wk 9, lec 1 Flashcards
how common is hypertension
Affects > 1 billion people, prevalence in those older
than 60 is > 60%
risk factors for hypertension
▪ Ischemic heart disease and congestive heart failure ▪ Peripheral arterial disease
▪ Dementia, stroke, and chronic kidney disease
effects of medications on hypertesnion
antihypertensive therapy reduces the risk of the above complications
▪ However, it is estimated that over half are not treated at all or are inadequately treated
what organ systems are involved in hypertension
▪ Central and peripheral nervous system
▪ Endocrine system
▪ Kidney
▪ Vascular system
▪ Digestive system, microbiome, and DIET
▪ Immune system
common factors in primary hypertension
▪ Arteriolar vasoconstriction and altered endothelial function
▪ Increased sodium retention & increased renin secretion
▪ Increased activation of the sympathetic nervous system
hypertension ____ resistance and ____ lumen size and ____ average resting muscle tone
increase, decrease, increase
increase in vessel wall thickness increases the resistance
what is the major site where total peripheral resistance is regualted
arterioles
what is vascular tone under the control of
hormonal, neural and local endothelial factors
what remodelling happens to the arteriole wall in hypertension
arteriosclerosis;;
▪ Hypertrophy and sometimes hyperplasia of smooth muscle cells
▪ Increased deposition of extracellular matrix
in hypertension the vascular endothelium releases ___ vasodilator susbtances (i.e. Nitric oxide)
less
remodelling of larger vessels in hypertension
become more stiff
arteriosclerosis
what organs can vascular changes to arterioles and arteries be seen in a lot
kidneys (regulate blood pressure)
initial vs chronic hypertesnion changes
initial: hypertrophy of smooth muscle cells –> hypererreactive to vascoactivite stimuli
chronic: arteriosclerosis; fibromuscular intimal thickening by new layers of elastin, reduplication of intimal elastic lamina, increased connective tissue, accumulate plasma proteins and basement membrane deposition
what happens with sodium intake increases beyond usual ability of kidney to excrete sodium
increased sodium –> increased blood volume –> increased mean arterial pressure
▪ Most arterioles will constrict in response to this increased pressure (remember autoregulation) to reduce flow to capillary beds
▪ Increased pressure at the kidney –> increased salt and water loss… however, it is thought that in hypertensive patients over time it takes higher and higher pressures to attain the same level of salt loss
what happens to the nervous system in hypertension? why?
increase SNS outflow; baroreceptors in brainstem reset to new higher normal
what do baroreceptor dysfunction causes
decrease afferent inhibitory signals
increase SNS
decrease limb blood flow
increase vasopressin, renin, angiotensin II
decrease renal blood flow
increase aldosterone secretion, sodium reabsorption, water reabsorption
Increased activation of the sympathetic nervous system leads to:
- Vasoconstriction of systemic arterioles (alpha-1 receptors)
- Increased ADH (vasopressin) release (increased water retention)
- Increased release of renin and AT2 (angiotensin II)
which receptor in RAAS is implicated in hypertension
the aldosterone receptor has been found in blood vessels outside the kidney and has been implicated in abnormal vascular function
where do leukocytes/WBC migrate into in hypertension
▪ The kidneys – well-known
▪ Vascular walls – knowledge is developing
what activates leukocytes (Th17 and ILC3) in hypertension and what are they implicated in
activated by increased extracellular sodium
mplicated and are likely involved in remodeling the vasculature both within and outside the kidney
how do insulin resistance and obesity link to hypertension
mpaired vasodilatory function of the vascular endothelium
▪ Weight loss and improved insulin sensitivity are associated with improved blood pressure, but there are many factors here to consider (i.e. improvements in diet)
▪ Interestingly, renal sodium-glucose cotransporters are closely integrated with sodium handling in the kidney
hypertension and atherosclerosis of renal arteries
Hypertension is one of the major risk factors for development of atherosclerosis, and atherosclerosis of the renal arteries can cause hypertension
▪ Reduced blood flow to the kidney –> increased secretion of renin –>vasoconstriction and sodium retention
primary vs secondary hypertension %
primary 90%
secondary 10%
causes of secondary hypertesnion impact which systems
kidneys and SNS mostly
SLIDE 16 chart
secondary causes of hypertesion
renal: chronic kidney disease (Na+ retention)
renovascular: atherosclerosis (increase renin)
obstructive sleep apnea (increase SNS)
endocrine: hypo/hyperthyroid, cushings etc (increase SNS or aldosterone)
congenital : aorta (hypoperfused renal)
medications/substances: decongestants, amphetamine, cocaine, TCAs, NSAIDs (impair vasodilation and icnrease SNS)
which BP (systolic or diastolic) does hyper and hypothryoid increase
Hyperthyroidism – increases SBP
Hypothyroidism – increases DBP
diagram on slide 17
shows secondary hypertension and mechanisms; i.e. Na+ retention, SNS< –> peripheral resistance and vasoconstriction
what gives an immediate diagnosis of hypertension
> 180/110 mm Hg
▪ Need multiple visits to diagnose hypertension, unless the
hypertension is severe
what factors to consider in BP measurement
- Home measurements are superior to medical office
measurements – less white coat HTN - automated measurements are superior to those done by a healthcare professional
- 24-hour measurements are very useful – BP that remains relatively high during sleep entails a higher risk of complications
hypertension value in diabetes vs non diabetic using automated BP
▪ In general, if mean awake automated systolic BP is 135 mm Hg or diastolic BP is 85 mm Hg –>
hypertension
* If measuring throughout a 24 hour period, average should be less than 130/80 mm Hg
▪ If diabetes, BP ≥ 130/80 mm Hg
office measurement BP value for hypertesnion
office measurements, takes 4-5 visits and average is 140 mm Hg systolic or 90 mm Hg diastolic
office vs automated BP for hypertension vs
office 140/90
auto 135/85
hypertesnion urgency vs hypertension emergency
Hypertensive urgency = greatly elevated blood pressure that should be treated urgently to minimize the likelihood of end-organ damage
Hypertensive emergency = hypertension with symptoms/signs that suggest end-organ damage is occurring due to high blood pressure
hypertesnion urgency
greatly elevated blood pressure that should be treated urgently to minimize the likelihood of end-organ damage
▪ i.e. stroke, IHD/heart attack, development of heart failure, acute kidney injury
▪ Usual definition is a systolic pressure > 180 mm Hg or a diastolic pressure > 120 mm Hg
hypertesnion emergency
hypertension with symptoms/signs that suggest end-organ damage is occurring due to high blood pressure
▪ Typical symptoms/signs: blurry/impaired vision, intractable headaches, stroke, worsening angina, polyuria or anuria
▪ No exact BP criteria – defined by hypertension in a setting of end-organ damage
malignant hypertesnion
▪ Rapid development of severe increases in blood pressure (> 180/120 mm Hg)
▪ Usually have signs of end-organ damage, and is often the cause of a hypertensive emergency
▪ Causes are not always clear, but may be linked to an insult (i.e. renal disease, discontinuation of antihypertensives)
- Pathological finding – severe remodeling of arterioles – known as hyperplastic or malignant arteriolosclerosis
4 antihypertensive medications
- alpha receptor blockers
- ace inhibitors
- angiotensin II receptor (ARB) blockers
4.calcium channel blockers
calcium channel blockers do what
▪ Block influx of calcium by inhibiting calcium channels in heart and in smooth muscle cells of coronary and peripheral arteriolar vessels
- Vascular smooth muscle relaxation and dilation
- Some blockers also inhibit calcium influx into heart’s conduction fibers and/or pacemakers resulting in negative dromotropy and negative chronotropy respectively
calcium channel blockers
block ca2+ influx to stop contraction
