Pharm Cardio

Question 1

Class 1a
Drugs

Answer 1

Quinidine
Procainamide
Disopyramide.

Question 2

Class 1a
Drugs:
Quinidine
Procainamide
Disopyramide.
–>MOA

Answer 2

Inhibit Na+ channels= slower depolarization

Inhibit K+ channels =slower rate of repolarization
on atrial & ventricular myocytes cells of the purkinje fibers.

Question 3

How is moa class 1a different
to class 1b&1c

Answer 3

Work also on Inhibit K+ channels =slower rate of repolarization = lengthen the QT (and QRS )
which mean more likely to cause torsade de point

Question 4

SE of 1a antiarrhythmics

Answer 4

longer QRS complex and a longer Q-T segment = torsade de pointes
Hypotension
Avoid in HF

Question 5

Procainamide use & side effect

Answer 5

Type 1a
Rx WWP
SE: SLE
(think caines)

Question 6

Action of 1B antiarrhythmics

Answer 6

Not as potent in blocking Na+ channel activity
Potency and selectiveness for ischemic tissue, c

Question 7

Examples 1B antiarrhythmics

Answer 7

(Na channels)
Mexiletine
Lidocaine.

Question 8

Action of 1C antiarrhythmics

Answer 8

Inhibit the Na+ channels in atrial and ventricular myocytes and purkinje fiber cells.
strongest potency
= dramatic decrease in the slope of phase 0.

Question 9

Examples 1C antiarrhythmics

Answer 9

Flecainide
Propafenone.

Question 10

SE 1C antiarrhythmics

Answer 10

• longer QRS complexes
• Avoid in ischemia = sudden death
  propafenone is that it causes a bitter or metallic taste

Question 11

SE: Quinidine

Answer 11

1A ANTIARRYTHMIC
Cinchonism (headache, tinnitus, thrombocytopaenia)

Question 12

Where are pacemaker cells found

Answer 12

SA node
AV NODE
Bundle of HIS

Question 13

Na channels on cardiac myocyte control what on ECG

Answer 13

the QRS
hence Na blocker=type 1 antiarrhythmics= prolong qrs

Question 14

K channels on cardiac myocyte control what on ECG

Answer 14

QT
1a drug long qt = torsade de point

Question 15

What channels do beta blockers work on and how do they alter myocyte and pacemaker AP
How is this reflected in the ECG

Answer 15

B- blocker decrease Decrease amount of Ca2+ Entering
Pacemaker cells = phase 4 take longer to get to threshold (decrease Rate of contraction)
–> Prolonged PR interval
Decrease amount of Ca2+ Entering Myocyte = affecting phase 2 = decreased force of contraction (recue O2 demand)

Question 16

Beta blcker effect on DM

Answer 16

decrease hypoglycemia awareness

Question 17

Beta blker contra indications (3)

Answer 17

pheochromocytoma
Cocaine toxicity
CBB use

Question 18

What receptor do b-blocker block

Answer 18

B1 adrenergic receptors - g proteins receptors

Question 19

What phase do K blker work on
Give examples of drugs

Answer 19

phase 3 of myocyte AP (prolonged repolarization)
Slower rate of K leaving the cell

amiodarone
sotalol

Question 20

Explain ECG changes with K blkers

Answer 20

Potassium blkers – phase 3 of myocyte contraction (repolarization)
Slower rate of K leaving the cell = slower repolarization = Longer QT = slower HR

Question 21

What type of antiarrhythmic is Amiodarone
What else does it block (4)

Answer 21

Amiodarone
1. blk K channels,
2. Blk Na channel,
3. Beta adrenergic receptors
4. Ca2+(L type)

Question 22

Half life of amiodarone

Answer 22

20-100 days

Question 23

SE: amiodarone
Hrt (3)
Lungs (1)
Endocrine (1)
Liver/GI (2)
Neuro (2)
Eyes (1)
Skin (2)

Answer 23

HRT: bradycardia, heart block, and HF.
Endo: thyroid dysfunction,hypo/hyperthyroidism;
Lung pulmonary fibrosis
GI& Liver:Liver dysfunction,constipation

Neurological
-tremor, paresthesia
Eyes corneal deposits; Skinblue-gray skin discoloration; & photosensitivity.

On the flip side, amiodarone can still cause

Question 24

MOA Sotalol

Answer 24

K blocker
Non selective Beta blker

Question 25

What phase do C2+ L channel in myocyte contract effect

Answer 25

Phase 2

Question 26

Adenosine MOA

Answer 26

increases K efflux & inhibits Ca2+ influx to hyperpolarize the cell and slow down t = HR

Question 27

Describe the 4 phases Myocyte depolarization

Answer 27

**phase 4-resting phase** - mainly **Ca2+ leak** = membrane slowly depolarizes **Phase 0-Depolarisation** Threshold potential met. **Na** channels open = Na in the cell = +ve membrane potential **Phase 1- initial repolarization** - Na channels close; - **K channels open** up, = K out of cell = Membrane potential falls **Phase 2 /plateau phase** - **Ca2+ channels open**, CA2+ into cell- counterbalances the k ions out, **Phase 3, or repolarization** - CA2+ channels close, - **K channels** remain open, = return to resting potential

Question 28

Describe depolarization of cardiac pacemaker cell 3 phases

Answer 28

**Phase 4-pacemaker potential** - Opening funny current (If) = Na in - T-type C2+ channels open up, = further depolarizing the pacemaker cell. **Phase 0 - depolarization phase** - SLOW influx of Ca2+ ions through the **L-type C2+** channels - **T-type C2+** channels close. **Phase 3 repolarization phase** - **L-type C2+** channels close - K channels open up, = +ve current.

Question 29

How do beta blker act on Pacemaker cell & Non- pace maker cells

Answer 29

Block B adrenergic receptors- ATP & adenylyl cyclase don’t make cAMP= Less Ca2+ enter the cell **Pacemaker Cell** – Decreased Ca2+ affects phase 4 = decrease HR SAN= Longer PR interval **Non pacemaker cell**- Less Ca2+ effects phase 2 = decrease contraction & cardiac O2 demand

Question 30

Anti arrhythmic effect of CCB

Answer 30

blk L- type Ca2+ channel Non Dihydropyridine- anti arrhythmic target: - **Pacemaker cells** - Decrease Ca entry into the cells = prolong effective refractory period = decrease SN firing rate and AV = Prolonged PR - In myocytes decrease Ca2+ = decrease contraction Slower action than b-blker

Question 31

Diff btwn verapamil an diltiazem ?

Answer 31

diltiazem affects smooth mscl; Used HTN & svt verapamil - is cardiac specific; Angina & SVT

Question 32

SE of Calcium channel Blockers

Answer 32

Constipation flushing Hyperprolactinemia Heart blk SA node depression

Question 33

MAO of Digoxin

Answer 33

Stim of vagal nerve

Question 34

MAO of nitrates (4)

Answer 34

Nitrates are Converted into NO to simulate cGMP = vasodilation of veins > Arteries = Decrease in afterload & preload = reduced cardiac O2 demand. Also vasodilate hrt vessel = increase o2 delivery

Question 35

Contraindications to Nitrates

Answer 35

R sided HF Erectile dysfunction meds

Question 36

what should be prescribed with nitrates to reduce SE

Answer 36

Beta blkers

Question 37

MOA Statins

Answer 37

1. inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis - Reduced Cholesterol= increase hepatic LDL receptors = increase uptake of LDL from body (Mild uptake of triglycerides ) - Increases HDL

Question 38

SE statins

Answer 38

myalgias - Coenzyme Q decrease in e-transport chain rhabdomyolysis. hepatotoxic. teratogenic.

Question 39

Indications for statins (4)

Answer 39

Indications * anyone with a 10-year cardiovascular risk >= 10% * Pts w. CVD (stroke, TIA, ischaemic heart disease, peripheral arterial disease) * DM2 Pts with assessed w/ QRISK2 * DM1 Pts w/ dx> 10 years ago OR are aged over 40 OR have established nephropathy

Question 40

MOA Ezetimibe

Answer 40

is a cholesterol absorption inhibitor

Question 41

MOA Fibrates Example

Answer 41

Agonist of PPAR-alpha therefore increases lipoprotein lipase expression used to reduce triglyceride levels bezafibrate and fenofibrate.

Question 42

Answer 42

Question 43

Answer 43

Question 44

Answer 44

Question 45

Answer 45

Question 46

Answer 46