intended vein, allowing the IV fluid into the surrounding tissue. A blood clot or venous inflammation can result from needle or cath- eter trauma, irritating medications, or insufficient vein size for the volume of medication required. Sign of inflammation at the IV site may indicate the presence of a thrombus, phlebitis or infiltration of particulate matter (Watkins, 2013, p. 195).
dicated in the presence of severe malnutrition, significant weight loss, inadequate tolerance of enteral nutritional application, bow- el obstruction and insufficient gastrointestinal absorption. Complications from intravenous administration may include in - filtration, thrombus/phlebitis, air emboli and vein irritation. In- filtration means an IV catheter has become displaced from the To review : The nervous system is divided and categorized in terms of location and function . The central nervous system (CNS) includes the brain and spinal cord, while the peripheral nervous system (PNS) includes spinal nerves and other neuronal tissues outside of the CNS. In addition, the autonomic nervous system functions to operate and incorporate visceral physiologic func- tions such as cardiac output and blood flow distribution. The so- matic nervous system consists of PNS structures that create vol- untary movement, respiration and posture (Katzung, 2018, p. 89). The nervous system also includes influx and efflux of chemical and electric signals, termed afferent and efferent inputs. Chemical transmission occurs between nerve cells, and between nerve cells and target cells. Autonomic activity can be stratified as central (occurring primarily in the midbrain and medulla), cardiovascular, presynaptic and postsynaptic. The autonomic nervous system (ANS) is composed of two divi- sions: The sympathetic/thoracolumbar division, and the parasym- pathetic/craniosacral division. The sympathetic division consists primarily of short paravertebral chains and longer prevertebral ganglia, and is associated with physiologic processes of energy- expenditure. This is the derivation of the common phrase “fight or flight” response. The majority of post-ganglionic parasympathetic fibers innervate target tissues in the form of grids within target organs. For example, the enteric nervous system lies within the gastrointestinal system, and includes more than 150 million neu- rons innervating the region from the esophagus to the distal co- lon (Katzung, 2018, p. 91). The enteric nervous system is involved with control of motor and secretion actions within the gastroin- testinal tract, as well as motor control of the colon. This design and distribution mediates energy-conserving physiology. Early scientific description of these processes used the word tropho- tropic, meaning “energy growth” (Katzung, 2018, p. 100). Current parasympathetic analogy includes the phrase “rest and digest.” While the chief autonomic transmitter molecules are acetylcholine and norepinephrine, many other neurochemicals are released and regulated within the ANS. Cholinergic fibers are ANS fibers that release acetylcholine. Near- ly all the efferent nerve fibers departing from the CNS are cho- linergic, including somatic fibers innervating skeletal muscle. In addition, the majority of parasympathetic postganglionic fibers are also cholinergic. Acetylcholine is synthesized and stored in large “quanta” capacity, often 1,000 to 50,000 molecules, in the nerve ending. This magnitude of formation and storage facilitates rapid transmitter release (Katzung, 2018, p. 95). Release of ace- tylcholine depends on calcium concentrations outside the cell. Action potentials trigger calcium influx along with efflux of acetyl- choline and other neurotransmitters. A single depolarization can release hundreds of quanta into the synaptic cleft. Acetylcholine receptors are currently termed cholinoreceptors , an update and departure from previous names such as muscarinic and nicotinic receptors. A common pharmaceutical that blocks the release pro- cess is botulinum toxin (Botox). Following release, acetylcholine molecules bind to cholinoreceptors to produce mechanism of ac- tion. The enzyme acetylcholinesterase then breaks down acetyl- choline en masse. Norepinephrine , also known as noradrenaline , is released along with dopamine by the most postganglionic sympathetic fibers; these fibers are termed adrenergic fibers . Adrenergic release is similarly induced by calcium influx during action potentials. Ad- renergic receptors are commonly termed adrenoceptors and are categorized based on agonist and/or antagonist selectivity. Norepinephrine transporter proteins are responsible for uptake
AUTONOMIC DRUGS
and reuptake of the neurochemical, which effectively terminates synaptic activity. Cocaine and certain anti-depressant drugs can block this neurochemical transporter, which leads to increased neurotransmitter activity (Katzung, 2018, p. 95). Drugs such as amphetamines and ephedrine act as sympathomimetics; they act as weak agonists and substrates for monoamine transporters. These drugs are thus taken up into the synaptic cleft, which in turn displaced norepinephrine, causing it to be ejected into synaptic space, and increasing neurotransmitter activity. Despite the upgrade in receptor nomenclature, cholinergic recep- tor categorization re-emerges when considering pharmaceuticals. Muscarinic and nicotinic receptors denote specifics regarding chemical affinities. Muscarinic receptors derive the name from the chemical alkaloid muscarine, which demonstrated effects that mimic parasympathetic nerve discharge. Therefore, pharmaceu- ticals that bind to muscarinic receptors are termed parasympa- thomimetic . Muscarinic receptors are primarily located at effector cells, including smooth muscles and glands. In contrast, nicotinic receptors are located along autonomic ganglia as well as skel- etal muscle neuromuscular junctions. Drugs that mimic the effects of acetylcholine are termed cholinomimetics . These medications either activate cholinoreceptors or inhibit break down of acetyl- choline by blocking acetylcholinesterase. Cholinomimetic agents fasten to and stimulate muscarinic or nicotinic receptors (Katzung, 2018, p. 109). As mentioned previously in this section, the majority of post-gan- glionic fibers are cholinergic. In turn, the effects of cholinomimetic drugs primarily stimulate parasympathetic effects for the nervous system and various organs, which follow: ● Eyes : Contraction of the iris and ciliary muscles; enacting near vision. ● Heart : Sinoatrial and atrioventricular nodes. ● Atria : Decreased heart rate, contractile strength and conduc- tion velocity. ● Blood vessels : Arteries and veins; dilation and/or constriction. ● Lung : Bronchial muscle and glands; bronchoconstriction and mucus secretion. ● Gastrointestinal tract : Increased motility, sphincter relax- ation, secretion stimulant. ● Urinary bladder : Detrusor contraction, trigone and sphincter relaxation. ● Glands : Salivary, lacrimal, sweat, nasopharyngeal; secretion. With regards to physical movement, cholinomimetics are effective in prolonging the presence and intensifying the effects of acetyl- choline by inhibiting acetylcholinesterase. This pharmacodynamic action can increase muscular contraction force and induce muscu - lar fibrillation at higher doses (Katzung, 2018, p. 119). Cholinomi- metics are a primary pharmacologic intervention in the presence of myasthenia gravis. Primary effects of this autoimmune pathol- ogy include breakdown of the post-synaptic membrane, binding of pathologic antibodies to nicotinic receptors and cross-linking receptors. Symptoms of the pathology often include muscular weakness, ptosis, diplopia, and trouble speaking and swallowing. Common therapeutic pharmaceuticals include pyridostigmine and neostigmine. These drugs may also be employed to reverse the effects of non-depolarizing agents, which may be employed during surgical procedures and induce acute post-surgical paraly- sis. In contrast, choline receptor-blocking agents block the effects of parasympathetic autonomic discharge and are primarily em- ployed to block muscarinic receptors. Atropine is the most well- known cholinoreceptor-blocking agent. Termed antimuscarinic
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