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CVS > Lecture 11 > Flashcards

Lecture 11 Flashcards

1
Q

Who can have hypertension?

A

Anyone

Steroids-gym attenders OR elevated BMI

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2
Q

Why is hypertension dangerous?

A

Because it is a silent killer- there are no symptoms

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3
Q

What is hypertension?

A

Sustained increase in BP

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4
Q

What is BP measured in?

A

MmHg

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5
Q

What is the normal BP range?

A

90/60 mmHg - 120/80 mmHg

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6
Q

What are the different classifications of hypertension?

A

High normal is near the stage 1 cut off
Stage 1: >/= 140/90 mmHg (135/85 mmHg for in ambulance/at home as it is lower here than in the GP)
Stage 2: >/=160/100 mmHg n
Severe hypertension: >/= 180/110 mmHg

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7
Q

What is hypertensive urgency/emergency?

A

Any rapid change in BP associated with damage to body

Rather than sustained increased in BP

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8
Q

What is primary/essential hypertension?

A

When the cause of the high BP is unknown

95% of cases

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9
Q

What is secondary hypertension?

A

Cause of BP is found (important to identify & treat underlying cause)
E.g. renovascular disease, chronic renal disease, hyperaldosteronism, Cushing’s syndrome

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10
Q

What effects does hypertension have?

A

-damage to heart and vasculature
(Potentially leading to heart failure, MI, stroke, renal failure, retinopathy)

-that is why it is essential that we primary prevent, rather than secondary prevent (after a health issue has occured)

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11
Q

Which major diseases do people with high BP tend to experience?

A

All vascular diseases

  • stroke
  • heart failure
  • cerebral haemorrhage
  • chronic kidney failure
  • MI
  • coronary heart disease
  • retinopathy
  • aortic aneurism
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12
Q

How does hypertension cause heart failure?

A

Increased afterload

-left ventricular hypertrophy

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13
Q

How does hypertension lead to MI/myocardial ischaemia?

A
  • increased afterload
  • increased myocardial oxygen demand due to increased workload
  • arterial damage
  • atherosclerosis
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14
Q

How does hypertension cause aneurysm/retinopathy/renal failure/stroke?

A

Atherosclerosis/weakened vessels

-arterial damage

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15
Q

What do you examine when a patient comes in with hypertension?

A

Look at their vasculature and take history of any vascular diseases

  • brain: stroke/vascular dementia
  • eyes: retinopathy
  • heart/ECG
  • chest pains/MI
  • urine tests/image kidneys
  • look at HR
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16
Q

What is vascular target organ damage?

A
  • left ventricular hypertrophy
  • retinopathy
  • MI
  • atherosclerosis of aorta
  • ischaemic stroke
  • inter-cerebral haemorrhage
  • chronic kidney disease
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17
Q

Is treating high BP effective?

A

Yes it lowers changes of end target organ damage
For every 10 mmHg reduction in BP:
-17% reduction for coronary heart disease
-27% reduction for stroke
-28% heart failure
-13% reduction in all cause mortality

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18
Q

What is the equation for your mean arterial blood pressure?

A

Mean arterial BP = CO x TPR

CO = SV x HR

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19
Q

How is blood pressure regulated short term?

A

Baroreceptor reflex
(Short term- bleeding to death/septic shock)
-body senses low BP via baroreceptors
-increased stretch by increased BP of baroreceptors stimulates them, decreased BP stretches them less
-baroreceptors send messages to medulla in brain, feeds back to heart/peripheral vessels to adjust HR/TPR-via dilation

Bradycardia/vasodilation counteract increased mean arterial pressure

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20
Q

Where are baroreceptors abundantly found?

A

-carotid sinus
-aortic arch
(Sensitive to stretch: monitor BP coming out of the heart)

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21
Q

What does the baroreceptor reflex control?

A

Acute changes in BP

  • doesn’t control long term changes to BP
  • threshold for baroreceptor resets and accepts what your BP is
22
Q

How is blood pressure controlled long term?

A

Control sodium balance and extracellular fluid

  • plasma is part of extracellular fluid
  • water follows Na+ so controlling Na+ levels controls plasma volume
23
Q

How many neurohumoral pathways are there to control circulating volume + therefore BP?

A

4

  1. Renin-angiotensin-aldosterone system
  2. Sympathetic nervous system
  3. ADH
  4. ANP (atrial natriuretic peptide)
24
Q

How does increasing extracellular fluid increase BP?

A

If fluid volume is increasing, then SV is increasing, therefore your BP increases

25
Q

What is the RAAS?

A

Renin-angiotensin-aldosterone system
-commenced by sensors in juxtaglomerular apparatus (JGA) in afferent arteriole of kidney
-renin released from granular cells of JGA in response to low BP
-renin catalyses angiotensin > angiotensin 1
-ACE converts angiotensin 1 > angiotensin 2
-angiotensin 2 causes vasoconstriction, stimulates Na+ reabsorption, stimulates adrenal glands to produce aldosterone which stimulates further Na+ absorption
= increases BP

26
Q

What stimulates renin release?

A
  • reduced NaCl transport to distal tubule (so less Na+ in reabsorbed and therefore less water)
  • reduced perfusion pressure
  • sympathetic stimulation to JGA to release renin
27
Q

What is ACE?

A

Angiotensin converting enzyme

28
Q

How does angiotensin 2 work?

A

AT1/AT2 receptors (predominantly AT1 receptors): G-coupled
Arterioles: vasoconstriction
Kidney: stimulates Na+ reabsorption
Sympathetic NS: increased release of NA
Adrenal cortex: release of aldosterone
Hypothalamus: increases thirst sensation (stimulates ADH release)

29
Q

How does aldosterone act on the kidney?

A
  • acts on cells of collecting duct
  • stimulates Na+ and therefore water reabsorption
  • activates apical Na+ channels (EPAC: epithelial Na channels) and apical K+ channel
  • increases basolateral extrusion of Na+ via Na/K/ATPase
30
Q

What is bradykinin and where is it found?

A

Found in lungs (is also present elsewhere)

-stimulation of ACE causes more breakdown of bradykinin and reduced vasdilating properties of it

31
Q

What breaks down bradykinin into peptide fragments?

32
Q

What does bradykinin in the lungs cause?

A

Cough as it vasodilates your lungs

33
Q

What animal can cause a severe drop in BP?

A

In venom of Brazilian viper is something that causes the build up of bradykinin- vasodilation (blocks conversion of angiotensin 1 to angiotensin 2 via ACE- inhibitor of ACE)

34
Q

How could you treat high blood pressure theraputically?

A

ACE inhibitor: Block ACE to treat high BP (as this stops conversion of Bradykinin to peptide fragments and bradykinin is a vasodilator- which builds up gradually)

35
Q

How does the sympathetic nervous system control BP?

A
  • high levels of sympathetic stimulation reduce renal blood flow
  • stimulating renin production
  • constriction of arterioles/increase in HR/increase in CO/increased Na+ reabsorption
36
Q

What is the function of ADH?

A
  • stimulated by increases in plasma osmolality/low BP
  • stimulates Na+ reabsorption via thick ascending limb of loop of Henle via Na/K/Cl co transporters + therefore water
  • causes vasoconstriction
  • increasing SV and therefore BP
37
Q

What is ADH also known as?

A

Arginine vasopressin

38
Q

What are natriuretic peptides?

A

ANP stimulated from sensors within atria of heart
-response to stretch
-released from atrial cells in response to stretch
-reduced volume inhibits release of ANP
Try to lower BP

39
Q

What are the actions of ANP?

A

-vasodilation of afferent arteriole
-inhibits sodium reabsorption along nephron
-low BP ANP release is inhibited
Acts in opposite direction to other neurohumoral regulators

40
Q

What are prostaglandins?

A

-act as local vasodilators

41
Q

What is dopamine?

A

Formed in kidney

-causes vasodilation (short acting)

42
Q

What is renovascular disease and what does it cause?

A 
It is occlusion of the renal artery 
-causes a fall in perfusion pressure leading to increase in renin production
-activation of RAAS + baroreceptors 
-vasoconstriction 
= raise BP
43
Q

What is renal parenchymal disease?

A

Direct damage to kidney (recurrent infection to kidney/polycystic kidney disease)

  • body thinks you are losing too much Na+ and water, fluid retention pathways start
  • causing hypertension
44
Q

What are some arsenal causes of secondary hypertension?

A

Conn’s syndrome - benign fatty tumours of adrenal glands which overproduce aldosterone (hypokalaemia-lose potassium at expense of retaining sodium)
Cushing’s syndrome-excess of glucocorticoid cortisol (act on aldosterone receptors at high levels)
Tumour of adrenal medulla- secretes NA/A which stimulate sympathetic nervous system

45
Q

How do you treat hypertension non-pharmacalogically?

A
  • exercise
  • diet
  • reduced salt intake
  • reduced alcohol intake
46
Q

How do you target the RAAS theraputically to reduced hypertension?

A
  • ACE inhibitors

- ANG2 antagonists

47
Q

What are the side effects of ACE inhibitors?

A

Dry cough due to build up of bradykinin
(Do not see this with ANG2 antagonists because they don’t block the bradykinin pathway- so if the patient can’t deal with the cough use this method)

48
Q

How do you reduce your TPR via dilation?

A

-L-type Ca2+ channel blockers (reduce calcium entry to vascular smooth muscles causing relaxation)
(VERAPAMIL/NIFEDIPINE)
-alpha1 receptor blockers (relaxes vascular smooth muscle)
(DOXAZOSIN)

Can cause postural hypotension

49
Q

How do you treat hypertension through diuretics?

A
  • thiazides (increase sodium excretion and therefore water excretion)
  • aldosterone antagonists will lower BP
50
Q

What are diuretics?

A

Increase urine production

51
Q

How do you use beta-blockers to treat hypertension?

A

-block beta1 receptors in heart- reduce sympathetic output
(Reduce HR & SV)
-don’t have as good effect as other antihypertensives
-use them if you have MI

CVS (16 decks)

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