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
Secondary hypertension: renovascular disease?
Occlusion of renal artery decreases perfusion pressure. Juxtaglomerular apparatus tricked into thinking BP is low and so renin produced etc
26
Renal parenchymal disease?
Early stage lose vasodilator, later stage retain sodium and water due to inadequate glomerular filtration
27
Give examples of adrenal causes of secondary hypertension?
Cushing syndrome and a tumour of the adrenal medulla
28
First approaches to treatment of hypertension?
Diet Exercise Reduce sodium intake Reduce alcohol
29
Pharmacological treatments for high BP?
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
What pharmacological BP treatments for what age groups?
Younger= ACE inhibitors Over 55= vasodilator and diuretics Most people require multiple drugs to bring about desired effect