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81 Cards in this Set

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BP varies with:
Temperature
time of day
meals
activity
posture
emotions
stressors (white coat)
Follow up recommendations
Normal HTN: 2 yrs
Pre-HTN: 1 year
Stage 1: confirm w/in 2 months
Stage 2: evaluate or refer to source of care w/in one month, if >180/110 evaluate/treat immediately
HTN Evaluation Components
Med History
Duration/Classification of HTN
Pt history of CVD
FH
Sx suggesting causes of HTN
Lifestyle factors
Current and previous meds
HTN Eval Components: PE
BP readings, 2 or more
Verification in contralateral arm
Ht, wt, waist circumference
Funduscopic exam
Exam of neck, heart, lungs, abdomen, extremities
neurological assessment
HTN Eval Components: Routine Lab tests
determine presence of Target Organ Damage and other risk factors
Specific Causes of HTN
Urinalysis, complete blood count, blood chem (K, Na, Ca, Scr, Hematocrit, fasting glucose)
FLP
12 lead ECG
HTN Eval Components: Optional tests
microalbuminuria
24 hr urinary protein
Serum Ca
Serum uric acid
Fasting triglycerides
LDL
Glycosylated hemoglobin
TSH
Plasma renin activity/urinary sodium determination
limited echocardiography
ultrasonography
measurement of ankle/arm index
Identifiable causes of HTN
Sleep apnea
drug induced
CKD
Primary aldosteronism
renovascular disease
Chronic steroid therapy
Cushing's syndrome
pheochromocytoma
coarctation of aorta
thyroid or parathyroid disease, esp hyperthyroid
Target Organ Damage
Heart: CAD, LVH, CHF
Cerebrovascular: transient ischemic attack, stroke
Peripheral: claudication, aneurysm
Renal: Scr >1.5, proteinuria,
Retinopathy: exudates, papilledema
JNC7 Guideliens
Pre-HTN: no drug, lifestyle changes
Stage 1: thiazide for most, consider ACE-I, ARB, BB, CBB or combo, drugs for compelling indications
Stage 2: Two drug combo for most: thiazide + ACEI, ARB, BB, CBB, w/compelling indication other drugs as needed
Lifestyle Modifications
Weight reduction
DASH
Dietary sodium reduction
physical activity
moderation of alcohol consumption
tobacco cessation
Goals for HTN managment
reduce morbidity and mortality by least intrusive means possible
Achieve and maintain goal BP
Controlling other CV risk factors
Preserve QoL: cost effective, least intrusive
Goal BP
<140/90
<130/80 for pts with Diabetes or CKD
Pharmacological Treatment Benefits
Decrease CV mortality and morbidity
protects against stroke, coronary events, heart failure, progression of renal disease, progression to more severe HTN, all cause mortality
ACCELERATE Study
New school of thought: combo therapies provide faster sustained BP reductions with fewer AE
Follow Up on HTN therapy
1-2 months after initiating
Certain meds may require earlier monitoring diuretics, ACEI and ARBS
Recognize high risk pts need high dose or combo
Drugs to use with Prior MI
ACEI
BB
Aldosterone Antagonist
Drugs to use with High Risk Coronary Disease
Going to be on one of each:
Diuretic, BB, ACE-I, CCB
Drugs to use with Diabetes
1. AceI or ARB
2. CCB
3. Diuretic
4. BB
Drugs to use with CKD
ARB or ACEI
Drugs to use with prior stroke
Diuretic and ACE/ARB
Drugs to use with Heart Failure
ACE or ARB
BB
Aldosterone Blocker
Diuretics (loop, used for Sx)
Angina comorbid
BB, CBB
Atrial tachycardia and fibrillation comorbid
BB
Non dihydro CBB
ACE and ARB
Cyclosporine induced HTN comorbid
CBB
Thiazide?
Dyslipidemia comorbid
alpha blockers
Prostatism comorbid
alpha blockers
Essential tremor comorbid
non cardioselective BB
Hyperthyroidism comorbid
BB
Migraine comorbid
Non cardioselective BB (propranolol)
Non-dihydro CBB
Osteoporosis Comorbid
Thiazides
Perioperative HTN comorbid
BB (slow HR)
Caution in bronchospastic disease
BB
Caution in Depression
BB, reserpine
Caution in dyslipidemia
BB
diuretics
Caution in Diabetes
BB
high dose diuretics
Caution in Gout
diuretics
Caution in Heart Failure
BB (except carvedilol, metoprolol, bisoprolol)
CBB (except amlodipine, felodipine)
Diuretic pharmacotherapy issues
high dietary Na+ can reverse benefits
NSAIDs can antagonize effects
Effects on electrolytes, cholesterol, glucose: monitor K+, creatinine
SHEP study
Systolic Hypertension in the Elderly Program:
Goal BP reached by 65-72% of active tx group vs 32-40 of placebo (using chlorthalidone)
Doses in Diuretics
use less than 25 mg
low dose diabetes, gout, hyperlipidemia

DONT use when GFR < 30
Diuretics Drug Interactions
Cholestyramine: reduced HCTZ absorption
Lithium: increased [Li]
NSAIDS: reduced diuresis
Digoxin: increased risk toxicity
Sulfonylureas: reduced sulfonylurea efficacy
Cyclophosphamide, fluorouracil, methotrexate: myelosuppression
Beta Blockers Non selectives
ISA-: propranolol, timolol, nadolol
ISA+: pindolol, carteolol, penbutolol
Beta Blockers Selective
ISA-: atenolol, metoprolol, bisoprolol, betaxolol
ISA+: acebutolol
Liver metabolized BB
propranolol
metoprolol
labetolol
some acebutolol
Kidney metabolized BB
atenolol
nadolol
Advantages of BB
Decrease CAD morality
Decrease mortality post MI (avoid ISA+)
Decrease M&M in CHF(metoprolol, bisoprolol, carvedilol)
no lab monitoring
Disadvantages of BB
mask hypoclycemia in diabetes (sweat)
Increase lipids
Dont use in asthma/COPD
Caution in CHF
Angina with ISA+
Sexual dysfunction
Decreased exercise capacity
Rebound HTN
BB SE
bradycardia, tiredness, cold extremtities
sweating
Questions about Atenolol and BB
less effective than others in reducing stroke
maybe because its only dosed 1 time daily
Authors argue: BB should not be first line or the second drug added to diuretic
BB Drug Interactions
Cimetidine: decreased metab of metoprolol, labetolol, propranolol
Amiodarone: hypotension, bradycardia
Ritonavir: increased [metoprolol]
Digoxin: AV nodal block
2D6 inhibitors: SSRI's, increased [metoprolol]
St John's Wort: decreased BB effectivness
Diltiazem, Verapamil: increased bradycardia, hypotension, AV conduction abnormalitiles
ACE-I Pharmacotherapy issues
Decrease mortality in CHF
Decrease progression of DM nephropathy
Decrease progression of CKD
decrease mortality from CV causes, MI, stroke
ACE-I drug interactions
Don't use salt substitutes
Careful with K+ supplements, K+ sparing diuretics, spironolactone
Advantages of ACE-I
Neutral on lipids
DM nephropathy--renal protective
Improve surivival in Heart Failure
Disadvantages of ACE-I
cough in 10%
Contraindicated in pregnancy and bilateral RAS
Monitoring ACE-I
Scr, K+
ACE-I SE
rash
angioedema
hyperkalemia
renal failure if bilateral RAS
dry cough
ARB Advantages
no lipid or glucose changes
useful in combo
ARB SE
dizziness,
cough but less than ACE
angioedema
Hyperkalemia
CCB non dihydros
diltiazem
verapamil
Decreased contractility, HR, AV node conduction
CCB dihydros
amlodipine, nifedipine, felodipine
much less decrease in contractility, slight increase in HR, no effect on AV node
INSIGHT and NORDIL Studies
Showed decrease mortality in HTN similar to conventional drugs, (with CCBs)
Which CCB may increase mortality?
nifedipine primarily (short acting CCB) increase risk of MI
CCB Advantages
Increase response in elderly for systolic HTN
effective in CAD, decreases angina (esp non dihdryos)
neutral lipids and glucose
CCB disadvantages
Increase MI with short acting agents
Caution in HF, use amlodipine or felodipine
CCB SE
constipation, bradycardia, AV block, CHF (verapamil, diltiazem)

edema, dizziness, HA, tachycardia (esp dihydros)
gingival hyperplasia (esp nifedipine)
Edema
angioedema
Alpha 1 antagonists
Advantages
positive impact on lipids
improve BPH Sx
Alpha 1 antagonist disadvantages
first dose hypotension
not recommended as initial monotherapy
diuretics superior immediately to decrease CV events
Alpha 1 antagonist SE
HA
fatigue
drowsiness
weakness
vivid dreams
Central alpha 2 agonists
Clonidine and methyldopa
Alpha 2 agonists advantages
neutral on lipids
clonidine patch
Methyldopa--pregnancy
Alpha 2 agonists disadvantages
Rebound HTN
alpha 2 agonist SE
CNS: sedation, decreased alertness, depression
Dry mouth, bradycardia, sodium and fluid retention (monitor)
Renin Inhibitors
Aliskirien
Renin inhibitors AE
GI
cough
rash
hyperuricemia
gout
kidney stones
Renin inhibitor Advantages
well tolerated
no dose reduction in elderly, hepatic impairment or mild-mod renal impairment
Safe in combo with ARB, CCB, thiazide--unless diabetic
Reduced rash, cough, angioedema compared to ACE and ARB
Direct vasodilators
hydralazine, minoxidil
Direct vasodilators disadvantages
reflex symptathetic activation: leads to increased HR, increased CO, renin release

Increased angina in pts with CAD
direct vasodilators SE
hypertrichosis (minoxidil)
lupus like syndrome (hydralazine)
dermatitis, drug fever, peripheral neuropathy, hepatitis, HA
Postganglionic sympathetic inhibitors
guanethedine, guanadrel
postganglionic sympathetic inhibitors disadvantages
ortho hypo
syncope
impotence, diarrhea, weight gain
Reserpine
cheap, efficacious

sedation, depression, Na/fluid retention, diarrhea, depression