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Sem 2 - The Cardiovascular System > Control Of Blood Pressure > Flashcards

Control Of Blood Pressure Flashcards

1
Q

What is the standard hypertensive patient?

A

There is no standard hypertensive patient.

Can be anyone (although does increase with age..).

It is know as “the silent killer” because it has no symptoms.

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2
Q

What is hypertension?

A

This is a sustained increase in blood pressure.

BP is measured in mmHg

The normal or ideal adult BP is considered to be between 90/60 - 120/80

Stage 1 hypertension - >140/90 mmHg (avg > 135/85)

Stage 2 hypertension - >160/100mmHg (avg > 150/95)

Severe hypertension - > 180 systolic or 110 diastolic.

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3
Q

What are the causes of hypertension?

A

In around 95% of cases, the cause is unknown.

This is called ‘essential’ it primary hypertension. This will be due to a variety of factors.

Secondary hypertension is when the cause can be identified. e.g.

  • Renovascular discease
  • Chronic renal disease
  • Hyperaldosteronism
  • Cushing’s syndrome

With secondary hypertension it is important to identity it and treat the underlying cause.

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4
Q

Why is it important to treat hypertension?

A

Hypertension - the silent killer.

Although hypertension may be asymptomatic, it can have unseen damaging effects on the heart and vasclature.

It can potentially lead to heart failure, MI, Stroke, Renal failure and retinopathy.

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5
Q

What diseases are attributable to hypertension?

A
  • Coronary heart disease
  • Heart failure
  • Stroke
  • Cerebral haemorrhage
  • Chronic kidney failure
  • Hypertensive encephalopathy
  • Retinopathy
  • Peripheral vascular disease
  • Aortic anuerism
  • Left ventriuclar hypertrophy
  • MI
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6
Q

What organs are targeted in high blood pressure?

A
  • Brain
  • Heart
  • Eyes
  • Kidneys - do a urine dip to identify changes.
  • Arteries

These organs should be assessed by clinical history and physical examination.

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7
Q

What are the effects of intervention of high blood pressure?

A

For every 10mmHg reduction on blood pressure, it results in:

  • 17% reduction in coronary heart disease
  • 27% reduction for stroke
  • 28% reduction for heart failure
  • 13% reduction in all causes of mortality.
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8
Q

How is blood pressure regulated?

A

pressure = flow x resistance

Mean arterial BP = CO x TPR

CO = ST x HR

Both short term and long term resistance.

E.g. in emergency department - Tachycardic and vasoconstriction.

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9
Q

Where are baroreceptors located?

A

Carotid sinus andaortic arch.

They are very sensitive to stretch.

Increased arterial pressure stretched these receptors and with decreased pressure is stretched less.

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10
Q

Medium and longer term control of blood pressure.

A

Complex interaction of neurohumoral responses.

Directed at controlling sodium balance and thus extracellularly fluid volume.

Plasma is part of the extracellular fluid conpartment.

  • control of extracellular fluid volume control plasma volume
  • Water follows Na+ therefore controlling total body Na+ levels controls plasma volume.
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11
Q

What are the four parallel neurohumoral pathways involved in controlling circulating volume and hence BP?

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

Control of BP in part by controlling Na+ balance and extracellular fluid volume.

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12
Q

What factors stimulate renin release? From where is it relesed?

A

Renin is released from granular cells of juxtaglomerular apparatus (JGA)

  • Reduced NaCl delivery to distal tube
  • Reduced perfusion pressure in the kidney causes the release of renin. (This is detected by baroreceptors in afferent arterioles.)
  • Sympatheic simulation to JGA increases release of renin
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13
Q

Why does decreased circulating volume stimulate renin release?

A
  • Decreased NaCl delivery to the macula densa
  • Sympathetic stimulation to juxtaglomerular apparatus
  • Decreased renal perfusion pressue (sensed by baroreceptors).

Renin is then released from the granular cells of the afferent arteriole in response to reduced perfusion pressure.

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14
Q

What is the renin-angiotensin aldosterone system?

A

Renin causes angiotensinogen to convert to angiotensin I.

ACE then causes the conversion of angiotensin I to angiotensin II.

Angiotensin II then stimulates:

  • Vasoconstriction
  • Na+ reabsorbtion in the kidney
  • Aldosterone release from the adrenal cortex.
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15
Q

What effect do angiotensin II receptos have?

A

There for two types of Ang II receptors, AT1 and AT2. The main action is via the AT1 receptor. This is a G protein couples receptor.

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16
Q

What are the actions of aldosterone on the kidney?

A

AngII stimulates aldosterone release from the adrenal cortex.

Alderstorone:

  • Acts in principle cells of collecting ducts
  • Stimulates Na+ and therefore water reabsorbtion
  • Activates apical Na+ channels (ENaC = Epithelial Na Channels) and apical K+ channels)
  • Also increases basolateral Na+ extrusion via Na/K/ATPase.
17
Q

What effect does ACE have on bradykinin?

A

As well as converting Ang I to Ang II, ACE catalizes the breakdown of bradykinin to peptide fragments.

This means that, a cough can occur if ACE in inhibited because bradykinin accumulates.

Also, the vasoconstriction effects of AngII are further augmented becayse ACE is also one of the kinase enzymes that breaks down the vasodilator bradykinin.

BUT, are bypass mechanisms which are not ACE mediated so still get some angiotensin II

18
Q

Sympathetic nervous system, effects on BP?

A
  • High levels of sympathetic stimulation reduce renal blood flow.
    • -Vasoconstriction of arterioles
    • -Decrease GFR - decrease Na excretion.
  • Activates apical Na/H- exchanger and basolateral Na/K ATPase in PTC.
  • Stimulates renin release from JGcells
    • Leading to increased AngII levels.
    • Leading to increased aldosterone levels which caused increased Na+ reabsorbtion.
19
Q

Role of ADH on BP?

A
  • Main role is formation of concentrated urine by retaining water to control plasma osmolarity.
    • Increases water reabsortion in distal nephron (AQP2)
  • ADH release is stimulated by increases in plasma osmolarity or severe hypovolaemia (decreased vol of circulating blood)
  • ADH also stimulates Na+ reabsorbtion.
    • Acts in thick ascending limb
    • Stimulates apical Na/K/Cl co-transporter
  • Also called arginine vasopressin and it causes vasoconstriction.
20
Q

What are natriuretic peptides?

A

Atrial netriuretic peptide (ANP) promotes Na+ excretion.

Synthesised and stored in atrial myocytes.

Released from atrial cells in response to stretch

Low pressure volume sensors in the atria

Reduced effective circualting volume inhbits the release of ANP to support BP.

-reducing filling of the heart - less stretch - less ANP released

21
Q

What are the actions of ANP on BP?

A

Causes vasodilation of afferent arterioles

Increased blood flow increases GFR

Also inhibits Na+ reabsorbtion along the nephron

Acts in popposite direction to the other neurohumoral regulators -causes natriuresis (loss of Na into urine)

If circulating volume is low, ANP release in inhibited - This supports BP.

22
Q

What is the role of prostaglandins?

A

Act as vasodilators.

More clinically than physiologically (no oral yet)

Locally acting prostaglandins (mainly PGE2) enhance glomerular filtration and reduce Na+ reabsorbtion.

May have important protective functions

Act as a buffer to excessive vasoconstriction produced by SNS and RAA system

Important when levles of Ang II are high.

Less important

23
Q

Dopamine?

A

Dopmine is formed locally in the kidney from circulating L-DOPA

Dopamine receptors are present on renal blood vessles and cells of PCT and TAL.

Vasodilation and increase renal blood flow

It also reduces the absorbtion of NaCl -inhibits NH exchanger and Na/K ATPase in principle cells of PCT and TAL.

Less important

24
Q

Renovascular disease?

A

Occlusion of the renal artery (renal artery stenosis) causes a fall in perfusion pressure in that kidney.

Decreased perfusion pressure leads to increased renin production.

Activation of renin-angiotensin-aldosterone system.

Vasoconstriction and Na retention at other kidney,

If ACE inhibitor - renal failure.

25
Q

Renal parenchymal disease?

A

Earlier stages may be a loss of vasodilator substances

Later stage Na+ and water retention due to inadequate glomerulat filtration. -Vol dependant hypertension.

Need to get rid of Na is most important

26
Q

Adrenal causes of high BP?

A

Conn’s syndrome - aldosterone secreting adenoma -= hypertension and hypokalemia

Cushing’s syndrome - excess secretion of glucocorticoids cortisol = t high cost acts on aldosterone receptors - Na and water retension

Tymours of adrenal medulla - Phaeochomacytoma - secretes catacholamines (noradrenaline and adrenaline)

27
Q

How to treat non-pharmacologically?

A

Exercise

Diet

Reduced Na intake

Reduced alcohol intake

BUT, limited effect - max 10mmHg reduction.

BUT, if on meds - failure to undergo lifestyle changes may undo the effects of meds.

28
Q

First line treatment?

A
  1. ACE inhibitor - prevent angiotensin I to angiotensin II.
  2. Angiotensin II receptor antagonist (all antagonists)
    - This is a powerful vasoconstrictor, has direct actions not he kidney and promotes the release of aldosterone, thus leading to NaCl H2O retention.

Blocking production or action of AngII has diuretic and vasodilator effects.

29
Q

C drugs?

A

L-type Ca channel blockets (e.g. Verapamil and Nidedipine)

They reduce Ca entry to vascular smooth muscle cells and therefore cause their relaxation.

-Can also use a1 receptor blockers (add-ons) e.g. Doxazosin.

These reduce sympathetic time (relaxation of vascular smooth muscle). But, they can cause postural hypotension.

30
Q

D drug?

A

Diuretics?

Thiazides diuretics - reduce circulating volume

Inhibit NaCl co-transporter on apical membrane of cells in distal tubule

Other diuretics e.g. aldosterone antagonists (spironnolactone) will also lower BP.

-But, not a first line choice.

31
Q

Beta blockers?

A

No longer used alone in hypertension as found that they dont reduce central blood pressure.

They reduce the effects of sympathetic output. So, they reduce heart rate and contractility.

They would only be used if there are other indications such as a previous MI.

Sem 2 - The Cardiovascular System (20 decks)

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