HT diagnosis Flashcards
(42 cards)
HT is a “silent killer”, how can we help the public?
- ) screen those at risk
- ) Increase public awareness of risk factors
- ) Make diagnsois based on clinical guidelines
- ) Promote lifesyle changes in pre-hypertensives
- ) Ensure compliance even though they won’t feel effect
Following diagnosis, what else should be assessed?
Cardiovascular risk and end organ damage
The aim of treatment is to reach target BP and reduce CV risk. What does the target BP depend on?
Age, end organ damage, diabetes and other perpheral vascular diseases
Prehypertensives won’t have any end organ damage. Lifestyle changes should be promoted (as in all other groups) What are the lifestyle changes?
- ) Smoking cessation
- ) aLCOHOL
- ) Reducing dietary sodium
- ) diet
- ) Exercise
- ) Reduction in stress
In what case would you not offer treatment for stage 1 hypertension?
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
What angiotensin II receptor subtype is important in CV regulation?
Type I (AT1)
What is the MoA of ACE inhibitors?
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
Angiotensin 2 can be produced from 1 independently of ACE, how?
Chimase interaction
How does ACE affect bradykinin? How do ACE inhibitors effect BK?
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.
What is the SE associated with lisinopril?
Dry cough - ACE inhibitor
What receptor does angiotensin ii blocker (ARB’S) antagonise?
AT1
What is thought to cause the dry cough associated with ACE?
BK through bronchoconstriction
Do ARB’s have an effect on BK?
No, this is why they are less effective in low-renin hypertensives than ACE inhibitors
Why do ARB’s more effectively control Ang II mediated vasoconstriction?
Because ARB’S directly target the AT1 receptors and so we can block the angiotensin 2 produced by ACE and chymase.
Name an angiotensin receptor blocker
Candesartan
What do L-type calcium channels do?
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
What does the large influx of calcium through calcium channels and the sarcoplasmic reticulum do in muscle cells?
Activates the contractile proteins myosin and actin and causes contraction of muscle cells
What do Calcium channel blockers (CCB’s) target?
The calcium initiated contraction of smooth muscle
What subunit on the VOCC do the 3 distinct classes of CCB’s interact with?
The alpha subunit (this is the pore that lets calcium in
What are the 3 distinct classes of CCB’s?
- ) Dihydropiridines
- ) Non-dihydropyridines
- ) Benzothiazapine
What are dihydropyridines selective for and what does this mean?
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)
What are non-dihydropyridines selective for and what does this mean?
Cardiac muscle = affects chronotropy and inotropy. (used in other CV diseases
What are benzothiazapines selective for and what does this mean?
Sit in the middle = have some selectivity for vasculature and muscle cells
How do dihydropyridines work?
They target different vascular beds and cause peripheral vasodilation which leads to reduced peripheral resistance (reduced TPR).
