Brainscape's Knowledge GenomeTM

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


See full index

eLCRS - 팜 > PHARM 11: Drugs + CVS - HEART > Flashcards

PHARM 11: Drugs + CVS - HEART Flashcards

1
Q

Describe the mechanism by which the HR is regulated

in response to sympathetic and parasympathetic stimulation:

A

Sympathetic response:
increased cAMP, increase If, Ica

Parasympathetic response:
decreased cAMP, increased Ik

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

What is a primary determinant of myocardial oxygen demand?

A

myocyte contraction

more work –> more O2 required

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

What is the effect of Beta blockers on If and Ica

what effect does this have?

A

decreases both If and Ica

decreases HR

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

What is the effect of calcium antagonists on Ica

what effect does this have?

A

decreases Ica

decreases HR

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

What is the effect of Ivabradine on If?

What effect does this have?

A

decreases If

decreases HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does Beta blockers effect contractility of the Heart?

A

decreases contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 2 classes of calcium antagonists?

A

a) rate slowing

b) non-rate slowing

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

give examples of rate slowing calcium antagonists

A
  • phenylalkylamines
  • benzothiazepines

–> blocks receptors on cardiac and smooth muscle tissue

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

give examples of non rate slowing calcium antagonists

A
  • dihydropyridines
  • -> has powerful effect on smooth muscle
  • -> but little effect on the heart itself

note: profound vasodilation can lead to reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how does organic nitrate + K-channel openers influence Myocardial O2 supply/ demand

(3 ways)

A
  • they increase coronary blood flow
  • decreases amount of work heart has to do
  • increases delivery of oxygen to the heart
  1. Organic nitrates increase NO available –> more cGMP –> relaxation + opens K+ channels
  2. K+ Channel Openers –> hyperpolarisation
    • Both ↑ blood flow in general
  3. Both also cause:
    o Vasodilation, meaning ↓ afterload
    o Venodilation, meaning ↓ preload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What two different effects of nitrates/potassium channel openers influence preload and afterload?

A 
Vasodilation = ↓ afterload
Venodilation = ↓ preload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are medications you would use to treat angina?

A
  • beta blockers
  • calcium antagonist
  • ivabradine
  • nitrate (symptomatic treatment) –> immediate dilation of coronary vessels to match oxygen demand
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some side effects of beta blockers?

why do they occur?

A

actions on B1:

  • CO reduction –> cardiac failure exacerbation
  • removes capacity to dilate –> increases vascular resistance –> increased strain on heart
  • less AV node conduction –> bradycardia

action on B2:

  • blockade of B2 –> bronchoconstriction
  • impairs glucose control = hypoglycemia –> in diabetics
  • blockade of B2 (skeletal muscle vessels) –> less peripheral vasodilation –> cold extremities

others:
- fatigue
- impotence
- depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some side effects of calcium channel blockers?

A

Verapamil (rate limiting) –> heart consequences

  • bradycardia + AV block = acts on Ca2+ channel block
  • constipation = acts on gut Ca2+ channels

Dihydropyridines (non rate limiting) –> blood vessels

  • ankle oedema = due to vasodilation, large amount of fluid leakage from capillaries –> enters lymph –> oedema
  • headache = vasodilation –> excessive blood flow to brain / peripheries
  • palpitations –> reflex tactic ardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe the vaughan williams classification

A

class 1: Na+ channel blockade

class 2: Beta adrenergic blockade

class 3: Prolongation of repolarisation

class 4: Ca2+ channel blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how is adenosine used as an anti-arrythmics?

A
  • IV
  • terminates supraventricular tachyarrhythmias
  • short lived

2 mechanisms
a) Acts on A2 receptors in VSMC –> cause vasodilation of vascular smooth muscle

b) Acts on A1 receptors in SAN/AVN –> decreased Ca2+ channel opening, but prolonged K+ channel opening –> causes prolonged depolarisation + repolarisation (relaxation) of heart

–> decreases chronotropic + dromotropic effect

17
Q

how is verapamil used as an anti-arrythmics?

A
  • used to reduce ventricular responsiveness to atrial arrhythmias
  • by depressing SA automaticity –> and subsequent AV node conduction

reduces calcium entry into tissues –>

18
Q

What is an amiodarone used for?

A
  • class 3

- used for supraventricular + ventricular tachyarrhythmias

19
Q

How do amiodarones work as an anti arrythmics ?

mechanism

A
  • multiple channel block
  • prolongs Repolarisation step
  • less likely to get reentry rhythm
20
Q

what are some side effects of amiodarones?

A
  • skin rashes
  • hypo/hyperthyroidism
  • pulmonary fibrosis
21
Q

How do digoxins (cardiac glycosides) work as an anti arrythmics ?

(mechanism)

A

2 mechanism

a) blocks Na-K ATPase
- there is accumulation of Na+
- excess Na+ is removed by Na+/Ca2+ exchanger –> which increases intracellular Ca2+ conc –> thus causes increases inotropic effect

b) - central vagal stimulation –> increases refractory period + reduces rate of AV node conduction

22
Q

What is a digoxin (cardiac glycosides) used for?

A
  • a.fib + flutter –> can cause increase in ventricular rate –> impairs ventricular filling –> causes cardiac output
  • so digoxin acts to reduce Cardiac Output
23
Q

what are some side effects of Digoxin (cardiac glycosides) ?

A
  • dysrhythmias

e. g AV conduction block

24
Q

Hypokalaemia (usually a consequence of diuretic use) lowers the threshold for digoxin toxicity WHY?

A

if you are hypokalaemic you need to be careful with digoxin

K+ and digoxin compete for the same site on Na-K ATPase
when you are have less K+,
there is increase binding of digoxin instead —> which can cause digoxin toxicity

25
Q

In SA node + AV node depolarisation = largely driven by :

A

calcium

26
Q

describe the graph relating different channels and the action potential elicited in the heart

(ik, if, ica etc)

A

If = hyperpolarised causes HCN channels to open

  • Na+ enters through these channels
  • slow inflow of Na+
    as it becomes more positive - - ca2+= channels open
  • and then calcium enters via the L-type channels

around 0mv
Ik = potassium K+ channels = there is depolarization –> back to resting state

27
Q

how is contractility maintained

A

Ca2+ flows in
- initiate contraction
also directly activates RyR channels –> to increase Ca2+ release (CICR)

  • Ca2+ binds to troponin –> initiates contraction
  • relaxation occurs when Ca2+ unbinds form troponin
  • Ca2+ = pumped back into SR for storage
  • rest of Ca2+ exchanged for Na+
  • Na+ gradient = maintained by Na+-K+ ATPase
28
Q

what can increase myocardial work demand?

A

increase in

  • heart rate
  • preload (less effect)
  • afterload
  • contractility
29
Q

How do calcium antagonists affect contractility

A
  • decreases Ica
30
Q

what is the effect organic nitrate

A

produce NO in tissues
activates guanylate cyclase

or K+ channel opens –>K+ efflux –> hyperpolarised
tissue remains relaxed for longer period of time

31
Q

what is angina usually due to?

A
  • when myocardial oxygen supply isn’t met with demand

- due to insufficient blood flow/ delivery to the heart

32
Q

patients has arrhythmia associated with heart failure - what 2 MAIN drugs would you use?

why are they used?

A
  • beta blocker
  • ivabraine
  • -> slows heart down to restore normal pattern of contraction
33
Q

why is pindolol a good beta blocker to use for heart failure

A

acts on B1 + B2

restores dilating effect –> less work needed to bring blood back to the heart

34
Q

why is carvedilol a good beta blocker to use for heart failure

A

acts on B1 + B2 + a1

has antagonistic effect on a1 –> which causes vasodilation –> less work needed to bring blood back to the heart

35
Q

when should beta blockers be avoided?

A

asthmatics

hypoglycaemic individuals

36
Q

non rate limiting Calcium antagonists –> have similar side effect profiles to:

A

Nitrates

37
Q

rhythms disturbance due to increased HR

A
  • tachyarrhythmias
38
Q

rhythms disturbance due to decreased HR

A
  • bradyarrhythmias
39
Q

adenosine is usually used to for what type of arrhythmia?

A

supraventriular arrhythmias

eLCRS - 팜 (36 decks)

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