Lecture 11- Controlling Blood Pressure In Patient With Hypertension Flashcards

1
Q

What is hypertension?

A

Sustained increase in blood pressure

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2
Q

What is the normal range for blood pressure in an adult?

A

90/60mmHg to 120/80 mmHg but normal can vary

Stage 1= over 140/90

Stage 2= over 160/100

Severe= over 180 systolic or 110 diastolic

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3
Q

Primary vs secondary hypertension?

A

With primary the cause is unknown in 95% of cases

Secondary cause can be defined eg chronic renal disease, Cushing syndrome etc

Treat cause in secondary

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4
Q

Some diseases attributable to hypertension?

A
MI
Coronary heart disease
Aortic aneurysm 
Retinopathy 
Peripheral vascular disease 
Heart failure
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5
Q

How do you know if you have hypertension?

A

It is asymptomatic

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6
Q

How does high blood pressure lead to damage?

A

Increased afterload- LV hypertrophy and heart failure. O2 demand increased leading to MI and ischaemia

Arterial damage- atherosclerosis and weakened vessels leading to aneurysm, MI, retinopathy etc

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7
Q

How do you check for organ damage with hypertension?

A

Look at functioning of kidneys, brain, arteries, heart and eyes

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8
Q

What is blood pressure?

A

Flow X resistance

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9
Q

Calculating mean arterial BP?

Calculating cardiac output?

A

CO X TPR

CO= SV X HR

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10
Q

How is blood pressure regulated in the short term?

A

Baroreceptors reflex involving sympathetic and parasympathetic inputs to heart and vasculature

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11
Q

How is blood pressure regulated in the medium to long term?

A

Through neurohumoral responses and sodium balance and so extracellular fluid volume

Controlling sodium levels controls extracellular fluid volume

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12
Q

What are the four parallel neurohumoral pathways that control circulating volume and BP?

A

Renin angiotensin-aldosterone system

Sympathetic nervous system

ADH

ANP (lowers, others raise)

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13
Q

Renin angiotensin aldosterone system (RAAS)?

A

Can be targeted by ACE inhibitors which reduces sodium reabsorption and prevents the breakdown of bradykinin which acts as a vasodilator.

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14
Q

What stimulates renin release from the juxtaglomerular apparatus?

A

Reduced NaCl delivery to distal tubule

Reduced perfusion pressure in kidney

Sympathetic stimulation to JGA

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15
Q

How does the RAAS work?

A

Angiotensinogen converted to angiotensin I by renin. Angiotensin I is converted to angiotensin II by ACE (angiotensin converting enzyme).
Angiotensin II then causes vasoconstriction sodium reabsorption and stimulates aldosterone which also helps retain sodium

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16
Q

What angiotensin II receptors are there?

A

AT1 and AT2.

AT1 has main actions.
Arterioles=vasoconstriction
Kidney= sodium reabsorption 
Sympathetic= adrenaline secretion
Adrenal cortex=aldosterone release 
Hypothalamus=thirst and ADH secretion
17
Q

How does ACE (angiotensin converting enzyme) interact with bradykinin?

A

Converts angiotensin I to angiotensin II and causes bradykinin to be broken down into fragments

18
Q

Role of bradykinin in blood pressure?

A

Acts as a vasodilator

19
Q

Why are ACE inhibitors effective drugs and give an example of one?

A

They prevent angiotensin I being converted to angiotensin II and they also prevent bradykinin from being broken down which prevents those compounds from exerting their BP elevating actions.

EG Ramipril and lisinopril

20
Q

Sympathetic nervous system control of BP?

A

Vasoconstriction and reduced renal blood flow and glomerular filtration.
Increased sodium reabsorbance and stimulation of renin release from juxtaglomerular cells.

21
Q

ADH and blood pressure?

A

Increased water reabsorption
Stimulated by increased plasma osmolarity or severe hypovolaemia
Stimulates sodium reabsorption and causes vasoconstriction

22
Q

Natriuretic peptides and BP control?

A

Produced and stored by atrial myocytes. Release in response to stretch of low pressure sensors. Cause sodium excretion to reduce circulating volume. Opposite effects to others (vasodilation etc)

23
Q

Role of prostaglandins?

A

Oppose effects of RAAS and sympathetic nervous system.

Reduce sodium reabsorption and cause vasodilation etc

24
Q

Dopamine?

A

Formed in kidney from L-Dopa. Causes vasodilation, reduces NaCl absorption etc

25
Q

Secondary hypertension: renovascular disease?

A

Occlusion of renal artery decreases perfusion pressure. Juxtaglomerular apparatus tricked into thinking BP is low and so renin produced etc

26
Q

Renal parenchymal disease?

A

Early stage lose vasodilator, later stage retain sodium and water due to inadequate glomerular filtration

27
Q

Give examples of adrenal causes of secondary hypertension?

A

Cushing syndrome and a tumour of the adrenal medulla

28
Q

First approaches to treatment of hypertension?

A

Diet
Exercise
Reduce sodium intake
Reduce alcohol

29
Q

Pharmacological treatments for high BP?

A

Ace inhibitors

L-type channel blockers like verapamil to relax smooth muscle

Alpha 1 receptor blockers like doxazosin to relax smooth muscle

Thiazides diuretics to reduce circulating volume

Beta blockers usually only used if other indication like MI

30
Q

What pharmacological BP treatments for what age groups?

A

Younger= ACE inhibitors

Over 55= vasodilator and diuretics

Most people require multiple drugs to bring about desired effect