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HMS120: Pharmacology > Pharmacodynamics- Dosage > Flashcards

Pharmacodynamics- Dosage Flashcards

1
Q

Define Drug Dose

A

amount of drug administered to produce a certain degree of response in a patient

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2
Q

The Dose-Response relationship has 2 components. What are they?

A
  1. Dose-Plasma Concentration relationship

2. Plasma Concentration-Response relationship

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3
Q

Define Response

A

change in the activity of a cell/tissue due to the selected dose of a drug

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4
Q

What are some pharmacological factors that affect drug response?

Hint: I went to the pharmacy because I wasn’t responding to the drugs and saw the trio (TRIAD)

A 
T: treatment duration
R: route of administration
I: (drug) interaction
A: administration time
D: dose
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5
Q

What are some individual factors that affect drug response?

Hint: BADDie

A
  • Age & weight
  • gender
  • Diet
  • tolerance
  • Blood flow
  • Disease state

BADDie

  • Blood flow
  • Age & weight
  • Disease state
  • DIEt
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6
Q

4 types of drug dosages

Hint: STaRT

A

S: standard dose
Ta: target level dose
R: regulated dose
T: titrated dose

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7
Q

What is Standard Dose?

A

dose is same for most patients (drug has a wide margin of safety)

e.g. Mebendazole

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8
Q

What is Target Level Dose?

A

dose adjusted as per the required target plasma level of the drug

e.g. Lithium

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9
Q

What is Regulated Dose?

A

dose regulated as per response of the patient

e.g. antihypertensive drug’s dose adjusted as per BP response

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10
Q

What is Titrated Dose?

A

maximum tolerated dose is given by upward or downward titration

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11
Q

What should be given before dose is gradually increased or decreased?

A

loading dose

e.g. corticosteroids, anticancer drugs

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12
Q

What is the Dose Response Curve?

A

curve showing the direct relationship between DOSE INTENSITY and RESPONSE

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13
Q

What is the relationship between the dose intensity and response? (dose response curve)

A
  • directly proportional

- drug intensity increases with dose

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14
Q

What is the use of a Drug Response Curve?

A

useful in predicting the potency, efficacy and safety of a drug

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15
Q

What does a leftward shift on the Drug Response Curve show?

A

metabolic response occurring at lower doses, higher potency

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16
Q

Define Potency

A

measure of the amount of drug that has to be present to produce a desired effect

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17
Q

What is Potency also known as?

A

strength of the drug

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18
Q

How can you produce the desired clinical effect for a more potent drug?

A

lower the dose to be administered

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19
Q

Define EC50

A

concentration producing an effect that is 50% of the maximum; used to determine potency

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20
Q

What is used to determine potency?

A

EC50

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21
Q

How is the relative potency determined?

A

by comparing the dose of two agonists at which they produce half maximum response (EC50)

[comparing the EC50 of two agonists]

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22
Q

Define Efficacy

A

ability of a drug to produce an effect at a receptor

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23
Q

What is efficacy also known as?

A

intrinsic activity or power

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24
Q

When comparing efficacy between drugs, how can you tell which is more efficacious?

A

the one with the higher maximum effect

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25
Q

The upper limit of DRC is the index of ________ and refers to the _______________

A

the upper limit of DRC is the index of drug efficacy and refers to the maximal response that can be elicited by the drug

e.g. morphine is more efficacious than aspirin

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26
Q

What is a more decisive factor in the choice of a drug, and why? Efficacy or Potency?

A

Efficacy

  • the potency measures the amount of drug that has to be present, meaning this can always be changed to produced the desired effect, whereas efficacy is the ability to produce an effect at the receptor (i.e. if a drug has low efficacy, it doesn’t matter the amount of drug that is administered, the efficacy will remain the same)
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27
Q

What is the difference between agonist and antagonist?

A
  • agonist has an affinity for a receptor and has efficacy

- antagonist has affinity but cannot have efficacy

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28
Q

Difference between potency and efficacy?

A

potency looks at the minimum dose that can produce desired effect, whereas efficacy looks at the response it can produce

(see potency vs efficacy graph pg 11)

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29
Q

Define Therapeutic Index (TI)

A

ratio that compares the blood concentration at which the drug becomes toxic and the concentration at which the drug is effective

  • toxic concentration : effective concentration
  • TI = TD50/ED50
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30
Q

What does a larger TI mean about the safety of the drug?

A

larger the TI = safer the drug

  • indicates a wide margin between doses)
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31
Q

What does a small/narrow TI indicate?

A

difference between the two concentrations is very small, safety of the drug decreases

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32
Q

If the TI of a drug is small/narrow, what must be done?

A
  • drug must be dosed carefully

- person receiving the drug should be monitored close for signs of drug toxicity

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33
Q

How is the TI of a drug determined?

A

by measuring the
: frequency of desired response
: toxic response
at various doses

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34
Q

Define ED50

A
  • effective dose

: dose that produces the therapeutic/desired effect in 50% of the population

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35
Q

Define TD50

A
  • toxic dose

: dose that produces the toxic effect in 50% of the population

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36
Q

How is the TI calculated in animal experiments?

A

TI = LD50 (lethal dose) / ED50 (effective dose)

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37
Q

Define Therapeutic Window / Safety Window

A

range of doses that produce therapeutic response without causing any significant adverse effect in patients

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38
Q

How do you calculate the Therapeutic/Safety Window?

A

minimum effect concentrations (MEC) : minimum toxic concentration

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39
Q

If the dose is less than the therapeutic range, what happens to the response? And if greater? Why?

A
  • dose < therapeutic range = less response
  • dose > therapeutic range = less response
  • the therapeutic range is the optimal concentrations that will produce a therapeutic effect
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40
Q

Define Tolerance

A

state in which an organism no longer responds to the drug; a higher dose is required to maintain the same effect

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41
Q

Is drug tolerance reversible or irreversible?

A
  • reversible

e. g. through a drug holiday

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42
Q

What are the types of drug tolerances?

A
  1. Reverse tolerance (drug sensitisation)
  2. Tachyphylaxis (acute tolerance)
  3. Innate tolerance
  4. Acquired tolerance
    : pharmacokinetic tolerance
    : pharmacodynamic tolerance
    : learned tolerance
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43
Q

Define Reverse Tolerance (Drug Sensitisation)

A

subject’s increased tolerance (positive or negative) to a drug following its repeated use

e.g. cocaine, amphetamine

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44
Q

Define Tachyphylaxis (Acute Tolerance)

A

acute development of tolerance after a rapid and repeated administration of a drug in shorter intervals

e.g. ephedrine, tyramine

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45
Q

Define Innate Tolerance

A

genetically determined sensitivity (or lack of sensitivity) to a drug that is observed the first time the drug is administered

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46
Q

Types of Acquired Tolerance

A
  • pharmacokinetic tolerance
  • pharmacodynamic tolerance
  • learned tolerance
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47
Q

Define Pharmacokinetic Tolerance

A
  • refers to changes in the distribution or metabolism of the drug after repeated drug administrations
  • results in reduced concentrations in the blood and then at the sites of drug action (higher metabolism)

e.g. barbiturates (increase in rate of metabolism), alcohol

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48
Q

Define Pharmacodynamic Tolerance

A
  • refers to adaptive changes that take place within systems affected by the drug (i.e. drug-induced changes in receptor density)
  • response to a given concentration of the drug is reduced

e.g. morphine, caffeine, nicotine

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49
Q

Define Learned Tolerance

A
  • refers to a reduction in the effects of a drug
  • results from compensatory mechanisms that are learned

e.g. behavioural tolerance
: describes the skills that can be developed through repeated attempts to function, when in a state of mild to moderate intoxication

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50
Q

Individuals differ both in the degree and character of the response that a drug may elicit (between different patients and even in the same patient on different occasions). What are the factors that are responsible for the variation in drug response in individuals?

A
  • differ in pharmacokinetic handling (one may metabolise faster than another person)
  • variation in number/state of receptors, coupling proteins, or other components of response
  • variation in neurogenic/hormonal tone or concentrations of specific constituents
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51
Q

What two ways can drug action be modified in individuals?

A
  1. Quantitatively

2. Qualitatively

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52
Q

How can drug action be modified quantitatively?

A

plasma concentration and/or the drug action is increased/decreased

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53
Q

How can drug action be modified qualitatively?

A

type of response is altered

e.g. drug allergy

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54
Q

What are factors that affect Dose & Action of Drugs?

Hint: my DAD is a dealer and distributes in BAGS

A

B: body weight/size
A: age (infants/children & elderly)
G: gender
S: surface area (body)

DAD: dose & action of drug

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55
Q

What are factors that modify the effects of the drugs?

Hint: my PUG ate food and it effected the drugs

A

P: pregnancy, psychological state
U: underlying disease
G: genetic factors

  • food
  • cumulation
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56
Q

How does body weigh/size affect the dose and action of drugs?

A
  • influences concentration of drug attained at site of action
  • for obese/lean individuals and children, dose may be calculated on body weight
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57
Q

What does the Average Adult Dose refer to?

A

individuals of medium build

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58
Q

How does the age of children and infants affect the dose and action of drugs?

A
  • infants & children have important physiological differences
    : higher proportion of water
    : lower plasma protein levels (more free drug)
    : immature liver/kidneys (liver metabolises more slowly; kidneys excrete more slowly)
59
Q

How is the drug dose for children calculated?

A

calculated from the adult dose

60
Q

What is Body Surface Area (BSA)?

A

the total tissue area

61
Q

How is BSA calculated?

A
  • nomogram used to calculate the BSA in square meters
62
Q

What is the formula to calculate child drug dose using BSA?

A

child dose = (child BSA / 1.73 m2) x adult dose

*1.73 m2 is the average adult BSA

63
Q

What is Bastedo’s formula?

A

child dose = (age in years + 3) / (adult dose x 30)

64
Q

What is Clark’s formula?

A

child dose = weight in pounds / (adult dose x 150)

65
Q

What is Cowling’s formula?

A

child dose = (age in years + 1) / (adult dose x 24)

66
Q

What is Fried’s formula?

A

child dose = age in months / (adult dose x 150)

67
Q

What is Young’s formula?

A

child dose = (age in years / (age + 12) ) x adult dose

68
Q

How does the age of elders affect the dose and action of drugs?

A
  • renal function declines (intact nephron loss)- drug doses have to be reduced
  • chronic disease states
  • decreased plasma-protein binding
  • slower metabolism
  • slower excretion
  • dietary deficiencies
  • use of multiple medications
  • lack of compliance
69
Q

How does gender affect the dose and action of a drug?

A
  • females have smaller body size compared to males (require doses of drugs on the lower side of the dose range)
  • females should not be given
    : uterine stimulants during menstruation
    : quinine during pregnancy
    : sedatives during lactation
70
Q

How does pregnancy modify the effects of drugs?

A 
- physiological changes
\: GI motility- reduced due to delayed absorption of orally administered drugs
\: plasma and ECF volume expands
\: albumin level falls
\: renal blood flow increase
\: hepatic microsomal enzyme is induced
71
Q

How does psychological state modify the effects of drugs?

A
  • efficacy of drugs can be affected by patients beliefs, attitudes and expectations
    : particularly applicable to centrally acting drugs
  • in some patients inert drugs (placebo) may produce beneficial effects equivalent to the drug, and may induce sleep in insomnia
72
Q

How does underlying disease modify the effects of drugs?

A
  • drug may aggravate underlying pathology
  • hepatic disease may slow down drug metabolism
  • renal disease may slow down drug elimination
  • acid/base abnormalities may change drug absorption/elimination
  • sever shock with vasoconstriction delays absorption (subcutaneous & intramuscular)
  • drug metabolism in
    : hyperthyroidism- enhanced
    : hypothyroidism- diminished
73
Q

How do genetic factors modify the effects of drugs?

A
  • lack of specific enzymes and lower metabolic rate
74
Q

How does food modify the effects of drugs?

A
  • delays gastric emptying, delays absorption (ampicillin)
  • calcium in milk: interferes with absorption of tetracyclines and iron by chelation (binding)
  • protein malnutrition
    : loss of body weight
    : reduced hepatic metabolising capacity
    : hypoproteinemia (abnormally low levels of protein in blood)
75
Q

How does cumulation modify the effects of drugs?

A
  • any drug will cumulate in the body if rate of administration > rate of elimination
    e. g. digitalis, heavy metals, etc.
76
Q

Where is the NT ACh stored?

A

in vesicles in nerve endings

77
Q

How is ACh released to cause contraction/relaxation of muscles?

A
  1. nerve impulse arrives at nerve ending (where vesicles of ACh are)
  2. ACh released and binds with receptors (muscarinic & nicotinic) on postsynaptic membrane of muscle fibre
  3. binding changes permeability of membrane, causing channels to open that allow sodium ions (+ve charged) to flow into muscle cell
78
Q

What determines whether or not the muscle is stimulated or inhibited by ACh?

A

the receptor

79
Q

Functions of ACh?

A
  • stimulate skeletal muscles
  • dilate blood vessels
  • increase bodily secretion
  • decrease heart
- influences mental processes 
\: learning
\: memory
\: sleeping
\: dreaming
80
Q

How is ACh recycled?

A

In the synaptic cleft, the enzyme ACETYLCHOLINESTERASE breaks ACh into acetic acid and choline

81
Q

What are Anticholinesterases and what they do? Give examples

A
  • Acetylcholinesterases breaks ACh into acetic acid and choline
  • inhibitors of acetylcholinesterases prolong the lifetime of acetylcholine

e.g. physostigmine and neostigmine: used to help augment contraction in GI conditions

82
Q

Example of a disease that anticholinesterases can be used in?

A

Alzheimer’s Disease

83
Q

What is the process of ACh?

A
  1. ACh is made from choline and acetyl CoA
  2. in the synaptic cleft, ACh is rapidly broken down by Acetylesterase into choline and acetate
  3. Choline is transported back into axon terminal and combined with Acetyl-CoA to make more ACh
84
Q

ACh is an ester composed of…

A

choline & acetic acid

85
Q

ACh is broken down by acetylcholinesterase into…

A

choline & acetate

86
Q

ACh is made formed when which two molecules combine?

A

acetyl-CoA & choline

87
Q

What are examples of cholinergic receptors?

A
  • muscarinic receptor

- nicotinic receptor

88
Q

Muscarinic receptors are what types of receptors?

A
  • cholinergic receptor

- G-coupled protein receptor

89
Q

Nicotinic receptors are what types of receptors?

A
  • cholinergic receptor

- ligand-gated cation channel

90
Q

Muscarinic receptors are blocked by…

A

atropine

91
Q

Nicotinic receptors are blocked by…

A

curare

92
Q

Where are muscarinic receptors located?

A
  • CNS (M1-M5)
  • secretory glands i.e. salivary, stomach & sweat glands-(M1)
  • cardiac tissue (M2)
  • smooth muscle (M3)
  • parasympathetic system
  • effector tissues in ANS & in CNS
93
Q

Where are nicotinic receptors located?

A
  • post-ganglionic cell membranes in both the sympathetic and parasympathetic systems (autonomic ganglia)
  • skeletal neuromuscular junction
  • CNS
  • adrenal medulla
94
Q

What is the mechanism of action for muscarinic receptors?

A
  • M1, M3 & M5: [activation of phospholipase C → IP3 & DAG generation →] increased calcium
  • M2 & M4: [inhibition of adenylate cyclase →] decreased cAMP
95
Q

What is the mechanism of action for nicotinic receptors?

A

[activation of nicotinic receptors → opening of sodium and potassium channels →] depolarisation

96
Q

M1 receptor

  • type?
  • location?
  • function?
A
  • muscarinic receptor
  • secretory glands
  • salivation, stomach acid, sweating, lacrimation (tears)
97
Q

M2 receptor

  • type?
  • location?
  • function?
A
  • muscarinic receptor
  • cardiac tissue
  • decreases heart rate (bradycardia)
98
Q

M3 receptor

  • type?
  • location?
  • function?
A
  • muscarinic receptor

1)
- smooth muscle (GIT/GUT/RT)
- contraction of smooth muscle (some) [→ diarrhoea, urination, bronchospasm]

2)

  • pupil and ciliary muscle
  • contraction (miosis), increased flow of aqueous humor
99
Q

Nm receptor

  • type?
  • location?
  • function?
A
  • nicotinic receptor
  • skeletal muscle end plate (NMJ)
  • contraction of skeletal muscle
100
Q

Nn receptor

  • type?
  • location?
  • function?
A
  • nicotinic receptor
  • autonomic ganglia, adrenal medula
  • secretion of adrenaline, controls of ANS
101
Q

What are other names for cholinergic drugs?

A
  • parasympathomimetic drugs

- cholinomimetic

102
Q

What are parasympathomimetic drugs?

A

drugs that mimic the action of the parasympathetic nervous system

103
Q

What are cholinomimetic drugs?

A

drugs that cause the effects similar to those resulting from the introduction of acetylcholine

104
Q

What are the 2 types of cholinergic agonists?

A
  • direct-acting

- indirect-acting

105
Q

Characteristics of direct-acting cholinergic receptors

A
  • lipid soluble
  • do not readily enter the CNS (effects are peripheral)
  • resistant to metabolism by ACh
  • effects longer acting compared to ACh
106
Q

Characteristics of indirect-acting cholinergic receptors

A
  • act through inhibition of ACh (increases ACh level in synapse)
  • accumulation of ACh in synapse enhances activation of nicotinic & muscarinic receptors
  • anticholinesterase drugs are reversible/irreversible inhibitors of acetylcholinesterase
107
Q

What are adrenergic receptors (adrenoceptors)?

A

a class of G protein-coupled receptors that are targets of many catecholamines (i.e. adrenaline, dopamine, etc.)

108
Q

Binding of catecholamine to a receptor is responsible for..

A

fight or flight response

109
Q

What are the classes of adrenergic receptors?

A

alpha & beta adrenergic receptors

110
Q

Types of alpha adrenoceptors?

A

alpha-1 & alpha-2 adrenoceptors

111
Q

Types of beta adrenoceptors?

A

beta-1, beta-2 & beta-3 adrenoceptors

112
Q

What type of G protein-coupled receptor is the alpha-1 receptor?

A

Gq coupled-receptors

113
Q

What type of G protein-coupled receptor is the alpha-2 receptor?

A

Gi coupled-receptor

114
Q

What type of G protein-coupled receptor is the beta-2 receptor?

A

Gi coupled-receptor

115
Q

What type of G protein-coupled receptor is the beta-3 receptor?

A

Gi coupled-receptor

116
Q

What receptors are Gq coupled-receptors?

A

alpha-1 adrenoceptors

117
Q

What receptors are Gi coupled-receptors?

A

alpha-2, beta-2 & beta-3 adrenoceptors

118
Q

All beta receptors are what type of G protein-coupled receptors?

A

Gs coupled receptors

119
Q

What does the binding of catecholamines to adrenergic receptors cause?

A

catecholamines to adrenoceptors cause fight/flight

  • bronchodilation
  • vasodilation
  • tachycardia
  • inhibition of digestion
  • glucose release from hepatocytes
120
Q

Mechanism of Alpha-1 adrenoceptors?

A
  1. alpha-1 adrenoceptor couples to Gq proteins resulting in activation of phospholipase C, causing
  2. induction of IP3 (inositol triphosphate) & DAG (diacyglycerol)
  3. results in increased intracellular calcium ions
  4. smooth muscle contraction
121
Q

Mechanism of Alpha-2 adrenoceptors?

A
  1. alpha-2 adrenoceptor couples to Gi proteins resulting in inactivation of adenylate cyclase, causing
  2. decrease in cAMP (cyclic adenosine monophosphate)
  3. muscle contraction
122
Q

Mechanism of beta adrenoceptors?

A
  1. stimulation of beta adrenoceptors by adrenaline, causing activation of Gs coupled proteins
  2. adenylate cyclase in stimulated, increasing cAMP
  3. cAMP then activates cAMP-dependent kinase (cAMP/PKA)
  4. cAMP/PKA phosphorylate serine and threonine residues on beta adrenergic receptor kinase (beta-ARK)
  5. this serine threonine kinase (beta-ARK) will then phosphorylate serine and threonine residues on the beta adrenoceptor itself
  6. this will facilitate beta-arrestin binding to the receptor
  7. additional stimulation by adrenaline will no be unable to activate Gs proteins (due to beta-arrestin)
  8. therefore beta-ARK is a negative feedback enzyme (prevents overstimulation of the beta adrenoceptor)
  9. results in heart muscle contraction, smooth muscle relaxation and glycogenolysis, etc.
123
Q

Alpha-1 adrenergic receptors

  • location?
  • action?
A

1)

  • most vascular smooth muscle (innervated)
  • contraction (vasoconstriction)

2)

  • pupillary dilator muscle
  • contraction (dilates pupil: mydriasis)

3)

  • pilomotor smooth muscle
  • contraction (erects hair)

4)

  • prostate
  • contraction

5)

  • heart
  • increases force of contraction
124
Q

Alpha-2 adrenergic receptor

  • location?
  • action?
A

1)

  • postsynaptic CNS adrenoceptors
  • multiple actions (decreased SNS outflow)

2)

  • platelets
  • aggregation

3)

  • adrenergic and cholinergic nerve terminals (presynaptic)
  • inhibition of transmitter release

4)

  • some vascular smooth muscle
  • contraction (vasoconstriction)
125
Q

Beta-1 adrenergic receptor

  • location?
  • action?
A

1)

  • heart
  • increases heart rate, cardiac contractility & AV node conduction

2)

  • kidney (juxtaglomerular cells)
  • increases renin release
126
Q

Beta-2 adrenergic receptor (not innervated)

  • location?
  • action?
A

1)

  • respiratory, uterine and vascular (skeletal muscle vessels and vessels to the liver), smooth muscle
  • promotes smooth muscle relaxation

2)

  • skeletal muscle
  • promotes potassium uptake

3)
- human liver
- activates gluconeogenesis (increase glucose)

4)

  • heart
  • increase heart rate, cardiac contractility and AV node conduction
127
Q

Beta-3 adrenergic receptor

  • location?
  • action?
A
  • fat cells

- activates lipolysis

128
Q

Delta-1 adrenergic receptor

  • location?
  • action?
A
  • smooth muscle

- dilates renal blood vessels

129
Q

Alpha-1 adrenoceptor

1) tissue distribution?
2) mechanism of action?
3) agonist potency?
4) physiological effects?
5) agonist?
6) antagonist?

A

1) vascular/visceral smooth muscles
2) Gq-protein coupled activates phospholipase C, IP3 + DAG
3) epinephrine ≥ norepinephrine ≫ isoproterenol
4) smooth muscle contractions, gluconeogenesis, vasoconstriction
5) norepinephrine, phenylephrine, methoxamine
6) doxazosin, phentolamine, prazosin

130
Q

Alpha-2 adrenoceptor

1) tissue distribution?
2) mechanism of action?
3) agonist potency?
4) physiological effects?
5) agonist?
6) antagonist?

A

1) pre-synaptic terminals, pancreas, platelets, ciliary epithelium, salivary glands
2) Gi-protein coupled inhibits adenyl cyclase
3) epinephrine ≥ norepinephrine ≫ isoproterenol
4) inhibits release of NT
5) clonidine, monoxidine
6) yohimbine, idazoxan, tolazoline

131
Q

Beta-1 adrenoceptor

1) tissue distribution?
2) mechanism of action?
3) agonist potency?
4) physiological effects?
5) agonist?
6) antagonist?

A

1) heart, kidney, some pre-synaptic terminals
2) Gs-protein coupled activates adenyl cyclase + PKA
3) isoproterenol > epinephrine ≥ norepinephrine
4) increase heart rate and renin secretion
5) isoproterenol, norepinephrine, dobutamine
6) propranolol, metoprolol, atenolol

132
Q

Beta-2 adrenoceptor

1) tissue distribution?
2) mechanism of action?
3) agonist potency?
4) physiological effects?
5) agonist?
6) antagonist?

A

1) visceral smooth muscles, bronchioles, liver, skeletal muscles
2) Gs-protein coupled activates adenyl cyclase + PKA, calcium-channels
3) isoproterenol > epinephrine ≫ norepinephrine
4) vasodilation, bronchodilation, inhibits insulin secretion
5) isoproterenol, salbutamol, salmeterol, albuterol, formoterol, terbutaline, levalbuterol
6) propanolol, nadolol, butoxamine

133
Q

Beta-3 adrenoceptor

1) tissue distribution?
2) mechanism of action?
3) agonist potency?
4) physiological effects?
5) agonist?
6) antagonist?

A

1) adipose tissue
2) Gs-protein coupled activates adenyl cyclase + PKA
3) Isoproterenol = norepinephrine > epinephrine
4) increase lipolysis
5) isoproterenol, amibegron, solabegron

134
Q

What are other names for adrenergic receptors?

A
  • adrenomimetics

- sympathomimetics

135
Q

3 types of adrenergic agonists?

A
  1. direct-acting
  2. indirect-acting
  3. mixed-acting (direct & indirect)
136
Q

What do direct-acting adrenergic agonists do?

A

directly simulate receptors (epinephrine or norepinephrine)

137
Q

What do indirect adrenergic agonists do?

A

stimulates release of norepinephrine from terminal nerve endings (amphetamine)

138
Q

What do mixed-acting adrenergic receptors do?

A

stimulates receptor sites & release of norepinephrine from nerve endings (ephedrine)

139
Q

Where are catecholamines derived from?

A
  • derived from the amino acid tyrosine (which is derived from sources as well as synthesis from phenylalanine [alpha-amino acid] )
140
Q

True or False?

Catecholamines are lipid soluble

A

False.

  • catecholamines are water soluble and are 5-% bound to plasma proteins
141
Q

Examples of catecholamines

A
  • dopamine
  • norepinephrine
  • epinephrine
142
Q

Formation of catecholamines dopamine, norepinephrine and epinephrine

A
  1. phenylalanine → L-tyrosine (via phenylalanine hydroxylase)
    or
    tyrosine can be ingested directly from dietary protein
  2. catecholamine-secreting cells convert L-tyrosine → L-Dopa (via tyrosine hydroxylase)
  3. L-dopa → dopamine (via L-aromatic amino acid decarboxylase {AAAD} )
  4. dopamine → norepinephrine (via dopamine beta-hydroxylase [DBH] )
  5. norepinephrine → epinephrine (via phenylethanolamine N-methyltransferase [PNMT] )
143
Q

Examples of catecholamine analogues

A

various stimulant drugs (such as amphetamines)

HMS120: Pharmacology (13 decks)

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