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
what is pheochromocytoma? how does it cause secondary HTN? how do you treat it?
it’s an adrenal tumor that secretes catecholamines (epinephrine and norepinephrine)
catecholamines cause vasoconstriction by activating alpha 1 = HTN
can be associated with other endocrine tumors (MEN syndromes)
patients may have sweating, anxiety, tachycardia, headaches with high BP (your SNS is being stimulated so you have sympathetic symptoms!)
treated with surgical removal
how does hyperaldosteronism cause secondary hypertension? how do you treat it?
caused by aldosterone producing adrenal adenoma or idiopathic bilateral adrenal hyperplasia
aldosterone stimulates sodium reabsorption and water follows increasing intravascular volume
it also stimulates potassium secretion in urine…always think of this when BP is high and potassium is low without an obvious cause
symptoms usually related to low potassium (muscle cramps, weakness, cardiac arrhythmias)
treatment can be surgical (adenoma) or medical
how does hypercortisolism cause secondary HTN? how do you treat it?
glucocorticoid cause increased BP by:
- increasing Na+ retention thus increasing intravascular volume
- stimulate angiotensin II receptors causing vasoconstriction,
- producing nitric oxide
this is Cushing syndrome!!
cause can be exogenous steroids, adrenal tumor, adrenal hyperplasia, or Cushing’s disease (adrenal glands make excess cortisol)
characteristic exam findings: Moon facies, stria, “buffalo hump”, abdominal fat
how can thyroid dysfunction cause secondary HTN?
both hypo and hyper thyroid states can cause HTN
mechanism of hypothyroid not well understood…
the theory for why this happens is that In hyperthyroidism, increased T3 hormone stimulates beta-2 receptors on vascular smooth muscle, decreasimg vascular resistance and overstimulating the heart increasing cardiac output
how can chronic kidney disease cause secondary HTN?
causes salt & water retention and dysregulation of RAAS
diagnosed by increased creatinine levels or protein in the urine
try to treat condition causing CKD along with BP management
who should you screen for secondary hypertension?
- severe or resistant hypertension –> resistant hypertension is defined as the persistence of hypertension despite concurrent use of adequate doses of three antihypertensive agents from different classes, including a diuretic
- an acute rise in blood pressure developing in a patient with previously stable values
- age less than 30 years in nonobese, nonblack patients with a negative family history of hypertension and no other risk factors (eg, obesity) for hypertension
- malignant or accelerated hypertension (eg, patients with severe hypertension and signs of end-organ damage such as retinal hemorrhages or papilledema, heart failure, neurologic disturbance, or acute kidney injury)
- proven age of onset before puberty
what are some of the complications of HTN? heart, kidney, brain and eyes
HEART: left ventricular hypertrophy –> arteriole system with increased SVR the heart will have to work harder to pump against the resistance
KIDNEY: thickening of arteries and arterioles leading to fibrosis and sclerosis due to overstimulation –> decreases GFR which can complicate medication clearance
BRAIN: narrowing of cerebral arteries that can lead to stroke and other vascular conditions
EYES: vessels become brittle and weak and can hemorrhage into eye causing retinopathy (basically they go blind)
what is hypertensive urgency? how do you treat it?
BP very high, but not associated with end organ damage; the patient is asymptomatic
usually incidental finding like during a routine checkup
not symptomatic
most often caused by people who stop taking their meds
treated outpatient because they’re asymptomatic; don’t need IV meds (adjust treatment & close follow up)
what is hypertensive emergency? how do you treat it?
BP high enough to cause immediate complications
> 180 SBP or >120 DBP
usually symptomatic: headache, vision changes
treated in hospital with IV meds to drop their BP in a controlled manner without a giant drop
