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Cardiovascular > SM 133 Hypertension Pathophysiology > Flashcards

SM 133 Hypertension Pathophysiology Flashcards

1
Q

What are the major side effects of ARBs?

A

Generally rare, Hyperkalemia only

No cough because ARB’s do not affect ACE, unlike ACE Inhibitors

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2
Q

What are the major side effects of ACE Inhibitors?

A

Cough, Angioedema, and Hyperkalemia + Kidney Damage

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3
Q

What is the Aortic Arch a readout for?

A

The Aortic Arch detects blood pressure to measure blood flow to the body

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4
Q

How should blood pressure be measured, procedurally, in clinic?

A

Patient should be seated, relaxed, with arm cuff used on sleeveless arm held at the same level as the heart

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5
Q

How do blood pressures in children compare to adults?

A

Blood pressure is lower in children than adults, so blood pressure is an age dependent measurement

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6
Q

How is hypertension related to CVD?

A

Hypertension is a risk factor for CVD

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7
Q

What is the major effect of a1 blockers?

A

Decreased PVR leading to decreased Blood Pressure

Increased Cardiac output due to Reflex Tachycardia

Increased Intravascular volume due to increased Capacitance

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8
Q

What are the blood pressure ranges for Stage 2 Hypertension?

A

Systolic >= 140 OR Diastolic >= 90mmHg

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9
Q

What are the side effects of Phenylalkylamine Calcium Channel Blockers?

A

Verapamil; Bradycardia

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10
Q

How does Hydralizine work?

A

Lowers blood pressure by relaxing arteriolar smooth muscle

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11
Q

Why do we treat hypertension?

A

To reduce the risk of cardiovascular events

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12
Q

How do ARBs differ from ACE inhibitors and why?

A

ARBs and ACE all decrease SNS stimulation, smooth muscle vasoconstriction, and Na/H2O retention

However, ARBs do not decrease Bradykinin because Angiotensin Converting Enzyme is not inhibited, only its receptor is

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13
Q

What clinical criteria must be met to diagnose Hypertension?

A

Hypertension is diagnosed if two elevated measurements are observed 1-4 weeks apart

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14
Q

Which class of Calcium Channel Blockers is most effective at lowering Cardiac Output?

A

Verapamil, similar to Beta Blockers

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15
Q

What are the major side effects of Furosemide and other drugs that target the Na-K-Cl symporter?

A

Hypokalemia
Hypocalcemia
Hypomagnesia

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16
Q

What are the three main processes that regulate arterial pressure?

A

Volume regulation, vascular tone, and cardiac output

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17
Q

Where are low pressure receptors found?

A

Low pressure receptors are found in:

The Cardiac Atria
Right Ventricle
Pulmonary Vessels

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18
Q

What are the blood pressure ranges for normal blood pressure?

A

Systolic < 120 AND Diastolic < 80mmHg

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19
Q

What are the main side effects of Loop diuretics?

A

Electrolyte abnormalities and volume depletion

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20
Q

When would Furosemide be used?

A

Rapid diuresis to treat volume overload, such as in Hypertension not controlled with Thiazides

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21
Q

How do Calcium Channel Blockers work?

A

Block L-type calcium channel Ca influx to keep MLC dephosphorylated, promoting vasodilation of smooth muscle

Decreases PVR

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22
Q

Where is Aldosterone produced?

A

The Zona Glomerulosa of the Adrenal Cortex

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23
Q

Why do labs evaluate for Hyperkalemia and Creatinine when ACE-I or ARB are used?

A

Hyperkalemia is a common side effect from blocking the effects of Aldosterone

Creatinine indicates Kidney damage, a less likely side effect

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24
Q

What drugs fall into the class known as Diuretics?

A

Hydrochlorothiazide (HCTZ) and Chlorthalidone

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25
Q

What causes secretion of Renin from the Juxtaglomerular Apparatus?

A

The composition of ions reaching the Macula Densa

Stretch of the Afferent Arteriole

SNS stimulation of the Juxtaglomerular Apparatus

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26
Q

What could cause secondary hypertension?

A

Renal Artery stenosis, Hyper Aldosteronism, Hyperthyroidism, Pheochromocytoma, and Medications

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27
Q

Why is hypertension relative to a patient’s population?

A

Reflects the idea that the evidence available is being tailored to each individual patient

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28
Q

What is the effect of Sympathetic Tone and Calcium on smooth muscle?

A

Sympathetic Tone and Calcium favor contraction of arterial vascular smooth muscle to increase blood pressure

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29
Q

Drugs that end with -pril are?

A

ACE inhibitors

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30
Q

What are the centrally acting agents?

A

Methyldopa and Clonidine

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31
Q

Where are a1 receptors found?

A

On postsynaptic neurons in the effector organ

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32
Q

What factors suggest secondary hypertension?

A

Elevated Blood Pressure in:

People younger than 40 or older than 60
Sudden onset with very high blood pressures

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33
Q

What are the effects of centrally acting sympatholytics?

A 
Major = decrease PVR via Vasodilate
Minor = increase Intravascular Volume via increased capacitance
Minor = decrease in Cardiac Output via Less Sympathetic Tone on the Heart
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34
Q

What are the effects of Alpha blockers?

A 
Major = decrease PVR
Minor = increase intravascular volume and CO
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35
Q

How does Amiloride effect water retention?

A

Amiloride inhibits Sodium transport from the lumen into Principal cells, leading to decreased sodium reabsorption and water loss to decrease blood volume

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36
Q

When should a thiazide diuretic be used instead of a loop diuretic?

A

Healthy people will compensate for the strong effects of loop diuretics, so Thiazides are better for controlling chronic hypertension

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37
Q

When are peripheral vasodilators used?

A

Last line in patients with difficult to control blood pressure

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38
Q

What are the side effects of Dihydropyridine Calcium Channel Blockers?

A

Nifedpine; Peripheral Edema

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39
Q

What are the effects of ACE Inhibitors and ARBs on Arterial pressure?

A 
Major = decreased PVR
Minor = decreased Intravascular Volume and reflex increased Cardiac Output
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40
Q

When should ACE Inhibitors and ARB not be used?

A

Women who are pregnant or may become pregnant

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41
Q

Where do Diuretics act?

A

The Distal Convoluted Tubule, Thick Ascending Loop of Henley, and the Collecting Duct

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42
Q

What is the Stage II Hypertension cutoff for high risk people?

A

130/80mmHg

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43
Q

What is the effect of inhibiting Aldosterone?

A

Aldosterone normally promotes Sodium reabsorption and Potassium excretion

Inhibiting Aldosterone leads to Sodium secretion and Potassium reabsorption

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44
Q

What is the Stage II Hypertension cutoff for low risk people?

A

140/90mmHg

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45
Q

What are the effects of Angiotensin II?

A

Sympathetic Activation
Smooth Muscle Vasoconstriction
Decreased Bradykinin = Vasoconstriction
Na/H2O Retention via Aldosterone

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46
Q

What are the side effects of Minoxidil?

A

Tachycardia and hypertrichosis

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47
Q

Why do ACE-I and ARBs work well with Thiazide diuretics?

A

Thiazides lower blood levels of K while ACE Inhibitors and ARB block Aldosterone to increase K, canceling out eachother negative effects

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48
Q

What reaction does Renin mediate?

A

Angiotensinogen to Angiotensin I

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49
Q

What is an example of a K sparing diuretic?

A

Spironolactone - inhibits Aldosterone receptor binding in the Late Distal Tubule and Collecting Duct

Amiloride inhibits sodium reabsorption in the late Distal Tubule and Collecting Duct

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50
Q

What are the effects of Peripheral Vasodilators

A

Nitroprusside, Minoxidil, Hydralizine

Major = decrease PVR
Minor = reflex tachycardia and increase intravascular volume
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51
Q

What reaction does ACE mediate?

A

Angiotensin I to Angiotensin II

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52
Q

What is the effect of Aldosterone on smooth muscle?

A

Aldosterone causes contraction of arterial vascular smooth muscle to increase blood pressure

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53
Q

Where are high pressure receptors found?

A

The Carotid Sinus, Aortic Arch, Left Ventricle, and the Juxtaglomerular Apparatus

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54
Q

What are side effects of Beta Blockers?

A

Bradycardia, cold extremities, bronchospasm

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55
Q

Where does Spironolactone act?

A

Spironolactone inhibits the Aldosterone receptor in the Distal Tubule and Collecting Duct

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56
Q

How can a diagnosis of hypertension be confirmed at home?

A

Blood pressure cuffs record measurements, and devices can monitor blood pressure over time for true values

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57
Q

What drugs target the Thick Ascending Loop of Henle?

A

Furosemide and Torsemide

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58
Q

What is the effect of Bradykinin?

A

Vasodilation

59
Q

What is the significance of Carvedilol a1 blocking activity?

A

Decrease SVR

60
Q

What drug interaction effects are dangerous with loop diuretics?

A

Electrolyte abnormalities and volume depletion, which worsen side effects

61
Q

What portion of Sodium reabsorption is attributable to the Thick Ascending Loop of Henle?

A

30% of Sodium reabsorption occurs in the Thick Ascending Loop of Henle

62
Q

How does the phosphorylation status of Myosin Light Chain affect vasoconstriction?

A

Calcium-dependent Myosin Light Chain Phosphorylation by MLCK leads to vasoconstriction

Phosphatase dephosphorylates Myosin Light Chain to cause vasodilation

63
Q

Where does Aldosterone act?

A

Aldosterone causes Na absorption and K/H secretion in the principal cells of the Collecting Tubule

64
Q

What is primary/essential hypertension?

A

Hypertension caused by genetic or environmental factors that worsen with age

Accounts for 95% of all hypertension

65
Q

What systems control the release of Renin?

A

The Renin-Angiotensin-Aldosterone System and the SNS control Renin release

66
Q

What are cardioselective Beta Blockers?

A

Affect b1 receptors found on heart, lead to Tachycardia, increased contractility, increased renin release

Increase HR, BV, and SV

67
Q

What is the target population for Beta Blockers?

A

Patients with CAD

Not for patients with Hypertension or Heart Failure

68
Q

Where does HCTZ act?

A

HCTZ inhibits the Na/Cl symporter in the DCT, leading to more Sodium and water excretion

69
Q

What age group is most susceptible to primary hypertension?

A

40 - 60 year olds

70
Q

What is secondary hypertension?

A

Hypertension caused by a specific defect

Accounts for 5% of all hypertension

71
Q

What is the major side effect of peripherally acting sympatholytics?

A

a1 blockers lead to orthostatic hypotension

72
Q

What is the Juxtaglomerular Apparatus a readout for?

A

The Juxtaglomerular Apparatus detects blood pressure to measure blood flow to the Kidney, allowing the Kidney to regulate volume

73
Q

What are the nonselective Beta Blockers?

A

Propanolol affects b1 and b2

74
Q

What is masked hypertension?

A

Normal blood pressure in clinic and elevated blood pressure at home

75
Q

How does Minoxidil work?

A

Activates a K channel in smoot muscle to cause K efflux, hyperpolarizing and vasodilating smooth muscle

76
Q

What are the side effects of Benzothiazepine Calcium Channel Blockers?

A

Diltiazem; Edema and Bradycardia

77
Q

How does Clonidine work?

A

Clonidine directly stimulates the central a2 receptor

78
Q

What does the -zosin suffix indicate?

A

Peripherally acting a1 blocker

79
Q

How does calcium regulate blood pressure?

A

Calcium influx into smooth muscle activates MLCK

MLCK phosphorylates Myosin Light Chain

Phosphorylated Myosin Light Chain leads to vasoconstriction of smooth muscle

80
Q

What are bronchodilative Beta Blockers?

A

Affect b2 receptors in lung and arterioles, lead to bronchodilation and decreased PVR

Increase O2 and decrease PVR

81
Q

How is hypertension defined?

A

Hypertension is defined based on a population

82
Q

What are the effects of blocking b2 receptors?

A

Vasoconstriction = increased BP

83
Q

How do a1 blokers work?

A

Prevent binding of Norepi to a1 Receptors, lowering Blood Pressure

84
Q

How is blood pressure measured using a cuff?

A

The cuff is inflated above systolic blood pressure, cutting off blood flow through the artery. As the cuff is deflated, the measurement at the first sound represents systolic blood flow, and as it continues to deflate, the second sound represents diastolic blood flow

85
Q

How do ARBs act?

A

They block AT1 receptors to prevent Angiotensin from exerting its effect

86
Q

What are the side effects of centrally acting sympatholytics?

A

Sedation, dry mouth, depression

87
Q

What are the sympatholytic a1 receptor blockers?

A

Prazosin, Terazosin, Doxazosin

88
Q

Why do smokers have a lower target blood pressure than non-smokers?

A

Smoking is a risk for CVD, so they compensate by targeting lower blood pressures

89
Q

What are the blood pressure ranges for Stage 1 Hypertension?

A

Systolic = 130 - 139 OR Diastolic = 80 - 89mmHg

90
Q

How do the kidneys manipulate intravascular volume?

A

The Kidneys can retain Sodium to increase intravascular volume and raise blood pressure

91
Q

Why are centrally acting agents not first line?

A

Despite minimal drug interactions, CNS side effects prevent first line usage

92
Q

Where is the Na-K-Cl symporter found?

A

The Thick Ascending Loop of Henle

93
Q

What are the effects of ACE Inhibitors?

A

Decreased Ang II leads to:

Decreased Sympathetic Activation = VasoDILATE
Decrease Smooth Muscle Contraction = VasoDILATE
Increased Bradykinin = Vasodilate
Decreased Na/H2O Retention = Lower Blood Volume

94
Q

Drugs that end with -artan are?

A

Angtiotenin II Receptor Blockers

95
Q

What are the effects of ARBs?

A

Decreased Sympathetic Activation = VasoDILATE
Decrease Smooth Muscle Contraction = VasoDILATE
Decreased Na/H2O Retention = VasoDILATE

96
Q

When should a loop diuretic be used instead of a Thiazide?

A

People with acute or complicated hypertension that have not controlled their hypertension with Thiazides should receive loop diuretics

97
Q

Are home blood pressures expected to be higher or lower than clinic blood pressures?

A

Home blood pressures should be lower than clinic

98
Q

What are the side effects of Nitroprusside?

A

Hypotension and lactic acidosis from Cyanide toxicity

99
Q

How do Thiazide Diuretics work?

A

Inhibit Na-Cl symporter in the Distal Convoluted Tubule to promote Sodium Excretion and water loss

100
Q

What portion of Sodium reabsorption is attributable to the DCT?

A

7% of sodium is reabsorbed in the DCT

101
Q

Why is the PCT not a good target for diuretics?

A

The PCT is responsible for 60% of sodium reabsorption, making it an attractive target

However, inhibition of the PCT leads to compensation by other areas to increase Na reabsorption, preventing a diuretic effect

102
Q

What is the Carotid Sinus a readout for?

A

The Carotid Sinus detects blood pressure to measure blood flow to the brain

103
Q

Why can Calcium Channel Blockers be effected by other drugs?

A

Depend on CYP450 metabolism; do not alter other drugs, but may be altered by other drugs

104
Q

How do risk factors effect target blood pressures for individual patients?

A

While there are overall guidelines for blood pressure, an individuals risk factors can result in lower target blood pressures to account for added individual risk

105
Q

What is the Juxtaglomerular Apparatus?

A

A group of cells found in the wall of the Afferent Arteriole that secrete Renin

106
Q

What are the b1 selective Beta Blockers?

A

Atenolol and Metoprolol

107
Q

What are Korotkoff sounds?

A

Sounds heard on a blood pressure cuff that correspond to Systolic and Diastolic blood pressure

108
Q

Which is more dangerous, white coat or masked hypertension?

A

Masked hypertension is more dangerous because in this scenario the patient’s blood pressure is elevated for longer periods of time when they are at home, and only briefly normal in clinic

109
Q

What are the side effects of K sparing diuretics?

A

Amiloride and Spironolactone lead to Hyperkalemia

110
Q

When is Methyldopa used?

A

During pregnancy

111
Q

What is hypertension?

A

Hypertension is the measured force against the walls of the arteries as the heart pumps blood through them

112
Q

What are side effects of diuretic drugs?

A

HCTZ and other diuretics can cause:

Hypokalemia
Hyponatremia
Hypercalcemia

113
Q

What are the peripheral vasodilators?

A

NMH

Nitroprusside
Minoxidil
Hydralazine

114
Q

What is a risk of Clonidine?

A

Withdrawal symptoms that lead to rebound high BP

115
Q

What is the risk of Hyperkalemia?

A

Arrythmias

116
Q

Why might clinic blood pressures be flawed?

A

White coat hypertension is falsely high while masked hypertension is falsely low in clinic

117
Q

Why can HCTZ cause Hypercalcemia?

A

HCTZ blocks the Na/Cl symporter, leading to low Na in the DCT cells

An Na/Ca antiporter results in Na being drawn into the DCT cells and an efflux of Ca into the bloodstream, resulting in Hypercalcemia

118
Q

How does Nitroprusside work?

A

Converted into Nitric Oxide, activating Guanyl Cyclase to increase cGMP and vasodilate

119
Q

What are the effects of blocking b1 receptors?

A

Decreased HR, Contractility, and SV

Decreased Renin Release = decreased SVR

120
Q

What three conditions lead to increased Renin release?

A

Decreased NaCl delivery to the Macula Densa

Hypotension/hypovolemia leading to decreased stretch of the Afferent Arteriole of the Kidney

Sympathetic stimulation

121
Q

How does volume regulation affect arterial pressure?

A

Kidneys maintain intravascular volume and can retain Sodium to increase intravascular volume, raising blood pressure

Renin, Angiotensin, and Aldosterone alter Kidney Sodium regulation

122
Q

What are the side effects of Hydralazine?

A

Headache, drug induced Lupus

123
Q

How does Cardiac Output affect arterial pressure?

A

Increased cardiac output results in increased blood pressure

Sympathetic tone increases HR which increases CO and blood pressure

124
Q

Are diuretics a first line treatment for hypertension?

A

Yes, they are a first line with the risk of causing hypokalemia in high doses

125
Q

When is Methyldopa used?

A

Prior to surgery

126
Q

How does Sodium movement regulate water reabsorption in the DCT?

A

Sodium movement from the lumen across the DCT and into circulation reabsorbs water

Na/Cl symporter first transports Sodium using Chloride to power the gradient, bringing water inside the DCT

Na/K ATPase then pumps the Sodium out into circulation

127
Q

Which class of Calcium Channel Blockers are most effective at lowering PVR?

A

Dihydropyridines; cause reflex Tachycardia

128
Q

Where are a2 receptors found?

A

On presynaptic neurons in the brain

129
Q

What are the major and minor effects of diuretics?

A

Major = decreased PVR due to decreased Na

Minor = decreased intravascular volume due to Na/Water loss

130
Q

How does Methyldopa work?

A

Methyldopa replaces Norepi in the secretory vesicles of Adrenergic neurons, causing vasoconstriction but inhibiting further activity from the brain, leading to overall vasodilation

131
Q

What are the target population for ACE Inhibitors and ARBs?

A

Hypertensive patients with:

Heart Failure
Diabetes
CAD/post MI

132
Q

How does altering sympathetic tone effect blood pressure?

A

Increased sympathetic tone leads to:

Increased Venous Return = Increased CO
Increased Cardiac Contractility + HR = Increased CO
Increased Arterial Contraction = Increased PVR

Combined, increased BP

133
Q

What is the effect of drugs that inhibit the Na-K-Cl symporter?

A

Decreased Sodium influx and ultimately water loss to decrease blood volume

134
Q

What are the major effects of Beta Blockers?

A

Decreased Cardiac output (b1) and decreased PVR (despite opposing effects of b1 decreased renin and b2 blockade)

135
Q

What are the blood pressure ranges for elevated blood pressure?

A

Systolic = 120 - 129 AND Diastolic < 80mmHg

136
Q

How does vascular tone affect arterial pressure?

A

Contraction of arterial vascular smooth muscle raises blood pressure while dilation of arterial vascular smooth muscle lower blood pressure

137
Q

Which class of Calcium Channel Blockers has roughly equal effects on Cardiac Output and PVR?

A

Diltiazem

138
Q

Why is hypertension considered a “silent killer”?

A

Effects 1/4 adults but presents no symptoms

139
Q

What is the danger of Hypercalcemia?

A

Kidney stones

140
Q

How does Sympathetic Activity alter blood pressure?

A

Sympathetic Activity:

Increases vascular resistance
Increases Sodium reabsorption
Promote Renin release by the JGA

141
Q

What is white coat hypertension?

A

Elevated blood pressure in clinic and normal blood pressure at home

142
Q

Where do Furosemide and Torsemide act?

A

They inhibit the Na-K-2 Cl symporter in the Thick Ascending Loop of Henle

Prevent Sodium reabsorption and lead to water loss

143
Q

How does blood pressure change in older adults?

A

Blood pressure rises as people get older, especially after 60 years old, and the cutoff is 140/90mmHg

144
Q

What population are Calcium Blockers contraindicated in and why?

A

Not safe in patients with Heart Failure due to risk of Bradycardia

Cardiovascular (25 decks)

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