Hypertension Flashcards

1
Q

why is HTN a problem

A

high pressure damages the walls of arteries = blocked

risk of stroke, heart attack, heart and renal failure increases with BP

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2
Q

definition and classificiations of HTN

A
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3
Q

Mx of HTN

A
  • Lower the bp = better risk reduction
  • Target between 85-80 is a good target
  • in dm - All risks were reduced in tight control gp

drug options

  • ACEi
  • ARB
  • B blocker
  • CCB
  • diuretic
  • (a blocker)

Evidence that 3 drugs at half standard dose better than 1 drug at normal dose

  • less SE
  • better compliance, fixed-dose combinations
  • heterogenous pts
  • additive/complementary pharmacology
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4
Q

mx of HTN in people who already have heart disease

A

in tightly controlled group risk of heart attack by 2%

and risk of all death by 2%

therefore aggressive mx of BP in people with heart disease improves survival

add thiazide diuretic - in 100 people witj CAD will save 2 lives oevr 5yrs

intensive lifestyle modification

aspirin

high dose statin - atorvastatin 40-80mg od

aspirin and statin prevent secondary MI

optimal BP control

assessment for t2dm

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5
Q

S3 heart sound

A
  • After s2
  • Suggest rapid ventricular filling
  • Happens when have large ventricle – HF/really fit people
  • LV dilatation – failing heart – heart dilates and CXR >50% thorax – feature of failing heart on PA film. – S3 – Kentucky – rapid ventricular filling
  • As blood hits the ventricular wall
  • During passive filling
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6
Q

s4 heart sound

A

Sound of atrial contraction – to overcome LV in ventricular hypertrophy or stiff ventrivle

Long standing HTN – muscle wall thicker and exercise hard against high pressure – grow thick inwards – v tall R waves. CXR normal – ie heart not bigger. S4 1 2 – Tennessee

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7
Q

what is galloping heart sounds

A

4 heart sounds – long standing HTN and then go into ischemia – have all 4 sounds – sound like a horse gallop – summation gallop of 3rd and 4th heart sound together

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8
Q

cardiac risk factors

A

BMI – obese

RF

  • HTN
  • Smoker
  • Lack of exercise
  • Weight
  • Male
  • Sedentary lifestyle
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9
Q

BMI cut offs

A

U shaped curve shape of survival – underweight = more at risk of infectious disease

Asian health risk start to raise >23

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10
Q

immediate approach to long standing HTN

A

encourage regular exercise

If a pt with long standing stable HTN and sent to casualty –diet and exercise and BP fall. Give drugs – but SE so use non-drug methods 1st

If diastolic >140 – accelerated HTN if have other clinical signs – casualty, check few times, see if S4, ECG – tall R waves, examine eyes. If chronic want to bring just down below 140.

If bring down too quickly = stroke. Need to drop slowly – reduce salt and then start on treatment if persistently high

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11
Q

signs of chronic HTN

A

seen on fundoscopy - hypertensive retinopathy

S4

heaves - R side of heart push through lungs

bruits

LVH cant be seen o/e

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12
Q

grade 1 hypertensive retinopathy

A

silver wiring in middle of the artery, around the disk

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13
Q

grade 2 hypertensive retinopathy

A

AV nipping

Artery crossing the vein – vein is nipped ie vein narrows where artery is because pressure in artery compresses the vein

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14
Q

grade 3 hypertensive retinopathy

A

Flame shaped haemorrhages

Patches of ischemia and cotton wool spots

Ischemia – blood not reaching retina = cotton wool (fluffy)

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15
Q

grade 4 hypertensive retinopathy

A

When really severe

Papilloedema – cant see the disk – edge is not visible

Also in obstructive hydrocephalus

  • When see papilloedema in casualty with headache and blurred vision – likely tumour blocking 3 or 4 ventricle = hydrocephalus so CT or MRI
  • If other features of HTN might be grade 4

Hard exudates are for diabetic not for HTN - deposits of cholesterol

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16
Q

sx of retinopathy

A

none until suddenly blind

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17
Q

what grade of HTN

A

Grade 3 HTN because cotton wool and flame shaped haemorrhages

18
Q

secondary causes of HTN

A

phaeochromocytoma

cushings

conns

acromegaly

renal artery stenosis

co-arctation of aorta

drugs - cocaine

19
Q

co-arctation of the aorta

A

aorta gets narrowed below arch = poor blood flow to legs and kidneys – act like renal artery stenosis

20
Q

basic Ix for HTN

A
  • FBC – polycythaemia
  • UE – K low because conns – a lot of endo causes. Renal func affected
  • ECG – LVH (tall R waves – deep 2 wave in V2 and tall R in V5. If add s and r – 40 or 45mm)
  • Urinalysis – nephritis or renal disease – haematuria. Nephritis is treatable
  • Fasting glucose – DM
  • Lipids – if also high it is an added RF

So start with the K – if K not low it wont be conns, cushings, phaeo

21
Q

summarise RAAs

A

ACE is in lungs

22
Q
A

CONN’S SYNDROME

If conns = high alsosterone – increase pressure because retain salt – HTN will suppress the renin

23
Q
A

RENAL ARTERY STENSOSIS

If K low – renal artery stenosis

Not conn’s because primary hyperaldosteronism,

This is secondary renal artery stenosis

Need ACE to vasoconstrict to maintain the eGFR

24
Q
A

angiogram with renal artery stenosis that has since been fixed

25
Q

how does salt cause HTN

A

System retains salt in form of RAAS

Kidney will excrete salt slowly but designed to retain salt – so have higher BP. Push out salt with thiazide diuretics.

26
Q

dx test for renal artery stenosis

A

On US can see the stenosis. MRI w/o contrast ie MR angiography is the dx test. Look at coarctation, renal artery and adrenal tumour -do one MR angio

27
Q
A

PHAEOCHROMOCYTOMA

Some drugs that give false positive – run on assay in same place – anti-depressants.

28
Q

sx/signs of phaeo

A
  • Tachy
  • Palpitations
  • Panic attacks
  • HTN that shoots up suddenly and then down again – episodes of sudden HTn
  • nervousness
  • sweat
  • Alpha receptor vasoconstrict = bowel infarction
  • Pul oedema
29
Q

Mx of phaeochromocytoma

A

A BLOCKADE

rehydrate - may need saline

B blcokade

localise lesion

surgery

  • Adrenaline has a and b receptor. If block a – prevent the severe HTN from vasoconstriction = safe*
  • B blocker – 2nd step. B2 receptor that cause peripheral dilation – if block = vasoconstriction = increase BP*

Can get sudden cardiac death – sudden vasoconstriction.

30
Q

why do you get episodic HTN in phaeochromocytoma

A

Adrenal medulla is neural tissue – whole tumour act like syncytium – wave spread through tumour and cells degranulate randomly or when stimulated.

When scare instead of getting normal blast get 10x normal amount – pulse of HTN. Then come down again.

in conns get constant aldosterone = constant HTN (also smaller on imaging than phaeo)

31
Q

indications and CI for a blocker for HTN

A

indication - BPH

caution - postural Hypotension, HF

CI - urinary incontinence

32
Q

indications and CI of ACEi

A

indications - HF, LV dysfunction, post MI or established CHD, t1dm nephropathy, secondary stroke prevention

possible indications - chronic renal disease, t2dm nephropathy, proteinuric renal disease

caution - renal impairment, PVD

CI - preg, renovascular disease

33
Q

indications and CI of ARB

A

indication - ACEi, t2dm nephropathy, HTN with LVH, HF in ACE intolerant, post-MI

possible indications - LV dysfunction post-MI, intolerance of otehr antihypertensive drugs, proteinuric renal disease, chronic renal disease, HF

caution - renal impairment, PVD

CI - pregnancy, renal vascular disease

34
Q

indications and CI of B blocker for HTN

A

indication - MI, angina

possible indication - HF

caution - HF if severe, PVD, dm (except with CHD)

CI - asthma/copd, heart block

35
Q

indications of CCB and CI for HTN

A

indication - elderly, ISH (isolated systolic HTN), angina

potential indications - elderly, angina, MU

caution - combination with B blockade

CI - heart block, heart failure

36
Q

indications and CI of thiazide/thiazide-like diuretics

A

indications - elderly, ISH, heart failure, secondary stroke prevention

CI - gout

37
Q

HTN med if dm

A

ACEi

ARB in pt who are ACE intolerant – have ACEi cough – leukotrienes.

38
Q
A
39
Q

Mx of HTN if microalbuminuria

A

ACEi unless CI

40
Q

what do you do if there is a statin intolerance

A

Problem with statins is that the SE are imaginary – nociceptive effect about muscle aches. Need to push them more

ezetemibe - drops lipids but not as well as statins

evolocumab - PCSK9 monoclonal Ab

41
Q

mechanism of proprotein convertase subtilisin kexin 9 (PCSK9) Ab (evolocumab)

A

Protein that sits on the LDL receptor – involved in the recycling of receptor – PC9SK9 tell cell to destroy the receptor.

gain of function mutations of PCSK9 reduce LDL receptors = high LDL in plasma and increased susceptibility of CHD

If don’t have it – LDL receptor recycled and more LDL is removed = low LDL cholesterol = protecton from CHD

evoculomab is an injection every 2wks - cholesterol falls to a low level

No difference in death – small difference in non-fatal heart attacks.

high NNT, absolute risk reduction small

so use if have statin intolerance, familial hypercholosteramia.

42
Q

statin intolerance

A

SE are imaginary

nociceptive effect about muscle aches.

Need to push them more