Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

notes to flashcards year 2 - LCRS1 > drugs and the heart > Flashcards

drugs and the heart Flashcards

1
Q

what are If channels?

A

hyperpolarisation-activated cyclic nucleotide gated channels
“funny channels”
predominantly Na channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are Ica (t or l) channels

A

transient T-type Ca channel or long-lasting L-type

mediate fast calcium influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does the SNS do in terms of these channels?

A

inc. cAMP

this inc. If and Ica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what does PNS do in terms of these channels?

A

dec. cAMP

this inc. If

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what do beta-1 adrenergic stimulation activate?

A
  • activated adenylate cyclase
  • creates cAMP
  • this activated PKA
  • PKA then has 2 actions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the 2 actions of PKA then?

A
  • phosphorylates proteins in myofibril
  • induces CICR in SR by stimulating Ca influx into SR
  • most Ca is from CICR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what mediates removal of Ca from cells?

A
  • PMCA (ATPase Ca channel)

- NCX (Na/Ca exchanger)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the primary determinant of myocardial oxygen?

A

myocyte contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what influences contraction?

A
  • inc. HR = inc. contractions
  • inc. afterload/contractility = inc. force of contractions
  • inc. preload = small inc. force of contractions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what 3 classes of drugs have an effect on the HR?

A
  • beta blcokers: dec. If and Ica
  • Ca antagonists: dec. Ica
  • Icabradine: dec. If
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how do these drugs reduce the HR?

A

by prolonging the extent of the depolarisation

dec. SNS drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the 2 classes of drugs that have an effect on contractility?

A
  • beta blockers: dec. contractility - reduce phosphorylation and cross bridge formation
  • Ca antagonists: dec. Ica - stops further entry of Ca into myofibrils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the 2 classes of Ca antagonists?

A
  1. rate slowing - cardiac and VSM: phenylalkylamines (Verapamil) and benzothiazepines (Diltazem)
  2. non rate slowing - VSM (more potent): dihydropyridines (Amlodipine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

even though non-rate slowing have no effect on the heart, how do they cause tachycardia?

A

they cause a lot of vasodilation and can lead to a reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the classes of drugs that have an effect on myocardial oxygen supply/demand?

A
  • organic nitrates (directly supply NO, inc. cGMP which stimulates K+ channel opening and relaxation directly)
  • potassium channel openers (stimulates hyperpolarisation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does these drugs do?

A

stimulates hyperpolarisation (ability of coronary arteries to contract is impaired)

17
Q

what effect do these drugs have on preload and afterload? How?

A

drugs dec. preload and afterload (demand) and inc. oxygen supply (inc. blood flow)

  • vasodilation = dec, afterload as less TPR
  • venodilation = dec. preload
18
Q

what is angina caused by?

A
  • angina is classic mismatch b/ myocardial supply and demand
19
Q

what classes of drugs are used in angina treatment?

A
  • beta blocker or CCA: background treatment
  • nitrate: symptomatic treatment (i.e. exercise)
  • K channel openers
20
Q

what are the side effects of beta blockers?

A
  • cardiac failure worsening (beta 1)
  • bradycardia (beta 1)
  • bronchoconstriction (beta 2)
  • hypoglycaemia (beta 2)
  • cold extremities
21
Q

what are the side effects of rate limiting calcium channel blockers? e.g. Verapmil

A
  • bradycardia and AV block (heart Ca channels blocked)

- constipation (gut Ca channels blocked)

22
Q

what are the side effects of non-rate limiting calcium channel blockers? e.g. Dihydropyridines

A
  • ankle oedema (vasodilation so more capillary pressure in extremities)
  • headache/flushing (vasodilation)
  • palpitations (reflex SNS adrenergic activation due to vasodilation)
23
Q

what are the side effects of potassium channel openers and nitrates?

A
  • ankle oedema (vasodilation, capillary pressure in extremeities)
  • headache/flushing (vasodilation)
24
Q

what are the aims of treatment in rhythm disturbances?

A
  • reduce sudden death

- alleviate symptoms

25
Q

what is the simple classification of rhythm disturbances?

A

based on site of origin

  • supraventricular e.g. amiodarone, verapmil
  • ventricular e.g. flecainide, lidocaine
  • comples (supra and ventricular) e.g. disopyramide
26
Q

Describe the Vaughan Williams Classification of antiarrhythmic drugs

A

Class 1: Na+ channel blockers
Class 2: beta blockers
Class 3: K channel blockade (prolong repolarisation)
Class 4: Ca channel blockade

27
Q

why is this classification of limited significance?

A

due to significance of cross overs in rhythm disturbances

28
Q

what is the MoA of adenosine (selective anti-arrhythmics)?

A
  • activates A1 receptors in SA and AV nodes
  • Gi protein activation to reduce AC conversion of ATP to cAMP
  • dec. cAMO
  • dec. ionotropic and chronotropic effect
29
Q

describe facts of adenosine

A
  • IV given
  • targets SVT
  • short action so safer than Verapmil
  • class V anti-arrhythmic
30
Q

what are the uses of verapamil?

A

reduces ventricular responsiveness to atrial arrhythmias

31
Q

what is the MoA of verapamil?

A
  • blocks VGCC and so depresses SA firing and subsequent AV node conduction
  • Class 4 anti-arrhythmic
32
Q

what are the uses of amiodarone?

A
  • SVT and VT
33
Q

what is the MoA of amiodarone?

A

complex but probably involving multiple ion channel block

prolongs hyperpolarisation which reduces chance of re entry

34
Q

what are the adverse effects of amiodarone?

A
  • accumulation in body
  • skin rashes (photosensitive)
  • hypo/hyperthryroidism
  • pulmonary fibrosis
35
Q

what is the MoA of digoxin?

A
  • inhibits Na/K ATPase
  • inc. intraceullar Na
  • reversal of Na/Ca exchanger
  • Na effluxed and Ca influx
  • inc. intraceullar Ca
  • this lengthens class IV are of ventricular muscle graph so lower chronicity
  • but inc. ionotropic effect as more Ca inside cell
36
Q

what is the other MoA of digoxin?

A

central vagal stimulation –> inc. refractory period and reduced rate of conduction through AVN

37
Q

what are the uses of digoxin?

A
  • atrial fibrillation and flutter lead to rapid ventricular rate
  • this impairs ventricular filling and reduces CO
  • digoxin via vagal stimulation reduces conduction within AVM so fewer impulses get to ventricles
  • slows down ventricular tachyarrhyth,ia
38
Q

what are the side effects of digoxin?

A

dysrhythmias e.g. AV conduction block

39
Q

what happens if digoxin is co-administered with diuretics?

A
  • get hypokalaemia
  • can lower threshold for digoxin toxicity
  • digoxin is a K receptor antagonist
  • low blood potassium means less competition, so effects of digoxin are enhanced

notes to flashcards year 2 - LCRS1 (58 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions