Hypertension Flashcards
Is a single measurement of ↑ BP sufficient to diagnose Hypertension?
NO!!
What is the process for determing a patient’s BP in clinc?
- Measure BP in both arms
- If difference in BP is > 20 mmHg –> repeat measurements
- If difference remains > 20 mmHg on the 2nd measurement –> measure subsequent BPs in the arm with the higher BP
- If BP is measured as 140/90 or higher –> take 2nd measurement during consultation
- If 2nd measurement is substantially different from the 1st –> take a 3rd BP measurement
- Record the lower of the last 2 measurements (2nd or 3rd) as the BP
How do you confirm a diagnosis of HTN after a recorded clinic BP of 140/90 or higher?
- If clinic BP is 140/90 or higher –> offer ABPM (ambulatory blood pressure monitoring) to confirm diagnosis, ensure that:
- At least 2 measurements per hour - during ususal waking hours
- Use average of at least 14 measurements to confirm diagnosis
- If pt unabale to tolerate ABPM –> HBPM (home blood pressure monitoring), ensure that:
- For each BP recording, 2 consecutive measurements are taken, at least 1 minute apart and with the person seated
- BP is recorded twice/day (ideally in the morning and evening)
- BP recording continues for at least 4 days (ideally for 7 days)
- Discard measurements taken on the 1st day + use the average value of all the remaining measurements to confirm a diagnosis of HTN
What are the grades for severity of Hypertension?
- Isolated Systolic HTN = >140 / >90
-
Grade 1 (mild) = clinic BP 140-159 / 90-99
- and ABPM daytime average / HBPM average of > 135/85
-
Grade 2 (moderate) = clinic BP >/= 160
- and ABPM / HBPM average of >/= 150/95
- Grade 3 (severe) = >180 / >110

For what 2 reasons is staging the severity of HTN important?
Severity grade impacts:
- Risk stratification of patient
- Guides next step in management
When a patient’s hypertension is stage 3 (severe) it can result in hypertensive emergency - what is this also known as? What does it involve?
Also known as Malignant Hypertension it is severe hypertension (BP ≥ 180/110 mmHg) WITH target organ damage
- Very high BP - systolic >180 or diastolic >120
-
Aetiology:
- Vasocontrictors intiate abrupt ↑ systemic vascular resistance
- Results in –> endothelial injury, deposition of platelets/fibrin, ischaemia –> prompts further release of vasoactive substances
- Involves organ damage:
- Encephalopathy - ↑ BP in cerebral arteries causes cerebral oedema –> ↑ ICP –> neurological disturbances / change in conciousness
-
Symptoms / Signs:
- Eye signs (opthalmoscopy):
- Papilloedema (must be present for diagnosis to be made)
- Retinal bleeding
- Cotton wool spots
- Chest pain - crushing/pressure
- Extreme ↑ BP
- SoB
- Pulmonary oedema
- Numbness/weakness of face/limbs - changes in power/tone
- Blurred vision
- Change in GCS/mental status:
- Anxiety, confusion, ↓ concentration, fatigue, lethargy
- Signs of ↑ ICP:
- Headache
- Nausea + vomiting
- Seizure
- Eye signs (opthalmoscopy):
-
Epidemiology:
- M > F
- Affects 1% of those with HTN
-
Management:
- BP needs to be ↓ within a few minutes up to 2hrs using IV antihypertensives
- Labetalol (alpha and beta adrenergic antagonist) –> ↓ peripheral vascular resistance via vasodilation (in short term use) + ↓ HR (in long term use)
- Nicardipine (Ca2+ channel blocker) - more selective for cerebral and coronary vessels than other Ca2+ antagonists –> causes vasodilation, ↓ BP
Severe hypertension (BP ≥ 180/110 mmHg) WITHOUT target-organ damage is defined as what?
Hypertensive urgency (not emergency)
- BP needs to be ↓ gradually over 24-48 hrs with ORAL antihypertensives (as opposed to minutes-2hrs and IV in hypertensive emergency)
What factors affect Cardiac Output?
CO = HR x stroke volume
What factors affect blood pressure?
MAP (mean arterial blood pressure) = CO x PVR (peripheral vascular resistance)
Which 4 organs in the body are common sites of damage/modification as a result of high BP?
-
Eyes
- Retinopathy/maculopathy
-
Brain
- Strokes
- Microaneurysms
-
Heart
- Compensative/adaptive cardiomegaly
- Ischaemic heart disease
- CCF (followed by pulmonary HTN)
- Sudden death
-
Kidneys
- Hypertensive nephropathy (HTN causing kidney pathology)
- Nephron arteriosclerosis –> ischaemia –> kidney atrophy (small kidneys)
- Glomerular ischaemia due to renal artery stenosis caused by plaques or stiffening
- Glomerular HTN can result in glomerular damage –> causing blood and protein leakage into urine
What 4 signs on the retina can be produced by high BP (seen on Opthalmoscopy)?
-
Papilloedema - optic disc swelling
- Venous engorgement (often 1st sign)
- Blurring of optic disc margin
- Paton’s lines - concentric/radial lines cascading from optic disc
-
Flame Haemorrhage - intraretinal haemorrhage (looks like bruise)
- Feather/flame shape indicates bleed occurs at level of nerve fibre layers
-
Hard exudates - small white/yellowish lipid deposits with sharp margins, which form due to capillary leakage (i.e. ↑ retinal vascular permeability)
- Often appear; waxy / shiny / glistening
-
Cotton wool spots - white spots which represent swelling of retinal nerve fibres due to microinfarctions
- Usually near optic disc

What are the 2 causes of Primary Hyperaldosteronism?
What metabolic disturbance does it cause?
- Conn’s Syndrome = Unilateral Aldosterone producing adenoma (~30% of cases) –> adrenalectomy
- Bilateral adrenal hyperplasia (~70% of cases) –> spironolactone
High aldosterone –> ↓ K+ and ↓ H+ but ↑ Na+ and ↑ BP = Hypokalaemic Alkalosis
Features:
- Alkalosis
- Hypertension (↑ BP)
- Hypokalaemia
- Muscle weakness, hypotonia
- Palpitations
- Hypokalaemia induced nephrogenic DI: polyuria + polydipsia
- ECG:
- T-wave flattening or inversion
- Prolonged PR interval
- Apparent Long QT - it only appears to shown long QT, but due to fusion of the T+U waves it is actually the QU segement not QT being viewed
- ST depression
- U-waves
What is Addison’s Disease?
Addison’s Disease = autoimmune destruction of adrenal glands causing –> hypoadrenalism (↓ cortisol + ↓ aldosterone)
Causes of Primary Hypoadrenalism:
- 80% of primary hypoadrenalism = Addison’s Disease
- TB, metastases, meningococcal septicaemia, HIV, antiphospholipid syndrome
Treatment:
- Ongoing: hydrocortisone (glucocorticoid) + fludrocortisone (mineralocorticoid)
- Mineralocorticoid dose is impacted by mineralocorticoid activity of glucocorticoid given
- Adrenal Crisis: 50-100mg IV every 6 hours for 1-3 days
Features:
- Lethargy + weakness
- Anorexia
- Weight loss
- Hyperpigmentation (especially palmar creases)
- ↓ BP
- ‘Salt-craving’ due to hyponatraemia
- Nausea / vomiting
- Hyperkalaemia + acidosis
- Hypoglycaemia
- Vitiligo
How do you test for Addison’s Disease?
Short SynACTHen Test
- Administer tetracosactide (synacthen) 250 micrograms IV/IM
- Check blood cortisol at time 0 and +30 mins
- Cortisol at +30min should be > 600 nmol/L (in normal person)
- If cortisol < 600 nmol/L –> Addison’s Disease
What % of cases are essential/primary hypertension vs secondary hypertension?
- Essential/primary hypertension = 90-95%
- Cause unknown
- Secondary hypertension = 5-10%
- This is hypertension due to an underlying pathology
What are some common causes of Secondary Hypertension?
Causes + some signs:
-
Renal diseases: - ↑ creatinine + abnormal urinalysis
- Polycystic kidney disease (PKD)
- Chronic glomerulonephritis
- Pyelonephritis
- Renovascular disease e.g. renal artery stenosis
- Presence of atherosclerotic disease elsewhere
- Asymmetry in renal size of > 1.5cm (without other cause)
- Renal artery bruit
-
Endocrine diseases:
- Cushing’s Syndrome - moon face, striae, central obesity, proximal muscle weakness, facial plethora, thin skin, bruising, ↓ libido
-
Primary hyperaldosteronism: (most common cause of secondary hypertension)
- Conn’s syndrome
- Bilateral idipathic adrenal hyperplasia
- Pheochromocytoma
-
Neurological disease:
- Brainstem lesion
- Space occupying lesion –> ↑ ICP –> ↑ resistance to cranial bloodflow –> heart ↑ BP to compensate
-
Drugs:
- Steroids
- MAO inhibitors (antidepressants)
- COCP
- NSAIDs
-
Pregnancy:
- Pre-eclampsia
-
Aorta coarctation
- Diminished femoral or left brachial pulse with high BP in right arm (subject to location of coarctation)
- Obesity
-
Sleep apnoea - ↓ oxygen supply to body –> heart tries to compensate by ↑ BP (noctural ↑BP)
- Obese men, loud snoring, daytime somnolence, fatigue, morning confusion
- Licorice (excessive consumption)
What is a Pheochromocytoma?
A neuroendocrine tumour of the chromaffin cells of the adrenal medulla
- Hypertension + Hyperglycaemia are common
- 90% unilateral vs 10% bilateral
- 10% present without hypertension
- FHx of such tumours is suggestive of –> Multiple endocrine neoplasia syndromes (MENs)
What lifestyle changes can be suggested to patients with Hypertension?
Those in bold ↓ risks associated with HTN
- Smoking cessation
- Diet:
- ↓ salt / switch to low-salt
- ↓ caffeine
- ↓ Fat
- ↓ Alcohol intake
- ↓ weight
- Exercise
- Find relaxing hobbies
When should Pharmacological antihypertensive treatment be offered for the following situations:
- Patient < 80yrs old with stage 1 HTN (BP 140-159/90-99) or ABPM/HBPM >= 135/85 mmHg
- Patient with stage 2 HTN (BP 160-179/100-109) or ABPM/HBPM >= 150/95 mmHg
- Offer antihypertensive in pts < 80yrs with stage 1 HTN who have 1 or more of the following:
- Target organ damage
- Established CVD
- Renal disease
- Diabetes
- 10-year cardiovascular risk > 10%
- Offer antihypertensive in everyone with stage 2 HTN

Describe the NICE pathway for choosing what type of antihypertensive medication to prescribe:
- What is the cut-off age that influences drug choice
- What ethnicity influences drug choice
- What type of diuretic is involved in the pathway
- What drug can be used instead of an ACE-I e.g. if patient is intolerant due to cough?
- What should you do if patient has grade/stage 1 hypertension and is < 40yrs?
- 55yrs is the cut-off for guiding drug choice
- Black African or Afro-Caribbean origin influence drug choice
- Thiazide [-like]
- Angiotension II receptor blocker
- Refer to specialist - if no evidence of target organ damage, CVD, renal disease or diabetes
Common Antihypertensive drugs include Ca2+ channel blockers, Thiazide diuretics and ARBs
- What are the common side effects of each drug?
- What are some important notes, if any for each drug?
-
Ca2+ channel blockers: - side effects for dihydropyridines (end in -pine)
- Ankle oedema
- Headache
- Flushing
-
Thiazide-diuretics:
- Hyponatraemia
- Hypokalaemia
- Dehydration
- Postural hypotension
- ↑ Urea reabsorption –> ↑ Uric acid –> can worsen gout
- Agranulocytosis (rare)
- Notes:
- Thiazides actually have very weak diuretic action
-
ARBs (end in -sartan)
- Hyperkalaemia
- Note: avoid in pregnancy
When is Methyl-dopa used to treat HTN?
In Pregnant Women
- Methyl-dopa = compeititve inhibitor of DOPA decarboxylase (which converts L-DOPA –> dopamine)
- Dopamine is a precursor for noradrenaline + adrenaline
- Methyl-dopa ↓ dopaminergic + adrenergic neurotransmission –> vasodilation + ↓ BP
The plan after a diagnosis of HTN is to 1) Assess CV risk 2) Assess target organ damage. To do this all pts with HTN should be offered which tests?
-
Urine tests: - check for renal disease
- Urine sample for albumin:creatinine ratio (tests for proteinuria)
- Urine dipstick for haematuria
-
Blood tests:
- Serum glucose + HbA1c
- U+Es: Electrolytes, creatinine, eGFR
- Serum cholesterol and HDL and LDL
-
Fundoscopy:
- Hypertensive retinopathy
- 12-lead ECG
- Check for left ventricular hypertrophy or ischaemic heart disease
With treatment what should a patient’s target BP be for;
- Age < 80yrs
- Age > 80yrs
-
< 80yrs:
- < 140/90 via clinic BP
- < 135/85 mmHg via ABPM or HBPM
-
> 80yrs
- < 150/90 via clinic BP
- < 145/95 mmHg via ABPM or HBPM

What is the ‘normal’ range for Blood Pressure?
- Most healthy people have a BP between 90/60 and 140/90 mmHg
- Some sources describe being between 120/80 and 140/90 as ‘pre-hypertensive’
- BP varies depending on; Age, gender and physiology
In which 2 populations of people is HTN more common?
- Black Afro-carribean
- Elderly (BP rises with age, up to the 7th decade)
What are the most important side-effects of ACE-Is?
-
ACE-inhibitors (end in -pril):
- Cough
- Angioedema - swelling of lower layer of skin; face, tongue, larynx, abdomen, arms, legs
- Hyperkalaemia
- Agranulocytosis (rare)
- Notes:
- Avoid in pregnancy
- Renal function check at 2-3 weeks due to risk of ↓ renal function in renal artery stenosis (up to 30%↑ in creatinine and ↑ in potassium expected)