HTN Flashcards

1
Q

HTN doubles the risk of CV diseases

A

CHD, CHF, ischemic and hemorrhagic strokes, renal failure and peripheral artery disease.
Mortality rate for stroke and coronary heart diseases have decreased by 50-60% over the past decade
The number of patients w/ end stage kidney disease and heart failure continues to rise

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2
Q

Why is there such a low rate of control of HTN?

A

Poor access to health care and medications
Lack of adherence w/ long term therapy
“Silent Disease”

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3
Q

HTN- Systolic BP

A

Systolic BP tends to rise as we age
After age 60, SBP of women>males

Systolic BP is a better predictor of morbid events than diastolic BP in older patients

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4
Q

HTN- Diastolic BP

A

Diastolic blood pressure increases progressively with age until age 55, then it tends to decrease.
Consequence is a widening of pulse pressure beyond age 55
Diastolic BP is a more important cardiovascular risk factor than is elevated SBP in younger patients w/o major comorbidities

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5
Q

Major Complications of HTN (4)

A

Hypertensive Cardiovascular Disease
Hypertensive Cerebrovascular Disease and Dementia
Hypertensive Kidney Disease
Atherosclerotic Complications

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6
Q

Hypertensive Cardiovascular Disease (4)

A

Most common cause of death in HTN patients
Major cause of morbidity and mortality in primary HTN
Result of LVHCHFVentricular arrhythmiasmyocardial ischemiasudden death
Occurrence of heart failure can be reduced by 50% w/ antihypertensive therapy
LVH regresses w/ therapy

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7
Q

Hypertensive Cerebrovascular Disease and Dementia (5)

A

Stroke is the 2nd most frequent cause of death in the world
HTN is the most common and most important risk factor for ischemic stroke
More closely correlates to systolic vs diastolic BP
Incidence of both ischemic and hemorrhagic strokes decreases w/ therapy
HTN is the most important risk factor for the development of a hemorrhagic stroke
HTN is associated w/ a higher incidence of both vascular and Alzheimer types dementia

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8
Q

Hypertensive Kidney disease (6)

A
  • The kidney is both a target and a cause of HTN
  • Primary renal disease is the most common etiology of secondary HTN
  • Related to systolic BP as opposed to diastolic.
  • HTN is a risk factor for renal injury and end stage renal disease.
  • More common in blacks than whites
  • Proteinuria is a reliable marker of the severity of chronic kidney disease and is a predictor of it’s progression.
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9
Q

Atherosclerotic Complications (4)

A

Blood vessels may be a target organ for atherosclerotic disease secondary to long standing elevated BP
Most Americans w/ HTN die of complications of atherosclerosis
Hypertensive therapy has a lesser impact on these complications
Reduction of atherosclerosis requires control of multiple risk factors including but not limited to HTN alone

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10
Q

Definition of HTN (2)

A

A systolic blood pressure of 140mmHg or higher, or a diastolic blood pressure of 90mmHg or higher

*Need 2 or more readings on 2 separate occasions over one to several weeks to diagnose HTN

Home monitoring is better correlated w/ target organ damage than clinic-based values

Ambulatory BP recordings provide a more comprehensive assessment of HTN than office readings

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11
Q

3 Types of HTN

A

Primary or Essential Hypertension
“White Coat Syndrome”
Secondary Hypertension

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12
Q

Essential HTN (8)

A

80-95% of patients w/ hypertension
No single, reversible cause
Specific etiology is unknown
Secondary to multiple genetic and environmental factors
Occurs in 10-15% of white adults in the US
Occurs in 20-30% of black adults in the US
Onset is usually b/w ages 25-55 years of age
Prevalence increases w/ age

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13
Q

Risk Factors for HTN (12)

A
Race (more common in blacks)
Age (> 55 for men, >65 for women)
First degree relative w/ HTN
Obesity/Weight gain
Diet high in sodium/salt
Excess ETOH intake
Metabolic Syndrome
Cigarette smoking
Inactivity/sedentary lifestyle
Dyslipidemia, independent of obesity
Polycythemia
Vitamin D deficiency
Low potassium intake
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14
Q

White Coat HTN (3)

A

20-25% of patients w/ stage 1 office HTN have “white-coat” or isolated office HTN
repeatedly normal when measured at home, work or by ambulatory BP monitoring)

Patients have increased risk of developing sustained primary HTN

Ambulatory BP Monitoring (ABPM) which records the BP at preset intervals during the day and night can be used to confirm or exclude the presence of white coat HTN in pts w/ persistent office HTN but normal BP readings out of the office

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15
Q

Secondary Causes of HTN (9)

A
Primary Renal Disease
Drug induced
Renovascular
Adrenal
Rare genetic D/O
HTN with pregnancy
Obstructive Sleep Apnea (OSA)
Other endocrine D/O
Coarctation of the aorta
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16
Q

Primary Renal Disease

A

Renal parenchymal disease (CKD) is the most common cause of secondary HTN
Others: renal cysts, renal tumors, obstructive uropathy

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17
Q

Drug Induced Secondary HTN (6)

A
Oral Contraceptives
NSAIDS
Antidepressants (MAO-I, and TCA)
Decongestants 
Cocaine
Glucocorticosteroids
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18
Q

Renovascular (renal artery stenosis) (5)

A

1-2% of hypertensive patients and secondary to:
Arteriosclerosis- older patients w/ obstructing plaque
Fibromuscular dysplasia- strong predilection for young white women, may be unilateral or bilateral
Renal arteriography is the definitive diagnostic test
Treated either medically or surgically

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19
Q

Renovascular should be suspected if… (6)

A

Onset of HTN before age 20 or after age 50
HTN is resistant to 3 or more drugs
If there are epigastric or renal artery bruits
If there is atherosclerotic dz of the aorta or peripheral arteries
If there is an abrupt increase in the level of serum creatinine after administration of ACE inhibitors
If episodes of pulmonary edema are associated w/ abrupt surges in BP

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20
Q

Adrenal Cause of HTN (Secondary) (3)

A

Pheochromocytoma:
D/t catecholamine-secreting tumors in the adrenal medulla

Primary aldosteronism:
Increased aldosterone production resulting in sodium retention, HTN, hypokalemia and low PRA (plasma renin activity)
Should be suspected in any patient w/ a triad of HTN, unexplained hypokalemia and metabolic alkalosis

Cushing’s Syndrome:
Related to excess cortisol production d/t either excess ACTH secretion (pituitary tumor) or to ACTH-independent adrenal production of cortisol
- HTN occurs in 75-80% of patients

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21
Q

Other endocrine disorders (Secondary Cause of HTN)

A

Hypothyroidism, hyperthyroidism, and hyperparathyroidism (hypercalcemia)

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22
Q

Obstructive Sleep Apnea (OSA) (2nd cause of HTN)

A

Independent of obesity

HTN occurs in >50% of patients w/ OSA

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23
Q

HTN Associated with Pregnancy

A

Preeclampsia and Eclampsia: one of the most common causes of maternal and fetal morbidity and mortality

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24
Q

Coarctation of the aorta (2nd cause of HTN)

A

Most common congenital cardiovascular cause of HTN

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25
Q

Screening: 2007 USPSTF

A

The USPSTF recommends blood pressure screening in adults 18 years and older because there is good evidence that it can identify adults at increased risk of cardiovascular disease from high blood pressure.
every 2 years for persons w/ systolic and diastolic pressures below 120mmHg and 80mmHg respectively and
yearly for persons w/ a systolic pressure of 120-139 or a diastolic pressure of 80-89.

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26
Q

Measurement of HTN (3)

A

Proper measurement and interpretation of the BP is essential in the dx and mgmt of HTN

Proper way: Preferably in a sitting position w/ arm at the level of heart after 5+ minutes of rest and 20-30 minutes after smoking/caffeine consumption

Systolic BP in the left and right arms should be roughly equivalent. A discrepancy of >15mmHg indicates subclavian stenosis  peripheral arterial dx

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27
Q

What do we do if we determine our patient has HTN? (3)

A

Assess the presence or absence of target organ damage and CVD
Assess lifestyle (diet, exercise, habits) and identify other CV risk factors or current disorders that may affect prognosis and guide treatment
Rule out identifiable/secondary causes of high BP (often curable)

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28
Q

PT History for HTN (6)

A

Duration of HTN (if ongoing)
Previous therapies (if any), responses and side effects (if any)
FH of HTN or CVD
Dietary and psychosocial Hx

Other risk factors: weight change, dyslipidemia, smoking, diabetes, physical inactivity

Evidence of Secondary HTN:
Hx of renal dz, change in appearance, muscle weakness, spells of sweating, palpitations, tremor, snoring, erratic sleep, symptoms of thyroid disease, medication use (Rx and OTC), etc

Evidence of Target organ damage:
Hx of TIA, stroke, angina, MI, CHF, kidney disease

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29
Q

Symptoms of HTN (3)

A

Silent disease; therefore most patients do not have any symptoms
Headache can occur in patients w/ severe HTN (characteristic in the morning and in the occipital region)
Other non-specific symptoms: dizziness, palpitations, easily fatigued and impotence
When symptoms are present, they are typically related to hypertensive cardiovascular disease or manifestations of secondary HTN

30
Q

Physical Exam for HTN (12)

A

Body habitus
Weight/height/BMI
BP measured in both arms
HR
Fundoscopic exam (AV nicking, hemorrhages, exudates, papilledema- malignant HTN)
Thyroid
Signs of thyroid disease
Displaced apical impulse/PMI (LVH)
Palpate distal pulses
Auscultate the heart
Auscultate for bruits (carotid and femoral)
Asses for abdominal bruit that lateralizes
Kidneys (palpable in polycycstic kidney dz)
Signs of CHF

31
Q

HTN Lab Summary

A
Urinalysis
CBC
BMP(fasting)- electrolytes/renal fx
Fasting Lipids
TSH
EKG
32
Q

Primary and Secondary Goal for HTN

A

Primary Goal:
Prevent end organ damage

Secondary Goals:
Minimize side effects, minimize patient cost
Increases adherence
Treat comorbid conditions
May choose different medication classes for pts w/ other conditions (e.g., DM, BPH, anxiety)

33
Q

Benefits of HTN Treatment

A

Lowering SBP by 10-12mmHg and DBP by 5-6mmHg confers relative risk reduction of:
35-40% for stroke
12-16% for CHD w/in 5 years of initiation of tx
Risk of heart failure is reduced by >50%
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.

34
Q

Lifestyle Modification (5)

A

Dietary salt restriction (≤100mmol/d)- 2.4g Na/6g Chl
Weight loss (maintain normal BMI, 18.5-24.9)
DASH Diet (fruits/veg, high protein/high fiber, low fat dairy, reduced saturated and total fat, low in red meat)
Exercise (regular aerobic physical activity, 30min/day)
Decrease alcohol intake (≤2/day in males, ≤1/day in fm)
Educate your patient

Other:  
proper Vitamin D intake
Adequate potassium intake
Smoking Cessation
Limit NSAID use
35
Q

Drug Therapies for HTN (10)

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
36
Q

Diuretics will…

A

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

37
Q

Side Effects of Thiazides (4)

A

hypokalemia, insulin resistance, increase cholesterol, increase uric acid

38
Q

3 Types of Diuretics

A

Thiazides (Hydrochlorothiazide, Chlorthalidone)
Loop (Furosemide, aka Lasix)
K+ retaining (Amiloride and Triamterene)

39
Q

Contraindications in Thiazides (4)

A

Use w/ caution in diabetics, dyslipidemia, gout, hypokalemia

40
Q

K+ retaining diuretic

A

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

41
Q

Loop Diuretics

A

Used in pts w/ reduced GFR(renal failure) and CHF

Same SE/Cautions as thiazides

42
Q

Thiazides

A

first line tx in most patients w/ uncomplicated HTN
Chlorthalidone is the drug of choice
Hydrochlorothiazide is an alternative
More potent in blacks, older individuals, and obese patients
Reduce the risk of CV events and all cause mortality

43
Q

Side Effects of Beta 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

CNS symptoms: nightmares, excitement, depression and confusion
Fatigue, lethargy and erectile dysfunction may occur

44
Q

MOA of Beta Blockers

A

Decreases heart rate and cardiac output (contractility)

45
Q

Beta Blockers Indicated in Pts with…

A

patients w/ Angina pectoris, post MI, CHF, sinus tachycardia, ventricular tachyarrhythmias
Significantly reduces CV morbidity and mortality

46
Q

Beta Blockers contraindicated by:

A

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

47
Q

Beta Blockers should be used cautiously in pts with?

A

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

48
Q

ACE Inhibitors

A

Inhibit the renin-angiotensin-aldosterone system
Effective as monotherapy or in combo w/ diuretics, CCBs and alpha blocking agents
More potent when combined w/a thiazide or CCB
Renoprotective
Results in a significant reduction in all cause mortality

49
Q

Side Effects for ACE Inhibitors

A

hyperkalemia, cough, skin rashes, angioedema

50
Q

ACE Inhibitors contraindicated

A

in pregnancy, b/l renal artery stenosis and hyperkalemia
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

51
Q

ACE Inhibitors indicated for?

A

Drug of choice in CHF and diabetics
(they delay the progression of end stage renal disease)
Other Indications: Post-MI, coronary syndromes, CHF and nephropathy

52
Q

Angiotensin II Receptor Blockers

A

Indications, efficacy and contraindications of ARBs are similar to ACE Inhibitors
Used in patients who do not tolerate ACE inhibitors d/t cough, skin rashes or angioedema
Do not reduce all cause mortality like ACEI do, but they are renoprotective (delay onset of kidney failure)

53
Q

Renin Inhibitors

A

Blockade of the renin-angiotensin system
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

54
Q

Aldosterone Antagonists

A

Other Indications: CHF d/t systolic dysfunction and primary aldosteronism
Caution/contraindicated: Renal failure and hyperkalemia
Side effects: Hyperkalemia, gynecomastia, impotence and menstrual irregularities (binds to progesterone and androgen receptors)

55
Q

CCB MOA

A

MOA: Act by causing peripheral vasodilation
2 Types:
Dihydropyridines (Nifedipine)
Nondihydropyridines (Verapamil & Diltiazem)

56
Q

CCB Side Effects

A

Side effects: headache, peripheral edema, bradycardia and constipation

57
Q

α-Adrenergic Antagonists

A

MOA: Decrease peripheral vascular resistance
Effective as monotherapy only in men w/ symptomatic BPH (benign prostatic hypertrophy)
Other indications: Pheochromocytoma

58
Q

Side Effects of α-Adrenergic Antagonists

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”

59
Q

Sympatholytic Agents MOA

A

Centrally acting α-2 sympathetic agonists decrease peripheral resistance

60
Q

Direct Vasodilators MOA

A

MOA: Decrease peripheral vascular resistance

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

61
Q

Initial Monotherapy

A

Used only in the absence of a specific indication and if the BP is <20/10mmHg above goal BP
3 main classes used for initial monotherapy
Thiazide Diuretic- recommend Chlorthalidone
Long acting CCB (most commonly dihydropyridine)- more effective in elderly and blacks
ACE inhibitor or ARB- more effective in younger pts

62
Q

First Line Combo Therapy

A

Used when the BP is more than 20/10mmHg above goal or SBP is >160 and/or DBP is >100
Fixed dose combos are available and may improve patient compliance, BP control and reduce SE if given at low dosages
Typically consists of a Diuretic plus either an ACEI/ARB or CCB

63
Q

Addition of a Second Drug

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

64
Q

Patient Follow Ups for HTN

A

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

Once BP is controlled on a well-tolerated regimen:
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 condition

65
Q

Indication and Contraindications for CCB

A

Blacks respond well to CCB
Indications:
Nondihydropyridines are also used post-MI, in supraventricular tachycardias and angina
Caution/contraindications:
Nondihydropyridines: 2nd or 3rd degree heart block

66
Q

Age ≥ 60 yrs (goal <150/90)

Initiation of Therapy

A

Nonblack: Thiazide diuretic or ACEI or ARB or CCB alone or in combo
Black: Thiazide diuretic or CCB alone or in combo

67
Q

Age < 60 yrs (goal <140/90)

Initiation Therapy

A

Nonblack: Thiazide diuretic or ACEI or ARB or CCB alone or in combo
Black: Thiazide diuretic or CCB alone or in combo

68
Q

All ages with DM and no CKD: <140/90

Initiation Therapy

A

Nonblack: Thiazide diuretic or ACEI or ARB or CCB alone or in combo
Black: Thiazide diuretic or CCB alone or in combo

69
Q

All ages with CKD w/ or w/o DM: <140/90

Initiation Therapy

A

All races: ACEI or ARB alone or in combo w/ other drug class

70
Q

Resistant HTN

A

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

One or more reasons may contribute to this:
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

71
Q

Step Down Therapy for HTN

A

Some 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.
Need to be monitored closely off the meds
Gradual tapering indicated if taking mult drugs
5-55% of pts remain normotensive for at least 1-2 years
*Abrupt cessation of therapy w/ a short acting B-Blocker or short acting α2 agonist can lead to a potentially fatal w/d syndrome; therefore, gradually d/c over a period of weeks is required