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Controlling blood pressure Flashcards

1
Q

What is the definition of hypertension?

what is stage 1 hypertension?

What is stage 2?

what is sever hypertension?

what is a hypertensive emergency?

A
  • A sustained Increase in blood presssure
  • more than 140/90 - at home = 135/85
  • 160/100 - at home = 150/95
  • 180+/110+
  • A rapid change in blood pressure associated with body damage
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2
Q

What is primary hypertension?

what is s3condary hypertension

what is more common?

A
  • Primary hypertension is when the cause is unknown
  • secondary is when the cause is know
  • primary (95% of the hypertension cases)
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3
Q

Why is it important to treat hypertension?

A

It is a silent killer - often have no symptoms

it can result in a massive vasulcular attack and have damaging effects on vasulature e.g stroke, MI, renal failure

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4
Q

Describe the why hypertension can cause vascular disease.

A
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5
Q

What controls medium and longer term hypertension?

A

Sodium - water follows Na+ therefore it controls extracellular and plasma volume therefore blood pressure

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6
Q

What are the 4 neurohumoral processes that control BP

A
  1. Renin-angiotensin-aldosterone system (RAAS)
  2. Sympathetic nervous system
  3. Antidiuretic hormone (ADH)
  4. Atrial natriuretic peptide (ANP)
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7
Q

Where is renein released from?

What triggers the system

Describe how the renin-angiotensin-aldosterone system (RAAS) works to increase blood pressure

what does angiotensin II do ?

what does acivateion of AT1 receptors do?

A
  • Renin is released from granular cells from the juxtaglomerular apparatus (JGA) - afferent artery to kidney
  • reduced NaCl delivery to distal tube triggers renin, reduced perfusion to kidney (from baroreceptors), increase sympathetic activity on JGA
  • angiotensinogen is converted to angiotensin I by renin - angiotensin I is converted to angiotensin II by ACE (angiotensin converting enzyme)
  • angiotensin II causes vasoconstriction, the increase absorption of Na+ and aldosterone release from adrenal cortex
  • AT1 and AT2 are the receptors for angiotensin II - binding tiggers the above points and increases sympathetic release of NA and thirst !!
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8
Q

What is the action of aldosterone ?

A

Acts in the collecting duct of the kidney

it increases Na+ uptake from ENaC and K+ channel, increases Na+ gradient into the cells by increasing Na/K ATPase

therefore increases water uptake

therefore increases blood volume

therefore increases blood pressure

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9
Q

What is the action of Bradykinin ?

what does the RAAS cause with relation to Bradykinin?

A
  • Bradyinin is a vasodilator
  • ACE is activated in he RAAS. ACE also breaks down brakykinin into peptide fragments therefore losing the vasodilator effect = more vaso constriction
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10
Q

What class of drugs did the Brazilian viper help to discover?

how?

A
  • ACE inhibitors
  • The venom from the snake induced shock (drop in blood pressure) - this was because the drug was found to inhibit AGTI to AGTII therefore is inhabiting ACE

this stopped the effects of AGTII and allowed badykinin to cause vasodilation = low BP

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11
Q

How do ACE inhibitors work ?

A

They prevent angiotensin I converting to angiotensin II

this means AGTII cant bind to AT1 and produce its hypertensive effects

also ACE is used to break down bradykinin - now cannot so bradykinin effect is potentiated and continues to drop BP via vasodilation

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12
Q

How does activation of the sympathetic nervous system raise blood pressure?

A

High levels of sympathetic activation reduced blood flow to kidneys via vasoconstriction of arterioles- this reduces the amount of Na+ excreted

sympathetic also acts on transporters in PCT to absorb more Na+ via NHE and Na/K ATPase

also induces renin release from JGV and the RAAS

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13
Q

How does ADH increase blood pressure?

when is ADH released?

A
  • It increases water absorption in he kidney via aquaporin 2, also stimulates Na+ absorption via the NKCC2 in thick ascending limb
  • Increase in plasma osmolality (conc) and hypovolaemia (low circulating blood volume) - low BP
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14
Q

How does Natriuretic peptides (ANP) reduce BP?

where is it made/released?

How does ANP work?

A
  • More ANP(atrial natriuretic peptide) increases Na+ excretion - lower BP
  • Made and released from atrial myoctes - low pressure volume sensors in the atria sens the BP
  • reduced circulating volume of blood = reduced filling and less stretch = sensors not activated = no ANP released - not lower BP anymore
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15
Q

What do prostaglandins do in relation to BP?

what does dopamine do?

A
  • Causes vasodilation and inhibits Na+ Absorption, they usually work loacally and can prevent damage to damage tissue by restoring blood flow, act as a buffer against excessive vasoconstriction from SNS and RAAS
  • Dopamine is formed locally in the kidney from circulating L-DOPA

DA receptors are present on renal blood vessels and cells of PCT &TAL
DA causes vasodilation and increases renal blood flow, it also reduced Na+ absorption in PCT and TAL by NHE

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16
Q

How do you treat secondary hypertension?

A
17
Q

Describe secondary hypertension: Renovascular disease

A

renal artery stenosis causes a fall in perfusion pressure in that kidney

Decreased perfusion pressure leads to increased renin production

Activation of the RAAS

Vasoconstriction and Na+ retention at other kidney and aldosterone = hypertension

18
Q

Decribe secondary hypertension: Renal parenchymal disease

A

Earlier stage may be a loss of vasodilator substances

In later stage Na+ and water retention due to inadequate glomerular
filtration =high blood volume = high BP

19
Q
  • Descibe secondary hypertension: adrenal causes

Conns syndrome

Cushings syndrome

Tumor of adrenal medulla

A
  • Conn’s = excessive aldosterone production
  • Cushing’s = excessive cortisol production - acts like aldosterone at high conc
  • Tumor of adrenal medulla = phaeochromocytoma
20
Q

Non pharmacological ways to treat hypertension

A
  • Exercise
  • Diet
  • Reduced Na+ intake - salt
  • Reduced alcohol intake

Lifestyle changes above can have limited effect

Failure to implement lifestyle changes
could limit the effectiveness of
antihypertensive therapy

21
Q

Drugs to treat hypertension - specifically RAAS

A

ACEi

and Ang II antagonists

22
Q

Treating hypertension with drugs : vasodilators

wht is the issue?

A

L type Ca2+ blockers in BV

reduces vasocontriction e.g. verapamil

also a1 receptor antagonists e.g. doxazosin to reduce sympathetic vascular tone - can cause postural hypotension

23
Q

Treating hypertension : diuretics

A

Thiazide diuretics
– reduce circulating volume

Inhibit Na/Cl co-transporter (NCCT) on apical membrane of cells in
distal tubule

Other diuretics eg aldosterone antagonists (spironolactone)
will also lower BP– not first line choice

24
Q

Treating hypertension : beta blockers

A

Less common

they act and block B1 receptors in the heart to reduce HR and contractility cause by sympathetic innervation

reduce CO therefore BP

not used along to treat hypertension - used if previous MI

25
Q
A
26
Q

Diagram of anti hypertensive drugs just to help visualise

A

cvs (19 decks)

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