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MRCP Master > Pharm Cardio > Flashcards

Pharm Cardio Flashcards

1
Q

Class 1a
Drugs

A

Quinidine
Procainamide
Disopyramide.

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2
Q

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

A

Inhibit Na+ channels= slower depolarization

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

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3
Q

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

A

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

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4
Q

SE of 1a antiarrhythmics

A

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

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5
Q

Procainamide use & side effect

A

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

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6
Q

Action of 1B antiarrhythmics

A

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

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7
Q

Examples 1B antiarrhythmics

A

(Na channels)
Mexiletine
Lidocaine.

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8
Q

Action of 1C antiarrhythmics

A

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

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9
Q

Examples 1C antiarrhythmics

A

Flecainide
Propafenone.

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10
Q

SE 1C antiarrhythmics

A
  • longer QRS complexes
  • Avoid in ischemia = sudden death
    propafenone is that it causes a bitter or metallic taste
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11
Q

SE: Quinidine

A

1A ANTIARRYTHMIC
Cinchonism (headache, tinnitus, thrombocytopaenia)

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12
Q

Where are pacemaker cells found

A

SA node
AV NODE
Bundle of HIS

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13
Q

Na channels on cardiac myocyte control what on ECG

A

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

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14
Q

K channels on cardiac myocyte control what on ECG

A

QT
1a drug long qt = torsade de point

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15
Q

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

A

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)

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16
Q

Beta blcker effect on DM

A

decrease hypoglycemia awareness

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17
Q

Beta blker contra indications (3)

A

pheochromocytoma
Cocaine toxicity
CBB use

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18
Q

What receptor do b-blocker block

A

B1 adrenergic receptors - g proteins receptors

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19
Q

What phase do K blker work on
Give examples of drugs

A

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

amiodarone
sotalol

20
Q

Explain ECG changes with K blkers

A

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

21
Q

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

A

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

22
Q

Half life of amiodarone

A

20-100 days

23
Q

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

A

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

24
Q

MOA Sotalol

A

K blocker
Non selective Beta blker

25
Q

What phase do C2+ L channel in myocyte contract effect

A

Phase 2

26
Q

Adenosine MOA

A

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

27
Q

Describe the 4 phases Myocyte depolarization

A

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

28
Q

Describe depolarization of cardiac pacemaker cell
3 phases

A

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.

29
Q

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

A

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

30
Q

Anti arrhythmic effect of CCB

A

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
31
Q

Diff btwn verapamil an diltiazem ?

A

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

32
Q

SE of Calcium channel Blockers

A

Constipation
flushing
Hyperprolactinemia
Heart blk
SA node depression

33
Q

MAO of Digoxin

A

Stim of vagal nerve

34
Q

MAO of nitrates (4)

A

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

35
Q

Contraindications to Nitrates

A

R sided HF
Erectile dysfunction meds

36
Q

what should be prescribed with nitrates to reduce SE

A

Beta blkers

37
Q

MOA Statins

A
  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
38
Q

SE statins

A

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

39
Q

Indications for statins (4)

A

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
40
Q

MOA Ezetimibe

A

is a cholesterol absorption inhibitor

41
Q

MOA Fibrates
Example

A

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

42
Q
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43
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47
Q
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MRCP Master (47 decks)

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