Term
decrease TG 7-30%
increase HDL 5-15%
decrease LDL 18-55% |
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Definition
| How much do HMG CoA reductase inhibitors affect TG, HDL, and LDL? |
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Term
HMG CoA reductase inhibitors
this drug can reduce TG, however normally only with simvastatin at high doses or any dose of atorvastatin or rosuvastatin |
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Definition
use this drug if primary issue is LDL.
this drug needs to be first line in CHD or CHD risk equivalent patients unless contraindicated in the individual patient |
|
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Term
no change in TG or increase 3-10%
increase HDL 3-5%
decrease LDL 15-30% |
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Definition
| How much do bile acid sequestrants affect TG, HDL, and LDL? |
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Term
bile acid sequestrant
colesevelam (Welchol) is not to be used if TGs are > 500 |
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Definition
could be used first line in someone that has a contraindication to statin therapy or in some one who is not a CHD or CHD risk equivalent patient
do not use in patients with TGs >200 or 400
this agent could be an add on therapy for someone who already is on a statin, TG are stable and needs further reduction with LDL |
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|
Term
decrease TG 20-50%
increase HDL 15-35%
decrease LDL 5-25% |
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Definition
| How much does niacin affect TG, HDL, and LDL? |
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Term
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Definition
could use first line in someone that does not need that much attention in lowering LDL however needs bid increase in HDL and moderate reduction in TG
could also be a great add on therapy for someone who is already on a statin and needs further increase HDL and only moderate reduction in TGs
would want to stay away from this agent if DM is not controlled (A1c > 9%), active or recent history of PUD (due to irritation of GI) or if patient had severe gout
remember to titrate these patients up to 1.5-2g per day to get the best cholesterol lowering benefits
remember to educate patient to take ASA 30-60 minutes prior to administration to reduce flushing |
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|
Term
decrease TG 20-50%
increase HDL 10-20%
decrease LDL 5-20% |
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Definition
| How much do fibric acid derivatives affect TG, HDL, and LDL? |
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Term
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Definition
this agent is very similar to niacin in how it greatly affects TG and HDL.
could be used first line in patients who need extensive TG lowering, moderate HDL increase and little LDL reduction. A lot of time if the patient is not a CHD or CHD risk equivalent and TGs are too elevated even after TLC for 3 months we would start this agent because we would need to correct the TGs before we can even calculate their LDL to find out if LDL is close to goal.
could also be a great add on therapy for someone who is already on a statin and needs extensive decrease in TGs and moderate increase in HDL. Just remember to educate patient about possibility of myopathies. Safe if monitored and educated properly. Remember do not exceed 10mg of simvastatin/rosuvastatin while on gemfibrozil per package insert. All other statins you can go to max dose because package insert does not say anything about dose limits, however need to know the higher the statin dose in combination, the increase chance of myopathies.
RULE of thumb: if patient's TGs are > 500 or 600 and only need moderate HDL increase then start this agent over niacin, assuming there are no contraindications or major drug interactions. |
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|
Term
decrease TG 8%
increase HDL 1%
decrease LDL 18% |
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Definition
| How much does zetia affect TG, HDL, and LDL? |
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Term
zetia
ENHANCE trial indicated that vytorin was not any better in intima regression, therefore at this point a statin is always preferred, however some cases may warrant vytorin usage. |
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Definition
this agent has no data stating reduction in morbidity or mortality. Therefore if patient's risk for CHD is not that high, you could use if for monotherapy. However, best to use statin as first line.
this agent is a great agent for patients who are already on a statin and just have problems of LDL lowering and are not able to achieve goal on statin. |
|
|
Term
decrease TG 51%
increase HDL 9%
increase LDL 49% |
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Definition
| How much does lovaza affect TG, HDL, and LDL? |
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|
Term
|
Definition
FDA approved for patients with TGs > 500 mg/dL as monotherapy or if TG > 200 mg/dL and are on a statin
when selecting an OTC product, you would like the sum of DHA and EPA to be as close to that of the mg on the tablet. If not many times the fillers are saturated fats, which is not what a person with cholesterol needs. Also notice the caloric intake and pill burden with OTC products |
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Term
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Definition
| If the patient has CHD (h/o MI, unstable/stable angina, h/o coronary procedure, h/o acute coronary syndrome) and no other risk factors what is their LDL goal? |
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Term
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Definition
| If a patient has and CHD risk equivalents: PAD, AAA, CAD (transient ischemic attack or stoke), carotid stenosis > 50%, diabetes, or Framingham > 20% but do not have CHD what is their LDL goal? |
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Term
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Definition
| If a patient has CHD (h/o MI, unstable/stable angina, h/o coronary procedure, h/o acute coronary syndrome) and any of the following: multiple major risk factors (diabetes), severe and poorly controlled risk factors (smoking), multiple risk factors of metabolic syndrome (TG >200, non-HDL > 130, HDL < 40), h/o ACS what is their LDL goal? |
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|
Term
men waist circumference >40 inches
women waist circumference >35 inches
TG > 200
HDL < 40
BP > or equal to 130/> or equal to 85
fasting glucose >110 |
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Definition
| signs of metabolic syndrome |
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Term
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Definition
If a patient does not have CHD or CHD risk equivalent and 0-1 of the following risk factors what is their LDL goal?
smoking (past month)
HTN or on meds
HDL < 40
man > or equal to 45
female > 55
CHD in male first degree relative <55 or female <65
*may subtract 1 risk factor is HDL > or equal to 60 |
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|
Term
if Framing ham score is less than or equal to 20% LDL goal is <130
if Framingham score is >20% LDL goal is <100 |
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Definition
If a patient does not have CHD or CHD risk equivalent and have > or equal to 2 of the following risk factors, what is their LDL goal?
smoking (past month)
HTN or on meds
HDL < 40
man > or equal to 45
female > 55
CHD in male first degree relative <55 or female <65
*may subtract 1 risk factor if HDL > or equal to 60 |
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|
Term
thiazides
oral contraceptives
alcohol
accutane |
|
Definition
| medications that increase lipids |
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|
Term
diabetes
alcoholic hyperlipidemia
obtrusive liver disease (primary biliary cirrhosis and extrahepatic biliary obstruction)
hypothyroidism |
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Definition
| disease states that alter lipids |
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Term
| As preload increases, contractility increases. As an adaptive mechanism to HF, the body will increase preload (extra volume) to help with contractility. Eventually this effect plateaus. |
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Definition
adaptive mechanisms of heart failure:
frank startling curve |
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Term
| the heart tries to pump harder to compensate for HF. this leads to increased muscle mass but not increased pumping ability. Instead, the actin and myosin become fibrotic. |
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Definition
| adaptive mechanisms of heart failure: myocardial hypertrophy |
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Term
| SV and CO are low in HF = decreased tissue perfusion. Body’s normal response = activate adrenergic nervous system. Higher levels of NE and catecholamines are produced. Increased contractility and heart rate. Harmful long term b/c heart cannot relax enough to allow filling of the ventricles. |
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Definition
adaptive mechanisms of heart failure:
adrenergic nervous system |
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Term
| : if your body can’t get enough blood flow to vital organs it will try to conserve blood for the brain and heart. Body starts to shunt blood away from less important organs. May lead to kidney failure. |
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Definition
adaptive mechanisms of heart failure:
redistribution of blood flow |
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Term
starts a chain of events due to decreased CO and vasoconstriction (SNS).
Angiotensin II will increase afterload, trying to build up pressure and get more profusion to the rest of the body.
Leads to Na/water retention = increased blood volume. Eventually this will cause pulmonary congestion and systemic edema (preload no longer good)
Increased renal vascular resistance.
Since GFR is decreased more Na reabsorption in proximal tubule and loop of Henle. |
|
Definition
adaptive mechanisms of heart failure:
renin-angiotensin system |
|
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Term
starts days to months after an MI, insidious alterations of left ventricular dilation and hypertrophy.
at first these alterations help to preserve the heart.
after long periods of time the shape of the heart becomes spherical and heart failure occurs |
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Definition
| concept of cardiac remodeling |
|
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Term
|
Definition
| what type of heart failure occurs when ejection fraction is <40%? |
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|
Term
|
Definition
| what type of heart failure occurs when ejection fraction is >40%? |
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|
Term
| right ventricular dysfunction |
|
Definition
symptoms: abdominal pain, nausea, constipation, anorexia, bloating, ascites
signs: peripheral edema, hepatomegaly, jugular venous distension (JVD), hepatojugular reflux (HJR)
right or left ventricular dysfunction? |
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Term
| left ventricular dysfunction |
|
Definition
symptoms: dyspnea on exertion (DOE), paroxysmal nocturnal dyspnea (PND), orthopnea, tachypnea, cough, hemoptysis (coughing up blood)
signs: bibasilar rales (crackling), pulmonary edema, S3 gallop, pleura effusion, cheyne-stokes respiration
right or left ventricular dysfunction? |
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|
Term
symptoms: exercise intolerance, fatigue, weakness, nocturia, CNS symptoms
signs: tachycardia, pallor, cyanosis of the digits, cardiomegaly |
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Definition
| non specific signs and symptoms of heart failure |
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|
Term
|
Definition
no limitations to physical activity
NYHA Class ? |
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Term
|
Definition
ordinary activities leads to slight limitations and positive symptoms
NYHA Class ? |
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Term
|
Definition
less than ordinary activities leads to positive symptoms, however comfort at rest
NYHA Class ? |
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Term
|
Definition
any activity leads to discomfort, possible discomfort even at rest
NYHA Class ? |
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Term
|
Definition
high risk patient that does not yet have HF.
no identified structural/functional abnormalities
no signs/symptoms of HF
example: HTN, CAD, DM, cardiotoxic drug therapy, alcohol abuse, h/o rheumatic fever, family history of cardiomyopathy.
need to treat current disease states and control them.
AHA Stage ? |
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Term
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Definition
developed structural heart disease associated with HF, but never had any signs or symptoms of heart failure.
example: LVH or fibrosis, LV dilation or hypocontracility, asymptomatic valvular heart disease, previous MI
AHA Stage ? |
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Term
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Definition
current or prior symptoms of HF and underlying structural heart disease
example: dyspnea or fatigue due to LV systolic dysfunction, asymptomatic patients who are undergoing treatment for prior symptoms of HF
AHA Stage ? |
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Term
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Definition
advanced structural heart disease and marked symptoms of HF at rest despite treatments and require interventions
example: frequently hospitalized for HF, cannot be safely discharged from the hospital, in hospital awaiting heart transplant, at home receiving IV support for symptomatic relief, mechanical ventilation, hospice setting.
AHA Stage ? |
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Term
regular exercise is encouraged for patients with STABLE HF
sodium restriction close to 2g/day
sodium intact should not exceed 3g/day in any CHF patient
avoid excessive fluid, however fluid restriction is not advisable unless the patient has hyponatremia |
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Definition
| non pharm therapy for HF patients |
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|
Term
1) diuretics
2) thiazides
3) loop diuretics
**goal of diuretics is symptomatic control** |
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Definition
patients with significant volume over load should be treated with ( )
mild overload can be treated successfully with ( )
( ) should be started when there is sever volume overload, severe renal insufficiency (CrCl < 30ml/min), persistent edema despite thiazide diuretics |
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|
Term
chem7 + Mg
BP
S/sx of dehydration
body weight |
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Definition
| what should you monitor in patients on diuretics? |
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Term
| ACEi, B Blocker, and spironolactone |
|
Definition
| what are the cornerstone drugs that should be used for heart failure? |
|
|
Term
prevent progression (decrease remodeling)
improve exercise tolerance
improve sx
reduce morbidity/mortality
reduce hospitalization |
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Definition
| goals of using ACEi in heart failure |
|
|
Term
Chem7 (K, SrCr, Na)
BP
cough |
|
Definition
| what lab values should be monitored while on an ACEi? |
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|
Term
intolerance of ADEs
bilateral renal artery stenosis
K > 5.5
SBP < 90 |
|
Definition
| contraindications for ACEi use |
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|
Term
EF < 40%
if no signs of volume overload could possibly use as monotherapy
caution in SrCr > 3 or CrCl < 30, however could still see benefit from ACEi (ATLAS trail)
class effect
dose can be titrated over 2-3 weeks |
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Definition
| When should ACEi be definitely used for patients with HF? |
|
|
Term
their lack of effects on bradykinin
NOT EQUIVALENT to ACEi |
|
Definition
| what may alter the effectiveness of ARBs on morbidity and mortality in CHF? |
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|
Term
the patient is on ACEi, +/- loop, but still has bothersome symptoms
digoxin has NO effect on mortality
does improve: EF, exercise tolerance, quality of life
appropriate digoxin level: 0.5-1 |
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Definition
| when would you add digoxin to a regimen for a patient with HF? |
|
|
Term
GI: anorexia, N/V/D, Abd Pain
CNS: mental confusion, hallucinations, restlessness, weakness
visual: yellow/green halos, altered colors of objects, hazy, photophobia
cardiac: 2nd or 3rd AV block, premature ventricular beats |
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Definition
|
|
Term
Chem7 (K - hypokalemia will make digoxin toxicity worse)
HR
EKG
digoxin levels |
|
Definition
| what labs do you monitor for a patient on digoxin? |
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Term
| do not protect against cardiac remodeling like B Blockers do b/c they have no effect on catecholamine binding. |
|
Definition
| why are non DHP CCB contraindicated for HF? |
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Term
|
Definition
| ACEi have a cardioprotective effect at any dose, whereas ( ) have to titrated up every 2 weeks to the maximum daily dose of 200mg/day to achieve cardioprotection |
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|
Term
depression
decreased libido
confusion
glucose control |
|
Definition
|
|
Term
|
Definition
| what labs should be monitored for a patient on a B blocker? |
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