Final

Question 1

arterial BP

Answer 1

primarily a function of cardiac output and systemic vascular resistance

arterial BP = CO x SVR

Question 2

cardiac output

Answer 2

volume of blood ejected from the heart per min

Question 3

short term mechanisms that control BP

Answer 3

effects from the SNS and vascular endothelium

Question 4

long term mechanisms that control BP

Answer 4

renal and hormonal processes that regulate arteriolar resistance and blood volume

Question 5

how does the SNS control BP

Answer 5

when BP drops the SNS kicks in

• increases HR and cardiac contractility
• triggers vasoconstriction in peripheral arterioles
• promotes release of renin from the kidneys

Question 6

norepinephrine (NE) effects on SNS

Answer 6

NE is a neurotransmitter released from sympathetic nerve endings

activates the adrenergic receptors (betas and alphas)

increases BP

Question 7

alpha adrenergic receptors

Answer 7

are located in peripheral vasculature and cause vasoconstriction when stimulated by norepinephrine

Question 8

beta 1 adrenergic receptors

Answer 8

are found in the myocardium and respond to NE by increasing HR (chronotropic) effect and increased force of contraction (inotropic) effect, and increased speed of conduction (dromotropic effect)

Question 9

sympathetic vasomotor centre

Answer 9

located in the medulla

maintains normal BP

changes in BP are sensed by baroreceptors and are transmitted to the vasomotor centre

Question 10

baroreceptors

Answer 10

aka pressorecceptors

specialized nerve cells located in the carotid sinus and the arch of the aorta

are sensitive to stretching and when stimulated by an increase in BP send inhibitory impulses to the vasomotor centre

a fall in BP leads to activation of the SNS

in HTN the receptors become used to the high level and recognize it as “normal”

Question 11

vagus nerve

Answer 11

increases PNS activity and reduces HR

Question 12

vascular endothelium

Answer 12

a single layer of cell layer that lines blood vessels

produces nitric oxide which causes vasodilation, and inhibits platelet aggregation

also produces endothelin which is a vasoconstrictor and causes aggregation of neutrophils

Question 13

renal system and BP regulation

Answer 13

control sodium excretion and extracellular fluid volume

plays a part in the RAAS system -> in response to SNS stimulation, decreased blood flow through the kidneys, or decreased serum sodium concentration - the kidneys will secrete renin from the juxtaglomerular apparatus

also secrete prostaglandins from the renal medulla, which has a vasodilator effect -> lowers BP

Question 14

endocrine system and BP regulation

Answer 14

stimulation of the SNS causes the release of epinephrin and NE from the adrenal medulla -> epinephrine activates beta 2 receptors in peripheral arterioles in skeletal muscles and cause vasodilation, but with alpha 1 receptors (kidneys and skin) cause vasoconstriction

cause release of aldosterone from the adrenal cortex -> stimulates the kidneys to retain sodium and water, increasing blood volume and CO

increased serum sodium levels stimulates release of ADH -> increases ECF volume by promoting reabsorption of water in the kidneys

Question 15

HTN

Answer 15

sustained elevation of BP and is the leading cause for visits to primary care physicians

systolic BP equal or greater than 140 or a diastolic BP equal or greater than 90

Question 16

normal BP

Answer 16

BP less than 120/80

Question 17

stage 1 HTN

Answer 17

140-159 systolic
90-99 diastolic

Question 18

stage 2 HTN

Answer 18

160 systolic
100 diastolic

Question 19

target BP for someone with HTN and DM

Answer 19

systolic = less or equal to 130
diastolic = less or equal to 80

the established level at which anti-hypertensive therapy is effective at decreasing CV morbidity and mortality

Question 20

isolated systolic hypertension

Answer 20

a sustained elevation in systolic BP equal to or greater than 140 with a diastolic less than 90

an increase in SBP but not DBP increased the pulse pressure

is associated with an increased risk for cardiomegaly, MI, or stroke

Question 21

pulse pressure

Answer 21

the difference between SBP and DBP

a high pulse pressure is considered an independent risk factor for CVD and end organ damage

loss of elasticity of large arteries contributes to the widening of the pulse pressure

Question 22

primary hypertension

Answer 22

aka essential HTN

is elevated BP and accounts for the majority of all cases of HTN

exact cause not identified

is considered to be a complex interaction between genes and the environment

contributing factors included increased SNS activity, overproduction of sodium-retaining hormones and vasoconstrictors, increased sodium intake, high body weight, DM, excessive alcohol use

Question 23

secondary HTN

Answer 23

elevated BP with a specific cause that often can be identified and corrected

accounts for 5 to 10% of HTN in adults and 80% in children

if HTN occurs in someone younger than 20 or older than 50, suspect a secondary cause

clinical finding that may suggest secondary HTN:
unprovoked hypokalemia, abdominal bruit, variable pressures with history of tachycardia, sweating, tremors, family history of renal disease

treat by fixing underlying cause

Question 24

causes of secondary HTN

Answer 24

• congenital narrowing of the aorta
• renal disease
• endocrine disorders (cushings syndrome)
• neurological disorders like brain tumour or injury
• sleep apnea
• medications (MAOs, birth control, NSAIDs)
• pregnancy induced HTN

Question 25

factors that contribute to primary HTN

Answer 25

genes - primary HTN is polygenic - if both parents and a sibling has HTN, there is a 40 to 60% chance of developing HTN - most likely from multiple genes, not just one sodium and water retention - excessive intake of sodium -> linked to the initiation of HTN - high sodium intake = retained water = elevated BP - some degree of sodium sensitively must be present for high sodium to trigger development of HTN altered RAAS stress and increased SNS activity - stress can trigger SNS activity which will lead to prolonged effects from the SNS and hormones insulin resistance and hyperinsulinemia - high insulin concentration in the blood stimulates SNS and RAAS activity and impairs nitro oxide vasodilation - strong genetic component in hyperinsulinemia - insulin resistance has to due with endothelial dysfunction endothelial cell dysfunction - impaired release of effect of nitric oxide (vasodilation) or ET (vasoconstriction) obesity

Question 26

risk factors for primary HTN

Answer 26

- old age - heavy alcohol use - cigarette smoking - DM - elevated serum lipids -high dietary sodium intake - gender - family history - obesity - ethnicity -> black or south asian descent are 3x more likely - sedentary lifestyle - socioeconomic status - psychosocial stress

Question 27

lanthanic related to HTN

Answer 27

HTN is a lanthanic, or silent, disease it is usually asymptomatic until it is very severe and target organ disease has occurred

Question 28

secondary symptoms of primary HTN

Answer 28

pts with severe HTN will experience secondary symptoms to the effects on the blood vessels - fatigue - reduced activity - dizziness - palpitations - angina - dyspnea

Question 29

complications of HTN

Answer 29

most common are target organ diseases -> occur in the heart, brain, peripheral vasculature, kidneys, and eyes - coronary artery disease - left ventricular hypertrophy - heart failure - cerebrovascular disease -> atherosclerosis most common cause - stroke - hypertensive encephalopathy - peripheral arterial disease -> aortic aneurysm, aortic dissection - intermittent claudication (ischemic muscle pain precipitated by activity and relieved with rest) - nephrosclerosis -> end stage renal disease - retinal damage

Question 30

diagnosis of HTN

Answer 30

not based on one elevated reading, but several elevated BPs over several weeks

Question 31

tests used to diagnosis HTN

Answer 31

- history and physical exam -routine lab tests - urinalysis and serum creatinine -> see if kidneys are involved and get baseline - electrolyte levels -> test for hyperaldosteronism - blood urea - fasting blood glucose -> see if pt has DM - fasting total cholesterol, HDL, LDL, triglycerides -> risk of atherosclerosis - urinary albumin in pt with diabetes standard 12 lead ECG

Question 32

ambulatory BP monitoring

Answer 32

24hr ambulatory BP reading are more accurate than office BP helps diagnosis HTN faster fully automated system that tests at intervals over a 24 hour period helpful to avoid white coat hypertension -> elevated BP at doctor offices

Question 33

masked hypertension

Answer 33

lower BP at the doctor office, elevated at home

Question 34

lifestyle modifications for HTN

Answer 34

used as definitive or adjunctive therapy - dietary changes -> reduce sodium intake - limit alcohol ->2 drinks or fewer per day, dont exceed 14 standard drinks per week for men, 9 for women - regular physical activity -> 30min- 1 hour 4 to 7 days a week, higher intensity workouts aren't more effective - avoid tobacco use - stress management -> relaxation techniques, CBT - weight reduction -> ideal BMI = 18.5 to 24.9, waist circumference of <102 for men and <88 for women

Question 35

DASH diet

Answer 35

helps reduce HTN emphasized consumption of fruits, veg, low fat dairy products, dietary and soluble fibres, whole grains, protein from plant sources reduce saturated fat and cholesterol intake

Question 36

sodium intake for reducing HTN

Answer 36

daily adequate sodium intake is 1200 mg to 1500 mg for healthy adults average sodium intake for Canadians is 3500 mg a day sodium restriction may be enough to control high BP in stage 1 HTN or if meds are needed, reducing sodium can decrease the dosage of med

Question 37

med therapy for HTN

Answer 37

general BP goal for med therapy if 140/90, 130/80 for those with CKD and NM 2 main actions - to reduce SVR - decrease volume of circulating blood