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Pathophysiology of Hypertension > HT diagnosis > Flashcards

HT diagnosis Flashcards

1
Q

HT is a “silent killer”, how can we help the public?

A
  1. ) screen those at risk
  2. ) Increase public awareness of risk factors
  3. ) Make diagnsois based on clinical guidelines
  4. ) Promote lifesyle changes in pre-hypertensives
  5. ) Ensure compliance even though they won’t feel effect
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2
Q

Following diagnosis, what else should be assessed?

A

Cardiovascular risk and end organ damage

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3
Q

The aim of treatment is to reach target BP and reduce CV risk. What does the target BP depend on?

A

Age, end organ damage, diabetes and other perpheral vascular diseases

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4
Q

Prehypertensives won’t have any end organ damage. Lifestyle changes should be promoted (as in all other groups) What are the lifestyle changes?

A
  1. ) Smoking cessation
  2. ) aLCOHOL
  3. ) Reducing dietary sodium
  4. ) diet
  5. ) Exercise
  6. ) Reduction in stress
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5
Q

In what case would you not offer treatment for stage 1 hypertension?

A

Under 80 with no end organ damage and a CV risk of less than 20%. Would offer lifestyle changes and review annually. Target BP = UNDER 140/90
NOT if have renal disease or diabetes

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6
Q

What angiotensin II receptor subtype is important in CV regulation?

A

Type I (AT1)

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7
Q

What is the MoA of ACE inhibitors?

A

Inhibit the conversion of Angiotensin 1 to Angiotensin 2. So we dont get angiotensin 2 ‘s effect on e.g. SNS, ALDOSTERONE, vasopressin, arteriolar vasoconstricion

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8
Q

Angiotensin 2 can be produced from 1 independently of ACE, how?

A

Chimase interaction

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9
Q

How does ACE affect bradykinin? How do ACE inhibitors effect BK?

A

ACE is a kinase enzyme and so breaks down bradykinin. ACE inhibitors will lead to an increase in BK and so an increase in its vasodilatory effects via NOS/NO and COX/PGI2. This makes them effective in low renin hypertensives.

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10
Q

What is the SE associated with lisinopril?

A

Dry cough - ACE inhibitor

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11
Q

What receptor does angiotensin ii blocker (ARB’S) antagonise?

A

AT1

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12
Q

What is thought to cause the dry cough associated with ACE?

A

BK through bronchoconstriction

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13
Q

Do ARB’s have an effect on BK?

A

No, this is why they are less effective in low-renin hypertensives than ACE inhibitors

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14
Q

Why do ARB’s more effectively control Ang II mediated vasoconstriction?

A

Because ARB’S directly target the AT1 receptors and so we can block the angiotensin 2 produced by ACE and chymase.

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15
Q

Name an angiotensin receptor blocker

A

Candesartan

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16
Q

What do L-type calcium channels do?

A

They allow the influx of calcium into all muscle cells especially smooth muscle (which are expressed throughout the body). They are voltage operated calcium channels VOCC

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17
Q

What does the large influx of calcium through calcium channels and the sarcoplasmic reticulum do in muscle cells?

A

Activates the contractile proteins myosin and actin and causes contraction of muscle cells

18
Q

What do Calcium channel blockers (CCB’s) target?

A

The calcium initiated contraction of smooth muscle

19
Q

What subunit on the VOCC do the 3 distinct classes of CCB’s interact with?

A

The alpha subunit (this is the pore that lets calcium in

20
Q

What are the 3 distinct classes of CCB’s?

A
  1. ) Dihydropiridines
  2. ) Non-dihydropyridines
  3. ) Benzothiazapine
21
Q

What are dihydropyridines selective for and what does this mean?

A

Peripheral vasculature = show little chronotropic (have llittle effect on the contraction of the heart = don’t affect HR) or inotropic effect (don’t effect the force of muscle contraction)

22
Q

What are non-dihydropyridines selective for and what does this mean?

A

Cardiac muscle = affects chronotropy and inotropy. (used in other CV diseases

23
Q

What are benzothiazapines selective for and what does this mean?

A

Sit in the middle = have some selectivity for vasculature and muscle cells

24
Q

How do dihydropyridines work?

A

They target different vascular beds and cause peripheral vasodilation which leads to reduced peripheral resistance (reduced TPR).

25
Q

What is the problem with dihydropyridines?

A

The reduced TPR can lead to tachycardia = the body’s attempt to increase heart rate in order to maintain cardiac output.

26
Q

For what groups of peolpe are CCB’s the primary treatment?

A

Low renin grouo - typicaly over 55 african-carribeans

27
Q

Give and example of a CCB?

A

Amlodipine

28
Q

What is the MoA of thiazide diuretics?

A

They effect the distal convoluted tubule of the kidney by inhibiting Na reabsorption = icreased production of urine = decreased blood volume = decreased BP

29
Q

What group of drugs do not play a part in primary treatment anymore?

A

B-blockers

30
Q

What is the MoA of B-blockers?

A

They reduce sympathetic tone by blocking noradrenalin and reducing myocardial contraction = decrease CO

31
Q

Why do we not use B-blockers anymore?

A

They are contraindicated in asthmatics, COPD patients and people who have heart block because they cause bronchoconstriction.
They can mask tachycardia (increased HR) which is a sign of insulin induced hypoglycaemia (care in diabetics)

32
Q

What is the first step treatment for patients who are under 55?

A

Group A = ACE (cheaper), if not tolerated give ARB. if neither of these then consider b-blocker in young patients.

33
Q

What is the first step treatment for patients who are over 55 or from african/caribbean decent?

A

Group C = CCB’s because renin dependance is low in this group. If not tolerated - consider thiazides

34
Q

What is the second step treatment for patients who are under 55?

A

Add group C or if not tolerated group D

35
Q

What is the SECOND step treatment for patients who are over 55 or from african/caribbean decent?

A

Add group A

36
Q

What is step 3 for both groups after checking compliance?

A

A + C + D

37
Q

What do we call step 4 hypertension?

A

Resistant HT

38
Q

What is step 3 for both groups after checking compliance?

A

A + C + D plus an additional diuretic or a higher dose thiazde diuretic. If still no improvement consider a beta blocker or and alpha1 antagonist

39
Q

What are the three types of HT during pregnancy?

A
  1. )Pre-existing HT
  2. ) Gestational HT (appears post 20 weeks_
  3. ) Pre-eclampsia ( gestational plus proteinriea = excess protein in urine)
40
Q

What anti-hypertensives are contraindicated in pregnancy?

A

Group A plus chlorothiazide (diuretic)

41
Q

What is the treatment for sever HT with end organ damage?

A

IV vasodilator within 2 hours to reduce the risk of haemorrhagic stroke etc

42
Q

What is the treatment for sever HT without end organ damage?

A

See GP or go to A&E urgently for oral b-blocker or CCB

Pathophysiology of Hypertension (5 decks)

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