Hypertension Flashcards

(40 cards)

1
Q

What is hypertension?

A
  • Defined as sustained BP >140/90 mmHg
  • Raised BP in the systemic vascular bed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the most common form of hypertension?

A

Essential/primary HTN - 95% cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the stages of hypertension?

A
  • Optimal = < 120/80
  • Normal = < 130/85
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

What is the step 1 pharmacological treatment of hypertension?

A
  • if pt <55yrs old: ACEi
  • pt >=55yrs old or afro-caribbean: Ca Ch blocker
20
Q

What is step 2 pharmacological treatment for hypertension?

A
  • ACEi + calcium channel blocker (A+C), OR
  • ACEi + diuretic (A+D)
21
Q

What is step 3 pharmacological treatment of hypertension?

A
  • add a thiazide diuretic (ie. A + C+ D)
  • NICE now advocate using either chlorthalidone or indapamide in preference to a convential thiazide diuretic such as bendroflumethiazide
22
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
23
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
24
Q

In summary, what is the step-wise treatment algorithm for hypertension?

25
ACE inhibitors: examples + indications
* ramipril, lisinopril, perindopril 1. hypertension 2. chronic heart failure 3. ischaemic heart disease 4. diabetic nephropathy + CKD w/ proteinuria
26
**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
27
**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,
28
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
29
**Calcium channel blockers**: examples and common indications?
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
30
**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
31
**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
32
**Thiazide diuretics**: examples and indications?
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
33
**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)
34
**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
35
**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
36
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**
37
Alpha-blockers: important adverse effects?
* postural hypotension * dizziness * syncope particularly prominent after first dose (rather like with ACEi and ARBs)
38
Beta-blockers: examples and indications?
eg. bisoprolol, atenolol, propranolol, metoprolol 1. ischaemic heart disease 2. chronic heart failure 3. atrial fibrilation 4. supraventricular tachycardia 5. hypertension
39
Beta-blockers: mechanism of action?
* b**1**-adrenoreceptors located mainly in heart * b**2**-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 b**1**-receptors
40
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