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PHAR 152* > Hypertension > Flashcards

Hypertension Flashcards

1
Q

What is the frequency of SA node depolarization?

A

70 times per minute (it is the pacemaker of the heart and sets its contraction rate)

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2
Q

What is sick sinus?

A

It is characterized by a low heart rate due to lower SA depolarization rate. These patients will usually have pacemakers (“artificial pacemakers”)

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3
Q

What is the AV node and what is its function?

A

The AV node is located between the atria and it is the gateway for electrical impulse into ventricles

The AV node effectively delays ventricular contraction (allowing the ventricles to fill with blood before contraction)

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4
Q

What happens if AV node depolarization rate is reduced?

A

Some drugs can delay the SA node’s signals for ventricle contraction. This allows for the ventricles to fill with blood before contraction

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5
Q

Before conduction, what is the polarization of the heart muscle cells?

A

80-90 mV negative compared to outside the cells.

Ion pumps work to maintain this resting membrane potential (pump out cations(+) and bring in more anions(-))

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6
Q

What is the flow of Na+ before contraction (closed channel gates)?

A

Due to the negative cell interior, Na+ is magnetically attracted to the surface of the polarized cells

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7
Q

How does the muscle cell loose its polarization?

A

K+ loss diminishes negative charge (gradual depolarization)

An abrupt increase in Na+ permeability will occur when a certain threshold potential is reached (rapid depolarization)

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8
Q

What types of channels are responsible for Na+ channels in muscle cells?

A

Voltage-gated

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9
Q

What occurs in Phase 0 of contraction?

A

Increase in muscle cell permeability to Na+

Ca2+ channels open at around -60mV

This effectively reduces depolarization, which in turn causes muscle contraction

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10
Q

What occurs in muscle cells during Phase 1 of contraction?

A

Brief re-polarization (cells gets a bit more negative) due to K+ loss

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11
Q

What occurs in muscle cells during Phase 2 of contraction?

A

At this point, contractions cannot occur despite neuronal impulses

Ca+ continues to enter the cell (started in phase 0)

Ca2+ enters the cell via L type calcium channels (Ca2+ movement initiates muscle contraction)

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12
Q

What occurs in muscle cells in Phase 3 during contraction?

A

Membrane remains permeable

Na+ and K+ ejected to repolarize (get back to 80-90mV)

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13
Q

What occurs in muscle cells during Phase 4 of muscle contraction?

A

Na+ is cleared from the cell and K+ loss slows

Eventually, an abrupt increase in Na+ permeability will occur when a certain “threshold potential” is reached

Phase 4 preps the cell for Phase 1, this cycle between all 4 phases allows for heart muscle contraction

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14
Q

What ion is the most responsible for muscle contraction?

A

Calcium entry causes muscle contraction

More Ca2+ =stronger contraction (contractility)

Faster Ca2+ =faster contraction (chronotropy)

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15
Q

What is an ECG?

A

Graph of electrical activity in heart

Detected by electrodes(leads) attached to the patient (6-12 leads are often used)

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16
Q

Where are the leads generally placed?

A

6 limb leads

6 precordial leads

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17
Q

What is the P-wave on an ECG reading?

A

It represents the depolarization of atria (atrial contraction)

Normal duration = 0.12s

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18
Q

What does the Q-T interval on an ECG reading?

A

It represents depolarization of ventricles (ventricular contraction)

Normal duration is less than 0.12s

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19
Q

Should the Q-T interval be narrow or wide in normal functioning hearts?

A

Narrow, if it is wide then an aberrant heat rate can develop independent of the heart (arrythmia can occur)

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20
Q

What does the T-wave on an ECG reading?

A

It represents the repolarization of ventricles (relax)

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21
Q

What are the different BP measurement methods?

A

Office (attended, OBPM)

Office Automated (unattended, AOBP)

Ambulatory BP monitoring (ABPM)

Home blood pressure monitoring (HBPM)

Pharmacy blood pressure machines

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22
Q

Should readings from pharmacy BP machines be used to make treatment decisions?

A

It is highly unlikely they can be relied upoon for determineing risk or deciding about treatment (lack the precision and accuracy)

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23
Q

What are some qualities of home BP monitors?

A

Considered highly accurate

Highly correlated with usual resting BP levels

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24
Q

Whn should BP be measured at home?

A

Conditions:
Resting, low stimulation/stimulants/irritants
Duplicate measures

Timing:
Before doses of antihypertensives (will show BP that has the lowest effect by drugs)
Morning and night

Duration:
One week blocks during times of interest (after dose changes, drug changes, taking other drugs)
Do not have to measure everyday for extended periods

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25
Q

Are wrist BP monitors used to make therapeutic changes?

A

No, unless patients have large arm circumference that cannot fit in brachial BP monitor cuffs

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26
Q

How many Canadians have hypertension?

A

23%

4 million prescriptions every month in Canada

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27
Q

What are some causes of hypertension?

A

Fluid and electrolyte balance

Sympathetic nervous system/baroreceptor function (Increased SNS activity)

Metabolic syndrome (diabetes, high cholesterol)

Vascular endothilial function (Prostacyclin and NO production)

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28
Q

What is the effect of a single antihypertensive drug on BP?

A

These regimen often have limited success in control (-10/-5)

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29
Q

What is treatment-resistant hypertension?

A

a lack of BP control despite a combination of 3 antihypertensive medications, one of which being a diuretic

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30
Q

How do risk factors impact incidence of heart attacks?

A

90-100% of heart attacks happen in patients that have have at least one of the following:

Hypertension, dyslipidemia, diabetes, and smoking

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31
Q

Are most CV risk factors very obvious when patients have them?

A

No, most are silent (makes early screening difficult)

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32
Q

What is the benefit of early detection in hypertension?

A

It can control risk factors before it develops into full-blown hypertension

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33
Q

At what stage can one manage risk factors that can best help reduce the risk for the development of hypertension?

A

Changes in earlier life stages have the biggest impact

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34
Q

What are some modifiable risk factors fo developing hypertension?

A

Obesity
Poor dietary habits
High sodium intake
Sedentary lifestyle
High alcohol consumption
High-normal blood pressure
Diabetes or metabolic syndrome
Smoking

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35
Q

What are some non-modifiable risk factors for developing hypertension?

A

Over 55 years old
Male
Family history of premature cardiovascular disease

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36
Q

What are the goals of therapy for hypertension?

A

Reduce/prevent myocardial cell dysfunction

Reduce/stabilize atherosclerosis burden and endothelial cell dysfunction

Reduce/prevent weakened vessel walls

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37
Q

Can one be diagnosed with hypertension after a single high blood pressure reading?

A

No, it is a trend

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38
Q

What does class mean in recommendations for hypertension therapy?

A

It suggests the strength of reccomendations

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39
Q

What does level mean in recommendations for hypertension therapy?

A

It suggests the amount and quality of evidence in support of the reccomendation

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40
Q

Can hypertension be diagnosed in a pharmacy?

A

No

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41
Q

At what BP does a patient get immediately diagnosed for hypertension without any other assessments?

A

BP>180/110

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42
Q

What is white-coat hypertension?

A

BP reading taken in a clinic may be higher than resting due to anxiety

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43
Q

What is masked hypertension?

A

BP reading taken at clinic are lower than normal resting.

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44
Q

What is metabolic syndrome?

A

Hypertension is often accompanied by metabolic syndrome.

They are a combination of risk factors and include at least three of the following:

Insulin resistance
Low HDL
Abdominal obesity
High triglycerides
High BP

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45
Q

What types of organ damage do people with long-standing hypertension develop?

A

Cerebrovascular disease

Hypertensive retinopathy (retinal hemorrhaging)

LVD and LVH

Coronary artery disease

CKD

Peripheral artery disease

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46
Q

Is target organ damage reversible?

A

No

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47
Q

What is the Framingham risk calculator?

A

A widely used tool to assess overall CV risk in Canada.

A simple algorithm that estimates an individuals’ 10-year risk of experiencing a major CV event (MI, stroke, etc) or death

It is usually performed on people who might ve developing diseases or have risk factors alone, but no disease

48
Q

What are some variables that are evaluated under the Framingham risk score?

A

Age

HDL-C

Total cholesterol

Systolic Blood Pressure

49
Q

What is problematic about telling patients to change their habits for them to avoid CV events altogether?

A

It is impossible to determine who will have a CV event with full certainty

We cannot predict how people will die or what age they will die. But we can give people the risk they are at for a major CV event/death

50
Q

What is the ultimate goal of CV risk reduction?

A

A complete elimination of risk is impossible, but significant reductions in risk are expected

51
Q

What are relative risk reductions?

A

This is the reduction in risk relative to what it was before intervention

52
Q

What are absolute risk reductions?

A

It is the absolute percentage drop in risk from what it was before intervention

53
Q

What are some symptoms of concern relating to major CV events?

A

Neurologic:
Severe headache, numbness, weakness, slurred speech
Vision problems

Cardio-respiratory:
Chest pain, difficulty breathing

54
Q

What is the difference between hypertensive urgency and emergency?

A

Hypertensive urgency (Situations where BP should be reduced within hours):
BP >180/130 and papilledema (optic nerve swelling) or other target organ damage

Hypertensive emergency (Situations that require immediate BP reduction):
Hypertensive encephalopathy, intracranial bleed, unstable angina/MI, acute heart failure

55
Q

Should stable patients be rushed to the ER for high blood pressure?

A

No, a stable human can tolerate high BP well, so send them to walk-in clinic instead

56
Q

What are the two types of clinical assessment performed at a physician’s office?

A

Physical assessment

Laboratory testing/imaging

57
Q

What is a pharmacist’s responsibility in relation to clinical assessments?

A

Be able to interpret the documentation collected from these tests as a minimum requirement

58
Q

What are some common physical assessments commonly documented in medical charts?

A

Jugular Venous Pressure (indirect assessment of right atrial pressure)

Edema (represents fluid volume)

Pulse (Heart rate and pressure/circulation)

Heart sounds (Normal: S1(systole), S2(diastole), Abnormal: S3 or S4 (murmur, may indicate disease)

BP

Point of maximal impulse

Bruit (carotid and renal)

59
Q

What can cause increased intravascular volume/preload?

A

Heart failure, kidney disease, and hypertension

Jugular venous pressure is often used to assess blood volume/preload (if less than 2cm, then increased volume/preload is not likely)

60
Q

What does a lowered arterial pulse indicate?

A

Reduced peripheral pulse pressure can indicate reduced stroke volume or peripheral artery disease

Ankle-brachial index is used to assess CV risk (ankle pressure/arm pressure)

61
Q

What causes the S1 and S2 sounds?

A

S1 (lub): It represents the start of ventricular contraction. It is caused by the closure of the mitral and tricuspid valves

S2 (dub): It represents ventricular relaxation. It is caused by the aortic and pulmonary valves

62
Q

What causes the sounds of murmurs?

A

Result from turbulent flow of flow within the heart

They are usually due to pulmonic and aortic stenosis, hypertrophic obstructive cardiomyopathy, etc.

63
Q

What are bruits, and what affect do they have on sound?

A

They are narrowings in arteries, and they cause turbulent flow. Sounds caused by bruits can be detected in the carotid and renal artery

64
Q

What are some baseline lab tests recommended for hypertension patients?

A

Urinalysis (broad spectrum analysis of metabolites and waste found in urine)

Electolyte levels (Na+ and K+)

Creatinine (renal function)

Glucose (screening for diabetes)

Cholesterol (screening for dyslipidemia)

Urinary albumin excretion (possible kidney dysfunction)

65
Q

What is the utility of baseline lab tests for hypertension patients?

A

Urgency for treatment (do we need drugs or can we make lifestyle changes)

BP target (depending on risk factors, BP targets are set differently)

Drug selection for hypertension that takes into consideration other risk factors

66
Q

What drugs can elevate BP?

A

NSAIDs
Steroids
Oral contraceptives
Decongestants
Certain antidepressants (MAOIs, SNRIs, and SSRIs)
Stimulants (ex. methylphenidate and dextroamphetamine)
Excessive alcohol

67
Q

How do NSAIDs elevate BP?

A

NSAIDs inhibit renal prostaglandin production, which reduces renal perfusion.

Lower renal perfusion = lower GFR = more blood volume = high BP

68
Q

How do steroids elevate BP?

A

They can mimic the effects of aldosterone and activate RAAS

69
Q

How do oral contraceptives elevate BP?

A

They trigger angiotensinogen production from liver (indirect activation of RAAS)

70
Q

How do decongestants and stimulants lower BP?

A

They have increased SNS activity (vasocontriction nd increased cardiac output)

71
Q

How does alcohol elevate BP?

A

In excess, it can overwhelm the ADH system and other mechanisms

72
Q

What are the BP targets for different patient profiles?

A

Review table on pg 165 in the Hypertension slide deck

73
Q

What are some indications for Stage 1 hypertension (140-159/90-99mmHg)?

A

Lifestyle modification alone can be considered in lower risk factor patients if BP is under 160/100

Use medication without delay if target organ damage present or BP is above 160/100

74
Q

What are the first line pharm treatments for adults with Systolic/Diastolic Hypertension without any risk factors?

A

ACEi + CCB

ARB + CCB

ACEi or ARB + diuretic

75
Q

What are some non-pharmacological treatments in hypertension?

A

Being more physically active

Weight Reduction

Moderation in alcohol intake

Eating healthier

Relaxation therapies

Smoking cessation

76
Q

When should combo therapy for hypertension be started?

A

BP drugs are relatively weak in their reduction of BP, so combo therapy is used in 2/3 of patients

Adding combo agents is preferred over maxing one drug/pathway. Multi-pathway treatment allows lower doses of multiple drugs.

Lifestyle modification can help reduce the necessity of combo therapy

77
Q

What hypertensive drugs can be safely combined?

A

Anti-hypertensive drugs can be split into two groups (non-renin and renin-active). Drugs from the same category cannot be used without risking damage

Non-renin:
Thiazide diuretic
DHP CCBs

Renin-active:
beta-adrenergic blocker (BB)
ACEi
ARB

78
Q

What drugs are preferred for being added as the second agent for hypertension management?

A

In most patients, ACEi and ARBs will be chosen 2nd line over BB for BP control as long as no other conditions precluding their use exist (pregnancy, bilateral renal stenosis, and hyperkalemia)

79
Q

What are the clinical difference between ACEi and ARBs?

A

They are very similar agents, but ACEi are associated with chronic cough

80
Q

What are some possible causes of combination anti-hypertension therapy failure?

A

Nonadherance
Secondary hypertension
Interfering drugs or lifestyle
White coat effect

81
Q

What is a required drug class in triple therapy for hypertension

A

It must contain a diuretic

82
Q

If a patient has a resting BP of 163/100, but want to get to 140/90?

A

Start with two drugs because the target BP is 20/10 lower (2 agents x 10/5 BP drop per agent)

Try to find a pill that contains to agents to help increase convenience and adherence

83
Q

What is the definition of treatment-resistant hypertension?

A

Poor response despite:
Three anti-hypertensive drugs used in combination (a relatively common therapeutic option)

One of the drugs are diuretic (requirement of triple therapy)

Non-adherence has been ruled out

This situation requires referral to a cardiologist for reevaluation for secondary causes of hypertension.

84
Q

What are some possible causes of treatment-resistant hypertension?

A

Hyperaldosteronism

Pheochromocytoma (Unregulated SNS activity)

CKD (these patients always have high BP due to electrolyte imbalance)

Renovascular disease

Onstructive sleep apnea (low O2, heart beats harder and correct underlying problem)

Hyper/hypo-thyroidism (correct underlying problem)

85
Q

What are some drugs used in treatment-resistant hypertension?

A

Spironolactone (or mineralocorticoid/aldosterone receptor antagonists):
This drug is the most effective in managing treatment resistance, likely due to the condition being caused by aldosterone excess

Clonidine/methyldopa (alpha-2 agonists)

Hydralazine/minoxidil + BB

86
Q

What is isolated systolic hypertension (ISH)?

A

It is common in the elderly because as you age, the arteries loose compliance (become stiffer). BP inside arteries increases because the arterial walls do not stretch as much in response to pressure.

This means BP is only elevated above normal levels during systole

87
Q

What is the treatment strategy for isolated systolic hypertension?

A

Virtually the same as any other uncomplicated cases

88
Q

Why should HCPs be concerned if diastolic BP falls below 60mmHg in patients with coronary heart disease?

A

If pressure at diastole is low, coronary arteries wont fully fill (potential for ischemia)

89
Q

What is the utility of diuretics?

A

Excellent efficacy in reducing BP and edema

Reduces K+ and Na+ levels

OD dosing (take in AM to avoid PM urination)

90
Q

What are the unique properties of different classes of diuretics?

A

TZD (best for BP reduction): gentle diuretic effect that is les likely to activate RAAS. Longer half-life, less frequent dosing

Loop (best for fluid excretion): great for patients with CKD and hypertension

K+ sparing: (hypokalemia is a concern in diuretic use, so it needs to be conserved): no significant diuretic effect on its own, but commonly used in combo with other diuretics to limit K+ loss

91
Q

How does diuretic monotherapy cause hypokalemia?

A

Diuretic-induced Na+ and water loss = reduced blood volume = body attempts to re-establish blood volume by activating RAAS (diuretics do not block RAAS) = Increased Na+ reabsorption (body replaces these positive ions from the urine with K+) = Increased K+ loss

Check slide 209 for a diagram

92
Q

What are some non-diuretic induced caused of hypokalemia?

A

Inadequate K+ intake
Excessive Na+ intake
Low magnesium
Prolonged diarrhea
Hyperaldosteronism (secondary hypertension)
Heart Failure (HF)
Insulin

93
Q

What concentrations of K+ warrant action in hyperkalemia?

A

under 3.0 mmol/L: is always imdesirabel
3.0-4.5 mmol/L: is usually treated
3.5-4.0 mmol/L: action can be taken

94
Q

What can be done to rectify hypokalemia?

A

General measures (reduce Na+ and increase K+ intake)

Switch TZD (Indapamide) for ARB (more liekly to maintain monotherapy with ARB)

Add K+ supplement (additional pill vs. switching to ARB)

Add K+ sparing diuretic

95
Q

What are the consequences of hyperkalemia?

A

Can cause ventricular arrhythmia by delaying conduction of signals (widening QRS)

96
Q

What are some drugs that increase K+?

A

RAAS drugs
NSAIDs
Vitamins/supplements
K+ sparing diuretics
TMP/SMX

97
Q

What are some conditions that affect how we treat hypertension?

A

Diabetes with/without nephropathy
Non-diabetioc kidney disease
Coronary artery disease
Heart Failure
LVH
Stroke

98
Q

How does diabetes affect how drug decisions for hypertension are made?

A

Diabetes causes vascular remodelling and can cause nephropathy

ACEi or ARBs are first line

99
Q

How does CKD affect how drug decisions for hypertension are made?

A

Due to the kidney’s contribution to maintaining fluid volume, ACEi and ARBs are always used when kidney function is involved in hypertension

100
Q

How does long-standing hypertension + diabetes increase the risk for CKD?

A

The two diseases both cause damage to the kidneys (via pressure and glucose toxicity respectively). Over time kidney function declines due to this damage

101
Q

What are some signs of CKD from lab tests?

A

Increased serum creatinine (easily secreted by normal kidneys)

Leakage of protein and large molecules (these can be toxic in the tubule, causing further damage)

102
Q

How do ACEi and ARBs have renal protection?

A

ACEi and ARBs prevent Angiotensin I from converting into Angiotensin II (a chemical that will usually bind to Angiotensin II binding sites can cause efferent vasoconstriction)

103
Q

What are the different types of hypertension experienced in pregnancy?

A

Pre-eclampsia (High BP with proteinuria)

Gestational Hypertension (High BP without proteinuria)

Chronic Hypertension (HTN was present before pregnancy)

People who develop pre-eclampsia or gestational hypertension are more likely to develop hypertension following their pregnancy

104
Q

What are some safe anti-hypertensive drugs in pregnancy

A

Labetalol, methyldopa, loong-acting nifedipine, enalapril or captopril all show efficacy without posing fetal harm

105
Q

What are some changes that can prevent pre-eclampsia?

A

Ca2+ 1-2g/day

Low dose ASA starting late in the first trimester (especially in women with risk factors like high BMI, diabetes, and other chronic conditions)

106
Q

How do centrally acting anti-hypertensive drugs work?

A

Stimulate alpha-2 receptors in the brain (lowers SNS outflow and increase cholinergic effects)

This results in lower HR, CO, and BP

107
Q

What are some centrally acting anti-hypertensives (alpha-2 agonists)?

A

Clonidine and Methyldopa

These drugs can cause sedation and dry mouth

108
Q

What are some side effects that should be measured for all anti-hypertensive drugs?

A

BP

Kidney, heart, and arterial health

Dizziness/headache/hypotension (can be caused when standing up)

Erectile dysfunction

Exercise (self-test)

109
Q

What are some specific monitoring parameters for different drug classes?

A

ACE/ARB: K+, SCr, chronic cough

Diuretics: (gout, electrolyte imbalance, SCr, urination)

DHP CCBs: edema

BB and non-DHP CCBs: Low heart rate

Alpha-2 agonists: fatigue

Vasodilators: tachycardia

110
Q

What are some examples of beta-1 selective blockers?

A

MOst commonly agents used in this drug class
Atenolol
Bisoprolol
Metprolol

Other b-1 selective blockers
Acebutolol
Esmolol

111
Q

What are some examples of non-selective beta blockers?

A

Nadolol
Pindolol
Propranolol
Timolol

*Carvedilol is a non-selective BB that also blocks a-1 receptors

112
Q

When can beta blockers be used in hypertension treatment?

A

Canadian guidelines recommend as an alternative for patients under 60 (minimal role in uncomplicated patients even if under 60)

but its used in controversial in terms of efficacy compared to placebo

113
Q

What are some vasodilator drug classes?

A

DHP CCBs (first line)

Alpha blockers (not recommended as first line)

Smooth muscle relaxants (Hydralazine and MInoxidil (used in treatment-resistant hypertension)

114
Q

How is b-1 and a-1 receptor activation affect vessel diameter?

A

b-1 activation causes dilation

a-1 activation causes contriction

115
Q

What are some alpha-1 blockers?

A

Doxazosin
Prazosin
Terazosin

not recommended for first-line b/c less efficacy

116
Q

Are BP targets lower in patients with lower CV risk factors?

A

No, they are lower in higher-risk patients

117
Q

How can the effects of ACEi or ARBs be a double-edged sword?

A

Decreased GFR can slow long-term kidney damage.

However excessive reduction in glomerular pressure can reduce pressure in arterioles. If excessively low pressure is not reversed, acute renal failure can result (nephron collapse).

Nephron collapse causes urine production to halt

PHAR 152* (16 decks)

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