Physiology of Hypertension Flashcards

1
Q

Definition of hypertension

A

140> mmHg systolic / >90 mmHg diastolic

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2
Q

What are the causes of hypertension

A
Multifactorial causes - genetic/foetal 
Environmental facors 
- obesity 
-XS alcohol 
-XS Na + intake `
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3
Q
What happens to the following in chronic hypertension
CO
PR
Lumen diameter
Wall thickness
A

CO - normal
PR- increase
Lumen diameter- decrease
increase in wall thickness “resitance” vessels - sclerosis

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4
Q

What are the consequences of hypotension?

A

Increase in Na+
increase in ECF/ BV
Increase in CO

barorecptor adaptation

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5
Q

Where does secondary hypertension occur

A
Renal disease 
Coarctation of the aorta 
Endocrine disease
Pregnancy 
drugs
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6
Q

What endocrine diseases can cause secondary hypertension

A

Primary hyperaldosteronism
Phaeochromocytoma
Cushings syndrome

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7
Q

What happens in renal disease

A

decrease in GF - leading to fluid retention
increase BV
increase in CO

increase in RAAS increases PR and increases CO

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8
Q

What happens in primary hyperaldosterone

A

Increase renal fluid absorption and increases BV and increases CO

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9
Q

What happens in phaeochromocytoma

A

Increase in catecholamines - vasoconstriction increasing PR

increase in catecholamines will also cause cardiac stimulation and increase CO

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10
Q

What is cushings syndrome

A

XS CG
increase in renal fuid absporption
increase in BV increase in CO

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11
Q

What does coarctation of the aorta mean

A

INcrease in BP proximal to stricture
decrease in BP/ perfusion distal to strcture
renally mediated general hypertension

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12
Q

What drugs can cause secondary hypertension

A
NSAIDs
substance abuse 
herbal remedies 
steroids 
COC pill
sympathomimetrics
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13
Q

What are the consequences of hypertension

A

LVH/cardiac failure

arterial wall thickening and reduced vascular compliance - increase in pulse wave veolcity

atheroma

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14
Q

What happens in endothelial dysfunction

A

Reduced dilators
Increase in constrictors
increase in risk atheroma/thrombosis

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15
Q

What happens in renal damage

A

Reduced perfusion/filtration
positive feedback from RAAS
further increase in blood pressure

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16
Q

What happens in cerebral vascular disease

A

Dementia
TIA
stroke

17
Q

What happens in hypertensive retinopathy

A

Thickening of arterial walls
Haemorrhages
“soft” exudates

18
Q

signs of hypertension

A

Headache/nosebleed
NONE
elevated BP
Hypersensitive retinopathy

19
Q

Symptoms of hypertension

A

Cardiac cerebrovascular
renal disease
Peripheral vascular disease
Coronary vascular disease

20
Q

How do we reduce cardiac output

A

Thiazide diuretics -
Beta adrenoreceptors
ACE inhibitors
All receptor inhibitors

21
Q

What do thiazide diuretics do

A

Decrease cardiac output initially and decrease peripheral resistance long term

22
Q

What do beta- adrenoreceptors blockers do

A

reduce cardiac sympathetic stimulation

23
Q

What do ace inhibitors do

A

reduce aldosterone production

24
Q

What do all receptor inihibitors do

A

reduced vasoconstriction

25
Q

How do we reduce peripheral resistance

A

L-type calcium channel blockers
alpha-1- adrenoreceptors blockers
vasodilators

26
Q

How do we treat hypertension

A

Lifestyle after diagnosis is confirmed

Implant baroreceptor after stimulation drive
Percutaneous transluminal RDN of renal artery