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CVS > 10 - Controlling Hypertension > Flashcards

10 - Controlling Hypertension Flashcards

1
Q

What is hypertension defined as?

A
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2
Q

What are the two types of hypertension?

A

- Primary (essential) hypertension: unknown

- Secondary hypertension: causes can be defined, e.g renovascular, Cushing’s, hyperaldosteronism

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3
Q

Why is it important to treat hypertension?

A
  • Asymptomatic but can lead to heart failure, renal failure, MI, stroke
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4
Q

Which type of hypertension causes the biggest problems?

A

Systolic hypertension

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5
Q

How does hypertension lead to MI, heart failure, aneurysm etc?

A
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6
Q

What should you do when a patient presents with hypertension?

A
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7
Q

What is an effective decrease in blood pressure?

A

10mmHg

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8
Q

What are longer term controls of blood pressure? (short term being baroreceptor reflex)

A

- Neurohumoral response

  • Works by controlling the plasma volume by controlling sodium balance
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9
Q

What are the four pathways of the neurohumoral response?

A

ALL OCCUR SIMULATENOUSLY

1. Renin-angiotensin-aldosterone system

2. Sympathetic nervous system

3. Antidiuretic hormone (ADH)

4. Atrial Natriuretic Peptide (ANP)

(ANP only one that lowers b.p)

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10
Q

How is the renin-angiotensin-aldosterone system get stimulated?

A
  • Reduced NaCl delivery to distal tubule
  • Reduced perfusion pressue detected by baroreceptors in afferent arteriole
  • Sympathetic stimulation to JGA

RENIN RELEASED FROM GRANULAR CELLS OF JUXTAGLOMERULAR APPARATUS

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11
Q

How does the renin-angiotensin-aldosterone system increase blood pressure?

A
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12
Q

What actions do the angiotensin II receptors have at different sites?

A

Main actions via AT1 receptor

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13
Q

What is the action of aldosterone?

A
  • Acts on cells of collecting ducts
  • Activates ENaC, K+ channel and Na/K ATPase so increased Na absorption and low K+ levels
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14
Q

What other molecules does ACE cleave, apart from angiotensin I?

A

Breaks bradykinin down into peptide fragment so it cannot have a vasodilation effect

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15
Q

What is one of the main side effects of taking ACE inhibitors and why does this occur?

A

Dry cough as there is a build up of bradykinin in the lungs

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16
Q

Why do you go into hypotensive shock when bitten by the brazillian viper?

A
  • Contains bradykinin potentiation factors blocking the conversin of angiotensin I to angiotesin II by ACE
  • Can cause pulmonary oedema, disseminated intravascular coagulation, activation of hypotensive substances, blood loss so hypovolemia
17
Q

What is disseminated intravascular coagulation?

A
  • Small blood clots develop throughout the bloodstream blocking small blood vessels
  • The extra clotting depletes platelets and clotting factors leading to excessive bleeding
18
Q

What are some examples of ACE inhibitors?

A
  • Ramipril, Captopril, Lisinopril, Perindopril
19
Q

How does the sympathetic nervous sytem cause an increase in blood pressure?

A
  • High levels of sympathetic stimulatuon reduce renal blood flow, so decreased GFR and decreased Na excretion.
  • Stimulates renin release from JG cells
20
Q

How does ADH increase blood pressure?

A
  • ADH release is stimulated by increase in plasma osmolarity or severe hypovolaemia
  • Increases water reabsorption in distal nephron (AQP2), stimulates Na reabsorption in thick ascending limb (Na/K/Cl) and causes vasoconstriction
21
Q

How do atrial natriuretic peptides decrease blood pressure?

A
  • Stored in atrial myocytes and are released in response to stretch

- Causes vasodilation of the afferent arteriole and increased blood flow increases GFR

- Inhibits Na reabsorption along nephron

  • If circulating volume is low ANP release is inhibited
22
Q

What are some local vasodilators?

A

- Prostagladin: reduce Na reabsorption and enhance glomerular filtration. Act as buffer to excess vasoconstriction by SNS and RAA. Important when Ang II high

- Dopamine: Formed in kidney and causes vasodilation and increased renal blood flow. Reduces reabsorption of NaCl

23
Q

How can renal artery stenosis cause hypertension?

A
  • Fall in perfusion pressure due to artery occlusion
  • Renin production so activation of RAA
  • Need to repurfuse kidney to treat, e.g via a stent
24
Q

How can renal parenchymal disease lead to secondary hypertension?

A
  • Early stage may be due to loss of vasodilator substances
  • Later stage Na and water rentention due to inadequate glomerular filtration
25
Q

What are some issues with the adrenal glands that can lead to secondary hypertension?

A

- Conn’s Syndrome: Aldosterone secreting adenoma

- Cushing’s Syndrome: excess secretion of cortisol, which can act on aldosterone receptors in highconcentration so Na and water retention

- Phaeochromocytoma: releases catacholamines

26
Q

What are treatments for hypertension?

A

1st - Exercise, Diet, reduce Na and alcohol intake. Failure to implement could limit effect of mediciation

2nd: ACE inhibitors, Ang II receptor antagonist (diuretic and vasodilator effects due to blocking release of aldosterone), vasodilators, diuretics, beta blockers

27
Q

What are some examples of vasodilators?

A

- L-type Ca Channel blockers (Nifedipine)

- a1 blockers (Doxazosin) to reduce sympathetic tone but cause postural hypotension

28
Q

Why is spironolactone not the first line of therapy for hypertension and when is it normally used?

A
  • Diuretic so decreases blood volume
  • Bad side effects of developing breast tissue in men due to sex hormones being affected
  • Used in hyperaldosteronism
29
Q

How do beta blockers help to relieve hypertension?

A
  • Blocking b1 receptors in the heart will reduce effects of sympathetic output (hr and contractility)
  • Would only be used if other indications
30
Q

What are some issues that can arise from hypertension?

A

CVS (19 decks)

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