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Clin Med-Cardiology Exam 1 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Epidemiology of HTN

A

prevalence increases with age
MC Dx in primary care
More common in black than whites

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2
Q

HTN doubles the risk of what diseases

A

CV diseases
CHD
CHF
ischemic and hemorrhagic strokes, renal failure and PAD

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3
Q

what happens to systolic BP as we age

A

it rises

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4
Q

what happens wit SBP of women compared to men

A

after 60 SBP of women>men

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5
Q

distolic blood pressure increase until when

A

until age 55 then it decreases

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6
Q

SBP is a better predictor of what

A

better predictor of morbid events than DBP in older patients per JNC7

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7
Q

why is there such a low rate of control of HTN

A

poor access to health care and med
lack of adherence w/long term therapy
its a silent disease

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8
Q

major complications of HTN

A

hypertensive cardiovascular disease
Hypertensive cerebrovascular disease and dementia
kidney disease
atherosclerotic complications

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9
Q

what is the most common cause of death in HTN patients

A

hypertensive cardiovascular disease.

Major cause of morbidity and mortality in primary HTN

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10
Q

what is the result of Hypertensive cardiovascular disease

A

LVH-CHF-Ventricular arrhythmias-myocardial ischemia- sudden death
LVH regresses with therapy

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11
Q

complications from hypertensive cerebrovascular disease and dementia

A

stroke
important risk factor for ischemic stroke
more closely related to systolic vs diastolic
most important risk factor for the development of hemorrhagic stroke
high incidence of vascular and dementia

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12
Q

what is the second most frequent cause of death in the world

A

stroke

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13
Q

hypertensive kidney disease

A

the kidney is both a cause and a target of HTN

related to systolic BP

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14
Q

what is the secondary most common etiology of secondary HTN

A

Primary renal disease

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15
Q

who is HTN kidney disease more common in

A

blacks than whites

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16
Q

Diastolic BP is a more important cardiovascular RF than elevated SBP in who

A

younger patients w/o major comorbidities

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17
Q

what is the most important RF for development of hemorrhagic stroke

A

HTN

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18
Q

HTN is associated with a higher incidence of what 2 diseases

A

vascular and Alzheimers type dementia

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19
Q

what is a reliable marker of the severe chronic kidney disease

A

proteinuria

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20
Q

What are complications of Atherosclerotic

A

blood vessels may be a target organ for atherosclerotic disease secondary to long standing elevated BP
Aortic aneurysms/dissection

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21
Q

What effect does hypertensive therapy have on atherosclerosis

A

has a lesser impact on this type of complication

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22
Q

how is atherosclerosis controlled

A

control of multiple risk factors including but not limited to HTN alone

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23
Q

what is the definition of hypertension

A

a systolic BP of 140mmHg or higher or a diastolic BP of 90mmHg or higher

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24
Q

How is HTN diagnosed

A

need 2 or more reading on 2 separate occasions over one to several weeks to diagnose HTN

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25
Q

Prehypertension BP is

A

120-139 or 80-89

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26
Q

Stage 1 HTN is

A

140-159 or 90-99

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27
Q

Stage 2 HTN is

A

> 160 or >100

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28
Q

Isolated systolic HTN

A

> or= 140 and <90

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29
Q

What is essential HTN

A

makes up 80-95% of patients w/HTN
no single reversible cause, etiology unknown
secondary to multiple genetic and environmental factors

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30
Q

what are the risk factors for HTN

A 
race (more common in blacks)
Age (>55 for men, >65 for women)
1st degree relative w/HTN
Obesity/Weight gain
Diet high sodium/salt
Excess ETOH intake
Metabolic Syndrome
Cigg Smoking
Inactivity/sedentary lifestyle
Dyslipidemia independent of obesity
Polycythermia
Vit-D deficiency
Low potassium intake
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31
Q

what is metabolic syndrome

A

central obesity, hyperinsulinemia, insulin resistance, hypertriglyceridemia

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32
Q

what is white coat HTN

A

20-25% of patients w/stage 1 office HTN have white coat or Isolated office HTN

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33
Q

what are secondary causes of HTN

A 
Primary Renal Disease
Drug Induced 
Renovascular
Adrenal
Endocrine Disorders
Obstructive Sleep Apnea
Coarc of the Aorta
Pregnancy HTN
Genetic Disorders
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34
Q

What is primary renal disease (both acute and chronic)

A

renal parenchymal disease, (CKD) is the most common cause of secondary HTN

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35
Q

what is the most common cause of Secondary HTN

A

Chronic Kidney Disease

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36
Q

What drugs cause secondary HTN

A 
Oral contraceptives
NSAIDS
Antidepressants
Decongestants
Cocaine
Glucocorticosteroids
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37
Q

Arm to leg systolic BP Difference >20mmHg
*Delayed or absent femoral pulses
*Murmur
possible cause

A

Coarctation of the aorta

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38
Q

*Increase in serum creatinine concentration (≥0.5 to 1mg/dL) after starting ACEI or ARB
*Renal artery bruit
�

A

Renal artery stenosis

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39
Q

What are the 2 types of HTN treatment

A

Nonpharmacological

Pharmacological

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40
Q

What is the primary goal in HTN treatment

A

prevent organ damage

41
Q

What is the secondary goals of HTN treatment

A

Minimize side effects, minimize patient cost
Increases adherence
Treat comorbid conditions

42
Q

What are the benefits of treatment

A

Lowering SBP by 10-12mmHg and DBP by 5-6mmHg confers relative risk reduction of
HTN control is the single most effective intervention for slowing the rate or progression of HTN-related chronic kidney disease
Short term reductions of BP in hypertensive patients over 65 provide greater benefits than that observed in younger patients

43
Q

What are nonpharmacological lifestyle modifications

A 
Dietary Salt restriction 2.4-6g
Weight loss (BMI 18.5-24.9)
DASH diet(fruits/Veg, high protein/fiber, low fat dairy, reduced saturated and total fat low red meat)
Exercise (30min/day regular)
Decrease Alcohol intake <1/day female
Vit-D intake
Adequate Potassium intake
Smoking cessation
Limit NSAID
Educate patients
44
Q

What are the pharmacological options?

A 
Diuretics
β-Blockers
Angiotensin-Concerting Enzyme Inhibitors (ACE-I)
Angiotensin II Receptor Blockers (ARB’s)
Renin Inhibitors
Aldosterone Receptor Antagonists
Calcium Channel Blockers (CCB)
α-Adrenergic Antagonists
Drugs w/ Central Sympatholytic Action
Direct Vasodilators
45
Q

How much do most drugs reduce SBP by

A

7-13mmHg and DBP by 4-8mmHg

Most patients require combination agents to achieve goal BP

46
Q

How do Diuretics work

A

Decrease plasma volume initially, but in long term use they reduce peripheral vascular resistance

47
Q

What are type of Diuretics

A

Thiazides
Loop
K+ retaining

48
Q

What are side effects with Thiazides and Loop and who should you be careful using them with

A

hypokalemia, insulin resistance, increase cholesterol, increase uric acid
Use w/ caution in diabetics, dyslipidemia, gout, hypokalemia

49
Q

Who do you use Loop diuretics with

A

pts w/ reduced GFR and CHF

50
Q

What are K+ retaining diuretics used for

A

Weak anti-hypertensives, but may be used in combo w/ a thiazide to protect against hypokalemia

51
Q

What is 1st line treatment for patients with uncomplicated HTN

A

Thiazide diuretics
Chlorthalidone is drug of choice
More potent in black and older individuals and obese pts

52
Q

Beta blockers MOA

A

Decreases heart rate and cardiac output

53
Q

What are the side effects of B-blockers

A

Induce or exacerbate bronchospasm in predisposed patients, bradycardia or AV block, nasal congestion, Raynaud’s phenomenon and CNS symptoms
Abrupt withdrawal can precipitate acute coronary events and severe increases in BP therefore if/when d/c medication, taper slowly

54
Q

What are beta blockers indicated for?

A

patients w/ Angina pectoris, post MI, CHF, sinus tachycardia, ventricular tachyarrhythmias

55
Q

Who do we cautiously use beta blockers with

A

in patients w/ Type I DM and patients w/ advanced peripheral vascular disease associated w/ rest pain or non-healing ulcers

56
Q

who are beta blockers contraindicated with?

A

in asthma, COPD, 2nd or 3rd degree heart block and sick sinus syndrome

57
Q

how does ACE-Inhib work

A

Inhibit the renin-angiotensin-aldosterone system

�Effective as monotherapy or in combo w/ diuretics, CCBs and alpha blocking agents

58
Q

What are the Benefits ACE-I

Side effects

A

Benefits: Renoprotective
Results in a significant reduction in all cause mortality
�
S/E:hyperkalemia, cough, skin rashes, angioedema

59
Q

Who do ACE-I/Angiotensin II RB work best for

A

More effective in younger white patients and less effective in blacks and older patients

60
Q

Who are ACE-I/Angiotensin II RB the drug of choice for?

A

CHF and Diabetics

they delay the progression of end stage renal disease

61
Q

Who is ACE-I/Angiotensin II RB contraindicated with

A

in pregnancy, b/l renal artery stenosis and hyperkalemia

62
Q

ACE-I others info

A

Severe hypotension can occur in patients w/ renal artery stenosis (induce acute renal failure that reverses with d/c of ACE-I)
Abrupt increase in creatinine

63
Q

Angiotensin II receptor blockers MOA

A

Provide selective blockade of angiotensin receptors

64
Q

Angiotensin II RB Side effects

A

hyperkalemia

Do not reduce all cause mortality like ACEI do, but they are renoprotective (delay onset of kidney failure)

65
Q

Renin inhibitors MOA

A

Blockade of the renin-angiotensin system

66
Q

Renin inhibitors info

A

Aliskiren is the first oral renin inhibitor
As effective as an ACEI or ARB in monotherapy, but not more effective
Not considered a first line agent

67
Q

Aldosterone Antagonists

A

Ex. Spironolactone

Effective in resistant HTN and can be used in combination w/ other classes

68
Q

What other conditions are Aldosterone antagonists indicated for

A

CHF due to systolic dysfunction and primary aldosteronism

69
Q

What are the contraindications of Aldosterone antagonists

A

renal failure and hyperkalemia

70
Q

what are the side effects of Aldosterone antagonists

A

Ex. Spironolactone

Effective in resistant HTN and can be used in combination w/ other classes

71
Q

CCB MOA

A

Act by causing peripheral vasodilation

72
Q

What are the 2 types of CCB

A

Dihydropyridines

Nondihydropyridines

73
Q

Dihydropyridines

A

nifedipine

74
Q

nonDihydropyridines

A

Verapamil & Diltiazem

75
Q

Nondihydropyridines should not be combined with

A

beta blockers because the risk of bradycardia

76
Q

what are side effects with CCB

A

H/A, peripheral edema, bradycardia, constipation

77
Q

CCB indications

A

Black people respond well to CCB

78
Q

Nondihydropyridines are also used post

A

-MI, in supraventricular tachycardias and angina

79
Q

CCB Caution/contraindications:

A

Nondihydropyridines: 2nd or 3rd degree heart block

80
Q

A-adrenergic antagonist MOA

A

Decrease peripheral vascular resistance

81
Q

A-adrenergic antagonist indications and benefits

A

Effective as monotherapy only in men w/ symptomatic BPH (benign prostatic hypertrophy)
Other indications: Pheochromocytoma
Benefits: Increase HDL cholesterol and lower TC

82
Q

α-Adrenergic Antagonists side effects

A

Common and include marked hypotension after the 1st dose, post dosing palpitations, HA and nervousness.
Previous and current use can complicate patients undergoing cataract removal resulting in “floppy iris syndrome

83
Q

Sympatholytic agents MOA

A

Centrally acting α-2 sympathetic agonists decrease peripheral resistance

84
Q

Sympatholytic agents

A

Infrequently used d/t drug intolerance (sedation, fatigue, dry mouth, postural hypotension, erectile dysfunction and drug-drug interactions)
*Methyldopa- used in pregnancy

85
Q

Direct Vasodilators MOA

A

Decrease peripheral vascular resistance

86
Q

Direct vasodilators
Use
Side effect

A

Not used as monotherapy, but in combo w/ diuretics and B-blockers in resistant pts

87
Q

What to start initial mono therapy

A

Used only in the absence of a specific indication and if the BP is <20/10mmHg above goal BP

88
Q

what are the 3 main classes used to initial mono therapy

A

Thiazide diuretics
Long lasting CCB
ACE inhibitor or ARB

89
Q

When to use combo therapy

A

Used when the BP is more than 20/10mmHg above goal or SBP is >160 and/or DBP is >100

90
Q

What drugs are used for combo therapy

A

Typically consists of a Diuretic plus either an ACEI/ARB or CCB

91
Q

Adding a second drug in combo therapy info

A

Combo therapy from drugs from different classes has a better BP lowering effect than doubling the dose of a single agent
Higher doses results in increased side effects and it does not mean you will get double the effect
Recommend adding an ACE-I/ARB to a Thiazide or CCB

92
Q

Resistant HTN deifinition

A

DBP >90mmHg despite 3 or more anti-hypertensive medications including a diuretic

93
Q

One or more reasons for resistant HTN

A

Suboptimal therapy
Volume Overload
Poor compliance w/ medical or dietary therapy
Secondary HTN
Pseudoresistance: Office or “white coat” HTN
Ingestion of substances that can elevate the BP
Associated Conditions: smoking, weight gain, increased ETOH intake, DM, Sleep Apnea, Anxiety, or chronic pain

94
Q

What to do when following up with a patient with HTN

A

Reinforce lifestyle modifications at EVERY visit
Reassess risk factors at every visit
Screen for side effects at every visit

95
Q

Once BP is controlled on a well tolerated regiment

A

Recommend f/u q6months if at low risk
Recommend f/u q3 months if at high risk
Yearly monitoring of labs (BMP, lipids) if at low risk
Biannual monitoring of labs (BMP, lipids) if at high risk or there are underlying medical conditions
EKG q2 years unless otherwise indicated (risk factors, age or hx of an abnormal EKG)

96
Q

What is step down therapy

A

ome pts w/ Stage I HTN are well controlled on a single med or combo
After a period of years w/ a successful lifestyle modification and BP lowering medication, you can consider decreasing the dosage and/or d/c med.

97
Q

The best way to treat high risk HTN pts

A

Aggressive Tx early in high risk patients to prevent cardiovascular problems and target organ damage
Consider other medications such as low dose ASA and lipid-lowering agents, etc to treat underlying/co-morbid conditions
�Patient Education is the key to better compliance and BP control!!!

98
Q 
HTN Treatment Goals
As per JNC8 guidelines:
General population ≥ 60 y:  
General population <60 y:  
Population aged ≥18 y with CKD or DM
A

<140/90

Clin Med-Cardiology Exam 1 (8 decks)

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