Severe HTN and the investigations to perform Flashcards
Categorise BMI
18.5 Underweight
18.5-24.9 Healthy weight
25–29.9 Overweight
30-34.9 Obese (class 1 obesity)
35-39.9 Severe obesity (class 2 obesity)
40-50 Morbid obesity (class 3 obesity)
50-60 Super obesity
>60 Super-morbid obesity
What happens to usual circadian BP rhythm if you have essential HTN
It is lost
What would you look for if the BP is high
Fundoscopy
What is seen on fundoscopy at each of the 4 grades of HTN
Grade 1: silver wiring (white bit in the artery)… shows it’s chronic
Grade 2: av nipping… the artery compresses the vein so vein narrows
Grade 3: Flame haemorrhae
Grade 4: Papilloedema
When is papillodema seen
Can be seen when high ICP due to brain tumour, as well as in HTN
Other signs in a patient with longstanding HTN
- LVH cannot be detected on clinical examination
- Heave
- S4
- Bruits
What happens to make S4 sound
S4 is caused by the atria contracting forcefully in an effort to overcome an abnormally stiff or hypertrophic ventricle
T/F in HTN you might feel a displaced apex beat
F.
Remember that in HTN you might get LVH over long term. This is not detectable on examination
Contrastingly, in HF you get dilated left ventricle which causes the shift apex beat
How can you tell if papilloema
Cannot see outline of optic disc
What does hypertensive retinopathy suggest
That the hypertension is severe and prolonged…
Causes of HTN
Conn's disease Phaeochromocytoma Cushings Renal artery stenosis Cushings Acromegaly Coarctation of the aorta Essential
What investigations for HTN and why
FBC (polycythaemia)
U + E (potassium might be low, renal function might be affected).. MOST USEFUL because a low potassium makes endocrine more likely
ECG (LVH)
Urinalysis (nephritis or renal disease)
Fasting glucose (risk of diabetes)
Lipids
What percentage of hypertensive patients have secondary hypertension
Under 30 (probably 30%) In older people (probably under 5%)
What is the renin and aldosterone in conns and why
Aldosterone high and the renin is low because it s suppressed by the high BP
When is the renin and aldosterone high
RAS
What is the presentation of phaeochromocytoma
Nervousness
Sweat pouring down face
Racing heartbeat (palpitations)
Episodic severe hypertension
It’s sudden episodes because it’s neural tissue degranulating, not like conns’s where it’s a constant tumour
What can happen to the bowel in phaeo
severe vasoconstriction could cause necrotic bowel
First therapeutic step with a phaeo
what is the other management
(Rehydrate if dehydrated) FIRST: Alpha blockade Beta blockade Localise the lesion surgery
What test could we do for a patient with a phaeo
MIBG
65 yo patient with a previous MI has a BP of 140/80 on atenolol.
Would you add a thiazide
Yes….. intensive control is better than standard control and it prevents deaths
“AGGRESSIVE” management of BLOOD PRESSURE and LIPIDS improves SURVIVAL
Using thiazides in 100 people with CAD will save 2 lives over 5 years.
Optimum medical therapy for those with previous CAD
Intensive lifestyle modification
Aspirin
High dose statin (Atorvastatin 40-80mg od)
Optimal blood pressure control to 120/80
Assessment for probable T2D
Outline the physiology of PCSK9
It controls the digestion of the LDLR.
Normally, PCSK9 will bind to the LDLR and, when the LDLR is recycled, causes it to be digested in the lysozyme so it can no longer bind cholesterol in the blood
How do PCSK9i work
It is a monoclonal antibody, it prevents PCKS9 binding to LDLR and thus prevents the digestion of this protein in the lysozome.
So it can stay and continue to remove cholesterol from the bloodstream and thus is lipid lowering
Is PCSK9 useful
No, wasn’t shown to
