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Drugs affecting BP and vasculature Flashcards

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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
What is RAAs involved in the regulation of?
Sodium excretion and vascular tone
26
Which enzyme converts angiotensin I into angiotensin II?
ACE - angiotensin converting enzyme
27
How does angiotensin II cause contraction of vascular smooth muscle?
Activates smooth muscle AT1 receptors (GPCR) | Increases release of noradrenaline from sympathetic fibres
28
Where is aldosterone secreted from?
Adrenal cortex
29
What does aldosterone stimulate?
tubular reabsorption of Na+ and salt retention
30
Is angiotensin II a vaso dilator or constrictor?
vasoconstrictor
31
What does ACE inactivate?
bradykinin - a vasodilator
32
What type of drug if Lisinopril?
ACE inhibitor
33
What is the suffix for AT1 receptor antagonists?
sartan(s)
34
What does Losartan do?
blocks the agonist action of angiotensin II at AT1 receptors in a competitive manner
35
What do ACEI cause?
Venous + arteriolar dilatation | -> decreasing arterial BP and cardiac load
36
What is the effect of ACEIs on cardiac contractility?
no effect
37
Where do ACEI have greatest effect?
angiotensin-sensitive vascular beds (brain, heart, kidneys)
38
In which patients may ACEI cause hypotension?
patients treated with diuretics
39
What is a common adverse effect of ACEIs?
dry cough
40
In which conditions should ACEIs and ARBs not be used?
pregnancy - foetal toxicity | bilateral renal artery stenosis
41
Cardiac failure is associated with inappropriate activation of what?
RAAS
42
what are adrenoceptors activated by?
the sympathetic transmitter noradrenaline and the hormone adrenaline
43
B1 adrenoceptors are found where and when bound cause an increase in what?
the heart | Increase heart rate, force and AV node conduction velocity
44
Which b-blockers are particularly useful in angina pectoris?
b1-selective agents
45
Why are these b-blcokers used in angina?
decreased oxygen consumption of heart counter elevated sympathetic activity assoc. with ischaemic pain increase amount of time spent in diastole
46
What is the effect of increasing the length of diastole?
decrease HR | Improves oxygenation of myocardium - prolong interval between systolic events
47
What are the 3 main clinical uses of b-adrenoceptor antagonists?
angina pectoris hypertension heart failure
48
How might b-blockers restore normal BP?
``` reduce CO (MAP = CP x SVR) reduce renin release from kidneys ```
49
how are b-blockers used in heart failure?
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
How do calcium antagonist drugs work?
prevent the opening of L-type channels in excitable tissues in response to depolarisation and so limit the increase of intracellular calcium
51
So if calcium antagonists reduce the influx of Ca2+...what effect do they have on cardiac action potentials?
Phase 2 of ventricular AP - reduce force of contraction - negative inotropes Upstroke in pacemaker AP - reduce rate and conduction through the AVN
52
Examples of calcium antagonists?
verapamil amlodipine diltiazem
53
Amlodipine is which type of compound and which L-type channels is it selective for?
Dihydropyridine | smooth muscle L-type channels
54
Verapamil is selective for which type of L-type channel?
cardiac L-type channels
55
What are the main clinical uses of calcium antagonists?
Hypertension Angina Dysrhythmias
56
What is the role calcium antagonists in the treatment of angina?
prophylactic treatment, often used in combo with GTN - particularly if b-blockers are contra-indicated
57
What makes calcium blockers of particular value in angina prophylaxis?
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
Which calcium antagonist is used in dysrhythmias?
verapamil
59
For which condition would you avoid using verapamil, especially when combined with a b-blcoker?
heart failure
60
What is the effect of a calcium channel blocker on ventricular rate in rapid AF?
reduced ventricular rate by suppression of conduction through the AV node
61
Nicorandil and Minoxidil are part of which class of drugs?
potassium channel openers
62
How do potassium channel openers cause relaxation?
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
Potassium channels openers act potently and primarily upon..?
arterial smooth muscle
64
When is Minoxidil used?
last resort in severe hypertension
65
What are the side effects of using Minoxidil for unresolved hypertension?
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
Which potassium channel opener has NO donor activity and when is it used?
Nicorandil | angina
67
Prazosin and doxazosin are of which drug class?
a1-adrenoceptor receptor antagonists
68
What is the effect of a1-ADRs?
vasodilatation - reduced sympathetic transmission - decreased MABP
69
What is benign prostatic hyperplasia?
an abnormally enlarged prostate that compresses the urethra
70
Which drugs that affect the vascular are indicated for benign prostatic hyperplasia?
a1-adrenoceptor antagonists - provide symptomatic relief - particularly indicated for hypertensive patients with this condition
71
What is the main adverse effect of a1-adrenoceptor antagonists?
postural hypotension
72
Diuretics increase excretion of what?
Na, Cl and H2O
73
What are the major classes of diuretic?
loop and thiazide
74
Which diuretic type inhibits NaCl reabsorption in the distal tubule?
thiazides
75
What do thiazide diuretics block to prevent reabsorption?
Na+/Cl- co-transporter
76
Which diuretics inhibit NaCl reabsorption in the thick ascending limb of the loop of Henle?
Loop diuretics
77
Which channel do loop diuretics block?
Na+/K+/2Cl- co-transporter
78
which diuretic type causes the stronger diuresis?
loop
79
Diuretics can produce an undesirable loss of K+...where does this occur?
the late distal tubule through Na/K exchange
80
How can this undesirable loss of K+ be corrected?
co-administration of a 'potassium sparing diuretic' or K+ supplements
81
Which cardio conditions are thiazides commonly used in?
mild heart failure hypertension severe resistant oedema (+ loop agent)
82
Wich cardio conditions would require a loop diuretic?
Used to reduce salt and water overload associated with: acute pulmonary oedema (IV) chronic heart failure
83
Bendroflumethiazide is a .... diuretic?
thiazide
84
Furosemide is a ... diuretic?
loop

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