Hypertension (renal) Flashcards
1
Q
What is hypertension?
A
- Defined as sustained BP >140/90 mmHg
- Raised BP in the systemic vascular bed
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
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
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.
5
Q
What is the most common form of hypertension?
A
Essential/primary HTN - 95% cases
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
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
8
Q
What is the flowchart/diagram for managing suspected hypertension / when should you act?
A
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
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
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
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
13
Q
What are the stages of hypertension?
A
- Optimal = < 120/80
- Normal = < 130/85
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
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
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
- hypertension
- chronic heart failure
- ischaemic heart disease
- 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
**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
26
**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
27
**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
28
**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
29
**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)
30
**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
31
**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
32
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**
33
Alpha-blockers: important adverse effects?
* postural hypotension
* dizziness
* syncope
particularly prominent after first dose (rather like with ACEi and ARBs)
34
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
35
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
36
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
37
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.
38
Hypertension **Management**
