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Year 2 Collin > Pharm 11/12 - Drugs and the Cardiovascular system > Flashcards

Pharm 11/12 - Drugs and the Cardiovascular system Flashcards

1
Q

Through what channels does calcium enter the myocyte upon depolarisation?

A

Dihydropyridine receptors (DHPR)

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2
Q

Explain the movement of calcium in a myocyte contraction

A
  1. Ca enters via DHPR
  2. Ca then binds to calcium release channels (Ryanodine receptors Ryr) - stimulates Ca release from sarcoplasmic reticulum
  3. Ca then removed via Plasma Membrane Calcium ATPase (PMCA) or Na+ - Ca2+ exchangers (both found on plasma membrane) OR taken back into SR by SERCA2A
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3
Q

70% of myoplasmic Ca is removed via?

A

SERCA2A

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4
Q

How is SERCA2A regulated?

A

Via its interaction with Phospholamban (PLN)

Dephosphorylated PLN = inhibitor of PLN

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5
Q

PLN is phosphorylated by?

A

PKA

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6
Q

In the heart, what ion drives depolarisation?

A

Ca

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7
Q

What are the 4 channel types involved in regulating SAN AP?

A
  1. If channel = “hyperpolarization-activated cyclic nucleotide-gated (HCN) channels”
    2/3. ICa (transient / long-lasting L type) Calcium channel
  2. Ik - Potassium K channels
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8
Q

What type of channel is the If channel?

A

Sodium

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9
Q

Explain how the channels are involved in SAN AP

A
  1. If channel begins depolarisation
  2. T type and then L type Ca channels become involved
  3. Once voltage is over threshold voltage, Ik channels become involved and cause repolarisation
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10
Q

Which ion is responsible for repolarisation in the heart?

A

K

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11
Q

How does a SNS nerve increase HR?

A

Releases NA, which increases cAMP conc in If & ICa channels, which increases the pacemaker potential gradient (phase 4)

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12
Q

What is phase 4

A

The pacemaker potential - spontaneous depolarisation that triggers AP

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13
Q

How does parasympathetic decrease HR?

A

Negatively coupled to cAMP via M2 receptor. Acts on Ik channels . Prolongs repolarisation step - bigger gaps between depolarisation steps

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14
Q

Out of HR, Preload, Afterload and contractility, which one has the least impact on the heart work

A

Preload

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15
Q

Currents in which channels do B-blockers stop

A

If and ICa

They block the amount of cAMP being produced

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16
Q

Which channel do calcium channel blockers block

A

ICa

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17
Q

Which channel does Ivabradine block

A

If

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18
Q

How do B blockers and Ca antagonists decrease heart contractility

A

B blockers - Decrease contractility as less cAMP produced so less downstream signalling of Ca influx

Ca antagonists block L type Ca channels - also means less Ca released from SR

Therefore B blockers and Ca antagonists reduce heart work

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19
Q

What are the 2 classes of Ca antagonists

A
  1. Rate slowing - cardiac and smooth muscle

2. Non-rate slowing - exclusive to SM

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20
Q

What are 2 types of rate-slowing Ca antagonists

A
  1. Phenylalkylamines (e.g. Verapamil)

2. Benzothiazepines (e.g. Diltiazem)

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21
Q

What is a type of non-rate slowing Ca antagonist

A
  1. Dihydropyridines (e.g. amlodipine)
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22
Q

Why can non-rate slowing Ca antagonists cause reflex tachycardia

A

No effects on heart but can cause profound vasodilation

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23
Q

Which 2 drugs influence myocardial oxygen supply/demand by influencing coronary blood flow

A

Organic nitrates

Potassium channel openers

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24
Q

How do organic nitrates cause smooth muscle relaxation?

A

Activates guanylate cyclase

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25
Q

When are organic nitrates given?

A

In angina - profound atherosclerosis which reduces blood supple to the heart - causes coronary vessels to dilate

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26
Q

How do potassium channel openers work?

A
  1. Promote potassium efflux - leads to hyperpolarisation

2. Thus reduces its ability to contract

27
Q

Organic nitrates and K channel openers increase the amount of blood reaching the heart but also decrease the amount of work the heart needs to do. How?

A
  1. Decreases preload (venodilation)

2. Decreases afterload (vasodilation)

28
Q

Which group of drugs are used for immediate vasodilation and is short acting?

A

Nitrates

29
Q

5 side effects of taking beta blockers

A
  1. Worsening Heart failure - reducing CO and increased vascular resistance (blockade of B2 receptors which cause vasoconstriction)
  2. Bradycardia
  3. Bronchoconstriction
  4. Hypoglycaemia
  5. Cold extremeties
30
Q

What do b2 receptors do when stimulated?

A

They cause SM relaxation - i.e. bronchodilation, vasodilation, etc

31
Q

in vascular SM, increased cAMP leads to?

A

SM relaxation

cAMP inhibits MLCK which phosphorylates SM myosin

32
Q

Which 2 groups of patients should not be given B blockers?

A

Asthmatics and diabetics

33
Q

What are side effects of Ca channel blockers

A

Rate limiting - (Verapamil)

  1. AV block
  2. Constipation

Non-rate limiting (DHPs - Amlodipine)

  1. Ankle oedema
  2. Headache/flushing
  3. Palpitations (reflex adrenergic activation)
34
Q

K channel openers and nitrates, what side effects may they give rise to?

A
  1. Ankle oedema

2. Headache/flushing

35
Q

How can arrhythmias be classified by site of origin?

A
  1. Supraventricular arrhythmias
  2. Ventricular arrhythmias
  3. Complex arrhythmias (supraventricular + ventricular)
36
Q

What are the mechanisms of action of each class of Vaughan-Williams drugs

Vaughan-Williams classification is of limited clinical significance

A
  1. Class 1 - Na channel blockade
  2. Class 2 - Beta adrenergic blockade
  3. Class 3 - Prolongation of repolarisation (membrane stabilisation - due to K channel blockade)
  4. Class 4 - Ca channel blockade
37
Q

Adenosine is a good acute antiarrhythmic. It doesn’t sit within the Vaughan-Williams classification. How does it work

A
  1. Binds to A2 receptor in VSMC - up regulates cAMP which causes VSMC relaxation
  2. Binds to A1 receptors in SAN/AVN and down regulates cAMP, causing decreased chronotropy and dromotropy
38
Q

Why is adenosine safer than Verapamil?

A

Its actions are short lived (20s - 30s)

39
Q

Which drug is used intravenously to terminate supraventricular tachyarrhythmias?

A

Adenosine

40
Q

Verapamil mainly acts on the L-type Ca channels. How does it work

A

Slows down the ability of nodal tissue to depolarise - useful in tachyarrhythmias

41
Q

Amiodarone is a class 3 antiarrythmic (VWC) - but it is quite messy. How does it work

A
  1. Complex action - probably involves multiple ion blockade.
  2. Prolongs repolarisation by blocking K channels
  3. Heart CAN’T depolarise when it is hyperpolarised / during prolonged repolarisation
  4. Prolonging repolarisation aims to reduce likelihood of re-entry
42
Q

What are adverse effects of amiodarone

A
  1. Photosensitive skin rashes
  2. Hypo/hyperthyroidism
  3. Pulmonary fibrosis
43
Q

How does digoxin/cardiac glycosides work?

A
  1. Inhibit Na/K ATPase.
  2. Causing Na buildup inside the cell.
  3. Na/Ca exchanger is also present and more heavily used - causing buildup of Ca in the cell
  4. This causes increased inotropy (contractility)
  5. Digoxin also causes vagal stimulation - increases refractory period and reduces rate of conduction through AVN
44
Q

Why must you be careful if you are hypokalaemic when taking Digoxin

A
  1. Digoxin competes w/ K for K binding site

2. If hypokalaemic = less competition for digoxin, so digoxin has a much more powerful effect - could be toxic

45
Q

What conditions may digoxin be used for

A

Atrial fibrillation and flutter

46
Q

BP = ?

A

BP = CO x TPR

47
Q

What is the clinical definition of hypertension

A

Consistently above 140/90 mmHg

48
Q

What is the most common RF for strokes?

A

Hypertension

49
Q

Where does renin come forom and what does it do?

A

Comes from juxtaglomerular cells in kidney and converts angiotensinogen into Ang 1

50
Q

3 things that stimulate renin release from the kidney

A
  1. Decreased Na reabsorption
  2. Decreased renal perfusion pressure
  3. Increased SNS drive
51
Q

What are 4 actions of Ang 2

A
  1. SNS activation / thirst
  2. Powerful vasoconstriction
  3. Salt and water retention
  4. Aldosterone secretion
52
Q

Drugs ending in -pril are usually?

A

ACEi

53
Q

How do ACEi decrease BP

A
  1. Reduces vasoconstriction (decreases TPR)

2. Reduces salt and water retention - less venous return - less CO

54
Q

How can ACEi treat heart failure

A
  1. Decreased TPR = less afterload = less work heart has to do
  2. Less venous return = less preload, heart doesn’t have to work as hard
55
Q

How do ARBs work and give an example of one

A

ARBs are AT1 receptor antagonists - block renal and vascular actions of Ang 2

e.g. Iosartan

56
Q

What is a problem with ACEi

A

ACE also converts bradykinin into metabolites.

ACEi causes bradykinin buildup, which can cause cough

57
Q

What is a risk when taking ARBs or ACEi

A

Hypotension, hyperkalaemia, renal failure in patients with renal artery stenosis

58
Q

Why can ARBs or ACEi cause hyperkalaemia

A

Less aldosterone secreted = less Na reuptake and less K excretion, caused K buildup in the blood

59
Q

How can ARBs or ACEi cause renal failure

A

Prevents ability of efferent arteriole to constrict - less GF pressure, less GF, causing renal failure

60
Q

Which CCB would you give to treat hypertension

A

Amlodipine (Non-rate limiting)

Non-rate limiting CCBs can cause reflex tachycardia and increase myocardial oxygen demand

61
Q

Why are ARBs or ACEi not given to over 55s or afro-carribeans?

A

They tend to have low plasma renin - Hypertension not linked to RAS

62
Q

Give an example of a mixed beta-alpha blocker

A

Carvedilol

A1 blockade = additional vasodilator properties

63
Q

Name 2 types of a blockers

A

Prazosin

Phentolamine

Year 2 Collin (114 decks)

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