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Lecture 13 Flashcards

Drugs for hypertension (81 cards)

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1
Q

What is hypertension?

A

elevated systemic arterial blood pressure

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2
Q

How is blood pressure measured and with what?

A

measurement of the force against the walls of your arteries as your heart pumps blood through your body
- use a sphygmomanometer

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3
Q

What steps need to be taken to accurately measure blood pressure?

A
  1. patient seated for at least 5 min
  2. no caffeine or nicotine within 30 min of measurement
  3. feet touching the floor
  4. arm elevated to heart level
  5. two measures in each arm taken 5 min apart
  6. repeat 3 times at least 2 weeks apart b4 diagnosis
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4
Q

What is blood pressure defined by?

A
  • systolic/diastolic pressure in mm Hg
  • systole: when the heart contracts (pumps blood out)
  • diastole: period of time when the heart fills after contraction
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5
Q

What is primary hypertension characterized by?

A
  • has no known cause
  • most cases of hypertension are primary
  • most people over 55 have high blood pressure
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6
Q

What is secondary hypertension characterized by?

A
  • has an identifiable cause
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7
Q

What are some of the causes of secondary hypertension?

A
  • kidney disease
  • hyperthyroidism
  • pregnancy
  • erythropoietin
  • pheochromocytoma (tumor on adrenal gland = excess epinephrine release)
  • sleep apnea
  • contraceptive use
  • water and salt in the body
  • stress, smoking, obesity, diabetes, African descent
  • conditions of CNS and blood vessels
  • NSAIDS, cold medicines with pseudoephedrine
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8
Q

Consequences of Hypertension?

A
  • increased morbidity and mortality
  • myocardial infarction
  • kidney failure
  • stroke
  • renal damage
  • known as a “silent killer”
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9
Q

Why do we want to lower blood pressure?

A
  • saves lives
  • decreasing blood pressure decreases patient morbidity and mortality, decreases incidence of stroke, myocardial infarction, and heart failure
  • minor decreases in blood pressure = huge beneficial effect
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10
Q

What are the determinants of Blood Pressure?

A
  • cardiac output
  • peripheral resistance

blood pressure = cardiac output x PR

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11
Q

What is cardiac output?

A
  • determined by heart rate, heart contractility, blood volume and venous return
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12
Q

What is peripheral resistance?

A
  • determined by arteriolar constriction

constriction of the arteries and arterioles will cause blood pressure to rise

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13
Q

What are the 3 systems that our body has to regulate blood pressure?

A
  1. sympathetic nervous system
  2. the renin-angiotension-aldosterone system (RAAS)
  3. Renal regulation of blood pressure (kidney)
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14
Q

What does the sympathetic nervous system do?

A
  • helps us respond to stress (fight or flight)
  • constantly active for body functions in homeostasis
  • has a reflex circuit called the baroreceptor reflex that helps keep blood pressure at a set level
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15
Q

How does the SNS affect our body when we’re stressed?

A
  • pupils dilate (far vision)
  • eyes water, tears form
  • mouth gets dry
  • sweating increases
  • heart rate increases
  • adrenaline rush
  • breathing quickens
  • bronchial passage dilates
  • digestive functions inhibited
  • digestive activity decreases
  • bladder relaxes
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16
Q

What are baroreceptors and where are they located?

A
  • located on aortic arch and carotid sinus (in
    the carotid arteries of the neck)
  • sense blood pressure and relay the info back to brainstem
  • respond rapidly (s to min) to changes in BP
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17
Q

What does the brainstem do if baroreceptors perceive BP as being too low?

A
  • sends impulses along sympathetic neurons = stimulate heart to increased cardiac output and vasoconstriction of arteries = INCREASED BP
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18
Q

What does the brainstem do if baroreceptors perceive BP as being too high?

A
  • sympathetic activity decreases = decreased cardiac output and vasodilation = DECREASED BP
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19
Q

Baroreceptors and drug interactions

A
  • activity of baroreceptors can oppose our attempts to lower BP with drugs (since “set point” in patients with hypertension is high
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20
Q

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

A
  • is a system comprised of a series of protein hormones that plays a critical role in regulating BP, blood volume, and electrolyte balance
  • RAAS activation affects kidney and vascular smooth muscle to control blood pressure
  • can take hrs - days
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21
Q

Step one of the RAAS pathway

A

RATE LIMITING STEP

- angiotensinogen cleaved by RENIN into inactive angiotensin I

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22
Q

Step two of the RAAS Pathway

A
  • angiotensin I converted to active angiotensin II by ANGIOTENSIN CONVERTING ENZYME
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23
Q

Step three of the RAAS pathway

A
  • action angiotensin II stimulates the release of aldosterone and antidiuretic hormone (ADH)
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24
Q

What is renin?

A
  • enzyme that catalyzes the formation of angiotension I from angiotensinogen (rate limiting step)
  • synthesized and secreted by the juxtaglomerular (beside the glomerulus) cells of the kidney into the blood
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25
What increases renin release?
1. decreased blood volume 2. low blood pressure 3. stimulation of beta 1 receptors on the juxtaglomerular cells of the kidney
26
What is the angiotensin converting enzyme (ACE)?
- converts inactive angiotensin I into the active angiotensin II
27
What does active angiotensin II do?
- is a potent vasoconstrictor when binding its receptor (AT1) - stimulates release of aldosterone from the adrenal cortex (which acts on the kidneys to increase sodium and water retention) - acts on posterior pituitary gland to release antidiuretic hormone (ADH/vasopressin) causing water retention by the kidneys
28
How does vasoconstriction increase blood pressure?
- by increasing peripheral resistance
29
How does increased sodium and water retention increase cardiac output?
- by increasing blood volume
30
How is blood pressure regulated renally?
- when blood pressure is decreased for prolonged period, kidneys retain water = increased blood volume = increased cardiac output = increased blood pressure
31
What are the non-pharmacologic interventions for hypertension?
- decreasing body weight - restricting sodium intake - physical exercise - potassium supplementation - the DASH diet - smoking cessation - alcohol restriction
32
How can obesity cause hypertension?
1. obesity = increased insulin secretion = tubular reabsorption of NA+ = Water reabsorption and higher blood volume 2. obesity = increased SNS activity
33
How can restricting sodium intake get rid of hypertension?
- when salt levels are too high water is reabsorbed from kidney into blood = increased blood volume = increased blood pressure
34
How can physical exercise mitigate hypertension?
- decreased blood pressure by decreased blood volume and circulating levels of plasma catecholamines (like epinephrine) - benefits seen without weight loss or sodium changes
35
How can potassium levels affect blood pressure?
- inversely correlated = high K+ = lower BP by increasing sodium excretion, decreasing renin release, and causing vasodilation * high potassium diets and ACE inhibitors should NOT be taken together!!!
36
What is the DASH diet?
- Dietary Approaches to Stop Hypertension - 3 diets given during study: 1. standard north american diet 2. standard north american diet + extra fruit and veggies (K+) 3. all diet rich in fruits, veggies, low fat dairy, lean meats, whole grains, nuts and legumes - most patients saw lower blood pressure within 14 days - best results seen in those with pre-hypertension - severe hypertension = dash diet + medications
37
smoking and blood pressure?
- elevates BP but not linked to be causal in hypertension | - still good to quit
38
Alcohol and BP
- consumption increases BP | - also decreases response to some antihypertensive medications
39
What are the sites of action of antihypertensive medications?
- vascular smooth muscle (calcium channel blockers; thiazide diuretics) - RAAS ( beta blockers; direct renin inhibitors; ACE inhibitors; ARBs; aldosterone receptor antagonists) - Brainstem ( centrally acting alpha 2 agonists) - heart (beta blockers, calcium channel blockers) - kidney (thiazide diuretics; loop diuretics; potassium spakring diuretics)
40
What are the 3 main classes of diuretics?
1. loop diuretics 2. thiazide diuretics 3. potassium sparing diuretics/aldosterone antagonists
41
How do diuretics work?
- block sodium and chloride ion reabsorption from the nephron in the kidney = osmotic pressure within the tubule (attracts the water) prevents reabsorption of water = water retention of water in nephron promotes excretion of water and Na+/Cl- ions
42
What are the sites of action for diuretics?
look at paper notes for diagram - mostly in ascending limb of the loop of henle, distal tubule and late distal tubule - most absorbed in early, some in middle, less in late
43
How do loop diuretics work?
- by blocking sodium and chloride ion reabsorption in the thick ascending limb of the loop of henle - most effective available
44
When are loop diuretics 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 - fluid then excreted out in the urine
45
What are the adverse effects of loop diuretics?
1. hypokalemia (low K+ levels) - may cause fatal cardiac dysrhythmias (occurs bc transporter responsible for reabsorbing Na+ and Cl- also transports K+ into blood) 2. hyponatremia (low Na+ blood lvls) 3. dehydration 4. hypotension (low BP)
46
How do thiazide diuretics work?
- two main mechanisms: 1. blocking Na+ and Cl- ion reabsorption in the distal tubule 2. decreasing vascular resistance (mechanism unknown) - most commonly used - less urine production - usually good enough to be used alone
47
What are the adverse effects of thiazide diuretics?
1. hypokalemia 2. dehydration 3. hyponatremia
48
How do potassium sparing diuretics/ aldosterone antagonists work?
- act by inhibiting aldosterone receptors (normally cause sodium reuptake and K+ secretion) in the collection duct = increased Na+ excretion and K+ retention - usually used in combination with thiazide and loop diuretics to counteract hypokalemia side effect - should NOT be used with ACE or renin inhibitors (also conserve K+)
49
Adverse effects of PSD/AA?
- hyperkalemia
50
What are the 2 mechanisms by which beta blockers (antagonists) treat hypertension?
1. blocking cardiac beta 1 receptors | 2. blocking beta 1 receptors on juxtaglomerular cells
51
How does blocking cardiac beta 1 receptors treat hypertension?
- binding of catecholamines (like epinephrine, norepinephrine) to cardiac beta receptors = increased cardiac output - blocking receptors decreases cardiac output = decreased BP
52
How does blocking beta 1 receptors on juxtaglomerular cells treat hypertension?
- JG cells release renin = activation of RAAS pathway = vasoconstriction = increased BP - decreasing renin release by blocking receptors = decreased RAAS mediated vasoconstriction (peripheral resistance)
53
What suffix to beta blocking drugs have?
- olol | ex. propanOLOL, metoprOLOL
54
What are the 2 different classes of beta blockers?
- 1 st generation: produce non-selective blockade of beta receptors; inhibit both beta 1 and beta 2 recept. - 2nd gen: produce selective blockade of beta 1 recepts
55
Adverse effects of 2nd gen beta blockers
- same adverse events as non-selective 1st gen but also: 1. bronchoconstriction in the lung 2. inhibition of hepatic and muscle glycogenolysis
56
Adverse effects of 1st gen beta blockers
- bradycardia (slow heart rate) - decreased cardiac output - heart failure (rare) - rebound hypertension/cardiac excitation if withdrawn abruptly
57
What are the two mechanisms by which Angiotensin concerting enzyme inhibitors (ACE inhibitors) decrease blood pressure?
1. decreasing the production of angiotensin II | 2. inhibiting the breakdown of bradykinin
58
How does decreasing the production of angiotensin II decrease BP?
- angiotensin II is a potent vasoconstrictor so decreasing it = vasodilation - also decreasing total blood volume - so ACEI decrease cardiac output AND peripheral resistance
59
How does inhibiting the breakdown of bradykinin decrease DP?
- elevated levels cause vasodilation
60
What suffix do all ACEI drugs have?
- pril | ex. captoPRIL
61
What are the adverse effects of decreasing angiotensin II?
- 1st dose hypotension | - hyperkalemia (decrease AII = decreased aldosterone = K+ retention)
62
What are the adverse effects of increased bradykinin?
- persistent cough | - angioedema
63
What happens if you use ACEI and NSAIDS together?
- potential decrease of ACEI effects
64
How do angiotensin receptor blockers (ARBs) work?
-block the actions of angiotensin II (but not synthesis) by binding to its receptor (AT1) = vasodilation - also decrease aldosterone release form the adrenal cortex causing increased sodium and water excretion
65
what suffix do all ARBs have?
- sartan | ex. loSARTAN
66
What are the adverse effects of ARBS
- dont inhibit bradykinin breakdown like ACEIs so no cough - no hyperkalemia - incidence of angioedema is much lower
67
How do direct renin inhibitors (DRIs) work?
- bind to renin to block conversion of angiotensin to angiotensin I - DRIs influence entire pathway bc it the rate limiting step - BP lowering effects the same as the other classes
68
What are the adverse effects of DRIs?
- hyperkalemia ( not to be used in combo with K+ sparing diuretics, ACEI, K+ supplements) - diarrhea - low incidence of cough ) angioedema
69
What are calcium channel blockers ?
- block entry of calcium into heart cells and smooth muscle cells, decreasing contraction of he heart
70
What are the two categories of calcium channel blockers?
1. dihydropyridine calcium channel blockers | 2. non-dihydropyridine calcium channel blockers
71
How do dihydropyridine calcium channel blockers work?
- significantly decrease Ca+ influx into smooth muscle of arteries = relaxation of the muscle around the arteries = vasodilation - do not act on the heart
72
What suffix do dihydropyridine CCBs have?
- dipine | ex. nifeDIPINE
73
What are the adverse effects of DCCBS?
- flushing - dizziness - headache - peripheral edema - reflex tachycardia - rash
74
How do non-dihydropyridine calcium blockers work?
- block calcium channels in both the heart and smooth muscle of the arteries - in addition, also decrease cardiac output
75
What are the adverse effects of NDCCBS?
- constipation - dizziness - flushing - headache - edema - may compromise cardiac function
76
What are centrally acting alpha 2 agonists?
- bind to a activate alpha 2 receptors in the brainstem = decreased sympathetic outflow to the heart and blood vessels - decrease cardiac output and peripheral resistance
77
What are the adverse effects of CAA2As?
- drowsiness - dry mouth - rebound hypertension if withdrawn abruptly
78
Treatment algorithm for prehypertension
prehypertension -> lifestyle modifications -> thiazide diuretics
79
Treatment algorithm for stage 1 hypertension
stage 1 hypertension -> lifestyle modifications -> thiazide diuretic -> thiazide diuretic + ACEI, ARB, BB, or CBB
80
Treatment for stage 2 hypertension
stage 2 hypertension -> lifestyle modification + thiazide diuretic + ACEI, ARB, BB, or CBB
81
Treatment algorithm for diabetes and renal disease
lifestyle modification + thiazide diuretic + ACEI or ARB

Pathology 2060A (18 decks)

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