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BSMS 103 > Theme 3 - drug treatment for CVD > Flashcards

Theme 3 - drug treatment for CVD Flashcards

1
Q

what blood pressure is classified as hypertension?

A

150/95 mmHg

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2
Q

what the blood pressure equation?

A

BP = CO x TPR

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3
Q

what does TPR measure?

A

degree of constriction or dilation of arterioles

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4
Q

where are the main baroreceptors that detect blood pressure found?

A

aortic arch, kidney and carotid sinus

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5
Q

what hormone is released when low blood pressure is low and what does this cause?

A

when baroreceptors detect low BP - noradrenaline is released which causes construction of arterioles which increases BP

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6
Q

what receptors does NA simulate when released in response to low BP?

A
  • alpha1 adrenergic receptors

as well as beta 1 adrenergic receptors on the SA node and ventricular myocytes in the heart

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7
Q

what is the main aim of the sympathetic NS when decreased aortic blood flow is detected?

A

to increase preload (blood back to the heart) therefore increasing CO

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8
Q

by what mechanism does activation of B1 receptors on the heart increase blood pressure?

A
  • via cAMP
  • increases calcium entry to the SA node cells
  • increases frequency and force of contraction
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9
Q

what NT is released by the parasympathetic NS to decrease blood pressure and what receptors does it act on?

A

Ace release which acts on M2 receptors

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10
Q

what branch of the ANS solely regulates peripheral resistance and what does this result in?

A
  • sympathetic NS

- NA release works on alpha 1 receptors which increases calcium via IP3 = vasoconstriction

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11
Q

which receptors can the sympathetic NS act via to cause vasoconstriction?

A
  • alpha 1 adrenergic (IP3)

- beta 2 receptors (cAMP)

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12
Q

what does decreased renal perfusion cause?

A

the juxtaglomerular apparatus to release renin

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13
Q

what does renin do?

A

converts angiotensinogen to AG I

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14
Q

where is ACE found?

A

in the endothelium

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15
Q

what NS response does AGII stimulate and what does this lead to?

A
  • sympathetic NS
  • causes aldosterone release from the adrenals (increased Na retention)
  • ADH release from posterior pituitary (increased waer reabsorption)
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16
Q

what does activation of ADH and aldosterone by the sympathetic NS ultimately lead to?

A

increased blood volume, increased stroke volume, increased cardiac output and therefore increased blood pressure

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17
Q

what receptor does AGII work on and what does stimulation of these receptors cause?

A

AT1 receptors that increases arteriole and venous constriction increased blood pressure

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18
Q

what cells does aldosterone work on and what receptor does it bind?

A

works on principal cells in the DT and CD and binds a mineralocorticoid receptor

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19
Q

what is the result of aldosterone binding to its receptor in principal cells?

A
  • upregulates Na/K ATPase on the BL membrane
  • upregulates ENac in apical of CD cells
  • results in increased reabsorption of Na+ and water in the blood
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20
Q

what would be the first choice of hypertensive drug for someone under 55

A

ACE inhibitor or angiotensin receptor blocker

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21
Q

what would be first choice hypertension treatment for those over 55 or from black origin?

A

calcium channel blockers/thiazide diuretics

22
Q

what is the mechanism of action of ACE inhibitors and give an example

A
  • reduced AGI –> AGII (doesn’t block it)

- RAMIPRIL

23
Q

what is first dose hypotension, what drugsf class is it associated with and how can it be avoided?

A
  • associated with ACE inhibitors
  • patient can get very big drop in BP the first time they take an ACE inhibitor
  • can be avoided by telling the patient to take it at night - prevents fainting
24
Q

what is the main side effects of ACEIs and why does this occur?

A
  • dry tickly cough (25-40%)
  • occurs as ACEIs also reduces kininase II levels which breakdown bradykinin - results in increased bradykinin which is an irritant = cough
25
Q

what is the main contraindication of ACEIs?

A

renal impairment/renal artery stenosis

26
Q

what parameter in the blood needs to be carefully monitored when giving ACEIs?

A

creatinine

27
Q

what is the action of angiotensin receptor antagonists?

A

blocks AG II action on AT1 receptors

28
Q

Give an example of an ARB and what situation may these be given in?

A

may be given if a patient cant tolerate ACEIs

- LOSARTAN

29
Q

give an example of an aldosterone antagonist and when would this be given

A
  • SPIRONOLACTONE
  • uncommon as a hypertensive but may be added on for resistant hypertension or front line for patients with primary aldosteronism
30
Q

give an example of a calcium channel antagonist and when might this be used?

A
  • AMILOPDIPINE or VERAPAMIL

- may be used in over 55s and patients from black origin

31
Q

what channel do calcium channel antagonists target and what does this cause?

A
  • target L type calcium channels in smooth muscle of arterioles
  • causes relaxation
  • no calcium means MLC cant be phosphorylated therefore no contraction
32
Q

what is the main side effect of calcium channel antagonists?

A

peripheral oedema

33
Q

by which mechanism do calcium channel blockers cause peripheral oedema?

A
  • block L type calcium channels which are found on pre capillary sphincters
  • lack of constriction disrupts the pressure balance in pre cap sphincters
  • less fluid moves back into the capillary at the venous end as there is already lots of water
  • fluid stays in tissue = OEDEMA
34
Q

give two other side effects of calcium channel blockers

A
  • flushing (due to dilation of blood vessels)

- headaches - blocking of blood vessels that perfuse the meninges

35
Q

what effect would cytochrome P450 blockers have on calcium channel antagonists?

A

increase its activity as CCB are metabolised by CP450 so reducing its activity means drug is more active

36
Q

what part of the nephron do thiazide diuretics work on?

A

DCT

37
Q

by what mechanism do thiazides work?

A
  • inhibit activity of Na/Cl co-transporter on the apical of DCT cells
  • Less Na moves into cells therefore more is in the tubular fluid
  • water therefore also stays in the tubular fluid
  • produces lots of dilute urine - decreases venous return, CO and BP
38
Q

Apart from the Na/Cl co-transporter - what other channels may thiazides work on and how does this lower BP?

A
  • K+ ATP channels
  • cause channel to open and K+ leaves
  • cell becomes more negative therefore L type calcium channels are less likely to open
  • less calcium in means less contraction
  • vasodilation and decreased BP/TPR
39
Q

what should be monitored in a patient on thiazides?

A

ions levels

40
Q

what are two side effects of thiazides?

A
  • hypokalaemia

- increased urate

41
Q

what does bendrofumathiazide cause an increase in the blood?

A

increased blood glucose and lipids - can therefore increase risk of MI and stroke

42
Q

what is the main contraindication for use of thiazides?

A

diabetes

43
Q

why are thiazides contraindicated in diabetics?

A

normally - glucose stimulates GLUT2 which increases ATP and closes K+ channels
- K+ doesn’t leave cells - calcium and insulin release to decrease blood glucose
THIAZIDES CAUSE K+ ATP CHANNELS TO BE OPEN
- K+ therefore leaves the cell and hyperpolarises it
- this causes decreased insulin release and an increase in blood glucose

44
Q

what do beta blockers cause?

A

decrease HR, FOC and therefore decreased CO and BP

45
Q

what receptors do beta blockers work on?

A

beta 1 and beta 2 adrenergic receptors

46
Q

give an example of both a selective and a non selective beta blocker

A
  • PROPANOLOL - non selective (targets beta 1 and 2 receptors)
  • BISOPROLOL - selective - only targets beta 1 receptors
47
Q

what is the main side effect of beta blockers?

A

fatigue

48
Q

which three conditions are contraindicated to beta blockers?

A

diabetes, asthma and reynaulds disease (sensitive BVs)

49
Q

why shouldn’t beta blockers be given to diabetics?

A

they block the warning signs of hypoglycaemia as they prevent adrenaline release

50
Q

give an example of a vasodilator and when may it be used?

A

DOXAZOSIN

- may be used in benign prostatic hypertrophy

51
Q

why are vasodilators used in benign prostate hypertrophy?

A
  • alpha 1 R antagonists
  • the prostate is surrounded by a muscular sheath with alpha R receptors on it
  • antagonising the receptors relaxes the sheath and prevents prostate pushing on urethra

BSMS 103 (23 decks)

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