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Pharmacology I > Exam 2 Prep - CV > Flashcards

Exam 2 Prep - CV Flashcards

1
Q

Name three loop diuretics

A

Lasix

Bumex

Torsemide

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2
Q

Why are loop diuretics potassium wasting?

A

They increase the amount of sodium that’s reaching the DCT, and when that increased sodium reaches the DCT, it thinks the body is volume down

It reacts by releasing aldosterone, reabsorbing Na and getting rid of K+ and H+

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3
Q

Which drug class decreases the action of loop diuretics?

Why?

A

NSAIDs

Prostaglandins do something similar to Lasix: they increase sodium reabsorption in the loop

If you block prostaglandins, Lasix is basically just doing the amount of work they usually do, and you don’t get a big diuretic effect

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4
Q

Name two thiazides diuretics

A

Diuril

HCTZ

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5
Q

How do the MOAs of Loop diuretics and Thiazide diuretics differ?

A

Same mechanism, different place

Loop diuretics are in the thick ascending

Thiazides are in the DCT

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6
Q

What electrolyte changes do loop diuretics and thiazides cause?

A

Hypokalemia

Hyponatremia

Hyperglycemia

Hyperuricemia

Thiazides only: Increased LDLs and hypomagnesemia

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7
Q

Which diuretic may turn urine blue?

A

Spironolactone

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8
Q

What class of Diuretic is spironolactone?

A

Aldosterone ANTagonist

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9
Q

How can you reduce the potassium wasting effects of loop and thiazide diuretics?

A

Give a potassium sparing diuretic, blocking aldosterone’s ability to react to overreact to increased sodium in the tubule and start wasting K

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10
Q

Potassium sparing diuretics should not be given with _____

A

ACE inhibitors

They increase potassium levels

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11
Q

How can you tell if a drug is an ACE inhibitor?

A

It ends in “-pril”

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12
Q

How can you tell if a drug is an ARB?

A

It ends in “-artan”

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13
Q

How doe the MOAs of ACEIs and ARBs differ?

A

ACEIs block the production of Angiotensin II

ARBs block the binding sites of Angiotensin II (fewer adverse effects)

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14
Q

What are the two classes of CCBs?

A

Nondihydropyridines (which impact arterioles AND the heart)

Dihydropyridines (which only impact arterioles)

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15
Q

List two Nondihydropyridine CCBs

A

Verapamil

Diltiazem

These impact vasculature AND the heart

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16
Q

List two dihydropyridine CCBs

A

Amlodipine

Nifedipine

Nicardipine

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17
Q

You are transitioning a patient off Spironolactone and onto an ACE inhibitor. What should be done to facilitate this?

A

Stop the spironolactone at least a week before starting the ACE inhibitor to prevent hyperkalemia

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18
Q

What are the adverse effects of Beta 2 Blockade?

A
  1. Bronchoconstriction (usually insignificant, but in patients with asthma any increase in airway resistance can be life threatening)
  2. Hypoglycemia from inhibition of glycogenolysis (this is really only a concern in diabetic patients, who are dependent on beta 2 mediated glycogenolysis as a way of overcoming insulin-induced hypoglycemia. Diabetic patients should get Beta 1 blockers if possible
19
Q

Which vasodilator carries a risk for cyanide toxicity?

A

Nipride

20
Q

Which drugs can decrease the effectiveness of beta blockers?

A

Rifampin

Antacids

Barbiturates

Anti-inflammatories

21
Q

How does digoxin impact cardiac function

A
  1. Positive Inotrope
  2. Negative Chronotrope (Inhibits AV conduction, depresses the SA)
22
Q

What are signs of Digoxin toxicity?

A

Bradycardia

Tachydysrhythmias and PVCs

N/V

Confusion and visual disturbances

23
Q

What is a therapeutic digoxin level?

A

0.5-2

24
Q

What is the antidote for digoxin poisoning?

A

Digibind

25
Q

What are contraindications to digoxin?

A

2nd or 3rd degree block

THYROID disease (will most likely cause hypothyroidism)

Hypokalemia

26
Q

What kind of foods should patients taking digoxin eat in large quantities?

A

Food high in potassium

27
Q

A patient taking Verapamil is being started on digoxin. What should be done?

A

Reduce the dose of digoxin

28
Q

CLASS 1 ANTIDYSRHYTHMICS

A

Sodium Channel Blockers

Lidocaine

29
Q

CLASS 2 ANTIDYSRHYTHMICS

A

Beta Blockers

Propranolol, Metoprolol, Labetalol

30
Q

CLASS 3 ANTIDYSRHYTHMICS

A

Potassium Channel Blockers

Amiodarone

31
Q

CLASS 4 ANTIDYSRHYTHMICS

A

Calcium Channel Blockers

Only Nondihydropyridines are used, obviously

Diltiazem, Verapamil

32
Q

How will Lidocaine impact an EKG?

A

It won’t

33
Q

How will a beta blocker impact an EKG?

A

Prolong PR

Bradycardia

34
Q

How will amiodarone impact the EKG?

A

Prolong QT

35
Q

How will verapamil impact an EKG?

A

Prolong PR

36
Q

What will digoxin impact an EKG?

A

Prolong PR

Depress St

37
Q

What four classes of drugs are used to treat Angina?

A

Nitroglycerin

Beta Blockers

CCBs

Ranolazine

38
Q

When should statins be given?

A

At night, when LDL levels are highest

39
Q

Major AE of statins:

A

Liver Problems

Rhabdomyolysis

NEVER IN PREGNANCY

40
Q

Which drugs are used to treat Atherosclerosis?

A

Statins

Fibrates

Niacin

41
Q

What is a normal aPTT? What is a therapeutic aPTT?

A

Normal 40

Therapeutic 60-80

42
Q

Which class I antiarrhythmic would you use for Wolf-Parkinson White?

Which would you use for VTach?

A

A class 1a, like procainamide. These effect atrial sodium channels.

A class 1b, like lidocaine. These effect ventricular sodium channels.

43
Q

How can you tell from its name whether a beta blocker is Beta 1 selective or nonselective?

A

Selective beta blockers start with letters from A-M

Nonselective beta blockers start with letters from N-Z

44
Q

Why is it so dangerous to give a beta blocker to a patient who’s high on cocaine?

A

Alpha 1 receptors on blood vessels are counterbalance by Beta 2 receptors

Patients high on Cocaine have extremely high alpha 1 stimulation, that’s being mediated by Beta 2. If you give a beta blocker, you cause unopposed Alpha 1 activity, leading to extreme hypertension - potentially causing a stroke or aortic dissection

Pharmacology I (29 decks)

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