ICL 3.4: Clinical Pathophysiology and Treatment of HTN & HTN Syndromes Flashcards
what is primary hypertension?
aka essential hypertension
- hypertension without an identifiable cause
- most common disease seen in US medical practice –> 90% of hypertension cases
more than 75 million Americans effected.
- usually asymptomatic = the “Silent Killer”
what is secondary hypertension?
specific cause is identified for the hypertension
what is white coat hypertension?
blood pressures measured in the office are high, but BP’s measured at home or other settings normal
not uncommon
what is the definition of hypertension?
normal = <120/80
elevated = 120-129 and >80
HTN stage 1: 130-139 or 80-89
HTN stage 2: >140 or >90
what is the formula for CO?
CO = SV x HR
what is the systemic vascular resistance?
opposing resistance of vessels
what is the formula for BP?
BP = CO x SVR
this means anything that affects SV, HR or SVR can affect BP!
what causes elevated BP due to increased HR?
- generally transient
- checking BP after exercise can result in temporary elevation from tachycardia
- elevated BP after consumption of caffeine.
how can increased BP cause increased SV?
BP increases usually via Na retention which causes expansion of extracellular fluid/blood volume increasing stroke volume
ECF or blood volume is increased which means SV is increased
what can cause increased SVR and consequently lead to increased BP?
- arteries harder as you get older
- catecholamines released from adrenal medulla and sympathetic nervous system bind to alpha receptors in vascular smooth muscle causing vasoconstriction and increased SVR
- RAAS (Renin Aldosterone-Angiotensin System)
- genetics
what are the genetic factors that can cause elevated BP?
- family history (first degree relatives especially)
2. race –> high BP in african americans
what is simple explanation of RAAS?
renin-angiotensin-aldosterone system –> it’s a really important mechanism for regulating BP and shows how the heart, kidneys and lungs function together
blood flower through kidney –> kidney sevens BP and volume status –> kidney responds by releasing or inhibiting renin and regulating Na ions to affect BP
what is the blood flow through the kidney?
renal artery off the aorta –> afferent arteriole into the glomerulus of the nephron –> efferent arteriole –> capillaries –> renal vein
Bowman’s capsule
where does renin come from?
juxtaglomerular cells in the afferent arteriole of the nephron make and secrete renin!
how do nephrons sense BP and react?
- sympathetic nerve fibers in aortic arch (baroreceptors) stretch with BP and relax with BP; relaxation stimulates renin release in juxtaglomerular cells
- the juxtaglomerular cells themselves also act as baroreceptors –> low BP (relaxation) stimulates renin release
- chemoreceptors in Macula densa cells in loop of henle sense NaCl in filtrate (increased GFR = increased BP = increased NaCl ions and visa versa) –> macula dense cells release prostaglandins which stimulate renin in juxtaglomerular cells
what happens to renin once it’s released from the juxtaglomerular cells in the kidney?
- renin released from nephron into the blood
- renin fragments angiotensinogen made by the liver to make angiotensin I
- angiotensin I binds to receptors in the lungs where angiotensin converting enzyme (ACE) cleaves it to make angiotensin II
- angiotensin II circulates in the blood to effect things in other areas of the body
what are the effects of angiotensin II?
- smooth muscle in vessels increase resistance, thus increasing BP
- causes vasoconstriction of afferent and efferent arterioles in kidney (efferent > afferent) leading to increased BP
- acts on hypothalamus to stimulate thirst, increasing ADH, thus increasing H2O reabsorption in kidney, thus increasing volume and BP
- acts on adrenal gland to cause release of aldosterone which binds in the kidney activating the Na-K+-ATPase pump causing NaCl reabsorption, K+ excretion leading to H20 retention and increased BP
what are the best non-pharmacological interventions for prevention and treatment of HTN?
- weight loss
- healthy diet (DASH diet)
- reduced intake of dietary sodium
- enhanced intake of dietary K+
- physical activity
- moderate alcohol intake
smoking isn’t something that effects BP!
what are the goals of HTN treatment?
guidelines differ!
for adults with confirmed HTN and known CVD or a 10 year ASCVD event risk of 10% or higher a BP target of less than 130/80 is recommended –> this is for patients with CVD, DM or renal disease UNDER 65 years old
when you get older your arteries harden and you get isolated systolic hypertension where the top number is 150 but bottom number is in the 70s –> ACE inhibitors and Ca+2 channel blockers work well for this –> so you know that laying down to standing with low BP you might get dizzy – with older people who are on meds to drop their BP this is bad because they could fall and hit their head or break a hip so you always need to way risks vs. benefits
what are some of the causes of secondary hypertension?
- Obstructive Sleep Apnea (OSA)
- Renal Artery Stenosis (RAS)
- Pheochromocytoma
- Chronic Kidney Disease (CKD)
- Medications/Drugs
- Hyperaldosteronism
- Hypercortisolism
- Thyroid Dysfunction
- Coarctation of Aorta
how does obstructive sleep apnea cause HTN? how do you treat it?
pharyngeal muscles collapse during sleep causing cessation of breathing
this results in drop in O2 (hypoxia) and increase in CO2 (hypercapnia)
this stimulates sympathetic nervous system leading to vasoconstriction increasing BP
treated with CPAP
how does renal artery stenosis cause HTN?
decreased blood flow to kidneys stimulates baroreceptors causing renin secretion and activation of RAAS (so the stenotic artery is making the kidney think its not getting enough blood and BP is low)
may have a renal bruit
diagnosed with ultrasound, MRA, or captopril nuclear medicine scan
treated with renal angioplasty with stent which will basically cure it
WARNING: if ACE inhibitors are given and RAS is bilateral, you further decrease the GFR which causes creatine levels to increase which can cause kidney damage
which drugs can cause secondary hypertension?
- oral contraceptives
- NSAIDS
- pseudoephedrine
- corticosteroids
- antidepressants
- amphetamines
- cocaine
how do NSAIDs cause secondary HTN?
macula densa cells monitor Na/Cl/H2O levels and when they sense hypotension they send prostaglandins to juxtaglomerular cells to release renin
so if you’re taking lots of NSAIDs, you’re limiting production of prostaglandins and the end result is decreased GFR which can cause increase creatinine –> this is because prostaglandins normally vasodilator so without them you have vasoconstriction of the arteries feeding the kidneys and lower perfusion –> kidneys sense hyperperfusion and think the whole body isn’t getting enough blood flow and activate RAAS system which increases BP
