Hypertension Flashcards
(98 cards)
1
Q
Epidemiology of HTN
A
prevalence increases with age
MC Dx in primary care
More common in black than whites
2
Q
HTN doubles the risk of what diseases
A
CV diseases
CHD
CHF
ischemic and hemorrhagic strokes, renal failure and PAD
3
Q
what happens to systolic BP as we age
A
it rises
4
Q
what happens wit SBP of women compared to men
A
after 60 SBP of women>men
5
Q
distolic blood pressure increase until when
A
until age 55 then it decreases
6
Q
SBP is a better predictor of what
A
better predictor of morbid events than DBP in older patients per JNC7
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
8
Q
major complications of HTN
A
hypertensive cardiovascular disease
Hypertensive cerebrovascular disease and dementia
kidney disease
atherosclerotic complications
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
10
Q
what is the result of Hypertensive cardiovascular disease
A
LVH-CHF-Ventricular arrhythmias-myocardial ischemia- sudden death
LVH regresses with therapy
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
12
Q
what is the second most frequent cause of death in the world
A
stroke
13
Q
hypertensive kidney disease
A
the kidney is both a cause and a target of HTN
related to systolic BP
14
Q
what is the secondary most common etiology of secondary HTN
A
Primary renal disease
15
Q
who is HTN kidney disease more common in
A
blacks than whites
16
Q
Diastolic BP is a more important cardiovascular RF than elevated SBP in who
A
younger patients w/o major comorbidities
17
Q
what is the most important RF for development of hemorrhagic stroke
A
HTN
18
Q
HTN is associated with a higher incidence of what 2 diseases
A
vascular and Alzheimers type dementia
19
Q
what is a reliable marker of the severe chronic kidney disease
A
proteinuria
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
21
Q
What effect does hypertensive therapy have on atherosclerosis
A
has a lesser impact on this type of complication
22
Q
how is atherosclerosis controlled
A
control of multiple risk factors including but not limited to HTN alone
23
Q
what is the definition of hypertension
A
a systolic BP of 140mmHg or higher or a diastolic BP of 90mmHg or higher
24
Q
How is HTN diagnosed
A
need 2 or more reading on 2 separate occasions over one to several weeks to diagnose HTN
25
Prehypertension BP is
120-139 or 80-89
26
Stage 1 HTN is
140-159 or 90-99
27
Stage 2 HTN is
>160 or >100
28
Isolated systolic HTN
>or= 140 and <90
29
What is essential HTN
makes up 80-95% of patients w/HTN
no single reversible cause, etiology unknown
secondary to multiple genetic and environmental factors
30
what are the risk factors for HTN
```
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
```
31
what is metabolic syndrome
central obesity, hyperinsulinemia, insulin resistance, hypertriglyceridemia
32
what is white coat HTN
20-25% of patients w/stage 1 office HTN have white coat or Isolated office HTN
33
what are secondary causes of HTN
```
Primary Renal Disease
Drug Induced
Renovascular
Adrenal
Endocrine Disorders
Obstructive Sleep Apnea
Coarc of the Aorta
Pregnancy HTN
Genetic Disorders
```
34
What is primary renal disease (both acute and chronic)
renal parenchymal disease, (CKD) is the most common cause of secondary HTN
35
what is the most common cause of Secondary HTN
Chronic Kidney Disease
36
What drugs cause secondary HTN
```
Oral contraceptives
NSAIDS
Antidepressants
Decongestants
Cocaine
Glucocorticosteroids
```
37
Arm to leg systolic BP Difference >20mmHg
*Delayed or absent femoral pulses
*Murmur
possible cause
Coarctation of the aorta
38
*Increase in serum creatinine concentration (≥0.5 to 1mg/dL) after starting ACEI or ARB
*Renal artery bruit
�
Renal artery stenosis
39
What are the 2 types of HTN treatment
Nonpharmacological
| Pharmacological
40
What is the primary goal in HTN treatment
prevent organ damage
41
What is the secondary goals of HTN treatment
Minimize side effects, minimize patient cost
Increases adherence
Treat comorbid conditions
42
What are the benefits of treatment
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
What are nonpharmacological lifestyle modifications
```
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
What are the pharmacological options?
```
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
How much do most drugs reduce SBP by
7-13mmHg and DBP by 4-8mmHg
| Most patients require combination agents to achieve goal BP
46
How do Diuretics work
Decrease plasma volume initially, but in long term use they reduce peripheral vascular resistance
47
What are type of Diuretics
Thiazides
Loop
K+ retaining
48
What are side effects with Thiazides and Loop and who should you be careful using them with
hypokalemia, insulin resistance, increase cholesterol, increase uric acid
Use w/ caution in diabetics, dyslipidemia, gout, hypokalemia
49
Who do you use Loop diuretics with
pts w/ reduced GFR and CHF
50
What are K+ retaining diuretics used for
Weak anti-hypertensives, but may be used in combo w/ a thiazide to protect against hypokalemia
51
What is 1st line treatment for patients with uncomplicated HTN
Thiazide diuretics
Chlorthalidone is drug of choice
More potent in black and older individuals and obese pts
52
Beta blockers MOA
Decreases heart rate and cardiac output
53
What are the side effects of B-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
54
What are beta blockers indicated for?
patients w/ Angina pectoris, post MI, CHF, sinus tachycardia, ventricular tachyarrhythmias
55
Who do we cautiously use beta blockers with
in patients w/ Type I DM and patients w/ advanced peripheral vascular disease associated w/ rest pain or non-healing ulcers
56
who are beta blockers contraindicated with?
in asthma, COPD, 2nd or 3rd degree heart block and sick sinus syndrome
57
how does ACE-Inhib work
Inhibit the renin-angiotensin-aldosterone system
| �Effective as monotherapy or in combo w/ diuretics, CCBs and alpha blocking agents
58
What are the Benefits ACE-I
| Side effects
Benefits: Renoprotective
Results in a significant reduction in all cause mortality
�
S/E:hyperkalemia, cough, skin rashes, angioedema
59
Who do ACE-I/Angiotensin II RB work best for
More effective in younger white patients and less effective in blacks and older patients
60
Who are ACE-I/Angiotensin II RB the drug of choice for?
CHF and Diabetics
| they delay the progression of end stage renal disease
61
Who is ACE-I/Angiotensin II RB contraindicated with
in pregnancy, b/l renal artery stenosis and hyperkalemia
62
ACE-I others info
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
Angiotensin II receptor blockers MOA
Provide selective blockade of angiotensin receptors
64
Angiotensin II RB Side effects
hyperkalemia
| Do not reduce all cause mortality like ACEI do, but they are renoprotective (delay onset of kidney failure)
65
Renin inhibitors MOA
Blockade of the renin-angiotensin system
66
Renin inhibitors info
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
Aldosterone Antagonists
Ex. Spironolactone
| Effective in resistant HTN and can be used in combination w/ other classes
68
What other conditions are Aldosterone antagonists indicated for
CHF due to systolic dysfunction and primary aldosteronism
69
What are the contraindications of Aldosterone antagonists
renal failure and hyperkalemia
70
what are the side effects of Aldosterone antagonists
Ex. Spironolactone
| Effective in resistant HTN and can be used in combination w/ other classes
71
CCB MOA
Act by causing peripheral vasodilation
72
What are the 2 types of CCB
Dihydropyridines
| Nondihydropyridines
73
Dihydropyridines
nifedipine
74
nonDihydropyridines
Verapamil & Diltiazem
75
Nondihydropyridines should not be combined with
beta blockers because the risk of bradycardia
76
what are side effects with CCB
H/A, peripheral edema, bradycardia, constipation
77
CCB indications
Black people respond well to CCB
78
Nondihydropyridines are also used post
-MI, in supraventricular tachycardias and angina
79
CCB Caution/contraindications:
Nondihydropyridines: 2nd or 3rd degree heart block
80
A-adrenergic antagonist MOA
Decrease peripheral vascular resistance
81
A-adrenergic antagonist indications and benefits
Effective as monotherapy only in men w/ symptomatic BPH (benign prostatic hypertrophy)
Other indications: Pheochromocytoma
Benefits: Increase HDL cholesterol and lower TC
82
α-Adrenergic Antagonists side effects
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
Sympatholytic agents MOA
Centrally acting α-2 sympathetic agonists decrease peripheral resistance
84
Sympatholytic agents
Infrequently used d/t drug intolerance (sedation, fatigue, dry mouth, postural hypotension, erectile dysfunction and drug-drug interactions)
*Methyldopa- used in pregnancy
85
Direct Vasodilators MOA
Decrease peripheral vascular resistance
86
Direct vasodilators
Use
Side effect
Not used as monotherapy, but in combo w/ diuretics and B-blockers in resistant pts
Hydralazine: GI disturbance and may induce a lupus like syndrome
Minoxidil: Hirsutism and fluid retention
87
What to start initial mono therapy
Used only in the absence of a specific indication and if the BP is <20/10mmHg above goal BP
88
what are the 3 main classes used to initial mono therapy
Thiazide diuretics
Long lasting CCB
ACE inhibitor or ARB
89
When to use combo therapy
Used when the BP is more than 20/10mmHg above goal or SBP is >160 and/or DBP is >100
90
What drugs are used for combo therapy
Typically consists of a Diuretic plus either an ACEI/ARB or CCB
91
Adding a second drug in combo therapy info
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
Resistant HTN deifinition
DBP >90mmHg despite 3 or more anti-hypertensive medications including a diuretic
93
One or more reasons for resistant HTN
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
What to do when following up with a patient with HTN
Reinforce lifestyle modifications at EVERY visit
Reassess risk factors at every visit
Screen for side effects at every visit
95
Once BP is controlled on a well tolerated regiment
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
What is step down therapy
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
The best way to treat high risk HTN pts
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
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HTN Treatment Goals
As per JNC8 guidelines:
General population ≥ 60 y:
General population <60 y:
Population aged ≥18 y with CKD or DM
```
<140/90
