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Cardio > Drugs affecting BP and vasculature > Flashcards

Drugs affecting BP and vasculature Flashcards

1
Q

What is CICR?

A

Calcium induced calcium release

Intra-cellular calcium increases via L-type Ca2+ channel which induces calcium release from SR.

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2
Q

CaM binds to what?

A

Ca2+ forming Ca2+-Calmodulin complex

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3
Q

Which form of MLC results in contraction?

A

phosphorylated MLC

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4
Q

Which enzyme is needed to cause relaxation of vascular smooth muscle?

A

Myosin-LC-phosphatase;

dephosphorylates MLC -> relaxation

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5
Q

What are some examples of vasodilating substances?

A

bradykinin
ADP
5-HT

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6
Q

What is the effect of vasodilating substances diffusing into an endothelial cell?

A

Increase intra-cellular Ca2+ concentration

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7
Q

Which enzyme is needed to form NO?

A

L-Arginine

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8
Q

What effect do organic nitrates have on smooth muscle?

A

relax all type of smooth muscle via their metabolism to nitric oxide

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9
Q

What are the main effects of organic nitrates of vasculature?

A

venorelaxation
arteriolar dilatation
increased coronary blood flow

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10
Q

How do organic nitrates cause venorelaxation?

A

decreased preload reduces SV, but CO is maintained by increasing HR - no change in arterial pressure

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11
Q

How do organic nitrates cause arteriolar dilatation?

A

decreases arterial pressure reducing after load

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12
Q

When is blood redirected towards an ischaemic zone?

A

organic nitrates increase coronary blood flow in angina - no overall increase

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13
Q

How do organic nitrates decrease myocardial oxygen requirement in angina?

A

Decreased preload
Decreased afterload
Improved perfusion of the ischaemic zone

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14
Q

What are the main examples of organic nitrates?

A

Glyceryltrinitrate (GTN)
Isosorbide mononitrate (ISMN)
Isosorbide dinitrate

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15
Q

Which organic nitrate is resistant to first-pass metabolism?

A

isosorbide mononitrate

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16
Q

Which organic nitrate is short acting?

A

GTN (30 min)

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17
Q

When is GTN administered sublingually as a tablet or spray?

A

for rapid effect before exertion - stable angina

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18
Q

When is GTN given by IV infusion?

A

in acute coronary syndrome - in conjugation with aspirin

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19
Q

how can you achieve a sustained effect from GTN?

A

transdermal patch

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20
Q

How and when is isosorbide mononitrate administered?

A

Orally for prophylaxis of angina

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21
Q

What is the risk of repeated administration of organic nitrates?

A

diminished effect

tolerance can be finished by ‘low nitrate’ periods

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22
Q

What are some of the unwanted effects of organic nitrates?

A

postural hypotension
headaches (initially)
formation of methaemoglobin (rarely)

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23
Q

Examples of ETa receptors antagonists and their effects on vascular smooth muscle?

A

Bosnian and ambrisentan

Used in the treatment of pulmonary hypertension

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24
Q

Which drugs act on RAAS?

A

ACE inhibitors and Angiotension receptor antagonists

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25
Q

What is RAAs involved in the regulation of?

A

Sodium excretion and vascular tone

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26
Q

Which enzyme converts angiotensin I into angiotensin II?

A

ACE - angiotensin converting enzyme

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27
Q

How does angiotensin II cause contraction of vascular smooth muscle?

A

Activates smooth muscle AT1 receptors (GPCR)

Increases release of noradrenaline from sympathetic fibres

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28
Q

Where is aldosterone secreted from?

A

Adrenal cortex

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29
Q

What does aldosterone stimulate?

A

tubular reabsorption of Na+ and salt retention

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30
Q

Is angiotensin II a vaso dilator or constrictor?

A

vasoconstrictor

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31
Q

What does ACE inactivate?

A

bradykinin - a vasodilator

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32
Q

What type of drug if Lisinopril?

A

ACE inhibitor

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33
Q

What is the suffix for AT1 receptor antagonists?

A

sartan(s)

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34
Q

What does Losartan do?

A

blocks the agonist action of angiotensin II at AT1 receptors in a competitive manner

35
Q

What do ACEI cause?

A

Venous + arteriolar dilatation

-> decreasing arterial BP and cardiac load

36
Q

What is the effect of ACEIs on cardiac contractility?

A

no effect

37
Q

Where do ACEI have greatest effect?

A

angiotensin-sensitive vascular beds (brain, heart, kidneys)

38
Q

In which patients may ACEI cause hypotension?

A

patients treated with diuretics

39
Q

What is a common adverse effect of ACEIs?

A

dry cough

40
Q

In which conditions should ACEIs and ARBs not be used?

A

pregnancy - foetal toxicity

bilateral renal artery stenosis

41
Q

Cardiac failure is associated with inappropriate activation of what?

A

RAAS

42
Q

what are adrenoceptors activated by?

A

the sympathetic transmitter noradrenaline and the hormone adrenaline

43
Q

B1 adrenoceptors are found where and when bound cause an increase in what?

A

the heart

Increase heart rate, force and AV node conduction velocity

44
Q

Which b-blockers are particularly useful in angina pectoris?

A

b1-selective agents

45
Q

Why are these b-blcokers used in angina?

A

decreased oxygen consumption of heart
counter elevated sympathetic activity assoc. with ischaemic pain
increase amount of time spent in diastole

46
Q

What is the effect of increasing the length of diastole?

A

decrease HR

Improves oxygenation of myocardium - prolong interval between systolic events

47
Q

What are the 3 main clinical uses of b-adrenoceptor antagonists?

A

angina pectoris
hypertension
heart failure

48
Q

How might b-blockers restore normal BP?

A 
reduce CO (MAP = CP x SVR)
reduce renin release from kidneys
49
Q

how are b-blockers used in heart failure?

A

in combination with other drugs to suppress the adverse effects associated with elevated activity of the sympathetic system and RAAS

Start low, go slow

50
Q

How do calcium antagonist drugs work?

A

prevent the opening of L-type channels in excitable tissues in response to depolarisation and so limit the increase of intracellular calcium

51
Q

So if calcium antagonists reduce the influx of Ca2+…what effect do they have on cardiac action potentials?

A

Phase 2 of ventricular AP - reduce force of contraction - negative inotropes

Upstroke in pacemaker AP - reduce rate and conduction through the AVN

52
Q

Examples of calcium antagonists?

A

verapamil
amlodipine
diltiazem

53
Q

Amlodipine is which type of compound and which L-type channels is it selective for?

A

Dihydropyridine

smooth muscle L-type channels

54
Q

Verapamil is selective for which type of L-type channel?

A

cardiac L-type channels

55
Q

What are the main clinical uses of calcium antagonists?

A

Hypertension
Angina
Dysrhythmias

56
Q

What is the role calcium antagonists in the treatment of angina?

A

prophylactic treatment, often used in combo with GTN - particularly if b-blockers are contra-indicated

57
Q

What makes calcium blockers of particular value in angina prophylaxis?

A

preload is not significantly changed - even though they cause arteriolar dilatation -> reduce after load and myocardial oxygen requirement

produce coronary vasodilatation - useful in variant angina

58
Q

Which calcium antagonist is used in dysrhythmias?

A

verapamil

59
Q

For which condition would you avoid using verapamil, especially when combined with a b-blcoker?

A

heart failure

60
Q

What is the effect of a calcium channel blocker on ventricular rate in rapid AF?

A

reduced ventricular rate by suppression of conduction through the AV node

61
Q

Nicorandil and Minoxidil are part of which class of drugs?

A

potassium channel openers

62
Q

How do potassium channel openers cause relaxation?

A

antagonise intracellular ATP - closure of K-ATP channels

cause hyper polarisation - switches off L-type Ca2+ channels

reduces amount of Ca entering cell -> relaxation

63
Q

Potassium channels openers act potently and primarily upon..?

A

arterial smooth muscle

64
Q

When is Minoxidil used?

A

last resort in severe hypertension

65
Q

What are the side effects of using Minoxidil for unresolved hypertension?

A

reflex tachycardia and salt and water retention

these can be alleviated by a b-blocker and diuretic - but this means more medication for patient

66
Q

Which potassium channel opener has NO donor activity and when is it used?

A

Nicorandil

angina

67
Q

Prazosin and doxazosin are of which drug class?

A

a1-adrenoceptor receptor antagonists

68
Q

What is the effect of a1-ADRs?

A

vasodilatation - reduced sympathetic transmission - decreased MABP

69
Q

What is benign prostatic hyperplasia?

A

an abnormally enlarged prostate that compresses the urethra

70
Q

Which drugs that affect the vascular are indicated for benign prostatic hyperplasia?

A

a1-adrenoceptor antagonists - provide symptomatic relief - particularly indicated for hypertensive patients with this condition

71
Q

What is the main adverse effect of a1-adrenoceptor antagonists?

A

postural hypotension

72
Q

Diuretics increase excretion of what?

A

Na, Cl and H2O

73
Q

What are the major classes of diuretic?

A

loop and thiazide

74
Q

Which diuretic type inhibits NaCl reabsorption in the distal tubule?

A

thiazides

75
Q

What do thiazide diuretics block to prevent reabsorption?

A

Na+/Cl- co-transporter

76
Q

Which diuretics inhibit NaCl reabsorption in the thick ascending limb of the loop of Henle?

A

Loop diuretics

77
Q

Which channel do loop diuretics block?

A

Na+/K+/2Cl- co-transporter

78
Q

which diuretic type causes the stronger diuresis?

A

loop

79
Q

Diuretics can produce an undesirable loss of K+…where does this occur?

A

the late distal tubule through Na/K exchange

80
Q

How can this undesirable loss of K+ be corrected?

A

co-administration of a ‘potassium sparing diuretic’ or K+ supplements

81
Q

Which cardio conditions are thiazides commonly used in?

A

mild heart failure
hypertension
severe resistant oedema (+ loop agent)

82
Q

Wich cardio conditions would require a loop diuretic?

A

Used to reduce salt and water overload associated with:
acute pulmonary oedema (IV)
chronic heart failure

83
Q

Bendroflumethiazide is a …. diuretic?

A

thiazide

84
Q

Furosemide is a … diuretic?

A

loop

Cardio (15 decks)

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