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SA 107 Pharm Cards
| Question | Answer |
|---|---|
| Anticoagulation (Heparin) Area of influence: | Thrombin |
| Define Thrombin- | Enzyme critical for forming the basis of a blood clot. Factor IIa. |
| Anticoagulation (Heparin) physiologic response to medication: | Antithrombin. Directly inhibits the blood coagulation cascade. Inhibits the enlargement of existing and /or development of new clots. |
| Anticoagulation (Heparin) pharmacologic goal: | Prevent continued thrombus formation thru increased antithrombin. |
| Anticoagulation (Warfarin) area of influence: | Vitamin K. |
| Why is vitamin K important? | It's an important enzyme in the blood clotting and uncontrolled hemorrhaging. |
| Anticoagulation (Warfarin) physiologic response to medication: | Inhibits Vitamin K. Inhibits the synthesis of functional clotting factors. Inhibits the enlargement of existing and / or development of new clots. |
| Anticoagulation (Warfarin) pharmacologic goal: | Prevent continued thrombus formation thru inhibited Vitamin K synthesis. |
| Novel / New Oral Anticoagulants (NOACs) area of influence: | Factor Xa. First step of the common coagulation pathway. Thrombin IIa. Critical path that creates the fibrin lattice of a clot. |
| NOACs physiologic response to medication: | Inhibits Factor Xa. Inhibits initiation of the common coagulation pathway. Inhibits Thrombinn IIa. Inhibits the creation of a fibrin lattice of a clot. |
| NOACs pharmacologic goal: | Prevent continued thrombus formation thru inhibited Factor Xa and Thrombin IIa. |
| Antiplatelet area of influence: | Thromboxane A(2). |
| What is Thromboxane A(2)? | Enzyme critical for forming the basis of a blood clot. |
| Antiplatelet Physiologic response to medication: | Inhibits Thromboxane A(2). Decreases platelet aggregation. Causes vasodilation. |
| Antiplatelet pharmacologic goal: | Prevent platelet aggregation thru Thromboxane A(2) inhibition. |
| Thrombi area of influence: | Fibrin. |
| What does Fibrin do? | Creates a whitish filamentous lattice of protein which creates the framework for blood clots to form. |
| Thrombi physiologic response to medication: | Fibrinolytics. Lyse fibrin clots thru the proteolytic action of plasmin. In theory, breaks up the fibrin lattice. Thrombolytics. Lyse fibrin clots. In theory, breaks up the clot rather than the fibrin lattice. |
| Thrombi pharmacologic goal: | Lyse thrombi thru fibrinolysis or thrombolysis. |
| Factor XII hemostatic agent area of influence: | Kaolin. |
| What does Kaolin do? | Activates the coagulation cascade. |
| Factor XII hemostatic agent physiologic response to medication: | Blood clotting. Increase platelet aggregation. Causes vasoconstriction. Creates a cross linked fibrin clot. |
| Factor XII hemostatic agent pharmacologic goal: | Activate the coagulation cascade by introducing kaolin. |
| Muchoadhesive hemostatic agent area of influence: | Chitosan. Actives clotting. |
| Muchoadhesive hemostatic agent physiologic response to medication: | Blood clotting. Initiates clotting without activating the clotting cascade. |
| Muchoadhesive hemostatic agent pharmacologic goal: | Initiate clotting without activating the coagulation cascade by introducing chitosan. |
| Delaying sodium influx area of influence: | Sodium channels. Sodium channels are critical for propagating initial phase of depolarization. |
| Delaying sodium influx physiologic response to medication: | Sodium channel inhibition. Inhibits excitation of neural cells. |
| Delaying sodium influx pharmacologic goals: | Inhibits seizure activity thru sodium inhibition. |
| Increased neurotransmitter inhibition area of influence: | GABA-BZ receptors. Chloride channels hyperpolrize neutral cells. |
| Increased neurotransmitter inhibition physiologic response to medication: | Increased neurotransmission inhibition. Neural cells cannot function properly due to hyperpolarization from influx of chloride. |
| Increased neurotransmitter inhibition pharmacologic goals: | Inhibit seizure activity thru GABA-BZ receptor stimulation. |
| Reducing excitation area of influence: | N-methyl-D-asparate receptors (NMDA-glutamate). Increase neurotransmission. |
| Reducing excitation physiologic response to medication: | NMDA-glutamate inhibition. Inhibits excitation of neural cells. |
| Reducing excitation pharmacologic goals: | Inhibit seizure activity thru glutamate receptor inhibition. |
| Delaying calcium influx area of influence: | Calcium channels. L-type channels. Coronary artery tone. Increased myocardial inotropy. Responsible for phase 2 plateau in the cardiac action potential. T-type cells. Highest abundance in SA and AV nodes. N-type cells. Normal tissue. |
| Delaying calcium influx physiologic response to medication: | Calcium channel inhibition. L-type. Coronary artery dilation. Decreased myocardial inotorphy. T-type. Decrease automaticity of the SA and AV nodes. Decrease thalamic transmission. N-type. Decreased neural transmission. |
| Delaying calcium influx pharmacologic goals: | Inhibit seizure activity thru calcium channel inhibition. |
| Increased neurotransmission inhibition area of influence: | GABA-BZ receptors. Chloride channels hyperpolarize neural cells. |
| Increased neurotransmission inhibition physiologic response to medication: | Increased neurotrasmission inhibition. Neural cells cannot function properly due to hyperpolarization from influx of chloride. |
| Increased neurotransmission inhibition pharmacologic goals: | Reduce neural activity thru GABA-BZ receptor stimulation. |
| Opioid analgesia (Mu receptors) area of influence: | Nocieceptors associated with C fibers. |
| Describe C fibers: | unmyelinated. Dull, visceral pain. Slow transmission to the humonculus. |
| Opioid analgesia (Mu receptors) physiologic response to medication: | Decreases synthesis of cAMP. Increases K+ conductance. Decreases Ca+ conductance. |
| Opioid analgesia (Mu receptors) pharmacologic goal: | Reduce pain thru opioid Mu receptor stimulation. |
| Opioid analgesia (Kappa receptors) area of influence: | Nociceptors associated with A-delta fibers. |
| Describe A-delta fibers: | Myelinated. Sharp, severe somatic pain. Fast transmission to the humonculus. |
| Opioid analgesia (Kappa receptors) physiologic response to medication: | Decreases synthesis of cAMP. Increases K+ conductance. Decreases Ca+ conductance. |
| Opioid analgesia (Kappa receptors) pharmacologic goal: | Reduce pain thru opioid kappa receptor stimulation. |
| Opioid analgesia (Delta receptors) area of influence: | Nociceptors associated with mouse vas deferens. |
| Opioid analgesia (Delta receptors) physiologic response to medication: | Decreases synthesis of cAMP. Increases K+ conductance. Decreases Ca+ conductance. |
| Opioid analgesia (Delta receptors) pharmacologic goal: | no therapeutic response. |
| Non-steroidal anti-inflammatory drugs (NSAIDs) area of influence: | Prostaglandin. |
| What does prostaglandin do? | Produces inflammation thru vasodilation and increased cell permeability. Sensitizes a person to stimuli that normally would not produce pain. |
| NSAIDs physiologic response to medication: | Inhibits prostaglandin synthesis thru decreased COX synthesis. Reduces inflammation thru vasoconstriction De-sensitizes a person to stimuli that normally produces pain. |
| NSAIDs pharmacologic goal: | reduces pain response thru inhibition of prostaglandin synthesis. |
| NMDA analgesia area of influence: | NMDA receptors. |
| What do NMDA receptors due: | Responsible for pain response as well as wind up pain phenomenon. |
| NMDA analgesia physiologic response to medication: | Inhibit NMDA receptors. Inhibits the activation of NMDA receptors which are associated with causing pain as well as "wind up" pain / phenomenon. |
| NMDA analgesia pharmacologic goal: | Reduce pain response as well as "wind up"pain / phenomenon through inhibiting NMDA receptors. |
| Centrally acting medications area of influence: | Exerts effects directly within the brain and spinal cord. |
| Centrally acting medications Physiologic response to medication: | Unknown |
| Centrally acting medications pharmacologic goal: | reduce pain thru unclear measures. |
| Local anesthesia area of influence: | Sodium channels. |
| Local anesthesia physiologic response to medication: | Sodium channel inhibition. Inhibits excitation of ascending pain response. |
| Local anesthesia pharmacologic goal: | Reduce pain thru sodium channel inhibition. |
| General anesthesia area of influence: | GABA receptors. Chloride channels. |
| General anesthesia physiologic response to medication: | Increased neurotransmission inhibition. Neural cells cannot function properly due to negative hyper-polarization from influx of chloride. |
| General anesthesia pharmacologic goal: | create state of analgesia, LOC, amnesia. relaxation of skeletal muscles, suppress smoatic -autonomic endocrine reflexes with hemodynamic stability. |
| Inhalational anesthesia area of influence: | unknown |
| Inhalational anesthesia physiologic response to medication: | unknown |
| Inhalational anesthesia pharmacologic goal: | reduce pain thru unclear mechanism |
| Class Ia area of influence: | Sodium channels. Sodium channels are critical for propagating phase 0 depolarization of the cardiac cell. |
| Class Ia physiologic response to medication: | Sodium channel inhibition. Intermediate binding kinetics. Potassium channel inhibition. Intermediate binding kinetics. Moderately prolongs the cardiac action potential. |
| Class Ia pharmacologic goal: | Cardiac stabilization thru intermediate sodium channels and moderately prolonging the cardiac action potential. |
| Class Ib area of influence: | Sodium channel. |
| Class Ib physiologic response to medication: | Sodium channel inhibition. Rapid binding kinetics. Potassium channel inhibition. No binding kinetics. Shortens the cardiac action potential. |
| Class Ib pharmacologic goal: | Cardiac stabilization thru rapid sodium channel inhibition and shortening the cardiac action potential. |
| Class Ic area of influence: | Sodium channels. |
| Class Ic physiologic response to medication: | Sodium channel inhibition. Slow binding kinetics. Potassium channel inhibition. Minimal binding kinetics. Minimally prolongs the cardiac action potential. |
| Class Ic pharmacologic goal: | Cardiac stabilization thru slow sodium channel inhibition and minimally prolonging the cardiac action potential. |
| Class II area of influence: | Adrenergic system Alpha-1 receptors. Vasoconstriction. Beta-1 receptors. Increased chronotrophy, dromotrophy, inotropy. Beta-2 receptors. Vasodilation. Bronchodilation. |
| Class II physiologic response to medication: | Adrenergic system inhibition Alpha-1 receptor inhibition. Vasodilation. Beta-1 receptors. Decreased chronotrophy, dromotropy, inotropy. Beta-2 receptors. Slight vasoconstriction. Bronchoconstriction. |
| Class II pharmacologic goal: | Cardiac stabilization thru adrenergic system inhibition. |
| Class III area of influence: | Potassium channels. Potassium channels are critical for propagating phase 1 repolarization of the cardiac action potential. |
| Class III physiologic response to medication: | Potassium channel inhibition. Increased refractory period. Increased inotropic effects of the myocardium as a secondary byproduct. Markedly prolongs the cardiac action potential. |
| Class III pharmacologic goal: | Cardiac stabilization thru potassium channel inhibition and markedly prolonging the cardiac action potential. |
| Class IV area of influence: | L-type channels. T-type channels. N-type channels. |
| What are L-type channels responsible for: | Vascular tone. Increased myocardial inotropy Responsible for phase 2 plateau in the cardiac action potential. |
| What are T-type channels responsible for? | Highest abundance in SA and AV nodes. Also located in the thalamic neurons. |
| What are N-type channels responsible for: | Tend to be found in the neural tissue. |
| Class IV physiologic response to medication: | L-type inhibition. Vascular dilation. Decreased myocardial inotropy. T-type inhibition. Decreased automaticity of the SA and AV nodes. Decreased thalamic transmission. N-type. Decreased neural transmission. |
| Class IV pharmacologic goal: | Cardiac stabilization thru calcium channel inhibition. |
| Non-depolarizing area of influence: | Cholinergic nicotinic receptors. Causes muscle contraction. |
| Non-depolarizing physiologic response to medication: | Cholinergic nicotinic receptor inhibition. Decrease neuromuscular activity resulting in muscular paralysis. |
| Non-depolarizing pharmacologic goal: | Muscular paralysis thru cholinergic nicotinic receptor inhibition. |
| Depolarizing area of influence: | Cholinergic nicotinic receptors. |
| Depolarizing physiologic response to medication: | Cholingergic nicotinic receptors stimulation. Completely depolarizes the cell membrane thus preventing transmission of another action potential in muscular paralysis. |
| Depolarizing pharmacologic goal: | Muscular paralysis thru cholinergic nicotinic receptors stimulation. |
| Adenosine area of influence: | Cardiac pacemakers. SA and AV node |
| Adenosine physiologic response to medication: | Potassium channel activation. Prematurely moves the potassium polarity out of the cell. Adenylate cyclase inhibition. Decreases inward flow of calcium. |
| Adenosine pharmacologic goal: | Cardiac stabilization thru potassium channel activation and inhibiting calcium channels thru adenylate cyclase. |
| Cardiac glycosides area of influence: | Sodium/potassium pump. |
| What does the sodium/potassium pump do: | Exchanges 3 intracellular Na+ for 2 extracellular K+ions. |
| Cardiac glycosides physiologic response to medication: | Sodium/potassium pump inhibition. Increases intracellular sodium. Increases inotropy. Hyper-sensitized baroreceptors. Decreases chronotropy. |
| Cardiac glycosides pharmacologic goal: | cardiac stabilization thru sodium/potassium pump inhibition. |
| Statins area of influence: | HMG-CoA reductase. Enzyme that plays a critical role in producing cholesterol. |
| Statins physiologic response to medication: | HMG-CoA reductase inhibition. Decreases the level of LDL. |
| Statins pharmacologic goal: | Lower lipid levels thru HMG-CoA reductase inhibition. |
| Fibrates area of influence: | PPAR-alpha receptors. Increase lipoprotien lysolysis and increases HDL. |
| Fibrates physiologic response to medication: | PPAR-alpha stimulation. Decrease levels of triglycerides and increases levels of HDL. |
| Fibrates pharmacologic goal: | Lower lipid levels through PPAR-alpha receptor stimulation. |
| Niacin area of influence: | Niacin receptor. Inhibition of lipolysis in adipose tissue. Inhibits hepatic synthesis of LDL. Inhibits hepatic uptake of HDL. |
| Niacin physiologic response to medication: | Niacin receptor stimulation. Decreased levels of triglycerides. Increase levels of HDL. |
| Niacin pharmacologic goal: | Lower lipid levels thru niacin receptors stimulation. |
| Bile sequestrants area of influence: | Bile is equally ionized to be reabsorbed in the small intestines. |
| Bile sequestrants physiologic response to medication: | Ionization exchange of bile. Exchanges the negative ionization of bile. |
| Bile sequestrants pharmacologic goal: | Lower lipid levels thru changing the ionized structure of bile. |
| Cholesterol absorption inhibitors area of influence: | Cholesterol absorption at the brush border of the small intestines. |
| Cholesterol absorption inhibitors physiologic response to medication: | Cholesterol absorption inhibition. |
| Cholesterol absorption inhibitors pharmacologic goal: | Lower lipid levels thru inhibiting the absorption of cholesterol in the brush border of the small intestine. |
| Sympathomimetic area of influence: | Adrenergic system Alpha-1 receptors. Vasoconstriction of skin and viscera. Beta-1 receptors. Increase chronotrophy, dromotrophy and inotropy. Beta-2 receptors. Vasodilation of skeletal muscles and bronchodilation. |
| Sympathomimetic physiologic response to medication: | Adrenergic system stimulation. Alpha-1 receptors. Vacosconstrition of skin and viscera. Beta-1 receptors: Increased chronotropy, dromotropy, inotropy. Beta-2 receptors. Vasodiliation of skeletal muscles and bronchodilation. |
| Sympathomimetic pharmacologic goal: | Sympathetic nervous system like effects thru adrenergic receptor stimulation. |
| Parasympathomimetic area of influence: | Cholinergic-nicotinic and cholinergic- muscarinic |
| What do cholinergic nicotinic receptors do: | Cardiovascular. Increase chronotropy, dromotropy, inotropy. GI system: decreases GI motility. Neuromuscular junction: Enhances transmission. Continued stimulation of nicotinic receptors causes parasympathetic effects. |
| What do choliergic muscarinic receptors do: | CNS and Nerves: inhibition of current. Cardiac: decrease chronotropy, dromotropy, inotropy. GI system: increase motility. |
| Parasympathomimetc physiologic response to medication: | Cholinergic nicotinic receptor stimulation Cholinergic muscarinic stimulation. |
| Parasympathomimetic pharmacologic goal: | Parasympathetic nervous system like effects thru cholinergic receptor stimulation. |
| Sypatholytic area of influence: | Adrenergic system. Alpha-1 receptors: Vasoconstrction of skin and viscera. Beta-1 receptors: increased chronotropy, dromotropy, inotropy. Beta-2 receptors: Vasodilation of skeletal muscles and bronchodilation. |
| Sympatholytic physiologic response to medication: | Adrenergic system inhibition Alpha-1 receptor: vasodilation of skin and viscera. Beta-1 receptors: decrease chronotropy, dromotropy, inotropy. Beta-2 receptors: slightly vasoconstriction of skeletal muscles and bronchoconstriction. |
| Sypatholytic pharmacologic goal: | Blocks actions of sympathetic nervous system thru adrenergic receptor inhibition. |
| Parasympatholytic area of influence: | Cholinergic nicotinic and muscarinic. |
| Parasympatholytic physiologic response to medication: | Nicotinic inhibition. decrease heart and neuromuscular and increase GI. Muscarinic inhibition. |
| Parasympatholytic pharmacologic goal: | Blocks actions of parasympathetic nervous system thru cholinergic receptor inhibition. |
| Calcium chloride area of influence: | Essential element for regulating excitation threshold of nerves and muscles. |
| Calcium chloride physiologic response to medication: | Stabilizes neuromuscular function. |
| Calcium Chloride pharmacologic goal: | Increases calcium levels in acute situations which require neuromuscular stabilization. |
| Dextrose area of influence: | Is the principle glucose used by the body to create energy. |
| Dextrose physiologic response to medication: | Increases circulating levels of glucose. |
| Dextrose pharmacologic goal: | Increase glucose levels in acute situations where glucose levels are depleted. |
| Magnesium sulfate area of influence: | Calcium channels. Essential element for regulating the excitation threshold of nerves and muscles. |
| Magnesium sulfate physiologic response to medication: | Calcium channel inhibition. |
| Magnesium sulfate pharmacologic goal: | Increase magnesium levels in acute situation which require inhibition of neruomuscular transmission. |
| Sodium bicarbonate area of influence: | Primary buffer in the body. |
| Sodium bicarbonate physiologic response to medication: | immediately raises the pH of blood plasma. |
| What are the 2 situation to give Sodium bicarbonate? | DKA and cardiac arrest |
| Sodium bicarbonate pharmacologic goal: | Raises pH of blood during a bicarbonate responsive acidosis. |
| Thiamine area of influence: | Essential coenzyme required for carbohydrates metabolism |
| Thiamine physiologic response to medication: | Allows carbohydrates to be metabolized in a normal manner |
| Thiamine pharmacologic goal: | Prevent serious neurologgic conditions associated with abnormal metabolism of carbohydrates. |
| Cytolytic and non-cytolytic histamine degranulation area of influence: | H1, H2 and H3 receptors |
| What is the difference between cytolytic and non-cytolytic? | Cytolytic is extrinsic and non-cytolytic is intrinsic. |
| What are H1 receptors responsible for? | Bronchoconstriction peripheral vasodilation Increase GI motility Increased neurotransmission |
| What are H2 receptors responsible for? | Increased cardiac stimulation Increased GI acid secretion |
| What are H3 receptors responsible for? | Decreased neurotransmission |
| Cytolytic and non-cytolytic histamine degranulation physiologic response to medication: | H1 inhibition. Bronchodilation, peripheral vasoconstriction, decreased GI motility decreased neurotransmission. H2 inhibition: decreased cardiac stimulation decreased GI acid secretion. H3 inhibition: Increased neurotransmission |
| Cytolytic and non-cytolytic histamine degranulation pharmacologic goal: | Antihistamine effects thru histamine receptor inhibition. |
| Glucagon area of influence: | Glycogen. The form in which carbohydrate is stored in the body for future conversion into sugar. |
| Glucagon physiologic response to medication: | Increasing glucose: caused by the breakdown of stored glycogen to create increasing levels of circulating blood glucose. Increased cAMP synthesis independent of the adrenergic receptors. |
| Glucagon pharmacologic goal: | Increase circulating blood glucose thru the break down of glycogen. Stimulate cAMP synthesis independent of the adrenergic receptors. |
| Insulin area of influence: | Produced in beta cells within the islets of Langerhans in the pancreas. |
| Insulin physiologic response to medication: | Promotes glucose entry into the cell by stimulating insulin receptors located within the cell membrane. |
| Insulin pharmacologic goal: | Increased glucose utilization by stimulating insulin receptors located within cell membranes. |
| Alpha-glucosidase inhibition area of influence: | Alpha-glucosidase. breakdown of disaccharides into monosaccharides. |
| Alpha-glucosidase inhibition physiologic response to medication: | Inhibits the release of alpha-glucosidase. Prevents the break down of disaccharides into monosaccharides. |
| Alpha-glucosidase inhibition pharmacologic goal: | Decrease circulating blood glucose thru inhibiting alpha-glucosidase. |
| Biguanide area of influence: | Area of influence is not fully known. |
| Biguanide physiologic response to medication: | unknown |
| Biguanide pharmacologic goal: | Decrease circulating blood glucose thru unclear mechanisms. |
| Sulfonylureas area of influence: | Affects the beta cells within the pancreas |
| Sulfonylureas physiologic response to medication: | Positively hyper-polarize beta cells within the pancreas. Decease efflux of potassium. Increase efflux of calcium. Results in increased secretion of insulin. |
| Sulfonylureas pharmacologic goal: | Decrease circulating blood glucose thru positively hyper-polarizing beta cells within the pancreas. |
| Oxytocin area of influence: | Oxytocin is produced in the hypothalamus and stored in thr posterior pituitary gland. |
| Oxytocin physiologic response to medication: | Directly affects the myofibrils in the uterus which produces phasic contractions characteristic of normal delivery. |
| Oxytocin pharmacologic response: | Increase phasic contractions thru stimulation of myofibrils in the uterus. |
| Acetylcholinesterase inhibition area of response: | Responsible for the biotransformation of AcH. Increased AcH levels stimulate the parasympathetic nervous system. |
| Acetylcholinesterase inhibition physiologic response to medication: | inhibit Acetylcholine. Inhibits the effects of AcH at the site of parasympathetic receptors. Reactivates the acetylcholinesterase cascade. Begins biotransforming accumulated acetylcholine. |
| Acetylcholinesterase inhibition pharmacologic goal: | Inhibit the effect of Acetylcholine at the site of the parasympathetic receptors. Biotransform acetyllcholine through reactivating the acetylcholinesterase cascade. |
| Beta blocker overdose area of influence: | Adrenergic system inhibition. Alpha 1: vasodilation Beta 1: decrease chronotropy, dromotropy, inotropy Beta 2: slight vasoconstriction broncho-constriction |
| Beta blocker overdose physiologic response to medication: | Competes against sympathetic inhibition. Stimulates cAMP synthesis independent of the adrenergic receptors. Increase chronotropic and inotropic effects within the cardiac system. Increases vascular tone. |
| Beta blocker overdose pharmacologic goal: | Stimulates cAMP synthesis independent of adrenergic receptors. Increase chronotropy and inotropy thru sympathomimic or parasympatholytic effects. Manage vascular tone thru alpha receptor stimulation. |
| Calcium channel blocker overdose area of influence: | Calcium channel inhibition. L-type: vascular dilation and decreased myocardial inotropy. T-type: Decreases automaticity of the SA and AV nodes and thalamic trasmission. N-type: Decreased neural transmission. |
| Calcium channel blocker overdose physiologic response to medication: | Compete against calcium channel inhibition. Increase therapeutic levels of calcium Manage vascular tone by stimulating alpha adrenergic receptors. Stimulates cAMP synthesis independent of adrenergic receptors. |
| Calcium channel blocker overdose pharmacologic goal: | Compete against calcium channel inhibition. Increase therapeutic levels of calcium Manage vascular tone by stimulating alpha adrenergic receptors. Stimulates cAMP synthesis independent of adrenergic receptors. |
| Cyanide toxicity area of influence: | Cytochrome oxidase. Final enzyme in the electron transport chain. Facilitates oxygen exchange at the cellular level. |
| Cyanide toxicity physiologic response to medication: | Manage cyanide toxicity. Binds with cyanide so it cannot interfere with cytochrome oxidase. Convert cyanide into cyanocobalamin. |
| Cyanide toxicity pharmacologic goal: | Binds with cyanide so it cannot interfere with cytochrome oxidase. Convert cyanide into cyanocobalamin. |
| Opioid narcotic overdose area of influence: | Hyperactive state of opioid receptor stimulation. Decreased cAMP increased K+ conductance decreased Ca+ conductance |
| Opioid narcotic overdose physiologic response to medication: | Hyperactive narcotics effects are decreased thru opioid receptor inhibition. |
| Opioid narcotic overdose pharmacologic goal: | Antagonize the effects of opioid narcotics thru opioid receptor inhibition. |
| Tricyclic overdose area of influence: | TCA toxicity inhibits the following: Histamine receptors, GABA receptors, Alpha andrenergic receptors, Acetylcholine receptors, sodium and potassium channels, serotonin receptors. |
| Tricyclic overdose physiologic response to medication: | Competes with the inhibition of TCA toxicity. |
| Tricyclic overdose pharmacologic goal: | Reverse metabolic acidosis. Compete with sodium channel inhibition by increasing therapeutic levels of sodium. |
| G.I. poisoning area of influence: | Ingested poisons. Affects only ingested poisons. |
| G.I. poisoning physiologic response to medication: | Inhibits G.I. absorption inhibits absorption thru enterohepatic circulation. |
| G.I. poisoning pharmacologic goal: | Prevent bioavalibility of G.I. poisons thru adsorpting toxic substances. |
| Butyrophenone and phenothiazine area of influence: | Bilateral vomiting centers. Chemoreceptor Trigger Zone (CTZ). Visceral afferents in G.I. tract and outside G.I. tract. Afferents from extra medullary centers in the brain. |
| Butyrophenone and phenothiazine physiologic response to medication: | Dopamine receptor inhibition. Inhibit CTZ. Increase tone in cardiac sphincter. Increase force of G. I. contractions. Improve coordination of G.I. contractions. Enhance gastric emptying. |
| Butyrophenone and phenothiazine pharmacologic goals: | Antiemetic effects thru dopamine receptor inhibition. |
| Serotonin area of influence: | Bilateral vomiting centers. CTZ Visceral efferents in and outside of G.I. tract Afferents from extra medullary centers in the brain. |
| Serotonin physiologic response to medication: | Serotonin receptor inhibition. (5-HT3) diminishes the feedback loop associated with the act of vomiting. |
| Serotonin pharmacologic goal: | Antiemetic effects thru serotonin receptor inhibition. |
| Cytolytic and non-cytolytic histamine degranulation pharmacologic goal: | Antiemetic effects thru histamine receptor inhibition |
| Cytolytic and non-cytolytic histamine degranulation area of influence in ulcers: | H2 receptors. Increased G.I. acid secretions. |
| Cytolytic and non-cytolytic histamine degranulation physiologic response to medication in ulcers: | H2 receptor inhibition. Decrease G.I. acid secretions. |
| Cytolytic and non-cytolytic histamine degranulation pharmacologic goal in ulcers: | Decrease gastric acid secretions thru H2 receptor inhibition. |
| Proton pumps area of influence: | Proton pumps Responsible for moving protons (HCL) into the stomach. |
| Proton pumps physiologic response to medication: | Proton pump inhibition. Decrease G.I. acid secretions. |
| Proton pump pharmacologic goal: | Decrease gastric acid secretions thru proton pump inhibitors. |
| Thiazide diuretics area of influence: | Distal convoluted tubule: 4.5% sodium and 14% water |
| Thiazide diuretics physiologic response to medication: | Inhibits the reabsorption of sodium and water through the distal convoluted tubules. |
| thiazide diuretics pharmacologic goal: | Diuresis thru inhibiting the reabsorption of sodium and water thru the distal convoluted tubules. |
| Loop diuretics area of influence: | The loop of henle. 25% sodium 15% water |
| Loop diuretics physiologic response to medication: | Inhibits the reabsorption of sodium and water thru the loop of henle |
| Loop diuretics pharmacologic goal: | Diuresis through inhibition of reabsorption of sodium and water thru the loop of henle. |
| Potassium sparing diuretics area of influence: | Cortical collecting tubules. 4.5% sodium 14% water. |
| Potassium sparing diuretics physiologic response to medication: | Inhibit the reabsorption of sodium and water thru cortical collecting tubules. |
| Potassium sparing diuretics pharmacologic goal: | Diuresis thru inhibition of reabsorption of sodium and water thru the cortical collecting tubules. |
| Carbonic anhydrase inhibitors area of influence: | Proximal tubules. 70% sodium and water |
| Carbonic anhydrase inhibitors physiologic response to medication: | Inhibits the reabsorption of sodium and water thru the porximal tubules. |
| Carbonic anhydrase inhibitors pharmacologic goal: | Diuresis thru inhibiting the reabsorption of sodium and water thru thr proximal tubules. |
| Osmotic diuretics area of influence: | Proximal tubules 70% sodium and water Loop of henle 25% sodium 15% water |
| Osmotic diuretics physiologic response to medication: | increase osmotic pressure within the proximal tubules and the loop of henle |
| Osmotic diuretics pharmacologic goal: | Diuresis thru increasing osmotic pressure within the proximal tubules and the loop of henle. |
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