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ESA2 > CVS - Control of BP - Hypertension > Flashcards

CVS - Control of BP - Hypertension Flashcards

1
Q

What two methods can you use to determine MABP?

A

1/3 pulse pressure + diastolic pressure

CO x TPR

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2
Q

How does the baroreceptor reflex alter CO and TPR?

A

CO - via sympathetic/parasympathetic

TPR - via sympathetic tone to vessels to alter resistance

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3
Q

What are the 4 neurohumoral pathways that control BP longterm? How do they do this?

A

Sympathetic NS
RAAS
ADH
ANP

By increasing circulating plasma volume

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4
Q

Where is renin released from? Which 3 factors stimulate it’s release?

A

Released from granular cells of juxtaglomerular apparatus

In response to:

1) Reduce perfusion pressure in kidney afferent arteriole
2) Reduced NaCl delivery to distal tubule
3) Sympathetic stimulation of JGA

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5
Q

How does angioteninogen get to angiotensin I and ang I to ang II?

A

Angioteninogen is cleaved to ang I by renin

Ang I converted to Ang II by ACE

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6
Q

Name 4 effects of Ang II to increase BP?

A

1) Sympathetic stimulation
2) Increases ADH release
3) Stimulates aldosterone from the adrenals (Na+ reabsorption)
4) Vasoconstriction

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7
Q

Which types of Ang II receptors are there? Which is the main one? What type of receptor are they? Where would you find Ang II receptors in the body (5)?

A

AT1 (main actions)
AT2

GPCR

Hypothalamus - ADH
Kidney - increases Na+ reabsorption 
Sympa NS - NA release
Adrenal cortex - Aldosterone release
Arterioles - Vasoconstriction
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8
Q

What type of hormone is aldosterone? What is is made from?

A

Steroid hormone made from cholesterol

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9
Q

What stimulates the release of aldosterone and from where?

A

Plasma Ang II stimulates release of aldosterone from adrenal cortex - acts on Na+ reabsorption.
Increased plasma ACTH
Increased K+ also stimulates aldosterone

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10
Q

What are 4 roles of aldosterone? What cells and location do they act on?

A

Act on principal cells of distal convoluted tubule and collecting duct

  • Upregulate NaKATPase activity in basolateral membrane (K+ out of blood
  • Increase ENacs - therefore increase H20 reabsorption
  • Acts on apical K+ channels - K+ extrusion into urine
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11
Q

Which 2 ways does ACE increase BP?

A

Converts Ang I to Ang II - vasoconstrictor

Also is a kininase that breaks down the vasodilator bradykinin

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12
Q

How do ACE inhibitors work? What is a side effect and why? Name one ACEi

A

Block conversion of Ang I to Ang II, and block breakdown of bradykinin - side effect dry cough due to increased bradykinin. Ramipril

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13
Q

How does the SNS control blood pressure via the kidneys (4)?

A

Vasoconstriction of afferent arterioles - reduced GFR so reduced Na excretion

Activates Na/H+ exchanger in apical membrane of proximal tubule and NaKATPase in basolateral - enhances Na+ reabsorption into blood

Less renal perfusion also leads directly to reduced Na+ and less urine

Stimulates renin release from JG cells - stimulates Ang II and stimulates aldosterone levels - increased Na+ reabsorption

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14
Q

State three functions of ADH on blood pressure control. What stimulates release of ADH?

A

Main role is to stimulate translocation of aquaporins in collecting duct and distal convoluted tubule (AQP2) to enhance water reabsorption

Also has a vasoconstriction role (other name vasopressin)

Also acts to increase Na+ reabsorption by stimulating apical NaKCl co-transporter on thick ascending limb

Reduces blood osmolarity is detected by osmoreceptors in the hypothalamus that stimulate release of ADH from post pituitary. Also severe hypovolaemia can stimulate/ Ang II

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15
Q

How does ANP control BP (2)? Where is it synthesised and released?

A

Has opposite effect to others - acts to decrease BP
If circulating vol is low - ANP inhibited - so acts to support BP in this way

Synthesised and stored in atrial myocytes and released in response to stretch receptors.

Causes vasodilation in afferent arteriole
Inhibits Na reabsorption along nephron

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16
Q

What two other substances in the body have an effect on BP? How?

A

Dopamine - Vasodilation and increases renal blood flow, reduces reabsorption of NaCl

Prostaglandins - Vasodilators - locally acting PG (mostly PGE2) enhance glomerular filtration and reduce Na+ reabsorption

17
Q

When are prostaglandins important?

A

Protective function - act as a buffer against excessive vasoconstriction by SNS and RAAS - important when Ang II levels are high

18
Q

What is hypertension?

A

Sustained increase in BP e.g. over 140/90

19
Q

What is accelerated hypertension?

A

Hypertensive emergency - significant rise in BP over a small amount of time accelerates damage to blood vessels

20
Q

What is primary vs secondary hypertension?

A

Primary - 95% unknown cause - or multifactorial (genetic, environment, potentially DA receptors)

Secondary - to disease e.g. renal artery stenosis, chronic renal disease, hyperaldosteronism, Cushings disease

21
Q

How does renal artery stenosis lead to hypertension?

A

Reduced renal blood flow at that kidney stimulates renin release –> vasoconstriction and increased Na+ reabsorption at other kidney leads to increased BP

22
Q

How does renal parenchymal disease lead to hypertension?

A

Early stage might be loss of vasodilator substances

Later stage Na+ retention due to inadequate GFR - vol dependent hypertension

23
Q

What is conns syndrome?

A

Aldosterone secreting adenoma

Hypertension and Hypokalaemia (due to effects on increased K+ excretion by aldosterone)

24
Q

What is Cushings syndrome?

A

Excess cortisol

At high concentrations it acts on aldosterone receptors so increases Na+ reabsorption and water retention

(aldosterone receptors are sensitive to aldosterone and cortisol but normally have a mechanism to prevent overstimulation by cortisol)

25
Q

What is Pheochromocytoma?

A

A tumour of the adrenal medulla that secretes catecholamines - vasoconstriction - increased BP

26
Q

Why is hypertension called the silent killer?

A

Because it has no symptoms

27
Q

What secondary diseases are caused by hypertension?

A

Vasculature - e.g. stroke, MI, AAA, retinopathy

28
Q

What effect does HTN have on after load? how does this affect the heart?

A

Increases afterload

Leads to LVH - Heart failure

29
Q

What non-pharmacological ways could you treat hypertension?

A

Diet - reduced salt and alcohol

Lifestyle - exercise

30
Q

Which 4 pharmacological ways can you treat hypertension?

A

ACEi

Ca2+ channel blockers - smooth muscle relaxation in vasculature

Diuretics - K+ sparing and non sparing

Beta-blockers - not used alone - reduce HR and contractility

31
Q

How do thiazide diuretics work?

A

Block NaCl co transporter on apical membrane of cells in distal tubule - reduce Na+ reabsorption

32
Q

How does Spironolactone work?

A

Aldosterone antagonist

ESA2 (37 decks)

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