control of BP Flashcards

1
Q

what is normal range for BP and what is high

A

normal = 90/60 - 120/80 mmHg and high is anything over 140/90 mmHg (its mainly systolic pressure responsible for death in hypertension

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2
Q

causes of hypertension

A
primary hypertension = unknown cause 
secondary hypertension is usually due to disease;
renovascular 
chronic renal failure 
hyperaldosreronism 
bushings syndrome
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3
Q

which organs does hypertension affect

A

eyes, brain, heart, kidneys and arteries

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4
Q

How can hypertension cause heart failure

A

It creates a larger after load which then means the ventricles have to work harder to pump blood out leading to left ventricular hypertrophy. This eventually leads to heart failure

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5
Q

Which clinical defects can hypertension cause

A

Heart failure, coronary disease, stroke, cerebral haemorrhage, chronic kidney failure, retinopathy, peripheral vascular disease, aortic aneurysm, left ventricular hypertrophy and myocardial infarction

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6
Q

How can hypertension cause retinopathy

A

High BP causes damage to retinas blood vessels limiting retinas function and putting pressure on the optic nerve causing vision problems

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7
Q

How can hypertension cause nephrosclerosis and renal failure

A

Walls of blood vessels thicken and fat becomes deposited in the degenerated walls. Causes blood supply to kidney to be blocked= tissue necrosis and renal is ease/failure

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8
Q

How can hypertension cause an aneurysm

A

Over time weakened artery can cause a section to enlarge= aneurysm. V dangerous if ruptures. Is. Bubble in blood vessels

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9
Q

How can hypertension cause cerebral a scalar disease/ stroke

A

Atherosclerosis blocks blood supply to brain = stroke

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10
Q

How can hypertension cause myocardial infarction

A

More o2 needed and fatty streak in aorta lead to loss of elasticity and reduced function of Herat

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11
Q

Physiological effects of hypertension

A

Greater after load on Herat and arterial damage. Greater after load leads to left ventricular hypertrophy and increased myocardial oxygen demand. Arterial damage leads to weakened vessels and atherosclerosis.

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12
Q

Short term regulation of blood pressure and why this mechanism is not long term

A

Use of baroreceptors. - baroreceptor reflex. Affects para/sympathetic input into heart and alters cardiac output and adjusts sympathetic output to peripheral resistance to alter TPR. This is a rapid response BUT does not control sustained high BP because threshold for baroreceptor just resets and higher BP.

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13
Q

Equation for mean arterial BP and equation needed to find cardiac output

A

Mean arterial pressure= CO x TPR

To find CO for this; CO = SV (circulating volume) x HR

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14
Q

What are the long term ways of regulating BP

A

Neurohumoral response composes of 4 pathways. Mainly uses mechanism to control Na+ balance because water flows in or out o plasma following it

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15
Q

What are the 4 pathways involved in the neurohumoral response to high BP

A
  1. Renin-angiotensin-aldosterone system
  2. Sympathetic nervous system
  3. Antidiuretic hormone (ADH)
  4. Atrial natriuretic peptide (ANP)
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16
Q

explain the factors releasing renin activating the renin-angiotensin-aldosterone system

A

Renin is released from granular cells of the juxtaglomelular apparatuses (in kidney).
Factors releasing renin;
Reduced NaCl delivery to distal tubule
Reduced blood flow pressure in the kidney (baroreceptors in afferent arteriole)
Sympathetic stimulation to JGA to increase renin release.

17
Q

How does renin release increase BP

A

Renin used to convert angiotensinogen to angiotesin 1 and then ACE (enzyme) will convert this to nighters in 2. This will then cause vasoconstriction, stimulates Na+ reabsoprtion in the kidney and stimulates aldosterone release when angiotensin 2 binds to Ang 2 or ang1 receptors.

18
Q

Explain the actions of aldosterone

A

Stimulates water reabsorption by activating Na+ channels and K+ channels (bit of leakage) as well as some ATP driven sodium/potassium channels.

19
Q

How can bradykinin be used to increase BP

A

Bradyknin is a vasodilator and if its broken down by ACE vasodilation will stop augmenting action of vasoconstriction. However, breaks down into peptide fragments which give you a cough.

20
Q

Why are ACEihibitors and what is the problem with this

A

They block the actions of ACE preventing Randy kin in from being broken down increasing vasodilation. However, build up of bradykinin can give you a cough. Examples of ACE inhibitors are captopril, lisinopril, perindopril ect.

21
Q

How does the sympathetic nervous system cause blood pressure increase

A

Acts on arterioles to reduce blood flow (vasoconstriction), stimulates granule cells of afferent arteriole to release renin, stimulates Na+ reasorption and decreases its excretion

22
Q

How does ADH increase BP (also known as vasopressin)

A

Increases water resorption in distal nephron and increases Na+ resorption in the ascending limb. Also stimulates vasoconstriction

23
Q

How natriuretic peptides (also known as ANP) lowerBP

A

Promote Na+ excretion and released by arterial cells in response to stretch. More stretch= more heart filling = more ANP released (because more heart filling will increase BP)
It also inhibits Na+ resorption and causes vasodilation

24
Q

Rule of prosteoglandins and dopamine

A

They are vasodilators. Prosteoglandins also buffer if SNS and RAAs too high causing excessive vasoconstriction.
Dopamine also reduces NaCl resorption

25
Q

How renovascular disease causes secondary hypertension

A

Occlusion of renal artery= fall in perfusion pressure in kidney = more renin produced = vasoconstriction and Na+ retention

26
Q

How renal parenchymal disease leads to hypertension

A

Inadequate glomelualr filtration = Na+ and water retention = volume dependent hypertension. ***

27
Q

Adrenal causes of hypertension - conns syndrome and Cushing syndrome

A

Cons syndrome - aldosterone secreting adenoma results in hypertension and hyperkalaemia
Cushing’s syndrome - glucococorticoid cortisol excess acting on aldosterone receptors= Na+ and H2O retention

28
Q

How should you treat hypertension if to secondary

A

For all these you must treat the underlying disease cause

29
Q

Non pharmological treatments of primary hypertension

A

Exercise, diet, reduced Na+ intake, reduced alcohol intake - these may not reduce BP by that much but if not carried out may limit effectiveness of antihypertensive therapy

30
Q

List all the different types of treatment or hypertension and a bit about how they work

A

Beta blockers - reduce heart rate and contraction try (used less these days)

Renin inhibitors - inhibit renin from increasing BP

ACE inhibitors (used less give cough)

Aldosterone antagonists - prevent aldosterone from increasing BP

Antagonists of angiotensin 2

Vasodilators- L type Ca2+ channel blockers for example reduce contraction of vessel walls and alpha blockers reduce sympathetic tone BUT also cause postural hypotension (dizzy when stand up becasue blood pools in venous system.

Diuretics- reduce circulating volume