Give some secondary causes of hypertension
Conn’s syndrome (or primary hyperaldosteronism), phaeochromocytoma, hyperthyroid, coarctation Ao, renal artery stenosis
What is QRISK2?
Someone’s risk of developing CVD (MI/Stroke/PVD) over next 10 years
What is malignant HTN?
rapid rise in BP w/ some form of end-organ damage
Give an example of thiazide-like diuretic?
Indapamide
If you are astute 4 of HTN management, how will you decide what extra thiazide to give? Why is this?
If K+ >4.5 –> another thiazide diuretic
If K+ <4.5 –> spironolactone
This is because thiazide (and loop) cause hypokalaemia - so you want to make sure their K+ levels are ok
Why should you not give thiazide(-like) diuretics w/ loop diuretics?
Can cause hypokalaemia
Give an example of a CCB?
Amlodipine or nifedipine
What is a big symptom caused by Amlodipine?
Swollen ankles (uncomfortable) [oedema]
Give an example of an alpha blocker
Doxazosin
Why should you never give an ACE-i w/ ARB?
Nephrotoxic –> renal failure
Also hyperkalaemia
What does angiotensin II do?
What does it do to the glomerulus (and GFR) - hence, what do ARBs and ACE-i’s do?)?
Vasoconstriction
Release of aldosterone (from zone glomerulosa)
Glomerulus: constriction of the efferent arteriole causing ^ GFR (therefore ARBs/ACEi’s cause dilatation and decrease GFR)
What does aldosterone do?
Aldosterone ^ ENAC expression on collecting ducts –> ^ Na+/water into cell –> blood
also causes ^ K+ excretion
What is the problem with first taking ARB/ACE-i?
first dose hypotension (take at night)
What should you advise patients not to take with ARB/ACE-I?
NSAIDs (risk of renal failure)
Give 2 contraindications of ACE-I?
Pregnancy
Renal artery stenosis
Why is ACE-i/ARB CI’ed in renal artery stenosis?
RAS relies on AngII to ^ GFR by causing vasoconstriction of the efferent arteriole. ACE-i prevents formation of Ang II (and ARB antagonises AngII)
Therefore if ACE-i used in RAS –> renal failure
What is the mechanism of an ARB?
Ang II receptor blocker
How do ARBs/ACE-I’s affect K+? how?
Cause hyperkalaemia - prevent formation of aldosterone (which causes excretion of k+)
How do CCBs work?
prevents Ca2+ influx into smooth muscles (acts on L-type calcium channels)
How do thiazide diuretics affect K+ and Na+ levels?
Hyponatraemia and hypokalaemia
How do thiazide diuretics work?
inhibit the Na+/Cl- transporter in the DCT
Do loop or thiazide diuretics cause hypokalameia more?
Loop - therefore thiazide are used in HTN Mx
What type of diuretics are used in HTN Mx
Thiazide(-like) + spironolactone (not loop [used in HF])
How do loop diuretics work?
Act on the ascending limb of henle loop (LOOP DIURETICS) inhibiting the Na+/K+/2Cl- co-transporter
How does spironolactone work?
Aldosterone antagonist (so no ^ in ENAC –> therefore sodium not excreted)
What is a side effect of spironolactone?
GYNAECOMASTIA (problem with adherence to Tx)
Hyperkalaemia
What are some CI’es of Beta-blockers?
ASTHMA
How do beta-blockers treat HTN?
bind to beta 2 receptors –> smooth muscle relaxation (vasodilatation)
+ beta-1 receptors in kidney –> prevent renin secretion
How do beta-blockers treat hf?
Bind to beta-1 receptors
Negatively inotropic (reduce force) + decrease HR (negatively chronotropic) –> reduces cardiac work / O2 demand
what else are alpha blockers used in?
BPH
Give some causes of HF
Coronary artery disease / MI
HTN
Thyrotoxicosis, pregnancy, anaemia, AF, alcohol…
What is used to assess the severity of HF?
New York HF association classification
What is the 1st line treatment for HF?
ACEi/ARB OR beta blocker
What guides your decision for first line treatment for HF?
ACEi/ARB if DM or fluid overload
Beta blocker if angina
What is the second line treatment of HF?
ARB
Spironolactone
Hydralazine + long-acting nitrate
What is 3rd line Tx for HF?
Digoxin
Pacemaker ± defibrilator
Give an example of a long and short acting nitrate
Short: GTN
Long: isosorbide mononitrate
What drug should be avoided in someone taking nitrates?
Sildenafil (viagra) –> hypotension
Give some issues surrounding polypharmacy
Poor adherence/compliance (can give drug nomad)
Therapeutic cascade
Hypotension
^ risk of adverse effects
^ risk of interactions
How is someone’s risk of CVD (MI/PAD/Stroke) in next 10years measured?
QRISK2
What is QRISK 2 used in?
Primary prevention
Describe the primary prevention of Coronary heart disease?
Treat co-morbidities
Lifestyle advise
If QRISK2 <10%: no statin
If QRISK2 10% or more: 20mg atorvastatin
Describe secondary prevention of CAD?
Treat co-morbidities
Lifestyle advise
Drugs:
- ACE-I
- 80mg atorvastatin
- Beta blocker
- Dual antiplatelet (aspirin + clopidogrel)
What dose of atorvastatin is recommended for primary and secondary CAD prevention?
Primary: 20mg
Secondary: 80mg
What are two ways of approaching primary prevention?
Population approach
High risk approach
What is the population approach and give some example?
Strategies to decrease the risk of developing e.g. CHD in an entire population
e.g. Change4Life, nationwide ban on smoking packaging
What is the high-risk approach and give some example?
Some indidviuals are at higher risk of developing the disease. This approach identifies them and decrease their risk (rather than the population)
E.g. QRISK2 –> identifies those w/ >10% risk –> given statin
How does a statin work?
HMA-CoA reductase inhibitor
What is a risk with statins?
Muscle aches –> myopathy –> rhabdomyolysis
What drugs CI’ed with statins?
Cytochrome P450 inhibitors (e.g. clarithromycin) –> causes ^ of statin within the blood (so increased risk of rhabdomyolysis)
What are some risks of prolonged falls?
DVT
Rhabdomyolysis + renal failure
dehydration
Give some features of digoxin toxicity
Yellow vision Fatigue N+V Confusion arrythmia (palpitations)