Cardiology

Question 1

Nifedipine and amlodipine

Answer 1

-Block L type Ca channels mosty on smooth muscle of arteris, acts like a nitrate

Question 2

Verapamil and Diltiazam

Answer 2

-Block cardiac L type Ca channel and leads to decrease ionotropy and slowed conduction at AV node

Question 3

Hydralazine

Answer 3

• Increase cGMP leading to vasodilation
• Used in malignant HTN and pregnancy
• Often co-administered with beta blockers to prevent reflex tachycardia

Question 4

Nitroprusside

Answer 4

• Release of nitrate for rapid vasodilation

- Can caues cyanide poisoning, treat with thiosulfate to generate thiocyanide which is less toxic

Question 5

Fendolopam

Answer 5

• D1 agonist, Increase cAMP causing vasodilation (B2)

- Used in malignant HTN

Question 6

Nitrates and beta blockers

Answer 6

-Often given together in angina to decrease work of heart. Combined cause decrease in all parameters.

Question 7

Lipoprotein E

Answer 7

• Mediates uptake by liver

- On all but VLDL

Question 8

Lipoprotein C

Answer 8

-Cofactor for LPL on HDL, Chylpmicrons, VLDL

Question 9

A-1

Answer 9

-Esterifies lipids only on HDL

Question 10

B-48

Answer 10

-Necessary for chylomicron assembly

Question 11

B-100

Answer 11

-Necessay for LDL uptake

Question 12

Statins

Answer 12

• Competetive inhibitors of HMGCOA reuctase. Decreased melovenate
• Decrease LDL levesl
• Can cause rhabdomyolysis and liver damage

Question 13

Niacin

Answer 13

• Mainly increases HDL
• Inhibits lypolysis in adipose tissue leading to increased VLDL secretion (contain apo E and can become HDL)
• Flushing is most common S/E (Give aspirin)
• Hyperglycemia and hyperuricemia

Question 14

Bile Acid binders (Cholestyramine)

Answer 14

• Prevent Bile reabsorption in terminal llleum leading to increased secretion.
• Lowers LDL levels
• Causes GI disturbance, foul taste, and may predispose to cholesterol gal stones

Question 15

FIbrates

Answer 15

• Decrease triglycerides
• Increase LPL and removes circulating triglycerides
• May cause myostis and hepatic injury

Question 16

Ezetimibide

Answer 16

-Prevents cholesterol absorption in the gut

Question 17

Digoxin mechanism and use

Answer 17

• Binds to K binding site of ATPase leading to increased intracellular Na levels and an impaired Na/Ca exchange. Elevated intracellular Ca leads to increased contractility.
• Also has stimulatory effects on vagus leading to block at AV node and bradychardia
• Use CHF, A FIb (rate control)

Question 18

DIgoxin S/E

Answer 18

• Hyperkalemia
• Yellowing of vision
• Vagal activit leading to GI distress
• AV block and arryhtmia
• Elevated PR and depressed QT

Question 19

Digoxin overdose Tx

Answer 19

• fAB to digoxin
• normalize K
• Lidocaine
• Mg

Question 20

Factors that cause digoxin overdose

Answer 20

-Poor renal function
-hypokalemia
-Quinidine
-

Question 21

Class I Antiarrythmics

Answer 21

• Na Channel blockers leading to alterations in AP duration, blockage of conduction (phase 0) and increase firing threshold.
• If patient is hyerkalemic will increase toxicity

Question 22

Quindine, Procainamide, Disopyramdie (Class IA)

Answer 22

• Cause an increase in AP duration leading to longer refractory period
• Used in SVT ectopic and re-entry rythms
• Toxicity is Torsades because of longer QT interval
• Quinidine Specifically has Tinnitus and Headaches
• Procaianamide has reversible lupus like syndrome (Hydralazine)
• Disopyramide can cause heart failure

Question 23

Lidocaine, Tocanide, mexiletene, phenytoin (Class IB)

Answer 23

• Decrease AP duration and refracractory period, especially in damaged tissues
• Used to prevent Arrythmia post MI and Digoxin overdose

Question 24

Flecainide, Propafenone (class IC)

Answer 24

• Rarely used except if others have failed

- Can cause torsades and other arryhtmias, contraindicated post MI

Question 25

Beta Blockers (Class 2)

Answer 25

-Decrease cAMP intracellularly leading to decreased contractility, decreased slope of phase 4 and decreased HR
-Used as rate control in SVT and ventricular arrythmias
-Strongest at AV node and cause a prolonged PR interval
Tox: Sedation, may exacerbate asthma, exercise intolerance, impotence, masks hypoglycemia
-Overdose Tx with glucagon. Increase intracellular cAMP
-Esmolol has short half life
-

Question 26

Amiodarone, Sotalol, Dofetilitide (Class III)

Answer 26

• Block K channels leading to elongated refractory period
• Generally used if others have failed
• All can cause torsades

Question 27

Amiodarone

Answer 27

• Has properties of all types of anti-arrythmics (structurally similair to thyroid hormone)
• Commonly given if conventional have failed
• Tox: Pulmonary fibrosis, hyper or hypothyroidism, Corneal and skin deposits, Bradycardia, constipation, hepatotox

Question 28

Verapamil and Diltiazem (Class 4)

Answer 28

• Decrease contractility and conduction velocity
• Increase refrctory period and PR interval
• Most commonly used as rate control in nodal arryhmias, similar to beta blockers
• Tox: AV nodal block, flushing, constipation, hypotension, etc

Question 29

Adenosine

Answer 29

• Causes K efflux from cardiomyocytes leading to hyperpolarization and abolish of rythm
• Abolishes SVT, makes heart stop
• Effects blocked by caffeine/theophyline
• Short acting, 15 seconds
• Tox: Flushing, hypotension, chest pain

Question 30

Mg

Answer 30

Used to treat torsades and Siezures of eclampsia

-Similiar structurally to K