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CV Basics + Hypertension > Drug Therapy + Management of Common Comorbidities > Flashcards

Drug Therapy + Management of Common Comorbidities Flashcards

1
Q

Non-pharmacologic treatments to help reduce BP include:

Think simple

A

Physical activity, weight reduction, improved diet/alcohol use, relaxation therapy, smoking cessation

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2
Q

Common classes of drugs that reduce BP are:

A

Thiazide diuretics, ACEI/ARB, CCB’s, B-Blockers

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3
Q

Majority of antihypertensive drugs usually lower BP by this much…

A

-10/-5

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4
Q

The time to maximal effect for most antihypertensives is…

A

Around a month

Therefore do not change doses quickly!

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5
Q

50% of an antihypertensive maximal dose achieves this % of its effect…

A

80% of effect achieved with 50% of max dose

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6
Q

What is preferred: Adding therapy, or switching drugs?

A

Additional therapy (BP drugs are weak) - target different HTN pathway

Lifestlye modification can help ALOT

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7
Q

What is the AB-CD rule?

A

Combining antihypertensives drugs based on mechanism; renin-based (ACEI/ARB, BB) with non-renin (TZD, DHP-CCB)

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8
Q

A non-DHP CCB and a BB should be cautioned because:

A

Their pharmacology is similar and increases risk of adverse effects

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9
Q

These two drugs should be avoided in combination:

A

ACEI and ARB

VERY similar mechanism

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10
Q

A notable evidence-based combination is:

A - C

A

ACEI + DHP-CCB

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11
Q

ACEI’s or ARB’s will be chosen to be added over a BB unless…

A

Patient has a specific condition that requires a BB

HF, Cirrhosis, AFib

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12
Q

The biggest difference between ACEI’s and ARB’s are…

A

Frequency of cough with ACEI

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13
Q

ACEI’s + ARB’s should be avoided in these three scenarios…

A

Pregnancy, Bilateral renal artery stenosis, Hyperkalemia

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14
Q

If therapy is added on and still not uncontrolled, these factors need to be considered:

A

Nonadherence
Secondary HTN
Interfering drugs or lifestyle
White coat effect

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15
Q

Triple/Quadruple therapy should contain…

A

A diuretic

Volume control

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16
Q

Single pill combinations should be used as often as possible, to…

A

Increase compliance

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17
Q

The best addition for treatment resistance with the most success is…

A

Spironolactone (or MRA)

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18
Q

Other additions besides an MRA for treatment resistance include:

A

Alpha-2 agonists (clonidine/methyldopa) or Non-DHP CCB + Beta-blocker

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19
Q

The three drugs that have shown benefit in isolated systolic hypertension are:

A

Thiazide diuretic, ARB, Long-acting DHP-CCB

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20
Q

Caution should be taken if DBP drops to… in ISH treatment

A

Below 60 mmHg

Analyze and modify drug therapy accordingly

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21
Q

Efficacy of thiazide diuretics state for HTN state:

A

Excellent effectiveness with added benefit of decreasing edema/fluid overload

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22
Q

Thiazide diuretics may have reduced effectiveness when…

A

CrCl drops below 30 mL/min

Switch to loop diuretics

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23
Q

The MOA of a thiazide diuretic is as follows:

A

Blocks sodium reabsorption in the distal tubule of the nephron, thereby blocking water reabsorption as well

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24
Q

The most common electrolytes that may be affected by a thiazide diuretic are:

A

Decreases in potassium and sodium

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25
Q

Other electrolytes (rather than sodium and potassium) may be affected by thiazide diuretics:

A

Decreases in magnesium and chloride, increases in calcium

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26
Q

Other adverse effects of thiazide diuretics are:

A

Slight increase in BG
May increase uric acid
Increase urinary frequency

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27
Q

Drug interactions with thiazide diuretics include:

A

Other BP drugs (enhance effect)
Electrolyte interactions with K+ and Na+

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28
Q

Diuretics will impact urine production by:

A

Increasing urine production - excretion of more fluid

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29
Q

The major driver of fluid retention is…

A

Reabsorption of sodium

Wherever sodium goes, water follows

And 99% of filtered fluid is reabsorbed

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30
Q

Mechanism of commonly used diuretics will impact sodium reabsorption by…

A

Inhibiting sodium reabsorption

More sodium in urine = more fluid excreted

High BP often involves high blood volumes so can help lower BP

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31
Q

The MOA of loop diuretics is:

A

Inhibiting sodium reabsorption in the ascending loop of henle

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32
Q

Loop diuretics can have adverse effects such as:

Electrolytes and… (gout)

A

Loss of calcium and magnesium
Increased potassium loss
Uric acid retention

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33
Q

Most common loop diuretic used is…

A

Furosemide

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34
Q

Loop diuretics are NOT good for BP control because…

2 reasons

A

Short half-life
Stimulator of RAAS

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35
Q

Loop diuretics could be used for BP control in a specific group of patients…

A

Poor kidney function

Prolongation of half-life

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36
Q

Compared to loop diuretics, thiazide diuretics are usually better for BP control because…

A

Longer half-life + more gentle action

Weaker due to location of action

Loop diuretics are best for fluid excretion

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37
Q

Thresholds for hypokalemia treatment are usually:

A

Consider treating 3.5-4.0, usually treat 3.0-3.5, always treat <3.0

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38
Q

Ways to help treat hypokalemia include:

3: natural, diuretic itself, other drugs

A

Dietary measures
Lowering diuretic dose or d/c if very low
Add K+ sparing drugs or supplement

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39
Q

Hyperkalemia is dangerous because…

A

Affect conduction - delays, Ventricular arrythmia

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40
Q

Drugs that increase potassium include:

A

RAAS drugs, NSAID’s, vitamins
K+ sparing diuretics, TMP/SMX

Also consider baseline potassium AND kidney function

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41
Q

RAAS is a system that…

A

Increases blood pressure

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42
Q

The major hormone products of RAAS include the two fololowing hormones:

A

Alodsterone + Angiotensin 2

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43
Q

Angiotensin 2 is derived from…

A

Angiotensinogen

In 2 steps

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44
Q

Angiotensinogen is converted to Angiotensin 1 via…

A

Renin activation

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45
Q

Angiotensin 1 is converted to angiotensin 2 via…

A

Angiotensin converting enzyme (ACE)

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46
Q

The three major actions of angiotensin 2 include:

A

Rapid pressor response
Slow pressor response
Cardiac hypertrophy/remodelling

Rapid = vasoconstriction. Slow = Kidney

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47
Q

RAAS is related to kidneys, as low blood pressure in the afferent blood vessel means that…

A

Low blood volume (fluid depletion) is suspected - low blood pressure in the kidney (afferent arteriole)

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48
Q

Consequences of low pressure to the kidney includes:

A

Decreased filtration, excretion of substances, collapse of tubules

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49
Q

Low pressure in the glomerulus will trigger…

A

Release of renin into the blood

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50
Q

Renin release is triggered by 3 pathways:

A

Low renal pressure
Low sodium in the loop
SNS activation

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51
Q

After conversion to angiotensin 2, the hormone will cause ____ in the kidney.

A

Preferential vasoconstriction of the EFFERENT arteriole

Exit blood vessel

Will also cause vasoconstriction in several tissues (receptors all over the body)

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52
Q

Vasoconstriction of the efferent arteriole will cause…

A

Increased pressure on the glomerulus - increase in BP without increasing blood volume, more fluid will be filtered (GFR increased)

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53
Q

Angiotensin 2 will also cause the release of _____.

Another hormone

A

Aldosterone

Slow pressor response, stimulation of angiotensin-type 1 receptor

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54
Q

Aldosterone will cause reabsorption of ____ and excretion of ____

A

Reabsorption of sodium and excretion of potassium

…water follows sodium

Increased activity and synthesis of sodium channels

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55
Q

Aldosterone is considered a ____ hormone.

A

Mineralocorticoid

Secreted from the adrenal gland

56
Q

The three drugs that directly inhibit RAAS activity are…

A

ACE inhibitor (ACEI)
Angiotensin receptor blocker (ARB)
Direct renin inhibitors (DRI)

57
Q

MOA of an ACE inhibitor is to…

A

Inhibit Angiotensin converting enzyme, preventing conversion to ANG2

Also inhibits kininase 2

Occurs on endothelial cells throughout circulation

58
Q

ACE inhibitors can be identified by the suffix…

A

-pril

59
Q

ACEI/ARB helps with HTN by:

A

Vasodilation + lowered aldosterone secretion

60
Q

ACEI/ARB helps with CKD by…

A

Decreasing glomerular pressure by decreasing vasoconstriction on efferent arteriole

CAUTION! May decrease renal perfusion to dangerous levels

61
Q

ACEI/ARB can help with heart failure and ischemic heart disease by…

A

Decreasing adverse effects of ANG2 and aldosterone on heart tissue + blood vessels

62
Q

Dry cough may occur in ACEI usage due to…

A

Bradykinin accumulation

Inhibition of kininase 2

63
Q

This electrolyte may be increased with ACEI/ARB usage due to…

A

Potassium (hyperkalemia), due to aldosterone inhibition

ALL Drugs that inhibit RAAS will increase potassium

Remember that aldosterone reabsorbs sodium and excretes potassium.

64
Q

Reduced BP with ACEI/ARB may be a nuisance because…

A

Drug can be used for other conditions than just HTN

65
Q

ARB MOA is…

A

Inhibiting the AT-1 receptor, blocking actions of ANG2

VERY similar effect as ACEI

66
Q

ARB adverse effects are similar to ACEI, except for…

A

Lower incidence of cough

Likely due to bradykinin able to be degraded

67
Q

ARB suffix is…

A

-sartan

68
Q

DRI MOA is…

A

Binding active site of renin, blocking conversion of angiotensinogen to ANG1

Not widely used, minimal use

69
Q

Common mineralocorticoid-receptor antagonists (MRA) are these two:

A

Spironolactone
Eplerenone

70
Q

MOA of MRA is…

A

Inhibiting aldosterone receptor

71
Q

Usage of MRA is usually reserved for

In relation to CV

A

Resistant HTN due to aldosterone excess
Heart failure

72
Q

Primary adverse effects of MRA include:

A

Increased potassium
Hormonal effects (stimulation of progesterone + androgen receptors)

Gynecomastia, impotence, menstrual irregularities

73
Q

If a patient presents with HTN and Diabetes together, it is important to identify…

Proteins in urine are???

A

Nephropathy

Urinalysis: urinary albumin to creatinine ratio, or CKD present

74
Q

Diabetes with nephropathy or renal disease indicates the following drugs…

A

ACEI or ARB

75
Q

Add-on therapy of HTN with diabetes + nephropathy recommends this drug rather than…

A

DHP-CCB
Add-on TZD

76
Q

HTN treatment with diabetes WITHOUT nephropathy recommends these drugs…

A

1st line drugs - ACEI, ARB, DHP-CCB, or TZD
Combination if appropriate (ACEI + CCB preferred)

77
Q

First-line therapy for HTN and CKD includes:

A

ACEI/ARB for proteinuria
Diuretics as add-on

Beneficial effects proven of lowering glomerular pressure proven

78
Q

Long-standing HTN and diabetes can increase risk for CKD because…

A

Increased pressure can damage glomerulus (and glucose harms vessels)

Proteinuria, as protein escapes

79
Q

Renal harm is possible from ACEI/ARB usage, because…

A

Decreased pressure may lower filtration and GFR too much - nephron collapse, urine production halted, toxin accumulation

Acute renal failure - reversible if caught early

NO direct damage to tubules, just lowered pressure

80
Q

The following should be monitored when starting an ACEI/ARB, and in 1-2 weeks after starting:

Kidney !

A

SCr, BUN, fluid balance, and electrolytes (sodium and potassium)

81
Q

Pre-eclampsia is related to HTN because…

A

In pregnancy - high BP with proteinuria, after 20 weeks

Associated with poor outcomes + can progress to seizures (eclampsia)

82
Q

Gestational HTN is…

A

In pregnancy - high BP without proteinuria after 20 weeks

83
Q

Chronic HTN is…

Pregnancy !

A

HTN was present before pregnancy began

84
Q

The following drugs should be avoided for HTN during pregnancy:

A

ACEI’s + ARB’s

85
Q

First line options for HTN during pregnancy include…

3!

A

Labetalol, methyldopa, long-acting oral nifedipine

Other beta-blockers could also be used

Same options for lactation, plus enalapril or captopril

86
Q

2nd line options for HTN during pregnancy include…

A

Clonidine, hydralazine, and thiazide diuretics

87
Q

Two things that could help lower risk of pre-eclampsia are…

A

Calcium 1-2g/day
Low-dose ASA starting late in 1st trimester

88
Q

The SNS impacts tissues via:

A

Alpha and beta receptors

89
Q

Activation of beta-receptors in HEART MUSCLE will result in…

A

Increased cardiac contractility and rate of contractions

BETA1 RECEPTORS

Increased cyclic AMP, increased intracellular calcium

90
Q

Activation of beta-receptors in ARTERIAL WALLS will result in…

A

Relaxation - vasodilation

BETA2 RECEPTORS

Increased cyclic AMP, decreased intracellular calcium

91
Q

Beta-1 receptor stimulation causes…

A

Incresaed heart rate + contractility
Renin release from pancreas

92
Q

Beta-2 receptor stimulation causes

A

Vasodilation

93
Q

Alpha-1 receptor stimulation causes

A

Vasoconstriction

94
Q

Beta-receptor antagonists work by…

Beta-blockers

A

Blocking the effects of beta-receptors

95
Q

Beta-blockers can be differentiated by…

A

Selectivity for Beta1 and Beta2
Blockade of alpha receptors
Intrinsic sympathomimetic activity

96
Q

Beta-1 selective blockers would impact the body by…

A

Inhibiting beta-1 receptor activity; lower heart rate and contractility, and renin release

97
Q

Most common uses for beta-1 selective blockers include:

A

HTN, High Heartrate
Cardiac workload/demand (angina)
Cardiac damage (HF, heart attack)

Shield from negative effects of norepinephrine

98
Q

Beta-1 selective blockers may be helpful for HTN due to:

A

Decrease in cardiac output, and renin production

Exact mechanism is unclear

99
Q

Beta-1 selective blockers may be helpful for an increased cardiac workload and damage

A

Block negative effects of norepinephrine - prevent further damage, and decrease demand for blood to heart muscle

100
Q

Non-selective beta-blockers include…

A

Nadolol, pindolol, propranolol, timolol

101
Q

Addition of beta-2 receptor blockade include:

A

Smooth muscle - Constriction of blood vessels
Lung - Inhibition of beta2 receptors in airways

Possible interaction between non-selective beta-blockers and beta2 agon

102
Q

Non-selective beta blockers are not used much for CV conditions anymore because…

A

Not much benefit over selective, and tolerability issues

103
Q

Beta1 selectivity is not absolute, especially when…

A

Using increased doses of beta-1 selective beta-blocker

104
Q

Non-selective beta + alpha blockers include these two…

A

Carvedilol + Labetalol

105
Q

Compared to selective beta-blockers, non-selective beta + alpha blockers are expected to…

…related to BP

A

Cause a greater fall in BP expected to other beta-blockers

Primary dx: heart failure

106
Q

Notable adverse effects from beta-blocker usage includes…

A

Decreased BP
Decreased cardiac output
Bradycardia

FATIGUE

107
Q

AV block can occur from beta-blocker usage because…

AKA heart block

A

Beta-blocker can slow AV conduction further (too much)

108
Q

Beta-blockers could increase potassium levels because…

Related to kidney

A

There are beta-receptors in the glomerulus - blockage of RAAS (aldosterone) means less potassium excretion

109
Q

Circulation problems may arise with beta-blocker usage because…

A

Beta-2 receptors are responsible for vasodilation in smooth muscle

110
Q

Beta-blockers have a theoretical impact with respiratory medications because…

A

Beta-2 receptors are also present in lungs

Beta-2 agonists used in asthma

111
Q

A patient taking a non selective beta-blocker and a beta2 agonist should…

A

Watch for signs of decreased response

Typically not problematic

112
Q

A primary issue that needs to be addressed when using beta-blockers in people with diabetes…

A

Reduced recognition of hypoglycemia - SNS trigger

Slight increase in BG is secondary and minor.

113
Q

Alpha-1 receptor antagonists MOA is to…

A

Inhibit vasoconstriction induced by the SNS

But is usually involved with baroreceptor activation

Baroreceptor activation = increased heart rate, CO, and RAAS

114
Q

Alpha-1 receptor antagonists are not used often for BP control anymore because…

A

Little protection from CV disease

Just because a drug lowers BP does not mean it is CV protective

CAN be used for add-on therapy.

115
Q

Instead of being used for BP, alpha-1 receptor antagonists are often used for…

A

Benign prostatic hyperplasia

Urinary issues

116
Q

Alpha-2 agonists MOA works by…

A

Stimulating alpha-2 receptors - decrease SNS nerve transmission and circulating norepinephrine

117
Q

Alpha-2 agonist usage results in:

A

Lowered BP, HR, and cardiac output

118
Q

Alpha-2 agonists are most commonly used for…

A

Pregnancy + treatment resistance

119
Q

Frequent adverse effects from alpha-2 agonists include…

A

Sedation
Anticholinergic effects (dry mouth)

120
Q

Alpha-2 agonists commonly used include these two…

A

Clonidine
Methyldopa

121
Q

DHP-CCB’s MOA works by…

A

Inhibiting L-type calcium channels, less intracellular calcium in vascular smooth muscle means less contraction

122
Q

DHP-CCB MOA impacts blood vessels by…

Also which blood vessel is it specific for??

A

Promoting vasodilation in arteries

123
Q

A major advantage of DHP-CCB’s over other vasodilators is…

A

Lack of impact on heart rate

NO reflex tachycardia

124
Q

In general, arterial vasodilators increase heart rate via…

EXCEPT DHP-CCB’s !

A

SNS stimulation - reflex tachycardia mediated by baroreceptors

125
Q

How do baroreceptors work?

A

Stretch receptors linked to nerve endings signalling CNS.
Increased stretch = vagal outflow (decreased HR). Decreased stretch = SNS outflow (increased HR)

Most vasodilators prevent baroreceptors from being stretched

126
Q

The three most common DHP-CCB’s are:

A

Amlodipine, felodipine, nifedipine

127
Q

Hydralazine and minoxidil are classified as… and work by…

A

Direct acting vasodilators - directly relax arteriolar smooth muscle

128
Q

The reason why hydralazine + minoxidil are never used as first line agents for HTN is because…

A

Reflex tachycardia (baroreceptors) and fluid retention (RAAS stimulation via vasodilation of kidney)

Typically used for resistance, in combination with drugs that prevent tachycardia + fluid retention (beta-blockers + diuretics)

129
Q

The two drugs classified as Non-DHP CCB’s are…

A

Diltiazem and verapamil

130
Q

Non-DHP CCB’s differ from DHP CCB’s due to…

A

Primary effect on cardiac smooth muscle vs vascular smooth muscle

131
Q

Usage of non-DHP CCB’s will result in…

A

Lowered heart rate + contractility - will lower BP but not commonly used for uncomplicated HTN

Useful where heart rate + myocardial demand is high - comorbid conditions

132
Q

The following should be monitored for ALL BP drugs in terms of adverse effects:

A

BP - dizziness, headache, hypotension
Orthostatic hypotension
Erectile dysfunction

Orthostatic hypotension = reduction of 20/10 upon standing
ED is usually caused by arterial dysfunction, not drugs

133
Q

A key adverse effect with DHP-CCB’s includes:

…Swelling

A

Edema

134
Q

Beta-blockers aren’t considered 1st line for uncomplicated HTN since…

A

The other 1st line drugs have shown better evidence of clinical outcomes.

Alternative for patients <60

NOTE that BB’s are extremely protective in certain complicated cases (Afib, HF)

135
Q

ACEI/ARB’s may even be used if BP is normal for high-risk CV patients because…

A

ACEI and ARB reduce CV injury beyond BP

136
Q

The following should be monitored when starting an ACEI/ARB for CKD patients:

A

SCr and K+ before starting, and within 1-2 weeks of starting drug/increasing dose

SCR expected to increase, but should be less than 20-25%

BP + Edema should get better, NOT worse

137
Q

Presence of orthostatic hypotension is a signal for us to…

A

Start with lower doses and titrate with caution

CV Basics + Hypertension (3 decks)

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