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CVS > Lecture 11 > Flashcards

Lecture 11 Flashcards

(51 cards)

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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?

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
A

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

25
What is the RAAS?
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
What stimulates renin release?
- 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
What is ACE?
Angiotensin converting enzyme
28
How does angiotensin 2 work?
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
How does aldosterone act on the kidney?
- 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
What is bradykinin and where is it found?
Found in lungs (is also present elsewhere) | -stimulation of ACE causes more breakdown of bradykinin and reduced vasdilating properties of it
31
What breaks down bradykinin into peptide fragments?
ACE
32
What does bradykinin in the lungs cause?
Cough as it vasodilates your lungs
33
What animal can cause a severe drop in BP?
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
How could you treat high blood pressure theraputically?
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
How does the sympathetic nervous system control BP?
- 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
What is the function of ADH?
- 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
What is ADH also known as?
Arginine vasopressin
38
What are natriuretic peptides?
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
What are the actions of ANP?
-vasodilation of afferent arteriole -inhibits sodium reabsorption along nephron -low BP ANP release is inhibited Acts in opposite direction to other neurohumoral regulators
40
What are prostaglandins?
-act as local vasodilators
41
What is dopamine?
Formed in kidney | -causes vasodilation (short acting)
42
What is renovascular disease and what does it cause?
``` 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
What is renal parenchymal disease?
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
What are some arsenal causes of secondary hypertension?
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
How do you treat hypertension non-pharmacalogically?
- exercise - diet - reduced salt intake - reduced alcohol intake
46
How do you target the RAAS theraputically to reduced hypertension?
- ACE inhibitors | - ANG2 antagonists
47
What are the side effects of ACE inhibitors?
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
How do you reduce your TPR via dilation?
-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
How do you treat hypertension through diuretics?
- thiazides (increase sodium excretion and therefore water excretion) - aldosterone antagonists will lower BP
50
What are diuretics?
Increase urine production
51
How do you use beta-blockers to treat hypertension?
-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

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