Treating hypertension Flashcards

1
Q

What are some complications of hypertension?

A

Stroke
Kidney disease
Diabetes

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2
Q

What is the difference btw primary and secondary hypertension?

A

Primary hypertension has no obvious cause and/or is not related to any other diseases.

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3
Q

What are some causes of secondary hypertension?

A

Renal/renal disease
Endocrine disease (Cushing’s)
Iatrogenic - NSAIDS/hormonal oral contraceptive.

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4
Q

What is the equation for BP?

A

BP = CO x TPR

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5
Q

What is the equation for CO?

A

CO = HR x SV

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6
Q

What are 4 drug types usually used to control blood pressure?

A

ACE inhibitors
Angiotensin II receptor blockers
Calcium channel blocker
Diuretics

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7
Q

Name 2 ACE inhibitors

A

Captopril

Enalapril

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8
Q

How do ACE inhibitors work?

A

They inhibit angiotensin I converting enzyme, to stop the formation of angiotensin II which has effects on the renal system which increase H20 absorption, causes vasoconstriction, increases aldosterone production.

However due to there being no angiotensin II, less Na and water is reabsorbed, less aldosterone produced and less vasoconstriction occurs meaning more water lost via urine - lowering blood volume and therefore reducing blood pressure.

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9
Q

What is a side effect of ACE inhibitors?

A

Hyperkalemia

Cough due to inhibition of bradykinin breakdown.

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10
Q

What is an example of an ATII receptor blocker?

A

Losartan

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11
Q

What is a benefit of using an ATII blocker compared to an ACE inhibitor?

A

No cough

Better tolerated

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12
Q

What are some side effects of ATII antagonists

A

Hyperkalaemia

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13
Q

What are some calcium channel blockers which we would use to cause peripheral vasodilation?

A

Dihydropyridines such as nifedipine - they are more selective for the periphery which makes them better for lowering blood pressures.

They also reduce preload of the heart (filling pressure).

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14
Q

What are some effects of using dihydropyridines (such as nifedipine)

A

Peripheral oedema (due to vasodilation)
Dizziness
Constipation (lack of gut smooth muscle contraction)
May worsen GORD (due to relaxation of the smooth muscle in the lower oesophageal sphincter).

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15
Q

What are the different classes of diuretics?

A

Loop agents - such as furosemide
- potent - up to 30% of filtered Na

Thiazide - hydrochlorothiazide

  • mild diuretic effect
  • direct vasoconstrictor

K+ sparing - spironolactone

  • weak diuretic
  • useful to control K+ loss due to other diuretics.
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16
Q

What is the method of action of thiazides?

A

Blocks Na+-Cl- symporter in the first part of DCT, leading to an increase Na+ load and therefore Increased water content in the nephron of the kidney.

Also had a vasodilation effect therefore more water filtered into the nephron.

17
Q

When are B blockers useful in treating hypertension?

A

B blockers are useful in hypertension where ACD has failed to achieve sufficient BP control.

  • b1 selective antagonists decrease cardiac output and also decrease renin secretion.
18
Q

Name a B1- selective B blocker?

A

atenolol

19
Q

Name a a1 selective B blocker?

A

Carvedilol - improves coronary perfusion.

20
Q

What are some side effects of B blockers

A

constipation

indigestion

hypotension

21
Q

Give an example of an alpha blocker?

A

Prazosin

Doxazosin

22
Q

When would we use alpha blockers to treat bp?

A

When bp has not been adequately controlled by ACD.

23
Q

Aldosterone antagonism method.

A

Studies show that primary aldosteronism is common in patients with resistive hypertension.

Spironolactone can help with resistant hypertension.

Blocks the effect of aldosterone at DCT.

24
Q

What are some side effects of spironolactone.

A

hyperkalemia - anti androgenic effect

25
Q

When would we use A2 agonists?

A

A2 adrenoceptor agonist action inhibits NE release - primary act via SNS

Not very selective due to CNS effects

Reserved for extreme resistant hypertension

26
Q

When can’t we use direct vasodilators to treat hypertension?

A

pregnancy

27
Q

What are some direct vasodilators we can use to treat hypertension?

A
NO donors (glyceroltrinitrate)
Hydralazine
K+ channel activators.