Pharmacology Quiz 3

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Preload: End diastolic ventricular volume; how much blood is in the ventricle after the heart has rested. Increasing preload increases cardiac output and b/p.

Preload is about volume. If the water pressure is low, the water output will be a trickle, not enough to water and sustain your pretty garden.
Afterload: Systemic vascular resistance; increase afterload and increase b/p.

Afterload is about pressure or resistance. If there is a link or narrowing in your garden hose, the volume will back up AND the output will drop.
Antihypertensives: Decrease preload and afterload. May decrease heart rate and decrease contractility.
What monitors blood volume?: Baroreceptors in the carotid.
What causes Renin to be released?: Decreased b/p and blood volume can cause renin to be released.
What happens after renin is released?: It stimulates AI, ACE transforms it into AII, which causes vasoconstriction and aldosterone to be released, which causes Na and H2O to be reabsorbed which increases b/p.
Arterial pressure: = cardiac output X peripheral resistance
Cardiac ouput: the amount of blood ejected from the left ventricle into the aorta per minute.
Another way to compute cardiac ouput (CO): Stroke volume (volume of blood ejected from LV with each contraction) X heart rate.

SV * h/r = CO
What factors influence cardiac output?: -Heart rate
-Force of the contraction
-Blood volume venous return to the heart

Increase any of these and increase cardiac output.
What systems control blood pressure?: 1. ANS
2. Renin angiotensin Aldosterone System
3. Endocrine. Release of epinephrine and NE from the adrenal medulla causes sympathetic stimulation.
Definition of hypertension: Increase b/p (140/90). Need to take at least 3 readings at least 1 week apart.
Blood pressure & hypertensive categories: Normal: <120/80
Blood pressure & hypertensive categories: Prehypertension: 120/80 - 139/89
Blood pressure & hypertensive categories: Stage 1 hypertension: 140/90 - 159/99
Blood pressure & hypertensive categories: Stage 2 hypertension: >= 160/100
Blood pressure & hypertensive categories: Hypertensive crisis: >210/120
Hypertension S/S: Asymptomatic (end stage - kidney failure, MI, heart attack, angina, stroke, vision). Headache in the morning, nose bleeds.
What's the most widely used diuretic and the first choice?: Thiazide diuretics
What are the drug classifications used for hypertension?: 1. Diuretics
2. Beta blockers
3. ACE inhibitors
4. Vasodilators
5. Alpha 2 agonist
6. Alpha 1 blocker
Diuretics: reduce volume overload
Beta blockers: They are selective, block Beta1 receptors: decrease heart rate, contractility, renin release. Causes vasodilation and diuresis.
Uses: HTN (first line drug), decreases preload & afterload, angina.
S/E: Hypotension, bradycardia (less than 60). High doses can cause bronchoconstriction & hypoglycemia.
NI: Safety, monitor h/r, never stop abruptly - can cause rebound effect.
ACE Inhibitors: MOA: prevents the conversion of angiotensin I to angiotension II by blocking ACE. End result is vasodilation and decreased reabsorption of Na and H2O.
Uses: HTN, CHF - reduces blood volume, decreases preload and afterload.
S/E: hypotension, first does effect - signif. drop in b/p, dry cough.
NI: Start w/ low dose, monitor b/p, best taken on empty stomach, b/w other drugs that cause hypertension.
Vasodilators: relaxes arterials, decreases venous return to the heart, reduces workload.
Alpha2 agonists: reduces sympathetic outflow from the brain
Alpha 1 blockers: vasoldilation
What are the different classifications of diuretics?: 1. Thiazide Diuretics
2. Loop Diuretics
3. Potassium Sparing Diuretics
4. Osmotic Diuretics
Thiazide Diuretics - MOA, Uses, and S/E: Most widely used; the first choice.
MOA: Blocks reabsorption of Na and Cl in the distal convoluted tubule. (won't reabsorb water, blood volume decreases)
Uses: Hypertension and edema
S/E: Lyte/H2O imbalance, increases uric acid (which causes gout), hypokalemia, increased blood sugar, (hyperglycemia inhibits release of insulin).
Thiazide Diuretics - NI: Monitor I&O and weight; monitor electrolytes especially K. Tell patient about increased voiding. Assess for hypokalemia; Not good for people with renal problems.
Loop Diuretics - MOA: Most effective & strongest; produces the greatest amount of diuresis.

MOA: Acts in the loop of Henle to block reabsorption of Na & Cl (where the most usually gets absorbed). Doesn't require good renal blood flow.
Loop Diuretics - Uses, S/E, & NI: Uses: Strong agent to mobilize fluid (a large amount rapidly). Also used for hypertension.
S/E: Lyte and H2O imbalance.(loss of H2O and K), ototoxicity, fluid vol. def., increases blood sugar, increases uric acid, hypotension.
NI: Assess for FVD, lyte disturb.; IV does start to work within 5 min. and last up to 2 hrs. Oral dose takes 30-60 min. and lasts up to 8hrs.
Examples of loop diuretics: Lasix or Bumex
Potassium Sparing Diuretics: The degree of diuresis is small. It's used as an adjunct to loop or thiazide diuretics. Balances the potassium.

MOA: Blocks aldosterone in the distal tubule.

Uses: Also for edema. Primarily for fluid in the belly (ascites).

S/E: Can cause hyperkalemia, arrythmias.

NI: Monitor for hyperkalemia.
Ascites: Excess fluid in the space between the membranes lining the abdomen and abdominal organs (the peritoneal cavity). This is typically caused by liver disease.
Osmotic diuretics: Not used for hypertension. Decreases intracranial pressure.
MOA: Increases osmolarity of the plasma. Pulls water into the vascular space so that it can be excreted.
Uses: Decreases intracranial and cerebral pressure.
S/E: Fluid and lyte imbalance, headache, nausea, vomiting.
NI: Monitor neuro status.
A potassium sparing drug: Aldactone
An osmotic diuretic drug: Mannital
Angiotensin II receptor antagonist: MOA: blocks the receptors of AII, results in vasodilation and decreases reabsorption of Na and H2O.
Uses: HTN
S/E: Hypertension, headache, fatigue, dizziness, can increase triglycerides. Can cause neutropenia. 2-3 weeks for full effect.
NI: Instruct patient about multiple drug interactions.
Examples of ACE inhibitors: Captopril, Vasotec
An example of Angiotensin II receptor antagonist: Avapro
An example of a beta blocker: Inderal
3 types of lipid lowering agents: 1. Cholesterol-Synthesis Inhibitors (statins)
2. Bile sequestering agents
3. Fibric acid derivatives
Cholesterol-Synthesis Inhibitors (statins): (Most effective)
MOA: Interferes with cholesterol synthesis. Inhibits hepatic HMG COA reductase (enzyme), causes hepatocytes to synthesize more LDL receptors, therefore more LDL is removed from the blood.
Lowers: primarily LDL, also decreases VLDL, increases HDL.
Use: Decrease LDL cholesterol (dose dependent). Effects are seen in 2 weeks, full effects in 4 weeks.
S/E: Few: GI, headache, rash
NI: Check LGTs. Admin in the evening.
What's an example of a Cholesterol-Synthesis Inhibitors (statins) drug?: Lovastatin, Simvastatin
Bile Sequestering Agents: MOA: Forms insoluable complexes with bile acids in the GI tract, prevents the reabsorption of bile acids and will increase the excretion. This triggers the liver to synthesize bile acids from cholesterol and the cholesterol plasma levels will decrease.
USE: Decrease LDL, may increase VLDL temporarily. Effects are seen in the first week, full effects in a month.
S/E: r/t GI (not systemic effects), constipation, nausea, indigestion, bloating (Decrease uptake of fat soluable vitamins.)
NI: Not usually given to patients with high VLDL levels. Need to watch for fat soluable vitamin deficiencies.
An example of a bile sequestering agent: Questran
Fibric Acid Derivatives: MOA: inhibits peripheral lipolysis and decreases hepatic extraction of fatty acids, reducing hepatic triglyceride production, increase the removal of cholesterol.
Use: Decrease VLDL, increase HDL. Effects are seen in 1 month.
S/E: GI problems, abnormal levels of LFT, hyperglycemia.
NI: Can increase the risk of hepatic malignancy and cholithiasis. Close monitoring with diabetic patients.
An example of a Fibric Acid Derivative drug: Gemfribrozil (Lopid)
Beta 2 Stimulation: Lung: Bronchial dilation, vasodilation, glycogenolysis (increases blood sugar)
Beta 1 stimulation: Cardiac: increase heart rate, force of contraction, and velocity of the A-V node.

Kidney: release of renin.

S/E: tachycardia, arrythmias, increase b/p, HTN, increase angina.
alpha 2 stimulation: Regulates transmitter release. Decreases NE. Blocks sympathetic stimulation.

S/E: Hypotension, headache, fatigue.
alpha 1 stimulation: vasoconstriction: increase b/p, HTN
What effect does Lopid (Fibric Acid Derivative) produce?: moderate hyperglycemic effect
Some nursing diagnoses for hyperlipidemia: - Risk for injury r/t increased blood lipid levels
- Risk for injury to skeletal muscles r/t adverse effects of drug therapies.
- Risk for altered nutrition...
Whay should Lovastatin be administered in the evening?: Because that is when most cholesterol synthesis occurs.
Explain why nicotinic acid can cause vasodilation and flushing.: This is attributed to histamine release.
Explain why CK levels may be evaluated in a patient receiving a statin?: Increased blood levels can cause an adverse effect. Increased CK levels cause myositis and rhabdomyelsis, which can be lethal.
2 contraindications for statins: Hypersensitivity, liver disease, and preganancy.
2 research findings involving the role of statins: + effect on vascular endothelium, have an antioxidant effect, inhibit inflammatory response, a role in preventing alzheimers, treating MS, and moderate diabetes.
List some therapeutic lifestyle changes that are recommended by NCEP: decrease intake of fats and cholesterol, decrease weight, increase physical activity, increase fiber, increase plant sterols.
What lab work would be ordered for a patient to evaluate lipid levels?: A total cholesterol level, an LDL level, and HDL level.
What is a statin?: (or HMG-CoA reductase inhibitors) form a class of hypolipidemic agents, used as pharmaceuticals to lower cholesterol levels in people at risk for cardiovascular disease because of hypercholesterolemia.

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