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7-5-10 Pharm II #2

7-5-10 Pharm II Test 2

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