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Semester 2 Cardiovascular System > L11: Control of BP > Flashcards

L11: Control of BP Flashcards

1
Q

What is hypertension?

A

Sustained high blood pressure (mmHg)

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2
Q

What is normal blood pressure considered to be?

A

Between 90/60mmHg - 120/80mmHg

  • Continuum–> no cut of score
  • Closer to the upper limit more at risk
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3
Q

What are the difference classifications of high blood pressure?

A

Stage 1 hypertension–> >140/90mmHg
Stage 2 hypertension –> >160/100mmHg
Severe hypertension–> >180 systolic or >110/120 diastolic

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4
Q

What causes hypertension?

A

Primary hypertension–> 95%
–> Cause unknown
Secondary hypertension–> 5%
–> Cause defined–> important to identify cause and treat
–> E.g. renovascular disease, chronic renal disease, hyperaldosteronism, Cushings disease

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5
Q

Why is it important to treat hypertension?

A

Silent killer
Assymptomatic but can have unseen damaging effects (heart and vasculature–> HF, Stroke, Renal failure and retinopathy)
3rd biggest risk factor for premature death
affects >1/4 people

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6
Q

What disease are caused by hypertension?

A 
HF
Stroke
Coronary Heart Disease
MI
Left Ventricular Hypertrophy
Aortic Aneurysm
Peripheral vascular disease
Retinopathy
Hypertensive encephalopathy
Chronic kidney failure
Cerebral Haemorrhage
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7
Q

How does it lead to these diseases?

A

Hypertension–> ↑ afterload–> LVH (–> HF) and ↑Myocardial oxygen demand (–>Myocardial ischemia and MI)
Hypertension–> arterial damage–> arthersclerosis and weakened vessels–> cerebrovascular disease, stroke, aneurysm, nephrosclerosis and renal failure and retinopathy

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8
Q

What areas of the body are usually the target for hypertensive disease?

A 
Brain (ischemia, haemorrhage), 
Heart (left ventricular hypertrophy), 
Arteries (atherosclerotic plaques), 
Eyes
Kidneys
--> should be checked-->  clinical history and physical examination
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9
Q

How effective are the interventions?

A

For every 10mmHg reduction in blood pressure

  • -> 17%↓ CHD
  • -> 27%↓ stroke
  • -> 28%↓ HF
  • -> 13%↓ in all case mortality
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10
Q

What is blood pressure?

A 
Pressure= Flow X Resistance
BP= CO X TPR
(CO= SV x HR)
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11
Q

How is blood pressure regulated?

A

Short and long term regulation –> baroreceptor reflex

–> adjust para- and sympathetic output to heart to alter CO and peripheral vessel to alter TPR

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12
Q

What is the baroreceptor reflex?

A

Reflex that controls acute changes in BP
BP↑–> baroreceptors detect stretch–> medulla–> efferent vessels ↓BP via vasodilation, decreased HR and CO
Opposite for BP↓

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13
Q

Where are the baroreceptors located?

A

Aortic Arch

Carotid sinus

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14
Q

What is the problem with sustained high blood pressure and the baroreceptor reflex?

A

Baroreceptor reflex resets

Elevated blood pressure no longer causes stretch and AP firing

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15
Q

How is the blood pressure controlled in the medium and long term?

A

Neurohumoral Response
Control sodium balance and thus extracellular fluid volume
–> plasma part of ECF volume
–> control Na+ control H2O and ECF volume so plasma volume (BP)

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16
Q

What are the 4 neurohumoeral pathways controlling circulation and hence volume?

A

1) Renin-Angiotensin-Aldosterone system
2) Sympathetic nervous system
3) Antidiuretic Hormone
4) Atrial Natriuretic Peptide

17
Q

How does the renin-angiotensin-aldosterone system work?

A

LOW BP
Renin released from glands of Juxaglomerular appartus
Converts angiotensinogen –> angiotensin 1
Angiotensin 1–> angiotensin 2 by ACE
Angiotensin 2–> vasoconstriction, stimulates Na+ reabsorption from kidneys, stimulates aldosterone (adrenal cortex)–> Na+ reasborption from kidneys

18
Q

What causes renin to be released?

A

Reduced NaCl delivery to renal tubules- macula densa detect
Reduced perfusion pressure across kidneys–> baroreceptors detect
Sympathetic stimulation to JGA
Released from granular cells/JGA cells–> afferent arterioles–> in response to reduced perfusion pressure

19
Q

What are the angiotensin 2 receptors? Where does angiotensin act and what does it do?

A

Two types AT1 and AT2
Main action via AT1
GPCR –> increase BP
Aterioles–> vasoconstriction
Kidney–> Stimulates Na+ reabsorption
Sympathetic NS–> Increased release of NA
Adrenal Cortex–> Stimulates release of aldosterone
Hypothalamus–> Increased thirst sensation (stimulate ADH release)

20
Q

How does aldosterone work?

A

AngII–> Aldosterone release from adrenal cortex
Actions:
- Principle cells of collecting duct
- Stimulate Na+ reabsoprtion–> H2O follows
- Activates apical Na+ channel (epithelial Na Channel (ENaC)) and apical K+ channels
- ↑ basolateral Na+ extrusion via Na/K ATPase

21
Q

How does ACE impact on bradykinin? What is significant about this?

A

Bradykinin broken down into peptide fragments by ACE

Bradykinin–> Vasodilator further increase vasoconstriction

22
Q

How do ACE inhibitors work? What are they used for?What is the significance of these with Bradykinin?

A

ACE inhibitors prevent the conversion of angiotensin 1- angiotensin 2 therefore reducing vasoconstriction–> reducing high blood pressure
Method for treating hypertension
Also inhibits conversion of bradykinin–> peptide fragment –> bradykinin builds up–> vasodilator so vasodilation of BV

23
Q

How does the sympathetic system work to increase blood pressure?

A

Sympathetic stimulation–>reduced renal blood flow

  • -> Vasoconstriction of arterioles
  • -> Decrease GFR–> less Na+ excreted so less H2O excreted

Activated apical Na/H exchanger and basolateral Na/K ATPase in PCT (increase Na+ reabsorption)

Stimulate renin release from JGA cells–> increase angiotensin 2 levels via pathway–> increased aldosterone levels–> Increased Na+ reabsoprtion

24
Q

How does antidiuretic hormone (ADH) increase blood pressure? What stimulates its release?

A

Formation of concentrated urine
Reabsorption of water in distal nephron (AQP2)
Stimulates Na+ reabsorption (thick ascending limb)–> stimuates apical Na/K/Cl co-transporter
Vasoconstriction (alternative name arginine vasopressin)

ADH release stimulated–> increase in plasma osmolarity or severe hypovolaemia (decreased volume)

25
Q

How do natriuretic peptides decrease blood pressure? What causes it to be released?

A

ANP –> excretion of Na+ –> water follows

Stored in atrial myocytes–> released upon stretch–> low pressure volume sensors in the atria

26
Q

How do natriuretic peptides increase blood pressure?

A

ANP released in response to stretch

Reduced circulating volume–> inhibits release for ANP–> supports increase in volume

27
Q

What are the actions of ANP?

A

1- Vasodilation of afferent arterioles
2- Increased blood flow increase GFR
3- Inhibits Na+ reabsorption along nephron
4- Causes natriuresis (loss of Na+ in urine)
If BP low ANP release inhibited

28
Q

What do prostaglandins do?

A

Vasodilators –> reduced BP
Important clinically rather than physiologically
Enhance glomerular filtration rate and reduce Na+
Protective function
Act as buffer–> excessive vasoconstriction produced by SNS and RAA system –> important when AngII↑

29
Q

What does dopamine do?

A

Formed from L-DOPA
Locally–> kidney produced acts on renal blood vessels and cells of PCT and TAL
Vasodilaion and ↑ renal blood flow
Reduced NaCl reabsorption (Inhibits Na/H+ exchanger and Na/K ATPase)

30
Q

How can secondary hypertension be treated?

A

Depends on cause

31
Q

How is renovascular disease treated?

A

Occlusion of Renal artery–> stenosis
Fall in kidney perfusion pressure (JGA detects)
Leads to ↑ renin production –> angiotensin aldosterone system –> vasoconstriction and Na+ reabsorption–> ↑BP–> hypertension
therefore remove occlusion–> surgery, drugs to dissolve, stent etc…

32
Q

What happens during renal parenchymal disease?

A

Caused initally by loss of vasodilator substances
Later stage–> Na+ and water retention–> inadequate glomerular filtration
Large Na+ loss –> body thinks its too much so reabsorbs it–> H2O follows

33
Q

What are the adrenal causes of hypertension?

A

Conn’s Syndrome–> aldosterone secreting adenoma
Cushing’s syndrome–> Excess secretion of glucocoticoid cortisol–> high conc acts on aldosterone receptors–> Na+ and water retention
tumour–> Phaeochromocytoma–> secrete catecholamine–> NA and A–> over production leads to vasocontriction α1 receptors

34
Q

What are the non pharmacological approaches to treating hypertension?

A

Exercise
Dietary advice
Lifestyle changes
Reduced NaCl intake

35
Q

How does an ACE inhibitor reduce BP?

A

Prevent angiotensin 1 conversion to Angiotensin 2
AngII powerful vasoconstrictor–> inhibited no vasoconstriction
AngII also controls release of aldosterone–> Na+ reabsorption–> inhibited no aldosterone release therefore no Na+ reabsorption and reduced H2O uptake

Also used for bradykinin to peptide fragments conversion
Inhibited –> bradykinin builds up–> vasodilator

36
Q

What other vasodilators can be used?

A

L-type Ca2+ channel blockers–> Verapamil and Nifedipine –> Reduce Ca2+ entry to SM cells–> relaxation of vascular SM

α1 receptor blockers–> Doxazosin
–> reduced sympathetic tone–> relaxation of vascular smooth muscle (Adrenaline at high levels= vasoconstriction)
Causes postural hypotension

37
Q

How do diuretics work?

A

Thiazide
Inhibit Na/Cl transporter–> Na+ released –> H2O follows
Aldosterone antagonists–> spironolactone–> inhibit angiotensin effect (not first choice)

38
Q

How do beta blockers work?

A

Block β1 receptors in heart–> reduce HR and contractility (sympathetic effects)
NOT used in hypertension alone
Only used if there are other indications such as MI

Semester 2 Cardiovascular System (21 decks)

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