6 Hypertension - Pharmacology Flashcards

1
Q

Define and describe Hypertension

A

Hypertension
- Abnormal elevation of systolic and/or diastolic blood pressure

can be asymptomatic for many years

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2
Q

Describe how a diagnosis of Hypertension is made

A

Diagnosed by:

  • repeated BP of >140/90mmHg
  • confirmed on an ambulatory BP recording
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3
Q

Define and describe secondary hypertension

A

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
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4
Q

Define and describe Essential HTN

A

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
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5
Q

Give some risk factors for developing Essential Hypertension

A
  • Advancing age
  • low birth-weight
  • low socio-economic class
  • high salt diet
  • obesity
  • sedentary lifestyle
  • excessive alcohol intake
  • stress + anxiety
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6
Q

Give some lifestyle measurements which are advocated in hypertension

A

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)
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7
Q

How is a diagnosis of Hypertension made?

A

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)

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8
Q

Describe what to do if a person’s BP is 180/120mmHg or higher

A

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
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9
Q

Describe the treatment aims of Hypertension

A

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
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10
Q

Which drug/drug class would you initially prescribe to a 46-year-old man of Caucasian origin recently diagnosed with hypertension?

A

ACE inhibitor
or
ARB (angiotensin receptor blocker)

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11
Q

Which drug/drug class would you initially prescribe to a 65-year-old woman of Caucasian origin recently diagnosed with hypertension?

A

Calcium channel blocker (CCB)

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12
Q

Which drug/drug class would you initially prescribe to a 51-year-old man of Afro-Caribbean origin recently diagnosed with hypertension?

A

Calcium Channel Blocker (CCB)

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13
Q

Describe ACE inhibitors, and give their MOA

A

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

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14
Q

Describe any contraindications/SE of ACEi’s

A

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)
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15
Q

Describe AT1 receptor blockers/Angiotensin Receptor Blocker (ARB)

+ give their MOA’s

A

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)
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16
Q

Describe Calcium Channel Blockers (CCB’s),

and give their MOA’s

A

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

17
Q

Describe Thiazide-like diuretics

and give their MOA

A

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
18
Q

Give some Side Effects of Thiazide-like diuretics

A
  • Hypokalaemia
  • Postural hypotension
  • Impaired Glucose control (diabetogenic)
  • Alter lipid profile
19
Q

Describe alpha-blockers

give MOA

A

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
20
Q

Describe beta-blockers

give MOA

A

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

21
Q

Give some SE of CCB’s

A
  • Peripheral oedema
  • Postural hypotension
  • Constipation (some)
22
Q

Give some SE of B-blockers

A

Bronchospasm

23
Q

Give SE of Alpha-blockers

A

Widespread

Postural hypotension