7-5-10 Pharm II Test 2
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| Pathogenisis of hypertension - 5 causes | Increase sympathetic activity, sodium retention with increased circulating volume, increased vascular rigidity and reactivity, increased circulating catecholamines and activation of renin-angiotesin-aldosterone system, and abnormal baroreceptor responces
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| What organ systems are effected by HTN that decrease life span (4 of them) | Stroke, CAD, renal failure, and retinopathy
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| When should surgery be delayed regarding diastolic BP | >110 mmHg
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| What are 3 classifications of drugs used for controlling BP (3 of them) | Diuretics, Vasodilators, and Adrenergic blocking agents
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| What are the first line of drugs to treat HTN | Diuretics
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| Name 4 vasodilator type of drugs | ACE-inhibitors, AT receptor antatagonists, calcium antagonists, and the direct vasodilator hydralazine (Apresoline)
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| Name an alpha 1 antagonist drug | Prozosin (Minipress)
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| Name 2 types of arterial HTN | 1)Systolic and 2)systolic and diastolic
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| What is a sign of systolic htn | A wide pulse pressure
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| Name 3 conditions that increase stroke volume | Thyrotoxicosis, Fever, and Aortic regurgitation
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| What is the cause of "systolic and diastolic" HTN | Increased peripheral vascular resistance
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| What are causes of increased PVR (5 of them) | Renal dz, Endocrine dz, Neurogenic dz, hypervolume, and hypercalcium
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| What are the other names of essential HTN (2 of them) | Primary hypertension and idiopathic hypertention
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| Physiological factors influencing arterial BP | Preload and contractility, HR, and PVR
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| "Increased ventricular strech usually leads to increased contractility" is what law | Starlings Law
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| What drugs decrease HR | Beta blockers
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| What is a principal mechanism for arterial BP control | Baroreceptor reflex
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| Baroreceptors are located where | Walls of most large arteries and in th neck
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| Where is the carotid sinus | Just above the carotid bifurcation
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| What is in the carotid sinus | A high density of baroreceptors in the wall of the sinus
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| When BP rises (esp. rapidly) where do the baroreceptors send their message | To the tractus solitarius of the medulla
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| What does the tractus solitatius of the medulla cause in HTN | Inhibition of the vasoconstrictor center and also excitement the vagal centers
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| Inhibition of the vasoconstrictor center and excitement the vagal centers cause | Vasodilatation of the veins and arterioles in the peripheral vascular beds and negative chronotropic and inotropic effects on the heart occurs. (slower heart rate with reduced force of contraction).
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| What are some concerns with giving anesthesia with HTN meds (3 of them) | Reduced SNS activity, Altered responses to SNS drugs (sympathomimetic), and Sedation
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| Reduced SNS activity includes(4 things) | Orthostatic hypotension, Excessive hypotension responces, Reduced responces to indirect acting drugs (ephedrine) because of depleted norepinephrine, and enhanced responce to catecholamines
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| T/F: Previously effective antihypertensive drug therapy should be continued during the perioperative period | True
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| Non-pharmacological ways to treat HTN (5 of them) | Diet, Stress reduction, Regular aerobic exercise, Wt reduction, smoking cessation, and lowering blood lipids
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| The first line of drug sequence to treat HTN is to first use | Ca blockers, beta blockers, ACE inhibitors, or AT antagonists (unless other dz processes contradict)
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| COPD should not receive what HTN med | Beta blockers
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| CHF pt should not receive which HTN med | Beta blockers or Ca blocker
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| How many miles of blood vessles are in a pound of fat | Orlando to Tampa and back (200 miles)
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| What USED to be the first line of drugs given to treat HTN | Thiazide diuretics (they cause too much potassium loss and increase serum lipids)
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| Diastolic pressure > 130 mmHg is defined as | Hypertensive crisis or Malignant hypertention
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| A Diastolic pressure >130 mmHg should be treated how and why | Emergently with parental agents and with A-lne monitoring because of end organ damage
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| What is the first drug of choice in hypertensive crises | Nipride (sodium nitroprusside)
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| What are the CNS causes of HTN crises | intracranial hemorrhage, head trauma, CNS tumor, thromboembolic stroke, subarachnoid hemorrhage
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| What are the CV causes of HTN crises | myocardial infarction, dissecting aortic aneurysm
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| What are the Renal causes of HTN crises | renal artery stenosis, parenchymal renal disease
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| What are Other causes (besides CNS, CV, and Renal) of HTN crises | ingestion of tyramine-rich foods in patients taking MAO inhibitors, preeclampsia, recreational drug use, hyperautonomic syndromes (chronic smoker or dysfunction), pheochromocytoma
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| THe two main classes of Diuretics used in chronic HTN | 1)thiazides and 2)potassium sparing drugs
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| What is the objective of using diuretics | Alteration of Sodium load - A reduction in sodium leads to reduced intravascular volume and a decrease in blood pressure
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| Thiazide (Hydroclorthiazide (Hydrodiuril)) diuretics cause an inhibition of NaCl transport in the | distal convoluted tubule
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| Long-term antihypertensive effects of thiazides appear due to | reduced vascular resistance - The exact mechanism responsible for the reduction in vascular resistance is not known
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| Thiazides, due to their inhibition of ??? increase sodium and chloride excretion | Na+-Cl- transport system
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| Since thiazides increase the sodium load at the distual tubule an indirect excretion of what happens because of what | an increase of potassium is excreted via the sodium/potassium exchange mechanism
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| Name potassium sparing drugs used in combination with Thiazide diuretics (2 of them) | Amiloride (Midamor) and Triamterene (Dyrenium)
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| Reducing what luminal charge in the distal tubule will cause "potassium sparing" | Potassium sparing drugs reduce the net negative luminal charge in the disal tubule
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| Name 3 Loop diuretics | Furosemide (Lasix), Bumetanide (Bumex), and Ethacrynic (Edecrin)
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| With Loop diuretics, 30-40 % of the sodium and chloride is reabsorbed in the | Ascending loop
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| T/F: Loop diuretics also increase renal blood flow by decreasing renal vascular resistance | True
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| T/F: Loop diuretics increase urinary Ca++ in contrast to the action of thiazides | True
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| Adverse effects of Loop diuretics | Ototoxicity, Potassium depletion, and Lasix and Edecrin can cause gout (blocking excretion of uric acid)
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| What receptors do HTN sympatholytic agents stimulate | Alpha 2
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| Name central acting sympatholytic HTN meds (3 of them) | Aldomet, Catapress, and Wytensin
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| In the initial phase of treatment Aldomet, Catapress, and Wytensin cause | sedation and dry mouth (aka xerostomia)
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| Sudden withdrawl of Aldomet, Catapress, and Wytensin cause | rebound HTN
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| How is the rebound HTN caused by sudden discontinuation of Aldomet, Catapress, and Wytensin corrected | Alpha and beta andrenergic antagonists
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| Name a central acting sympatholytic HTN med you can give epidural/spinal for analgesia | Clonidine 150-450 mcg (preservative free)
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| what are 2 other names for Nitroprusside | Nipride and Nitropress
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| Stopped hypertensive slide 30 ish |
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