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Pharm Unit 2 Terms

Pharmacology: Unit 1 terms + drugs

QuestionAnswer
Nervous system functions to control, coordinate, and communicate among all systems within the body.
Structural divisions of the nervous system central and peripheral
Central nervous system (CNS) brain and spinal cord
Peripheral nervous system (PNS) cranial nerves (12 pairs) and spinal nerves (31 pairs)
Peripheral nerve pathways afferent and efferent pathways
Afferent pathway pathway of peripheral nervous system; ascending pathways—carry sensory impulses toward the CNS
Efferent pathways pathway of peripheral nervous system; descending pathways—innervate skeletal muscle or effector organs by carrying impulses away from the CNS
Functional divisions of peripheral nervous system somatic and autonomic
Somatic nervous system division of PNS; nerves are branches of cranial and spinal motor nerves that innervate skeletal muscle; under voluntary control of the cerebral cortex
Autonomic nervous system (visceral, vegetative, involuntary) branches of the cranial and spinal motor nerves that innervate cardiac and smooth muscle and secretory glands; involuntary; regulated by hypothalamus and medulla oblongata
System that innervates smooth and cardiac muscle autonomic nervous system
Automaticity/autorhythmicity special property of smooth and cardiac muscle allowing them to initiate their own contractions
Autonomic nervous system function regulates rate at which organs work, either increasing or decreasing activity in order to maintain homeostasis
Innervation of visceral organs two different types of autonomic nerves—sympathetic and parasympathetic—innervate most internal organs; each organ/gland receives a nerve from each division; effect of division depends on stimulus
Sympathetic division “fight or flight”; increases activity of some organs, decreases activity of others, in attempt to conserve energy. Activated during times of stress, anxiety, illness, even if “fight or flight” is not truly needed. All nerves activated at same time
Parasympathetic division more active during periods of “rest and digest.” Nerves regulate body functions such as digestion and elimination. Only selected nerves can be stimulated, and stimulation can be confined to particular body system (i.e. bladder during urination)
Structural arrangements preganglionic neuron and postganglionic neuron
Preganglionic neuron neuronal fiber leaving brainstem and spinal cord synapse outside the CNS at ganglion
Postganglionic neuron second neuron that impacts on effector organ
Sympathetic (thoracolumbar) division fibers originate in the thoracic and lumbar regions of the spinal cord
Sympathetic division ganglia are located near the spinal cord (distant from effector organ
Sympathetic division preganglionic neurons innervate the adrenal medulla which is embryonically and anatomically analogous to other ganglia of the same division
Sympathetic division One preganglionic neuron may act on many post ganglionic neurons
Sympathetic division diffuse distribution pattern lead to widespread massive responses (desirable if organisms is confronted with a sudden emergency
Parasympathetic (craniosacral) division fibers originate in the brain stem (oculomotor III, facial VII, glossopharyngeal IX, vagus X, and sacral segments of the spinal cord
Parasympathetic division ganglia are located near the end effector organs (distant from spinal cord)
Parasympathetic division generally 1 preganglionic to 1 postganglionic neuron ratio
Parasympathetic division discrete distribution leads to fine and limited responses
Parasympathetic division functionally important in protection, conservation, and restoration of bodily resources
Neurotransmission communication b/t cells in nervous system accomplished by chemical mediators (transmitter, neurotransmitter, NT) released by nerve terminals; NT interacts w/specific receptor on second neuron (synapse) or on target tissue (neuroeffector junction)
Neurotransmitters of the ANS acetylcholine (ACh), norepinephrine (NE); epinephrine (Epi) is released into circulation, so is a neurohormone
Cholinergic neurons that release ACh
Adrenergic neurons which release norepinephrine (NE)
Sympathetic division neurotransmitter release preganglionic release ACh; postganglionic release NE (ACh—NE); ACh at sweat glands (ACh—ACh); adrenal medulla releases Epi, NE (ACh—Epi, NE)
Parasympathetic division neurotransmitter release preganglionic neurons release ACh; postganglionic neurons release ACh (ACh—ACh)
Adrenergic (sympathetic) receptors target organ receptors for norepinephrine and/or/ epinephrine; subdivided into Alpha and Beta receptors
Alpha adrenergic receptors subdivided into Alpha-1 and Alpha-2 based on the action produced.
Alpha-1 receptors adrenergic; assocd w/ excitation/stimulation; causes contraction of smooth muscle in blood vessels, glands, organs; smooth muscle contractions result in vasoconstricition/elevated blood pressure; most receptors on effector organs belong to this class
Alpha-2 receptors adrenergic; associated w/ relaxation/inhibition; negative feedback stimulation of these receptors leads to decreased contraction of smooth musclelower blood pressure; stimulated by NE or Epi
Beta adrenergic receptors adrenergic receptor subdivision according to location
Beta-1 receptors adrenergic receptors; located in cardiac muscle; facilitate increased heart rate in cardiac muscle + increased HR and contractility + causes release of rennin from kidney; stimulated by NE or Epi
Beta-2 receptors adrenergic receptor; located in lungs and cause bronchodilation as well as facilitating all remaining effects attributed to beta adrenergic receptors; stimulated by Epi or NE
Cholinergic (parasympathetic) receptors target organ receptors for ACh; subdivided into muscarinic, nicotinic I, and nicotinic II
Muscarinic receptors cholinergic; located on smooth muscle of internal organs, cardiac muscle, glands; w/ stimulation cause decreased heart rate, increased GI motility, increased salivary gland activity; stimulated by ACh
Nicotinic I receptors cholinergic receptor; located in ganglia of post-synaptic nerve body in both sympathetic and parasympathetic systems; stimulated by ACh
Nicotinic II receptors cholinergic receptors; located at the neuromuscular junction of skeletal muscles; when stimulated cause contraction of skeletal muscles; stimulated by ACh
Sympathetic nervous system function innervates the heart, increasing heart rate & contraction; innervate all large and small arteries/veins, causing constriction of vessels except arterioles supplying skeletal muscles; innervate smooth muscle of gutdecreased motility
Sympathetic nervous system function innervate smooth muscle of respiratory tract, causing bronchial relaxation/decreased bronchial secretions; stimulation affects liver, stimulates sweat glands, ejaculation
Parasympathetic nervous system functions innervates heart, slowing heart rate; innervate the gut, increasing motility; innervate bronchial smooth muscle, causing airway constriction; innervates genitourinary tract, causing erection in males.
Somatic nervous system functions efferent motor neurons synapse on skel. muscle cells & release ACh @ NMJ; binds w/ receptors on muscle cell; cell reaches threshold, causes action potential, opening of Ca channels in membrane; increase in IC Ca and contraction of skel. Muscle fiber
Autonomic nervous system regulates regulates the physiological functions of the body—vegetative functions; respiration, perspiration, body temp, carbohydrate metabolism, digestion, bowel motility, pupil size, blood pressure, heart rate, glandular secretions.
Autonomic nervous system divisions sympathetic and parasympathetic; normally in balance and maintain homeostasis
Sympathetic nervous system fight or flight; also called adrenergic; closely associated with the quick regulation of the expenditure of energy during emergencies
Parasympathetic nervous system vegetative; rest and digest; also called cholinergic; more involved with storage and conservation of energy
SNS neurotransmitters norepinephrine (NE), epinephrine (Epi); dopamine; these are all considered catecholamines and are metabolized by monoamine oxidase (MAO) and catechol-Omethyl-transferase (COMT)
Monoamine oxidase (MAO) enzyme that metabolizes NTs; works within the adrenergic nerve ending
Catechol-Omethyl-transferase (COMT) enzyme that metabolizes NTs; works outside the nerve ending in the synapse
Norepinephrine (NE) neurotransmitter of SNS; catecholamine; released at the postganglionic synapse
Epinephrine (Epi) neurotransmitter of SNS; catecholamine; released by adrenal glands
Dopamine neurotransmitter of SNS; catecholamine; present in the brain and also formed as a precursor in synthesis of NE in the postganglionic adrenergic nerve ending
PSNS neurotransmitter acetylcholine (ACh)
Acetylcholine (ACh) PNS neurotransmitter; inactivated by release of acetylcholinesterase in the synaptic cleft.
Autonomic drug categories adrenergic (sympathomimetic); adrenergic blocking (sympatholytic); cholinergic (parasympathomimetic); cholinergic blocking (parasympatholytic, anti-cholinergic); ganglionic; serotonergic; skeletal muscle reactants, anti-Parkinson’s
Adrenergic (sympathomimetic) MOA acts like NE;induces response 3 ways; direct-acting (receptor binding, causes physio response); indirect-acting (causes release of catecholamine from nerve ending); dual-acting (mixed acting, binds to receptor, stimulates release of NT from nerve ending
Adrenergic (sympathomimetic) Drug Therapeutic Uses appetite suppression, bronchodilation, reduce intraocular pressure (glaucoma), nasal decongestant, temp. relief of conjunctiva congenstion (red eyes), support heart during cardiac failure (resuscitation) or shock (to increase BP)
Adrenergic (sympathomimetic) Drug side/adverse effects—Alpha most frequent side/adverse effects—headache, restlessness, insomnia, euphoria; others inc. palpatations, dysrhythmias, vasoconstriction, hypertension, loss of appetite, dry mouth, nausea, vomiting
Adrenergic (sympathomimetic) drug side/adverse effects—Beta mild tremors, headache, nervousness, dizziness
Adrenergic (sympathomimetic) toxicity/management of overdose seizures (treat with diazepam); hypertension that can cause intracranial bleeding (treat with rapid acting alpha adrenergic blocker)
Adrenergic blocking (sympatholytic) MOA alpha and beta blockers are antagonists—they bind to adrenergic receptors & inhibit/block stimulation of SNS via competitive or non-competitive inhibition; neuronal blockers inhibit the release from the nerve terminal
Adrenergic blocking (sympatholytic) Alpha blockers therapeutic use treatment of hypertension, vascular headaches, pheochromomcytoma
Adrenergic blocking alpha blocker side/adverse effects nausea, vomiting, diarrhea; orthostatic hypotension, reflex tachycardia, dizziness
Adrenergic blocking Beta blockers cardioselective blockers work primarily in heart; nonspecific or nonselective blockers block both beta 1 & beta 2 receptors; nonselective blockers can cause bronchial constriction and vasoconstriction
Beta blocker therapeutic use treatment of hypertension, protection of heart after MI, treatment of dysrhythmias, chronic open angle glaucoma, migraine headaches, mitral valve prolapse syndrome
Beta blocker side/adverse effects NVD; possible bradycardia and cardiac arrest; agranulocytosis; thromcytopenia; give cautiously to patients w/ asthma or CAD
Cholinergic (parasympathomimetic) MOA mimics PNS; mimics actions of ACh; can induce response in 2 ways—direct acting (binds to receptors) and indirect-acting (makes more ACh available at receptor site by blocking acetylcholinesterase in synaptic cleft.
Cholinergic therapeutic uses—direct acting treatment of glaucoma—decreases intraocular pressure through inducing miosis
Cholinergic therapeutic uses—indirect-acting diagnosis and treatment of myasthenia gravis; antidote to curare type muscle relaxants
Cholinergic drug side/adverse effects these limit the use of cholinergic drugs; NVD; blurred visions, excessive sweating, flushing, excessive salivation, bradycardia, bronchoconstriction
Signs and symptoms of cholinergic poisoning Salivation and sweating; Lacrimation, Urinary incontinence; Diarrhea; GI cramps; Emesis (vomiting)—SLUDGE; antidote is atropine (anti-cholinergic drug)
Cholinergic Blocking (parasympatholytic, anti-cholinergic) MOA block or inhibit the actions of ACh; in large part these agents are competitive antagonists at muscarinic receptors of PSNS
Cholinergic Blocking Therapeutic Uses drugs used to treat Parkinson’s disease; treatment of some dysrhythmias, pre-op med before general anesthesia
Cholinergic blocking side/adverse effects cotton mouth, constipation, NV, tachycardia, palpitations, dizziness, drowsiness, blurred vision; oldest agents are atropine and scopolamine
Ganglionic blocking agent MOA though to inhibit nerve transmission at nicotinic receptors
Ganglionic blocking agent therapeutic uses potent antihypertensive but use limited because of extreme adverse effects (usually used in emergency situations)
Ganglionic blocking agent adverse effects paralytic ileus, dry mouth, constipation, urinary retention, impotence
Serotonergic Drug MOA believed to bind w/ one serotonin receptor subtype on cranial blood vessels; effect is vasoconstriction and perhaps cerebral blood vessel constriction resulting in reduction of pulsation associated w/ pain from vascular headaches
Serotonergic Drug therapeutic uses vascular headaches, i.e. migraines
Serotonergic side/adverse effects NV, dizziness, weakness, drowsiness, fatigue
Skeletal muscle relaxants—centrally acting MOA unknown; possibly blocking of signal from spinal cord, but not sure
Skeletal muscle relaxants—centrally acting therapeutic uses relaxation of spastic muslces caused by trauma, overexertion, or nervous tension.
Skeletal muscle relaxants—peripherally/direct acting MOA inhibits skeletal muscle fiber; prevents actin and myosin contraction
Skeletal muscle relaxants—peripherally/direct acting therapeutic uses treatment of spastic diseases (MS, cerebral palsy, spinal cord injury
Skeletal muscle relaxants—peripherally/direct acting side/adverse effects dizziness, vomiting, fatigue, weakness, hepatotoxicity
Parkinson’s Disease disease caused by excess cholinergic activity b/c of ACh & dopamine imbalance; decrease in dopamine & increase in ACh causes muscle rigidity, muscle tremor; treated w/ anti-cholinergic, dopaminergic, monoamine oxidase B inhibitor, antihistamine, antiviral
Anti-Parkinson’s anti-cholinergic agent MOA inhibit/block effects of ACh; readily cross blood brain barrier and can produce some improvement in functional capacity
Dopaminergic MOA 3 types—release dopamine, increase brain levels of dopamine, dopamine agonists; have major effect on akinesia (difficulty in or lack of ability to initiate muscle movement)
Dopaminergic therapeutic uses treatment of Parkinson’s disease
Dopaminergic side/adverse effects drowsiness, headache, nausea, sedation, confusion, hallucinations
Monoamine oxidase B inhibitor (dopamine conserver) MOA irreversibly inhibits monoamine oxidase B, thereby preventing breakdown of dopamine
Monoamine oxidase B inhibitor therapeutic use used in combo with levodopa or levodopa-carbidopa to treat Parkinson’s
Monoamine oxidase B inhibitor side/adverse effects dry mouth, NV, insomnia, dizziness, mood alterations, dyskinesias
Myasthenia gravis progressive, incurable autoimmune disease that results in skeletal muscle weakness and chronic fatigue; cause by lack of ACh; treated w/ anticholinesterase agents
Anticholinesterase MOA inhibits/blocks acetylcholinesterase in synaptic cleft which in turn inhibits reuptake of ACh back into nerve terminal; results in increased levels of ACh in synaptic cleft
Anticholinesterase therapeutic use treatment of myasthenia gravis
Action of histamine found throughout body in mast cells and basophilic white blood cells; largest concentrations of mast cells are in the lungs, the GI tract, and skin.
Histamine receptors 2 types—H1 receptors in blood vessels, bronchiolar smooth muscle, intestinal smooth muscle; H2 receptors—found in stomach, heart, blood vessels, uterine tissue
Anti-allergic agents—mast cell stabilizer cromolyn sodium (Intal/Nasalcrom); must be given before histamine release has begun; used for prophylaxis
Mast cell stabilizers allergic reactions can be blocked by preventing mast cells from releasing contents (histamine) or H1 receptors can be blocked from interacting w/ histamine.
Capsule (spinhaler); solution (nasalcrom); oral capsule (gastrocrom) routes of administration for Cromolyn (anti-allergic agent)
Anti-allergic agent therapeutic use used as prophylactic adjunct in mgmt of chronic bronchial asthma & allergic rhinitis to prevent bronchospasms; pulmonary function tests must show that patient has a bronchodilator reversible component to the airway obstruction for cromolyn to be benefit
Anti-allergic side/adverse effects minimal, include wheezing, nasal itching, nasal burning, nausea, drowsiness, headache; rare bronchospasms; rash—discontinuation of drug
Antihistaminic used to releave acute reaction in which histamine has already been released; all available specifically block histamine from interfacing w/ H1 receptors preventing H1 mediated allergic response.
Antihistaminic routes of administration usually orally; few for parenteral administration; metabolized rapidly by liver, so repeat administration necessary to maintain therapeutic response
Antihistamine therapeutic use used in acute allergic reactions including urticarial (hives), hay fever, insect bites, rhinitis, dermatitis; can induce sleep or relieve motion sickness; also anti-emetic.
Antihistamine adverse reactions drowsiness, sedation and xerostomia/dry mouth; hypotension rapid heartbat, anorexia, apigastric distress, urinary retention
Antihistamine precautions/contraindications s/b used with caution in patients w/ cardiovascular disease or hypertension/patients predisposed to developing increase in intraocular pressure or urinary retention.
Decongestant drugs vasoconstrictor; reduce blood flow to edematous mucous membrane in nose, sinuses, pharynx; produce vasoconstriction by stimulating alpha receptors in smooth muscle around blood vessels; decrease swelling of mucous membranes, alleviate nasal stuffiness
Chronic obstructive pulmonary disease (COPD) common respiratory condition caused by emphysema and chronic bronchitis.
Chronic bronchitis caused by chronic irritation of respiratory tract by cigarette smoke or environmental pollutants
Emphysema deases involving destruction of alveolar walls; difficulty expelling air from lungs; respiratory exchange is reduced and shortness of breath occurs. Irreversible lung damage.
Asthma respiratory condition characterized by shortness of breath and wheezing; effects caused by bronchiolarChronic obstructive pulmonary disease (COPD)
Chronic bronchitis caused by chronic irritation of respiratory tract by cigarette smoke or environmental pollutants
Emphysema deases involving destruction of alveolar walls; difficulty expelling air from lungs; respiratory exchange is reduced and shortness of breath occurs. Irreversible lung damage.
Asthma respiratory condition characterized by shortness of breath and wheezing; effects caused by bronchiolar constriction. Cause can be irritants, exercise, infections, aspirin, allergy.
Chemical mediators formed during inflammatory reaction and released from injured tissue, mast cells, and leukocytes in the respiratory tract; responsible for most of the symptoms and complications of asthma
Histamines produced by mast cells
Prostaglandins produced by almost all body cells (ex. leukotrines)
Beta-adrenergic drugs (sympathomimetics) bronchodilator drugs
Xanthine derivatives xanthine compounds are found naturally in tea, cocoa, and coffee; theophylline is used in treatment of asthma
Corticosteroids in treatment of asthma, inhibit inflammatory response that occurs in the respiratory airways; used in acute asthmatic conditions when bronchodilators have failed to provide relief or maintain control
Corticosteroid adverse effects fluid retention, muscle wasting, metabolic disturbances, increased susceptibility to infection.
Cysteinyl leukotriene receptor antagonists leukotrienes are prostaglandin derivatives and cause bronchoconstriction, mucus production, inflammation; these agents interfere w/ leukotriene formation
Mucolytics chemical agents that liquefy bronchial mucus so can be removed by coughing or suctions
Expectorants stimulate the production of respiratory secretions, which then decrease irritation and cough caused by excessive dryness of the airways; increase output of respiratory tract secretions which indirectly suppresses cough
Antitussives depress the coughing center in the medulla; should be used only for non-productive cough
Inotropic increases or decreases FORCE of myocardial contraction
chronotropic increases or decreases HEART RATE
dromotropic increases or decreases SPEED of electrical conduction
Created by: mbtrimm
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