Peripheral Nervous System Flashcards
Discuss properties of A-beta fibers
A-beta fibers are myelinated second largest fibers responsible for proprioception, touch, and pressure
Discuss properties of A-alpha fibers
A-alpha fibers are myelinated large fibers with fast conduction speeds.
The motor (efferent) control muscle length and force of contraction
The sensory (afferent) control proprioceptin
Discuss the properties of a-gamma fibers
A-gamma fibers are myelinated 3rd largest fibers responsible for skeletal muscle tone
Discuss properties of a-delta fibers
A-delta fibers are myelinated small fibers responsible for temperature and sharp prickling pain sensation
Discuss B fibers
B fibers are myelinated preganglionic autonomic neurons responsible for various autonomic functions
First fibers to be blocked by LA
Discuss sC fibers
sC fibers are small unmyelinated postganglionic sympathetic neurons responsible for various autonomic functions
Discuss dC fibers
dC fibers are small unmyelinated afferent (sensory) neurons responsible for temperature and throbbing pain
List the different nerve fiber type in order of size and conduction speed.
A-alpha, A-beta, A-gamma, A-delta, B, sC, dC
Nerves with LARGER diameter conduct AP faster than fibers with smaller diameter
Myelinated fibers conduct AP faster than unmyelinated fibers
Discuss the anatomy of the sympathetic nervous system
The sympathetic thoracholumbar nervous system arises from T1-L2(3) and the cardio accelerator fibers are from T1-T4
Most sympathetic presynaptic neurons synaps with post ganglionic fibers at the paravertebral ganglia formed by the inferior cervical and first thoracic ganglia
What are the S/S if Horners syndrome?
Ipsilateral miosis, ptosis, flushing, increased skin temperature, enophathalamos, and nasal congestion due to stellate ganglion blockade.
Discuss where sympathetic preganglionic fibers arise and how the intersect the white and gray rami communicans
Sympathetic preganglionic fibers arise from the intermediolateral horn of the spinal cord. All Sympathetic PREganglionic fibers pass though the white rami, while some but not all POSTganglionic fibers pass through the grey rami. PREganglionic white rami are distributed to spinal nerves from T1-L2. Gray rami are distributed to ALL spinal nerves from the ganglia. Gray rami allows coordinated massive discharge of the sympathetic nervous system
Describe the synthesis of epinephrine
Tyrosine -> dopa -> dopamine -> norepinephrine -> epinephrine (only in adrenal medulla)
Norepinephrine is stored in presynaptic vesicles. In the adrenal medulla NE is 20% and Epi is 80% of totals storage
Describe events of sympathetic neurotransission
1) AP arrives at sympathetic nerve terminal
2) Depolarization opens Ca+ channels and ca+ rushes into cell.
3) Ca+ unites with calmodulin to cause NE filled vesicles to merge with cell membrane and spill NE into synaptic cleft
4) presynaptic alpha 2 receptors activated by NE cause a decrease in NE release (neg feed back loop)
5) NE diffuses down concentration gradient to post synaptic membrane receptors
6) adrenergic receptor activation causes ion channels to open, or activation of adenylate cyclase
7) NE diffuses away from receptors (1st step in termination) NE is actively reuptaken inside presynaptic terminal (80%) small amounts are metabolized by MAO in the synaptic cleft, and small amounts diffuse into the blood stream and are metabolized by COMT
Sympathetic nervous system activation acts to:
Increase HR, CO, BP, blood glucose, dilate bronchial tree, shunt blood away from intestine and viscera to supply skeletal muscle
Flight or flight
Discuss location and activity of alpha-1 receptors
Alpha-1 receptors are found a variety of tissues (vascular smooth muscle, glands) and are inervated by sympathetic postganglionic neurons. Stimulation is usually excitatory
Arterial and venous constriction, increased preload, SV, CO,and BP
Discuss location and actively of alpha-2 receptors
Found on PREsymaptic nerve terminals of sympathetic postganglionic neurons, but also found in post synaptic membranes of brainstem and peripheral tissue.
stimulation of sympathetic postganglionic, presynaptic nerve varicosities inhibits the release of NE (neg feed back loop). Stimulation of postsynaptic receptors in the brainstem inhibits sympathetic outflow.
Stimulation of receptors in the substantial gelatinosa of the spinal cord promotes analgesia
Discuss location and function of beta-1 receptos
found in heart, kidney, and adipose tissue. Stimulation is excitatory –> increased HR, CO, contractility –> increased CO and BP
Discuss location and function of beta-2 receptors
Found in smooth muscle and in glandular tissue. Stimulation is inhibitory –> vasodilitation, bronchodilation, relaxation of pregnant uterus, glycogenolysis, and gluconeogenisis.
beta-2 receptor stimulation promotes hyperglycemia, and hypokalemia
Discuss the renin-angiotensin-aldosterone System
85% of resting BP Is controlled by renin.
In response to low BP the kidney releases renin –> converting angiotensinogen ( produced in the liver) into angiotensin-I, in the lungs ACE converts angiotensin-I to angiotensin-II –> causes vasoconstriction, and release of aldosterone from adrenal gland, aldosterone promotes K+ excretion in exchange for Na+ retention, Na+ retention results in fluid expansion and combined with vasoconstriction in increased BP
Phenylephrine
Alpha-1 +++
Clonidine
Minimal alpha-1 with strong alpha-2
Isoproterenol
Strong beta-1 and beta-2
Doubutamine
Strong beta-1
Terbutaline
Minimal beta-1 strong beta-2
Ritodrine (yutopar)
Minimal beta-1 strong beta-2
Epinephrine
Strong alpha-1, weak alpha-2 strong beta-1and beta-2
Leads to increased SBP (beta-1), decreased DBP (beta-2 vasodilation more pronounced than alpha-1 constriction at low doses), an increased in HR (beta-1) MAP is variable
Norepinephrine
Alpha-1 alpha-2 and beta-1
Leads to increased SBP (beta-1) increased DBP (alpha-1) and increased MAP
Dopamine
Alpha-1, alpha-2, beta-1 and minimal beta-2
Ephedrine
Indirect acting, strong alpha and weak beta
Metarminol (aramine)
Indirect acting, strong alpha and wean beta
Sympathetic stimulation of heart
Beat-1
SA node increase HR
AV node increase conduction
Muscle fibers increase contractility
Sympathetic stimulation of arterial blood vessels
Alpha-1
Vasoconstriction and inc. SVR in most systemic blood vessels
Beta-2
Vasodilation and decreased SVR in skeletal muscle vessels
Sympathetic stimulation of veins
Alpha-1
Vasoconstriction increased preload
Sympathetic stimulation of lungs
Beta-2
Bronchodilation and increased secretions
Sympathetic stimulation of kidney
Beta-1
Increased renin release
Alpha-1
Decreased renin release
Sympathetic stimulation of Liver
Beta-2
Gluconeogenisis
Glycogenolysis
Sympathetic stimulation of uterus
Beta-2
Muscle relaxation
Alpha-1
Contraction
Sympathetic stimulation of Na-K ATPase pump
Beta-2
Hypokalemia
What are the side effects of Ritodrine (Yutopar)
Tachycardia, Hypokalemia, hyperglycemia (ketoacidosis is a risk in insulin dependent diabetics), and pulmonary edema
Crosses placenta side effect to fetus
What are the actions and uses of Phenoxybenzamine (Dibenzyline)?
Phenoxybenzamine, is a long acting non-selective alpha-adrenergic antagonist it is used to control BP in patients with pheochromocytoma
What are the uses and action of Yohimbine?
Yohimbine is a selective alpha-2 adrenergic antagonist used to treat ED
What are the uses and action of timolol
Non-selective beta-1and beta-2 antagonist
What are the uses and action of propranolol?
Non-selective beta antagonist.
Generally to be avoided in patients with irritable airways due to possible bronchoconstriction
What are the uses and action of Esmolol
Non-selective beta blocker, very short acting because it’s metabolized by plasma non-selective esterases
What are the uses and action of Labetalol?
Competitive antagonist at alph-1 and beta-1 and beta-2. Alpha to beta 1:7
May be used to TX hypertensive emergencies or to produce controlled hypotension. Decreases HR, contractility, and SVR
Discuss the anatomy of the parasympathetic nervous system
The parasympathetic craniosacral nervous system out flow arrives from
Oculomotor cranial nerve (III) from midbrain Facial cranial nerve (VII) from the pons Glossopharyngeal nerve (IX) from medulla Vagus nerve (X) from medulla S2-S4
What are the responses to Parasympathetic stimulation to the eye.
The pupil constricts (miosis)
What are the responses to Parasympathetic stimulation to the heart?
Decreased HR, conduction speed, contractility
What are the responses to Parasympathetic stimulation to smooth muscle
Bronchoconstriction, gallbladder contraction, increased motility, contraction of bladder destructor muscles
What is the effect on secrearions in response toare the Parasympathetic stimulation?
Increased salivary, pharyngeal, laryngeal and bronchial secretions. Increased gastric acid secretions. Increased secretions of digestive enzymes and bicarbonate from pancrease and small intestine
What the action of pilocarpine and what is it used for
Pilocarpine is a parasympathetic used to treat some forms of glaucoma
What are the cholinesterase inhibitors?
Endrophonium (Tensilon) Neostigmine (prostigmin) Pyridostigmine (Mestinon, Regonol) Physostigmine (Antilirium) Echothoiphate (Echodide, Phospholine)
What is the mechanism of action of the cholinesterase inhibitors and what are they used for?
Cholinesterase inhibitors inhibit both true AchE and plasma AchE. Since true AchE is found postsynaptically these agent have postsynaptic activity. They act indirectly by raising the concentration of Ach.
Muscarinic effects: bradycardia, increased gastry secretions, hyperperistalsis, miosis, salivation
Nicotinic effects: stimulation of autonomic ganglia and neuromuscular junction
Uses: NMB reversal, tx anticholinergic syndrome, myasthenia gravis, Alzheimer’s, ileus, glaucoma, atonic bladder
What is the significance of the effect that cholinesterase inhibitors have on plasma AchE?
Neostigmine and pyridostigmine but not endrophonium, produce marked prolonged inhibition of plasma AchE. Succinylcholine and mivacurium would have prolonged effects. A result.
What is cholinergic syndrome and how is it treated?
Cholinergic syndrome can be a result of organic pesticides, “nerve gas”, or excess physostigmine. Symptoms include:
Muscarinic: Miosis, difficulty focusing, salivation, bronchoconstriction, bradycardia, ABD cramps
Nicotinic: Weakness mild to paralysis
CNS: dysphoria, confusion, ataxia, seizure, coma
Treatment: atropine, pralidoxime (reactivates Ach) and diazepam for seizures
How will excessive doses of acetycholinesterase inhibitors effect nondepolarizing neuromuscular blocked?
In excess doses acetycholinesterase inhibitors can paradoxically potentate the blockade
What are the antimuscarinic agents and what is their mechanism of action?
Atropine, scopolamine and glycopyrolate combine with muscarinic receptors and prevent Ach from interacting with the receptors, acting as competitive inhibitors
Lead to responses opposite those seen with parasympathetic stimulation
What is anticholinergic syndrome and how is it Tx?
Anticholinergic syndrome may develop in response to high doses of atropine or scopolamine.
Central manifestations include: mania, hallucinations, delirium, drowsiness, come, agitation, disorientation.
Peripheral manifestations include: blurred vision,dry mouth, tachycardia, flushed skin, rash over face and neck, and hypotension.
Pediatric and elderly most sensitive
Tx with physostigmine 15-60mcg/kg IV (lipid soluble and will cross BBB)
What is the effect of antimuscarinic agent on esophageal sphincter tone?
Tone is decreased –> increasing the likelihood of reflux
Describe the process of bronchial smooth muscle relaxation via beta-2 stimulation
1) First messenger (ie Terbutaline) binds to beta-2 receptor
2) Gs activates adenylate cyclase
3) adenylate cyclase transforms ATP to cAMP ( second messenger)
4) cAMP activates protein kinase resulting in Bronchodilation
5) phosphodiesterase breaks down cAMP ending dilation
Phosphodiesterase inhibitors such as aminophylline block the breakdown of cAMP therefore promoting dilation
Describe the process of bronchial smooth muscle relaxation via nitric oxide
1) First messenger Nitric oxide diffuses into cell
2) NO activates GTP into cGMP resulting in Bronchodilation
Nitroglycerin and nitroprusside promote bronchodilation by donating NO and increasing cGMP
Describe the process of bronchial smooth muscle constriction via muscarinic activation
1) Ach bings to muscarinic receptor activating protein G
2) Protein G activates phospholipiase-C transforming PIP into IP3
3) IP3 stimulates release of intracellular Ca+ stores into the sarcoplasm activating the contractile mechanism
Atropine and the inhaled antimuscarinic agent ipratropium (atrovent) produce Bronchodilation by competitively inhibiting muscarinic receptors
