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
Screening: 2007 USPSTF
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.
26
Measurement of HTN (3)
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
27
What do we do if we determine our patient has HTN? (3)
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)
28
PT History for HTN (6)
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
29
Symptoms of HTN (3)
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
Physical Exam for HTN (12)
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
HTN Lab Summary
``` Urinalysis CBC BMP(fasting)- electrolytes/renal fx Fasting Lipids TSH EKG ```
32
Primary and Secondary Goal for HTN
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
Benefits of HTN Treatment
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
Lifestyle Modification (5)
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
Drug Therapies for HTN (10)
``` 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
Diuretics will...
Decrease plasma volume initially, but in long term use they reduce peripheral vascular resistance
37
Side Effects of Thiazides (4)
hypokalemia, insulin resistance, increase cholesterol, increase uric acid
38
3 Types of Diuretics
Thiazides (Hydrochlorothiazide, Chlorthalidone) Loop (Furosemide, aka Lasix) K+ retaining (Amiloride and Triamterene)
39
Contraindications in Thiazides (4)
Use w/ caution in diabetics, dyslipidemia, gout, hypokalemia
40
K+ retaining diuretic
Weak anti-hypertensives, but may be used in combo w/ a thiazide to protect against hypokalemia
41
Loop Diuretics
Used in pts w/ reduced GFR(renal failure) and CHF | Same SE/Cautions as thiazides
42
Thiazides
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
Side Effects of Beta Blockers
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
MOA of Beta Blockers
Decreases heart rate and cardiac output (contractility)
45
Beta Blockers Indicated in Pts with...
patients w/ Angina pectoris, post MI, CHF, sinus tachycardia, ventricular tachyarrhythmias Significantly reduces CV morbidity and mortality
46
Beta Blockers contraindicated by:
in asthma, COPD, 2nd or 3rd degree heart block and sick sinus syndrome
47
Beta Blockers should be used cautiously in pts with?
in patients w/ Type I DM and patients w/ advanced peripheral vascular disease associated w/ rest pain or non-healing ulcers
48
ACE Inhibitors
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
Side Effects for ACE Inhibitors
hyperkalemia, cough, skin rashes, angioedema
50
ACE Inhibitors contraindicated
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
ACE Inhibitors indicated for?
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
Angiotensin II Receptor Blockers
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
Renin Inhibitors
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
Aldosterone Antagonists
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
CCB MOA
MOA: Act by causing peripheral vasodilation 2 Types: Dihydropyridines (Nifedipine) Nondihydropyridines (Verapamil & Diltiazem)
56
CCB Side Effects
Side effects: headache, peripheral edema, bradycardia and constipation
57
α-Adrenergic Antagonists
MOA: Decrease peripheral vascular resistance Effective as monotherapy only in men w/ symptomatic BPH (benign prostatic hypertrophy) Other indications: Pheochromocytoma
58
Side Effects of α-Adrenergic Antagonists
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
Sympatholytic Agents MOA
Centrally acting α-2 sympathetic agonists decrease peripheral resistance
60
Direct Vasodilators MOA
MOA: Decrease peripheral vascular resistance | Not used as monotherapy, but in combo w/ diuretics and B-blockers in resistant pts
61
Initial Monotherapy
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
First Line Combo Therapy
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
Addition of a Second Drug
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
Patient Follow Ups for HTN
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
Indication and Contraindications for CCB
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
Age ≥ 60 yrs (goal <150/90) | Initiation of Therapy
Nonblack: Thiazide diuretic or ACEI or ARB or CCB alone or in combo Black: Thiazide diuretic or CCB alone or in combo
67
Age < 60 yrs (goal <140/90) | Initiation Therapy
Nonblack: Thiazide diuretic or ACEI or ARB or CCB alone or in combo Black: Thiazide diuretic or CCB alone or in combo
68
All ages with DM and no CKD: <140/90 | Initiation Therapy
Nonblack: Thiazide diuretic or ACEI or ARB or CCB alone or in combo Black: Thiazide diuretic or CCB alone or in combo
69
All ages with CKD w/ or w/o DM: <140/90 | Initiation Therapy
All races: ACEI or ARB alone or in combo w/ other drug class
70
Resistant HTN
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
Step Down Therapy for HTN
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