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diphenylhydramine/ benedryl
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H&N Pharm
Pharm H&N, lecture 10
| Question | Answer |
|---|---|
| Body % water, % ICF, % ECF | 60% water, 40% ICF, 20% ECF |
| diphenylhydramine/ benedryl | anti histamine Histamine type 1 receptor inverse agonist |
| Cimetidine | Acid reducer H2 receptor blocker |
| Tamulosin | increase urine flow |
| nifedipine -dipine | decrease BP, anti-hypertensive block Ca channels |
| sildenafil | treat erectile dysfunction increases cGMP |
| cholinergic nicotinic receptor type | ligand gated ion channel |
| -caine | local anesthetics block Na channels |
| -zepam (benzos) | anti-anxiety drugs open Cl channels |
| tolbutamide -amide | sulfonyl ureas treats Type 2 diabetes increase insulin from beta cells in pancreas close K channels |
| nitroglycerin | nitric oxide causes vasodilation via opening K channels |
| Beta 1 mechanism | Gs increases cAMP |
| alpha 2 mechanism | Gi decreases cAMP |
| alpha 1 mechanism | GQ increases Ca |
| Insulin receptor mechanism | tyrosine kinase recruits glucose transporters to cell membrane from intracellular reserves |
| Aspirin | irreversible inhibition of COX (cyclooxygenase) |
| Acetaminophen | competitive inhibitor of COX (cyclooxygenase) |
| Reversible COX inhibitors | ibuprofen, acetaminophen |
| Caffeine | non specific inhibitor of PDEs, stimulant, increases HR |
| Theophylline | specific to cAMP PDE in lungs, bronchodilation |
| PDE inhibitors | caffeine, theophylline, sildenafil |
| sildenafil | cGMP PDE5 inhibitor on corpus cavernosum |
| enalapril -april | ACE inhibitor |
| ciproflaxacin | fluoroquinolone, inhibits DNA gyrase & topoisomerase |
| fluoxetine | SSRI, antidepressant |
| chloroquine | antimalarial |
| Advantages of gene therapy | replace a dysfunctional gene, create continuous production of deficient protein, target specific cells, maximize compliance |
| Gene therapy vectors | Plasmids: does not integrate into host DNA Virus- based vectors: Retrovirus: RNA virus integrates into host DNA Adenovirus: double strand DNA that can transfer to non-dividing cells, largest segments, but not integrative |
| Adenovirus adv & disadvantages | -capable of integrating in both dividing and nondividing cells -can insert a large piece of DNA -Not integrative, so effect is transient |
| Full vs partial agonist | Full agonist only binds to active receptors |
| Noncompetitive or uncompetitive antagonist | Prevents receptor activation, reduces max response |
| Inverse agonist vs antagonist | Antagonist has no effect without agonist Inverse agonist has effect without agonist |
| Therapeutic index | LD50/ ED50 Bigger is better |
| Low therapeutic index drugs | "The Queen Likes Digging Low" Low therapeutic index Theophylin (asthma), Quinine (anti-arrhythmic), Lithium (bipolar), Digoxin (cardiac) |
| succinylcholine | only depolarizing NMJ blocker, "flaccid paralysis" by inhibiting stimulation by Ach at NMJ, half life of one minute, used in surgery |
| curare | non-depolarizing NMJ blocker, half life 1 hours, patients come off by achetylcoline esterase inhibitor and muscarinic antagonist |
| gallamine | non-depolarizing NMJ blocker, half life 1 hours, patients come off by achetylcoline esterase inhibitor and muscarinic antagonist |
| Atropine | competitive inhibitor of ach at muscarinic receptors, blocks M2 muscarinic receptors; increase HR by blocking vagal affect on SA node (dec HR at low levels), decrease secretion, decrease mictutition, decrease accomodation; can enter CNS; can treat nerve |
| Cholinergic antagonists/ antimuscarinics | inc HR, inc CV, mydriasis, cycloplegia (inability to focus), dec GI motility, dec secretions, urinary retention; include atropine, scopolamine, glycopyrollate, scopolamine; ipratroprium for bronchiodilation in COPD |
| Depolarizing NMJ antagonist | succinylcholine, binds Nm receptor, opens channel in end plate, depolarizes endplate, blocks receptor so desensitized to effect of ach, transient fasciculations then flaccid paralysis |
| Non-depolarizing NMJ antagonist | competitive antagonist, bind Nm receptor, do not open ion channel, produce skeletal muscle relaxation, include -"cur"- drugs, *d-tubocurarine* and *gallamine*; toxicity causes respiratory paralysis so mechanical ventilation required, |
| bring patient off *d-tubocurarine* and *gallamine* | half life 1 to 2 hours, bring patient off with cholinesterase inhibitors & muscarinic antagonist (to prevent overstimulation at muscarinic receptors) |
| Malignant hyperthermia | autosomal dominant disorders with rapid increase temp and serum potassium in response to inhalation anesthesics or muscle relaxants (succinylholine) increase in Ca, muscle contraction; treat with ice & dantrolene to block Ca from SR |
| PAM | regenerates Ach Esterase, does not enter CNS, treat nerve gas |
| Sarin | nerve gas, inhibits cholinesterase, stopping Ach degradation, build up of Ach at synapses |
| Cholinergic agonist/ cholinomimetics | dec HR, dec CV, miosis, accomodation, increase GI motility, bronchoconstriction, increaase secretions, promote urination |
| Cholinergic antagonists/ antimuscarinics | inc HR, inc CV, mydriasis, cycloplegia (inability to focus), decrease GI motility, dec secretions, urinary retention; include atropine, scopolamine, glycopyrollate to dec secretions; scopolamine for motion sickness; ipratropprium for bronchiodilation in C |
| Cholinergic antagonist for asthma | block constriction (dilation) via blocking muscarinic receptor on central airways, muscarinic receptor constant rate through aging, e.g. ipratropium |
| Adrenergic agonist for asthma | bronchodilation via activating beta 2 receptors in small peripheral airways, incrases adenyl cyclase, incraeses cAMP to promote relaxation, beta 2 receptors in airways reduce with age, e.g. albuterol |
| Xanthines | inhibit PDE, which breaks down cAMP to increase cAMP and promote smooth muscle relaxation, includes caffeine, theophylline, , and theobromine |
| Albuterol | adrenergic agonist on beta 2 receptors, bronchodilation for asthma and COPD with side effect of chest pain |
| Ipratroprium | cholinergic antagonist on M3 receptors for bronchodilation for asthma & COPD, side efects of dry mouth and sedation |
| Theophylline | methyl xanthine, acts on adenosine receptors for bronchodilation, treats asthma & COPD, side effects inc heart rate, inc force of contraction, increase gut secretions |
| Scopolamine | patches, treats motion sickness |
| How do you treat an atropine overdose | 1) treat symptoms 2) provide cholinesterase inhibitor eg psysotigmine, in small doses 3) blankets for cold and diazepam for seizure control |
| Ganglionic blockers | interfere with post synaptic action of Ach at Nicotinic Nn receptors of all autonomic ganglia, treat hypertension in ER or during surgery, side effects include Nm blockade, hypotension, impotence; include nicotine, mecamylamine, trimethaphan |
| NMJ blockers | drugs that bind competitively to nicotinic receptor, classified as de-polarizing or non-depolarizing |
| Depolarizing NMJ antagonist | binds Nm receptor, opens channel in end plate, depolarizes endplate, and blocks receptor so desensitized to effect of ach, produces skeletal muscle transient fasciculations followed by flaccid paralysis; eg succinylcholine |
| Non-depolarizing NMJ antagonist | competitive antagonist, bind Nm receptor, do not open ion channel, produce skeletal muscle relaxation, include -"cur"- drugs, *d-tubocurarine* and *gallamine*; toxicity causes respiratory paralysis so mechanical ventilation required, |
| Malignant hyperthermia | autosomal dominant disorders with rapid increase in temp and serum potassium in response to inhalation anesthesics or muscle relaxants (succinylholine) caausing increase in Ca, muscle contraction, heat cycles; treated with ice packs & dantrolene to block |
| Dantrolene | treats malignant hypothermia |
| Botulinum toxin | prevents release of acetylcholine in synaptic terminal by cleaving SNAP 25 to |
| Atropine | competitive inhibitor of ach at M2 muscarinic receptors; increase HR by blocking vagal affect on SA node (dec HR at low levels), dec secretion, decrease mictutition, decrease accomodation; can enter CNS; treat nerve gas (excess Ach) |
| ANS on SA node, | b1 (b2) Increased heart rate & M2 Decreased heart rate |
| ANS on Atria | b1 (b2) Increased contractility & M2 Decreased contractility |
| ANS on AV node | b1 (b2) Increased Conduction Velocity & M2 Decreased Conduction Velocity |
| ANS on His-Purkinje | b1 (b2) Increased Conduction Velocity & M2 Decreased Conduction Velocity |
| ANS on Ventricles | b1 (b2) Increased Contractility & little effect on contractility |
| Sympathetic stimulation of Arterioles | blood supply increases, decreases, or same due to a1/b2 receptor rato & local demand) |
| ANS on Arterioles | a1 Constriction, b2 dilation* ; No PS innervation |
| ANS on Veins | a1 Constriction*, b2 dilation ; No PS innervation |
| ANS effects on Eye | pupil dilation mydriasis via sympathetic for far vision; Constriction & accommodation via parasympathetic for near vision, reading |
| ANS on Radial muscle-iris | a1 Contraction (mydriasis) ; no PS innervation |
| ANS on Sphincter muscle-iris | no sympathetic innervation, PS stimulation causes Contraction / miosis M3 |
| ANS on Ciliary muscle | b2 relaxation (far vision), Contraction (reading) M3 |
| ANS on Lung Smooth muscle | b2 relaxes – bronchodilation, M3 bronchoconstriction |
| ANS on GI Motility & tone | decreases –a2 inhibition, b2 relaxation, PS increases motility, increases secretions |
| ANS on GI Sphincters | a1 contraction of sphincter, PS relaxation of sphinters |
| ANS on GI Secretions | a2 decrease, PS Stimulation M3 on M3 increases secretions |
| ANS effect on Bladder | sympathetic – difficult to urinate; parasympathetic – facilitates urination |
| ANS on bladder Detrusor muscle | symp b2 relaxation; PS M3 Contraction |
| sympathetic effect on Pancreas | keep glucose levels up; less insulin, more glucagon |
| ANS effect on b-cells producing insulin in pancraes | a2 inhibits release, PS Stimulates release |
| ANS effect on a-cells producing glucagon in pancreas | b2 stimulates release, PS inhibits release |
| ANS effect on Liver | sympathetic - increased glycogen breakdown & gluconeogenesis |
| ANS effect on Gluconeogenesis | sympathetic on b2 increases gluconeogenesis to increase glucose, PS increase Glycolysis |
| ANS effect on Glycogen breakdown | sympathetic on b2 – increase glycogenolysis, PS increase glycogen synthesis |
| ANS effect on Insulin receptors | sympathetic a1 inactivation of insulin receptors by dephosphorylation to increase blood glucose, PS insulin receptors activated |
| ANS effect on Adipose | sympathetic stimuation causes breakdown of triglycerides, supply fatty acids to rest of the body |
| ANS effect on Adipocytes | symp on b1, b3 lipolysis, PS stimulates fat synthesis, storage |
| ANS effect on Kidney | b1 – rennin secretion goes up |
| ANS effect on Pituitary | b1 – ADH secretion goes up |
| Where are MOST of the beta 1 receptors located in our body | Heart |
| Adrenergic nervous system is generally mediated by Norepinephrine and Epinephrine. Name an EXCEPTION to this general rule | Temperature control & Sweat glands by acetylcholine |
| What is the effect of an alpha 2 agonist on blood glucose levels | Increase, alpha 2 lowers insulin levels, lower insulin increases glucose levels |
| You prescribe Terazosin (Hytrin), an alpha-1 blocker to an elderly male for an enlarged prostate. What is the effect of an alpha-1 blocker on blood pressure | decrease |
| What is effect of prednisone on a. Blood pressure, b. Blood glucose levels, c. Blood lipid levels, d. Weight e. Blood CRH levels f. Blood Cortisol levels g. Blood ACTH levels h. Ability to fight infections i. Fluid retention | a. Blood pressure (incr), b. Blood glucose levels (incr), c. Blood lipid levels (incr)d. Weight (incr) e. Blood CRH levels (decr)f. Blood Cortisol levels (decr)g. Blood ACTH levels (decr)h. Ability to fight infections (decr)i. Fluid retention (incr) |
| The autonomic nervous system is responsible for ____ | homeostasis |
| Within the autonomic nervous system, there are always how many neurons needed to reach the target organ | _two |
| All preganglionic neurons release _______, which binds to ____ receptors on the postganglionic neurons | acetylcholine, nicotinic |
| The sympathetic nervous system is (catabolic/anabolic) and is often called the (craniosacral/thoracolumbar) system. The preganglionic fibers connect with (few/many) postganglionic fibers | catabolic, thoarcolumbar, many |
| The parasympathetic nervous system is (catabolic/anabolic) and is often called the (craniosacral/thoracolumbar) system. The preganglionic fibers connect with (few/many) postganglionic fibers | anabolic, craniosacral, few |
| Within the parasympathetic system, the postganglionic fibers release __, which interacts with ____ receptors | acetycholine, muscarinic |
| Within the sympathetic system, most of the postganglionic fibers release __, which interacts with __ _ receptors | norepinephrine, α or β |
| Noradrenaline is also called | _norepinephrine___ |
| Adrenaline is also called | _epinephrine__ |
| Acetylcholine is synthesized from ___ and ____. It's action is terminated by _____ (enzyme name) | acetylCoA, choline, cholinesterase |
| What is the rate-limiting step in the synthesis of epinephrine | tyrosine hydroxylase |
| How is the effect of norepinephrine terminated | reuptake |
| In the resting state, most dually innervated organs are controlled by the what system | parasympathetic |
| Which important organs/cells are not dually innervated | blood vessels (symp only, alpha 1 constrict and beta 2 relaxation), skin (symp only, beta 1?), radial/ dilator muscle (symp only, alpha 1 mydriasis or dilation), and sphincter/ constrictor muscle (PS only, M3 miosis or pupil constriction) |
| In the eye, the sympathetic nervous system innervates the __________ muscle, which causes _____________, or ___________. The parasympathetic nervous system innervates the ____________ muscle, which causes ________________, or __________ | sympathetic radial for mydriasis, parasympathetic sphincter for miosis |
| ß1 receptors are found predominantly in the _______ | heart |
| Activation of α1 receptors causes ______________________ | constriction of blood vessels, constriction of GI sphincters, constriction of urinary sphincter, inactivation of insulin receptor in liver causing blood glucose increase, |
| Activation of ß2 receptors causes _____________ of smooth muscle | relaxation |
| To stimulate dilation of the bronchioles in an asthmatic patient without causing stimulation of the heart, it would be best to give a selective ____ stimulant | beta 2 selective stimulant |
| Why do drugs that increase acetylcholine transmission, such as anticholinesterases, promote sympathetic as well as parasympathetic responses | both PS and sym use Ach at first synapse |
| A drug that can dilate the pupil and simultaneously block accommodation of the lens is a drug that (stimulates/blocks) (adrenergic/cholinergic) receptors | blocks cholinergic |
| Adrenomimmetics | drugs that produce response by interacting with alpha or beta adrenoreceptors on sympathetic effector cells, direct, indirect, reuptake inhibition or COMT & MAO inhibitors |
| Direct adrenomimmectis | eg epinephrine, norepinephrine, dopamine at high conc, isoproterenol |
| Indirect adrenomimetics | cause release of NE, eg tyramine, ephedrine, amphetamin |
| Cathecolamine reuptake inhibitors | cocaine, imiprisine, amirtryptyline, SSRIs |
| COMT & MAO inhibitors | increase catecholamine levels by inhibiting breakdown |
| Adrenergic receptors | G protein coupled receptors, alpha1, alpha2, beta1, beta2, beta3 |
| Norepinephrine | acts on alpha 1&2, beta 1, but not beta 2; most same effects as epinephrine but with beta2, it does not dilate bronchial smooth muscle to dilate airways and does not dilate blood vessels to skeletal muscles, |
| Epinephrine | all adrenergic receptors, beta1 to incr HR,CO,contract&lusitropy, alpha1 dilates pupil, beta2 dilates bronchial sm muscle, alpha1 constricts vessels to skin, beta2 dilates vessels to sk muscle, beta2 relax GI, alpha1 contracts sphincters, inc glucose |
| Sympathetic innervation blood vessels to skeletal muscle | primarily beta2 to dilate, at high levels of epinephrine, alpha1 to constrict blood vessels |
| Why do local anesthetic contain epinephrine | to achieve vasoconstriction through alpha1 receptors to keep anesthetic local |
| Isoproterenol | acts on adrenergic beta but not alpha, large group on amine nitrogen increases affinity for beta receptor, same effects as epinephrine except not dilate pupils, not constrict blood vessels to skin, not contract GI & bladder sphincters |
| Catecholamines on glucose level | epinephrine has strongest effect on glucose level because it acts on alpha1&2, beta 2 of pancreas to decrease insulin and increase glucagon, while norepinephrine doesnt act on beta2 and isoproterenol doesn't acts on alpha |
| Dopamine | acts on dopamine receptors, and with increasing concentrations Beta1 then alpha 1 then alpha2 |
| Sympathetic innervation of veins | alpha1 predominates on veins, so epinephrine and norepinephrine constrict veins to increase BP, alpha1 & beta2 together in capillaries |
| Epinephrine effect on vessels to skeletal muscle | dose dependent; at low dose, activates beta2 for dilation, and high dose, activates alpha1 for constriction |
| Sympathetic stimulation effect on blood supply to different organs | increase to heart, lungs and skeletal muscles, brain stays same, decrease to skin, GI, and genitals |
| Norepinephrine effect on heart | sudden increase in peripheral resistance due to contriction of blood vessels with stimulation of alpha1 & not beta2, increase in systolic, diastolic, & MAP, induces reflex bradycardia |
| Epinephrine effect on heart | peripheral resistance decreases through beta2 stimulation, systolic pressure increases, diastolic pressure decreases, MAP stays same, pulse increases with rate of contraction through beta1 |
| isoproterenol effect on heart | peripheral resistance decreases through vasodiation through beta2 receptors, significant decrease in diastolic and slight increase insystolic, slight overall decrease in MAP, increased pulse rate due to increase contraction rate through beta1 |
| presynaptic autoreceptors | alpha2 for NE on presynaptic terminal to monitor amount of NE being released to downregulate NE release when NE excess |
Created by:
rcconrad