enzymatic Activity is activated

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7
Q

How are protein tyrosine kinases turned off?

A

Receptor Down Regulation and endocytosis of receptors

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8
Q

Examples of ligand-gated channel drugs

A

Acetylcholine
GABA
Glycine, Aspartate, Glutamate

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9
Q

Acetylcholine causes the opening of the _____ channel

A

nicotinic acetylcholine receptor

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10
Q

Time delay between agonist binding an ligand gated channel opening?

A

milliseconds

Going very fast is important for things like nerve signalling

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11
Q

Three common second messengers of GPCRs

A

cAMP
Calcium Ion
Phosphoinositides

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12
Q

Describe the process of GPCR activity

A

G-GDP inactivity, G-GTP can activate

Phosphorylation inactivates

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13
Q

What is EPAC?

A

Exchange Protein Activated by cAMP

A cAMP stimulated kinase recently discovered that may influence many effects of GPCRs

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14
Q

Phospholipase C results in the release of _____ and _______

A

Phosphoinositides and Diacylglycerol

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15
Q

Downstream effect of photphoinositides

A

Release of Calcium

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16
Q

Downstream effect of diacylglycerol

A

Protein Kinase C activation

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17
Q

Quantal log-dose response relationships are…

A

Quantal log-dose response relationship

ex. sleep and death

18
Q

What is a drug threshold?

A

The minimum effective dose of the drug which evokes an all-or-none pharmacological response

19
Q

How are the doses required to produce a quantal effect typically distributed?

A

log-normally

The resulting cumulative frequency constitutes a quantal dose-response curve

20
Q

What is Median Effective Dose (ED50)

A

Dose required to produce the stated effect in 50% of the population

21
Q

What is the median lethal dose?

A

The dose required to produce death in 50% of the population

22
Q

What is the Therapeutic Index/Ratio?

A

LD50/ED50 OR TD50/ED50

23
Q

What does one look for in a therapeutic index in a potential drug

A

A larger ratio indicate a larger gap between effective and toxic doses that will imply a decreased likelihood of accidental patient harm when pursuing a maximal efficacy

24
Q

What is seen in graded log-dose response relationships

A

The responding system is capable of showing progressively increasing effects with increasing concentrations of the drug

25
Q

What is drug tolerance?

A

A condition of decreased responsiveness to a drug acquired after prior or repeated exposure to a given or related drug

26
Q

Two ways for development of drug tolerance

A
  • Decrease in effective concentration of the agonist at the site of action
  • Decrease in the normal reactivity of the receptor
27
Q

What drugs most commonly cause downregulation of receptors or changes in receptor affinity?

A

CNS drugs such as narcotics, depressants, and stimulants

28
Q

What is cross tolerance?

A

Tolerance developed to one drug that is also seen with drugs belonging to the same class

Ex. Morphine use leads to tolerance of all narcotics

29
Q

Important molecular steps in receptor downregulation

A

GPCR kinase is triggered. It phosphorylates beta arrestin, which binds to the receptor and internalizes it for degradation or recycling.

30
Q

What is tachyphylaxis?

A

Acute development of tolerance following a rapid, repeated administration of a drug. Ex. ephedrine

31
Q

What is a drug allergy?

A

An adverse response to a foreign chemical resulting from previous exposure to the substance.

32
Q

What happens at inital exposure when developing a drug allergy.

A

Drug or metabolite acts as a hapten and combines with a protein to generate an antigen. The antigen induces latent synthesis of antibodies.
Subsequent exposure to drug results in an antigen-antibody response.

33
Q

Describe the drug allergy dose response.

A

There isn’t an apparent one. A minute amount of drug results in response.

34
Q

How could you test for a drug allergy?

A

Skin Test

35
Q

Unique characteristic of Type I allergic response?

A

First exposure IgE to be produced
Becomes fixed to mast cells and basophils
Subsequent exposure causes drug to bind to Fab of IgE
Histamine, PGs released

36
Q

Unique characteristic of Type II allergic response?

A

Ab dependent cytolytic response
IgG and IgM mediated
Abs activate the complement system, resulting in cell lysis
Blood Cells are primary targets

37
Q

Unique characteristic of Type III allergic response?

A

Immune complex fomation
Drug reacts with soluble Ab (IgG)
Deposits in vasculat endothelium, Cell mediated inflamm.
Serum sickness, hemolysis, and allergic nephritis

38
Q

Unique characteristic of Type IV allergic response?

A

Hours or Day after exposure before reaction
Mediated with antigen contact with sensitized T lymphocytes and macrophages
Release of cytokines –> Neutrophils and macrophages

39
Q

Example of a Type IV drug reaction

A

Contact dermatitis with a topical cream

40
Q

Idiosyncratic reactions to drugs are often caused by…

A

differences in drug metabolizing enzymes

Pharmacology -- Test #1 (8 decks)

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