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103 Theme 3 - Cardiovascular System > Drug treatments for cardiovascular disease 1 & 2 > Flashcards

Drug treatments for cardiovascular disease 1 & 2 Flashcards

1
Q

What is the definition of hypertension?

A

Persistently higher than normal blood pressure

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2
Q

What is normal BP and what BP is treated?

A

Normal - 120/80

Treatment if mean BP>150/95mmHg

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3
Q

What is the equation for blood pressure?

A

BP = CO x TPR

Total Peripheral Resistance a measure of the degree of constriction of the arterioles

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4
Q

What is the equation for cardiac output?

A

Cardiac Output = Stroke Volume x Heart Rate

Stroke Volume regulated by Ventricles

Heart Rate by the SA-node

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5
Q

Complete the diagram on sympathetic control of blood pressure

A
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6
Q

Which nervous system controls extrinsic regulation?

A

Autonomic nervous system

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7
Q

Does the sympathetic / parasympathetic nervous system increase / decrease heart rate?

A
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8
Q

How does the sympathetic nervous sytem increase heart rate?

A

Sympathetic system increases frequency and force of contraction via

β1 receptors -> increase cAMP -> increase Ca2+ -> increase rate and force of contraction.

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9
Q

How does parasympathetic nervous system decrease heart rate?

A

Parasympathetic system decreases frequency by decreasing cAMP via M2 receptors.

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10
Q

Complete the diagram of the blood vessel

A
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11
Q

Draw the renin-angiotensin-aldosterone system

A
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12
Q

Complete the diagram on regulation of blood pressure by the renin-angiotensin-aldosterone system

A
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13
Q

How does the RAAS system cause vasoconstriction?

A

Increases in Ang II -> increase IP3 -> increase intracellular [Ca2+]

Causes constriction of arterioles and an increase in total peripheral resistance and an increase in BP

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14
Q

How does RAAS increase preload?

A

Constriction of venules via AT1-R

RAAS also facilitates Na+ and H2O retention

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15
Q

What 3 things is the choice of anti-hypertensive drug reliant on?

A

a) Age (<55 years old ACE inhibitor/angiotensin receptor blocker (ARB); >55 years old or all Black African/Americans calcium channel blocker)
b) Race (ACE inhibitors/beta blockers may be less efficacious in black African/Amercians).
c) Co-existing diseases

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16
Q

What are the 5 classes of hypertensives?

A

ACE inhibitors and Angiotensin receptor blockers.

Calcium channel antagonists

Diuretics

Beta Blockers

Vasodilators

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17
Q

Draw the 4 steps in the national guidelines for anti-hypertenive drugs

A
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18
Q

How do ACE inhibitors cause a dry cough?

A

Increase in bradykinin

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19
Q

Which anti-hypertensive agents cause a dry cough as a side-effect?

A

ACE inhibitors

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20
Q

What are the side-effects of ACE inhibitors?

A

Dry cough

First dose hypotension

Renal impairment

May cause hypokalaemia

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21
Q

What 2 anti-hypertensives work via the renin-angiotensin-aldosterone system?

A

ACE inhibitors

ARB (angiotensin receptor blockers)

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22
Q

ACE inhibitors are contraindicated in what condition?

A

Bilateral renal artery stenosis

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23
Q

What tests are measured bedore ACE inhibitors are presribed?

A

Renal function

Creatinine levels in blood

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24
Q

Which anti-hypertensive drug is the first line treatment for diabetics and why?

A

ACE inhibitors

No adverse effects on serum glucose or lipids

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25
Q

What suffix do all ACE inhibitor drugs have and name an example

A

_____pril

•Egs. RamiPRIL

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26
Q

How do ARB work?

A

Block the actions of Ang II on AT1-R

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27
Q

What does ARB stand for?

A

Angiotensin receptor blocker

28
Q

What is the suffix for ARBs and name an example

A

_____artan

•E.g. Losartan

29
Q

What are the side effects for ARBs?

A

Minimal

30
Q

What is spironolactone?

A

Aldosterone antagonist.

31
Q

When is spironolactone used?

A

Can be used as an add on for resistant hypertension but FRONTLINE for hypertension in patients with primary aldosteronism (excess production of aldosterone from adrenal glands)

32
Q

What is the main type of calcium channel blockers?

A

Dihydropyridines

33
Q

What is the suffix for calcium channel blockers and name an example

A

_______dipine

Amlodipine

34
Q

How do calcium channel blockers reduce hypertension?

A
  • Target L-type Ca2+ channels on smooth muscle of arterioles.
  • Phenylalkylamines (e.g. verapamil) and benzothiazepines (e.g. diltiazem) target L-type channels in the heart and decrease the frequency and force of contraction, less used to treat hypertension.
35
Q

How do calcium channel blockers decrease smooth muscle contraction in arterioles?

A
  1. Block L-type channels
  2. Reduce intracellular Ca2+
  3. Reduce activation of myosin light chain kinase (MLCK)
  4. Reduce phosphorylation of myosin light chain
  5. Muscles relax more
36
Q

What does this diagram show?

Which anti-hypertensive targets this?

A

Regulation of smooth muscle contraction in arterioles

Calcium channel blockers

37
Q

What are the side-effects of calcium channel blockers?

A

Peripheral oedema

Flushing and headaches

38
Q

How do calcium channel blockers cause peripheral oedema?

A

Preferential dilation of precapillary arteriole and impairment of the function of the pre-capillary sphincter increases hydrostatic pressure across the capillary and reducing fluid reabsorption.

39
Q

What happens when this goes wrong?

What anti-hypertensive causes this to go wrong as a side effect?

A

Peripheral oedema

Calcium channel blockers

40
Q

Combination of which class of anti-hypertensives is not recommened?

A

Calcium channel antagonists

41
Q

What are calcium channel blockers also known as?

A

Calcium channel antagonists

42
Q

What affect does grapefruit juice have on calcium channel blockers?

A

Enhances action (CYP3A4)

43
Q

How do thiazide and thiazide-like diuretics decrease hypertension?

A

Some diuretic action but also acts via activation of KATP in smooth muscle of blood vessel to dilate arterioles and decrease BP

44
Q

How does indapamide work?

A

Indapamide hyperpolarises smooth muscle cells causing a relaxation/dilation of the arteriole and a decrease in total peripheral resistance

45
Q

What are the side-effects of thiazide and thiazide-like diuretics?

A
  • Hypokalaemia
  • Increase in urate
  • Increase in glucose
  • Increase in blood lipids
46
Q

What is the suffix for thiazide diuretics and name an example

A

•E.g. bendroflumethiazide

47
Q

Name a thiazide-like diuretic

A

Indapamide

48
Q

How does indapamide cause relaxation of artereoles?

A
  • Diuretic causes more K+ to leave cell - cell more negative
  • Inhibits Ca2+ channel which normally opens up when cell depolarises
  • Less intracellular Ca2+
  • Smooth muscle cell relaxes
49
Q

Thiazide-like diuretics are contraindicated in which patients and why?

A

Diabetics

  • Less Ca2+ in cell
  • Less insulin
  • Increase in blood glucose levels
50
Q

What do beta blockers do?

A

Block B1 receptors

B1 receptors increase frequency and force of contraction.

51
Q

What are the side effects of beta blockers?

A

Fatigue

Vasocontriction

Bronchoconstriction

Hypoglycaemia

52
Q

What effects do beta blockers have on the SA node?

A

Decrease heart rate

Decrease O2 demand

53
Q

What effects do beta blockers have on vetricular myocardium?

A

Decrease contractility

Decrease O2 demand

54
Q

What effects do beta blockers have on arterioles?

A

Decrease in blood pressure (decreased afterload)

Decrease in myocardial 02 demand

55
Q

How do beta blockers cause fatigue?

A
  • Excerisise increases O2 demand
  • Patients on beta blockers can’t beat harder or faster - tissues lacking nutrients and O2
56
Q

How does adrenaline cause vaso/bronchodilation?

A
  • Stimulates B2 receptors on smooth muscle cell in the airways or peripheral arterioles perfusing skeletal muscle
  • Increase in cAMP
  • Increae in protein kinase A
  • PKA phosphorylises myosin light chain kinase
  • MLCK cannot phosphorylate mysoin light chain
  • Smooth muscle relaxation
57
Q

How do beta blockers cause vasoconstricton and bronchoconstriction?

A

Beta blockers are selective for B1 receptors but can also block B2 receptors

Adrenaline cannot cause vaso/bronchodilation on smooth muscle cell in the airways or peripheral arterioles perfusing skeletal muscle

58
Q

How can beta blockers cause hypoglycaemia?

A
  • Low blood glucose activates the release of adrenaline, mobilises glucose release from liver.
  • Leads to tremor, palpitations and sweats
  • Action of adrenaline is blocked by Beta Blockers
59
Q

Which anti-hypertensives are contraindicated in diabetes?

A

Combinations of beta blockers and thiazides

60
Q

What is the suffix for beta blockers?

A

_____olol

61
Q

What are the 2 types of beta blockers and name an example for each

A

Non-selective (b1 and b2) e.g. propranolol

Selective b1 antagonist e.g. bisoprolol

62
Q

How do vasodilatators work?

A

a1-antagonists

Noradrenaline -> a1 -> IP3 -> Ca2+ -> constriction

63
Q

What is a powerful vasoconstricter found in the body?

A

Noradrenaline

64
Q

What are vasodilatators used for?

A

Used to treat hypertension in patients with benign prostatic hypertrophy

(Doxazosin)

65
Q

What is the suffix for vasodilatators and name an example

A

______azosin

Doxazosin

66
Q

What is minoxidil?

A

Other vasodilators such as minoxidil open K+ channels

103 Theme 3 - Cardiovascular System (19 decks)

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