Hypercholesterolemia: Clinical (To be retired)
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Hypercholesterolemia: Clinical (To be retired)
Cardiology
Cardiology
Acute coronary syndrome: Clinical sciences
Advanced cardiac life support (ACLS): Clinical (To be retired)
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Coronary artery disease: Clinical (To be retired)
Heart failure: Clinical (To be retired)
Syncope: Clinical (To be retired)
Pericardial disease: Clinical (To be retired)
Infective endocarditis: Clinical (To be retired)
Valvular heart disease: Clinical (To be retired)
Cardiomyopathies: Clinical (To be retired)
Hypertension: Clinical (To be retired)
Hypercholesterolemia: Clinical (To be retired)
Pharmacology
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Sympathomimetics: Direct agonists
Muscarinic antagonists
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
Adrenergic antagonists: Beta blockers
cGMP mediated smooth muscle vasodilators
Calcium channel blockers
Adrenergic antagonists: Beta blockers
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Positive inotropic medications
Loop diuretics
Antiplatelet medications
Assessments
Hypercholesterolemia: Clinical (To be retired)
USMLE® Step 2 questions
0 / 4 complete
Questions
USMLE® Step 2 style questions USMLE
of complete
Reproduced from: Wikimedia Commons
Which of the following is the most appropriate high-dose supplementation to prevent further neurologic deterioration in this patient?
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Transcript
Content Reviewers
Rishi Desai, MD, MPHCholesterol is a lipid molecule that helps maintain the structure of cell membranes, and is a precursor to steroid hormones, bile acids, and vitamin D.
Although, every day, some new cholesterol comes in through the diet, most of the cholesterol we need is obtained through recycling existing cholesterol.
Most of that recycling happens in the intestines and is facilitated by bile acids which help us reabsorb cholesterol and bring it back into the bloodstream.
There are two main types of cholesterol: HDL or High Density Lipoprotein which is sometimes called “good cholesterol”, and LDL or Low Density Lipoprotein which is sometimes called “bad cholesterol”. But good and bad is overly simplistic, and like all things - the subtleties matter.
LDL is produced by the liver and it carries cholesterol out to the rest of the body.
If all of the cholesterol from LDL is not completely distributed to the peripheral cells, then HDL brings some of that cholesterol back from the peripheral tissues and sends it to the liver.
Now, what makes LDL bad and HDL good is that, whenever there’s a high blood concentration of LDL, the LDL can be ingested by macrophages that sit along vessel walls, forming atherosclerotic plaques.
Over decades, large atherosclerotic plaques can lead to myocardial infarctions, strokes, and peripheral vascular disease. That’s why we want to keep LDL blood levels under control.
On the other hand, HDL can remove cholesterol from cells and that can help reverse the process of atherosclerosis.
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