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2060B: Pharmacology > Module 13: Pharmacotherapy and Hypertension > Flashcards

Module 13: Pharmacotherapy and Hypertension Flashcards

1
Q

Define hypertension:

A

Hypertension is simply defined as elevated systemic arterial blood pressure.

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2
Q

Define blood pressure:

A

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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3
Q

How is blood pressure measured?

A

Blood pressure is measured with a sphygmomanometer.

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4
Q

What are the 5 steps to measuring blood pressuring?

- How is hypertension diagnosed?

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.

*Before a diagnosis of hypertension, the patient should have this repeated 3 times at least 2 weeks apart.

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5
Q

How is blood pressure classified?

A

By looking at the systolic and diastolic blood pressure

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6
Q

Explain systole and diastole:

- How is it read?

A

Systole – When the heart contracts.

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

*In clinical practice, blood pressure is read as the systolic pressure over the diastolic pressure.

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7
Q

Classification of Hypertension:

“Normal”

A

Systolic less than 120

AND

Diastolic less than 80

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8
Q

Classification of Hypertension:

“Pre-hypertension”

A

Systolic 120-129

OR

Diastolic 80-89

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9
Q

Classification of Hypertension:

“Stage 1 Hypertension”

A

Systolic 140-159

OR

Diastolic 90-99

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10
Q

Classification of Hypertension:

“Stage 2 Hypertension”

A

Systolic greater than 160

OR

Diastolic greater than 100

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11
Q

What are the two types of hypertension?

A

Primary

Secondary

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12
Q

What causes primary hypertension?

A

No known cause

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13
Q

What % accounts for primary hypertension?

A

92%

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14
Q

What age group does primary hypertension affect?

A

90% of people over the age of 55 have high blood pressure

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15
Q

What is secondary hypertension?

A

It has an identifiable cause including:

  • Kidney Disease
  • Hyperthyroidism
  • Pregnancy
  • Erythropoietin
  • Pheochromocytoma (i.e. tumour on adrenal gland = epinephrine release)
  • Sleep apnea
  • Contraceptive use
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16
Q

What are the consequences of hypertension?

A

Increased mobility and mortality

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17
Q

What occurs if hypertension is left untreated?

A
  • Myocardial infarction
  • Kidney failure
  • Stroke
  • Retinal damage
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18
Q

Why is hypertension a silent killer?

A

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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19
Q

What causes hypertension?

A
  1. Amount of salt and water in your body
  2. Conditions of kidneys, nervous systems, and blood vessels
  3. Hormone levels
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20
Q

What are risk factors of hypertension?

A
  • Obesity
  • Stress
  • Smoking
  • High salt diet
  • Diabetes
  • African Descent
  • Medications (i.e. NSAIDS, oral contraceptives, cold medicines with pseudoephedrine)
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21
Q

Why should we lower blood pressure?

A

SAVE LIVES

  • Decreases PT mobility and mortality
  • Decreases incidence of stroke, myocardial infarction, and heart failure
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22
Q

T/F
It is estimated that decreasing blood pressure by just 5 mmHg can reduce the risk of stroke and heart attack by 20 – 35%.

A

True

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23
Q

How is blood pressure determined?

A
  1. 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
  2. Peripheral Resistance: Is determined by arteriolar constriction
    - Constriction of the arteries and arterioles will cause blood pressure to rise

BLOOD PRESSURE = Cardiac Output x Peripheral Resistance

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24
Q

What 3 systems in our body help regulate blood pressure?

A
  1. The sympathetic nervous system.
  2. The renin-angiotensin-aldosterone system (RAAS)
  3. Renal Regulation of Blood Pressure
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25
Q

How does the sympathetic nervous system help regulate blood pressure?
- What reflex does it use?

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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26
Q

Sympathetic Nervous System: Baroreceptor Reflex

  • Where are they located and where do they relay info?
  • What if BP is too low? What occurs to increase BP?
  • What if BP is too high? What occurs to decrease BP?
  • How quickly does it respond?
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 baroreceptor reflex responds rapidly (seconds or minutes) to changes in blood pressure.
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27
Q

T/F
The activity of baroreceptors can not oppose our attempts to lower BP with drugs since the “set point” in patients with hypertension is high.

A

False
The activity of baroreceptors CAN oppose our attempts to lower BP with drugs since the “set point” in patients with hypertension is high.

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28
Q

What is the renin-angiotensin-aldosterone system (RAAS) comprised of?

A

The renin-angiotensin-aldosterone system (RAAS) is comprised of a series of protein hormones.

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29
Q

What does the renin-angiotensin-aldosterone system (RAAS) regulate? (3)

A

The renin-angiotensin-aldosterone system plays a critical role in regulating:

  1. blood pressure
  2. blood volume; and
  3. electrolyte balance.
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30
Q

What does activation of RAAS affect?

A

Kidney and vascular smooth muscles to control BP

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31
Q

T/F

The RAAS is a target for many blood pressure lowering drugs

A

True

32
Q

T/F

Unlike the baroreceptor reflex, activation of the RAAS may take hours or days to influence blood pressure.

A

True

33
Q

THE RAAS:

Renin

  • What does renin catalyze?
  • What is synthesized and secreted?
  • What increases renin release?
A

Renin 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.

The following increase renin release:

  1. Decreased blood volume.
  2. Low blood pressure.
  3. Stimulation of beta 1 receptors on juxtaglomerular cells of the kidney.
34
Q

THE RAAS:

Angiotensin Concerting Enzyme (ACE)

  • What does ACE concert?
  • What does activated Angiotensin II do? (2)
  • What does angiotensin II act on?
A

Angiotensin converting enzyme (ACE) converts the inactive angiotensin I into the active angiotensin II.

Activated Angiotensin II is:

  • potent vasoconstrictor by binding to its receptor (the AT1 receptor) to produce vasoconstriction.
  • 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.

35
Q

Briefly summarize the renin angiotensin aldosterone system:

A

The RAAS system is present to help our bodies regulate blood pressure.

  • When the RAAS system is activated it causes vasoconstriction and renal retention of sodium and water.
  • Vasoconstriction increases blood pressure by increasing peripheral resistance.
  • Increased retention of water and sodium cause an increase in blood volume, which in turn increases cardiac output.
36
Q

How does renal regulation of blood pressure occur?

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.
37
Q

What are 7 methods to treat hypertension (non-drug)?

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.
38
Q

T/F
Pharmacological interventions are the initial recommendation for patients with a diastolic blood pressure of approximately 90 – 95 mmHg.

A

False
NON-pharmacological interventions are the initial recommendation for patients with a diastolic blood pressure of approximately 90 – 95 mmHg.

39
Q

T/F

Non-pharmacological treatments augment the effectiveness of drug therapy in patients with higher blood pressure.

A

True

40
Q

What is the relationship between obesity and hypertension?

A

Direct relationship

41
Q

How does obesity cause hypertension? (2)

A
  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.
42
Q

T/F

Weight loss lowers blood pressure in up to 20% of obese patients.

A

False

Weight loss lowers blood pressure in up to 20% of obese patients.

43
Q

How does sodium increase BP?

- How should we limit salt intake?

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.

44
Q

How can physical exercise decrease 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.

45
Q

How does potassium regulate 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.

46
Q

What patients should avoid high potassium diets?

A

IMPORTANT

Patients taking ACE inhibitors should not be on a high potassium diet.

47
Q

How does the DASH diet influence BP?

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.
48
Q

How does smoking cessation reduce 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.
49
Q

How does alcohol restriction reduce 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

50
Q

How do drugs reduce blood pressure?

A

They reduce cardiac output or peripheral resistance

Cardiac Output - Decreasing:

  • Heart rate
  • Heart contractility
  • Blood volume
  • Venous return

Peripheral Resistance - Decreasing:
- Constriction
Increasing
- Dilation

51
Q

List the sites of action for antihypertensive medication

- Examples of meds in each category

A
  1. Vascular Smooth Muscle
    - Ca-Channel Blockers
    - Thiazide Diuretics
  2. RAAS
    - Beta-blockers
    - Direct Renin Inhibitors
    - ACE Inhibitors
    - ARB’s
    - Aldosterone receptor antagonists
  3. Brainstem
    - Centrally acting alpha-2 agonists
  4. Heart
    - Beta-blockers
    - Ca-Channel blockers
  5. Kidney
    - Thiazide diuretics
    - Loop diuretics
    - Potassium sparing diuretics
52
Q

What are the three main classes of diuretics?

A
  1. Loop diuretics
  2. Thiazide diuretics
  3. Potassium sparing diuretics/aldosterone antagonists
53
Q

T/F

Diuretics are the mainstay therapy for hypertension

A

True

54
Q

How do diuretics function?

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.
55
Q

Diuretics site of action:

  • Loop
  • Thiazide
  • Potassium
A

Diuretics produce more effective decreases in blood pressure at sites of high sodium reabsorption

  1. Loop =
  2. Thiazide = Distal Tubule
  3. Potassium = Collecting Duct
56
Q

Loop Diuretics:

  • Action?
  • Reserved for? (3)
  • Adverse Effects
A

The most effective diuretics available.

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

Loop diuretics are usually reserved for 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.

Remember, this fluid is then excreted out in the urine

Adverse effects include:

  1. *Hypokalemia – may cause fatal cardiac dysrhythmias
  2. Hyponatremia
  3. Dehydration
  4. Hypotension
57
Q

Thiazide Diuretics:

  • Mechanisms (2)
  • Diuresis production?
  • Used alone?
  • Adverse effects?
A

*Are the most commonly used class of drug to treat hypertension.

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.

Adverse Effects include:

  1. Hypokalemia – may cause fatal cardiac dysrhythmias
  2. Dehydration
58
Q
  1. Potassium Sparing Diuretics/Aldosterone Antagonists
    - Effective?
    - Action?
    - Used alone?
    - Should not be used with?
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.

The primary adverse event associated with potassium sparing diuretics is hyperkalemia, which may result in fatal dysrhythmias.

59
Q

How do beta-blockers treat hypertension?

A

Beta blockers are effective at treating hypertension by two distinct mechanisms:

  1. Blocking cardiac beta 1 receptors
    - Binding of catecholamines (i.e. epinephrine, norepinephrine) to cardiac beta receptors causes increased cardiac output.
    - Blocking beta receptors decreases cardiac output and therefore decreases blood pressure.
  2. Blocking beta 1 receptors on juxtaglomerular cells
    - Juxtoglomerular cells release renin which activates the RAAS pathway causing vasoconstriction.
    - Beta blockers decrease renin release therefore decreasing RAAS mediated vasoconstriction (peripheral resistance).
60
Q

T/F

Beta blocker drugs all have the suffix “olol”.

A

True

For example propanolol, metoprolol etc. Remember, these are antagonists since they block receptors!

61
Q

What are the classes of beta-blockers?

A

Beta blockers can be classified as either first generation or second generation.

1st generation beta blockers

  • These drugs produce non-selective blockade of beta receptors.
  • Inhibit both beta 1 (in the heart and juxtaglomerular cells) and beta 2 (in the lung) receptors.

2nd generation beta blockers
- These drugs produce selective blockade of beta 1 receptors.

62
Q

Adverse effects of beta-blockers?

- Selective vs. Non-selective

A

Selective beta 1 receptor blockers have the following adverse events:

  • Bradycardia (slow heart rate)
  • Decreased cardiac output
  • Heart failure (rare)
  • Rebound hypertension/cardiac excitation if withdrawn abruptly. The dose of beta blockers should be tapered slowly over 10 – 14 days to prevent this.

Non-selective beta blockers have the same adverse events as selective beta blockers but also cause:

  • Bronchoconstriction due to blockade of beta 2 receptors in the lung. Non-selective beta blockers should be avoided in patients with asthma or other pulmonary diseases.
  • Inhibition of hepatic and muscle glycogenolysis. This can be dangerous in patients with diabetes if they accidentally take too much insulin.
63
Q

How do ACEI decreased BP?

A

ACEI decrease blood pressure by two mechanisms:

  1. Decreasing the production of angiotensin II
    - Angiotensin II is a potent vasoconstrictor so decreasing it causes vasodilation.
    - Decreased angiotensin II also decreases total blood volume, therefore ACEI reduce cardiac output and peripheral resistance.
  2. Inhibiting the breakdown of bradykinin.
    - Elevated levels of bradykinin cause vasodilation.
64
Q

T/F

ACEI all have the suffix “pril”.

A

True

For example captopril, ramipril.

65
Q

Adverse effects of ACEI?

A

ACEI are generally well tolerated however there are some adverse effects.

Adverse effects can be linked to the reduction of angiotensin II or elevated bradykinin.

  1. Side effects from decreased angiotensin II
    - 1st dose hypotension – first few doses should be low.
    - Hyperkalemia – decreased angiotensin II causes decreased aldosterone release. Decreased aldosterone leads to potassium retention. Potassium supplements and use of potassium sparing diuretics should be avoided.
  2. Side effects from increased bradykinin
    - Persistent cough (in 5-10% of patients).
    - Angioedema (rare but potentially fatal).

Use with certain NSAIDs may decrease the effect of ACE inhibitors.

66
Q

How do ARBs reduce BP?

A

ARBs have a similar action to ACEI in that they decrease the actions of angiotensin II, although the mechanism differs.

  • ARBs act by blocking the binding of angiotensin II to its receptor (the AT1 receptor).
  • Therefore ARB’s block the actions of angiotensin II but do not affect its synthesis.

ARBs cause vasodilation by blocking the action of angiotensin II on arterioles.
- ARBs also decrease aldosterone release from the adrenal cortex causing increased sodium and water excretion.

67
Q

T/F

ARBs all have the suffix “sartan”.

A

True

For example losartan, valsartan etc.

68
Q

Adverse affects of ARB’s

A
  • ARBs don’t inhibit bradykinin breakdown as well as ACEI do, so they don’t produce persistent cough.
  • Incidence of angioedema is much lower than with ARBs than with ACEI.
  • ARBs still cause hyperkalemia due to the same mechanism as ACEI
69
Q

How do direct renin inhibitors decreases BP?

A

DRI’s bind to renin and block the conversion of angiotensinogen to angiotensin I.

  • Since conversion of angiotensinogen to angiotensin I is the rate-limiting step in the RAAS pathway, DRIs can influence the entire pathway.
  • Despite DRI’s decreasing plasma renin activity by 50-80%, its blood pressure lowering effect is the same as other classes of drugs (i.e. ACEI and ARBs).
70
Q

Adverse effects of DRIs

A
  • Hyperkalemia – should not be used in combination with other drugs that may cause hyperkalemia (i.e. potassium sparing diuretics, ACEI) and potassium supplements.
  • Very low incidence of persistent cough and angioedema (much lower than ACEI).
  • Diarrhea
71
Q

How does Ca-channe blockers lower BP?

A

Calcium channels bring calcium from outside the cell to inside the cell.

  • In the heart and smooth muscle that surrounds arteries, calcium is essential for contraction.
  • Therefore the activity of calcium channels plays an important role for contraction of the heart and smooth muscle that surrounds the arteries and arterioles.
  • Calcium channel blockers block the entry of calcium into heart cells and smooth muscle cells, therefore decreasing contraction.
72
Q

What are the 2 categories of Ca-channel blockers?

  • Suffix
  • Adverse effects
A
  1. Dihydropyridine calcium channel blockers
    - Dihydropyridine calcium channel blockers significantly decrease calcium influx into smooth muscle of arteries.
    - This results in relaxation of the muscle around the arteries and causes vasodilation.
    - At therapeutic doses they do not act on the heart.
    - Suffix of drug names is always “dipine”. For example, nifedipine, felodipine etc.
Adverse Effects
•	Flushing
•	Dizziness
•	Headache
•	Peripheral edema
•	Reflex tachycardia
•	Rash
  1. Non-dihydropyridine calcium channel blockers
    - These drugs block calcium channels in both the heart and smooth muscle of the arteries.
    - Therefore, in addition to producing vasodilation of arteries, non-dihydropyridine calcium channel blockers also decrease cardiac output.
Adverse Effects
•	Constipation
•	Dizziness
•	Flushing
•	Headache
•	Edema
•	May compromise cardiac function.  Should be used with caution in patients with cardiac failure.
73
Q

How do centrally acting alpha-2 antagonists lower BP?

A

These drugs bind to and activate alpha 2 receptors in the brainstem.

  • Activation of these receptors decreases sympathetic outflow to the heart and blood vessels.
  • Sympathetic activity normally causes increased cardiac output and vasoconstriction.
  • By inhibiting sympathetic outflow, centrally acting alpha 2 receptor agonists decrease cardiac output and peripheral resistance.
74
Q

Adverse Effects of centrally acting alpha-2 antagonists:

A
  • Drowsiness
  • Dry mouth
  • Rebound hypertension if withdrawn abruptly.
75
Q

How is treatment decided for BP?

  • Patient less than 140/90mg
  • Diabetes or chronic kidney disease
  • Renal disease
A

Deciding how to treat patients with hypertension can be difficult.

The target blood pressure that most patients should achieve is less than 140/90 mmHg.

Patients with diabetes or chronic kidney disease should achieve a blood pressure less than 130/80 mmHg.
- Keeping blood pressure below 130/80 mmHg in patients with chronic kidney disease slows the progression of kidney damage.

In patients with severe renal disease, thiazide diuretics are ineffective so loop diuretics should be used.

Treatment algorithms exist for patients with just hypertension and for patients with hypertension plus diabetes or kidney disease.
- These algorithms help guide dosing.

2060B: Pharmacology (18 decks)

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