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ANS Flashcards

1
Q

How do muscarinic receptors act

A

they are G-protein coupled receptors

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2
Q

How to nicotinic receptors act

A

They are ion-channel mediated (increase Na+ movement into cells)

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3
Q

Types of nicotinic receptors

A

NM and NN

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4
Q

Effects of M2 receptors

A

Heart: reduce HR, FOC and CO

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5
Q

Effects of M3 receptors

A
  1. blood vessel: vasodilation and and decrease BP 2. smooth muscle: contraction–> broncospasm, diarrhea, urination 3. Pupil: miosis 4. Glands: increase salivation (increase lacrimation), sweating, gastric acid
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6
Q

M1 receptor type

A

Gq

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7
Q

Effector enzyme at Gq

A

Gq–>stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.

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8
Q

Effector enzyme at M1

A

Gq–>stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.

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9
Q

M3 receptor type

A

Gq

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10
Q

Effector enzyme at alpha 1

A

Gq–>stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.

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11
Q

Effector enzyme at M3

A

Gq–>stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.

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12
Q

alpha 2 receptor type

A

Gi

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13
Q

Gq second messenger

A

stimulates PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.

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14
Q

alpha 1 receptor type

A

Gq

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15
Q

beta 1 effector enzyme

A

Gs–>stimulate adenylyl cyclase–>increase cAMP

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16
Q

M2 receptor type

A

Gi

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17
Q

Gi effector enzyme

A

Gi–>inhibit adenylyl cyclase–>decrease cAMP

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18
Q

alpha 2 effector enzyme

A

Gi–>inhibit adenylyl cyclase–>decrease cAMP

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19
Q

Receptors that act via Gs

A

beta 1, beta 2, beta 3

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20
Q

M2 effector enzyme

A

Gi–>inhibit adenylyl cyclase–>decrease cAMP

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21
Q

beta 2 effector enzyme

A

Gs–>stimulate adenylyl cyclase–>increase cAMP

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22
Q

Receptors that act via Gq

A

M1, M3 & alpha 1

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23
Q

beta 1 receptor type

A

Gs

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24
Q

beta 2 receptor type

A

Gs

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25
Q

beta 3 receptor type

A

Gs

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26
Q

M1: 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

A
  1. Gq 2. Stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity. 3. Neurons 4. CNS effects
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27
Q

Receptors that act via Gi

A

alpha 2, M2

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28
Q

Effect of tyrosine hydroxylase

A

converts Tyrosine–>DOPA RATE LIMITING STEP in formation of Dopamine ADRENERGIC TRANSMISSION

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29
Q

NN receptor 1. location 2. type

A
  1. ANS ganglia & Adrenal Medulla 2. Na/K channel
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30
Q

alpha 2 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

A
  1. Gi 2. Inhibit adenylyl cyclase–>decrease cAMP 3. presynaptic neurons 4. reduces release of norepinephrine–>bradycardia & hypotension
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31
Q

M3: 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

A
  1. Gq 2. Stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity. 3/4. Smooth muscle and; glands: –>contraction (except in bv–>vasodilation–>decrease BP); diarrhea, bronchoconstriction, urination, increase secretions, salivation, stomach acid, sweating, lacrimation Pupil and ciliary muscle: contracts–>miosis; increase flow of aqueous humor
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32
Q

alpha 1 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

A
  1. Gq 2. Stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity.[3] In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity. 3/4. blood vessels–> vasoconstriction–>increase BP pupil (iris)–>dilation (mydriasis) smooth muscle–>sphincter contraction–>constipation & urinary retention
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33
Q

Metyrosine

A

inhibits tyrosine hydroxylase–>so it can’t convert tyrosine to DOPA AFFECTS ADRENERGIC TRANSMISSION Tyrosine is co-transorted into pre-synaptic nerve terminal with Na+

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34
Q

beta 3 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

A
  1. Gs 2. stimulate adenylyl cyclase–>increase cAMP 3. fat tissue 4. Lipolysis
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35
Q

Rate-limiting step for ACh synthesis

A

choline uptake

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36
Q

M2: 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

A
  1. Gi 2. Inhibit adenylyl cyclase–>decrease cAMP 3. Heart 4. reduces HR, FOC and CO
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37
Q

Receptor in adrenal medulla & response

A

NN–>secretion of Epi & NE

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38
Q

beta 3 effector enzyme

A

Gs–>stimulate adenylyl cyclase–>increase cAMP

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39
Q

Where you find NN

A

Adrenal medulla & autonomic ganglia

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40
Q

beta 2 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

A
  1. Gs 2. stimulate adenylyl cyclase–>increase cAMP 3/4. smooth muscles–> relaxation–>bronchodilation, urinary retention, constipation, uterus relaxation liver–> heart–>
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41
Q

beta 1 1. receptor type 2. effector enzyme & second messenger 3. location 4. effects

A
  1. Gs 2. stimulate adenylyl cyclase–>increase cAMP 3. heart 4. contraction, increased HR increases renin release & juxtaglomeruluar apparatus
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42
Q

Reserpine

A

inhibits uptake of dopamine into vesicles (inhibits storage) AFFECTS ADRENERGIC TRANSMISSION

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43
Q

Bretylium

A

inhibits VAMPs & SNAPs which enable vesicles containing NE/ATP/E to bind to membrane & release–>inhibits release AFFECTS ADRENERGIC TRANSMISSION

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44
Q

Guanethidine

A

inhibits VAMPs & SNAPs which enable vesicles containing NE/ATP/E to bind to membrane & release–>inhibits release AFFECTS ADRENERGIC TRANSMISSION

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45
Q

cocaine

A

inhibits reuptake of messengers (NE/E/Dopamine) AFFECTS ADRENERGIC TRANSMISSION

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46
Q

Tricyclic antidepressants

A

inhibits reuptake of messengers (NE/E/Dopamine) AFFECTS ADRENERGIC TRANSMISSION

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47
Q

Where does NE work

A

at presynaptic alpha 2 (autoreceptors) & at postsynaptic alpha 1 receptors

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48
Q

Hemicholinium

A

AFFECTS CHOLINERGIC TRANSMISSION inhibits uptake of Choline into presynaptic nerve terminal (co-transorter with Na+); RATE-LIMITING STEP

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49
Q

Vesamicol

A

AFFECTS CHOLINERGIC TRANSMISSION inhibits storage of ACh in the presynaptic nerve terminal (ACh can’t be properly taken up & stored in vesicles)

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50
Q

Botulinum

A

AFFECTS CHOLINERGIC TRANSMISSION inhibits release of ACh (vesicles can’t properly dock & release)

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51
Q

rate limiting step for catecholamine synthesis

A

tyrosine hydroxylase

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52
Q

Cholinergic neurotransmission is terminated by

A

AChE

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53
Q

Adrenergic neurotransmission is terminated by

A

reuptake

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54
Q

DAG function

A

modulates action of protein kinase C

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55
Q

Myasthenia Gravis Symptoms; Dx; what makes it worse?

A

autoimmune disorder that involves antibody mediated disruption of NMJ receptors Production of antibodies that decreases the number of functional nicotinic receptors on the muscle end plates Sx: transient weakness with ptosis, diplopia, difficulty speaking, swallowing & extremity weakness. Severe disease may affect all muscles including those used in respiration infection and thyroid dysfunction worsen the symptoms Dx = blood ACh receptor antibody level

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56
Q

result of IP3

A

IP3–>Ca2+ release from intracellular storage–>smooth muscle contraction

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57
Q

Somatic nervous system receptors & are they cholinergic or adrenergic

A

NM–>cholinergic

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58
Q

Cholinergic nerves

A
  1. all nerve fibers in somatic nervous system = NM 2. All PRE-ganglionic fibers in ANS (SYMPATHETIC & PARASYMPATHETIC) = NN 3. All POSTganglionic fibers in PARAsympathetic nervous system = M1-3
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59
Q

Effect of acetylcholine

A

DUMBBELSS: D=diarrhea (Smooth muscle contraction & sphincter relax) U=urination (Smooth muscle contraction & sphincter relax) M=miosis (pupil & ciliary muscle contraction*) B=bradycardia (reduce HR, FOC, CO & vasodilation reduces BP) B=bronchoconstriction (Smooth muscle contraction) E=excitation of skeletal muscle L=lacrimation S=secretion S=sweating Sphincters: relaxation smooth muscle contraction EXCEPT in bv->VASODILATION *use for near vision

60
Q

M3 location & effects

A
  1. smooth muscles (GIT, Bronchial, detrussor): contraction–>diarrhea, bronchoconstriction & urination. EXCEPT BV–>vasodilation–>decrease BP due to release of NO 2. Glands–> increase salivation, lacrimation, sweating, gastric acid 3. Pupil–> Miosis–>increase outflow of aqueous humor–>decrease IOP 4. Ciliary Muscle–>contraction 5. Trigone & sphincters–>relaxation–>urination
61
Q

Indirect Cholinergic Agonists

A

act by inhibiting metabolism of ACh–>increases concentration in synapse–>increases action of ACh

62
Q

Direct Cholinergic agonists examples

A
  1. Acetylcholine (B) 2. Bethanechol (M) 3. Pilocarpine (naturally occurring alkaloid; M) 4. Carbachol (like bethanechol, M&N) 5. Methcholine 6. Nicotine (like pilocarpine, N) Direct cholinergic agonists = bind directly to cholinergic receptors
63
Q

Indirect Cholinergic Agonist Examples

A
  1. Neostigmine (B) 2. Physostigmine (B) 3. Pyridostigmine (B) 4. Edrophonium (B) 5. Tacrine, Donepezil (B) 6. Ecothiophate (B) 7. Malathion, Parathion, Sarin (B) 1-5 are used to treat Myasthenia Gravis, Alzheimers & Glaucoma
64
Q

Woman with: -dry skin. -tiredness and fatigue – which are common and can lead to total exhaustion. -muscle pain. -joint pain, stiffness and swelling. -vasculitis (inflammation of blood vessels)

A

Sjorgens syndrome

65
Q

Acetylcholine

A
  1. Direct Cholinergic Agonist 2. both Muscarinic & nicotinic actions 3. bc of non-specific actions & rapid inactivation by acetylcholinesterase, this drug has no clinical use 4. Vasodilation by ACh is due to the release of EDRF (endothelium derived relaxing factor, aka NO)
66
Q

Bethanechol DOA; Uses; MOA

A
  1. Direct Cholinergic Agonist 2. strong muscarinic action & little or no nicotinic action 3. orally active, poor lipid solubility 4. DOA = 30m-2h Therapeutic uses: 1. paralytic ileus 2. non-obstructive urinary retention (ie post-op) MOA = stimulates M3 receptors–>increase bowel movements & bladder contraction no N effects
67
Q

DOC for treating paralytic ileus or non-obstructive urinary retention

A

Bethanechol

68
Q

Pilocarpine Uses; DOA

A
  1. alkaloid 2. Has mucarinic activity only 3. lipid-soluble & penetrates cornea very well 4. DOA = 30m-2h 5. Therapeutic Uses: 1. Glaucoma: due to increased intraocular tension 2. Sjorgens syndrome: chronic, inflammatory autoimmune disorder characterized by dry mouth (xerostomia) & dry eye (keratoconjunctivitis sicca. Works to control these symptoms
69
Q

Drug used to reduce dry mouth

A

Pilocarpine

70
Q

Drug used to treat Sjorgens syndrome

A

Pilocarpine

71
Q

Reversible Indirect acting Cholinergic agonists

A
  1. Neostigmine 2. Physostigmine 3. Pyridostigmine 4. Edrophonium 5. Tacrine–used to treat alzheimers 6. Donepezil–used to treat alzheimers These are all short-acting & the enzyme is reactivated and hydrolyzes ACh as usual
72
Q

Irreversible Indirect acting Cholinergic agonists

A
  1. Ecothiophate–used to treat glaucoma 2. Malathion 3. Parathion 4. Sarin These are all long-acting; enzyme reactivation takes extremely long time or almost doesn’t take place–>persistent action of ACH in body Ecothiophate is the only one used therapeutically; the rest are insecticides or war gases
73
Q

Physostigmine: Use; MOA

A

tertiary amine; lipid soluble–>good eye penetration & CNS penetration; used to treat Glaucoma MOA = reversible inhibition of AChE–> increase ACh Used as a TOPICAL treatment in Glaucoma; Causes miosis–>increases outflow of aqueous humor–>decreases IOP reverses the central & peripheral signs of muscarinic blockade

74
Q

Neostigmine

A

quatrenary amine; lipid INSOLUBLE, NOT used to treat Glaucoma

75
Q

transient weakness with ptosis, diplopia, difficulty speaking, swallowing & extremity weakness

A

symptoms of myasthenia gravis Dx = blood ACh receptor antibody level

76
Q

Tx of Myasthenia Gravis

A
  1. AChE inhibitors: Neostigmine, pyridostigmine, edrophonium (these are all reversible) 2. immunosuppressants & corticosteroids 3. Thymectomy (bc thyroid dysfunction worsens symptoms)
77
Q

Neostigmine: use; method given

A

Reversible AChE Inhibitor used in acute cases of myasthenia gravis; given via IV

78
Q

Pyridostigmine: use; method given

A

Reversible AChE Inhibitor; has a longer duration of action than neostigmine, so good for maintenance/long term therapy in myasthenia gravis. 2. Given orally

79
Q

Edrophonium: use

A

Reversible AChE Inhibitor; shortest acting for 5 minutes 2. used in diagnosis of M. Gravis & to differentiate myasthenic & cholinergic crisis by doing a Tension test.

80
Q

Myasthenic Crisis

A

if drug therapy is inadequate patients develop severe muscle weakness

81
Q

Cholinergic crisis

A

if excessive amounts of drugs have been used, patients will become paradoxically weak because of nicotinic depolarizing blockade of motor end plate

82
Q

Tensilon test

A

Used to differentiate myasthenia crisis from Cholinergic crisis. small doses of edrophonium (1-2mg IV) will produce NO RELIEF or even WORSEN weakness if the patient is receiving EXCESSIVE AChE Inhibitor therapy = cholinergic crisis patient will improve with edrophonium if has myasthenic crisis–> may be indication for increase in AChE inhibitor dosage

83
Q

Patient with severe muscle weakness improves with edrophonium given by IV

A

Patient had myasthenia crisis–> may be indication for increase in AChE inhibitor dosage

84
Q

Patient with severe muscle weakness has no relief when edrophonium given by IV; may even have worsening of symptoms

A

patient had cholinergic crisis

85
Q

Alzheimers Disease

A

progressive disorder involving neural degeneration in the cortex leading to a marked loss of memory & of the ability to carry on ADL; MCC of degenerative dementia mostly due to loss of cholinergic neurons, thus mainstay of treatment is ACh therapy; Cause unknown Tx: AChE Inhibitors like Tacrine, Rivastigmine & Donepezil

86
Q

Tx for OP Poisoning

A
  1. Atropine: muscarinic receptor blocker (Anticholinergic drug) given via IV large doses until you observe mydriasis, tachycardia, & dryness of mouth Can’t control the nicotinic effects of OP poisoning, just blocks the muscarinic receptor) Also doesn’t have any role in reversing the CNS effects of OP poisoning 2. Pralidoxime (2-PAM): AChE reactivator; acts by hydrolyzing (reactivating) the drug bound enzyme. Should be given as early as possible, before “aging of the enzyme” OP antagonist.
87
Q

Treatment for Alzheimers

A

AChE Inhibitors like Tacrine, Rivastigmine & Donepezil

88
Q

Tacrine

A

AChE inhibitor used to treat Alzheimers (mostly due to loss of cholinergic neurons)

89
Q

Rivastigmine

A

AChE inhibitor used to treat Alzheimers (mostly due to loss of cholinergic neurons)

90
Q

Donepezil

A

AChE inhibitor used to treat Alzheimers (mostly due to loss of cholinergic neurons)

91
Q

fasciculations followed by paralysis

A

nicotinic toxicity

92
Q

Miosis, blurred vision, bradycardia, salivation, sweating, urination, bronchial constriction, vomiting, diarrhea

A

symptoms of organophosphate poisoning; mainly due to stimulation of muscarinic receptors Due to phosphorylation (irreversible inhibition) of the enzyme resulting in excess ACh

93
Q

3 cardinal signs of atropinization

A

mydriasis, tachycardia & dry mouth

94
Q

Pralidoxime (2-PAM)

A

AChE reactivator; acts by hydrolyzing (reactivating) the drug bound enzyme. Should be given as early as possible, before “aging of the enzyme” OP antagonist.

95
Q

Atropine

A

muscarinic receptor blocker (Anticholinergic drug) given via IV large doses to treat OP poisoning until you observe mydriasis, tachycardia, & dryness of mouth Can’t control the nicotinic effects of OP poisoning, just blocks the muscarinic receptor) Also doesn’t have any role in reversing the CNS effects of OP poisoning

96
Q

Features of toxicity of cholinergic drugs (OP poisoning)

A

DUMBBELSS D=diarrhea, abdominal cramps, vomiting (Muscarinic) U=urination (Muscarinic) M=miosis (Muscarinic) B=bradycardia (Muscarinic) B=bronchospasm (Muscarinic) E=excitation of skeletal muscle (Nicotinic)* L=lacrimation (Muscarinic) S=salivation (Muscarinic) S=sweating (Muscarinic) *Atropine can’t fix nicotinic symptoms bc just blocks muscarinic receptor

97
Q

methacholine challenge test

A

primarily used to diagnose bronchial hyperreactivity = hallmark of asthma & occurs in COPD subject inhales aerosolized methacholine–>bronchoconstriction other therapeutic uses are limited by its adverse cardiovascular effects = bradycardia & hypotension (bc it’s a cholinomimetic)

98
Q

Use of Edrophonium

A

diagnosis of M. gravis

99
Q

Use of neostigmine

A

Tx of M. gravis acts on cholinesterase; N&M effects

100
Q

43 yo unable to continue picking vegetables: unsteady gait, difficulty speaking, swallowing, blurry vision, watery eyes, tightness in chest–>difficulty breathing

A

OP poisoning irreversibly inhibits AChEsterase–>increase in ACh Tx with atropine & 2-PAM

101
Q

Use of pyridostigmine

A

Tx of M. gravis

102
Q

Use of Physostigmine

A

glaucoma & atropine overdose

103
Q

Malathion, paration

A

used as insecticides parathion more toxic than malathion. Very lipid soluble & rapidly absorbed through lungs & skin

104
Q

Drugs used to treat paralytic ileus

A

bethanechol & neostigmine

105
Q

causes miosis (constriction of pupillary sphincter m)

A

M3

106
Q

opposite of M3 in the blood vessel is

A

alpha 1

107
Q

increases outflow of aqueous humor–>decreases IOP

A

M3

108
Q

causes accommodation (contraction of ciliary muscle) for near vision

A

M3

109
Q

causes mydriasis (pupillary sphincter relaxation)

A

alpha 1

110
Q

causes urinary retention via sphincter contraction

A

alpha 1

111
Q

opposite of M3 in the pupil is

A

alpha 1

112
Q

reduces release of NE & consequences

A

alpha 2–>bradycardia, hypotension, also causes inhibition of liplysis in fat cells

113
Q

results in bronchodilation

A

beta 2

114
Q

results in bronchospasm

A

M3

115
Q

What happens when you increase IP3 & DAG?

A

Gq–>stimulate PLC–>increase IP3 & DAG–> Increase Ca++ DAG remains bound to the membrane, and IP3 is released as a soluble structure into the cytosol. IP3 then diffuses through the cytosol to bind to IP3 receptors, particularly calcium channels in the smooth endoplasmic reticulum (ER). This causes the cytosolic concentration of calcium to increase, causing a cascade of intracellular changes and activity. In addition, calcium and DAG together work to activate protein kinase C, which goes on to phosphorylate other molecules, leading to altered cellular activity.

116
Q

what’s the consequence of aldosterone secretion

A

aldosterone–>kidney tubules to increase sodium & water reabsorption–>increase in blood volume–>increase in BP

117
Q

Opposite of M2 in the heart is

A

beta 1

118
Q

opposite of M3 in smooth muscle is

A

beta 2

119
Q

opposite of M3 in sphincters is

A

alpha 1

120
Q

receptors found on blood vessels

A

M3 & alpha 1

121
Q

receptors found in smooth muscle

A

M3 & beta 2

122
Q

receptors found in sphincters

A

M3 & alpha 1

123
Q

receptors found in pupils

A

M3 & alpha 1

124
Q

receptors found in glands

A

M3

125
Q

Receptors found in the heart

A

M2 & beta 1

126
Q

D1 receptor 1. location 2. MOA 3. effect

A
  1. smooth muscle 2. Gs–> increase cAMP 3. relaxes renal vascular smooth muscle
127
Q

Reflex response to a drop in blood pressure how can you block this response?

A

increase in sympathetic outflow (–>increase in HR and FOC; from beta 1) and increase renin release (from beta 1; –> increase salt and water retention) and decrease in parasympathetic you can block this with ganglion-blocking drugs i.e. hexamethonium

128
Q

what happens in juxtaglomerular cells when renal blood flow decreases

A
  1. JG cells convert prorenin (found in blood) to renin and secrete it into circulation 2. renin converts angiotensinogen (secreted by liver) to angiotensin 1 3. AT1–>AT2 by ACE (found in lungs) 4. AT2–> BV constriction–>increase in BP 5. AT2 also stimulates secretion of aldosterone from the adrenal cortex 6. aldosterone–>kidney tubules to increase sodium & water reabsorption–>increase in blood volume–>increase in BP
129
Q

DAG modulates

A

DAG modulates action of PKC

130
Q

IP3 leads to

A

IP3–>Ca2+ release from intracellular storage–>sm contraction

131
Q

from where is angiotensinogen secreted?

A

liver

132
Q

where is ACE found

A

lungs

133
Q

what does AT2 do?

A
  1. AT2–>BV constriction–>increase in BP 2. AT2 also stimulates secretion of aldosterone from the adrenal cortex)
134
Q

from where is aldosterone secreted?

A

adrenal cortex (AT2 also stimulates secretion of aldosterone from the adrenal cortex)

135
Q

In ANS preganglionic fibers, ACh acts through ___ receptors?

A

Nn

136
Q

does neostigmine have nicotinic, muscarinic or both activity

A

both (all indirect, reversible cholinergic agonists do)

137
Q

drug used to treat atropine overdose

A

physostigmine

138
Q

D1 receptor location

A

smooth muscle

139
Q

D2 receptor location

A

nerve endings

140
Q

beta 2 affect on the human liver

A

activates glycogenolysis

bc increases pancreas insulin secretion

141
Q

alpha 2 affect on fat cells

A

inhibition of lipolysis

142
Q

alpha 1 affect on the prostate

A

causes contraction in ductus deferens and seminal vesicles –>ejaculation

143
Q

alpha 2 affect on vascular smooth muscle in the nasal mucosa

A

nasal decongestion

144
Q

beta 2 affect on skeleton muscle

A

promotes potassium uptake

also causes vasodilation of the vascular beds in skeletal muscle which –> decrease in TPR

145
Q

2 ways in which adrenergic system can affect PVR

A
  1. alpha 1–>vasoconstriction–>increases TPR–> increases BP
  2. beta 2–>vasodilation–> decreases TPR–> decreases BP
146
Q

receptors that act on fat cells and their actions

A

beta 3: activates lipolysis

alpha 2: inhibites lipolysis

Pharm (32 decks)

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