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CVS > Session 5: Control of Blood Pressure - The Patient with Hypertension > Flashcards

Session 5: Control of Blood Pressure - The Patient with Hypertension Flashcards

1
Q

Define hypertension.

A

A sustained increase in blood pressure. Blood pressure is measured mmHg.

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2
Q

What is a normal range of blood pressure?

A

90/60 to 120/80 mmHg.

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3
Q

What is stage 1 hypertension?

A

140/90 mmHg

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4
Q

What is stage 2 hypertension?

A

160/100 mmHg

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5
Q

What is severe hypertension?

A

>180 systolic >110 diastolic

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6
Q

What is primary hypertension?

A

It is also called essential hypertension. 95% of cases are primary hypertension and the cause is unknown.

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7
Q

What is hypertension where the cause is known called? Give examples.

A

Secondary hypertension. E.g. Renovascular disease Chronic renal disease Hyperaldosteronism Cushing’s syndrome

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8
Q

Explain how hypertension can have impact on organs and tissues.

A

Hypertension leading to an increase in afterload which can lead to left ventricular hypertrophy and subsequent heart failure. Or an increase in afterload can lead to an increase in myocardial oxygen demand and therefore myocardial ischaemia and myocardial infarction. Hypertension can also lead to arterial damage -> atherosclerosis and weakened vessels. Atherosclerosis and weakened vessels can lead to: Cerebrovascular disease stroke Aneurysm Nephrosclerosis and renal failure Retinopathy

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9
Q

Give examples of target organ damage and where to do physical examination.

A

Brain, eyes, heart (ECG), kidneys (listen, feel and test urine), arteries by palpating all peripheral arteries and checking for abdominal aneurysm.

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10
Q

How is mean arterial blood pressure calculated?

A

MAP = CO x TPR but also by: MAP = 1/3 SBP + 2/3 DBP

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11
Q

How is cardiac output calculated?

A

CO = SV x HR

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12
Q

How is the blood pressure regulated short term?

A

By baroreceptors found in the carotid sinus and aortic arch. They respond to the stretching of said vessels resulting in sensory nerves sending signals to the medulla oblongata to cause vasodilation and and bradycardia in order to counteract the increased mean arterial pressure.

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13
Q

Why is baroreceptors only effective in short term regulation?

A

Because they will adapt and reset to a higher level if the high blood pressure is sustained.

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14
Q

Give examples of medium and longer term control of blood pressure.

A

Interaction of neurohumoral responses that are directed at controlling the sodium balance and therefore also the extracellular fluid volume. The control of the extracellular fluid volume controls the plasma volume. This means that when sodium increases in blood stream the plasma volume will increase as water follows.

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15
Q

Give the names of the four parallel neurohumoral pathways that control circulating plasma volume and therefore also BP.

A
  1. Renin-angiotensin-aldosterone system 2. Sympathetic nervous system 3. Antidiuretic hormone (ADH) 4. Atrial natriuretic peptide (ANP) The first three raise blood pressure if they are stimulated. The last one decreases blood pressure if stimulated.
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16
Q

Where is renin released from?

A

From granular cells of the juxtaglomerular apparatus also known as JGA. Renin is released from the granular cells of the afferent arteriole in response to reduced perfusion pressure.

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17
Q

Give three factors that stimulate renin release.

A

Reduced NaCl delivery to the distal tubule Reduced perfusion pressure in the kidney that is detected by baroreceptors in afferent arteriole Sympathetic stimulation to JGA

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18
Q

What is the role of renin?

A

Renin is an enzyme that converts angiotensinogen to angiotensin 1.

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19
Q

Explain the angiotensinogen pathway.

A

Angiotensinogen -> angiotensin 1 by renin -> angiotensin 2 by ACE (angiotensin converting enzyme) Angiotensin 2 is the effective hormone that causes vasoconstriction etc.

20
Q

What are the roles of angiotensin 2 and what receptors does it act on?

A

Angiotensin 2 acts on two types of Ang 2 receptors called AT1 and AT2 which both are GPCRs. They main action however is via the AT1 receptor.

21
Q

Give sites where AT receptors can be found and what the actions of stimulation are.

A

Arterioles - Vasoconstriction Kidneys - Stimulates Na+ reabsorption at the kidney. Sympathetic NS - Increased release of NA Adrenal cortex - Stimulates release of aldosterone Hypothalamus - Increases thirst sensation (ADH release)

22
Q

What are the actions of aldosterone?

A

Acts on principal cells of collecting ducts Stimulates Na+ and hence water reabsorption Activates apical Na+ channels like ENaC and apical K+ channels Also increases basolateral Na+ extrusion via Na/K - ATPase All of this increases blood pressure.

23
Q

Angiotensin converting enzyme also called ACE has another name and another function than converting angiotensin 1 to angiotensin 2. What is that role?

A

It is also called kininase 2 and breaks down bradykinin into peptide fragments. Bradykinin is a vasodilator so ACE therefore further increases vasoconstriction by breaking down bradykinin.

24
Q

How can you counteract the function of angiotensin 2 and the breakdown of bradykinin to decrease blood pressure?

A

By ACE inhibitors which will inhibit the formation of angiotensin 2 and will also inhibit the breakdown of bradykinin.

25
Q

How does the sympathetic nervous system regulate blood pressure?

A

High levels of sympathetic stimulation reduce renal blood flow. This causes vasoconstriction of the arterioles and a decrease in glomerular filtration rate which will subsequently decrease Na+ excretion. It activates apical Na/H+ exchanger and basolateral Na/K - ATPase in proximal convoluting tubule. It also stimulates renin release from JGA which will then lead to an increase in Ang 2 and aldosterone levels causing Na+ reabsorption.

26
Q

How does ADH regulate blood pressure?

A

Formation of concentrated urine by retain water to control plasma osmolality. Stimulates Na+ reabsorption by acting on thick ascending limb and stimulating apical Na+/K+/Cl- co-transporter Also causes vasoconstriction

27
Q

What is ADH release stimulated by?

A

Increase in plasma osmolarity and severe hypovolaemia.

28
Q

How does natriuretic peptides regulate blood pressure?

A

Promotes Na+ excretion. Causes vasodilation of afferent arterioles. Increased blood flow increases glomerular filtration rate. It also inhibits Na+ reabsorption.

29
Q

What regulates natriuretic peptide release? How is it released?

A

It is synthesised and stored in atrial myocytes and released from atrial cells in response to stretch as low pressure volume sensors in the atria sense it.

30
Q

What happens to ANP when circulating volume is low?

A

ANP release is inhibited to increase BP.

31
Q

What is the role of prostaglandin in BP control?

A

Acts as a vasodilator and important when levels of Ang 2 are high. Means it lowers blood pressure.

32
Q

What is the role of dopamine in BP control?

A

Fomed locally in kidneys from circulating L-DOPA. Causes vasodilation and increases renal blood flow. Reduces reabsorption of NaCl. Means it lowers blood pressure.

33
Q

Explain the complication and treatments of renal artery stenosis.

A

Renal artery stenosis causes a fall in perfusion pressure in the affected kidney. This means that the body thinks that the BP is too high and not getting there although that is not the problem. In response renin production is increased and eventually forms Ang 2 which causes vasoconstriction and Na+ retention of the other kidney. It will therefore increase blood pressure even though that wasn’t a problem to begin with. It is treated by surgery - fixing the renal artery stenosis.

34
Q

Explain renal parenchymal disease.

A

Can be due to a loss of vasodilator substances. In later stage Na+ and water retention is due to inadequate glomerular filtration. This means that it is a volume-dependent hypertension.

35
Q

Give adrenal causes of secondary hypertension.

A

Conn’s syndrome Cushing’s syndrome Tumour of the adrenal medulla.

36
Q

Explain Conn’s syndrome.

A

It’s an aldosterone secreting adenoma that causes hypertension and hypokalaemia.

37
Q

Explain Cushing’s syndrome.

A

Excess secretion of glucocorticoid cortisol. At high concentration it acts on the aldosterone receptors causing Na+ and water retention.

38
Q

Explain tumour of the adrenal medulla (phaeochromocytoma)

A

Secretion of catecholamines which are NA and adrenaline.

39
Q

Give non-pharmacological approaches to treat hypertension.

A

Exercise Diet Reduced Na+ intake Reduced alcohol intake

40
Q

How do you treat hypertension by targeting the renin-angiotensin-adlosterone system?

A

By ACE inhibitors which prevents the production of Ang 2 from Ang 1. Also by Ang 2 (AT1/AT2) receptors antagonists. This means that blocking the production or action of Ang 2 has a diuretic and vasodilator effect.

41
Q

Give examples of pharmacological vasodilators.

A

Verapamil and Nifedipine which are L-type channel blockers that reduce entry of ca2+ into vascular smooth muscle causing dilation. Alpha 1 receptors blocker like Doxazosin which reduces sympathetic tone and vasodilation.

42
Q

Explain how to treat hypertension with diuretics.

A

Thiazide e.g. which reduces circulating volume and also BP. It inhibits Na/Cl- cotransporter on apical membrane of cells in distal tubule. There are other diuretics as well which acts as aldosterone antagonists such as spironolactone which also lowers BP.

43
Q

What is a less common treatment of hypertension?

A

Beta-blockers.

44
Q

Explain how beta-blockers are used as treatment for hypertension.

A

They are not very common and not used in hypertension alone.

They work by inhibiting b1 receptors in the heart reducing heart rate and contractility -> reduce in BP.

Would only be used if there are other indications such as previous MI.

45
Q

So to briely outline: Which are the most common antihypertensives?

A

ACE inhibitors, renin inhibitors, aldosterone antagonists, alpha-blockres, diuretics and beta-blockers.

46
Q

Label the diagram.

A

CVS (18 decks)

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