Term
| Framingham point scales used for? |
|
Definition
| estimating 10 year CHD risk |
|
|
Term
| LDL lipoprotein deposits cholesterol |
|
Definition
| on the artery walls, causing the formation of a hard, thick, substance called cholesterol plaque. |
|
|
Term
| these cholesterol particles prevent atherosclerosis by extracting cholesterol from the arterial walls and disposing of it through the liver |
|
Definition
|
|
Term
| class of drugs that lower the level of cholesterol in the blood by reducing the production of cholesterol by the liver. They block the enzyme in the liver that controls the production of cholesterol. |
|
Definition
|
|
Term
| typically includes high triglycerides, low HDL-C, and moderate elevations of total cholesterol and LDL-C. First line treatment should be |
|
Definition
Diabetic dyslipidemia
Statins |
|
|
Term
| a constellation of abdominal obesity, hypertension, insulin resistance, hypertriglyceridemia, and low HDL |
|
Definition
metabolic syndrome
Diet and exercise is #1 to do |
|
|
Term
| There is increased CHD risk associated with the presence of triglyceride levels > |
|
Definition
|
|
Term
| If triglycerides remain >200 mg/dL after the LDL-C goal is reached, further reduction in triglycerides may be achieved by |
|
Definition
| may be achieved by increasing the dose of a statin or of niacin. Combination therapy (statin plus niacin or statin plus fibrate) may be required, but caution is necessary with these combinations to avoid myopathy |
|
|
Term
| Statins are best restricted to use in patients who have only a moderate triglyceride elevation (e.g., 150–300 mg/dL), leaving treatment of patients with triglycerides above this level to triglyceride-lowering drugs: |
|
Definition
| niacin, fibrates, and fish oils. |
|
|
Term
| the enzyme catalyzing the rate-limiting step in hepatic cholesterol synthesis |
|
Definition
|
|
Term
| statins decrease synthesis of cholesterol by the liver, which results in two important effects: |
|
Definition
| the up-regulation of LDL receptors by hepatocytes and consequent increased removal of apolipoprotein (apo) E– and B–containing lipoproteins from the circulation, and a reduction in the synthesis and secretion of lipoproteins from the liver |
|
|
Term
| The net effect of statin therapy is to |
|
Definition
| lower plasma concentrations of cholesterol-carrying lipoproteins, the most prominent of which is LDL. Importantly, however, statins also increase the removal and reduce the secretion of remnant particles, i.e., very low density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL). |
|
|
Term
| elevated triglycerides indicates increased levels of? |
|
Definition
| indicating increased levels of triglyceride-rich VLDL and IDL remnants. |
|
|
Term
| Why are statins not effective in patients with Familial hypercholesterolemia? |
|
Definition
| due to defective LDL-receptor genes these drugs are not effective. |
|
|
Term
| In descending size and increasing density |
|
Definition
Chylomicrons-VDLD-IDL-LDL-HDL
LDL= TC- (HDL + TG/5) |
|
|
Term
| What Class: colesevelam (Welchol) |
|
Definition
Bile acid sequestrants
used to treat high blood cholesterol levels, especially high levels of LDL cholesterol. It does not lower cholesterol as much as the statin class of drugs, but when used in combination with a statin, it lowers cholesterol levels further than the statin alone. |
|
|
Term
| What Class: Colestipol (Colestid) |
|
Definition
Bile acid sequestrants
used for the treatment of high cholesterol in conjunction with dietary control; for the treatment of diarrhea due to increased intestinal bile acids after some types of surgery; for the treatment of itching associated with partial obstruction to the flow of bile due to liver disease. |
|
|
Term
| What Class:Atorvastatin (Lipitor) |
|
Definition
Statin
used for the treatment of elevated total cholesterol, LDL, triglycerides, and to elevate HDL cholesterol. The effectiveness of atorvastatin (Lipitor) in lowering cholesterol is dose-related. |
|
|
Term
| What Class: Rosuvastatin (Crestor) |
|
Definition
Statin
The most serious side effects are liver failure, muscle breakdown (rhabdomyolysis) and kidney failure |
|
|
Term
What Drug Class: Simvastatin Zocor
and Pravastatin (Pravachol) |
|
Definition
|
|
Term
| CHD risk reduction with a statin appears to occur as a result of several related changes: name some:) |
|
Definition
| restoration of endothelial function, reduction in inflammation, and stabilization of vulnerable plaque. The time course for these antiatherosclerotic effects of statins ranges from days to years. Within weeks to months after beginning statin therapy, endothelial function of coronary arteries is restored. |
|
|
Term
|
Definition
headache, upset stomach, fatigue, flu-like symptoms, and myalgia (without changes in creatine kinase [CK]).
One or both liver transaminases may be elevated to >3 times the upper limit of normal |
|
|
Term
| Myopathy a rare side effect of Statins can occur when: |
|
Definition
Myopathy is most likely to occur with higher doses, in patients with renal impairment, when a statin is combined with a fibrate, when a drug interfering with the metabolism of the statin is given concurrently (e.g., macrolide antibiotics, certain antifungal medications, gemfibrozil, cyclosporine), and in elderly women.
All patients started on statins should be instructed to report immediately muscle symptoms or brown urine and to have CK measured. If myopathy is present or strongly suspected, the statin should be discontinued immediately. |
|
|
Term
| Ezetimibe-Zetia works how? |
|
Definition
| cholesteral is kept from being absorbed through the brush border of the small intestine to inhibit dietary cholesterol absorption |
|
|
Term
| Ezetimibe (Zetia) is used for what? can it be combined with a statin? when is it not recommended? |
|
Definition
alone or in combinationwith statin to reduce TC, LDL and apo B. use with a statin to achieve additional small reductions in LDL cholesterol, compared to just the statin alone
Not recommended with statin in patients with moderate to severe liver disease |
|
|
Term
| Controversies with Ezetimibe Zetia: |
|
Definition
A study that pitted Vytorin against a placebo to compare the number of strokes and heart attacks that occurred in older people with narrowing of the heart’s aortic valveshowed that after five years, except for a decreased number of coronary artery bypasses in the Vytorin group, there were no differences in the incidence of strokes and heart attacks.
There is also a reported and currently studied possible association between increased cancer deaths in patients on Zetia. |
|
|
Term
Ezetimibe(Zetia) indications
Use with or without a statin for?
with a statin for?
with a fenofibrate for? |
|
Definition
Hypercholesterolemia
Familial hypercholesterolemia
Mixed Dyslipidemia |
|
|
Term
| What class: Cholestyramine (Questran) |
|
Definition
Bile acid sequestrants
Cholestyramine (Questran) is used for reducing cholesterol levels in the blood, to relieve the itching of liver and biliary disease, and to treat overdoses of digoxin or thyroid hormone.
The most common side effects are constipation, abdominal pain, bloating, vomiting, diarrhea, weight loss, and excessive passage of gas (flatulence). Long-term use of cholestyramine may cause a deficiency of vitamins A, D, E, and K. |
|
|
Term
Good choice for increased LDL esp. when combined with a statin. The combo can decrease LDL by more than 50%
Low potential for systemic SE’s
GI bloating and constipation limit compliance
Good choice for younger patients
Available in granules or tablets |
|
Definition
|
|
Term
| Disadvantages of Bile Acid Sequestrants: |
|
Definition
Can increase TGs (0-20%)
expensive
inhibits Vit A/D/K
binds to other drugs in the GI tract
Inconvenient dosing: multiple tabs mixing granules dosing away from other drugs
contraindicated in Hypertriglyceridemia/ pancreatitis |
|
|
Term
Bile Acid Resins MOA
Why would you add a statin? |
|
Definition
Bile acid resins bind bile acids in the intestine, are not absorbed and ar lost in the stool, which reduces the enterohepatic recirculation of bile acids. This promotes the upregulation of 7- hydroxylase and the conversion of more cholesterol in the hepatocyte into bile acids. This decreases the cholesterol content in the hepatocyte, which enhances LDL-receptor expression, which in turn increases the removal of LDL and VLDL remnant particles from the circulation.
The liver also increases its synthesis of cholesterol without statin interference, which partially negates the LDL-C–lowering efficacy of the bile acid resin. |
|
|
Term
| This drug Used alone, can raise HDL cholesterol levels by 30% or more. However, it is not as effective as a statin in lowering LDL cholesterol. |
|
Definition
|
|
Term
| niacin and lovastatin (Advicor) used for |
|
Definition
| Niacin and lovastatin (Advicor) is used for treating elevated blood levels of total cholesterol, LDL cholesterol, and triglycerides, and for raising low levels of HDL cholesterol. |
|
|
Term
best agent available for increasing HDL-C (increments of 30-40%); it also lowers triglycerides by 35-45% (as effectively as fibrates and the more potent statins) and reduces LDL-C levels by 20-30%.
What keeps it from being the #1 treatment? |
|
Definition
Niacin
Flushing, itching, headache (immediate-release, & Niaspan®)
Worse when initiating or increasing doses, taken with hot beverages or EtOH
Usually ceases within 1-2 weeks of steady dosing
Hepatotoxicity, GI (sustained-release)
Activation of peptic ulcer
Hyperglycemia and increased insulin resistance
May require insulin therapy in DM II |
|
|
Term
|
Definition
| Niacin appears to exert its effects by inhibiting lipoprotein synthesis and decreasing the production of VLDL particles by the liver. It inhibits the peripheral mobilization of free fatty acids, thus reducing hepatic synthesis of triglycerides and the secretion of VLDL. The net result is a reduction in VLDL particles secreted by the liver and thus less substrate to make LDL particles. It increases the production of HDL through mechanisms that are not clear. |
|
|
Term
| This disorder can contribute to hypertriglyceridemia by increasing free fatty acid delivery to the liver, which can either increase lipoprotein production or promote hepatic lipogenesis. A triglyceride-to-HDL ratio > 3.5 is a good predictor of this disorder |
|
Definition
|
|
Term
| What class: lower blood triglyceride levels by inhibiting production in the liver of VLDL and speeding up the removal of triglycerides from the blood. |
|
Definition
|
|
Term
| particles in the blood that carry triglycerides and lipoproteins |
|
Definition
|
|
Term
| Fibrates also are modestly effective in increasing blood HDL cholesterol levels; however, fibrates are not effective in lowering______ |
|
Definition
LDL
You may consider combining a fibrate with a statin. |
|
|
Term
what class:
Fenofibrate (Tricor)
Gemfibrozil (Lopid) |
|
Definition
|
|
Term
| Fibric Acid binds to what in the liver? |
|
Definition
Bind to PPARα in liver (regulates gene transcription in nucleus) resulting in:
Increased lipoprotein lipase (LPL) activity and TG clearance
decreases hepatic TG synthesis
lowers LDL (possibly by a reduction in LDL receptors affinity) |
|
|
Term
| Careful use of Fibrinc acid in patients that are prone to? |
|
Definition
|
|
Term
| Steps to minimize the risk of muscle toxicity with the Fibrate-Statin Combo? |
|
Definition
Use statin alone for non-HDL-C goals
Use fish oils or niacin rather than fibrates
Keep the doses of the statin and fibrate low
Dose the fibrate in the AM and the statin in the PM
Avoid (or cautiously use) combo in renal impairment
Assure no interactions
Teach the patient to recognize muscle symptoms
Discontinue therapy if muscle symptoms are present and CK is >10 times the upper limit of normal |
|
|
Term
| CHF is a condition in which the myocardium is not able to pump sufficient blood to provide oxygen and other nutrients to the vital organs of the body. The deficit can be caused by |
|
Definition
1) pump failure, where the heart muscle is just incapable of mechanically moving the blood around or
2) the cardiac workload is too much for the heart to overcome. These circumstances are usually caused by various conditions including a) arteriosclerosis b)HTN
3) valvular heart dx
4) dilated cardiomyopathy
5) congenital heart disease. |
|
|
Term
| Indeed, the most common cause of of right sided heart failure is |
|
Definition
| Left sided heart failure caused by coronary artery disease. |
|
|
Term
| The goal in treatment of CHF is to |
|
Definition
|
|
Term
| The three (3) classes of drugs that have proven to be of clinical benefit in treating CHF are |
|
Definition
Vasodialators (ie ACEI),
Diuretics (HCTZ),
Inotropic (Digoxin) agents as well as the newer Beta naturetic peptides |
|
|
Term
| The functional and therapeutic classification for prescription of physical activity for cardiac patients is? |
|
Definition
| NYHA: New York Heart Association Classification |
|
|
Term
| After an initial acute onset of CHF, there may be either progression |
|
Definition
| to death (fortunately in a small minority) or return toward baseline. Typically, this is followed by periodic exacerbations and ultimately death after later deterioration. At any time, sudden death can intervene. Traditionally 5 year mortalities are quoted as 50-75% with almost all patients dead by 10 years. |
|
|
Term
| This class of drugs is widely used to increase the strength of contraction of the heart. Inhibition of sodium pump activity in cardiac myocytes results in an increase in intracellular sodium concentration. This leads to an increase in intracellular calcium concentration by sodium-calcium exchange, which appears to be the proximal mechanism for enhancing cardiac contractility. |
|
Definition
|
|
Term
| Na/K pump rate is ______ in patients with CHF |
|
Definition
|
|
Term
| Name some cardiac compensation mechanisms to preserving Cardiac output? |
|
Definition
Increased Sympathetic Activity
Fluid Retention
Myocardial Hypertrophy |
|
|
Term
| Atrial and B-type natriuretic peptides are released from the myocardium in response to |
|
Definition
| stress –too great a preload and afterlood. |
|
|
Term
| Atrial and B-type natriuretic peptides do what? |
|
Definition
| inhibit aldosterone and renin secretion and serve as a physiologic antagonist of the RAAS. The natriuretic peptides also decrease endothelin levels, one of the most potent endogenous vasoconstrictors |
|
|
Term
| The hemodynamic actions of BNP include |
|
Definition
| a reduction in sympathetic tone to promote vascular relaxation and blood pressure reduction. |
|
|
Term
| neurohormonal blockers include what classes of drugs |
|
Definition
| ACE inhibitors, beta-blockers, and aldosterone blockers (eg, spironolactone) in the treatment of chronic HF |
|
|
Term
| the renin-aldosterone-angiotensin and adrenergic systems is counterbalanced by the? |
|
Definition
| natriuretic peptic system. |
|
|
Term
What does this?
Renal efferent arterioles constriction
Renal afferent arteriole dilation
Inhibit aldosterone and renin secretion
Physiologic antagonists of RAAS
Decrease endothelin secretion
Reduction in sympathetic tone |
|
Definition
| Atrial (atrium) and B-Type (ventricle) Natriuretic peptides |
|
|
Term
| dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND), hemoptysis are signs and symptoms of what type of HF |
|
Definition
|
|
Term
| ankle edema, abdominal pain/ swelling/ ascites, nausea are signs and symptoms of what type of HF |
|
Definition
|
|
Term
| What is the principal force driving fluid out of the vascular space into the interstitial space and into the alveolus to cause pulmonary edema |
|
Definition
| PCWP Pulmonary Capillary Wedge pressure |
|
|
Term
| Normal patients tend to have a PCWP of |
|
Definition
|
|
Term
| Asymptomatic LV dysfunction EF<40% treat with? |
|
Definition
| ACE inhibitor + Beta blocker (post MI) |
|
|
Term
|
Definition
| ACE Inhib. + beta block +/- digoxin |
|
|
Term
|
Definition
| ACEinh + diuretics + Beta blocker +/- digoxin + spiro |
|
|
Term
| Symptomatic CHF NYHA IV treatment |
|
Definition
| Inotropes + ACE Inhib+ diuretics + digoxin + beta blocker + spiro |
|
|
Term
| Drug class cause blood vessels to widen (dilate), thus decreasing the amount of work the heart has to do; they may also have direct beneficial effects on the heart. These drugs are the mainstay of heart failure treatment. They reduce symptoms and the need for hospitalization, and they prolong life. |
|
Definition
|
|
Term
| Reducing vasoconstriction reduces afterload of preload? |
|
Definition
|
|
Term
| reducing blood volume reduces preload or afterload? |
|
Definition
|
|
Term
| the amount of blood that fills the ventricles during diastole and stretches the myocardial fibers causing the heart to work harder to overcome this resistance is called? |
|
Definition
|
|
Term
| is the blood pressure in the systemic circulation that the heart must overcome in order to pump the blood out of the heart into the circulation is called |
|
Definition
|
|
Term
| All CHFers should take an______ unless they truly cannot. |
|
Definition
|
|
Term
| Take an ________ even if symptoms don't improve - it will help stop CHF from getting worse. |
|
Definition
|
|
Term
|
Definition
Postural Hypotension
Give 1st dose at bedtime
Renal Insufficiency
Decreased renal perfusion pressure by interfering with AT-II efferent arteriole vasoconstriction
Hyperkalemia
Monitor [K+] especially on thiazide/loop diuretics
Persistent Cough
Avoid use in Pregnancy |
|
|
Term
What drug class:
Decrease volume overload
Decrease Preload
Decrease Orthopnea
Decrease PND |
|
Definition
|
|
Term
| The goal of diuretics is to eliminate symptoms like |
|
Definition
| shortness of breath and signs of retaining fluid |
|
|
Term
| Proper diuretic dose is very important. Not taking enough can |
|
Definition
| reduce ACE inhibitor effectiveness |
|
|
Term
Used in the treatment of HTN, edema, CHF
Affects the distal renal tubular mechanism of electrolyte reabsorption |
|
Definition
|
|
Term
| When synthesis of prostaglandins is inhibited, as with nonsteroidal anti-inflammatory drugs , the efficacy of _______ decreases |
|
Definition
| diuretics—especially loop diuretics—decreases. |
|
|
Term
What class: Furosemide, bumetanide
Most powerful diuretics - up to 20% filtered sodium excreted. |
|
Definition
|
|
Term
|
Definition
thick segment (ascending) of loop of Henle
inhibits NaCl transport out of tubule by inhibition of Na/K/2Cl carrier by action on chloride-binding site.
Loop diuretics have a venodilator action which is seen clinically in the treatment of heart failure, with symptomatic relief occurring before the onset of diuretic action |
|
|
Term
What class:
Amiloride
Spironolactone
Triamterene |
|
Definition
| Potassium-sparing diuretics |
|
|
Term
| This drug is a competitive antagonist of aldosterone with a long half life. It is the only diuretic who's action is on vascular side of epithelium rather than luminal side. |
|
Definition
|
|
Term
| these drugs slow the heart rate and block excessive stimulation of the heart. They are appropriate for some people with heart failure. These drugs are usually used with ACE inhibitors and provide an added benefit. They may temporarily worsen symptoms but result in long-term improvement in heart function. |
|
Definition
Beta Blockers
Bisoprolol (Zebeta)
Carvedilol (Coreg)
Metoprolol (Toprol) (Lopressor) |
|
|
Term
What class:
General Cardiac Effects
Negative Inotrope
Reduces Myocardial Contractility
Negative Chronotrope
Reduces Heart Rate
Reduces Blood Pressure
Reduces Myocardial Oxygen Demand |
|
Definition
|
|
Term
| Beta Blocker contraindications: |
|
Definition
Asthma
Acute Congestive Heart Failure exascerbation
Concurrent Calcium Channel Blocker use |
|
|
Term
| All CHFers with stable class one to class 3 heart failure caused by left heart weakness should take a _________ unless they truly cannot. |
|
Definition
beta-blocker
Carvedilol is a beta blocker that is indicated for CHF |
|
|
Term
Increase Cardiac Contractility
Increase Cardiac Output
Increased levels of cyclic AMP
Increases Ca++ for increased contractility |
|
Definition
|
|
Term
| In most cases, therapy with ACEI’s and diuretics can control the symptoms of CHF so reserve__________ for those not controlled by these other drugs. |
|
Definition
|
|
Term
| What can increase the toxicity of digoxin predisposing the myocardium to ventricular arrhythmias |
|
Definition
|
|
Term
What Class:
inhibit PDE and increase cAMP in cardiac tissues
increase calcium influx and increase contractility
Has direct arterial vasodilator activity
Indicated for cardiac output maintenance and CHF |
|
Definition
| Phosphodiesterase Inhibitors like Milrinone IV and Inamrinone IV |
|
|
Term
What Class:
Increase cAMP and Ca++
Have inotropic and vasodilator effect
Increase CO
Decrease PCWP
Decrease symptoms & Increase exercise tolerance
Improve diastolic relaxation |
|
Definition
|
|
Term
| The Phosphodiesterase Inhibitor produces a prompt increase in cardiac output and decreases in pulmonary capillary wedge pressure and vascular resistance, without a significant increase in heart rate or myocardial oxygen consumption. The great majority of patients experience improvements in hemodynamic function within 5 to 15 minutes of the initiation of therapy. |
|
Definition
|
|
Term
| Name some Drugs used to treat Acute Severe Heart Failure: |
|
Definition
Amrinone
Milrinone
Dobutamine
Dopamine
Nitroglycerin
Nitroprusside |
|
|
Term
| This agent (a Phosphodiesterase inhibitor) is used for the short term treatment of congestive heart failure in patients who have not responded well to therapy with digitalis, diuretics, and vasodilators. |
|
Definition
|
|
Term
| Used in the short term treatment of patients with cardiac decompensation caused by depressed contractility from organic heart disease, cardiac surgical procedures, and acute MI. |
|
Definition
|
|
Term
| Stimulates both adrenergic and dopaminergic receptors, lower doses are mainly dopaminergic stimulating and produce renal and mesenteric vasodialation. Higher doses are both dopaminergic and beta-1 adrenergic stimulating to produce cardiac stimulation and renal vasodilation. Large doses are mainly alpha-adrenergic stimulants. |
|
Definition
|
|
Term
| Vasodilators cause blood vessels to dilate. These vasodilators are usually given to people who cannot take an ACE inhibitor or angiotensin II receptor blocker. |
|
Definition
Nitroglycerin
NITRO-BID (isosorbide dinitrate)
NITROL is particularly useful in people who have heart failure and angina. |
|
|
Term
| both arteriolar vasodilators that have no effect on veins. These drugs reduce blood pressure and afterload. They are used in combination with diuretics and beta-blockers (to decrease rebound tachycardia). |
|
Definition
| Hydralazine (Apresoline) and Minoxidil (Loniten |
|
|
Term
Vasodilator that
reduces preload
relieves ischemia
improves symptomatic HF |
|
Definition
|
|
Term
Vasodilator that
reduces afterload
reduces Bp
increases Cardiac output |
|
Definition
|
|
Term
Vasodilator that
reduces preload and afterload
increases Cardiac output
decreases neurohormonal activation
relieves dyspnea |
|
Definition
|
|
Term
| B-Natriuretic Peptide that is approved for acute decompensated CHF Results in increased CO and diuresis |
|
Definition
|
|
Term
Administered IV as an infusion or a bolus
Has a mean terminal T1/2 of 18 minutes
Effects:
Reduction in right atrial, pulmonary artery and capillary wedge pressures
Systemic and pulmonary vascular resistance |
|
Definition
|
|
