Severe HTN and the investigations to perform Flashcards

1
Q

Categorise BMI

A

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

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2
Q

What happens to usual circadian BP rhythm if you have essential HTN

A

It is lost

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3
Q

What would you look for if the BP is high

A

Fundoscopy

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4
Q

What is seen on fundoscopy at each of the 4 grades of HTN

A

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

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5
Q

When is papillodema seen

A

Can be seen when high ICP due to brain tumour, as well as in HTN

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6
Q

Other signs in a patient with longstanding HTN

A
  1. LVH cannot be detected on clinical examination
  2. Heave
  3. S4
  4. Bruits
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7
Q

What happens to make S4 sound

A

S4 is caused by the atria contracting forcefully in an effort to overcome an abnormally stiff or hypertrophic ventricle

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8
Q

T/F in HTN you might feel a displaced apex beat

A

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

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9
Q

How can you tell if papilloema

A

Cannot see outline of optic disc

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10
Q

What does hypertensive retinopathy suggest

A

That the hypertension is severe and prolonged…

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11
Q

Causes of HTN

A
Conn's disease 
Phaeochromocytoma 
Cushings 
Renal artery stenosis 
Cushings 
Acromegaly 
Coarctation of the aorta 
Essential
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12
Q

What investigations for HTN and why

A

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

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13
Q

What percentage of hypertensive patients have secondary hypertension

A
Under 30 (probably 30%)
In older people (probably under 5%)
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14
Q

What is the renin and aldosterone in conns and why

A

Aldosterone high and the renin is low because it s suppressed by the high BP

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15
Q

When is the renin and aldosterone high

A

RAS

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16
Q

What is the presentation of phaeochromocytoma

A

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

17
Q

What can happen to the bowel in phaeo

A

severe vasoconstriction could cause necrotic bowel

18
Q

First therapeutic step with a phaeo

what is the other management

A
(Rehydrate if dehydrated)
FIRST: Alpha blockade
Beta blockade
Localise the lesion
surgery
19
Q

What test could we do for a patient with a phaeo

A

MIBG

20
Q

65 yo patient with a previous MI has a BP of 140/80 on atenolol.

Would you add a thiazide

A

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.

21
Q

Optimum medical therapy for those with previous CAD

A

Intensive lifestyle modification

Aspirin

High dose statin (Atorvastatin 40-80mg od)

Optimal blood pressure control to 120/80

Assessment for probable T2D

22
Q

Outline the physiology of PCSK9

A

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

23
Q

How do PCSK9i work

A

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

24
Q

Is PCSK9 useful

A

No, wasn’t shown to