SNS drugs Flashcards

1
Q

where are andrenergic receptors found

A
  1. CNS and SNS

2. presynaptically on neuron or post-synaptically on effector organ

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2
Q

where do catecholamines come from

A

synthesized from tyrosine in sympathetic nerve endings

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3
Q

what are drugs that turn on SNS

A
  1. sympathicomimetics

2. a or B angonists

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4
Q

what are drugs that turn off SNS

A
  1. sympatholytics

2. a or B blockers

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5
Q

what are receptor types for each SNSr

A

a1 - Gq and i/o
a2 - Gi/o
B - Gs

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6
Q

tissues for a1

A
  1. vascular smooth muscle
  2. GU and GI smooth muscle
  3. heart
  4. liver
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7
Q

tissues for a2

A
  1. pancreatic B cells
  2. platelets
  3. nerve
  4. vascular smooth muscles
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8
Q

actions of a1 agonists

A
  1. vasoconstriction
  2. increased vascular resistance
  3. enlarged pupils
  4. sphincter closure
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9
Q

actions of a2 agonists

A

inhibit cAMP

- inhibits Ca channels , NE release, Ach release, insulin release

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10
Q

tissues for B1

A
  1. heart

2. juxtaglomerular cells

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11
Q

tissues for B2

A
  1. bronchi
  2. skeletal muscle
  3. liver
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12
Q

tissues for B3

A
  1. adipose
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13
Q

actions of B1 agonists

A

Gs > cAMP> opening of Ca channel - contractions

  1. tachycardia
  2. myocardial contraction
  3. lipolysis
  4. renin release
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14
Q

actions of B2 agonists

A

Gs > cAMP > PKA phosphoylate MLCK > inactive > relax

  1. vasodilation
  2. decrease peripheral resistance
  3. bronchodilation
  4. glycogenolysis
  5. release of glucagon
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15
Q

3 potential actions of sympathomimetics

A
  1. direct action - stim G receptor
  2. indirect - affect synthesis, storage, release of actitivy
  3. mixed
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16
Q

what are direct acting sympathomimetics (2)

A
catechoamines 
1. rapid onset
2. breif action
3. paraenterally
non - catecholamines
17
Q

5 important catecholamines

A
  1. NE
  2. E
  3. dopa
  4. isoproterenol
  5. dobutamine
18
Q

where does NE act and what does it do (2)

A
  1. a>B1»B2,3
  2. increase MAP and PVR
  3. increase HR but reflex bradycardia
19
Q

where does E act and what does it do (2)

A
  1. low dose mostly B and high dose mostly a

2. increase inotropy and chronotropy (B1), bronchodilates (B2), hyperglycemia, drops peripheral resistance (B2)

20
Q

what does dopamine do

A
  1. vasodilates peripheral renal, mesenteric, coronary vascular beds via D1
  2. inhibs NE release
  3. at high does B1 effects the biggest
  4. at higher dose a1 is most - good for treatment of shock
21
Q

what are a1 agonists (phenyephrine) used for

A

treatment of shock, nasal decongestants

22
Q

what are a2 agonists (clonadine) used for

A

hypertension by acting on CNS to inhibit sympathetic output

  1. CNS - inhibits excitatory outflow
  2. peripheral - inhibits release of catecholamines
23
Q

what are B1 agonists (dobutamine) used for

A

increase cardiac output - ionotropic effects more significant

24
Q

what are B2 agonists (salbutamol) used for

A

aerosols for bronchodilation

25
Q

what is a non-seletive B agonist

A

isoproterenol

- most prominent effects are B, but rarely used because of lack of selectivity

26
Q

what does and indirect andrenergic agonist (amphetamine) do

A

reverses the vesicular monoamine transporter > more NE and dopa

  • vasoconstriction, MAP, ionotropy
  • wakefulness, euphoria, anxiety, hypertension
27
Q

what are mixed sympathomimetics

A

ephedrine and pseudoephedrine

- increase release of NE and stim a1, B1, B2

28
Q

2 classes of sympatholytics and examples

A
  1. direct - a and B blockers

2. indirect - decrease release, change storage, decrease synthesis

29
Q

2 types of a blockers

A
  1. reversible - can be displaced by agonists - phenotolamine, prazolin
  2. irreversible - covalent bond - phenoxybenzamine
30
Q

what do non-selective a blockers do

A
  • both a1 and a2
  • lower PVR and reflex tachycardia
  • more profound effects when standing
  • more NE released because of a2 blockade
31
Q

what do a1 selective blockers do

A
  • good for hypertension
  • lower PVR
  • fewer adverse effects
  • lower lipid levels
  • ___-zosins
32
Q

what do a1A selective blockers do

A
  • tamulosin

- treatment of BPH by causing vasodilation of the prostate vascular smooth muscle

33
Q

what are effects of non-selective B-blockers (propranolol)

A
  • lower ionotropy, chronotropy, CO, SA and AV activity

- brochoconstrict problematically

34
Q

what are B1 blockers good for

A

avoid bronchoconstriction

- metoprolol, atenolol, bisprolol