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
how does salt cause HTN
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
dx test for renal artery stenosis
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
PHAEOCHROMOCYTOMA Some drugs that give false positive – run on assay in same place – anti-depressants.
28
sx/signs of phaeo
* 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
Mx of phaeochromocytoma
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
why do you get episodic HTN in phaeochromocytoma
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
indications and CI for a blocker for HTN
indication - BPH caution - postural Hypotension, HF CI - urinary incontinence
32
indications and CI of ACEi
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
indications and CI of ARB
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
indications and CI of B blocker for HTN
indication - MI, angina possible indication - HF caution - HF if severe, PVD, dm (except with CHD) CI - asthma/copd, heart block
35
indications of CCB and CI for HTN
indication - elderly, ISH (isolated systolic HTN), angina potential indications - elderly, angina, MU caution - combination with B blockade CI - heart block, heart failure
36
indications and CI of thiazide/thiazide-like diuretics
indications - elderly, ISH, heart failure, secondary stroke prevention CI - gout
37
HTN med if dm
ACEi ## Footnote ARB in pt who are ACE intolerant – have ACEi cough – leukotrienes.
38
39
Mx of HTN if microalbuminuria
ACEi unless CI
40
what do you do if there is a statin intolerance
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
mechanism of proprotein convertase subtilisin kexin 9 (PCSK9) Ab (evolocumab)
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
statin intolerance
SE are imaginary nociceptive effect about muscle aches. Need to push them more