ICL 3.4: Clinical Pathophysiology and Treatment of HTN & HTN Syndromes

Question 1

what is primary hypertension?

Answer 1

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”

Question 2

what is secondary hypertension?

Answer 2

specific cause is identified for the hypertension

Question 3

what is white coat hypertension?

Answer 3

blood pressures measured in the office are high, but BP’s measured at home or other settings normal

not uncommon

Question 4

what is the definition of hypertension?

Answer 4

normal = <120/80

elevated = 120-129 and >80

HTN stage 1: 130-139 or 80-89

HTN stage 2: >140 or >90

Question 5

what is the formula for CO?

Answer 5

CO = SV x HR

Question 6

what is the systemic vascular resistance?

Answer 6

opposing resistance of vessels

Question 7

what is the formula for BP?

Answer 7

BP = CO x SVR

this means anything that affects SV, HR or SVR can affect BP!

Question 8

what causes elevated BP due to increased HR?

Answer 8

1. generally transient
2. checking BP after exercise can result in temporary elevation from tachycardia
3. elevated BP after consumption of caffeine.

Question 9

how can increased BP cause increased SV?

Answer 9

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

Question 10

what can cause increased SVR and consequently lead to increased BP?

Answer 10

1. arteries harder as you get older
2. catecholamines released from adrenal medulla and sympathetic nervous system bind to alpha receptors in vascular smooth muscle causing vasoconstriction and increased SVR
3. RAAS (Renin Aldosterone-Angiotensin System)
4. genetics

Question 11

what are the genetic factors that can cause elevated BP?

Answer 11

1. family history (first degree relatives especially)

2. race –> high BP in african americans

Question 12

what is simple explanation of RAAS?

Answer 12

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

Question 13

what is the blood flow through the kidney?

Answer 13

renal artery off the aorta –> afferent arteriole into the glomerulus of the nephron –> efferent arteriole –> capillaries –> renal vein

Bowman’s capsule

Question 14

where does renin come from?

Answer 14

juxtaglomerular cells in the afferent arteriole of the nephron make and secrete renin!

Question 15

how do nephrons sense BP and react?

Answer 15

1. sympathetic nerve fibers in aortic arch (baroreceptors) stretch with BP and relax with BP; relaxation stimulates renin release in juxtaglomerular cells
2. the juxtaglomerular cells themselves also act as baroreceptors –> low BP (relaxation) stimulates renin release
3. 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

Question 16

what happens to renin once it’s released from the juxtaglomerular cells in the kidney?

Answer 16

1. renin released from nephron into the blood
2. renin fragments angiotensinogen made by the liver to make angiotensin I
3. angiotensin I binds to receptors in the lungs where angiotensin converting enzyme (ACE) cleaves it to make angiotensin II
4. angiotensin II circulates in the blood to effect things in other areas of the body

Question 17

what are the effects of angiotensin II?

Answer 17

1. smooth muscle in vessels increase resistance, thus increasing BP
2. causes vasoconstriction of afferent and efferent arterioles in kidney (efferent > afferent) leading to increased BP
3. acts on hypothalamus to stimulate thirst, increasing ADH, thus increasing H2O reabsorption in kidney, thus increasing volume and BP
4. 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

Question 18

what are the best non-pharmacological interventions for prevention and treatment of HTN?

Answer 18

1. weight loss
2. healthy diet (DASH diet)
3. reduced intake of dietary sodium
4. enhanced intake of dietary K+
5. physical activity
6. moderate alcohol intake

smoking isn’t something that effects BP!

Question 19

what are the goals of HTN treatment?

Answer 19

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

Question 20

what are some of the causes of secondary hypertension?

Answer 20

1. Obstructive Sleep Apnea (OSA)
2. Renal Artery Stenosis (RAS)
3. Pheochromocytoma
4. Chronic Kidney Disease (CKD)
5. Medications/Drugs
6. Hyperaldosteronism
7. Hypercortisolism
8. Thyroid Dysfunction
9. Coarctation of Aorta

Question 21

how does obstructive sleep apnea cause HTN? how do you treat it?

Answer 21

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

Question 22

how does renal artery stenosis cause HTN?

Answer 22

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

Question 23

which drugs can cause secondary hypertension?

Answer 23

1. oral contraceptives
2. NSAIDS
3. pseudoephedrine
4. corticosteroids
5. antidepressants
6. amphetamines
7. cocaine

Question 24

how do NSAIDs cause secondary HTN?

Answer 24

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

Question 25

what is pheochromocytoma? how does it cause secondary HTN? how do you treat it?

Answer 25

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

Question 26

how does hyperaldosteronism cause secondary hypertension? how do you treat it?

Answer 26

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

Question 27

how does hypercortisolism cause secondary HTN? how do you treat it?

Answer 27

glucocorticoid cause increased BP by:

1. increasing Na+ retention thus increasing intravascular volume
2. stimulate angiotensin II receptors causing vasoconstriction,
3. 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

Question 28

how can thyroid dysfunction cause secondary HTN?

Answer 28

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

Question 29

how can chronic kidney disease cause secondary HTN?

Answer 29

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

Question 30

who should you screen for secondary hypertension?

Answer 30

1. 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
2. an acute rise in blood pressure developing in a patient with previously stable values
3. 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
4. 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)
5. proven age of onset before puberty

Question 31

what are some of the complications of HTN? heart, kidney, brain and eyes

Answer 31

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)

Question 32

what is hypertensive urgency? how do you treat it?

Answer 32

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)

Question 33

what is hypertensive emergency? how do you treat it?

Answer 33

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