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Cardio Exam 1 > B-adrenergic Receptor Antagonists HTN > Flashcards

B-adrenergic Receptor Antagonists HTN Flashcards

1
Q

Define Sympathetic Adrenergic nervous System

A

Increases the bodies readiness for strenuous muscular activity and “fight or flight reaction”

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2
Q

SNS can make what kind of changes?

A

Increase arterial pressure, heart rate, cardiac output, blood flow to muscles and heart, respiration, oxygen consumption, blood glucose levels, glycolysis in liver and muscles and mental activity
Decreased blood flow to GI and kidneys

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3
Q

Main effectors of the SNS are?

A

NE and Epinephrine

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4
Q

Define NE

A

Synthesized in sympathetic nerve terminals and CNS as a neurotransmittor

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5
Q

Define Epi

A

Synthesized in adrenal medulla Chromaffin cells as a hormone and in CNS as a neurotransmitter

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6
Q

Who is Otto Loewi?

A

Father of neuroscience

Believe in neurotransmitters not electrical impulses

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7
Q

How do you make NE and Epi?

A

Tyrosine via tyrosine hydroxylase → DOPA via DOPA decarboxylase → Dopamine via dopamine beta hydroxylase→ NE via PNMT→ Epi

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8
Q

What is the rate limiting step of NE and Epi creation?

A

Tyrosine → DOPA via tyrosine hydroxylase

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9
Q

Where does the synthesis of NE and Epi occur?

A

Inside the sympathetic nerve terminal

Tyrosine has to come in via transporters

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10
Q

Release, action and termination of NE

A

NE is released into the synaptic cleft and binds to B1 or a1 on the postsynaptic cleft, uptaken by the postsynaptic cleft, bind to a2 or B2 or be reuptaken by receptor on the presynaptic cleft

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11
Q

NE binding to B2 stimulates?

A

Release more NE

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12
Q

NE binding to a2 stimulates?

A

Stop releasing NE

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13
Q

NE that is taken back up into the presynaptic cleft?

A

Either is recycled and used again or inactivated by MAO and released as metabolites

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14
Q

NE that is taken up into the post-synaptic cleft?

A

Is inactivated via COMT to normetanephrine and released to diffuse out

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15
Q

Alpha 1 Receptors

A

Post-synaptic

Coupled to Gq which increases stuff

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16
Q

Alpha 2 Receptors

A

Pre-synaptic

Coupled to Gi which decrease cAMP

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17
Q

Beta 1 Receptors

A

Post-synaptic

Myocardium

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18
Q

Beta 2 Receptors

A

Can be Pre or post-synaptic

SM

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19
Q

NE prefers?

A

Alpha receptors

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20
Q

Epi prefers?

A

Beta receptors

21
Q

NE and Epi can?

A

Bind to all 5 receptors

22
Q

Beta 3 Receptors

A

Adipose tissue

23
Q

All beta receptors are coupled to?

A

Gs which increased cAMP

24
Q

Alpha 1 Adrenoceptors expression and effects?

A

Blood vessels (arteries and veins) cause vasoconstriction and kidneys help with Na reabsorption

25
Q

Beta 1 Adrenoceptors expression and effects?

A

Heart cause + chrono, dromo and inotropic effects and juxtaglomerular cells in kidney causing renin release

26
Q

Beta 2 Adrenoceptors expression and effects?

A

SM of arterioles: vasodilation
Bronchial SM: dilation and increased secretion
Skeletal muscles and liver cells: glycogenolysis and gluconeogenesis
Ciliary muscle: relaxation and intraocular pressure

27
Q

Beta 3 Adrenoceptors expression and effects?

A

Adipocytes: lipolysis

28
Q

Renin does what?

A

Increase BP

29
Q

Beta-Adrenoceptor Antagonists 1st Generation

A

Non-selective B1 and B2 antagonists

30
Q

Beta-Adrenoceptor Antagonists 2nd Generation

A

Selective B1 Antagonists

31
Q

Beta-Adrenoceptor Antagonists 3rd Generation

A

Non-selective and selective Beta antagonists with additional effects

32
Q

Beta-Adrenoceptor Antagonists Site of Action

A

Cardiovascular system

Profound effect when sympathetic activity is high (HTN, stress, exercise)

33
Q

Beta-Adrenoceptor Antagonists Chronotropic effect

A

Decreased heart rate

34
Q

Beta-Adrenoceptor Antagonists Ionotropic effect

A

Decreased contractile force

35
Q

Beta-Adrenoceptor Antagonists Chronotropic + Ionotropic effect =

A

Decrease cardiac output

36
Q

Short term effect of non-selective beta-blockers?

A

Decrease cardiac output → decrease BP → reflector sympathetic activation → increase NE/Epi → activation of alpha receptors → increased peripheral resistance

37
Q

Long term effect of non selective beta blockers

A

Peripheral resistance returns to initial values and CO continues to be lowered

38
Q

Beta-Adrenoceptor Antagonists Dromotropic effect

A

Decrease cardiac rhythm and automaticity which reduce sinus rate, decreases automaticity, slow conduction velocity in AV node and increased AV node refractory period
All of which decreases CO

39
Q

Beta-Adrenoceptor Antagonists in HTN patients

A

Reduction of CO (Beta1)

Inhibition of renin release (Beta1)

40
Q

Beta-Adrenoceptor Antagonists in the respiratory system?

A

Bronchoconstriction and decrease secretion from bronchial glands
(non-selective blockers via B2 blockade)

41
Q

Beta-Adrenoceptor Antagonists in the eyes?

A

Reduction of intraocular pressure (non-selective blockers via B2 blockade)

42
Q

Beta Adrenoceptors Antagonists in Energy metabolism and endocrine systems?

A

Decrease glycogenolysis and gluconeogenesis (non-selective blockers via B2 blockade) –> delayed recovery from hypoglycemia
WATCH IN DIABETES PTS

43
Q

Beta Adrenoceptors Antagonists Uses?

A 
HTN
Angina pectoris
Cardiac arrhthmias
MI
Glaucoma
Migraine prophylaxis
44
Q

Beta Adrenoceptors Antagonists Name

A

End in -olol

45
Q

Beta Adrenoceptors Antagonists Adverse Reactions in CV?

A

Worse heart failure
Induce life-threatening arrhthmias
Worsen symptoms of peripheral vascular disease
Sexual dysfunction

46
Q

Beta Adrenoceptors Antagonists Abrupt discontinuation can induce?

A

Angina pectoris (myocardial ischemia) and increase the risk of death

47
Q

Beta Adrenoceptors Antagonists Adverse Pulmonary Effects?

A

Worsen problems in asthma or COPD

48
Q

Beta Adrenoceptors Antagonists Adverse CNS Effects

A

Sedation, sleep disurbances and depression

49
Q

Beta Adrenoceptors Antagonists Adverse Metabolic effects

A

Mask hypoglycemia-induced tachycardia in diabetes

Increase plasma levels of TGs

Cardio Exam 1 (7 decks)

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