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Fam Med: Hypertension > Pharmacotherapy > Flashcards

Pharmacotherapy Flashcards

1
Q

Describe the RAAS system

A
  • Renin is produced and stored in the juxtaglomerular cells of the kidney and its release is stimulated by impaired renal perfusion, salt depletion, and B1-adrenergic stimulation.
  • Release of renin is the rate limiting step in the eventual formation of angiotensin II, which is primarily responsible for the pressor effects mediated by the RAAS
  • Evidence indicates that renin’s pressor effects occur at a cellular level (autocrine), local environment (paracrine), and through systemic circulation (endocrine)
  • Role of RAAS in primary HTN
    • High levels of renin, suggesting that the system is inappropriately activated-possible mechanisms may include: sympathetic drive, defective regulation of RAAS, and existence of a subpopulation of ischemic nephrons that release excess renin
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2
Q

What is the equation for BP?

A

BP= CO x PR

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3
Q

Describe how the following factors affect HTN:

excess sodium intake

A

renal sodium retention –> increased fluid volume –> increased preload –> increased CO and increased BP

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4
Q

Describe how the following factors affect HTN:

decreased nephron count

A

renal sodium retention and decreased filtration surface –> increased fluid volume –> increased preload –> increased CO and increased BP

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5
Q

Describe how the following factors affect HTN:

Stress

A

SNS over-activity –> increased contractibility –> increased CO and increased BP

decreased filtration surface –> increased fluid volume –> increased preload –> increased CO and increased BP

Renin-angiotensin excess –> functional constriction –> increased PR and increased BP

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6
Q

Describe how the following factors affect HTN:

obesity

A

hyperinsulinemia –> functional constriction and structural hypertrophy –> increased PR and increased BP

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7
Q

Describe how the following factors affect HTN:

activation of SNS

A

direct activation of SNS may lead to enhanced sodium retention, insulin resistance, and baroreceptor dysfunction

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8
Q

Describe how the following factors affect HTN:

endothelium derived factors

A

hyperinsulinemia –> functional constriction and structural hypertrophy –> increased PR and increased BP

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9
Q

Where is renin stored?

A

juxtaglomerular cells of the kidney

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10
Q

What stimulates renins release?

A

impaired renal profusion, salt depletion, and B1-adrenergic stimulation

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11
Q

How do you take a good BP?

A
  • Instruct patients to avoid exercise, alcohol, caffeine, or nicotine consumption 30 mins before
  • Patients should be sitting comfortably with back supported and arm free of constrictive clothing with legs uncrossed and feet flat on the floor for a min of 5 mins before the first reading
  • Should not talk during to reduce deviations
  • Measurement arm should be supported and positioned at heart level
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12
Q

What happens when the BP cuff is too small?

A

Systolic and diastolic BP tend to increase

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13
Q

How do you know what the right size cuff is?

A

The cuff bladder should encircle at least 80% of the arms circumference

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14
Q

What are korotkoff sounds?

A

Noise heard over an artery by auscultation when pressure over the artery is reduced below the systolic arterial pressure

Heard over the brachial artery in the antecubital fossa – first and last audible are systolic and diastolic pressures

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15
Q

What labs do you want to order/monitor on a patient with hypertension?

A
  • Fasting lipid panel:
    • LDL >160mg/dL
    • Total >240mg/dL
    • HDL <40mg/dL
    • Triglycerides >200mg/dL
  • Fasting plasma glucose or A1c
  • Hypertension related damage:
    • Serum creatinine >1.2mg/dL
    • Microalbuminuria
  • 24-hour urine collection (20-200 microg/min) or from elevated concentrations on at least 2 occasions (30-300dg/L)
  • Albumin-to-creatinine ratio becoming MC
    • 30-300mg/g creatinine
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16
Q

For every __mmHg systolic or ___mmHg diastolic increase, there is a ______ of mortality for both ischemic heart disease or stroke

A

20, 10, doubling

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17
Q

How would you counsel a patient on lifestyle modifications?

A
  • Weight reduction
    • maintain normal body weight (BMI 18.5-24.9 kg/m2)
    • systolic BP reduction of 5-20mmHg/10 kg
  • Adopt DASH diet
    • consume a diet rich in fruits, vegetables, and low-fat dairy with a reduced content of saturated and total fat
    • systolic BP reduction of 8-14mmHg
  • Dietary sodium restriction
    • Reduce dietary sodium intake to no more than 100 mmol/day (2.4g sodium or 6g sodium chloride)
    • Systolic BP reduction 2-8mmHg
  • Physical activity
    • Engage in regular aerobic physical activity such as brisk walking (at least 30 mins/day, most days of the week)
    • Systolic BP reduction 4-9mmHg
  • Moderation of alcohol consumption
    • Limit consumption to no more than 2 drinks/ day in most men and no more than 1 drink/day in women and lighter persons
    • Systolic BP reduction 2-4mmHg
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18
Q

What is the DASH diet?

A

Diet Approaches to stop HTN

Diet high in fruits, vegetables, and low-fat dairy products with a reduced intake of total and saturated fat

Significant reduce in BP in 8 weeks

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19
Q

What effect do lifestyle modifications have on morbidity and mortality?

A

Never been documented to reduce cardiovascular morbidity and mortality in patients with HTN

but they do effectively lower BP to some extent and may obviate the need for drug therapy in those with mild elevations or minimize doses or number of anti-HTN agents in those with higher elevations

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20
Q

Describe the difference between chlorthalidone and HCTZ

A

Chlorathalidone 1.5-2x as potent as HCTZ

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21
Q

Describe the metabolic effects of thiazides

A

Hyperlipidemia and hyperglycemia

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22
Q

Describe the electrolyte effects of thiazides

A

Hypokalemia, hypomagnesemia, hyperuricemia, and hypercalcemia

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23
Q

How do you decrease the risk of diabetes with thiazides?

A

Keeping potassium in the normal range (above 4.0 mEq/L)

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24
Q

When are loop diuretics > thiazides?

A

Reduced renal function that occurs with age and an eGFR <30 mL/min

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25
Q

How do loop diuretics work?

A

Site of action is the thick ascending limb of the Loop of Henle

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26
Q

Describe the metabolic effects of loop diuretics

A

Potential for aggravating hyperglycemia, dyslipidemia, and hyperuricemia

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27
Q

Describe the electrolyte effects of loop diuretics

A

Excess diuresis leading to hyponatremia but may additionally cause hypokalemia, hypomagnesemia, and hypocalcemia

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28
Q

Describe the MOA of potassium sparing diuretics

A

Act on the late distal tubule and collecting duct, and have limited ability to affect sodium resorption

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29
Q

What are ADRs of potassium sparing diuretics?

A

Potential to contribute to hyperkalemia

Especially relevant in patients receiving other agents with K-sparing properties like ACE inhibitors, ARBs, K supplements and NSAIDs along with pts with renal impairment

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30
Q

Name the two potassium sparing diuretics

A

Triamterene

Amiloride

31
Q

Name the aldosterone antagonist

A

Spironolactone

32
Q

How does the aldosterone antagonist work?

A

Modulate vascular tone through a variety of mechanisms besides diuresis

Their K+ sparing effects mediated through aldosterone antagonism, complement the K+ wasting effects of more potent diuretics

33
Q

When is eplenerone indicated?

A

Used with increasing frequency in patients with heart failure following acute MI

34
Q

Contrast spironolactone and eplenerone

A

Spironolactone: MC used, more commonly associated with gynecomastia, greater risk of hyperkalemia

Eplenerone: contradicted with estimated creatinine clearance < 50mL/min or serum creatinine >1.8mg/dL for women or >2 mg/dL for men or T2DM with microalbuminuria

35
Q

Why aren’t beta blockers effective BP agents?

A

May be due to their tendency to reduce central aortic pressure and cardiac afterload to a less degree compared to other agents

36
Q

Which BB has the highest risk for stroke?

A

Atenolol

37
Q

When should beta blockers be used?

A

Patients with comorbidities such a HF and recent MI and other ischemic conditions

38
Q

Why are BB effective in CHF?

A

Inhibition of neurohormonal medicated cardiac remodeling reduces morbidity and mortality relative to standard HF therapies

39
Q

How do BB lower blood pressure?

A

Their modulation of renin which appears to result in reduction in CO and/or reduction in PR along with their negative inotropic/chronotropic actions

40
Q

What is the significant of ISA in beta blockers?

A

Intrinsic sympathomimetic activity

Effectively block the B-receptor at higher circulating catecholamine levels, such as during exercise, while having modest B-blocking activity at times of lower catecholamine levels, such as at rest

41
Q

When do you want a cardioselective beta blocker?

A

Consider in a patient with mild asthma, COPD, or PVD (intermittent claudication)

May achieve adequate blockage of B1-receptors in the heart and kidneys while minimizing the undesirable effects of B2-receptor blockade on the smooth muscle lining the bronchioles

42
Q

Describe the differences between beta-1 and beta-2 receptors

A

B1-receptors: found in heart and kidneys

B2-receptors: found in smooth muscle lining bronchioles

43
Q

What are the adverse effects of beta blockers?

A

Bradycardia

Various degrees of HB

Signs/sx of HF

44
Q

What are ADRs of ACE-Is?

A

Hyperkalemia

Persistent dry cough

45
Q

When is hyperkalemia more likely to occur?

A

Compromised renal function

Concurrent NSAIDs

Taking potassium supplements or using K+ containing salt substitute

46
Q

Why does a dry cough occur?

A

Caused by accumulation of bradykinin resulting from a direct effect of inhibiting ACE

47
Q

Discuss monitoring kidney function with ACE-Is

A

Inhibition of the generation of angiotensin II through ACE inhibition would reduce the efferent renal artery tone thereby changing the intraglomerular pressure à reduction in GFR which results in elevation of serum creatinine up to 30%

Need to monitor serum creatinine for needed dose reduction and ACE should be d/c if serum creatinine is >30% elevation

48
Q

Describe more rare effects on kidney function

A

More serious renal function effects (acute renal failure in those with pre-existing kidney dysfunction, bilateral or unilateral renal artery stenosis)

49
Q

How do ARBs work?

A

Inhibitors of the angiotensin-1 receptors

50
Q

What do AT1 receptors do?

A

AT1 receptor stimulation evokes a pressure response via a host accompanying effects on catecholamines, aldosterone, and thirst

Inhibition of AT1 receptors directly prevents this pressor response and results in upregulation of RAAS, which results in elevated levels of angiotensin II à added effect of stimulating AT2 receptors which are associated with anti-HTN activity

51
Q

How do ARBs differ from ACE-Is?

A

ARBs: cause up-regulation of the RAAS

ACE-I: blocks the breakdown of bradykinin

52
Q

List the renin inhibitors

A

Aliskiren

53
Q

What are you concerned about when prescribing renin inhibitors?

A

Because of its role in RAAS, there are recommendations and precautions for monitoring serum potassium and kidney function similar to ACE/ARBs

Long term clinical trials evaluating efficacy and safety yet to be completed and effects of morbidity/mortality are unknown

54
Q

When should alpha blockers be used?

A

Considered as add-on therapy when HTN is not controlled

55
Q

What is the risk with alpha blockers?

A

Increase in cardiovascular events

56
Q

What are ADRs of alpha blockers?

A

Syncope, Dizziness, Palpitations following first dose and orthostatic HoTN with chronic use

57
Q

How do central a2-agonists work?

A

They stimulate central alpha1-adrenergic receptors which leads to reduction of sympathetic outflow and enhance parasympathetic activity thereby reducing HR, CO, and total PR

58
Q

What role do direct vasodilators play in HTN?

A

Primarily relax smooth muscles in arterioles and activate baroreceptors

59
Q

What are the direct vasodilators?

A

Hydralazine

Minoxidil

60
Q

Why are the direct vasodilators combined with beta blockers and diuretics?

A

They are used to offset their tend to cause reflex tachycardia and fluid retention

61
Q

Describe the best hypertensive agents for specific populations and why:

HTN and angina

A

Beta-blockers and long-acting CCBAs

May also benefit from plaque stabilizing effects of Amlodipine

62
Q

Describe the best hypertensive agents for specific populations and why:

ischemic heart disease (diabetics)

A

ACE inhibitors useful in reducing risk of cardiovascular events

ARB if ACE cannot be tolerated

63
Q

Describe the best hypertensive agents for specific populations and why:

post-MI

A

Beta-blockers and ACE inhibitors

Proven reduction of cardiovascular morbidity and mortality in this population

Aldosterone with reduced LV systolic function and diabetes or s/sx of HF

64
Q

Describe the best hypertensive agents for specific populations and why:

asx LV systolic dysfunction

A

Beta-blocker and ACE inhibitor

65
Q

Describe the best hypertensive agents for specific populations and why:

HF

A

Drugs proven to also reduce the morbidity and mortality of HF, including beta-blockers, ACE-I, ARBs, aldosterone antagonists, and diuretics for sx control as well as anti-HTN effects

66
Q

AA with CHF and LV systolic dysfunction

A

Combo therapy with nitrates and hydralazine affects morbidity/mortality and HTN

67
Q

HF with preserved EF

A

Diuretics, beta-blockers, ACE-I, ARBs, CCBAs

68
Q

DM and HTN

A

Initially: ACE-I, ARBs, beta-blockers, diuretics, CCBAs

69
Q

CKD and HTN

A

ACE-I and ARBs usually in combo with a diuretic

70
Q

h/o stroke, TIA

A

ACE-I in combo with thiazide diuretic

Reduces risk of recurrent stroke

71
Q

What are the two categories of hypertensive crisis?

A

Hypertensive emergencies

Hypertensive urgencies

72
Q

What is the difference between hypertensive urgency and emergency?

A

Emergency: severe elevations in BP accompanied by acute of life-threatening target organ damage such as AMI, unstable angina, encephalopathy, intracerebral hemorrhage, acute LV failure with pulm. edema, dissecting AA, rapidly progressing renal failure, accelerated malignant HTN with papilledema, eclampsia. BP >220/140 mm Hg

Urgency: severe elevation in BP without evidence of acute or life-threatening organ damage

73
Q
A

Fam Med: Hypertension (2 decks)

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