6 Hypertension - Pharmacology Flashcards
Define and describe Hypertension
Hypertension
- Abnormal elevation of systolic and/or diastolic blood pressure
can be asymptomatic for many years
Describe how a diagnosis of Hypertension is made
Diagnosed by:
- repeated BP of >140/90mmHg
- confirmed on an ambulatory BP recording
Define and describe secondary hypertension
Secondary hypertension is when a specific cause for HTN is found,
- hence secondary to an underlying disease process
e.g. Renal disease (found in 5% of cases of all hypertension) other e.g. - tumour secreting hormones - OCP - cocaine - preeclampsia etc
Define and describe Essential HTN
Primary (Essential) Hypertension
- Cause - unknown (95% of cases)
- Can be benign or Malignant (> 180/110mmHg)
Aetiology of essential HTN not quite known, but there is a genetic component as evidenced by:
- Increased prevalence in the Afro-caribbean population
- those with family history
Give some risk factors for developing Essential Hypertension
- Advancing age
- low birth-weight
- low socio-economic class
- high salt diet
- obesity
- sedentary lifestyle
- excessive alcohol intake
- stress + anxiety
Give some lifestyle measurements which are advocated in hypertension
Modify the modifiable risk factors + offer lifestyle advice
- low salt diet
- more exercise (obesity, sedentary lifestyle)
- cut down on alcohol, smoking
- try and address stress + anxiety
Additional:
- Reduce consumption of caffeine-containing products
- inform people about local initiatives (that promote healthy lifestyle change)
How is a diagnosis of Hypertension made?
In people with a clinic BP of 140/90mmHg or higher
- if 1st measurement is higher, take 2nd one
- if the 2nd one is much different, take a 3rd one
- record lower of last 2 measurements as the clinic BP
AND
Ambulatory BP monitoring (ABPM) of 135/85mmHg or higher
- If clinic BP is between 140/90 and 180/120, offer ABPM (or HBPM)
Describe what to do if a person’s BP is 180/120mmHg or higher
Refer for same-day specialist assessment if there are:
- Signs of retinal haemorrhage and/or papilloedema (accelerated HTN)
- Life-threatening symptoms, such as new-onset confusion, chest pain, signs of heart failure, or acute kidney injury
Describe the treatment aims of Hypertension
To reduce and main BP to following targets
AGE < 80 years
- Clinic BP < 140/90mmHg
- ABPM/HBPM < 135/85mmHg
AGE > 80 years
- Clinic BP < 150/90mmHg
- ABPM/HBPM < 145/85mmHg
Specific goals:
- reduction in Cardiovascular damage
- preservation of renal function
- limitation/reversal of Left Ventricular Hypertrophy + further Heart Failure
- prevention of Ischaemic Heart Disease
- reduction in mortality due to Stroke and Myocardial Infarction
Which drug/drug class would you initially prescribe to a 46-year-old man of Caucasian origin recently diagnosed with hypertension?
ACE inhibitor
or
ARB (angiotensin receptor blocker)
Which drug/drug class would you initially prescribe to a 65-year-old woman of Caucasian origin recently diagnosed with hypertension?
Calcium channel blocker (CCB)
Which drug/drug class would you initially prescribe to a 51-year-old man of Afro-Caribbean origin recently diagnosed with hypertension?
Calcium Channel Blocker (CCB)
Describe ACE inhibitors, and give their MOA
ACE inhibitors
- e.g. Ramipril, enalapril, lisinopril, captopril
ACE inhibitors inhibit Angiotensin-Converting Enzyme (ACE)
- which converts Ang I to Ang II
ACE enables:
Ang II is a vasoconstrictor and releases aldosterone
- it increases total peripheral resistance = MAP
- aldosterone increases Na+ retention and H2O retention
- it also potentiates bradykinin (vasodilator), which ACE breaks down - cough
ACEi can increase K+
- can be given to diabetics
Describe any contraindications/SE of ACEi’s
AVOID ACEi’s
- in renovascular disease - bilateral renal artery stenosis
> renin-dependent hypertension
> ACEi’s lead to renal under perfusion and severe hypotension - if there is stenosis, kidey thinks there is low BP, so kidney release renin
- so if ACEi given, the BP drops lower - more hypotension in renal systems (so more renin - PROBLEM)
- Also be cautious in patients with low GFR
SE:
- Cough
- severe 1st-dose hypotension
- Renal damage (maybe)
Describe AT1 receptor blockers/Angiotensin Receptor Blocker (ARB)
+ give their MOA’s
ARB
- e.g. losartan, candesartan, valsartan
ARB’s block the action of Ang-II at the ATII receptor
- The AT1 subtype is found in the heart, blood vessels, kidney, adrenal cortex, lung, and brain
- AT1 mediates the vasoconstrictor effects
ARBs have a similar effect to ACEi’s, but do not give cough
- Less breakdown of Bradykinin (less ACE), which ACEi’s block
- BUT ARB’s no effect ACE (more breakdown of Bdarykinin)
Describe Calcium Channel Blockers (CCB’s),
and give their MOA’s
CCB’s
- e.g. Verapamil, diltiazem,
- e.g. Dihydropyridines (amlodipine)
They inhibit voltage gated Ca2+ channels on vascular smooth muscle
- leading to vasodilation and reduction in BP
There are 2 types of CCB’s
- Rate limiting (e.g. Verapamil)
> have greater effects on cardiac tissue - can decrease Cardiac contracility + HR
- Dihydropyridines [long-acting] (e.g. Amlodipine)
> have greater effects on vascular smooth muscle
Describe Thiazide-like diuretics
and give their MOA
Thiazide-like (e.g. indapamide, chlortalidone)
- these are second line anti-hypertensives
MOA
- they inhibit Na+/Cl- reuptake in DCT
- loss of Na+, loss of H20
- leading to a reduction in the circulating blood volume
- hence reduction in SV
Give some Side Effects of Thiazide-like diuretics
- Hypokalaemia
- Postural hypotension
- Impaired Glucose control (diabetogenic)
- Alter lipid profile
Describe alpha-blockers
give MOA
Alpha-blockers
e.g. Doxazosin, prazosin
These are competitive receptor antagonists of a1-adrenoceptors
- these are stimulated by Noradrenaline/Adrenaline - vasoconstriction
- inhibition of this by a-blockers
Last choice anti-hypertensives
- due to widespread side-effects
- making them poorly tolerated
Describe beta-blockers
give MOA
B-blockers
- no longer recommended as 1st line
e. g. Atenolol, propanolol - Atenolol - is B1 selective
- Propanolol is B-nonselective
MOA:
- reduction in sympathetic drive to the heart
- reducing Cardiac output
- a reduction in sympathetically evoked renin release
Beta-blockers may block bronchial B2 receptors, and are used with caution in:
- Asthma, COPD
Blockage of Peripheral B2-adrenoceptors opposes vasodilation to skeletal muscle
- cold
Give some SE of CCB’s
- Peripheral oedema
- Postural hypotension
- Constipation (some)
Give some SE of B-blockers
Bronchospasm
Give SE of Alpha-blockers
Widespread
Postural hypotension
