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Pharmacology > Adrenergic Antagonists > Flashcards

Adrenergic Antagonists Flashcards

1
Q

reseerpine inhibitor

A

NE

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2
Q

SYMPATHOMIMETIC DRUGS

A

Drugs that mimic the actions of Epinephrine or Norepinephrine

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3
Q

Alpha-1 Receptor Agonist

A 
1. Phenylephrine - nasal decongestant which causes
vasoconstriction.
2. Methoxamine
3. Midodrine (withdrawn) – can block ANS
4. Metaraminol
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4
Q

Alpha-2 Receptor Agonist

A
  1. Clonidine - present pre-synaptically; used for HTN, by the decrease of cAMP which reduces the release of Norepinephrine thereby reducing the BP (also considered sympatholytic)
  2. Methyldopa
  3. Guanabenz r
  4. Guanfacine
  5. Rilmerudine
  6. Dexmetomidine –combine with Opiates = prevent Resp.
    depression
  7. Brimonidine
  8. Moxonidine
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5
Q

Beta-1 Receptor Agonist

A
  1. Dobutamine

2. Dopamine CHF treatment, Inc. CO not HR

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6
Q

Beta-2 Receptor Agonist

A
  1. Fenoterol
  2. Formoterol
  3. Albuterol
  4. Terbutaline
  5. Salbutamol
  6. Pirbuterol
  7. Levalbuterol
  8. Metaproterenol
  9. Bitollerol
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7
Q

NON SELECTIVE DIRECT ACTING

A
  1. Epinephrine
  2. Norepinephrine
  3. Oxymetazoline (binds to α1 and α2)
    Xylometazoline – both are former a1, but has higher affinity to a2 receptor
  4. Isoproterenol- has higher affinity to β receptor
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8
Q

INDIRECT AGONISTS

A

they do not bind to the receptor instead they increase
the level and effect of Norepinephrine in the synaptic
cleft

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9
Q

Steps in IA

A
  1. By acting as a releasing agent/displacing agent, e.g.
    Amphetamine and Tyramine, they would stimulate release
    of NE from the vesicle
  2. by acting inhibitor they would inhibit the reuptake of NE
    like Cocaine and Tricyclic Anti-depressants
  3. By inhibiting the enzyme that will degrade your NE
     prevent enzymatic metabolism of NE (MAO and
    COMT).
    Ex: Entacapone (COMT inhibitor- used for Parkinson’s
    disease).
    Selegiline (MAO inhibitor- anti-depressant)
     they only prolong the effect of the NE that is released.
     actions are dependent on their ability to enhance the
    actions of endogenous catecholamine
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10
Q

Mixed Acting

A

they directly bind or indirectly stimulate the release
\1. Ephedrine
2. Pseudoephedrine
3. Phenylpropanolamine (PPA)

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11
Q

How do u differentiate the 3?

A

DIRECT ACTING AGONIST WITH PRIOR
TREATMENT TO RESERPINE: the response is not
reduced because even in the absence of NE stores since they directly bind to the
receptor their response is NOT AFFECTED

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12
Q

INDIRECT ACTING AGONIST WITH PRIOR TREATMENT

TO RESERPINE:

A

affected with NE stores; since Reserpine
blocks the storage of NE, so if you give Amphetamine that
displaces NE and there is decreased levels of NE the
response will be ABOLISHED/ DIMINISHED

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13
Q

WITH MIXED ACTING

A

since this directly stimulates the
adrenoceptor and may displace the NE the response will
still be there. However, it is REDUCED comparing it with
indirect acting

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14
Q

Reserpine will diminish effect of direct-acting adrenergic

agonist.

A

False.

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15
Q

Reserpine will diminish effect of mixed-acting adrenergic

agonist.

A

True

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16
Q

Reserpine will abolish the effect of indirect-acting

adrenergic agonist

A

True

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17
Q

DESENSITIZATION

A

● Decrease in response of the agonist receptor as you
increase the time of administration
● In a long term use of a drug the response of these drugs
to its agonist receptor binding will be diminished
● After a cell or tissue has been exposed to an agonist (in
this case, catecholamines and other sympathomimetic
drugs) for a period of time, it often becomes less
responsive to further stimulation by that agent

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18
Q

Tolerance

A

progressively reduced therapeutic
effectiveness due to enhancement of their
own metabolism

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19
Q

Refractoriness

A

lack of responsiveness to a drug

Clinical significance: May limit the therapeutic response to
sympathomimetic agents

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20
Q

Homologous desensitization-

A

refers to loss of
responsiveness EXCLUSIVELY OF THE RECEPTORS
that have been exposed to repeated or sustained
activation by a agonist
- E.g. is Arestine binding to G-protein
coupled receptorsleading to inhibition of the same
receptor

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21
Q

Heterologous desensitization

A

desensitization of 1
RECEPTOR BY ITS AGONIST ALSO RESULTS IN
DESENSITIZATION OF ANOTHER RECEPTOR that
has been directly activated by the agonist

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22
Q

Longer the side chain

A

e longer action of duration

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23
Q

PHENYLETHYLAMINE

A

not a catecholamine. It is
only a parent structure of your other catecholamines. it
consists of a benzene ring, with an ethylamine side
chain

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24
Q

Catecholamines are combination of

A

of CATHECOL and
phenylethylAMINE. The OH groups at 3 and 4 position
found in catechol is joined with the parent structure
phenylethylamine leading to the derivation of the structures
of your catecholamines: DOPAMINE, EPINEPHRINE,
NOREPINEPHRINE AND ISOPROTERENOL (NE and Epi
- most potent)

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25
Q

OH at 3 and 4 position

A

increases drug potency

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26
Q

-OH at 3 and 4 position:

A

increases susceptibility to

COMT (present in gut and liver) catabolism

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27
Q

Absence of -OH at 3 and 4 position:

A

reduction in drug
potency → NON-CATECHOLAMINES → these drugs are
not predisposed to the enzymatic action of COMT to
catabolize them. COMT enzyme acts on the -OH groups of
the catecholamines thereby inhibiting their actions → THUS
CAN BE GIVEN ORALLY

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28
Q

COMT is present

in the gut and liver.

A

If you give epinephrine orally, it will
be easily metabolized in the gut and liver, losing its
effects. The best way to elicit the effects of epinephrine
is via IV.

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29
Q

Absence of -OH at 3 and 4 position

A

: increase in plasma

concentration orally

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30
Q

All drugs entering blood-brain barrier

A

r act centrally in the
nervous systems will have CNS adverse effects such as
somnolence/sedation, appetite suppression.

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31
Q

Substitution at alpha carbon

A

Blocks oxidation by MAO
→ prolongs duration of action. Example is amphetamine:
there is methyl group substitution at the alpha carbon →
therefore is not susceptible to MAO catabolism making it
freely enter the blood-brain barrier

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32
Q

*MAO, as opposed to COMT

A

is found at the periphery

of the blood-brain barrier.

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33
Q

Prolonged alkyl group

A

Higher beta selectivity of the

drug *Isoproterenol

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34
Q

subs at beta

A

important for storage

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35
Q

α1

A

Gq ↑ cAMP, IP3, DAG → muscular contraction

can also cause mydriasis & increased closure of
internal sphincter of bladder- would cause decrease in
urine output or urinary retention
● The main effect of α1 receptor is
VASOCONSTRICTION

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36
Q

α2

A

Gi ↓ cAMP, Ca → inhibit transmitter release

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37
Q

β

A

Gs ↑ cAMP → contraction

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38
Q

D1

A

Gs ↑ cAMP → smooth muscle relaxation

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39
Q

D2

A

Gi ↓ cAMP and open k+ channels

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40
Q

Non selective Alpha receptor

A

oxymetazoline, Norepi, Epi

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41
Q

Alpha-1 AGONIST Drugs

A
  1. Phenylephrine- for hypotension and decongestion
  2. Methoxamine
  3. Midodrine (withdrawn) – can block ANS
  4. Metaraminol
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42
Q

Alpha-1 ANTAGONIST

A

“zosin”

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43
Q
  1. Doxasozin
  2. Prazosin
  3. Terazosin
A

Anti-HTN and tx for BPH

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44
Q
  1. Alfusozin

5. Indoramin

A

Anti-HTN

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45
Q
  1. Urapidil
  2. Silodosin
  3. Tamsulosin
A

Tx of BPH

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46
Q

Α1 RECEPTOR ACTIVATION EFFECTS

A

 Vascular Beds: Arterial and
venous vasoconstriction
 Heart: Modest positive inotropic action
 Skin and splanchnic vessels: Constricts in
response to Epi and NE
 Blood vessels of nasal mucosa:
Local vasoconstriction (explains decongestant
action of sympathomimetics)
 Do not prescribe for more than three days → may
cause Rhinitis medicamentosa or rebound
congestion (it is a compensatory mechanism of
your body if there is prolonged decongestion)

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47
Q

Alpha-2 AGONIST Drugs

A

“Sympatholytics” management of hypertension

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48
Q

Drugs A2

A
  1. Clonidine
  2. Methyldopa – anti-HTN for pregnant women
  3. Guanabenz
  4. Guanfacine
  5. Rilmerudine
  6. Dexmetomidine
  7. Tizanidine – central muscle relaxant
  8. Brimonidine
  9. Moxonidine
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49
Q

Alpha-2 ANTAGONIST Drugs

A

Yohimbine – combine with Papaverine = Erection
- second messenger involved: cAMP, which
is inhibited

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50
Q

EFFECTS of A2

A

● Autonomic neuromodulation by inhibiting cAMP, it
would inhibit norepinephrine release, so act as
inhibitory autoreceptor. Also inhibits Ach release (so it’s
a inhibitory heteroreceptor)
● inhibit insulin release
● inhibit renin secretion, so it can be used as
sympatholytic drug in treating hypertension

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51
Q

Rhinitis medicamentosa

A

or rebound
congestion (it is a compensatory mechanism of
your body if there is prolonged decongestion)

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52
Q

BETA RECEPTORS

A

These drugs can increase blood vessel supply on
muscle sites. Increase blood supply of skeletal muscle
may result to increase in the response of muscle →
more twitch responses → thus, one adverse effect of
beta-adrenoceptor agonists are tremors
 Palpitations may also result due to increased blood
supply
 Liver: Glycogenolysis

53
Q

Isoproterenol NON-SELECTIVE BETA AGONIST

A

net effect is to maintain or slightly

increase systolic pressure and to lower diastolic pressure, so that mean BP is decreased

54
Q

β1 receptor

A

mostly present in heart

55
Q

Reflex bradycardia in a1 antagonist

A

baroreceptor activation and bradycardia

56
Q

Dobutamine

Dopamine

A

for CHF patients with poor heart control, it
has greater effects on contractility over rate
- increases largely the effect on contraction
with lesser effect on heart rate.
- (+) Isomer: higher affinity on beta than
alpha, higher chronotropy than ionotropy.
- Enhanced automaticity and cardiac output
and stroke volume without marked increased in
heart rate

57
Q

EFFECTS of B1`

A

Heart: Increases cardiac output by increasing
contractility and by direct activation of the sinus
node to increase HR
● Vascular beds: Decrease peripheral
● Adrenoceptor Agonists & resistance leading to
vasodilation
● (+) chronotropic effect, (+) dromotropic effect, (+)
inotropic effect
● Increase heart rate
● Increase AV node velocity
● Positive chronotropic, dromotropic, inotropic.
● Increases renin release (BP increases due to
Angiotensin and Aldosterone).
●Indirectly increases Aldosterone, causing sodium
and water retention to increase blood volume and
cardiac output, blood pressure

58
Q

In what condition u give β1 agonist?

A

Mostly with person with decrease heart rate- e.g.

CHF

59
Q

BETA-2 RECEPTOR, relax

A
  1. Fenoterol
  2. Formoterol
  3. Albuterol
  4. Terbutaline
  5. Salbutamol
  6. Pirbuterol
  7. Levalbuterol
  8. Metaproterenol
  9. Bitollerol
60
Q

BROCHODILATION-

A

for asthma (Salbutamol)
- Lesser adverse effect if given as inhalations.
Patients given oral Salbutamol (2mg or 4mg tablets) frequently complain of tremors and palpitations.
- Absorption in lesser thru inhalation thus, mild adverse effects are felt by the patient.
● Promote K+ uptake in skeletal muscle

61
Q

Used for preterm delivery as TOCOLYSIS in uterine

muscles

A

Ritodrine/Terbutaline is given

62
Q

OTHER EFFECTS

A

● Bladder detrusor muscle: Relaxation
● Ciliary muscle: Relaxation (Mydriasis)
● GI: Decrease motility
● Uterus: Relaxation
● Liver: Increase Glc metabolism (enhance glucagon
secretion from pancreatic cells, diminish glucose
reuptake, enhance glycogenolysis, stimulates
lipolysis)

63
Q

ADE of b2

A

Tremor and Tachycardia.
 Why would be there tremor? They supply the
skeletal muscle. So increase blood supply to skeletal
muscle would cause increase in twitch response by
producing tremor and restlessness The effect of
tachycardia and tremor decrease if you give drug
through inhalation then comparing with systemic

3T- Tolerance, Tachycardia, Tremor

64
Q

BETA-3 AGONISTS

A

controlling urinary incontinence → relaxes the bladder smooth muscle, adipocyte
1. Mirabegron- tx for overactive bladder

65
Q

D1

A

Smooth muscle - Dilates renal blood vessels

  1. Fenoldopam – manages severe HTN
  2. Levodopa – converted into dopamine once it crossed
    the blood-brain barrier, managing Parkinson’s disease
    and Prolactinemia
66
Q

D2

A

Nerve endings - Modulates transmitter release, Inhibits
adenyl cyclase, Open K+ channels, decreased Calcium
influx

67
Q

non sel b1 and b2 dir acting

A

isoproterenol, norepi, epi

68
Q

B1 sel

A

Dobutamine

69
Q

B2 sel (SMART FIVE)

A

Salmetrol, Metaprotenol, Albuterol, Ritodiner, Terbutaline, formoterol,indacaterol

70
Q

B3 sel

A

Mirabegron

71
Q

Low concentration of Dopamine

A

Vascular D1 receptors (renal,
mesenteric, coronary beds) → activates adenylyl cyclase
→ Vasodilation
Higher doses: (+) Inotropic effect on myocardium acting on
Beta adrenergic receptors → DA causes release of NE from
nerve terminals → Effects on heart
Very high doses: DA activates vascular α1 receptors →
Vasoconstriction and Tachycardia

72
Q

β1 SELECTIVE AGONISTS

1. Dobutamine

A

 Initially considered a relatively β1-selective agonist
but its actions are more complex
 Chemical structure resembles dopamine, but its
actions are mediated mostly by α and β receptors
 Enhances automaticity of sinus node, increase CO,
Stroke volume w/o increasing heart rate
 Not all patients hooked to dopamine would be
hooked to dobutamine
 The only indication for dobutamine is SHORT
TERM TREATMENT OF CARDIAC
DECOMPENSATION that may occur after cardiac
surgery or patients with CHF or MI. So more on the
contractility and not HR
 If u want to increase HR start patient on dopamine.
If you give dopamine and and dose is too high it
may cause angina because of increased workload

73
Q

Short acting B2

A

Procaterol, Perbuterol, Albuterol, metaprotenrol, Terbutalinre, Isothearine, levabuterol, Fenoterol

74
Q

long Acting B2

A

Formoterol, Salmeterol, Aformetorol

75
Q

Veery long acting B2

A

Vilanterol, indacaterol, Oladeteol

76
Q

other B2

A

Tocholysis, ritodrine

77
Q

75 yrs old, female complains of decrease functionality and
quality of life caused by her incontinence, saying that it
prevents her from completing her task. She wants to spend
time away from home, to spent some time in public. Which
is the most appropriate agent for her?

A

A. Guanfacine
B. Prenalterol
C. Midodrine (α1 causes contraction of sphincter)
D. Xylometazoline

78
Q

MIXED-ACTING SYMPATHOMIMETIC

A

Two mechanisms:
1. Receptor binding
2. Increase NE release: main effect of mixed-acting
agonists is via this mechanism

79
Q

epi

A 
Oral- no
SQ- slow
Im- rapid
IV- emergency
inhalerd- Restricted to RT

a1=a2=b1=b2 receptor

COMT inhib

80
Q

Low Epi

A

B1: Inc. HR, SV, CO, Pulse P
B2: Low TotalPeriResis , BP

81
Q

high dose epi

A

a1 inc: TPR, BP (reflex brady)
B1: inc. HR, SV,CO, PP
B2: LOW TPR

82
Q

Norepi

A

a1=a2, b1»>b2

83
Q

Higher doses: D2

A

+) Inotropic effect on myocardium acting on
Beta adrenergic receptors → DA causes release of NE from
nerve terminals → Effects on heart

84
Q

VH d2`

A

Very high doses: DA activates vascular α1 receptors →

Vasoconstriction and Tachycardia

85
Q

INDIRECT-ACTING SYMPATHOMIMETICS

A
  1. Stimulate NE release- “Amphetamine-like”
  2. Inhibit NE reuptake
  3. Inhibit COMT activity
  4. Inhibit MAO activity
86
Q

Amphetamine-like

A

Methamphetamine
Phenmetrazine- Promoted as an ANOREXIANT and popular drug of
abuse

Methylphenidate-Appear to have efficacy in some children with
ATTENTION DEFICIT HYPERACTIVITY
DISORDER

Modafinil-IMPROVE
WAKEFULNESS IN NARCOLEPSY

Tyramine -Patients taking MAO inhibitors should avoid
tyramine-containing food

87
Q

MIXED-ACTING SYMPATHOMIMETIC

A

Two mechanisms:
1. Receptor binding
2. Increase NE release: main effect of mixed-acting
agonists is via this mechanism

88
Q

Ephedrine

A

Found in Ma-huang, a popular herbal medication
● Enhance the epinephrine release, which enhance
● HR & BP
● Can cause BRONCHODILATION
● Both α and β receptor stimulation
● FIRST ORALLY ACTIVE SYMPATHOMIMETIC
DRUG
● Ability to activate β receptors probably accounted
for its earlier use in asthma
● Has high bioavailability and a relatively long
duration of action
● Mild stimulant in CNS
● Banned by FDA

89
Q

Phenylpropanolamine

A 
● COMMON COMPONENT IN OTC APPETITE
SUPPRESSANTS
● Associated with Hemorrhagic Stroke
● Removed from the market
● The one that is available is Phenylephrine as a
nasal decongestan
90
Q

. Pseudoephedrine

A

● Has been available OTC AS A COMPONENT OF
MANY DECONGESTANT MIXTURES
● Restriction of sale for its use in ILLICIT
MANUFACTURE OF METHAMPHETAMINE

91
Q

What is the most appropriate agent used to relieve
bronchospasm, severe angioedema and hypotension in a
20 yrs. old individual that has been stung by a bee?

A

B. Intramuscular Epinephrine 1:1000 dilution

92
Q

All antagonist are competitive except

A

Phenoxybenzaminre (aplah blocker)

irreversible-covalent bonding
inhibut reuptake of NE by PS nerever
Blocks H1, ach, sero
Pheochromocytoma management

excess catecholemine- Sustained HPN
Headache
palpitatiomm
Sweating

best alternative to Phenotalimine- non cop-high efficacy

93
Q

ADVERSE EFFECTS in Phenoxybenamine

A 
● Postural hypotension
● Nasal stuffiness
● Nausea and vomiting
● Inhibit ejaculation
● The drug also may induce reflex
tachycardia, mediated by the baroreceptor
reflex, and is contraindicated in patients
with decreased coronary perfusion
94
Q

CARDIOVASCULAR EFFECT of Phenoxybenzamine

A

By blocking α receptors,
Phenoxybenzamine prevents
vasoconstriction of peripheral blood
vessels by endogenous catecholamines.
- The decreased peripheral resistance promotes
a reflex tachycardia
- The ability to block presynaptic inhibitory
α2 receptors in the heart can contribute to
an increased cardiac output

95
Q
  1. PHENTOLAMINE
A
  • Produces a competitive block of α1 and α2
    receptors
  • Produces postural hypotension and cause
    epinephrine reversal (decrease BP, increase heart
    rate)
96
Q

Phentolamine-induced reflex cardiac

A

stimulation
and tachycardia are mediated by the baroreceptor
reflex and by blocking the α2 receptors of the
cardiac sympathetic nerves
- Can also trigger arrhythmias and angina pain, and it
is contraindicated in patients with decreased
coronary perfusion (same with phenoxybenzamine)
- Also used for the short-term management
of Pheochromocytoma

97
Q

TAMSULOSIN Selective A1`

A
  • Competitive α1
  • relatively greater potency in inhibiting contraction
    in prostate smooth muscle versus vascular smooth
    muscle compared with other α1 selective
    antagonist
  • efficacy in BPH suggests that 1A subtype may be
    the most important subtype mediating prostate
    smooth muscle contraction
  • Half-life: 9-15 hours
98
Q

PRAZOCIN

A

Selective competitive blockers of the α1 receptor
- Relaxes both arterial and venous vascular smooth
muscle, as well as smooth muscle in the prostate
due to blockade of α1 receptors
- Half-life: 3 hours

99
Q

TERAZOCIN

A
  • Reversible α1-selective antagonist that is effective in
    hypertension
  • It is also approved for use in men with urinary
    symptoms due to benign prostatic hyperplasia
  • Half-life: 9-12 hours
100
Q

DOXAZOSIN

A
  • Treatment of hypertension and BPH (bENIGN PROSTATIC HYPERLLASIA)
  • Longer half-life: 22 hours
    long acting
101
Q

what is required for a1 blocker activity

A

Quinazoline-4-amine

102
Q

duration of action of Sel. Alpha ag

A

Acyl moeity

103
Q

other Antagonist a1

A

URADIPIL, LABETOLOL/CARVEDIOLOL, HAOPERIDOL/cH;OROPROMAIZE

104
Q

a1 blocker sideeffect

A

Vasodialation

first dose effect- dec dose of a1 antagonist
postural hypotensiomm
tachycardia
headache- cranial vasodialaitom
lowe ejaculatiom (vasoconstrictiom)
Nasal congestiom
105
Q

SELECTIVE ALPHA2 ANTAGONISTSYOHIMBINE

A

selective competitive α2 blocker
- Found as a component of the bark of the
Yohimbine tree and is sometimes used as a sexual
stimulant
- Works at the level of the CNS to increase
sympathetic outflow to the periphery
- It directly blocks α2 receptors and has been used to
relieve vasoconstriction
associated with Reynaud’s disease
- Used in the treatment of orthostatic hypotension
because it promotes NE release through blockade of
presynaptic α2 receptors

106
Q

URINARY OBSTRUCTION

A

● The mechanism of action in improving urine flow
involves partial reversal of smooth muscle
contraction in the enlarged prostate and in the
bladder base
● Prazosin, Doxazosin, and Terazosin are all
efficacious in patients with BPH
● These drugs are particularly useful in patients who also
have HTN
● Tamsulosin- also efficacious in BPH and has
relatively minor effects on blood pressure at a low
dose
● Almost all drugs with “zosin” can be used for BPH

107
Q

ERECTILE DYSFUNCTION

A

• Combination of Phentolamine with the
nonspecific smooth muscle relaxant Papaverine
when injected directly into the penis, may cause
erections in men with sexual dysfunction
• Alternative therapies for erectile dysfunction
include prostaglandins, Sildenafil (Viagra) and other
cGMP phosphodiesterase inhibitors, and
apomorphine

108
Q

BETA RECEPTOR ANTAGONISTS (beta blocker)

A

● ‘-olol’
● Primarily affects the heart
● Beta 2 in Lungs whereas Beta 3 in Bladder
● Effects are largely predictable, based on the sympathetic
nervous system (SNS) innervation and the adrenoceptor
subtypes present on the effectors.
● Heart: ↓ contractility, HR, CO, oxygen demand, and BP
(without orthostatic hypotension) Possible AV block and
heart failure
● Eye: ↓ ciliary epithelial secretions, ↓intraocular pressure,
use in glaucoma
● Lungs: bronchospasm in asthmatics, especially for nonselective
● Metabolism: delay hypoglycemia (↓glycogenolysis)

109
Q

RESPIRATORY TRACT:

A

• Bronchoconstriction- adverse effect
• Blocking β2 receptors in the lungs of susceptible
patients causes contraction of the bronchiolar
smooth muscle.
• This can precipitate a respiratory crisis in patients
with chronic obstructive pulmonary disease
(COPD) or asthma
• β-Blockers, and in particular nonselective ones,
are thus contraindicated in patients with COPD or
asthma

110
Q

EFFECTS ON EYE

A

EFFECTS ON EYE:
• Reduce intraocular pressure, especially
Glaucoma
• Decrease aqueous humor production Timolol

111
Q

METABOLIC AND ENDOCRINE EFFECTS

A

● Disturbances in glucose metabolism
● β-blockade leads to decrease glycogenolysis and
decreased glucagon secretion.
● Therefore, if a Type 1 (formerly insulindependent) diabetic is to be given propranolol, very
careful monitoring of blood glucose is essential,
because pronounced hypoglycemia may occur
after insulin injection.
● β-blockers also attenuate the normal physiologic
response to hypoglycemia

112
Q

Adverse effect ofn b blocker

A 
Bronchoconstrictiom
Bradycardia
Arrythmia
Lethargy
distubance in glucose
Fatigye
Insomnia
Sexual dysfuntion
113
Q

Beta blocker contraindicariom

A

ABCDE, Asthma, blok, COPD, DM, Hyperkalemia

114
Q

Full agonist

A

Max response- norepi, epi, isoprelaline

115
Q

Full antagonistq

A

Propanolol
Timolol
Atenolol
Metoprolol

116
Q

partial agonist

A

Sub maximal- pindolol, Penbutolol, Acebutolol

117
Q

intrinsic sympathomemtic- partial agonist

A

Celiprolol, oxeprenol, pindolol, Alprenolol, Acebutol

118
Q

1st gen non-sel b1=b2

A

● These are our (NPPPT) that is our
Nadolol, Penbutolol, Pindolol,
Propranolol, Timolol

● They are so called non selective as
they block both Beta 1 & 2 receptor.

● For their mechanism involved in
blocking of Beta 1 receptor, they
mainly decrease the CAMP, thereby
decreasing the adenyl cyclase,
eventually decreasing cytosolic
calcium thus helps in decreasing the
rate/force of contraction and at last
the cardiac output.
 ● Whereas similar effects seen in
beta 2 receptor in which blocking the
beta 2 receptor will decrease the
cyclic AMP thus causing
“Bronchospasm”
119
Q

2nd Generation
Selective Beta 1
Antagonist
Cardioselective

A 
● They include mainly
(BAAME) Bisoprolol, Acebutolol,
Atenolol, Metoprolol, Esmolol.
● Same mechanism as before they
act by decreasing levels of CAMP.
And the significant effect seen by this
drugs is “Bradycardia” but important
to note that bronchospasm doesn’t
come under their (Beta 1 selective)
side effects
120
Q

3rd Generation

Beta Antagonists non sel

A

Cartelolol, Carvedolol, labetolol

121
Q

rd gen Selective

A

Betaxolol, Celiproplol, nevibolol

122
Q

Dont stop B locker quickly

A

when antagonist given-upregulation,\more endogenous ligand bound-reebound hypertension

123
Q

HYPERTENSION

A

Propranolol lowers blood pressure in hypertension
by several different mechanisms of action
• Decreased cardiac output is the primary
mechanism decreasing blood pressure
• Inhibition of renin release from the kidney
• No Angiotensin= no vasoconstrictor, No
aldosterone= no Na reabsorption, decreasing also
water=resulting to low blood volume
• Decreased sympathetic outflow from the CNS

124
Q

ISCHEMIC HEART DISEASE

A

• Reduce the frequency of angina episodes and
improve exercise tolerance in many patients with
angina
• These actions relate to the blockade of cardiac
receptors, resulting in decreased cardiac work and
reduction in oxygen demand
• Slowing and regularization of the heart rate may
contribute to clinical benefits

125
Q

CARDIAC ARRHYTHMIAS

A

D. CARDIAC ARRHYTHMIAS
• Effective in the treatment of both supraventricular
and ventricular arrhythmias
• By increasing the atrioventricular nodal refractory
period, antagonists slow ventricular response
rates in atrial flutter and fibrillation
• These drugs can also reduce ventricular ectopic
beats, particularly if the ectopic activity has been
precipitated by catecholamines
• Sotalol has antiarrythmic effects involving ionchannel blockade in addition to its β-blocking
action

126
Q

HEART FAILURE

A

HEART FAILURE
• Etoprolol, bisoprolol, and carvedilol – are effective
in reducing mortality in selected patients with
chronic heart failure
• Although administration of these drugs may
worsen acute congestive heart failure, cautious
long-term use with gradual dose increments in
patients who tolerate them may prolong life

127
Q

OTHER CARDIOVASCULAR DISORDERS

A

• Increase stroke volume in some patients with
obstructive cardiomyopathy
• Results from the slowing of ventricular ejection and
decreased outflow resistance
• Β-antagonists are useful in dissecting aortic
aneurysm to decrease the rate of development of
systolic pressure
• Also useful in selected at-risk patients in the
prevention of adverse cardiovascular outcomes
resulting from noncardiac surgery

128
Q

HYPERTHYROIDISM

A

In a patient with hyperthyroidism there is mainly a
presence of palpitations and tremors. Give
propranolol as treatmen

129
Q

ereeuced response to epine[hrine

A

Propanolol- non sel bronchocontriction

Pharmacology (19 decks)

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