Hypertension Flashcards

1
Q

Epidemiology

Affects?

A

1 billion
Leading global cause of death
Distinction between hypertensive+ normatensive= arbitary
Updated guidelines= emphasis is on home BP monitoring vs office (5-10mmHg lower)

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2
Q

BP and age
BP and mortality risk
BP and attributable burden

A

Increase age= increase BP
Increase age= increase pulse pressure
(Increase age= increase SBP but increase age= no change in DBP which actually flattens out and decreases therefore increase difference between SBP and DBP)

No reliable threshold for mortality risk as BP increases

50% of attributable burden have a normal SBP

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3
Q

Hypertension classification

A
Primary= unidentifiable cause (85% cases)
Secondary= Identifiable cause  (15% cases)
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4
Q

General causes of primary hypertension?

A

1) Genetics: Monogenic (rare)/ Complex polygenic (common)

2) Environment: Dietary Na, Obesity, Alcohol etc

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5
Q

BP and dietary Na

A

Major factor in rise of BP with age

people with no Na in diet don’t have rise in BP with age

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6
Q

Established hypertension is associated with these changes in values:

A
Increased TPR
Decreased arterial compliance
Normal cardiac output
Normal blood volume/ ECV
Central shift in volume (Secondary to reduced venous compliance)
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7
Q

What causes the elevated TPR in hypertension?

A
Active narrowing of arteries ( Short term vasoconstriction)
Structural narrowing of arteries (lumen gets smaller and wall gets thicker)
Capillary loss (Blood going through reduced area of vessels)
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8
Q

Isolated systolic hypertension
Ranges?
Age of people with it?
Cause?

A

Systolic BP ≥ 140 mmHg, diastolic BP ≤ 90 mmHg
Condition of people over age 60
Due to increasing stiffness of medium/large arteries= pulse wave reflected and is greater by the time it reaches brachial artery
Does NOT mean that TPR increases

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9
Q

Specific causes of primary hypertension

A

Kidney
Regulates Na/H2O/ECF volume
Almost all monogenic causes of hypertension affect renal Na excretion (you can transplant hypertension)

Endocrine/ paracrine factors

Increased sympathetic nervous system activity

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10
Q

Hypertension associated with changes to…

A
Heart
Large arteries
Eye
Microcirculation
Kidney

MELKH

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11
Q

Hypertension and the heart

A

Increase in left ventricular wall mass (LVMI)= changes in chamber size= more likely to lead to arrhythmias= heart failure+ sudden death

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12
Q

Hypertension and large arteries

Causes?

A

Arterial rupture/ dilations (aneurysms)= thrombosis/ haemorrhage (e.g. strokes)

Increased thickness of large arteries= acceleration of atherosclerosis: result of it, not a cause

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13
Q

Hypertension and eye

A

Microvascular damage:
Thickening of the wall of small arteries
Arteriolar narrowing
Vasospasm (arterial spasm= vasoconstriction= tissue death)
Impaired perfusion
Increased leakage into the surrounding tissue

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14
Q

Hypertension and microcirculation

A

Reduction in capillary density= decreased perfusion in organs
Elevated capillary pressure= damage and leakage

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15
Q

Primary hypertension and kidney

A

Granular capsular surface
Cortical thinning, renal atrophy
Renal dysfunction- reduced glomerular filtration rate+ increase albumin loss into urine
NB: GFR declines with age even without high BP, which speeds up deterioration

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16
Q

Accelerated hypertension and kidney

A

Subcapsular haemorrhages

Rare but leads to rapidly progressive renal failure

17
Q

Lifestyle modification to treat hypertension

A

Weight loss
Eat healthy
Exercise
Less alcohol

18
Q

Hypertension drugs

A

ACE inhibitors
reduce amount of Ang II produced (which increases BP)
(AngII still produced because there are other mechanisms for it’s production)

Angiotensin receptor blockers- alleviate bad effects of Ang II in kidney

Diuretics

1) Loop diuretics: Used in patients experiencing hypertensive crisis (lots of fluid in body)
2) Thiazide diuretics- more common, don’t work through diuresis but because they slowly reduce PVR (uncertain mechanism)

Beta blockers- not that great in stroke reduction through

1) Blockage of β1 receptors in heart= Reduced rate and force of contraction= Reduced cardiac output
2) Blockage of β1 receptors in kidney= Reduced secretion of renin= Reduced activity of RAAS

Calcium channel blockers
1) Major mechanism
In vascular smooth muscle
Reducing Ca2+ influx reduces actin myosin cross bridge cycling
2) Minor mechanism
In the heart
Inhibition of Ca2+ influx reduces contractility (negative inotropy) and rate of conduction (negative dromotropy)

19
Q

Hypertension= increased risk of?

A
Coronary heart disease
stroke
peripheral vascular disease/atheromatous disease
heart failure
atrial fibrillation
dementia /cognitive impairment 
retinopathy