Pathophysiology of Hypertension

Question 1

systolic blood pressure

Answer 1

peak value in the arteries during cardiac contraction

Question 2

diastolic BP

Answer 2

pressure in arteries during ventricular filling

Question 3

pulse pressure

Answer 3

difference between systolic and diastolic pressure

Question 4

mean arterial pressure

Answer 4

tells us what the average BP is in a cardiac cycle

Question 5

the relationship between BP, cardiac output, and total peripheral resistance

Answer 5

BP = CO x TPR

Question 6

cardiac output

Answer 6

measurement of blood flow; determined by stroke volume (amount of blood pumped out of ventricle in one contraction)

Question 7

proper BP measurement technique

Answer 7

Patient’s back rested, feet flat on the ground for 5 minutes, arms need to be resting, cuff size must be appropriate, check BP in both arms initially (want to always check the arm that has the higher reading), important to get two readings

Question 8

primary hypertension

Answer 8

• essential / benign

- we don’t know what the discreet underlying cause is

Question 9

secondary hypertension

Answer 9

has a discrete and identifiable cause

Question 10

risk factors that increase hypertension

Answer 10

• overweight / obesity
• salt intake
• sedentary lifestyle
• alcohol intake
• aging
• stress
• Low K and Ca intake
• race (blacks / hispanics)

Question 11

the effects of angiotensin II

Answer 11

• direct vasoconstrictor if overly produced
• stimulates sympathetic nervous system: peripherally releases catecholamines, can increase activity in the medulla
• stimulates aldosterone (which can lead to water and sodium retention)

Question 12

triggers for renin release

Answer 12

• Released from juxtamedullary cells in kidney
• Decrease in renal perfusion will stimulate this process
• Renin is released when sodium or chloride is delivered to the nephron
• Direct stimulation of juxtamedullary cells
• Decreased circulation of angiotensin II

Question 13

effects of stimulating adrenergic receptors in the central nervous system

Answer 13

• Pre-synaptic alpha II inhibits NE release

- Pre-synaptic beta causes NE release

Question 14

effects of stimulating adrenergic receptors in the autonomic nervous system

Answer 14

Post-synaptic stimulation:

• Alpha I – vasoconstriction
• Alpha II – vasoconstriction
• Beta I – minimal peripheral effect
• Beta II – vasodilation

Question 15

baroreceptor reflex: acute increase in BP

Answer 15

Baroreceptors will send a signal to decrease sympathetic outflow and cause vasodilation of arterioles and venules.

Question 16

baroreceptor reflex: acute increase in BP -> Consequence if baroreceptors are not functioning adequately

Answer 16

Blood pressure will stay elevated.

Question 17

baroreceptor reflex: acute decrease in BP

Answer 17

Baroreceptors will send a signal to cause vasoconstriction, increased heart rate, and increase contractility to preserve organ perfusion.

Question 18

baroreceptor reflex: acute decrease in BP -> Consequence if baroreceptors are not functioning adequately

Answer 18

Organ perfusion may be reduced. Can result in syncope or near-syncope (passing out). Common among elderly patients and those with diabetes.

Question 19

other mechanisms that could have a role in the genesis of primary hypertension

Answer 19

• tissues and organs defective in self-regulating their own blood flow
• endothelial dysfunction

Question 20

causes of secondary hypertension

Answer 20

• Medications
• Renovascular / kidney disease
• Sleep apnea
• Hyperaldosteronism (primary or secondary)
• Endocrine (Cushing’s disease, excessive functioning thyroid)
• Pheochromocytoma
• Head injury
• Coarctation of the aorta

Question 21

medications that cause secondary hypertension

Answer 21

• adrenergic agonists (e.g., methylphenidate)
• amphetamines
• anorexiants (e.g., sibutramine)
• corticosteroids (e.g., prednisone)
• cyclosporin
• decongestants (e.g., pseudoephedrine)
• ergot alkaloids (e.g., ergonovine)
• erythropoiesis-stimulating agents (e.g., erythropoietin)
• estrogen-containing substances
• monoamine oxidase type A inhibitors (e.g., tranylcypromine is an older drug that is rarely used, but is one of the original MOA inhibitors). ▪ Type B inhibitors are much less likely to cause a hypertensive response at lower doses (e.g., selegiline)
• NSAIDs/COX-1 inhibitors (e.g., ibuprofen, celecoxib)
• some anti-depressants (e.g., venlafaxine, desvenlafaxine, bupropion)
• street drugs (e.g., cocaine, ephedra alkaloids, herbal ecstasy)
• tripans (for migraines) (e.g., sumatriptan)

Question 22

physiologic changes that occur in hypertension

Answer 22

• Endothelial dysfunction
• Stiffening / hardening of arteries
• Increased work on heart, leading to thickening of ventricular wall

Question 23

What happens in endothelial dysfunction?

Answer 23

Leads to development of atherosclerosis

Question 24

What effect is produced in the dysfunction of renal arteries?

Answer 24

thickening of the renal arteries will worsen hypertension by making the renal response to blood flow and pressure dysfunction (ineffective autoregulatory control)

Question 25

What effect is produced in the dysfunction of carotid arteries?

Answer 25

Provide the most blood flow to the brain. Dysfunction in the carotid arteries can cause cerebrovascular problems

Question 26

clinical consequences of hypertension

Answer 26

• Cerebrovascular disease: stroke
• Cardiovascular disease: left ventricular hypertrophy
• Nephropathy
• Retinopathy
• Peripheral Vascular Disease