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Drugs: From molecules to man > Antihypertensive drugs > Flashcards

Antihypertensive drugs Flashcards

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Organic Chemistry 101 flashcards
1
Q

Define hypertension

A

abnormally high blood pressure (increased systolic/diastolic/pulse pressure)

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2
Q

How is a blood pressure measurement given?

A

systolic over diastolic e.g. ‘120 over 80’

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3
Q

What’s systolic pressure?

A

pressure when the heart is contracting (max. pressure)

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4
Q

what’s diastolic pressure?

A

pressure when the heart is filling (min. pressure)

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5
Q

what’s pulse pressure?

A

the difference between systolic and diastolic BP

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6
Q

what’s hypotension?

A

abnormally low BP

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7
Q

What diastolic BP measurement would be severe hypertension?

A

> 120 mm Hg

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8
Q

what diastolic BP measurement would be moderate hypertension?

A

105- 120 mm Hg

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9
Q

what diastolic BP measurement would be mild hypertension?

A

90- 105 mm Hg

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10
Q

what’s normal/ optimal diastolic BP?

A

around 80 mm Hg

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11
Q

what are the 2 types of hypertension?

A

primary and secondary

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12
Q

what’s primary hypertension?

A

where the cause is unknown

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13
Q

what are 2 other names for primary hypertension?

A

essential or idiopathic hypertension

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14
Q

what’s secondary hypertension?

A

where the cause has been identified (due to another disorder/drugs) e.g. renal artery stenosis

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15
Q

what are the 2 important trials for Hypertensive drugs?

A

ASCOT and ALLHAT

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16
Q

what does ASCOT stand for?

A

Anglo-Scandinavian Cardiac Outcomes Trial

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17
Q

what was ASCOT testing?

A

compared Amlodipine (Calcium channel antagonist) and Perindropil (ACE inhibitor) with Atenolol (B-blocker) and Bedroflumethiazid (diuretic)

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18
Q

what were the findings of ASCOT?

A

both groups had reduced BP and reduced incidence of CVD (better with Amlodipine group)

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19
Q

what did ASCOT conclude?

A

that calcium agonists and ACE inhibitors should replace ‘older’ treatments (B- blockers and diuretics)

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20
Q

What does ALLHAT stand for?

A

Antihypertensive and Lipid Lowering treatment to prevent Heart Attack Trial

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21
Q

where was ALLHAT done?

A

USA

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22
Q

which had a wider ethnic range, ALLHAT or ASCOT?

A

ALLHAT (as it was done in the USA instead of UK/Scandinavia)

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23
Q

what was ALLHAT testing?

A

Compared Chlorthalidone ( thiazide-like diuretic) with Amlodipine (calcium channel antagonist) or Lisinopril (ACE inhibitor)

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24
Q

what were the findings of ALLHAT?

A
  • BP was controlled in all 3 groups, but Chlorthalidone was superior
  • risk of HA was similar for all 3
  • risk of some other CVDs was lower with chlorthalidone
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25
Q

what did ALLHAT conclude?

A

that thiazide diuretics are superior to calcium channel blockers and ACE inhibitors

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26
Q

What’s the NICE care pathway for hypertension?

A

https://www.google.com/search?safe=active&rlz=1C1CHBF_en-gbGB767GB767&biw=1280&bih=610&tbm=isch&sa=1&ei=ye3CXOn8CemBjLsP7u2gyAU&q=NICE+carepathway+hypertension+stage+1+and+stage+2&oq=NICE+carepathway+hypertension+stage+1+and+stage+2&gs_l=img.3…14350.18046..18160…0.0..0.87.1188.20……1….1..gws-wiz-img.g4LiWCP5BMw#imgrc=-Jhi0wDHD7aUOM:

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27
Q

what’s Peripheral resistance?

A

the resistance the heart has to push against

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28
Q

what is peripheral resistance controlled by?

A

resistance arteriole which can contract and dilate under the control of the ANS

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29
Q

what’s the chain of events which causes contraction of the resistance arteriole?

A

SNS releases Noradrenaline –> binds to the a1 adrenoreceptor –> activates Phospholipase C activation –> activates Inositol Triphosphate (INP3) release –> activates calcium store –> influx of calcium ions increases intracellular concentration –> causes calcium sensitive ion channels to open –> Cl- efflux –> causes membrane depolarisation –> causes opening of L-type calcium channels –> Ca2+ influx –> increases intracellular Calcium concentration –> causes contraction of arteriole, therefore increased resistance and BP

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30
Q

which part of the flow chart to calcium channel blockers act on?

A

causes opening of L-type calcium channels –> Ca2+ influx

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31
Q

what are the 3 main classes of calcium channel blockers?

A
  • Verapamil ( a phenylalkylamine)
  • Diltazen (a benzothiazepine)
  • Amlodipine (a dihydropyridine)
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32
Q

Give a summary of how Calcium Channel blockers work

A 
Reduce L-type calcium channel opening 
targets vasculature (BVs) and heart
inhibits Ca2+ entry in vessels and reduces contractility and AV conduction in the heart
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33
Q

what are 2 side effects of calcium channel blockers?

A
  • Headaches

- Hypotension (in early stages of treatment/ at high dosage) caused by a change in posture e.g. standing up from sitting

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34
Q

What’s Diuresis?

A

increased urine output

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35
Q

what’s the short-term effect of diuresis?

A

intravascular salt and water depletion

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36
Q

In what case can intravascular salt and water depletion be useful?

A

renal failure

37
Q

what effect does diuresis have in the long term?

A

Arterial dilation

38
Q

how does arterial dilation affect BP?

A

it reduces it

39
Q

As well as hypertension, what else can diuretics treat?

A

Oedema (removes excess fluid)

40
Q

Generally, what do diuretics do?

A

increase excretion of Na+, Cl- and water

41
Q

what are the 3 main classes of diuretics?

A

Thiazide, Loop and Potassium sparing

42
Q

what part of the renal system do loop diuretics act on?

A

Loop of Henle

43
Q

give 2 examples of loop diuretics

A

Frusemide and Bumetanide

44
Q

What do loop diuretics do?

A

inhibit Na+/K+/2Cl- cotransport in the ascending limb

45
Q

How does the loop of Henle work?

A

the descending limb has no active transport but is water permeable. The loss of water for the descending limb is driven by the movement of NaCl from the ascending limb. The ascending limp actively transports Na+ and passively transports Cl- and is water impermeable

46
Q

what are 4 clinical uses for loop diuretics?

A

Heart failure, Hypertension, Renal failure, Pulmonary Oedema

47
Q

which are the most powerful type of diuretics?

A

loop (up to 10 litres of urine produced a day)

48
Q

what do thiazide diuretics do?

A

inhibit Na+/Cl- cotransport in the distal convoluted tubule.
By inhibiting NaCl cotransport out of the convoluted tubule, more NaCl is passed onto distal segments. This means less difference in osmality between urine and plasma, reducing ability to reabsorb water in more distal portions

49
Q

what are the 2 main examples of Thiazide Diuretics

A

Bendroflumethiazide and Chlorthalidone

50
Q

what are 2 clinical uses of Thiazide diuretics?

A

Hypertension and Oedema due to heart failure

51
Q

how strong are thiazide diuretics?

A

mild

52
Q

what do potassium sparing diuretics do?

A

decrease trans-principal cell Na+ movement and decrease negative lumen potential

53
Q

what are the 2 main examples of Potassium sparing diuretics?

A

Spironolactone and Amiloride

54
Q

what does Spironolactone do?

A

it’s an aldosterone antagonist. It increases the expression of Na/K ATPase (genomic effect). This makes sodium channels in the membrane work better (non- genomic effect)

55
Q

what does Amiloride do?

A

Blocks sodium channels in lumenal membrane- conserves Potassium

56
Q

How strong are Potassium sparing diuretics?

A

weak (usually used in combination)

57
Q

what aspect of BP is Renin involved in?

A

slow ‘compensatory’ control of BP

58
Q

describe the overall flow cart in the renin-angiotensin system to increase blood pressure

A

Renin –> Angiotensin–> forms aldosterone and causes vasocontriction–> Aldosterone causes salt and water retention –> both vasoconstriction and salt and water retention increase BP

59
Q

describe the formation of angiotensin hormones

A

Angiotensinogen is cleaved by renin to form Angiotensin I (inactive decamer)
Angiotensin I is cleaved by Angiotensin Converting Enzyme (ACE) to produce the active octamer Angiotensin II.
This can be cleaved to make either Angiotensin III (heptamer active) or Angiotensin IV (active hexamer)
Angiotensin II and III bind to AT1R to increase Aldosterone secretion and cause vasocontriction
(if we can prevent active forms of Angiotensin, we can reduce BP- ACE inhibitors)

60
Q

What is Captopril?

A

an ACE inhibitor

61
Q

how was captopril discovered?

A

viper venom

62
Q

what do the names of all ACE inhibitors end with?

A

-pril

63
Q

name the 4 main ACE inhibitors

A

captopril, lisinopril, ramipril, anapril

64
Q

what are 2 common side- effects of ACE inhibitors?

A

Initial Hypotension and cough

65
Q

What do Angiotensin II receptor antagonists do?

A

the angiotensin II receptor type I

66
Q

give 2 examples of Angiotensin II receptor antagonists

A

Iosartan and Candesartan

67
Q

what’s a common side effect of Angiotensin II receptor antagonist?

A

Hypotension

68
Q

what’s a benefit of Angiotensin II receptor antagonists over ACE inhibitors?

A

no cough as a side effect

69
Q

How does alpha 1 adrenoreceptor activation affect BP?

A

it increases it as it causes vasocontriction

70
Q

name 2 competitive a1-adrenoreceptor antagonists

A

Phentolamine and chloropromazine

71
Q

name a non-competitive a1-adrenoreceptor agonist

A

Phenoxybenzamine

72
Q

what does Doxazosin do?

A

it’s an a1- adrenoreceptor antagonist that blocks the receptor

73
Q

when is Doxazosin used?

A

when other therapy has proved ineffective

74
Q

give 3 side-effects of Doxazosin

A
  • initial hypotension
  • urinary incontinence
  • retrograde ejaculation
75
Q

Give the 3 main adrenoreceptor Beta-blockers

A
  • Propranalol
  • Atenolol
  • Bisopropolol
76
Q

describe Propranalol

A

competitive antagonist, non-selective B- adrenoreceptor antagonist, relatively lipid soluble (good penetration of the CNS)

77
Q

describe atenolol and Bisopropolol

A

Competitive antagonists, B-selectivity, relatively water soluble (poor penetration of the CNS)

78
Q

what physiological effects do Beta adrenoreceptor antagonists have to reduce BP?

A

reduced cardiac output
reduced renin release
reduced sympathetic tone

79
Q

give 3 side-effects of beta-blockers

A
  • Bronchoconstriction (can’t be given to asthmatics)
  • precipitation of cardiac failure (heart block)
  • hyperglycaemia (can’t be given to diabetics)
  • reynauds
  • Vivid dreams (propranalol)
80
Q

What’s the NICE guidelines for antihypertensive drugs?

A

https://www.google.com/search?q=NICE+recommendations+for+antihypertensive+drugs&safe=active&rlz=1C1CHBF_en-gbGB767GB767&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiMo5r68-3hAhWDblAKHefXB5cQ_AUIDigB&biw=1280&bih=610#imgrc=2beLUpi82ZgSwM:

81
Q

what type of drug is chlorthalidone?

A

Diuretic

82
Q

what type of drug is verapamil?

A

calcium channel blocker

83
Q

what type of drug is phenoxybenzamine?

A

adrenoreceptor blocker

84
Q

what type of drug is doxazonsin?

A

adrenoreceptor blocker

85
Q

what type of drug is amiloride?

A

diueretic

86
Q

what;s the difference between pharmacodynamics and pharmacokinetics?

A

Pharmacodynamics focuses on what the drug does to the body whereas pharmacokinetics focuses on what the body does to the drug

87
Q

does phenoxybenzamine bind reversibly or irreversibly to adrenoreceptors?

A

irreversibly

88
Q 
which of the following isn't a cause of secondary hypertension?
tumours of the adrenal medulla
polycystic kidney disease
myocardial infarction
renal artery stenosis
A

Myocardial infarction (hypertension can cause IT but IT doesn’t cause hypertension)

Drugs: From molecules to man (10 decks)

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