| Term 
 | Definition 
 
        | damage to the heart and the blood vessels or circulation, including the brain, kidney, and the eye |  | 
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        | Term 
 | Definition 
 
        | a maximal dose of a drug beyond which it no longer exerts a therapeutic effect; however, it toxilogical effect does increase |  | 
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        | Term 
 | Definition 
 
        | a drug that prevents or breaks up blood clots in such conditions as thrombosis ot embolism, includes anticoagulants, antiplatelets, and thrombolytics |  | 
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        | Term 
 | Definition 
 
        | defined hemodynamically as the product of cardiac output and total peripheral resistance |  | 
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        | Term 
 | Definition 
 
        | Influencing the rate of rhythmic movement |  | 
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        | Term 
 | Definition 
 
        | human biological variations of rhythm within a 24-hour cycle |  | 
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        | Term 
 | Definition 
 
        | Measurement of the renal clearance if endogenous creatinine per unit time |  | 
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        | Term 
 | Definition 
 
        | Covalently cross-linked degradation fragments of cross-linked fibrin polymer during plasmin-mediated fibrinolysis |  | 
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        | Term 
 | Definition 
 
        | a max dose of a drug, beyond which it not longer exerts a therapeutic effect; however its toxic effect does increase |  | 
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        | Term 
 
        | Fibrin split or fibrinogen degredation products (FDPs) |  | Definition 
 
        | Small peptides that result following the action of plasmin on fibrinogen and fibrin in the fibrinolytic process. |  | 
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        | Term 
 
        | Glomerular filtration rate |  | Definition 
 
        | The volume of water filtered from the plasma by the kidney via glomerular capillary walls into bowmans capsule per unit time; considered to be 90% of creatinine clearance and equivalent to insulin clearance |  | 
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        | Term 
 | Definition 
 
        | Blood pressure above 180/120 mmHG when te elevation of blood pressure is accompanied by acute, chronic, or progressing target organ injury |  | 
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        | Term 
 | Definition 
 
        | Blood pressure above 180/120 without signs or symptoms of acute target organ complications |  | 
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        | Term 
 | Definition 
 
        | a drug influencing the contractility of a muscle (heart) |  | 
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        | Term 
 
        | intrinsic sympathomimetic activity |  | Definition 
 
        | Having the ability to activate and block adrenergic receptors, producing a net stimulatory effect on the sympathetic ns |  | 
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        | Term 
 | Definition 
 
        | treatment of disease by drug therapy |  | 
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        | Term 
 | Definition 
 
        | an enzyme also known as angioteninogenase, released by the kidney in response to a lack of renal blood flow, and responsible for converting angiotensin to angiotensin I |  | 
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        | Term 
 
        | Subtitute neurotransmitter |  | Definition 
 
        | neurotransmitter or hormone replacements that may be weak or inert |  | 
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        | Term 
 | Definition 
 
        | blood pressurre of 140/90 mmHG or greater |  | 
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        | Term 
 
        | first line agents to treat hypertension |  | Definition 
 
        | thiazide diuretics, B blockers, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin II receptors blockers (ARBs), a-B blockers, and calcium antagonists |  | 
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        | Term 
 
        | Second line antihypertensives |  | Definition 
 
        | a2 agonists, vasodilators, and antiadrenergics |  | 
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        | Term 
 
        | what are ACEIs and how do they work |  | Definition 
 
        | Angiotensin-converting enzyme inhibitors. Primarily act through suppression of renin-angiotensin-aldosterone system |  | 
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        | Term 
 
        | are ACEIs effective alone? |  | Definition 
 
        | Yes but they can be combined with other hypertensive agents, especially thiazide-type diuretics |  | 
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        | Term 
 
        | what is the most common ACEI-induced adverse effect? |  | Definition 
 
        | Persistent nonproductive dry cough (20-30%) |  | 
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        | Term 
 
        | what other drugs do ACEIs have a significant drug reaction with? |  | Definition 
 
        | NSAIDs. These increase renin release by inhibiting renal vasodilating prostaglandins and thereby blunting or negating the antihypertensive effects of ACEIs. |  | 
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        | Term 
 
        | describe nonrenin pathways to generate angiotensin II from angiotensinogen |  | Definition 
 
        | this is done via tissue plasminogen activator, cathepsin G, and tonin. |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | They are angiotensin II type 1 receptor antagonists. Helpful since there are nonrenin ways of making angiotenin II |  | 
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        | Term 
 | Definition 
 | 
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        | Term 
 
        | ARBs have been shown to reduce what? |  | Definition 
 
        | morbidity such as target organ damage, cardiovascular events in systolic heart failure pts, and progression of nephropathy in pts with type 2 diabetes |  | 
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        | Term 
 
        | what do L type calcium channel blockers do? |  | Definition 
 
        | They mediate coronary and peripheral vasodilation and may also cause reflex sympathetic activation or a negative inotropic effect |  | 
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        | Term 
 
        | what do conventional calcium channel blockers (CCBs) do? |  | Definition 
 
        | CCBs inhibit only L-channels |  | 
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        | Term 
 
        | what are 2 negative chronotropic effects? |  | Definition 
 
        | lowers SA node automaticity and decreases AV node conduction |  | 
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        | Term 
 
        | Name 2 negative inotropes and their effects |  | Definition 
 
        | Verapamil and diltiazem. they may exacerbate heart failure especially in pts with left ventricular dysfunction |  | 
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        | Term 
 
        | what kind of drugs lower the efficacy of calcium antagonist |  | Definition 
 
        | cytochrome P450 enzyme inducers since calcium antagonist are significantly metabolized by cytochrome P450 |  | 
        |  | 
        
        | Term 
 
        | what are the 3 antihypertensive effects of B blcokers? |  | Definition 
 
        | -Blockade of the B receptors on the renal juxtaglomerular cells -blockade of myocardial B receptors
 -blockade of central ns B receptors
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | an a-B blocker with B2ISA |  | 
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        | Term 
 
        | when is treatment with labetalol contraindicated? |  | Definition 
 
        | Contraindication: pts with asthma and COPD |  | 
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        | Term 
 
        | side effect of beta blockers include.. |  | Definition 
 
        | hyperglycemia and glucose intolerance |  | 
        |  | 
        
        | Term 
 
        | how are beta blockers metabolized and why is it important? |  | Definition 
 
        | by cytochrome P450. important because P450 inducers may decrease serum levels of B blockers |  | 
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        | Term 
 
        | what are 5 types of diuretics? |  | Definition 
 
        | Thiazides and thiazide like agents, loop diuretics, potassium sparing agents, carbonic anhydrase inhibitors, and osmotics |  | 
        |  | 
        
        | Term 
 
        | 2 diuretics that are primarily used for the management of hypertension are? |  | Definition 
 
        | thiazides and potassium sparing agents |  | 
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        | Term 
 
        | what kind effect will you have when combining diuretics with NSAIDs? |  | Definition 
 
        | effect of diuretic will be decreased |  | 
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        | Term 
 
        | what should potassium sparing agents be paired with and why? |  | Definition 
 
        | Thiazide diuretics since alone they are weak hypotensive agents. it can offset the potassium excretion effects of other diuretics |  | 
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        | Term 
 
        | how do potassium sparing agents work? |  | Definition 
 
        | they block sodium channels in the lumenal membrane of cells in the distal tubule and collecting duct, thereby attenuating the excretion of potassium, calcium, and magnesium. |  | 
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        | Term 
 
        | how do thiazide like diuretics work? |  | Definition 
 
        | their antihypertensive activity is caused primarily by direct vasodilation. |  | 
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        | Term 
 
        | what are indications for thiazide? |  | Definition 
 
        | hypertension, chronic edema, CHF, and ascites |  | 
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        | Term 
 
        | when do thiazides lose their antihypertensive potency? |  | Definition 
 
        | In pts with a creatinine clearance less than 30 ml/min |  | 
        |  | 
        
        | Term 
 
        | Loop diuretics are also referred to as.. |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | how do loop diuretics work? |  | Definition 
 
        | they act on the thick ascending limb of loop of henle where they decrease sodium reabsorption by competing for the chloride site on the Na+-K+-2Cl- symporter |  | 
        |  | 
        
        | Term 
 
        | what kind of diuretic potency do thiazides have? |  | Definition 
 
        | they have a limited diuretic potency |  | 
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        | Term 
 
        | where do aldosterone antagonists act? |  | Definition 
 
        | late distal tube and collecting duct |  | 
        |  | 
        
        | Term 
 
        | what affect to centrally acting adrenergic agents have? |  | Definition 
 
        | they affect CO and peripheral resistance. They have negative chronotropic and inotropic effects |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | they stimulate the brainstem a2 receptors resulting in a decrease in sympathetic outflow from the central NS |  | 
        |  | 
        
        | Term 
 
        | why are a2 agonist not considered 1st line therapy for antihypertensive? |  | Definition 
 
        | side effects like high incidence of anticholinergic-like side effects such as sedation, blurred vision, dry mouth, constipation, and urinary retention. also CNS side effects |  | 
        |  | 
        
        | Term 
 
        | what line of therapy are antiadrenergic agents considered to be? |  | Definition 
 | 
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        | Term 
 
        | why are vasodilators considered second line therapy for management of hypertension? |  | Definition 
 
        | because of their adverse effects |  | 
        |  | 
        
        | Term 
 
        | what are treatment for angina pectoris? |  | Definition 
 
        | nitrates, B blockers, calcium antagonists, and ranolazine. |  | 
        |  | 
        
        | Term 
 
        | why are vasodilators considered second line therapy for management of hypertension? |  | Definition 
 
        | because of their adverse effects |  | 
        |  | 
        
        | Term 
 
        | what are treatments for angina pectoris? |  | Definition 
 
        | nitrates, B-blockers, calcium antagonists, ranolazine |  | 
        |  | 
        
        | Term 
 
        | what does nitroglycerine do? |  | Definition 
 
        | reduces myocardial oxygen demand by causing venodilation or coronary arteries and collaterals, resulting in decrease end diastolic pressures |  | 
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        | Term 
 
        | dont forget to look at the questions at the end of the chpt |  | Definition 
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