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Semester 2 (3rd year) > case 24: the NHS health check (hypertension) > Flashcards

case 24: the NHS health check (hypertension) Flashcards

1
Q

what is the overall aim of the NHS well women/man health check

A

to identify evidence of CVD
to identify areas that need to be targeted with lifestyle/medical intervention
reduced risk of cardiovascular events

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2
Q

what is the leading cause of death of adults in the UK

A

CVD

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3
Q

what tool is used in general practice to determine someones cardiovascular risk

A

QRISK3

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4
Q

modifiable risk factors for CVD

A

hypertension
diet
alcohol
BMI
hypertension
physical activity
hypercholesterolaemia
smoking

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5
Q

non-modifiable risk factors for CVD

A

sex
age
family history

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6
Q

which blood vessels are responsible for generating the most resistance to blood flow

A

arterioles

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7
Q

which organs can be affected by systemic hypertension

A

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

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8
Q

what is the guidance for exercise per week

A

150 minutes of moderate intensity exercise per week

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9
Q

how to manage a high BP reading in GP

A

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

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10
Q

what investigations to order when investigating hypertension

A

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

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11
Q

how to calculate rate on an ECG

A

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

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12
Q

sings and symptoms of organ damage from hypertension

A

headache
dyspnoea
visual changes
chest pain
sensory/motor problems

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13
Q

the 2 classifications of hypertension

A

primary (essential) hypertension

secondary hypertension (there is an underlying often reversible cause)

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14
Q

adrenal causes of secondary hypertension

A

pheochromocytoma (adrenaline secreting tumour)
hyperaldosteronism
cushings

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15
Q

renal causes of secondary hypertension

A

renal artery stenosis
CKD
PCKD
nephritic and nephrotic syndrome

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16
Q

thyroid causes of secondary hypertension

A

hyperthyroidism
hyperparathyroidism

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17
Q

other causes of secondary hypertension

A

contraction of aorta

obstructive uropathy

obstructive sleep apnoea

oral contraceptives

chronic alcohol use

NSAIDs

illicit drugs (cocaine) can cause pseudohypertension)

preeclampsia

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18
Q

what type of hypertrophy in the heat can you see with hypertension

A

LVH

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19
Q

systolic BP vs diastolic BP

A

systolic= pressure when heart is contracting
diastolic= pressure when heart relaxing

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20
Q

what diet is particularly bad for hypertension

A

high salt

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21
Q

signs of pheochromocytoma

A

sweating
headaches
palpitations

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22
Q

first line treatment for hypertension

A

for under 55/diabetic= ACE inhibitor

for over 55/black= calcium channel blocker

23
Q

what is the first line agent used in a hypertensive emergency

A

labetalol (beta blocker)

24
Q

what electrolyte abnormality may be seen with ACEi

A

hyperkalaemia

25
Q

definition of refractory hypertension

A

the inability to achieve BP control despite maximum tolerated doses of at least 5 antihypertensive medications (including diuretics)

26
Q

symptoms suggesting a hypertensive emergency

A

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)

27
Q

how can IgA nephropathy cause hypertension

A

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

28
Q

criteria for diagnosing an MI

A

must have at least 2 of the 3:

chest pain

ischaemic changes on ECG

biochemical evidence of ischaemia (raised troponin)

29
Q

which drugs may precipitate a hypertensive emergency

A

amphetamines

cocaine

monoamine oxidase inhibitors (MAOI)

recent discontinuation of hypertensive agents

30
Q

hypertensive urgency vs hypertensive emergency

A

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

31
Q

how quickly does hypertensive urgency need to be managed

A

in hours-days

32
Q

management of asymptomatic hypertensive urgency

A

can start oral antihypertensives and discharge for outpatient management (needs early follow-up in ambulatory care/see GP in 1-2 days)

33
Q

management of hypertensive emergencies

A

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

34
Q

recurrent type of what infection can lead to hypertension

A

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

35
Q

(potential cause of secondary hypertension) examination finding of contraction of the aorta

A

unequal BP measurements in both arms and radio-femoral delay

36
Q

(potential cause of secondary hypertension) examination finding of renal artery stenosis

A

renal bruits

37
Q

(potential cause of secondary hypertension) examination finding of PDKD

A

ballotable kidneys

38
Q

(potential cause of secondary hypertension) examination finding of vasculitis

A

vasculitic rash

39
Q

(potential cause of secondary hypertension) examination finding of pheochromocytoma

A

tachycardia flushing and sweating

40
Q

(potential cause of secondary hypertension) examination finding of acromegaly

A

enlarged facial features

41
Q

what is the most common cause of secondary hypertension in young adults

A

primary hyperaldosteronism

42
Q

in the RAAS system what detects a reduction in blood pressure

A

it is detected by the juxtaglomerular apparatus (near the afferent arteriole)- this secretes renin

43
Q

the RAAS system

A

renin coverts angiotensinogen to angiotensin I

angiotensin I is converted to angiotensin II via ACE enzyme

44
Q

effects of angiotensin II

A

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

45
Q

in primary hyperaldosteronism what happens to renin levels

A

aldosterone is high therefore renin is low (due to negative feedback)

46
Q

what causes primary hyperaldosteronism

A

there is an adrenal cause

1/3= benign adenoma of the adrenal gland (Conns syndrome)

2/3= bilateral hyperplasia of the adrenal glands

47
Q

what causes secondary hyperaldosteronism

A

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

48
Q

hyperaldosteronism and Na+ and K+

A

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)

49
Q

what investigation would you do to distinguish between benign adrenal adenoma or bilateral adrenal hyperplasia

A

MRI of adrenals

50
Q

management of bilateral adrenal hyperplasia

A

spironolactone- mineralocorticoid receptor antagonist, reduced salt and therefore water retention so decreases the circulating volume

51
Q

what diet is recommended to all patients with hyperaldosteronism

A

salt restriction

52
Q

follow up after prescribing spironolactone for hyperaldosteronsim

A

review in 2 weeks to repeat renal profile and K+

53
Q

pneumonia vs pulmonary oedema on CXR

A

look similar but pneumonia will not be as symmetrical as a pleural effusion

54
Q

what simple test can you do for pre-clampsia first

A

urine dip (will see proteinuria)

Semester 2 (3rd year) (12 decks)

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