Hypertension Flashcards
When assessing a patient with newly diagnosed hypertension, what are important areas to address?
- Concomitant CVS risk factors
- Consider secondary causes if appropriate
- Assess for target organ damage
Cardiovascular risk factors
Non-modifiable: - Age - Gender (Male > female) - Family hx - Race Modifiable: - Obesity - Hypertension - Hyperlipidaemia - Alcohol - Smoking - Diabetes/ metabolic syndrome -Sedentary lifestyle
When to consider secondary causes of HTN?
- Pt <40yo
- Sudden changes in BP in previously well managed patient
- Rapid onset of HTN
- Resistant HTN, unresponsive to meds
What are secondary causes of HTN and what are features suggestive of each?
Renal artery stenosis: pulmonary oedema, widespread atherosclerosis (bruits)
Nephrotic syndrome: oedema, foamy urine
Obstructive uropathy: Prostatic enlargement, previous urethral instrumentation, renal calculi
CKD: Hx of renal impairment, uraemic sx
Coarctation of the aorta: poor feeding in children, radiofemoral delay, cold peripheries
Polycystic kidney disease: fhx of polycystic kidney, intracranial aneurysms, sub-arachnoid haemorrhages
- Hyperaldosteronism: Sx of low potassium (headaches, nocturia, parasthesiae)
- Cushing’s: Depression, wt gain, hirsutism, easy bruising, low libido, moon facies, buffalo hump, hyperglycaemia, osteporosis, etc.
- Hyperthyroidism: heat intolerance, sweating, palpitations, diarrhoea, wt loss, etc.
- Hypothyroidism: Depression, wt gain, constipation, etc.
- Hyperparathyroidism: Bone pain, parasthesiae, myalgia
- Toxic cause: OCP, NSAIDs, alcohol, other meds
Assessment of target organ damage in the hypertensive patient.
CVD
- CCF: any SOB, PND, orthopnoea, ankle oedema.
- IHD: chest pain/angina
- O/E: displaced apex beat, murmurs, thrills, heaves, pulmonary oedema
- LVH dx on ECG
Cerebrovascular Disease
- Ask about sx suggestive of CVA/TIA–> speech difficulties, visual disturbances, transient focal neurology (weakness)
- O/E: Carotid bruits, residual functional loss
Renal failure
- May be asymptomatic, pay have polyuria or oligouria, pruritus, lethargy, wt loss, nausea, vomiting, loss of appetite
Retinopathy
- Mostly asymptomatic, may have headaches or visual changes
- O/E: fundoscopy for hypertensive retinopathy
Initial investigations for patient with newly dx HTN?
- ECG: signs of previous MI, LVH (important prognostic factor), strain pattern (ST depression and T-wave inversion)
- Echo: if clinical suspicion of HF
- CXR: cardiomegaly
- Bloods: UEC with random BSL (kidney function {need to know baseline before commencing antihypertensive}, stratify risk), cholesterol, fasting BSL if diabetes suspected, LFTs if alcohol suspected, TFTs if thyroid suspected
- Urine dipstick: glycosuria, proteinuria, casts.
- Urinalysis: assessment of microalbuminuria
Physical examination on a patient with diagnosed HTN.
General Inspection:Body habitus
Vitals: BP, HR rhythm and character, RR, Temp, BMI, BSL
Hands: CRT, warm peripheries, nicotine staining
Face: Cushingoid or thyroid features
Neck: Elevated JVP, carotid bruits
Chest: Apex beat, thrills, heaves, heart sound (extra heart sounds, murmurs)
Back: auscultate lung bases for fluid
Abdo: hepatomegaly, ascites, pulsatile liver, abdominal aortic aneurysm, palpable kidneys (CKD), renal bruits
Legs: Absent femoral pulses, radiofemoral delay, peripheral oedema, peripheral pulses
Fundoscopy for hypertensive retinopathy
Neuro exam for focal neurological signs
ACE Inhibitor MOA
Blocks conversion of angiotensin I to angiotensin II, thereby reducing the effects of angiotensin II-induced vasoconstriction (reduced peripheral vascular resistance), sodium retention (reduced fluid load) and aldosterone release (reduced sodium and water retention)
ACE inhibitor Adverse effects
Common: hypotension, cough, hyperkalaemia, headaches, dizziness, fatigue, nausea, renal impairment.
Infrequent: Angiodema, anaphylaxis. Can rarely cause liver damage.
How to counsel a patient starting an antihypertensive medication.
Take the tablet at the same time every day. Most are a once daily dose.
You may feel dizzy when you start taking this medication. Get up gradually from sitting or lying to minimise this effect. Sit or lie down if you become dizzy or light-headed. For ACEI and ARB: Do not take potassium supplements while taking this medication.
ARB MOA
Competitively block binding of angiotensin II to type I angiotensin (AT1) receptors. Reducing angiotensin-induced vasoconstriction, sodium reabsorption and aldosterone release.
Side effects of ARBs.
Common: Dizziness, headache, hyperkalaemia.
Infrequent: First dose hypotension, rash, diarrhoea, dyspepsia, abnormal LFTs, muscle aches and pains.
MOA of thiazide diuretics.
Moderately potent diuretics. Inhibit reabsorption of sodium and chloride in the proximal segment of the distal convoluting tubule and produce a corresponding increase in potassium excretion –> lowers BP mostly by vasodilator effect.
Side effects of thiazide diuretics.
Common: Dizziness, weakness, muscle cramps, polyuria, hypotension, hyponatraemia, hypokalaemia, hyperuricaemia, hypochloricaemic alkalosis, hypomagnesaemia.
Calcium channel blockers MOA
Block inward current of calcium into cells in vascular smooth muscle, myocardium, and cardiac conducting system via L-type calcium channels. Dihydropyridines act mostly on smooth muscle. Verapamil has greater cardiac effect (reduces contractility, HR and contraction with less effect on smooth muscle). Diltiazem acts on both.
