Hypertension and hyperlipidemia Flashcards
What type of drug ends in -pril, lisinopril, and can be considered cardio and renoprotective?
ACE inhibitors
What do you need when putting a patient on ACE inhibitors?
baseline Cr and K+ levels and repeat 1-2 weeks after initiation
do NOT in pregnancy
What type of drug ends in -sartan that you can prescribe if someone cannot tolerate beta blockers or ACE-I but you CANNOT give with ACE-I and cannot be given in pregnancy?
ARBs - angiotensin II blockers
What type of drug has two types (dihydropyridine like –dipine + nondihydropyridine) with nondihydropyridine that affects cardiac contractility/conduction like diltiazem or verapamil?
calcium channel blocker
What is the only calcium channel blocker that is safe for CHF?
amlodipine
What is the first line diuretic for uncomplicated HTN?
thiazides like hydrochlorothiazide, chlorthalidone
What are side effects of thiazides?
hyponatremia, hypokalemia, hypercalcemia, hyperglycemia
What are the type of diuretics like furosemide, bumetanide that cannot be used in a sulfa allergy and are the strongest diuretics?
loop diuretics
What are some side effects of loop diuretics?
hypokalemia, volume depletion, hypocalcemia, hyponatremia, hyperuricemia, hyperglycemia
What are the weakest diuretics that can cause hyperkalemia?
potassium sparing diuretics
What are the drugs that end in -olol that treat HTN?
beta blockers
What beta blockers are cardioselective with beta one?
atenolol, metoprolol, esmolol
What beta blockers are non selective with beta 1 and 2?
propranolol
What beta blockers are both alpha and beta?
labetalol, carvedilol
What alpha antagonists can be used for HTN?
doxazosin, prazosin, terazosin
In who is primary HTN most common?
25-50 yrs old
What organs are involved in HTN?
heart, brain, kidneys, eyes, peripheral arteries
How may primary HTN present?
asymptomatic for years, with headache as the most frequent symptom
What is required for diagnosis of HTN?
more than one reading unless it’s an emergency or >220/115
What are risk factors for exacerbating of primary HTN?
obesity, sleep apnea, increased salt intake, excessive alcohol, polycythemia, NSAID therapy, low potassium
What can cause primary HTN?
genetic + environmental –> overactivation of SNS, RAAS, elevated Na/Ca levels, variation in development
What is considered normal BP?
<120/80
What is considered elevated BP?
120-129/<80
What is considered Stage 1 HTN?
130-139/80-89
What is considered Stage 2 HTN?
> 140/90
When should you treat with HTN medications?
all patients if lowers CV risk
BP above 160/100 needs 2 meds
those w/ 140-159/90-99 even if risk is low
What is non-pharmacological therapy for HTN?
weight loss, DASH diet, sodium intake, alcohol intake, exercise, mindfulness
When there is risk for advanced age when should you consider pharmacotherapy in BP?
> 130/80
When there is an increased risk for CV, when should you consider pharmacotherapy in BP?
> 130/80
When there is no risk when should you consider pharmacotherapy in BP?
> 140/90
What’s the #1 cause of secondary HTN?
renal disease – elevated BV, activity of RAAS, SNS activation
What can cause renal disease –> secondary HTN?
arteriosclerosis + fibromuscular dysplasia in women <50yrs
When should renovascular HTN be suspected?
- documented before 20 or after 50
- HTN resistant to maxed 3+ drugs
- epigastric or renal artery bruits
- atherosclerosis disease of aorta or peripheral arteries
-abrupt increase in serum creatine after ACE inhibitor administration - episodes of pulmonary edema = surge of BP
When should you suspect secondary HTN?
at a young age or >50 or previously controlled becomes refractory (resistant to max doses of 3 meds)
What can cause secondary HTN?
- primary hyperaldosteronism
- cushing syndrome
- pheochromocytoma
- coarctation of aorta
- estrogen use
What do you need to look for when you suspect coarctation of aorta?
radial-femoral delay in all younger patients w/ HTN
How do you diagnose renovascular HTN?
high suspicion –> renal arteriography (definitive diagnostic test)
moderate-low –> noninvasive angiography using MRI or CT
doppler sonography
When should you refer to cardiology with HTN?
severe, resistant to meds, or early/late onset
What can cause major risk for CV events?
HTN, smoking, obesity BMI>30, physical inactivity, dyslipidemia, diabetes, microalbuminuria or eGFR>60, age >55m, >65f
Where are you looking for target organ damage (HTN)?
heart (LVH, angina, MI, HF), brain (stroke), CKD, PAD, retinopathy
How do you treat CV risk factors?
statins (rosuvastatin) or low dose aspirin
What is step 1 in HTN treatment?
ACE inhibitor/ARB OR CCB OR thiazide diuretic
What is step 2 in HTN treatment?
ACE inhibitor/ARB + CCB OR thiazide
What is step 3 in HTN treatment?
ACE inhibitor/ARB + CCB + thiazide
What is step 4 in HTN treatment?
ACE inhibitor/ARB + CCB + thiazide + spironolactone
In a black patient, what is your first line treatment for HTN?
CCB or diuretic
What is your 2nd line HTN treatment for a black patient?
ARB or ACE inhibitor or beta blocker
What is your treatment of choice in ALL PATIENTS with resistance?
aldosterone receptor blocker
What would you add on for ALL PATIENTS with HTN?
central alpha agonist or peripheral alpha antagonist
How do you monitor a patient you just put on HTN meds?
follow up in 2 weeks, yearly monitoring of lipids, ECG every 2-4 years
What is first line for a HTN patient <55 “others”?
ACE inhibitor or ARB or CCB or diuretic
What’s second line for a HTN patient <55 “others”?
beta blocker
What’s first line for a HTN patient > 55 “others”?
CCB or diuretic
What’s second line for a HTN patient >55 “others”?
ARB or ACE inhibitor or beta blocker
What are some symptoms for hypertensive emergencies?
headache, somnolence, vomiting (HTN encephalopathy), seizures, altered consciousness, vision disturbance (posterior reversible encephalopathy syndrome), focal neurologic deficits (cerebral infarction or hemorrhage), angina and dyspnea (acute elevation of LV afterload), severe CP or ab pain (aortic dissection or rupture)
What can a difference between BP in arms (subclavian stenosis), orthostatic drop >20/10, have the osler sign (falsely elevated BP seen in older patients), narrowing of arterial diameter, copper/silver wiring, AV nicking, cotton wool spots, exudates, hemorrhages, papilledema, LV heave, aortic regurg, S4 gallop, radial femoral delay (coarctation of aorta), loss of peripheral pulse (atherosclerosis) mean?
hypertensive emergency
What are labs you should consider with HTN?
hemoglobin, electrolytes, creatinine, fasting glucose, lipids, serum uric acid, UA, BMP, lipid panel
further: ECG, CXR, echo
If tests indicate secondary/complicated HTN, what’s next?
24 hour urine free cortisol, urine or plasma metanephrines, plasma aldosterone and renin concentration, renal ultrasound
When should someone go to the ER for HTN?
vision changes, >180/120
How do you lower emergency HTN?
reduce no more than 25% within 1st hour and additional 5-15% over next 23 hours
What are the exceptions to slowly lowering BP?
acute ischemic stroke unless >180-200 or thrombolytics are given
acute aortic dissection and should be decreased to <120 and <60 within 30 minutes
What is used for emergency HTN?
combo of nicardipine or clevidipine + labetalol or esmolol
What sign could indicate hyperlipidemia?
xanthomas
Higher the level of ___, higher the risk of athlerosclerotic HD
LDL
What can predispose someone to hyperlipidemia?
alcohol use, beta blockers, cirrhosis, CKD, Cushing’s, DM, thyroid, obesity
What’s a normal cholesterol level?
<200
What’s a normal triglyceride level?
<150
What’s a normal HDL level?
60 or more is good
What’s a normal LDL level?
60-130, lower is better
What’s a normal cholesterol/HDL ratio?
4.0 – with more being worse
All adults should have what checked before middle age?
lipids
When should you test adults?
all adults 20+ that have risk factors q5 years or more if higher risk
What level of LDL needs to be treated?
> 190
What are calculators used to define risk of CVD?
lifetime risk, 10 year risk, coronary artery calcium score (best test for additional risk stratification with 0 being best)
q3 for high risk, q7y for low risk
What’s first line treatment for hyperlipidemia?
statins
based on : presence of CVD or diabetes, LDL>190, age, 10 year risk
What statins are used for high intensity (and adjusted for lower)?
atorvastatin (40-80mg) or rosuvastatin (20-40mg) high
What are 4 groups of patients who benefit from statin medications?
1) individuals w ASCD
2) individuals w/ LDL >190
3) individuals 40-75 w/ diabetes and LDL >70
4) individuals 40-75 w/o ASCVD or diabetes w/ LDL 70-189 and estimated 10 year risk of 7.5% or higher
What’s second line treatment for hyperlipidemia?
ezetimibe and bempedoic acid for:
- CVD whose LDL remains above relevant treatment threshold 55 or 70 on statin therapy
- possible familial hypercholesterolemia w/ LDL >190 baseline and still above 100 with treatment and remains above treatment threshold
- OR documented statin intolerance
-CAN add to therapy if at max statin and patient has high risk for CVD and high LDL
What are lifestyle recommendations for hyperlipidemia?
diet, exercise, smoking cessation, HTN control, weight loss, diabetes control, antithrombotic therapy
What can cause markedly high LDL levels and early ASCVD?
familial hypercholesterolemia - absent/defective LDL receptors resulting in unregulated metabolism
What do statins do?
reduce LDL
w/ CVD - need maximally tolerated dose
What are side effects of statins?
muscle aches, myositis, rhabdomyolysis, elevated risk of muscle injury or myopathy with highest dose, liver disease, DM
What does ezetimibe “zetia” do?
reduces LDL
When do you add ezetimibe/zetia to hyperlipidemia therapy?
max statin + high risk for CVD + high LDL
What do proportein convertase subtilisin/kexin type 9 inhibitors (alirocumba and evolocumab) do?
reduce LDL
When do you add proportein convertase subtilisin/kexin type 9 inhibitors (alirocumba and evolocumab) to statins?
- calcium scores >1000
- very high risk for recurrent CVD when on treatment for LDL and remains >55 or 70
OR >100 in patients w/ familial hypercholesterolemia w/o known CVD
What patients are considered very high risk for CVD?
- recent ACS within 12 months
- multiple prior MIs or strokes
- significant unrevascularized CAD
- polyvascular disease (CAD + cerebrovascular or PVD)
What do omega 3 fatty acids target?
triglycerides
What do bile acid binding resins target (cholestyramine, colesevalam, colestipol)?
reducing LDL
What do you HAVE to know about bile acid binding resins (cholestyramine, colesevalam, colestipol)?
- can increase TG levels so NO in high TG level patients
** only medication safe in pregnancy!!!! **
What do fibric acid derivatives (gemfibrozil, fenofibrate) target?
TGs by 40%
What do niacin/nicotinic acid target?
increasing HDL by 25-35%
BUT INTOLERANCE IS COMMON!!!
In these patients, what is indicated:
1) w/ hypercholesterolemia w/ LDL>100 w/ treatment
2) advanced subclinical atherosclerosis or high-risk patients w/ existing CVD where LDL>70 w/ treatment
3) very high risk patients w/ excisting CVD where LDL>55
4) many high risk patients w/ TG >150 or non HDL >100
combination therapy
When is someone at risk for pancreatitis with TG levels?
> 1000
When should treat high TGs fasting?
> 500
What are some treatment recommendations for high triglyceride levels?
avoid alcohol, simple sugars, refined starches, fatty acids, control secondary causes
How is drug treatment for TGs reserved?
> 150 but <500 is only for those w/ established CVD with well-controlled LDL on maximal tolerated therapy
