Ch 11 HTN, dyslipidemia, HF Flashcards
target organ damage form HTN: brain
stroke, vascular (multi-infarct) dementia
target organ damage from HTN: cardiovascular system
atherosclerosis, MI, Left ventricular hypertrophy, heart failure
target organ damage from HTN: kidney
HTN nephropathy, renal failure
target organ damage from HTN: Eye
HTN retinopathy with risk of blindness
hypertensive retinopathy
retinal vascular damage caused by poorly controlled HTN. if there’s damage in the retinal vessels, there’s damage everywhere else in body. examining eyes are the only way we see blood vessels
hypertensive retinopathy grade 1
common in longstanding poorly controlled HTN
reversible when txed
-narrowing of terminal arteriolar branches
-no vision change or permanent findings
ex: 165/98
hypertensive retinopathy grade 2
see MORE narrowing of arterioles with severe local constriction
no vision changes or permanent retinal findings
hypertensive retinopathy grade 3
DBP is 110 or greater = HTN EMERGENCY
-flame-shaped hemorrhages (bleeding behind eyes)
-potential for visual changes and retinal findings from bleeding scars
hypertensive retinopathy grade 4
DBP 130 or more= HTN EMERGENCY
-papilledema (bulging of optic disc; “vessels point arrows that point to optic disc”)
-bleeding behind eyes,
potential for visual change and permanent retinal findings
primary HTN initial diagnostic testing
need a baseline for med use and screening for secondary causes of HTN:
- fasting blood glucose (DM)
-CBC (anemia) - lipid (dyslipidemia)
- Cr, GFR (renal fxn)
- Na, K, Ca (e- disorder)
- TSH
- UA (proteinuria for HTN nephropathy; usually 1st warning)
- ECG (arrhythmia, infarction, chamber size)
primary prevention for lifestyle changes in HTN
-goal of <130/80
->150 mins/wk exercise or >75/wk vigorous
-low dose aspirin for high risk pts
-metformin (primary) or SGLT-2 or GLP-1 (secondary)
-diet
-tobacco
-cholesterol
BP meds: chlorthalidone (preferred), HCTZ: what are the adverse effects?
thiazide diuretics (peripheral vascular resistance reducers)
AE: depletes Na, K, Mg
-calcium SPARING so it’s good for older women who are fracture risk
lisinopril (prinivil), enalapril, losartan, telmisartan adverse effect
ace inhibitor / ARB (peripheral vascular resistance reducers)
AE: K sparing (hyperK risk with inadequate fluid intake, over diuresis, renal impairment), use with aldosterone antagonist
ACE: cough, angioedema (Black, Latino, hx of NSAID allergy), use ARB instead
no pregnancy
what HTN med is priority to use in diabetic patients?
ACE inhibitors/ARB
CCB (dihydropyridine; Amlodipine (Norvasc) -ipine, NonDHP (diltiazem) adverse effects
PVR reducers
-ankle edema with DPH, dose dependent with more edema in higher dose (max 2.5 mg of amlodipine)
-avoid use in HF, renal, hepatic impairment
priority HTN meds
diuretics (thiazide)
ACE/ARB
CCB
secondary HTN meds
use when pt is on all 3 priority meds but HTN still not under control
-Beta-blockers
-Aldosterone antagonist
for BP: beta adrenergic antagonist (beta blockers , -lol): atenolol, metoprolol, propranolol
-secondary HTN meds; not 1st line
-lowers HR and Stroke volume
do NOT use non cardioselective beta blockers (propranolol,pindolol, sotalol, timolol (O thru Z letters) in lower airway disease (asthma, COPD)
BB with 1st letter A-N are cardioselective
aldosterone antagonist: Spironolactone (Aldactone), eplerenone (Inspra) adverse effects
-secondary HTN meds; not 1st line
-hyperK risk, esp with ACE/ARB use or volume depletion, excessive diuresis
-gynecomastia risk with prolonged use
if pt on 1 HTN medication and still not under control, what can you do?
add a 2nd HTN drug. it’s usually more effective than increasing 1st drug dose (also minimizes side effects from 1st med). 2nd med can cause 10-15 mmgh drop.
which medication should be avoided with a pt with HTN?
a systemic vasoconstrictor: pseudoephedrine
hypertensive urgency
severe BP >180/>120
STABLE pt w/o acute or impending change in HTN target organ dysfunction
-long-standing stopped/nonadherent with meds, no labs or progressing HTN
hypertensive emergency
severe BP >180/>120
pt has evidence of impending or progressive HTN target organ dysfunction
-long-standing stopped/nonadherent, evidence of rapidly progressing TOD (SOB, crackles, vision changes)HF, pulmonary edema, retinopathy, intracranial hemorrhage, etc)
hypertensive urgency intervention
NO indication for immediate in-office BP reduction with short-acting antihypertensive meds (clonidine, hydralazine, nitroglycerine)
NO need to send to ED
tell them to get BACK on the meds they were on before. if they ran out, give them a diff or increase dose
NOT an emergency
hypertensive emergency intervention
NO indication for immediate in-office BP reduction with short-acting antihypertensive meds (clonidine, hydralazine, nitroglycerine) bc lowers BP too quickly and can lead to cardiovascular event
SEND TO ED ASAP!!
when to check BP again after prescribing HTN meds
4 weeks/1 mo
dysplipidemia screening
strong family hx, DM, HTN, obesity
-TC, LDL, HDL, TG
FASTING DOESN’T MATTER!
-triglycerides are affected if non fasting but only need to repeat in fasting state if TG are 400 or more
high-intensity statin therapy: caution
reduces LDL by 50% or more
-atorvastatin 40-80 mg
-rosuvastatin 20-40 mg
-avoid with higher risk for statin adverse effects: rhabdomyolysis, > 75 yrs, impaired renal/low GFR, frailty, multiple comorbidities, with fibrates
moderate intensity statin therapy: caution
reduces LDL by 30-49%
-atorvastatin 10-20mg
-rosuvastatin 5-10 mg
-simvastatin 20-40mg
-pravastatin 40-80 mg
preferred when there is high risk of adverse events with high intensity statins
which meds not advised in dyslipidemia therapy?
niacin, resins
HMG-CoA reductase inhibitor (statin): simvastatin (Zocor), atorvastatin (Lipitor), rosuvastatin (Crestor)
how much LDL does it lower? cautions/AE?
lowers LDL 50% or more
-check hepatic enzymes baseline before starting; no monitoring afterward
-caution grapefruit juice
AE: rhabdomyolysis, myositis (muscles inflamed)
selective cholesterol absorption inhibitor:
Ezetimibe (Zetia)
lowers LDL by 20%
-works at gut only, not systemically
-Zetia + simvastatin = Vytorin
proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors :
-cumab, Evolocumab, alirocumab
monoclonal antibody = $$$$
-lowers LDL 60% or more
for pts already on statin therapy
-SC injection only
-use as ADD ON to statin for hypercholesterolemia or clinical atherosclerotic.
ex: if uncorrectedLDL is 300 gets down to 150 with high intensity, then add in zetia to lower LDL 20% more, THEN consider PCSK9 inhibitor
adenosine triphosphate citrate lyase (ACL) inhibitors (non statin): Bempedoic acid (Nexletol)
-lowers LDL 33%
-adjunct to max tolerated statin and/or ezetimibe therapy , also able to use in statin intolerant pts
if statin intolerant and says they have muscle aches from going on statin but not a true rhabdo,
treating vitamin D deficiency usually takes care of it.
use rosuvastatin or pravastatin (less likely to get muscle aches)
which medication lowers triglycerides by 30%? and AE?
Omega 3 fatty acids at 4g/d dose at PRESCRIPTION strength (not OTC)
-AE: increase bleeding risk/antiplatelet effect.
which medication lowers triglycerides by 50% and increases HDL by 20%? and AE?
-fibric acid derivatives (fibrates): fenofibrate, (Tricor), Fenofibric acid
AE: myopathy (rhabdomyolysis esp if taken with statins)
what is the purpose of the ASCVD ?
use to estimate pt’s 10 year ASCVD risk at initial visit as a reference point and clinical pt discussion on risk and risk lowering interventions.
if have LDL 190 or more…
start on HIGH intensity statin
no risk assessment needed
if have diabetes mellitus and age 40-75 yrs old…
start on moderate-intensity statin
if 40-75 yrs old, with LDL 70-190, without diabetes, and is >20% “high risk” for ASCVD…
start HIGH intensity statin to reduce LDL by 50% or more
hypertriglyceridemia
mild, mod, severe
mild: 150-199
moderate: 200-999
severe: 1000-1999
-mod and severe is at risk for CVD
very severe = risk of CVD, acute pancreatitis
common causes of secondary hypertriglyceridemia
-DM with poor control
-untreated hypothyroidism
meds (2nd gen antipsychotics, systemic corticosteroids, estrogen supps, systemic retinoids)
-high carb diet, excess alcohol
-sedentary/obesity
hypertriglyceridemia intervention
-if moderate TG 199-499: (reduce sat fat, inc fish, alcohol, statin (lower LDL)
-if TG 500+: reduce risk of ASCVD and pancreatitis!! diet, alcohol, STATIN, consider omega 3 or fibrate therapy
familial hypercholesteremia
genetic coniditon causing super high LDL (LDL > 190)
-swollen or bumps around knuckles
-statin first line (then ezeteimab add on, then -umab (PSCK9) add on if LDL still no under control)
statin therapy lab monitoring
no need to monitor serum transminases if there are no sx’s or concerns from pt
Stage A & B of HF are goals of avoiding C &D HF. Stage B,C,D need cardiology consult
Stage A:
stage A: high risk but NO structureal or sx’s (HTN, atherosclerotic disease, DM, obesity, metabolic syndrome or using cardiotoxins, family hx of cardiomyopathy)
-Goal: good BP control to avoid LVH
-START ON ACE/ARB, statins are HEROS
stage B: if pt develops structural heart disease, such as having previous MI, LV remodeling with LVH and low EF, asx vascular disease…what is the goal?
goal: prevent HF sx’s, further remodeling
-ACE/ARB, Beta blockers
-in specific ptss…ICD, revascularization or vascular surgeries
ANYONE (doesn’t matter ethnicity) can benefit from ___ if have HTN, CKD
statins
protects kidney, brain, heart
suspected heart failure symptoms
dyspnea
fatigue
edema
HF clinical examination
tachycardia
increased JVP
displaced apex
S3 heart sounds
murmur
pulmonary crackles
dependent edema
HF labs
ECG
chest x ray
echo
hemoglobin
blood chemistry
thyroid function tests
if pt is 60 and OLDER, start BP meds if bp is…
SBP is 150+ or when DBP is 90+
target: < 150 and < 90
if pt is YOUNGER than 60 years old, start BP meds if bp is…
SBP 140 + or DBP is 90 +
target: < 140 / DBP < 90
