Module 13 Flashcards

1
Q

Define hypertension

A
  • Hypertension is simply defined as elevated systemic arterial blood pressure.
  • Blood pressure is a measurement of the force against the walls of your arteries as the heart pumps blood through the body.
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2
Q

What is blood pressure measured with?

A

A sphygmomanometer

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3
Q

List the steps for accurately obtaining blood pressure

A
  1. The patient should be seated for at least 5 minutes.
  2. No caffeine or nicotine within 30 minutes of measurement.
  3. Feet should be touching the floor (not dangling).
  4. Arm should be elevated to heart level.
  5. Two measurements in each arm should be taken 5 minutes apart.
  6. Before a diagnosis of hypertension, the patient should have this repeated 3 times at least 2 weeks apart.
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4
Q

Blood pressure is classified by looking at the systolic and diastolic blood pressure. Define systolic blood pressure

A

The blood pressure when the heart contracts.

Systole – When the heart contracts.

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5
Q

Define diastolic blood pressure

A

Measures the blood pressure in your arteries when your heart rests between beats.

Diastole – Period of time when the heart fills after a contraction.

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6
Q

How is blood pressure read?

A

Systolic/diastolic BP

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7
Q

What is considered a normal blood pressure?

A

Less than 120/80
Systolic = <120 mm Hg
Diastolic = < 80 mm Hg

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8
Q

What is considered prehypertension?

A

Systolic = 120-139 mm Hg
Diastolic = 80-89 mm Hg

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9
Q

What is considered Stage I hypertension?

A

Systolic = 140-159 mm Hg
Diastolic = 90-99 mm Hg

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10
Q

What is considered Stage II hypertension?

A

Systolic = > 160 mm Hg
Diastolic = > 100 mm Hg

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11
Q

What are the two types of hypertension?

A
  1. Primary Hypertension
  2. Secondary Hypertension
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12
Q

Describe Primary Hypertension

A
  • Hypertension of no known cause.
  • Approximately 92% of all cases of hypertension.
  • 90% of people over the age of 55 have high blood pressure.
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13
Q

Describe Secondary Hypertension

A
  • Hypertension with an identifiable cause.
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14
Q

What are some causes of secondary hypertension

A
  1. Kidney disease
  2. Hyperthyroidism
  3. Pregnancy
  4. Erythropoietin
  5. Pheochromocytoma – tumour on the adrenal gland that causes excess epinephrine release.
  6. Sleep apnea
  7. Contraceptive use
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15
Q

What are some consequences of hypertension?

A
  • Chronic hypertension is associated with increased morbidity and mortality.
  • If untreated, hypertension can cause myocardial infarction, kidney failure, stroke, or retinal damage.
  • Unfortunately, hypertension is a “silent killer” as many patients may have elevated blood pressure for years before they show any symptoms.
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16
Q

Why do we care about lowering blood pressure?

A

Lowering blood pressure saves lives.
* Clinical trials have conclusively demonstrated that decreasing blood pressure decreases patient morbidity and mortality.
* Lowering blood pressure decreases the incidence of stroke, myocardial infarction, and heart failure.
* It is estimated that decreasing blood pressure by just 5 mmHg can reduce the risk of stroke and heart attack by 20 – 35%.

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17
Q

Blood pressure is determined by what?

A

Cardiac output and peripheral resistance

BP is the product of cardiac output times peripheral resistance

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18
Q

Describe cardiac output

A

Cardiac Output
* Is determined by heart rate, heart contractility, blood volume and venous return.
* An increase in any of these results in an increase in blood pressure.

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19
Q

Describe peripheral resistance

A

Peripheral Resistance
* Is determined by arteriolar constriction.
* Constriction of the arteries and arterioles will cause blood pressure to rise.

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20
Q

What are the three systems that our body has to regulate BP?

A
  1. The sympathetic nervous system.
  2. The renin-angiotensin-aldosterone system (RAAS)
  3. Renal Regulation of Blood Pressure (kidney)
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21
Q

What is the sympathetic nervous system?

A
  • Helps us respond to stress, i.e. the fight-or flight response.
  • Is also constantly active to help keep body functions (including blood pressure) in homeostasis.
  • The sympathetic nervous system has a reflex circuit called the baroreceptor reflex that helps keep blood pressure at a set level.
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22
Q

Describe the Baroreceptor Reflex pathway used to affect BP

A
  • Baroreceptors on the aortic arch and carotid sinus (in the carotid arteries of the neck) sense blood pressure and relay the information back to the brainstem.
  • If BP is perceived to be too low, the brainstem sends impulses along sympathetic neurons that stimulate the heart to cause increased cardiac output and smooth muscle on arteries causing vasoconstriction. This increases BP.
  • If BP is perceived to be too high, sympathetic activity is decreased. This causes decreased cardiac output and vasodilation.
  • The activity of baroreceptors can oppose our attempts to lower BP with drugs since the “set point” in patients with hypertension is high.
  • The baroreceptor reflex responds rapidly (seconds or minutes) to changes in blood pressure.
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23
Q

What does RAAS stand for?

A

renin-angiotensin-aldosterone system

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24
Q

Describe RAAS

A
  • The renin-angiotensin-aldosterone system (RAAS) is comprised of a series of protein hormones.
  • The renin-angiotensin-aldosterone system plays a critical role in regulating blood pressure, blood volume and electrolyte balance.
  • Activation of the RAAS affects the kidney and vascular smooth muscle to control blood pressure.
  • The RAAS is a target for many blood pressure lowering drugs.
  • Unlike the baroreceptor reflex, activation of the RAAS may take hours or days to influence blood pressure.
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25
Q

What is the RAAS pathway?

A

Angiotensinogen -> Renin (synthesized/secreted from juxtaglomerular cells of kidney) -> Angiotensin I (inactive) -> Angiotensin Converting Enzyme -> Angiotensin II = Aldosterone and Antidiuretic Hormone (ADH)

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26
Q

What is Renin?

A
  • Catalyzes the formation of angiotensin I from angiotensinogen.
  • This represents the rate-limiting step in angiotensin II formation.
  • Renin is synthesized and secreted by the juxtaglomerular cells of the kidney into the blood.
27
Q

What increases renin release?

A
  1. Decreased blood volume.
  2. Low blood pressure.
  3. Stimulation of beta 1 receptors on juxtaglomerular cells of the kidney.

Note: juxtaglomerular = beside the glomerulus

28
Q

When the RAAS system is activated it causes what?

A

vasoconstriction and renal retention of sodium and water

29
Q

Vasoconstriction increases BP by what?

A

increasing peripheral resistance

30
Q

Increased retention of water and sodium cause an increase in BP, which in turn does what?

A

increases cardiac output

31
Q

Describe Angiotensin Converting Enzyme (ACE)

A
  • Angiotensin converting enzyme (ACE) converts the inactive angiotensin I into the active angiotensin II.
  • Activated Angiotensin II is:
    o potent vasoconstrictor by binding to its receptor (the AT1 receptor) to produce vasoconstriction.
    o stimulates release of aldosterone from the adrenal cortex. Aldosterone acts on the kidneys to increase sodium retention, which can increase water retention.
  • Angiotensin II also acts on the posterior pituitary gland to release antidiuretic hormone (ADH also called vasopressin). ADH causes water retention by the kidney.
32
Q

Describe the renal regulation of BP

A
  • The kidney is a critical organ in terms of blood pressure regulation.
  • If blood pressure decreases for a prolonged time period, the kidney retains water.
  • This increased water retention leads to increased blood volume.
  • Increased blood volume causes increased cardiac output and therefore increased blood pressure.
33
Q

What is the initial recommendation for patients with a diastolic BP of approx. 90-95 mm Hg?

A

Non-pharmacological interventions

34
Q

What are some non-pharmacologic interventions used to lower BP?

A
  1. Decreasing body weight.
  2. Restricting sodium intake.
  3. Physical exercise.
  4. Potassium supplementation.
  5. The DASH diet.
  6. Smoking cessation.
  7. Alcohol restriction.
35
Q

Describe how decreasing body weight affects BP

A
  • There is a direct relationship between obesity and hypertension.
  • Obesity is thought to cause hypertension by two mechanism:
  1. Obese patients have increased insulin secretion, which causes tubular reabsorption of Na+ and therefore water reabsorption and a higher blood volume.
  2. Obese patients also have increased activity of the sympathetic nervous system.
  • Weight loss lowers blood pressure in up to 80% of obese patients.
36
Q

Describe how restricting sodium intake affects BP

A
  • Salt is necessary to our bodies, however when sodium chloride (salt) intake is too high, it has a negative effect on blood pressure.
  • The kidney regulates the amount of salt in our body, eliminating excess salt in the urine.
  • When salt levels are too high, it causes water to be reabsorbed from the kidney into the blood.
  • This causes increased extracellular (blood) volume and therefore increased blood pressure.
  • Limiting salt intake to 5 g per day decreases systolic BP by approximately 12 mmHg and diastolic BP by 6 mmHg.
37
Q

Describe how physical exercise affects BP

A
  • Regular exercise decreases blood pressure by an average of 10 mmHg.
  • Regular exercise decreases extracellular fluid volume and circulating levels of plasma catecholamines (like epinephrine).
  • Importantly, the benefits of exercise are seen even if patients don’t restrict sodium or lose weight during the training period.
38
Q

Describe how potassium supplementation affects BP

A
  • Just as total body sodium levels are positively correlated with blood pressure, total body potassium levels are inversely correlated with blood pressure.
  • This means high total body potassium results in lower blood pressure.
  • High potassium diets decrease blood pressure by increasing sodium excretion, decreasing renin release and causing vasodilation.
  • Preferred sources of potassium are fresh fruits and vegetables.
39
Q

Patients taking which BP drug should NOT be on a high potassium diet?

A

ACE inhibitors

40
Q

Describe the DASH diet

A
  • The “DASH diet” was derived from the dietary approaches to stop hypertension studies.
  • These studies gave subjects one of three diets and evaluated blood pressure. The three diets included:
  1. Standard North American diet
  2. Standard North American diet plus extra fruit and vegetables.
  3. A diet rich in fruits, vegetables, low fat dairy, lean meats (poultry and fish), whole grains, nuts and legumes. The diet also excluded foods high in saturated fat, total fat and cholesterol.
  • The results were remarkable with most patients achieving lower blood pressure within 14 days without lowering salt intake.
  • The best results were seen in patients with prehypertension.
  • Patients with severe hypertension are encouraged to stick to this diet in combination with blood pressure lowering medications.
41
Q

Describe how smoking cessation affects BP

A
  • Smoking acutely elevates blood pressure but has not been linked to be causal in the development of hypertension.
  • Despite this, patients with hypertension should be encouraged to quit.
  • Both smoking and hypertension are risk factors for the development of cardiovascular disease.
42
Q

Describe how alcohol restriction affects BP

A
  • Excessive alcohol consumption increases blood pressure.
  • It also can decrease response to some antihypertensive medications.
  • Patients with hypertension or prehypertension should consume less than 2 drinks per day and less than 14 drinks per week for men and 9 drinks per week for women.
43
Q

Drugs that decrease BP do so by decreasing what?

A

cardiac output and peripheral resistance

44
Q

Which BP drugs target the vascular smooth muscle?

A
  • Calcium channel blockers
  • Thiazide diuretics
45
Q

Which BP drugs target the RAAS?

A
  • Beta blockers
  • Direct renin inhibitors
  • ACE inhibitors
  • ARBs
  • Aldosterone receptor antagonists
46
Q

Which BP drugs target the Brainstem?

A
  • Centrally acting alpha 2 agonists
47
Q

Which BP drugs target the Heart?

A
  • Beta blockers
  • Calcium channel blockers
48
Q

Which BP drugs target the Kidney?

A
  • Thiazide diuretics
  • Loop diuretics
  • Potassium Sparing diuretics
49
Q

What is the mainstay therapy for hypertension?

50
Q

What are the 3 main classes of diuretics?

A
  1. loop diuretics
  2. thiazide diuretics
  3. potassium sparing diuretics/aldosterone antagonists
51
Q

How do diuretics work?

A
  • Diuretics work by blocking sodium and chloride ion reabsorption from the nephron of the kidney.
  • By preventing reabsorption of Na+ and Cl- diuretics make an osmotic pressure within the tubule (“attracts the water”) that prevents the reabsorption of water.
  • The retention of water within the nephron promotes excretion of water and sodium/chloride ions.
52
Q

What is the most effective diuretic available?

A

Loop diuretics

53
Q

Loop diuretics are usually reserved for which situations?

A

Situations that require rapid loss of fluid such as:
1. Edema
2. Severe hypertension that does not respond to milder diuretics.
3. In severe renal failure.

54
Q

Describe how loop diuretics work?

A

They act by blocking sodium and chloride ion reabsorption in the thick ascending limb of the Loop of Henle.

55
Q

What are the adverse effects of loop diuretics?

A
  1. *Hypokalemia – may cause fatal cardiac dysrhythmias
  2. Hyponatremia
  3. Dehydration
  4. Hypotension

*The transporter responsible for reabsorbing Na+ and Cl-, also transports K+ into the blood which is why hypokalemia occurs

56
Q

What is the most commonly used class of drug to treat hypertension?

A

Thiazide diuretics

57
Q

Describe how thiazide diuretics work?

A
  • They act by two main mechanisms:
  1. Blocking sodium and chloride ion reabsorption in the distal tubule.
  2. Decreasing vascular resistance (the mechanism of which is unknown).
  • The maximum amount of diuresis (i.e. urine production) is much less than loop diuretics.
  • For many hypertensive patients thiazide diuretics alone are enough to control blood pressure.
58
Q

What are the adverse effects of thiazide diuretics?

A
  1. Hypokalemia – may cause fatal cardiac dysrhythmias
  2. Dehydration
  3. Hyponatremia
59
Q

What is the alternative name for potassium sparing diuretics?

A

Aldosterone Antagonists

60
Q

Describe potassium sparing diuretics

A
  • Produce minimal lowering of blood pressure.
  • Act by inhibiting aldosterone receptors in the collecting duct.
  • Aldosterone normally causes sodium reuptake and potassium secretion.
  • Blocking aldosterone receptors causes increased sodium excretion and potassium retention (hence “potassium sparing”) in the body.
  • The main use is in combination with thiazide and loop diuretics to counteract the hypokalemia side effect.
  • Potassium sparing diuretics should not be used with ACE inhibitors or renin inhibitors as these drugs also conserve potassium.
61
Q

What is the primary adverse event associated with potassium sparing diuretics?

A

hyperkalemia, which may result in fatal dysrhythmias

62
Q

Define hyperkalemia

A

Hyperkalemia is defined as a serum or plasma potassium level above the upper limits of normal, usually greater than 5.0 mEq/L to 5.5 mEq/L. While mild hyperkalemia is usually asymptomatic, high potassium levels may cause life-threatening cardiac arrhythmias, muscle weakness, or paralysis.

63
Q

Angiotensin II is a very potent what?

A

vasoconstrictor