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The source of this quiz is the notes for the Duke School of Medicine Exam 7 for Body and Disease 2011. If you are not in medical school at Duke, you won't enjoy or understand this quiz.
Therapy for angina
Name a type of angina
Name the molecule liberated in large amounts from ischemic myocytes that leads to the perception of pain
Name a type of angina for which pharmacotherapy without surgery is a good idea for treatment
What would you do in addition to giving drugs for unstable angina?
During what process are coronary arteries perfused? (You should have more than 60 and less than 100 each minute)
Doing this to the coronary arteries during hypoxia doesn't help - it's already maxed out.
The overall goal of therapy for angina is to reduce this
While your treatment for angina should help resolve the acute attack, it should also do this.
A drug that causes mitochondrial aldehyde dehydrogenase to release NO is this.
The duration of organic nitrate therapy is limited by:
The point of venodilation (what nitrates do) is this
If you want an organic nitrate to work, you must deliver it in a way that doesn't immediately send it to this organ
The one oral (not sublingual) organic nitrate we have is this
Name a side effect of nitrate therapy
Name a class of drug that can't be used for variant angina because it doesn't treat vasospasm but that aids in stable and unstable
Diabetes would make you think twice about a beta blocker, but you can still use it in most people. What condition would absolutely prevent you from using a beta blocker?
Name a drug that works only on vascular calcium channels to vasodilate and counteract vasospasm without directly affecting the heart
Name a drug that blocks cardiac AND vascular calcium channels
What kind of channel becomes increasingly important in the ischemic heart?
Name a drug that works on the late Na+ channel
Name the channel that causes the pacemaker current (If)
Name a drug that blocks the channels that cause the pacemaker current
What's the first line of therapy for stable angina (assume no comorbidities)?
What's the first line of therapy for unstable angina (assume no comorbidities)?
What's the first line of therapy for variant angina?
Anticoagulants and Hypercholesterolemia
What molecule is secreted from damaged endothelium that activates the coagulation cascade?
Clotting factors II, VII, IX, and X are carboxylated in a step dependent on what dietary substance?
What drug interferes with the carboxylation of the above-mentioned factors?
Arterial and venous thrombi differ in several ways. One of them is that arterial thrombi are made primarily of these cells (this has treatment implications).
tPA is often given as a 'clot buster.' It cleaves a precursor to produce what molecule?
What enzyme(s) does aspirin inhibit?
What platelet-activating molecule does asprin prevent the synthesis of?
Name another drug other than aspirin that prevents platelet activation by a different mechanism
The drug you just named prevents adenosine uptake and also inhibits another enzyme, Name that enzyme.
Name one of two drugs that inhibit platelet aggregation by antagonizing the P2T receptor.
Name a monoclonal antibody (ends in -mab) that inhibits GPIIb/IIa receptor, inhibiting platelet aggregation.
Monoclonal antibodies suck in one way - they can only be adminstered this way.
Inhibitors of platelet aggregation are particularly useful after what event?
Name a drug that blocks the GPIIb/IIIa receptor that is not an antibody
What does heparin accelerate the inactivation of?
Name a formulation of heparin (or a synthetic) that accelerates inactivation of factor Xa.
Heparin and its derivatives require this molecule as a suicide substrate to work.
Name a drug that, like a leech, prevents the binding of fibrinogen to thrombin.
This side effect of heparin makes the drugs you just named necessary alternatives in some patients.
Name a competitive inhibitor of thrombin.
If tPA is effective at cleaving plasminogen at the site of a clot, name a drug that cleaves it in the circulation
tPA + SK also cleaves what molecule that comprises the clot?
Estrogen, thyroid hormone, and what other hormone are required for maximal LDL receptor expression?
What type of cell expresses scavenger receptors that recognize LDL particles with oxidized lipid?
Familial hyperchylomicronemia results from a lack of this enzyme that is activated by ApoCII.
Which type of cholesterol particle is protective against heart disease when elevated?
Name a drug that reduces cholesterol by binding to bile acids and preventing their recirculation (but that can also raise triglycerides!).
Name a drug that inhibits HMG-CoA reductase, a critical enzyme for the biosynthesis of cholesterol.
The side effects of statins include drug interactions, liver dysfunction, and damage to this type of cell.
Name a drug that blocks intestinal absorption of cholesterol
Name a fibrate, a drug that activates PPAR-gamma to reduce trigylceride and LDL levels.
Name a drug that is more useful for raising HDL than for lowering LDL, though it does a little of that, too.
Below what number is the goal LDL level for a patient with coronary heart disease?
Above what value are at least dietary and lifestyle changes recommended for a patient with no other risk factors for heart disease?
In order to be a good osmotic diuretic, a substance should be nontoxic, pharmacologically and metabolically inert, and filtered, but not what?
Name an osmotic diuretic
Why isn't mannitol prescribed for outpatients? In other words, how is it delivered?
Mannitol can relieve cerebral edema or angle closure glaucoma because it doesn't enter what organs?
Thiazide Diuretics work in this part of the renal tubule.
Name a thiazide diuretic
Chlorthalidone works better than hydrochlorothiazide because it has a longer ____.
Thiazide diruetics reduce blood pressure by opening a channel in vascular smooth muscle that lets this ion through
ARBs and ACE inhibitors reduce aldosterone stimulation, preventing the side effect most diuretics have of reducing levels of this ion.
Name the prototypical loop diuretic
Name the ion channel blocked by the drug you just named
Name a molecule that is upregulated in endothelial cells by furosemide, leading to a drop in blood pressure.
Without the NKCC2 cotransporter, will the osmolarity of urine be greater than, less than, or the same as that of plasma?
Name a potassium-sparing diuretic.
What systolic pressure is the target for an individual with no comorbid conditions?
What systolic pressure is the target for an individual with diabetes or renal disease?
At what systolic pressure is a person said to have Stage 2 hypertension and need to be started on 2 drugs?
Name a condition for which a thiazide diuretic would not be your first choice for treating hypertension.
Name a beta-blocker that does nothing but antagonize beta1 receptors (and inhibit cardiac remodeling).
Name the beta-blocker that blocks EVERYTHING (Beta1, Beta2, Alpha1) and has anti-oxidant and anti-apoptotic effects.
Name the beta-blocker that is Beta1 selective but also increases NO availability.
Name the prototypical ACE inhibitor
Name the prototypical ARB
What does the ACE in ACE inhibitor stand for?
What side effect of ACE inhibitors most frequently causes them to need to switch to an ARB?
What class of drugs that can be used to treat hypertension relax the lower esophageal sphincter and can exacerbate GERD?
What class of second-line hypertension drugs have favorable effects on lipid profiles for unknown reasons?
Name a drug from the class you just named
Name a drug that increases inotropy by inhibiting the Na/K ATPase, thereby increasing availability of calcium for muscle contraction.
Traditionally, sCHF was treated by addressing inotropy, preload, and afterload. Inotropy was treated with digoxin, afterload with a vasodilator. What was used to reduce preload?
Digoxin also increases activity of the vagus nerve and slows conduction through what structure to treat arrhythmias?
A cardioprotective response to excess catecholamine signaling in CHF can include what receptors coupling to G proteins with Gi subunits?
Digoxin can cause tachyarrhythmias if a patient taking the drug has low levels of what ion?
True or false - Beta-blockers have use in both systolic and diastolic heart failure?
In CHF, calcium channel blockers are used in which kind of heart failure (systolic or diastolic)?
The calcium channel blockers that should be used for CHF include those that affect cardiac calcium channels. Name one.
Isosorbide dinitrate and hydralazine work together - isosorbide dinitrate is a source of this molecule and hydralazine inhibits ROS production, which would inactivate it.
The combination of isosorbide dinitrate and hydralazine is approved by the FDA for what population?
What drug is used in acute decompensated CHF for its ability to vasodilate by increaing cGMP and suppress the renin-angiotensin system?
In addition to oxygen, name two drugs you would want to use in acute decompensated CHF (you just named one)
True or false: All arrhythmias should be treated, whether or not they are symptomatic?
What is the EKG signature of digoxin-induced arrythmia?
Long QT, which can result from blocking potassium channels, can lead to what abnormal EKG reading?
Name a drug that is used as a local anesthetic that can also be used to terminate a ventricular arrhythmia.
What type of ion channel does the drug you just named block?
Name a drug that is both a class II and a class III antiarrhythmic because it blocks beta receptors AND potassium channels
Arrhythmias come in two flavors: supraventricular and ventricular. For which type are class II and IV antiarrhythmics used?
Class I antiarrhythmics all block Na+ channels; what other ion channels do class IC drugs block?
Slowing conduction through the AV node, an effect of class I drugs, can be bad because it can allow 1:1 conduction of this type of arrhythmia.
What kind of drugs are class II antiarrhythmics?
Class III antiarrhythmics, which prolong the QT interval, block this type of ion channel
Name a class III antiarrhythmic that works only on the channels you just named
Now name a class III antiarrhythmic that works on K+, Na+, and Ca++ channels, giving it less of a chance to cause torsade de pointes.
Class IV antiarrhythmics work on this type of calcium channel
Name a drug that is rapidly metabolized but can be used in the ED to terminate a supraventricular arrhythmia by activating inhibitory GPCRs (A1 receptors)
Instead of drugs, name a procedure that can be done to end an arrhythmia
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