Hypertension (renal) Flashcards
What is hypertension?
- Defined as sustained BP >140/90 mmHg
- Raised BP in the systemic vascular bed
How do you diagnose hypertension?
- Blood pressure has a skewed distribution within the population
- Don’t rely on single reading
- Assess over period of time
- Sustained BP >140/90mmHg on 2 separate readings
- Confirm with 24hr ambulatory BP monitoring
What is the target for BP control?
- < 140/90
- < 130/80 in diabetes
- 150/90 if aged >80
- Reduce BP slowly, rapid reduction can be fatal
- A target of 120/80 proven to be beneficial
Would you treat a patient with >140/90 mmHg BP?
The decision depends on the risk of coronary events, presence of diabetes, or end-organ damage.
Treat those with >160/100mHg (or ABPM >150/95).
BP on average is lower in young people and a study shows there is substantial benefit in treating 80+ age group.
What is the most common form of hypertension?
Essential/primary HTN - 95% cases
What is the aetiology of essential/primary hypertension?
No underlying cause but associated with:
- Genetic component - FHx
- Black ancestry
- Low birthweight
- Obesity
- Excess alcohol intake
- High salt intake
- Metabolic syndrome: obesity, DM2, hypercholesterolaemia
Secondary hypertension is ~ 5% of cases, what can it be caused by?
- Renal disease (most common): glomerulonephritis, diabetic nephropathy, polycystic kidneys, renovascular disease
- Endocrine: Cushing’s syndrome, acromegaly, thyroid disease, hyperparathyroid disease, Conn’s syndrome, Adrenal hyperplasia, phaeochromocytoma
- Others: Aortic coarctation, pregnancy, liquorice
- Drugs: NSAIDs, oral contraceptives, steroids, sympathomimetics, vasopressin, MAO inhibitors, carbenoxalone
What is the flowchart/diagram for managing suspected hypertension / when should you act?
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What are the signs and symptoms of hypertension?
- Usually asymptomatic
- Always examine CVS fully and check for retinopathy (haemorrhages, exudates, papilloedema)
- Renal disease: renal bruits, palpable kidneys, proteinuria, haematuria
- Endocrine disease: attacks of sweating, tachycardia in phaeochromocytoma, symptoms of Cushing’s, acromegaly etc
- Coarctation of aorta: radiofemoral delay, weak femoral pulses, mid-late systolic murmur
What is malignant hypertension and its effects on the kidney, brain, retina and CVS?
Described as rapid rise in BP with diastolic BP >120mmHg in conjunction with bilateral retinal haemorrhages and exudates. If untreated, it will result in end-organ damage to the:
- Kidneys: haematuria, proteinuria, progressive renal failure
- Brain: cerebral oedema, haemorrhage, seizures
- CVS: acute heart failure, aortic dissection
- Retina: flame shaped haemorrhages, cotton wool spots, exudates, papilloedema
What are the possible complications of hypertension?
- Coronary artery disease
- Cerebrovascular accident
- Left ventricular hypertrophy
- Congestive heart failure
- Retinopathy
- Peripheral artery disease
- Chronic kidney disease
- Aortic dissection
- Malignant hypertension
What investigations can be done to look for causes of hypertension and possible complications?
- Serum U&E: evidence of renal impairment (-> if so, do US, angiography), eg. hypokalaemia occurs in Conn’s
- Urine stix test: for protein + blood
- Fasting blood for lipids (total + HDL cholesterol) + glucose
- ECG: look for end-organ damage (LVH, MI)
- Fundoscopy: look for retinal changes
What are the stages of hypertension?
- Optimal = < 120/80
- Normal = < 130/85
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What characteristics might an ECG show for hypertension?
- left ventricular hypertrophy
- tall R waves in left lateral leads (I and V6)
- deep S waves in right-sided pericordial leads (V1 and V2)
- maybe left axis deviation
- if there is significant left ventricular ‘strain’ then there are also inverted T waves in V5 and V6 and possible ST depression
- QRS may be slightly prolonged
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What is the conservative, life-style management for hypertension?
- diet: high consumption of veg/fruits and low-fat diet, low salt diet, reduced caffeine intake
- regular exercise: 30min of mod-intensity aerobic exercise 5-7days/week
- reduction of alcohol intake per week
- stop smoking
- overall lose weight
What impact does reduced salt diet have?
- low salt diet is recommended
- aiming for less than 6g/day, ideally 3g/day
- average adult in UK consumes 8-12g/day of salt
- recent BMJ paper showed lowering salt intake can have significant effect on BP
- eg. reducing salt intake by 6g/day can lower systolic BP by 10mmHg
What do you do if a patient has an ABPM/HBPM of >= 135/85 mmHg (ie. stage 1 hypertension)?
- treat if <80 years of age AND any of following:
- target organ damage
- established cardiovascular disease
- renal disease
- diabetes
- 10-year cardiovascular risk equivalent to 10% or greater
What would you do if a patient had an ABPM/HBPM reading of >= 150/95mmHg (ie. stage 2 hypertension)?
- offer drug treatment regardless of age
NICE define a clinic BP >= 140/90mmHg after step 3 treatment w/ optimal or best tolerated doses as resistant hypertension. They suggest step 4 treatment or seeking exp advice.
What is the step 4 treatment?
- consider further diuretic treatment
- if potassium <4.5mmol/l add spironolactone 25mg od
- if potassium >4.5mmol/l add higher-dose thiazide-like diuretic
- if further diuretic therapy not tolerated, or is contraindicated or ineffective, consider an alpha or beta-blocker
What’s next for patients that fail to respond to step 4 measures?
- referred to specialist
- NICE:
- if blood pressure remains uncontrolled w/ optimal or max tolerated doses of four drugs, seek exp advice if it has not yet been obtained
ACE inhibitors: examples + indications
- ramipril, lisinopril, perindopril
- hypertension
- chronic heart failure
- ischaemic heart disease
- diabetic nephropathy + CKD w/ proteinuria
ACE inhibitors: mechanism of action
- ACE inhibitors block action of the ACE
- prevent conversion of ang I to ang II
- ang II = vasoconstrictor + stimulates aldosterone secretion
- blocking its action reduces peripheral vascular resistance -> lowers BP
- particularly dilates efferent glomerular arteriole -> reduces intraglomerular pressure + slows progression of CKD
- reducing aldosterone level promotes sodium + water excretion
- this can help to reduce venous return -> beneficial in HF
ACE inhibitors: side-effects?
- hypotension (particularly after firt dose)
- persistent dry cough (due to inc levels of bradykinin)
- hyperkalaemia (bc lower aldosterone -> K+ retention)
- cause or worsen renal failure too
- rare idiosyncratic effects = angioedema, other anaphylactoid rxns
Tend not to use ACEi in renal artery stenosis, AKI, pregnant women, breastfeeding,
What is the alternative drug choice when ACEi are not tolerated due to the persistent cough?
- Angiotensin receptor blockers (ARBs)
- eg. losartan, candesartan
- same indications
- similar MOA, instead of inhibiting Ang I -> II conversion, they block action of Ang II on AT1 receptor
- unlike ACEi, less likely to cause cough and angioedema
Calcium channel blockers: examples and common indications?
examples: amlodipine, nifedipine, diltiazem, verapamil
- amolidipine + nifedipine used for first/second line tx for hypertension
- all ca-ch blockers used to control symptoms of stable angina
- diltiazem and verapamil used to control cardiac rate in ppl w/ supraventricular arrhythmias incl supraventricular tachycaria, atrial flutter and atrial fibrilation
Calcium channel blockers: mechanism of action?
- they decrease Ca2+ entry into vascular and cardiac cells
- reducing intracellular calcium conc
- causes relaxation + vasodilation in arterial sm muscle -> lowering arterial pressure
- in heart, calcium channel blockers reduce myocardial contractility
- they suppress cardiac conduction across AV node -> slowing ventricular rate
- reduced cardiac rate, contractility + afterload -> reduce myocardial oxygen demand
- preventing angina
- CaCh blockers:
- dihydropryidines (amlodipine, nifedipine) - selective for vasculature
- non-dihydropyridines (verapamil) - more cardioselective
Calcium channel blockers: important side-effects?
amlodipine + nifedipine:
- ankle swelling, flushing, headache, palpitations
verapamil:
- constipation, bradycardia, heart block, cardiac failure
diltiazem has mixed effects so can cause both sets of adverse effects
Thiazide diuretics: examples and indications?
eg. bendroflumethiazide, indapamide, chlortalidone
- alternative first-line tx for hypertension where a ca-ch blocker would otherwise be used but is either unsuitable or there are features of heart failure
- thiazides also an add-on treatment for hypertension in pts whose BP not adequately controlled by a calcium-channel blocker plus an ACEi/ARB
Thiazide diuretics: mechanism of action?
- thiazide (bendro) vs thiazide-like (indapamide, chlortalidone)
- differ chemically but similar effects + uses
- thiazides inhibit the Na+/Cl- co-transporter in distal convoluted tubule of nephron
- prevents reabsorption of sodium + its osmotically associated water
- resulting diuresis causes initial fall in ECV
- over time, compensatory changes (eg. activation of RAAS) tend to reverse this, at least in part
- long-term antihypertensive effect prob mediated by vasodilatation (incompletely understood)
Thiazide diuretics: important side-effects?
- hyponatraemia (not usually problematic)
-
hypokalaemia
- increased delivery of sodium to distal tubule, exchanged for potassium, increases urinary potassium losses
- -> cardiac arrhythmias
- impotence in men
Alpha-blockers: indications and examples?
eg. doxazosin, tamsulosin, alfuzosin
- first line med option to improve symptoms in benign prostatic hyperplasia, when lifestyle changes insufficient. 5a-reductase inhibitors may be added in selected cases. surgical treatment also an option, particularly if there is evidence of urinary tract damage (eg. hydronephrosis)
- as an add-on tx in resistant hypertension, when other medicine (Ca-ch blockers, ACEi, thiazides) are insufficient
Alpha-bockers: mechanism of action?
- most drugs in this class highly selective for a1-adrenoreceptor
- a1-adrenoreceptors found mainly in sm muscle - blood vessels + urinary tract (bladder neck + prostate in particular)
- stimulation induces contraction; blockade induces relaxation
- a1-blockers therefore cause
- vasodilatation -> fall in BP
- and reduced resistance to bladder outflow
Alpha-blockers: important adverse effects?
- postural hypotension
- dizziness
- syncope
particularly prominent after first dose (rather like with ACEi and ARBs)
Beta-blockers: examples and indications?
eg. bisoprolol, atenolol, propranolol, metoprolol
- ischaemic heart disease
- chronic heart failure
- atrial fibrilation
- supraventricular tachycardia
- hypertension
Beta-blockers: mechanism of action?
- b1-adrenoreceptors located mainly in heart
- b2-adrenoreceptors found mostly in sm muscle of blood vessels + airways
- via the b1-receptor, B-blockers reduce force of contraction + conduction speed of heart
- this relieves myocardial ischaemia by reducing cardiac work + oxygen demand -> increasing myocardial perfusion
- improve prognosis in heart failure by protecting the heart from effects of chronic sympathetic stimulation
- they slow ventricular rate in AF mainly by prolonging refractory period of AV node
- SVT often involves a self-perpetuating circuit that takes in the AV node; B-blockers may break this and restore sinus rhythm
- in HT, B-blockers lower BP through variety of means, one of which is by reducing renin secretion from kidney since this is mediated by b1-receptors
B-blockers: adverse effects?
- fatigue
- cold extremeties
- headache
- GI disturbance (nausea)
- can cause sleep disturbance + nightmares
- may cause impotence in men
remember to avoid in pts w/ asthma, choose B1-receptor selective blocker (eg. all prev mentioned but propranolol which is non-selective) in COPD
What are Korotkoff sounds?
Korotkoff sounds are blood flow sounds that healthcare providers observe while taking blood pressure with a sphygmomanometer over the brachial artery in the antecubital fossa. These sounds appear and disappear as the blood pressure cuff is inflatedand deflated.
Hypertension Management