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7-5-10 Pharm II #2
7-5-10 Pharm II Test 2
| Question | Answer |
|---|---|
| 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 |
| What organ systems are effected by HTN that decrease life span (4 of them) | Stroke, CAD, renal failure, and retinopathy |
| When should surgery be delayed regarding diastolic BP | >110 mmHg |
| What are 3 classifications of drugs used for controlling BP (3 of them) | Diuretics, Vasodilators, and Adrenergic blocking agents |
| What are the first line of drugs to treat HTN | Diuretics |
| Name 4 vasodilator type of drugs | ACE-inhibitors, AT receptor antatagonists, calcium antagonists, and the direct vasodilator hydralazine (Apresoline) |
| Name an alpha 1 antagonist drug | Prozosin (Minipress) |
| Name 2 types of arterial HTN | 1)Systolic and 2)systolic and diastolic |
| What is a sign of systolic htn | A wide pulse pressure |
| Name 3 conditions that increase stroke volume | Thyrotoxicosis, Fever, and Aortic regurgitation |
| What is the cause of "systolic and diastolic" HTN | Increased peripheral vascular resistance |
| What are causes of increased PVR (5 of them) | Renal dz, Endocrine dz, Neurogenic dz, hypervolume, and hypercalcium |
| What are the other names of essential HTN (2 of them) | Primary hypertension and idiopathic hypertention |
| Physiological factors influencing arterial BP | Preload and contractility, HR, and PVR |
| "Increased ventricular strech usually leads to increased contractility" is what law | Starlings Law |
| What drugs decrease HR | Beta blockers |
| What is a principal mechanism for arterial BP control | Baroreceptor reflex |
| Baroreceptors are located where | Walls of most large arteries and in th neck |
| Where is the carotid sinus | Just above the carotid bifurcation |
| What is in the carotid sinus | A high density of baroreceptors in the wall of the sinus |
| When BP rises (esp. rapidly) where do the baroreceptors send their message | To the tractus solitarius of the medulla |
| What does the tractus solitatius of the medulla cause in HTN | Inhibition of the vasoconstrictor center and also excitement the vagal centers |
| 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). |
| What are some concerns with giving anesthesia with HTN meds (3 of them) | Reduced SNS activity, Altered responses to SNS drugs (sympathomimetic), and Sedation |
| 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 |
| T/F: Previously effective antihypertensive drug therapy should be continued during the perioperative period | True |
| Non-pharmacological ways to treat HTN (5 of them) | Diet, Stress reduction, Regular aerobic exercise, Wt reduction, smoking cessation, and lowering blood lipids |
| 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) |
| COPD should not receive what HTN med | Beta blockers |
| CHF pt should not receive which HTN med | Beta blockers or Ca blocker |
| How many miles of blood vessles are in a pound of fat | Orlando to Tampa and back (200 miles) |
| 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) |
| Diastolic pressure > 130 mmHg is defined as | Hypertensive crisis or Malignant hypertention |
| 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 |
| What is the first drug of choice in hypertensive crises | Nipride (sodium nitroprusside) |
| What are the CNS causes of HTN crises | intracranial hemorrhage, head trauma, CNS tumor, thromboembolic stroke, subarachnoid hemorrhage |
| What are the CV causes of HTN crises | myocardial infarction, dissecting aortic aneurysm |
| What are the Renal causes of HTN crises | renal artery stenosis, parenchymal renal disease |
| 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 |
| THe two main classes of Diuretics used in chronic HTN | 1)thiazides and 2)potassium sparing drugs |
| 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 |
| Thiazide (Hydroclorthiazide (Hydrodiuril)) diuretics cause an inhibition of NaCl transport in the | distal convoluted tubule |
| 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 |
| Thiazides, due to their inhibition of ??? increase sodium and chloride excretion | Na+-Cl- transport system |
| 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 |
| Name potassium sparing drugs used in combination with Thiazide diuretics (2 of them) | Amiloride (Midamor) and Triamterene (Dyrenium) |
| 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 |
| Name 3 Loop diuretics | Furosemide (Lasix), Bumetanide (Bumex), and Ethacrynic (Edecrin) |
| With Loop diuretics, 30-40 % of the sodium and chloride is reabsorbed in the | Ascending loop |
| T/F: Loop diuretics also increase renal blood flow by decreasing renal vascular resistance | True |
| T/F: Loop diuretics increase urinary Ca++ in contrast to the action of thiazides | True |
| Adverse effects of Loop diuretics | Ototoxicity, Potassium depletion, and Lasix and Edecrin can cause gout (blocking excretion of uric acid) |
| What receptors do HTN sympatholytic agents stimulate | Alpha 2 |
| Name central acting sympatholytic HTN meds (3 of them) | Aldomet, Catapress, and Wytensin |
| In the initial phase of treatment Aldomet, Catapress, and Wytensin cause | sedation and dry mouth (aka xerostomia) |
| Sudden withdrawl of Aldomet, Catapress, and Wytensin cause | rebound HTN |
| How is the rebound HTN caused by sudden discontinuation of Aldomet, Catapress, and Wytensin corrected | Alpha and beta andrenergic antagonists |
| Name a central acting sympatholytic HTN med you can give epidural/spinal for analgesia | Clonidine 150-450 mcg (preservative free) |
| what are 2 other names for Nitroprusside | Nipride and Nitropress |
| Stopped hypertensive slide 30 ish |
Created by:
smorrissey1
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