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MD Pharmacology > Kaplan-Lecture 2 > Flashcards

Kaplan-Lecture 2 Flashcards

1
Q

What can we use for IOP (open angle glaucoma) and ICP? How does it work

A

Mannitol, inhibits water reabsorption throughout the tubule. It increases urine volume. I pulls water out of eye and brain, so it can be used for increased intracerebral pressure.

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2
Q

What are the indications for acetazolamide and dorzolamide? MOA?

A

It blocks the production of aqueous humor, inhibits carbonic anhydrase, it eliminates the gradient Na/H.

They can also be used ofr acute mountain sickness.

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3
Q

Which medication causes hyperchloremic metabolic acidoses as a S.E.?

A

Carbonic anhudrase inhibitors : acetozolamide and dorzolamide.

Chloride is reabsorbed due to loss of bicarb.

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4
Q

What is the main difference in ions between loops and thiazides?

A

Hypocalcemia. It blocks the reabsorption of Ca and Mg. we will also have hypo K / mg with loop diuretics.

Thiazide diuretics will increase the reabsorption of Ca.

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5
Q

What is the only loop that is not a sulfonamide derivative?

A

Ethacrynate (Ethacrynic acid), can be given to people with sulfa allergic. SE: ototoxicity

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6
Q

What kind of drugs causes ototoxicity? Enhanced by?

A

Loops diuretics, enhanced by Aminoglycosides.

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7
Q

What kind of drugs interact with Li clearance?

A

Any loss of total body Na leads to decrease clearance of li. This will be a characteristic of loop diuretics. Furosemide/ Torsemide/ Ethacrynic acid.

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8
Q

What is the drug of choice for nephrogenic (ADH insensitive) DI?

A

Thiazide diuretics, except for li induced Nephrogenic DI. The preferred drug for li-induced is Amiloride (K sparing diuretic) it is Na channel blocker.

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9
Q

What diuretic blocks release of insulin in the pancreas and produce hyperglycemia?

A

Thiazide

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10
Q

What drug do we use in a pt. with hyperlipidemia?

A

Indapamide (thiazide diuretic) it is a lipid neutral. All of the other thiazides are lipid unfriendly causing hyperlipidemia.

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11
Q

What are the receptors inhibited by spironolactone in CHF and hirsutism?

A

CHF: aldosterone receptor blocker
Hirsutism: antiandrogenic

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12
Q

What are the drugs (Loops/thiazides - Ksparing) that produce alkalosis / acidosis?

A

Loops/Thiazides: alkalosis

K-sparing: acidosis

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13
Q

Names of ACE inhibitors? ARB?

A

Captopril / Lisinopril “Prils”

Losartan “Sartans” ARB

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14
Q

What are two major SE of ACE inhibitors? why do they cause this?

A

Dry cough and angioedema due to accumulation of bradykinin.

ARBs do not interefere with bradykinin degradation

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15
Q

What is the MOA of Aliskiren?

A

It is a direct renin inhibitor

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16
Q

What causes acute renal failure in renal artery stenosis and why?

A

ACE inhibitors as they block the efferent artery constriction maintaining RBF.

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17
Q

What are the two L-type ca cardiac channel blocker?

A

Verapamil and Diltiazem, we won’t see reflex tachy (they offset NE effects) Dipines (Nifedipine) has no way of doing that as it acts only in vascular ca channel blocker.

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18
Q

What can cause gingival hyperplasia?

What ca channel blocker causes constipation ?

A

Gingival (Nifidipine) - Dipine

Verapamil causes constipation

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19
Q

What are the name of alpha-1 blockers?

A

“Sins” Prazosin / Doxazosin/ Terazosin

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20
Q

What are two drugs that can cause orthostatic hypertension?

A

A drug directiy acting on SNS innervation of veins and drugs directly dilating veins. Alpha-1 inhibitors and nitroglycerin.

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21
Q

What drug is a selective arteriolar vasodilator?

A

Hydralazine, one of our HIP drugs that cause SLE. (ANA antihistone ab, fever, myalgia, and sore throat)

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22
Q

What is the MOA and uses of Minoxidil?

A

Open K channel, causing hyperpolarization of smooth muscle, resulting in arteriolar vasoldilation. Used for insulioma, severe HTN, and baldness.

23
Q

What are the worst drugs for dyspelipidimia? what are the ones that are lipid neutral?

A

Beta blockers and thiazides.
Lipid neutral are:
BB: Acetobutolol / Pindolol / Labetalol / carvedilol
THZ: Indapamide

24
Q

What are two drugs we can use to treat Primary pulmonary HTN?

A

Bosentan: endothelin -1 is a powerful vasocontrictor through ET-A and B receptors, bosentan blocks the ET-A receptor. SE: vasodilation, headache, flushing, hypotension)

Sildenafil: Inhibits type V PDE , increasing cGMP, relaxing pulmonary arteries and decrease pulmonary HTN.

25
Q

What drug causes yellow green vision as SE?

A

Digoxin (inhibitor of cardiac Na/K ATPase)

26
Q

What are the drugs that displaces digoxin from its tissue binding protein producing toxicity?

A

Verapamil / Quinidine

27
Q

What are the 5 classes of antiarrhytmic drugs?

A 
Class I: Fast Na channel blocker 
Class II: Beta blocker
Class III: K+ blocker
Class IV: Ca channel blocker
Class V: Adenosine
28
Q

What are the two drugs that present with ringing in the ears?

A

Tinnitus is a common early sign of intoxication with Aspirin and Quinidine.

29
Q

What are the class I drugs?

A

Ia: Block fast Na channels preferentially bind to open (state dependent) , Also blocks K channel, prolongs repolarization.
Quinidine and Procinamide (One of our HIP) drugs
Ib: Block inactivated channels. Lidocaine / Mexiletine

30
Q

Pt. presents post-MI, what’s the most indicated drug?

A

Beta blockers: Propanolol (nonselective) and cardioselective acebutolol and esmolol

31
Q

Which drugs increase ERP? What can it lead to?

A

K+ channel blockers, the prolong QT which can lead to Torsades. Class I and Class III antiarrhythmics.

32
Q

Pt. died from hepatic necrosis and pulmonary fibrosis. A week prior he presented to his physician with blue pigmentation mainly in the face, phototoxicity, and corneal deposits. What drug was this pt. on?

A

Amiodarone: K+ channel blocker. This happens because amiodarone has a large Vd and binds extensively to tissues.

33
Q

Pt. presents with increase thyroid levels which is causing hyperthyroidism symptoms, what is this pt. on?

A

Amiodarone, increases levels of iodine (5-10% of pts develop this symptoms). This drug also blocks 5’deiodinase and can cause hypothyrodism.

34
Q

What is the MOA of adenosine?

A

Activates adenosine receptors: causes Gi-coupled decreases in cAMP, decreases SA and AV nodal activity.

35
Q

What do we uses for paroxysmal supraventricular tachycardias and AV nodal arrythmias?

A

Adenosine

36
Q

How does caffeine promotes wakefullness?

A

Blocks adenosine in the brain , since adenosine promotes sedation , it will inhibit this effect.

37
Q

What is a treatment for Torsades?

A

Magnesium as it shortens the QT interval.

38
Q

What are three drugs that can cause Torsades?

A

Potassium-channel blockers (class 1A and class III)
Antipsychotics (thioridazine)
TCAs

39
Q

What causes Prinzmetal angina?

A

Vasospastic, due to a reversible decrease in coronary blood flow. Occurs at rest, transmural ischemia ST-elevation.

40
Q

Which type of angina present subendocardial ischemia ?

A

Stable or classic angina due to effort or exercise, due to coronary atherosclerotic occlusion. ST depression.

41
Q

What kind of angina will beta blockers are indicated for?

A

Stable angina, since it will decrease the effect of NE. In vasospactic they are contraindicated.

42
Q

What are three antianginal drugs?

A

Nitroglycerin (Nitrate)
Verapamil (CCB)
Beta blockers

43
Q

Pt. presents with familial hypercholesterimia type IIA, what is the DOC? why?

A

Bile acids inhibitors: Colestipol and cholestyramine. They decrease LPL but increase TGs (VLDL). It decreases LDL as cholesterol is used to make more B.A. and then this leads to an upregulation of LDL in the liver thus decreasing its’ levels.

44
Q

what is contradicted on familial hypercholesterimia type IIA? why?

A

Gemfibrozil, which increases lipoprotein lipase, it decreases TGs and increases LDL. Contradicted, it will exacerbate the problem.

45
Q

what kind of cholesterol lowering drugs can cause rhabdomyolysis?

A

HMG-COA Reductase inhibitors. Statins (atorvastatin, rosuvastatin).

46
Q

What exacerbates the side effects of statin drugs?

A

Gemfibrozil (increased rhabdomyolysis)

Cytochrome P450 inhibitors enhance toxicity.

47
Q

What kind of cholesterol lowering drug will cause malabsorption of lipid-soluble vitamins, hyperglycemia?

What will be elevated? LDL?HDL?

A

Cholestyramine and Colestipol

B.A. sequestrants, complexation of bile salts in the gut, results in decrease blood LDL, increase LDL-receptor expression, and decrease liver cholesterol.

SE: Increased VLDL, and TGs

48
Q

What is the MOA of Gemfibrozil and Fenofibrate?

A

Binds to the PPAR alpha and increase expression of lipoprotein lipases which results in:
Decreased VLDL and IDL
Increased LDL (contradicted in FH type II)
SE: gallstones.

49
Q

What is the DOC for benzodiazepines toxicity?

A

Flumazenil

50
Q

What are the DOC for seizure emergency?

A

Benzodiazepines. Tamazepam (status epilepticus)

51
Q

what causes profound amnesia and it used as a sedative?

A

Midazolam causes anesthesia and anterograde amnesia.

52
Q

What are the BZ-1 receptors agonist?

A

Zolpidem and Zaleplon, they induce hypnotic effects.

53
Q

What is used for General anxiety disorder?

A

Buspirone (5HT1 partial agonist) Takes about 1-2 weeks to kick in, non-sedating.

MD Pharmacology (7 decks)

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