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*Medicine: Cardiology & Vascular > Hypertension (renal) > Flashcards

Hypertension (renal) Flashcards

1
Q

What is hypertension?

A
  • Defined as sustained BP >140/90 mmHg
  • Raised BP in the systemic vascular bed
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2
Q

How do you diagnose hypertension?

A
  • 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
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3
Q

What is the target for BP control?

A
  • < 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
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4
Q

Would you treat a patient with >140/90 mmHg BP?

A

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.

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5
Q

What is the most common form of hypertension?

A

Essential/primary HTN - 95% cases

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6
Q

What is the aetiology of essential/primary hypertension?

A

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
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7
Q

Secondary hypertension is ~ 5% of cases, what can it be caused by?

A
  • 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
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8
Q

What is the flowchart/diagram for managing suspected hypertension / when should you act?

A
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9
Q

What are the signs and symptoms of hypertension?

A
  • 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
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10
Q

What is malignant hypertension and its effects on the kidney, brain, retina and CVS?

A

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
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11
Q

What are the possible complications of hypertension?

A
  • Coronary artery disease
  • Cerebrovascular accident
  • Left ventricular hypertrophy
  • Congestive heart failure
  • Retinopathy
  • Peripheral artery disease
  • Chronic kidney disease
  • Aortic dissection
  • Malignant hypertension
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12
Q

What investigations can be done to look for causes of hypertension and possible complications?

A
  • 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
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13
Q

What are the stages of hypertension?

A
  • Optimal = < 120/80
  • Normal = < 130/85
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14
Q

What characteristics might an ECG show for hypertension?

A
  • 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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15
Q

What is the conservative, life-style management for hypertension?

A
  • 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
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16
Q

What impact does reduced salt diet have?

A
  • 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
17
Q

What do you do if a patient has an ABPM/HBPM of >= 135/85 mmHg (ie. stage 1 hypertension)?

A
  • 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
18
Q

What would you do if a patient had an ABPM/HBPM reading of >= 150/95mmHg (ie. stage 2 hypertension)?

A
  • offer drug treatment regardless of age
19
Q

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?

A
  • 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
20
Q

What’s next for patients that fail to respond to step 4 measures?

A
  • 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
21
Q

ACE inhibitors: examples + indications

A
  • ramipril, lisinopril, perindopril
  1. hypertension
  2. chronic heart failure
  3. ischaemic heart disease
  4. diabetic nephropathy + CKD w/ proteinuria
22
Q

ACE inhibitors: mechanism of action

A
  • 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
23
Q

ACE inhibitors: side-effects?

A
  • 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,

24
Q

What is the alternative drug choice when ACEi are not tolerated due to the persistent cough?

A
  • 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
25
Q

Calcium channel blockers: examples and common indications?

A

examples: amlodipine, nifedipine, diltiazem, verapamil

  1. amolidipine + nifedipine used for first/second line tx for hypertension
  2. all ca-ch blockers used to control symptoms of stable angina
  3. diltiazem and verapamil used to control cardiac rate in ppl w/ supraventricular arrhythmias incl supraventricular tachycaria, atrial flutter and atrial fibrilation
26
Q

Calcium channel blockers: mechanism of action?

A
  • 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
27
Q

Calcium channel blockers: important side-effects?

A

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

28
Q

Thiazide diuretics: examples and indications?

A

eg. bendroflumethiazide, indapamide, chlortalidone

  1. 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
  2. thiazides also an add-on treatment for hypertension in pts whose BP not adequately controlled by a calcium-channel blocker plus an ACEi/ARB
29
Q

Thiazide diuretics: mechanism of action?

A
  • 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)
30
Q

Thiazide diuretics: important side-effects?

A
  • hyponatraemia (not usually problematic)
  • hypokalaemia
    • increased delivery of sodium to distal tubule, exchanged for potassium, increases urinary potassium losses
    • -> cardiac arrhythmias
  • impotence in men
31
Q

Alpha-blockers: indications and examples?

A

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
32
Q

Alpha-bockers: mechanism of action?

A
  • 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
33
Q

Alpha-blockers: important adverse effects?

A
  • postural hypotension
  • dizziness
  • syncope

particularly prominent after first dose (rather like with ACEi and ARBs)

34
Q

Beta-blockers: examples and indications?

A

eg. bisoprolol, atenolol, propranolol, metoprolol

  1. ischaemic heart disease
  2. chronic heart failure
  3. atrial fibrilation
  4. supraventricular tachycardia
  5. hypertension
35
Q

Beta-blockers: mechanism of action?

A
  • 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
36
Q

B-blockers: adverse effects?

A
  • 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

37
Q

What are Korotkoff sounds?

A

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.

38
Q

Hypertension Management

A

*Medicine: Cardiology & Vascular (17 decks)

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