case 24: the NHS health check (hypertension) Flashcards
what is the overall aim of the NHS well women/man health check
to identify evidence of CVD
to identify areas that need to be targeted with lifestyle/medical intervention
reduced risk of cardiovascular events
what is the leading cause of death of adults in the UK
CVD
what tool is used in general practice to determine someones cardiovascular risk
QRISK3
modifiable risk factors for CVD
hypertension
diet
alcohol
BMI
hypertension
physical activity
hypercholesterolaemia
smoking
non-modifiable risk factors for CVD
sex
age
family history
which blood vessels are responsible for generating the most resistance to blood flow
arterioles
which organs can be affected by systemic hypertension
eyes- hypertensive retinopathy can lead to blindness
brain- small vessel disease can progress to stroke or vascular dementia
heart- ischaemic heart disease, HF, Arrythmia (AF as a result of hypertension related atrial englargement)
kidneys- hypertensive nephropathy can lead to renal failure
what is the guidance for exercise per week
150 minutes of moderate intensity exercise per week
how to manage a high BP reading in GP
if 140/90 or higher:
take second reading
if this second reading is substantially different to the first take a third measurement (record the lowest 2 as their reading)
offer 24hr ambulatory BP to confirm diagnosis
if unable to tolerate ambulatory then can offer at home BP monitoring to confirm diagnosis
what investigations to order when investigating hypertension
Us and Es
HbA1C
Lipif profile
urine albumin:creatinine ratio (tells us whether excess protein is getting into the urine through the kidney- this indicates that the kidney is damaged and leaky
urine dip for microscopic haematuria
how to calculate rate on an ECG
300/number of large squares between 2 QRS complexes
1500/number of small squares between 2 QRS complexes
number of QRS complexes multiple by 6
sings and symptoms of organ damage from hypertension
headache
dyspnoea
visual changes
chest pain
sensory/motor problems
the 2 classifications of hypertension
primary (essential) hypertension
secondary hypertension (there is an underlying often reversible cause)
adrenal causes of secondary hypertension
pheochromocytoma (adrenaline secreting tumour)
hyperaldosteronism
cushings
renal causes of secondary hypertension
renal artery stenosis
CKD
PCKD
nephritic and nephrotic syndrome
thyroid causes of secondary hypertension
hyperthyroidism
hyperparathyroidism
other causes of secondary hypertension
contraction of aorta
obstructive uropathy
obstructive sleep apnoea
oral contraceptives
chronic alcohol use
NSAIDs
illicit drugs (cocaine) can cause pseudohypertension)
preeclampsia
what type of hypertrophy in the heat can you see with hypertension
LVH
systolic BP vs diastolic BP
systolic= pressure when heart is contracting
diastolic= pressure when heart relaxing
what diet is particularly bad for hypertension
high salt
signs of pheochromocytoma
sweating
headaches
palpitations
first line treatment for hypertension
for under 55/diabetic= ACE inhibitor
for over 55/black= calcium channel blocker
what is the first line agent used in a hypertensive emergency
labetalol (beta blocker)
what electrolyte abnormality may be seen with ACEi
hyperkalaemia
definition of refractory hypertension
the inability to achieve BP control despite maximum tolerated doses of at least 5 antihypertensive medications (including diuretics)
symptoms suggesting a hypertensive emergency
focal neurological symptoms- agitation, delirium, stupor (near-unconsciousness), visual disturbances and headache (SIGNS OF INTRACRANIAL BLEED)
vomiting, headache, agitation, delirium (SIGNS OF RAISED ICP)
visual disturbance (SIGN OF RAISED ICP/HYPERTENSIVE RETINOPATHY)
chest pain (SIGN OF MI/AORTIC DISSECTION
back pain (SIGN OF AORTIC DISSECTION)
SOB (SIGN OF PULMONARY OEDEMA)
how can IgA nephropathy cause hypertension
IgA antibodies circulate kidneys causing inflammation
this affects the kidneys ability to filter blood
inflammation allows blood and protein to lead through the glomeruli into the urine, and a damaged kidney cannot remove the fluid and produce urine so therefore the BP rises
criteria for diagnosing an MI
must have at least 2 of the 3:
chest pain
ischaemic changes on ECG
biochemical evidence of ischaemia (raised troponin)
which drugs may precipitate a hypertensive emergency
amphetamines
cocaine
monoamine oxidase inhibitors (MAOI)
recent discontinuation of hypertensive agents
hypertensive urgency vs hypertensive emergency
urgency= BP over 180/110 but there is no evidence of ACUTE end organ damage
emergency = there needs to be evidence of ACUTE end organ damage
how quickly does hypertensive urgency need to be managed
in hours-days
management of asymptomatic hypertensive urgency
can start oral antihypertensives and discharge for outpatient management (needs early follow-up in ambulatory care/see GP in 1-2 days)
management of hypertensive emergencies
admission and close monitoring
IV antihypertensives (nitroglycerine- GTN or labetolol)
after around 8-24hrs IV medication can be tapered down and oral medication given instead
recurrent type of what infection can lead to hypertension
recurrent UTIs
the kidneys can become chronically scarred and damaged meaning they are not able to remove fluid from the blood into the urine, therefore the autoregulatory mechanisms to increase GFR become deranged and lead to hypertension as a result
(potential cause of secondary hypertension) examination finding of contraction of the aorta
unequal BP measurements in both arms and radio-femoral delay
(potential cause of secondary hypertension) examination finding of renal artery stenosis
renal bruits
(potential cause of secondary hypertension) examination finding of PDKD
ballotable kidneys
(potential cause of secondary hypertension) examination finding of vasculitis
vasculitic rash
(potential cause of secondary hypertension) examination finding of pheochromocytoma
tachycardia flushing and sweating
(potential cause of secondary hypertension) examination finding of acromegaly
enlarged facial features
what is the most common cause of secondary hypertension in young adults
primary hyperaldosteronism
in the RAAS system what detects a reduction in blood pressure
it is detected by the juxtaglomerular apparatus (near the afferent arteriole)- this secretes renin
the RAAS system
renin coverts angiotensinogen to angiotensin I
angiotensin I is converted to angiotensin II via ACE enzyme
effects of angiotensin II
it is a vasoconstrictor so increases systemic vascular resistance and therefore BP
is also causes aldosterone production from the adrenal cortex- this leads to salt retention and therefore water retention which also increases the BP
in primary hyperaldosteronism what happens to renin levels
aldosterone is high therefore renin is low (due to negative feedback)
what causes primary hyperaldosteronism
there is an adrenal cause
1/3= benign adenoma of the adrenal gland (Conns syndrome)
2/3= bilateral hyperplasia of the adrenal glands
what causes secondary hyperaldosteronism
the cause is outside of the adrenal glands
there is excessive stimulation of RAAS pathway, with high renin levels triggering high aldosterone production
causes:
reduced blood flow to kidneys- renal artery stenosis, fibromuscular dysplasia
reduced cardiac output- CCF
reduced circuiting volume- cirrhosis, ascites
hyperaldosteronism and Na+ and K+
aldosterone acts on epithelial sodium channels (ENaC) in the collecting tubules leading to sodium reabsorption
therefore K+ is lost in urine to try and maintain the electrical neutrality
(will have low K+, and Na+ can be on higher side)
what investigation would you do to distinguish between benign adrenal adenoma or bilateral adrenal hyperplasia
MRI of adrenals
management of bilateral adrenal hyperplasia
spironolactone- mineralocorticoid receptor antagonist, reduced salt and therefore water retention so decreases the circulating volume
what diet is recommended to all patients with hyperaldosteronism
salt restriction
follow up after prescribing spironolactone for hyperaldosteronsim
review in 2 weeks to repeat renal profile and K+
pneumonia vs pulmonary oedema on CXR
look similar but pneumonia will not be as symmetrical as a pleural effusion
what simple test can you do for pre-clampsia first
urine dip (will see proteinuria)
