Brainscape's Knowledge GenomeTM

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


See full index

PMP 201 Patient-Centred Learning > Pharmaceutcial Chemistry of CVS drugs III > Flashcards

Pharmaceutcial Chemistry of CVS drugs III Flashcards

1
Q

Arrhythmia

A
  • Heart rhythm problems, abnormal heart rhythm, caused by different
    factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What diseases do you use beta blockers

A
  • Hypertension
  • Arrhythmia
  • Angina
  • MI
  • CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are Adrenoceptors?

A
  • G protien coupled receptors that conotain an amine group and a catechol group (benzene with 2 alcohols)
  • Small-molecule binding characteristics to be clinically significant in pharmacotherapeutics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Targets of Catecholamines

A
  • Norepinephrine with R group of H
  • Epinephrine with R group of CH3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

α-receptors

A
  • α1 = α1A, α1B, and α1D
  • α2 = α2A, α2B, and α2C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

β-receptors

A
  • β1, β2, and β3 subtypes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Adrenoceptors location

A
  • Various organs and tissues as well as on neurons of both the peripheral nervous system and central nervous system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

β1 major in the heart

A
  • All β-blockers affinity for β1 inhibit binding norepinephrine/epinephrine
  • Slow heart rate/decreased myocardium contractile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

β1 in kidney

A
  • All β-blockers affinity for β1
  • Decrease secretion of renin
  • Decrease plasma levels of angiotensin II causing vasodialation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

β2 major in CNS

A
  • Increased sympathetic activity
  • β1selective drugs can also
    produce CNS side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

β2 vascular, lungs, uterus smooth muscle

A
  • Arterial dilation
  • Bronchodilation
  • Uterus muscle relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

β2 agonist

A
  • Alleviating respiratory distress in
    persons with asthma or used to inhibit uterine contractions in premature labour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

𝛼1 stimulation of smooth muscle of the peripheral vasculature

A
  • Constriction
    causing a rise in blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

α1antagonist

A
  • Relaxation of the blood vessels and a drop in blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Extracelluar structure of Adrenoceptors

A
  • Crystal structure of the human β2 adrenoceptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Membrane structure of Adrenoceptors

A
  • 7 Trans Membrane (TM) helices
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Intracellular structure of Adrenoceptors

A
  • Contains Protein G
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Alcohol part alpha and beta adrenoceptor binding site

A
  • R-enantimer is more active compared to S-enantimer forming H-bond with Asn293
19
Q

Amine part alpha and beta adrenoceptor binding site

A
  • Protonated and ionised at physiological pH. Ionic bond with Asp113
  • Primay and secondary amines are better
20
Q

Phenols alpha and beta adenoreceptors binding site

A
  • H-bonds with Ser204 and
    207 able to form hydrogen bonds
21
Q

Catechol aromatic ring alpha and beta adrenoceptor

A
  • Stabilising hydrophobic
    interaction with Phe290
22
Q

Alkyl substitution on the side chain alpha and beta adrenoreceptor binding site

A
  • Decreases activity. Steric effect which blocks
    H-bonding to the alcohol
23
Q

Beta adrenoceptor Extra hydrophobic pocket

A
  • Required for Beta receptor increasing the size of the N-alkyl substituent (CH3)
  • A bulky alkyl group can fit
24
Q

Pharmacological response of beta blockers

A
  • Sympatholytic drugs
  • Dependent on the drug-receptor affinity and selectivity
  • Selectivity decreases at higher dose
25
Q

Examples of Antagonist of β1

A
  • Atenolol
  • Metoprolol
  • Bisoprolol
  • Nebivolol
26
Q

Examples of Antagonists of both, β1 and β2

A
  • Propranolol
  • Sotalol
  • Timolol
27
Q

Examples of Mixed antagonists of β1 and β2 and 𝛼1

A
  • Carvedilol
  • Labetalol
28
Q

Pronethanol

A
  • Arylethanolamines
  • Withdrawn cause tumor ether
29
Q

Propranolol

Aryloxypropanolamines

A
  • Aryl
  • Oxypropanol
  • amino
  • More potent B-blocker compared to arylethanolamines
30
Q

Low energy conformation of Beta blockers

A
  • Have overlapping critical functional groups which occupy the same approximate region of space
31
Q

R absolute configuration

A
  • Maximum effectiveness in
    receptor binding, the OH group must occupy the same region in space as it does for the Catecholamines
  • Groups still have the same
    spatial arrangements

Most beta blocker are racemic

32
Q

Requirement of beta blocker

A
  • At least one aromacic or hetroaromatic ring with hydrophobic interaction
  • Hydrogen bond with either R-enantiomer arylethanolamines or s-enantiomer aryloxypropanolaminesm
  • Amine forming ionic bond branched bulky N-alkyl substituents (beta antagonist require hydrophobic pocket)
  • para substitutions with phenyloxypropanolamine
  • Substitution on the side chain increases metabolic stability but lowers activity replace O with S or CH2 is detrimental
33
Q

Lipophilic beta blockers

A
  • Higher partion coefficient at 2.65 due to hydrocarbon naphthyl ring system
  • Ability to peetrate blood brain barrier higher
  • Extensive hepatic metabolism - shorter half life
34
Q

Hydrophilic beta blocker

A
  • Lower partion coefficient with LogP = 0.5
  • Polar acetamide less likely to cross CNS
  • ## Minimal metabolised by liver insttead cleared by kidney
35
Q

Class I Antiarrhythmic Drugs

A
  • Class based of elecrophysological effect
  • Sodium channel blocker
  • Affinity for Na+ channels in fast action potential tissue therefore decrease in influx of Na+
36
Q

Class II Antiarrhythmic Drugs

A
  • Beta adrenergic receptors
  • Blocking norepinepherine from binding to beta receptors
  • Decrease SA and AV nodes increase PR interval
  • Can be selective & non-selective Esmolol and propranolol
37
Q

Class III Antiarrhythmic Drugs

A
  • Potassium channel blocker
  • Block outflow of potassium increase refractory peroid of AP increase QT interval
38
Q

Class IV Antiarrhythmic Drugs

A
  • Non-dihydropyridine Ca2+ channel blockers by decreasing influx of Ca2+
  • Decease slope of phase 0 prolong refractory peroid
  • Decrease heart rate and prolong PR interval so longer to travel to atrial myocardium
  • Verapamil and Diltiazem
39
Q

Flecainide

A
  • Sold as acetate (CH3COO-) salt which causes increase in water solubility and oral adminsitration (Amine/carboxylic acid)
  • Well absorbed orally
  • metabolised by CYP2D6 most elimininated renally and some via feaces
40
Q

Amiodarone

A
  • Potassium channel blocker that is lilophilic by diiodinated benzofuran derivative Long-elimination half-life cause toxicity
  • HCl salt increase water
    solubility/oral administration
  • Incomplete oral absorption
  • Additive effects with CCB
41
Q

Metabolite of Amiodarone

A
  • Mono-Desethylamiodarone (May be more toxic) is metabolised to Amiodarone
  • CYP2C9,CYP2D6, and CYP3A4 inhibitors inhibits the metabolism of warfarin therefore increase plasma levels and anticoagulant effect
42
Q

Issues with Amiodarone vs Triiodothyronine

A
  • Similar to triiodothyronine T3 hormone for thyroid cause hyperthyroid
  • Very lithophilic drug causes risk of neurotoxicity
  • Long half life cardiovascular toxicity
43
Q

Counteract issues with Amiodarone to Dronedarone

Still not optimum causes mortality

A
  • Removal of iodine groups reduce risk of thyroid issue
  • reduces lipophilicity, the risks of neurotoxicity and shortens half-life significantly by Methylsulphonamide
  • Associated with an increased risk of mortality
44
Q

To overcome the problem of long elimination
half-life of amiodarone

A
  • Replacing the butyl chain with ester group can undergo ester hydrolysis decrease half life
  • Bulkier compound increase the steric effect for esterases and delaying inactivation
  • Inactive drug

PMP 201 Patient-Centred Learning (51 decks)

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