PNS General + Cholinergic Flashcards

Question

PNS cholinergic receptor: Nn

Answer 1

1. Tissue: Autonomic ganglia Response: Depolarizes postsynaptic neurons 2. Tissue: Adrenal medulla Response: Depolarizes medullary cells → secretion of catecholamines For both: Mechanism: Opens Na+/K+ channels →depolarization

Answer 2

Mechanism: ↑ PLC → ↑ IP3, DAG, Ca++ 1. Tissue: Smooth muscle (eye, vascular, urogenital, hair follicles) Response: Contracts smooth muscle (Increase BP, or keep it up enough to perfuse) 2. Tissue: Liver Response: ↑ Glycogenolysis, gluconeogenesis

Answer 3

Mechanism: ↓ AC → ↓ cAMP; ↑ K+ channel efflux (via Gβγ); ↓ L- and N type Ca++ channel influx; ↑ PLC → ↑ IP3, DAG, Ca++ 1. Tissue: Axon terminals (autoreceptors) Response: ↓ NE release 2. Tissue: Pancreatic b cells Response: ↓ Insulin release 3. Tissue: Vascular smooth muscle Response: Contracts smooth muscle (Increase BP, or keep it up enough to perfuse) 4. Tissue: Platelets Response: Aggregation

Answer 4

Mechanism: ↑ AC → ↑ cAMP → ↑ PKA →↑ L-type Ca++ channel influx 1. Tissue: Heart Response: ↑ Heart rate, conduction velocity, contractility 2. Tissue: Kidney (juxtaglomerular cells) Response: ↑ Renin release

Answer 5

Mechanism: ↑ AC → ↑ cAMP; in smooth muscle, inhibits MLCK → ↓ myosin-PO4 → relaxation 1. Tissue: Smooth muscle (eye, bronchioles, GI, urogenital, vascular) Response: Relaxes smooth muscle 2. Tissue: Heart Response: ↑ Heart rate, contractility 3. Tissue: Liver and skeletal muscle Response: ↑Glycogenolysis, gluconeogenesis (liver) 4. Tissue: Pancreatic b cells Response: ↑ Insulin release

Answer 6

Tissue: Lipocytes Response: activates lipolysis

Answer 7

Tissue: Vascular smooth muscle, especially renal vasculature Response: Dilates blood vessels, increasing RBF thus increasing GFR Mechanism: ↑ AC → ↑ cAMP

Answer 8

Tissue: Axon terminals (autoreceptors) and Cholinergic neurons in the gut Response: ↓ DA release ↓ GI motility Mechanism: ↑ AC → ↑ cAMP; ↑ K+ efflux; ↓Ca++ influx

Answer 9

``` 1. Iris circular muscle 􀁺 M3 activation → muscle contraction → miosis 􀁺 β2 activation → muscle relaxation → mydriasis (slight effect) -eases the way for a1 ``` 2. Iris radial muscle 􀁺 α1 activation → muscle contraction →mydriasis

Answer 10

1. Ciliary smooth muscle: 􀁺 M3 activation → muscle contraction → relaxes ligament → accommodation for near vision (rest and read) 􀁺 β2 activation → muscle relaxation → stretches ligament (slight effect) -flat lens for distance sight

Answer 11

1. Lacrimal glands | 􀁺 M3 (ACh) activation → lacrimation

Answer 12

``` 1. Bronchial smooth muscle 􀁺 M3 activation → muscle contraction → bronchoconstriction 􀁺 β2 activation → muscle relaxation → bronchodilation ``` ``` 2. Bronchial glands 􀁺 M3 activation → mucous secretion 􀁺 β2 activation → watery secretion via CFTR activation ```

Answer 13

``` 􀁺 Vagal Tone: M2 activation → bradycardia (SA node), ↓ AV node conductivity, ↓ atrial contractility *only in atria *overall relaxing effect ``` 􀁺 β1 and β2 activation → tachycardia (SA node), ↑ AV node automaticity and conductivity, ↑ His-Purkinje automaticity and conductivity, ↑ ventricular automaticity and contractility

Answer 14

􀁺 M3 activation (endothelial cells) → relaxation → ↓ blood pressure 􀁺 α1 and α2 activation (smooth muscle cells) → constriction → ↑ blood pressure 􀁺 β2 activation (liver and skeletal muscle) → relaxation → ↓ TPR → ↑ blood flow to these tissues 􀁺 D1 activation → dilation of renal arteries and arterioles → ↑ renal blood flow

Answer 15

Overall ACh relaxes the heart * Decreased cAMP results in less current through If (I funny) * decreases rate of depolarization * leads to slowed HR • ACh binds to M2R and then Beta gamma subunits act upon Ik to activate it and more K+ leaves the cell and causes hyperpolarization-->relaxing effect Decreased PKA-->decreased Phosphorylation of L-Ca2+ channels--> decreased contractility-->conduction-->Heart rate

Answer 16

Excitatory: Gprotein Increases cAMP activates PK PK phosphorylates L-type Ca2+ channel Increases HR, conduction velocity, force of contraction

Answer 17

1. Innervated by the SYMPATHETIC NS 2. Not innervated by parasymp. 3. Although no neurons, ACh still has influence 4. Because there is ChAT activity on vasculature allowing for local production of ACh 5. May perhaps be stretch activated

Answer 18

1. Rest: only NE - alpha-1 Receptors for NE control - vasoconstriction of vascular SMCs - this is balanced with vasodilation from ACh MR action on endothelial cells 2. Flight: Epi -B2 receptors in liver and skeletal muscle cause relaxation -↓ TPR → ↑ blood flow to these tissues

Answer 19

1. M3 activation → contraction of circular and longitudinal muscles in intestinal walls → ↑ motility 2. α1 and β2 activation → muscle relaxation→ ↓ motility 􀁺 In GI smooth muscle, hyperpolarization and relaxation is caused by activation of calcium-dependent K+ efflux channels

Answer 20

􀁺 M3 activation → relaxation | 􀁺 α1 activation → contraction

Answer 21

1. M3 activation → ↑ acid secretion from parietal cells, ↑ secretions from gastric and intestinal glands, gall bladder contraction 􀁺 β2 activation → ↓ gastric acid secretion, relaxes gall bladder, ↑amylase secretion (want more free glucose)

Answer 22

1. • M3 (ACh) receptors of the PNS are in the glands of the mucosa and submucosa, and in the circular and longitudinal muscle ◦ promotes peristalsis 2. SNS receptors (adrenergic) are in the circular and longitudinal muscle

Answer 23

􀁺 D1 activation → vasodilation → ↑ blood flow, GFR 􀁺 β1 activation → stimulates renin release from kidney 􀁺 M3 activation → contraction of bladder detrusor, relaxation of trigone and sphincter → promotes urination 􀁺 β2 activation → relaxes detrusor → urinary retention 􀁺 α1 activation → constricts trigone and sphincter → urinary retention

Answer 24

**Rare example of SNS and PSNS working together to stimulate! 􀁺 M3 activation → relaxation of vessels → erection 􀁺 α1 activation → contraction of seminal vesicles, prostatic capsule, vas deferens → ejaculation

Answer 25

1. Nonpregnant: β2 activation → relaxes uterus 2. Pregnant ***Rare example of SNS and PSNS working together to stimulate! 􀁺 M3 activation → contracts uterus 􀁺 α1 activation → contracts uterus 􀁺 β2 activation → relaxes uterus

Answer 26

1. M3 activation → stimulates watery secretions from salivary, nasopharyngeal, pulmonary, gastrointestinal, and eccrine sweat glands 2. α1 activation → stimulates secretion from apocrine sweat glands found in axillary and pubic regions; produces viscous salivary secretions

Answer 27

􀁺 α2 activation → ↓ insulin release from pancreatic b cells 􀁺 β2 activation → promotes glycogenolysis and gluconeogenesis in liver, glycogenolysis and K+ uptake in skeletal muscle, ↑ insulin release from pancreatic β cells -Want glucose available and insulin so skeletal muscles can take glu in 􀁺 β3 activation → stimulates lipolysis in adipocytes

Answer 28

Mainly run on ACh except vasculature. Overall body is under the control of the PSNS

Answer 29

Sympathetic (adrenergic)

Answer 30

Sympathetic (cholinergic)

Answer 31

Parasympathetic (cholinergic

Answer 32

Parasympathetic (cholinergic

Answer 33

Parasympathetic (cholinergic

Answer 34

Parasympathetic (cholinergic

Answer 35

Parasympathetic (cholinergic

Answer 36

Parasympathetic (cholinergic

Answer 37

􀁺 Prepares for strenuous activity, mobilizes energy stores (fight or flight) 􀁺 Widespread output 􀁺 ↑ Pupil diameter, ↑ respiration, ↑ heart rate, ↑ blood pressure, ↓ GI motility and secretions, ↓ urination, ↑ sweating

Answer 38

􀁺 Accumulation and conservation of energy (rest and digest) 􀁺 Discrete output 􀁺 Maintenance functions during periods of minimal activity 􀁺 ↓ Pupil diameter, accommodation for near vision, ↑ lacrimation, ↓ respiration, ↓ heart rate, ↓ blood pressure, ↑ GI motility and secretions, ↑ urination

Answer 39

􀁺 Cholinomimetic drugs: drugs that mimic ACh activity 􀁺 Cholinolytic drugs: drugs that inhibit ACh activity

Answer 40

􀁺 Muscarinic agonists: M receptor agonists 􀁺 Nicotinic agonists: N receptor agonists 􀁺 Drugs that slow the inactivation of ACh by blocking AChE

Answer 41

􀁺 Muscarinic antagonists: M receptor antagonists 􀁺 Nicotinic antagonists: N receptor antagonists 􀁺 Drugs that speed the inactivation of ACh by activating AChE

Answer 42

M3 agonism would exacerbate these conditions! ``` 􀁺 Acute cardiac failure; bradycardia -ACh slows HR 􀁺 Asthma -ACh causes vasoconstriction 􀁺 Hyperthyroidism -they increased sensitivity to catecholamines 􀁺 Peptic ulcer -ACh causes increased secretions 􀁺 Urinary tract obstruction 􀁺 Parkinsonism ```

Answer 43

-dysjunction between DA and ACh control in the basal ganglia ◦ decreased DA function ◦giving a cholinimimetic is like ACh running unrestrained and w/muscarinic receptor activation you can increase this

Answer 44

Chronic dry mouth due to autoantibodies against salivary glands

Answer 45

1. Open: Too much aqueous humor being produced 2. Closed: Angle is small but production may be normal Either condition , miosis (thus opening of the angle) is beneficial

Answer 46

``` 1. SImple Alcohols Quaternary amine -they're simple competitive inhibitors that drift in and out over time -Drug: edrophonium ``` 2. carbamic Acid Esters - covalently bonds but the bond is hydrolyzed water over time - Drugs: Neostigmine, Physostigmine 3. Organophosphates - Covalently bonds and modifies AChE

Answer 47

􀁺 “Irreversible” cholinesterase inhibitors covalently bind to AChE 􀁺 R groups may be alkyl, alkoxy, aryloxy, amido, and others 􀁺 X is the leaving group and can be halogen, cyano, thiocyanate, phenoxy, thiocholine, carboxylate, and others 􀁺 Uses: glaucoma, insecticides, nerve gases

Answer 48

• permanent phosphorylation of the serine in AChE-only one drug can reverse this (pralidoxime) • If not done within 24 hours (sooner the better) aging will occur ◦ the R groups will form a covalent bond to other parts of the enzyme's active site and will no longer be able to come back ◦ will need to make more enzyme (AChR) instead ◦ aging=irreversible inhibition

Answer 49

1. Atropine-muscarinic antagonist | 2. pralidoxime-reversal of the poison binding to the AChE

Answer 50

1. 1st synapse thought the PNS (peripheral) is always a Nicotinic cholinergic synapse (nAChR) 2. Ganglionic Antagonists block these 1st synapses 3. They DO NOT block NMJ: cannot affect somatic movement 4. Thus they can block all PSNS and SNS effects since they block the 1st synapse in PNS

Answer 51

1. Anything controlled by SNS will act like what it is under PSNS 2. Vice versa for things under control of PSNS

Answer 52

***normally SNS 1. Vasodilation, ↑ peripheral blood flow, hypotension 2. Vasodilation, peripheral pooling of blood, ↓ venous return, ↓ cardiac output 3. anhidrosis---need SNS stimulation to sweat

Answer 53

***normally PSNS 1. Tachycardia 2. mydriasis 3. cycloplegia b/c normally ACh from PSNS causes the ciliary muscle to contract allowing tendons to relax and lens to bulge; now they're just tonically relaxed by SNS 4. ↓ tone and motility, constipation, ↓ gastric secretions 5. xerostomia

Answer 54

1. in HTN, normally baroreceptors will inhibit the SNS = HTN + brady * vagal tone 2. However w/ganglionic blockade, you get HTN + unchanged HR or tachy: -because baroreceptors can no longer inhibit the SNS b/c they can't communicate (no baroreceptor reflex)

PNS General + Cholinergic Flashcards

(78 cards)