hypertension and hyperlipidemia Flashcards
(110 cards)
1
Q
elevated blood pressure
A
hypertension
2
Q
How is Hypertension Diagnosed?
A
- A single elevated blood pressure reading is NOT sufficient to establish the diagnosis
There are major exceptions to this:
* HTN presenting with obvious evidence of life-threatening end-organ damage (HTN emergency)
* In absence of life-threatening end organ injury, when BP is >220/125 mm Hg
- It typically requires more than one reading to diagnose (do this
as quickly as possible) - A 3-month delay in treatment in high-risk patients is associated with a
twofold increase in CV morbidity and mortalit
3
Q
normal BP
A
< 120/80
4
Q
elevated BP
A
120-129/<80
5
Q
stage 1 HTN
A
130-139/80-89
6
Q
stage 2 HTN
A
> 140/90
7
Q
white coat hypertension
A
only high at the doctors
8
Q
masked hypertension
A
normal at office and high at home
9
Q
labile hypertension
A
variable high and lows
10
Q
- 95% of hypertensive patients
- Results from complex interactions between multiple genetic and
environmental factors (no identifiable cause) (genetic) - Onset 25-50 years old
A
primary essential hypertension
11
Q
- Obesity
- Sleep apnea
- Increased salt intake
- Excessive alcohol use
- Polycythemia
- NSAID therapy
- Low potassium intake
Coffee and cigarette smoking may cause a transient increase in BP
but do not seem to be associated with sustained elevations
A
primary essential hypertension: exacerbating factors
12
Q
- 5% of hypertensive patients
- Results from identifiable specific cause
- Suspect in patients whom:
- HTN develops at a young age or >50 years of age
- Previously controlled becomes refractory to treatment
A
secondary hypertension
13
Q
causes of secondary hypertension
A
RENAL
13
Q
- Best understood pathways:
- Overactivation of sympathetic nervous system
- Overactivation of renin-angiotensin-aldosterone system (RAAS)
- Blunting of the pressure-natriuresis relationship
- Variation in cardiovascular and renal development
- Elevated intracellular sodium and calcium level
A
how primary essential hypertension occurs
14
Q
- Definition:
- Upper body obesity
- Insulin resistance
- Hypertriglyceridemia
- Associated with hypertension and increased risk of adverse CV
outcomes - Labs:
- Low HDL cholesterol
- Elevated catecholamines
- Elevated inflammatory markers (CRP)
A
metabolic syndrome
15
Q
- Suspect in patients if:
- Hypertension develops at an early age or after age 50
- Those previously well controlled who become refractory to
treatment - Hypertension resistant to maximum doses of 3 medications
is a clue - BUT keep in mind that multiple medications are usually required to
control HTN in persons with diabetes
A
secondary hypertension
16
Q
most common cause of
secondary hypertension
Blood pressure is elevated in CKD due to:
* Increased intravascular volume
* Increased activity of RAAS
* Activation of the sympathetic nervous system
A
renal parenchymal
Secondary HTN- Kidney Disease
17
Q
- Renal artery stenosis- present in 1-2% of hypertensive patients
- MC cause: arteriosclerosis
- Fibromuscular dysplasia should be suspected in women <50 years of age
- Excessive renin release occurs due to reduction in renal perfusion
pressure
should be suspected in the following circumstances:
* Documented onset is before age 20 or after age 50
* HTN is resistant to 3 or more drugs
* There are epigastric or renal artery bruits
* There is atherosclerosis disease of aorta or peripheral arteries
* Abrupt increase (>25%) in serum creatinine after administration of ACE inhibitor
* Episodes of pulmonary edema are associated with abrupt surges in blood pressure
A
secondary HTN –> renal vascular hypertension
18
Q
diagnostics If suspicion is high for secondary HTN renal vascular disease and endovascular intervention is a viable
option
A
renal arteriography (the definitive diagnostic test), is the
best approach
19
Q
diagnostics If suspicion is moderate to low for renal vascular disease
A
noninvasive angiography using
MR or CT
20
Q
Excess glucocorticoid
* Salt and water retention (via mineralocorticoid effects)
* Increased angiotensinogen levels
* Permissive effects in regulation of vascular tone
(Will discuss more in endocrinology module
A
secondary HTN- Cushing syndrome
21
Q
Increased aldosterone secretion from an adrenal adenoma or
bilateral adrenal hyperplasia
A
Secondary HTN- Primary
Hyperaldosteronism
22
Q
- The blood pressure elevation caused by the catecholamine excess
results mainly from alpha-receptor-mediated vasoconstriction of
arterioles, with a contribution from beta-1-receptor-mediated
increases in cardiac output and renin release - Chronic vasoconstriction of the arterial and venous beds leads to a
reduction in plasma volume and predisposes to postural hypotension - Hypertensive crisis in pheochromocytoma may be precipitated by a
variety of drugs, including tricyclic antidepressants, antidopaminergic
agents, metoclopramide, and naloxone
A
Secondary HTN- Pheochromocytoma
22
Q
- Small increase in blood pressure occurs in most women taking
oral contraceptives - 5% of women may have a more significant increase of 8/6 mm
Hg systolic/diastolic - Mostly obese
- > 35 years of age
- Treated >5 years
- Caused by increased hepatic synthesis of angiotensinogen
- Lower dose of postmenopausal estrogen does not generally
cause hypertension but rather maintains endothelium-mediated
vasodilation
A
Secondary HTN- Estrogen Use
22
* Uncommon cause of hypertension
* Evidence of radial-femoral delay should be sought in all
younger patients with hypertension
Secondary HTN- Coarctation of the Aorta
23
Hypertension- When to Refer?
* Severe
* Resistant
* Early-/late-onset hypertension
24
Complications of Untreated Hypertension
* Structural and functional changes in vasculature and heart
* Thrombosis
* ↑ vascular shear stress converts normally anticoagulant endothelium to a prothrombotic state
* Excess morbidity and mortality related to HTN approximately doubles for each 6 mm Hg increase in diastolic blood pressure
* Target-organ damage
24
Clinical and laboratory findings of HTN arise from involvement
of the target organs
* Heart
* Brain
* Kidneys
* Eyes
* Peripheral arteries
24
* Asymptomatic for years
* Headache most frequent symptom*
Mild to moderate primary (essential) hypertension
25
* Events where uncontrolled HTN results in end-organ damage
* Presenting symptoms depend on profile of organ injury
hypertensive emergencies
25
Usually asymptomatic and typically presents as incidental finding
uncontrolled HTN
26
Blood Pressure
* Difference of BP in the arms (subclavian stenosis)
* Orthostatic drop (20/10 mm Hg) (pheochromocytoma)
* Osler sign: falsely elevated BP seen in older patients
* Palpable brachial or radial artery when the cuff is inflated above SBP
Retina
* Narrowing of arterial diameter, copper or silver wiring, AV nicking, cotton wool spots, exudates, hemorrhages, papilledema, sausage-shaped veins (hypertensive retinopathy)****
Heart
* LV heave (severe hypertrophy)
* Aortic regurgitation murmur
* S4 gallop
Pulses
* Radial-femoral delay (coarctation of aorta)
* Loss of peripheral pulse (atherosclerosis, Takayasu arteries and aortic dissection)
signs of hypertensive emergencies
27
what labs to order for hypertension to check:
* Hemoglobin
* Serum electrolytes
* Serum creatinine
* Fasting glucose
* Plasma lipids
* Serum uric acid
* UA
CBC, BMP, CMP, lipid panel, UA
28
diagnostics for hypertension (you don't have to do this)
* ECG
* Chest X-ray
* Echocardiogram
29
who should be treated with BP medications
* All patients when BP reduction will reduce CV risk
* Office-based BP exceeding 160/100 mm Hg (regardless of CV risk)
29
nonpharmacologic therapy for hypertension
- weight loss if they are obese
- DASH diet (fruits, veggies)
- restrict sodium
- limit alchohol intake
- exercise
- mindfulness
29
* Hypertension
* Cigarette smoking
* Obesity (BMI ≥ 30)
* Physical inactivity
* Dyslipidemia
* Diabetes
* Microalbuminuria or eGFR <60
* Age (>55 y men; >65 y women)
* Family history of premature CV
disease (<55 men; <65 women)
Major Risk Factors of cardiovascular disease and probably should be put on meds
30
* Heart (LVH; angina or prior MI;
prior coronary revascularization;
HF)
* Brain (stroke or TIA)
* CKD
* Peripheral artery disease
* Retinopathy
target organ damage and you should be asking questions about this
31
how to treat risk factors of CV
(secondary prevention)
Statins (Rosuvastatin 10 mg)
* Reduces LDL-C and significantly reduces risk of multiple CV events
Low-dose aspirin (81 mg/day)
* No longer recommended in primary prevention of MI or stroke
* Is effective in prevention of recurrent CV events
* BP should be controlled first to minimize risk of cerebral hemorrhag
32
Antihypertensive Medications
initial therapy
* Many classes suitable for initial therapy
* ACE inhibitors
* ARBs
* CCB
* Diuretics
* BB
33
* Commonly used as the initial medication in mild to moderate HTN
* Names of medications--> -pril (lisinopril, enalapril, etc.)
* Both cardio- and renoprotective*
* Indications--> HTN in diabetes, nephropathy, CHF, post MI
* Initiating therapy--> baseline serum K+ and Cr levels
* Repeat levels 1-2 weeks after initiation
* S/E: first-dose hypotension, renal insufficiency, hyperkalemia, cough, skin rashes, angioedema, hyperuricemia
* CI: Pregnancy
Angiotensin-Converting Enzyme
Inhibitors (ACE Inhibitor)
34
* Blocks effects of angiotensin II
* Names of medications: -sartan (losartan, valsartan)
* Can improve CV outcomes in patients with HTN
* Also in HF, type 2 diabetes with nephropathy
* Indications: patients who cannot tolerate BB or ACE-I (do not
use in combo with ACE-I)
* SE: hyperkalemia, hypotension, renal insufficiency
* CI: Pregnancy
Angiotensin II Receptor Blockers (ARBs)
34
* Cause vasodilation
Two classes
Dihydropyridines
* Have little to no effect on cardiac contractility
* Ex: amlodipine, nifedipine, nicardipine
Nondihydropyridines
* Affect cardiac contractility and conduction (used in HTN with afib)
* Ex: diltiazem, verapamil
* Indications: HTN, angina, Raynaud’s phenomenon
* SE: vasodilation, headache, dizziness, flushing, peripheral edema, bradycardia, constipation (verapamil)
* CI: CHF, 2nd/3rd AV blocks
* Amlodipine ONLY CCB with established safety in patients with severe HF
calcium channel blocking agents (CCB)
35
increases sodium and water excretion by preventing reabsorption of Na and water at the distal diluting tubule
* First-line for uncomplicated HTN
* SE: hyponatremia, hypokalemia, hypercalcemia, hyperglycemia, caution in gout and DM
* Meds: Hydrochlorothiazide (HCTZ), Chlorthalidon
thiazide diuretics
36
inhibits water transport across loop of henle; increases water, Na, Cl, K
excretion
* Strongest class of diuretics
* SE: hypokalemia, volume depletion, hypocalcemia, hyponatremia, hyperuricemia, ototoxicity, do not
use in sulfa allergy
* Meds: Furosemide, Bumetanid
loop diuretics
37
inhibits aldosterone-mediated Na/water absorption
* Spares potassium, weakest
* SE: hyperkalemia, gynecomastia (do not use in renal failure or hyponatremia)
* Meds: Spironolactone, amlorine, eplernon
potassium sparing diuretics (mineralocorticoid receptor blockers)
38
Classes
* Cardioselective: beta-1 (atenolol, metoprolol, esmolol)
* Nonselective: beta 1 & 2 (propranolol)
* Both alpha and beta: (labetalol, carvedilol)
* Decrease renin release; decrease heart rate; decrease cardiac output
* Indications: HTN, angina, HF, MI, pheochromocytoma, migraines,
essential tremor
* SE: inducing/exacerbating bronchospasm; sinus node dysfunction and AV conduction depression (resulting in bradycardia or AV block), nasal congestion, Raynaud phenomenon, fatigue, depression, erectile dysfunction
* CI: 2nd/3rd AV blocks; decompensated HF; hypotension and pulse <50 bpm; asthma/COPD
beta blocking agents (BB)
38
Management of HTN with post MI
BB or ACE-1
39
Management of HTN with angina
BB or CCB
39
* Relax smooth muscle, reduce BP by lowering peripheral vascular resistance
* Indications: HTN with BPH, improves insulin sensitivity,
nightmares linked to PTSD
* Meds: Doxazosin, prazosin, terazosin
* SE: first-dose syncope, postural hypotension, dizziness,
palpitations, headache, drowsiness, sexual dysfunction
Alpha-Antagonists (Alpha blockers)
39
first line antihypertensive regimen
ACE/ARB or CCB or thiazide diuretic
--> lisinopril and hydroclorathiazide
39
first line antihypertensive regimen for black persons
CCB or diuretic
39
Management of HTN with systolic HF
ACE-1, ARB, BB, diuretics
39
Management of HTN with atrial fibrillation
BB or CCB
40
what to do Once blood pressure is controlled on a well-tolerated regimen
* Yearly monitoring of blood lipids is recommended
* ECG should be repeated at 2- to 4-year intervals
* Might consider reducing medications if patients have lost weight
and initiated favorable lifestyle modifications
40
what do to if you have resistant hypertension
* Failure to reach blood pressure control in patients who are
adherent to full doses of an appropriate three-drug regimen
(including a diuretic)
* Approach
* Confirm compliance
* Rule out “white coat hypertension”
* Exacerbating factors should be considered
* Identifiable causes of resistant hypertension should be evaluated
* If goal blood pressure cannot be achieved- refer or consul
41
Significant HTN (usually exceeding 180/120 mm Hg) is cause of injury
to
heart, retina, brain, kidneys, large arteries, or microcirculatio
41
* Improper blood pressure
measurement
* Nonadherence
* Volume overload and pseudo
tolerance
* Excess sodium intake
* Volume retention from kidney
disease
* Inadequate diuretic therapy
* Associated conditions
* Obesity
* Excessive alcohol intake
* Drug-induced or other causes
* Inadequate doses
* Inappropriate combinations
* NSAIDs, cyclooxygenase-2
inhibitors
* Cocaine, amphetamines, other
illicit drugs
* Sympathomimetics
(decongestants, anorectics)
* Oral contraceptives
* Adrenal steroids
* Cyclosporin and tacrolimus
* Erythropoietin
* Licorice
causes of resistant hypertension
42
Hospital admission is required to manage
consequences of organ
injury and to closely monitor blood pressure response to IV blood
pressure medications
43
Management of Hypertensive Emergency
* Goal
No more than 25% within first hour & additional 5-15% over the next 23
hours
* Exceptions:
* Acute ischemic stroke (often will fall spontaneously)
* Unless BP exceeds 180-200 mm Hg (reduced cautiously by 10-15% over 24 hours)
* Unless thrombolytics are given- BP maintained at <185/110 mm Hg during treatment and for 24 hours following treatment
* Acute aortic dissection
* Systolic BP and HR should be reduced within 30 min to <120 mm Hg and <60 bpm using combination of vasodilation and beta-blockade
44
Detecting End-Organ Injury
* History & Physical Examination
* Focal or global neurologic deficit
* Abnormal retinal examination
* Absent pulses
* Asymmetric blood pressure readings
* Severe chest pain
* Back pain
* Frank pulmonary edema
* Papilledema is one form of end-organ injury
* Blood test screening for thrombotic microangiopathy, AKI, myocardial
damage
* Urine exam- blood/protein; substances of abuse (cocaine)
* Imaging modalities may confirm:
* Pulmonary edema, myocardial dysfunction, aortic dissection, acute intracranial bleed,
thrombosis, or cerebral microvascular injury
45
In most situations, appropriate control of BP is best achieved
using combo
nicardipine or clevidipine + labetalol or esmolol
46
increased levels of lipids (fats) in the
blood, including cholesterol and triglycerides (the two main
types of lipids)
* does not cause symptoms, but it can increase risk of developing CV disease
* Coronary artery disease
* Cerebrovascular disease
* Peripheral vascular disease
* Cholesterol and TG are carried in lipoproteins, globular particles
that also contain proteins known as apoprotein
hyperlipidemia
46
usually classified by density, which is determined by the amounts of TG (makes them less dense) and apoproteins (makes them more dense)
lipoproteins
47
Cholesterol is carried primarily on
* VLDL (very low-density lipoproteins)
* LDL (low-density lipoproteins)
* HDL (high-density lipoproteins)
47
Total cholesterol
HDL cholesterol + VLDL cholesterol + LDL cholesterol
48
cholesterol normal
< 200
49
triglycerides normal
< 150
50
HDL cholesterol normal
60
51
LDL cholesterol normal
60-130
52
cholesterol/HDL ratio normal
4.0
53
Plaques in arterial walls of patients with atherosclerosis contain
large amounts of
cholesterol
54
The higher the level of LDL-C:
greater risk of atherosclerotic heart disease
55
The higher the level of HDL-C:
lower risk of heart disease
56
causes markedly high LDL-C
levels and early ASCVD
familial hypercholesterolemia
57
secondary causes of lipid abnormalities
alcohol
beta blockers
etc
58
Therapeutic Effects of Lowering
Cholesterol
* Primary prevention
reducing cholesterol levels without
coronary heart disease
58
Therapeutic Effects of Lowering
Cholesterol
Secondary prevention
reducing cholesterol levels in patients
with established CVD
59
hyperlipidemia clinical presentation
Most have no specific symptoms or sign
* Eruptive xanthomas
* Tendinous xanthomas
* Lipemia retinalis
60
how to diagnose hyperlipidemia
Laboratory testing typically leads to diagnosis
* Screening labs
* Work-up of patient with CVD
61
hyperlipidemia screening
* All adults should have their lipids checked before middle age
* Patients with documented atherosclerosis and diabetes should
have their lipids checked routinely- higher risk
* Best screening and treatment strategy for adults who do not
have ASCVD is less clear- several algorithms have been
developed to help guide clinicians, but management should be
individualized based on patients risk to maximize net benefi
62
hyperlipidemia screening guidelines
* 2018 AHA/ACC
* Screen all adults aged 20 years or older if they have risk factors
* Screening can be repeated every 5 years for those with
average or low risk and more often for those whose levels are
close to therapeutic thresholds
* Individuals without CVD should have 10-year-risk of CVD
calculated
* Individuals with LDL-C >190 mg/dL are recommended to be
treated independent of their 10-year risk
63
* Single best test for additional risk stratification (not initial thing)
* Simple noncontrast cardiac-gated CT scan (takes 10-15 min)
* Might help identify patients who are unlikely to benefit from
cholesterol-lowering therapy
* Calcium score of 0 in absence of smoking or diabetes- low risk and
less likely to receive net benefit from therapy
* Can be repeated in 3 years for higher-risk patients and 7 years
for lower-risk patients
* USPSTF does not endorse calcium scoring as a broad screening test
Coronary Artery Calcium Score
63
first line therapy for hyperlipidemia
* Statins nearly always first-line therapy
* Treatment decision based on:
* Presence of clinical CVD or diabetes
* LDL-C >190 mg/dL
* Patient age
* Estimated 10-year risk of developing CVD
63
* Define four groups of patients who should be treated with statin medications:
1. Individuals with clinical ASCVD
2. Individuals with primary elevation of LDL-C >190 mg/dL
3. Individuals aged 40-75 with diabetes and LDL-C ≥ 70 mg/dL
4. Individuals aged 40-75 without clinical ASCVD or diabetes, with LDL-
C 70-189 mg/dL and estimated 10-year CVD risk of 7.5% or higher
63
hyperlipidemia second line therapy
* Ezetimibe, PCSK9 inhibitors, and bempedoic acid have the
strongest recommendations as second-line therapy for patients
with:
* CVD whose LDL on statin therapy remains above relevant treatment
threshold of 55 mg/dL or 70 mg/dL
* Possible familial hypercholesterolemia with baseline LDL > 190 mg/dL
whose LDL remains above 100 mg/dL treatment threshold
* Documented statin intolerance (inability to tolerate at least two different
statin therapies, including at least one attempt at the lowest approved
dose or a trial of an alternate-day dosing strategy
64
Treatment of High LDL Cholesterol
* Reduction of LDL-C with statins is just one way to reduce risk of
CVD
* Should also include other measures:
* Diet, exercise, smoking cessation, hypertension control, weight loss,
diabetes control, and antithrombotic therapy
* Exercise and weight loss may reduce LDL-C and increase HDL
* Use of medication to raise HDL-C has not demonstrated to
provide additional benefit
65
* Inhibit rate-limiting enzyme in the formation of cholesterol
* Reduce MI and total mortality in secondary prevention
Statins (HMG-CoA reductase inhibitors)
high intensity statins:
atorvastatin 40-80 mg/day
rosuvastatin 20-40 mg/day
66
statin side effects
* Muscle aches
* Myositis and rhabdomyolysis
* Simvastatin at highest approved dose (80 mg) is associated
with elevated risk of muscle injury or myopathy
* Liver disease
* Diabetes mellitus (10% risk in those with metabolic syndrome
66
* Inhibits absorption of dietary and biliary cholesterol across the
intestinal wall by inhibiting a cholesterol transporter
* Reduces LDL-C between 15-20% when used as monotherapy
* Can further reduce LDL-C in patients taking statins in whom
therapeutic goal has not been reached
* Side effects uncommon
* Current guidelines recommend adding ezetimibe therapy to
maximally tolerated statin therapy in patients at high risk for
CVD whose LDL-C remains above the treatment threshold of 70 mg/dL
Ezetimibe (zetia)
66
* Inhibit PCSK9-mediated LDL-receptor degradation and lower
LDL-C levels by 50-60%
* Two agents (alirocumab and evolocumab) are FDA-approved
for use in patients with:
* Familial hypercholesterolemia
* Patients with CVD or high risk of CVD who require further lowering of
LDL-C
* SQ every 2-4 weeks
* Side effects uncommon
* EXPENSIVE
Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) Inhibitors
67
* Current guidelines recommend addition of these to statins at
maximally tolerated doses in patients with:
* Calcium scores >1000
* Very high risk for recurrent CVD when on treatment LDL-C remains
>55 or 70 mg/dL (or above 100 mg/dL in patients with familial
hypercholesterolemia without known CVD
Proprotein Convertase Subtilisin/Kexin
Type 9 (PCSK9) Inhibitors
67
Patients considered very high risk for CVD include
* Recent ACS within 12 months
* Multiple prior MIs or strokes
* Significant unrevascularized CAD
* Polyvascular disease (CAD plus cerebrovascular or peripheral vascular disease)
67
* Targets cholesterol synthesis in the liver
* Lowers LDL-C by 17-20% on top of lowering produced by
moderate-to-high-intensity statins
* Lowers LDL-C by 38% when combined with ezetimibe (on top
of statin therapy)
* Monitor for hyperuricemia and potential onset or worsening of
gout as well as cholelithiasis
* Increase risk of tendon rupture
* Should not be used with more than 20 mg of simvastatin or 40
mg of pravastatin daily
Bempedoic Acid
67
essential fatty acids that must be
consumed in the diet and are prominent feature of
mediterranean-style diets
* Can lower triglycerides up to 30% at pharmacologic doses
Omega-3 Fatty Acid Preparations
67
* Cholestyramine, colesevelam, colestipol
* Bind bile acids in the intestine- reduces the enterohepatic
circulation- causes liver to increase its production of bile acids,
using hepatic cholesterol
* Hepatic LDL-receptor activity increases, with decline in plasma LDL-C
levels
* Can reduce LDL-C by 15-25%
* Can increase TG levels- use in caution with patients who
have elevated TG
* Do not use in patients who have TG > 500 mg/dL
* Only medication for lipid lowering that is safe in pregnanc
Bile Acid-Binding Resins
* Cholestyramine, colesevelam, colestipol
68
Can increase TG levels- use in caution with patients who
have elevated TG
* Do not use in patients who have TG > 500 mg/d
Bile Acid-Binding Resins
* Cholestyramine, colesevelam, colestipol
69
Only medication for lipid lowering that is safe in pregnancy
Bile Acid-Binding Resins
* Cholestyramine, colesevelam, colestipol
70
* Result in significant reductions in plasma triglycerides and
increases in HDL-C
* Reduce LDL-C by 10-15%
* Reduce TG by 40%
* Increase HDL-C by 15-20%
* Examples: gemfibrozil, fenofibrate
* Side effects (more for gemfibrozil, less for fenofibrate)
* Cholelithiasis
* Hepatitis
* Myositis
Fibric Acid Derivatives
71
* Reduces production of VLDL particles
* Secondary reduction in LDL-C and increases in HDL-C
* LDL-C decrease by 15-25%
* HDL-C increase by 25-35%
* Intolerance is common
* Prostaglandin-mediated flushing (“hot flashes” or pruritis)
* Can be decreased with aspirin or NSAIDS taken an hour before Niacin dosing
* Can exacerbate gout and peptic ulcer disease (PUD)
* Can increase blood sugar
Niacin (Nicotinic Acid)
72
treatment for any patient requiring a lipid-modifying medication
statins
73
treatment for any patient requiring a lipid-modifying medication Combination therapy indicated for
* Patients with familial hypercholesterolemia in whom LDL-C remains
>100 mg/dL with treatment
* Patients with advanced subclinical atherosclerosis (coronary artery
calcium scores >100, particularly those >1000), or high-risk patients
with existing CVD in whom LDL-C remains >70 mg/dL with treatment
* Very high-risk patients with existing CVD in whom LDL-C remains >55
mg/dL with treatment
* Many high-risk patients with TG > 150 mg/dL or non-HDL-C > 100
mg/d
74
* Risk for pancreatitis when serum TG >1000 mg/dL
* Pathophysiology is not certain
* Most clinicians treat fasting levels >500 mg/dL
high blood triglycerides
75
Primary therapy for high blood triglycerides
* Dietary– avoiding alcohol, simple sugars, refined starches, saturated and
trans fatty acids, and restricting total calories
* Control secondary causes (discussed earlier)
* If still >500 despite compliance and certainly in those with previous episode of
pancreatitis- medication treatment is indicated
76
cholesterol absorption inhibitor (ezetimibe) used for
LDL
77
PCSK9 inhibitors used for
LDL
78
bile acid binding resins (cholestyramine, colestipol, colesevelam) used for
LDL
79
fibrates (gemfibrozil, fenofibrate, fenofibric acid) used for
TG
80
omega 3 fatty acids used for
TG
81
niacin used for
HDL
