unit 12 hypertension

• list modifiable and non-modifiable risk factors for essential hypertension?

  • Modifiable - Smoking, Alcohol, Exercise, Diet, Stress

  •Non-modifiable:

  ·Age: older age increases risk

  ·Ethnicity: African-Caribbean and South-Asian descent are at increased risk of high ABP

  ·Family history: having one or more close relatives with hypertension increases risk
• examination of a patient with hypertension:

  • most only finding is a high BP

  •Other patients' signs relate to cause: abdominal bruit in renal artery stenosis,

  -delayed femoral pulses in coarctation of aorta,

  -hypertensive heart disease could cause loud second heart sound, left ventricular heave, fourth heart sound, and retinal abnormalities.
• Retinal abnormalities grading:

  •Grade 1 – increased tortuosity and reflectiveness of the retinal arteries (silver wiring)

  •Grade 2 – grade 1 plus arteriovenous nipping

  •Grade 3 – grade 2 plus flame-shaped haemorrhages and soft ‘cotton wool’ exudates

  •Grade 4 – grade 3 plus papilloedema.

  
• comparison of a normal and pathological fundus in HT:

  
• ECG findings:

  • Left Ventricular Hypertrophy: One of most common findings. Increased voltage amplitudes in QRS complexes (wide QRS complex). In leads facing left side of the heart (I, aVL, V5, V6
  • Left Atrial Enlargement (LAE): Wide and notched P wave P mitrale). Leads II, III, and aVF
  • ST-T Changes: ST-segment depression or T-wave inversion. changes may not be specific to hypertension and can also be influenced by other cardiovascular conditions
  • Arrhythmias: Atrial fibrillation = Irregularly irregular R-R intervals and absence of distinct P waves.
• dx HT: by blood pressures

  1. BP ≥140/90 mmHg take a second measure
  2. BP 180/120 ≥ 140/90 mmHg offer ABPM to confirm diagnosis
  3. BP ≥180/120 mmHg -> consider same-day referral
  4. • if retinal damage or life-threatening symptoms -> refer
  5. • if no serious signs/symptoms -> more investigations ± immediate treatment
• how to stage different types of HT:

  
• Management of severe hypertension

  • malignant or severe hypertension (diastolic BP >140 mmHg), admitted to hospital for treatment.

  • aim to reduce diastolic BP slowly (over 24–48 hours) to 100–110 mmHg with oral antihypertensives, e.g. atenolol or amlodipine.

  • Sublingual and intravenous antihypertensives may produce a sever fall in BP, leading to cerebral infarction

  • When rapid control of BP is required (e.g. aortic dissection), the agent of choice is intravenous sodium nitroprusside or labetalol.
• Non-pharmacological management:

  • Weight reduction (aim for body mass index (BMI) <25 kg/m 2 )

  • Low-fat and low saturated fat diet

  • Low-salt diet

  • Limited alcohol consumption (<14 units per week)

  • Dynamic exercise (at least 30 minutes brisk walk per day)

  • Increased fruit and vegetable consumption

  • Reduce cardiovascular risk by stopping smoking and increasing oily fish consumption.
• Indications for tx based on BP readings:

  
• why is the NICE tx algorithm useful:

  • contraindications and indications for drugs
  • glycaemic control for diabetics
  • statins used to help with HT management
  • start with one drug and usually more drugs are added
• you have a 70yr M, black patient what is the treatment pathway you would follow from NICE if they had PROGRESSING symptoms of hypertension

  start them on calcium channel blockers (C) -> then to ACEI with the calcium channel blockers (A+C) -> then calcium channel blockers, ACEI and THIAZIDE-type diuretics (A+C+D) -> further tx of hypertension (further diuretic like spironolactone, alpha-blockers, beta blockers) for this seek specialist advie
• you have a 70yr M, black patient what is the treatment pathway you would follow from NICE if they had PROGRESSING symptoms of hypertension

  start them on calcium channel blockers (C) -> then to ACEI with the calcium channel blockers (A+C) -> then calcium channel blockers, ACEI and THIAZIDE-type diuretics (A+C+D) -> further tx of hypertension (further diuretic like spironolactone, alpha-blockers, beta blockers) for this seek specialist advice

  
• your 18yrs, white patient was coughing and could not tolerate it. You think this is an effect of a medication, what is the medication and what do you do?

  2 indicators

  young and white -> ACEI

  ACEI common side effect -> dry, tickly and bothersome cough

  switch the medication from an ACEI to an Angiotensin II RecepTor ANtagonist (ARTAN)
• Angiotensin II receptor antagonists (ARBs) -> SELECTIVELY block receptors for angiotensin II (ang II type 1 receptor - aka the AT1 receptor)
• your patient is a young, white male and is to be started on hypertensive drugs he has a diagnosis in his Hx which means you cannot prescribe what you would have normally according to the NICE pathway. What is his diagnosis, why can you not provided that drug and what would be the risk if you did?

  his dx is RENAL ARTERY STENOSIS -> narrowing of the renal artery

  ACEI is what he should have been prescribed BUT -> the effect of ACEI on the RAAS system can inadvertently decrease the blood flow to the kidneys putting the patient at risk of renal ischaemia and infarction
• ACEI have two paradoxical effects, what are the targets and effects of these?

  1. ACE enzymes -> inhibit ACE and prevent the conversion of Ang I to Ang II -> inhibit the RAAS (which causes vasoconstriction) -> leads to vasodilation
  2. prevent the breakdown of Bradykinin -> acts on endothelium of smooth muscle -> bradykinin is a vasodilator so then the blood vessels are in a constant state of vasodilation
• the patient in the PBL case is prescribed amlodopine, explain/describe the MOA of amlodopine:

  • amlodopine is a CCB acts on calcium channels
  • peripheral arterial vasodilator
  • is a dihydropyridine (DHP) -> possesses vascular selectivity (acts more on the vasculature than heart)
  • DHP calcium ANTAGONIST
  • prevents channels opening and allowing for influx of Ca across cell membrane
  • decreased Ca in the cells the vascular smooth muscle cells cannot contract
  • the vascular smooth muscle is in a relaxed state -> vasodilation
  • this decreases total peripheral resistance
  • decreasing blood pressure
• You patient is switched from ramapril to Valsartan due to complaints of (x), what is the mechanism of action of valsartan and why might they have been switched?

  may been switched due to dry, itchy and bothersome cough

  • ARB -> AT1 receptor antagonist
  • this prevents the Ang II from binding and exerting hypertensive effects (liek vasoconstriction, synth of aldoesterone and ADH, increased renal Na+ reabsorption)
  • lower TPR -> lower BP
  • Also ARBs cause a blockade on AT1 R this inhibits the negative feedback signalling in RAAS -> lowers BP
• what demographic of patient would you prescribe ramipril to for the tx of hypertesion?


  see the card
• what causes the characteristic dry, itchy and bothersome cough in ACEI?

  • the prevention of the breakdown of bradykinin
  • ACE enzymes breakdown the bradykinin normally as they all have been inhibited this function is inhibited too
• Your patient is struggling with managing their hypertension with ACEI and CCB so you decide to put them on a thiazide type diuretic, explain why?

  • It is the next stage on what is recommended by NICE
  • Thiazides are prefered over loops as : they have a longer activity time, they are cheaper, they are less likely to cause severe diuresis (severe urine produciton)
• After putting your patient on thiazide-type diuretics for their hypertension you look at their electrolytes, they have experienced side effects of thiazide-type diuretics. How have their electrolytes changed?

  • HYPOkalemia -> low k+
  • HYPOnatremia -> low Na+
  • HYPERcholesteremia -> high cholesterol
  • HYPERurecaemia -> high uric acid levels, may percipitate gout

  you may also see IMPAIRED GLUCOSE TOLERANCE
• A young patient was given a drug to tx their hypertension this was changed due to a side effect to another drug this drug was then changed to their current medication, what where they precribed across the case?

  • 1st - ACEI which was changed due to coughing side effect possibly
  • 2nd - Ang II Receptor Antagonist (ARB) - patients can present with intolerance OR contraindications to ACEI and ARBS so given...
  • 3rd - BETA BLOCKERS - to treat the hypertension -> reduce renin production and sympathetic activity
• A patient is prescribed Beta blockers for their hypertension, what could be the reasons for this?

  • the patient is intolerant or contraindicated for ACE or ARBs
  • the patient is a woman of childbearing age
  • the patient is young and its okay
  • there is evidence of increased sympathetic drive in the patient (beta blockers can reduce sympathetic activity)
• what are side effects of beta blockers?

  all of these kind of link to sympathic system

  • cold extremities
  • bradycardia
  • bronchospasm
  • fatigue and weakness
• what are examples of some agents that may be used in treating hypertension? (NOT ACEI, ARBs/ Angiotension II Receptor Antagonists, CCB or beta blockers)

  • Alpha-blockers
  • hydralazine
  • Aldosterone antagonists (spironolactone)
  • Centrally-acting agents (clonidine)
• A patient comes in with nose bleeds, headaches, dizziness and a littel visual disturbances. He is referred from his optician to see the doctor, they believe he has Hypertension.

  what should the doctor do in the Hx?

  • take account of symptoms, these can be seen in hypertension
  • take a family history - believed genetic link
  • it is a man but if they were female are they pregnant - pre-eclampsia?
  • SHx - exercise, smoking, drinking, ethnicity, age, weight/BMI, stress, drugs
  • do they already have a dx? Are they adhering to anti-hypertensives?
• A patient comes in with nose bleeds, headaches, dizziness and a littel visual disturbances. He is referred from his optician to see the doctor, they believe he has Hypertension.

  what is really important to consider in the differential dx?

  it could be essential/ primary hypertension but just because they are hypertensive it does not mean that's it - need to investigate and ask about symptoms that could lead to the diagnosis of secondary hypertension (hypertension secondary to another pathology)
• A patient comes in with nose bleeds, headaches, dizziness and a littel visual disturbances. He is referred from his optician to see the doctor, they believe he has Hypertension.

  which types of BP investigations/measurents can be carried out?

  • office/surgery - taken at a healthcare setting
  • home - patient takes their own and reports, could be for: long-term, engaging the patient, identifying phenotypes
  • ambulatory - portable device worn, measures BP over 24hrs, can measure a daytime and nocturnal BP - better diagnosis and recommended for diagnosis in the UK
• give 2 causes of a Renal secondary hypertension:

  • Acute glomerulonephritis
  • Chronic renal disease
  • Polycystic disease
  • Renal artery stenosis
  • Renal vasculitis
  • Renin-producing tumours
• give 2 causes of endocrine secondary hypertension:

  • Adrenocortical hyperfunction (Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, liquorice ingestion)
  • Exogenous hormones (glucocorticoids, oestrogen [including pregnancy-induced and oral contraceptives], sympathomimetics and tyramine-containing foods, monoamine oxidase inhibitors)
  • Pheochromocytoma
  • Acromegaly
  • Hypothyroidism (myxoedema)
  • Hyperthyroidism (thyrotoxicosis)
  • Pregnancy-induced (pre-eclampsia)
• give 2 CVS causes of secondary hypertension:

  • Coarctation of the aorta
  • Polyarteritis nodosa
  • Increased intravascular volume
  • Increased cardiac output
  • Rigidity of the aorta
• give 2 examples of neurological causes of secondary hypertension:

  • Psychogenic
  • Increased intracranial pressure
  • Sleep apnoea
  • Acute stress, including surgery
• you take a histological slide of a (severely) hypertensive patient, what can you see?

  hyperplastic arteriosclerosis

  • see 'oninon-skinning'
  • as a response to the constant hypertension, the smooth muscle cells proliferate concentrically and thickens the layer under then intense and prolonged BP

  
• you take a histological slide of a hypertensive patient, what can you see:

  hyaline arteriosclerosis - deposition of proteinaceous material (can see its pink, eosin=protein) hyalinizes the walls of the blood vessels, thickens the walls, lumen is noticeably narrowed

  
• A patient comes in with nose bleeds, headaches, dizziness and a littel visual disturbances. He is referred from his optician to see the doctor, they believe he has Hypertension.

  after doing a Hx how would you calculate the risk to the patient?

  QRISK3:

  Your QRISK score will tell you whether you are at low, moderate or high risk of developing CVD in the next 10 years. Low risk – QRISK3/less than 10% means you have less than a one in ten chance of having a stroke or heart attack in the next 10 years. Moderate risk – QRISK3 of 10-20% and high risk >20%
• A patient comes in with nose bleeds, headaches, dizziness and a littel visual disturbances. He is referred from his optician to see the doctor, they believe he has Hypertension.

  which lab investigations would you carry out?

  • U&Es - Na increases BP
  • Urine - blood and protein
  • ECG - left ventricular heave or ischaemia
  • blood glucose - (high BG -> artherosclerosis, narrows vessels, increased BP)
  • serum lipids/lipid profile - (seen to be high in hypertension, increases the risk of other CVD, LDL cholesterol upregulates AT1 receptor, increased BP)
• A patient has tachycardia and has attacks of sweating, what is their hypertension most likely secondary to?

  Phaemochromocytoma
• Malignant/accelerated HT:

  • severely high BP
  • when untreated results in end-organ failure
  • fibroid necrosis of the vessel walls