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cardiology > hypertension and hyperlipidemia > Flashcards

hypertension and hyperlipidemia Flashcards

1
Q

elevated blood pressure

A

hypertension

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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
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3
Q

normal BP

A

< 120/80

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4
Q

elevated BP

A

120-129/<80

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5
Q

stage 1 HTN

A

130-139/80-89

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6
Q

stage 2 HTN

A

> 140/90

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7
Q

white coat hypertension

A

only high at the doctors

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8
Q

masked hypertension

A

normal at office and high at home

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9
Q

labile hypertension

A

variable high and lows

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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

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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

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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

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13
Q

causes of secondary hypertension

A

RENAL

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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

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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

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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

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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

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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

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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

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19
Q

diagnostics If suspicion is moderate to low for renal vascular disease

A

noninvasive angiography using
MR or CT

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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

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21
Q

Increased aldosterone secretion from an adrenal adenoma or
bilateral adrenal hyperplasia

A

Secondary HTN- Primary
Hyperaldosteronism

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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

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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

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22
Q
  • Uncommon cause of hypertension
  • Evidence of radial-femoral delay should be sought in all
    younger patients with hypertension
A

Secondary HTN- Coarctation of the Aorta

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23
Q

Hypertension- When to Refer?

A
  • Severe
  • Resistant
  • Early-/late-onset hypertension
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24
Q

Complications of Untreated Hypertension

A
  • 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
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24
Q

Clinical and laboratory findings of HTN arise from involvement
of the target organs

A
  • Heart
  • Brain
  • Kidneys
  • Eyes
  • Peripheral arteries
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24
Q
  • Asymptomatic for years
  • Headache most frequent symptom*
A

Mild to moderate primary (essential) hypertension

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25
Q
  • Events where uncontrolled HTN results in end-organ damage
  • Presenting symptoms depend on profile of organ injury
A

hypertensive emergencies

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25
Q

Usually asymptomatic and typically presents as incidental finding

A

uncontrolled HTN

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26
Q

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)

A

signs of hypertensive emergencies

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27
Q

what labs to order for hypertension to check:
* Hemoglobin
* Serum electrolytes
* Serum creatinine
* Fasting glucose
* Plasma lipids
* Serum uric acid
* UA

A

CBC, BMP, CMP, lipid panel, UA

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28
Q

diagnostics for hypertension (you don’t have to do this)

A
  • ECG
  • Chest X-ray
  • Echocardiogram
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29
Q

who should be treated with BP medications

A
  • All patients when BP reduction will reduce CV risk
  • Office-based BP exceeding 160/100 mm Hg (regardless of CV risk)
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29
Q

nonpharmacologic therapy for hypertension

A
  • weight loss if they are obese
  • DASH diet (fruits, veggies)
  • restrict sodium
  • limit alchohol intake
  • exercise
  • mindfulness
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29
Q
  • 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)
A

Major Risk Factors of cardiovascular disease and probably should be put on meds

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30
Q
  • Heart (LVH; angina or prior MI;
    prior coronary revascularization;
    HF)
  • Brain (stroke or TIA)
  • CKD
  • Peripheral artery disease
  • Retinopathy
A

target organ damage and you should be asking questions about this

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31
Q

how to treat risk factors of CV
(secondary prevention)

A

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

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32
Q

Antihypertensive Medications
initial therapy

A
  • Many classes suitable for initial therapy
  • ACE inhibitors
  • ARBs
  • CCB
  • Diuretics
  • BB
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33
Q
  • 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
A

Angiotensin-Converting Enzyme
Inhibitors (ACE Inhibitor)

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34
Q
  • 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
A

Angiotensin II Receptor Blockers (ARBs)

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34
Q
  • 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
A

calcium channel blocking agents (CCB)

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35
Q

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

A

thiazide diuretics

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36
Q

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

A

loop diuretics

37
Q

inhibits aldosterone-mediated Na/water absorption
* Spares potassium, weakest
* SE: hyperkalemia, gynecomastia (do not use in renal failure or hyponatremia)
* Meds: Spironolactone, amlorine, eplernon

A

potassium sparing diuretics (mineralocorticoid receptor blockers)

38
Q

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
A

beta blocking agents (BB)

38
Q

Management of HTN with post MI

A

BB or ACE-1

39
Q

Management of HTN with angina

A

BB or CCB

39
Q
  • 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
A

Alpha-Antagonists (Alpha blockers)

39
Q

first line antihypertensive regimen

A

ACE/ARB or CCB or thiazide diuretic
–> lisinopril and hydroclorathiazide

39
Q

first line antihypertensive regimen for black persons

A

CCB or diuretic

39
Q

Management of HTN with systolic HF

A

ACE-1, ARB, BB, diuretics

39
Q

Management of HTN with atrial fibrillation

A

BB or CCB

40
Q

what to do Once blood pressure is controlled on a well-tolerated regimen

A
  • 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
Q

what do to if you have resistant hypertension

A
  • 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
Q

Significant HTN (usually exceeding 180/120 mm Hg) is cause of injury
to

A

heart, retina, brain, kidneys, large arteries, or microcirculatio

41
Q
  • 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
A

causes of resistant hypertension

42
Q

Hospital admission is required to manage

A

consequences of organ
injury and to closely monitor blood pressure response to IV blood
pressure medications

43
Q

Management of Hypertensive Emergency
* Goal

A

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
Q

Detecting End-Organ Injury

A
  • 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
Q

In most situations, appropriate control of BP is best achieved
using combo

A

nicardipine or clevidipine + labetalol or esmolol

46
Q

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
A

hyperlipidemia

46
Q

usually classified by density, which is determined by the amounts of TG (makes them less dense) and apoproteins (makes them more dense)

A

lipoproteins

47
Q

Cholesterol is carried primarily on

A
  • VLDL (very low-density lipoproteins)
  • LDL (low-density lipoproteins)
  • HDL (high-density lipoproteins)
47
Q

Total cholesterol

A

HDL cholesterol + VLDL cholesterol + LDL cholesterol

48
Q

cholesterol normal

A

< 200

49
Q

triglycerides normal

A

< 150

50
Q

HDL cholesterol normal

A

60

51
Q

LDL cholesterol normal

A

60-130

52
Q

cholesterol/HDL ratio normal

A

4.0

53
Q

Plaques in arterial walls of patients with atherosclerosis contain
large amounts of

A

cholesterol

54
Q

The higher the level of LDL-C:

A

greater risk of atherosclerotic heart disease

55
Q

The higher the level of HDL-C:

A

lower risk of heart disease

56
Q

causes markedly high LDL-C
levels and early ASCVD

A

familial hypercholesterolemia

57
Q

secondary causes of lipid abnormalities

A

alcohol
beta blockers
etc

58
Q

Therapeutic Effects of Lowering
Cholesterol
* Primary prevention

A

reducing cholesterol levels without
coronary heart disease

58
Q

Therapeutic Effects of Lowering
Cholesterol
Secondary prevention

A

reducing cholesterol levels in patients
with established CVD

59
Q

hyperlipidemia clinical presentation

A

Most have no specific symptoms or sign

  • Eruptive xanthomas
  • Tendinous xanthomas
  • Lipemia retinalis
60
Q

how to diagnose hyperlipidemia

A

Laboratory testing typically leads to diagnosis
* Screening labs
* Work-up of patient with CVD

61
Q

hyperlipidemia screening

A
  • 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
Q

hyperlipidemia screening guidelines

A
  • 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
Q
  • 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
A

Coronary Artery Calcium Score

63
Q

first line therapy for hyperlipidemia

A
  • 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
Q
  • Define four groups of patients who should be treated with statin medications:
A
  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
Q

hyperlipidemia second line therapy

A
  • 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
Q

Treatment of High LDL Cholesterol

A
  • 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
Q
  • Inhibit rate-limiting enzyme in the formation of cholesterol
  • Reduce MI and total mortality in secondary prevention
A

Statins (HMG-CoA reductase inhibitors)

high intensity statins:
atorvastatin 40-80 mg/day
rosuvastatin 20-40 mg/day

66
Q

statin side effects

A
  • 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
Q
  • 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
A

Ezetimibe (zetia)

66
Q
  • 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
A

Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) Inhibitors

67
Q
  • 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
A

Proprotein Convertase Subtilisin/Kexin
Type 9 (PCSK9) Inhibitors

67
Q

Patients considered very high risk for CVD include

A
  • Recent ACS within 12 months
  • Multiple prior MIs or strokes
  • Significant unrevascularized CAD
  • Polyvascular disease (CAD plus cerebrovascular or peripheral vascular disease)
67
Q
  • 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
A

Bempedoic Acid

67
Q

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

A

Omega-3 Fatty Acid Preparations

67
Q
  • 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
A

Bile Acid-Binding Resins
* Cholestyramine, colesevelam, colestipol

68
Q

Can increase TG levels- use in caution with patients who
have elevated TG
* Do not use in patients who have TG > 500 mg/d

A

Bile Acid-Binding Resins
* Cholestyramine, colesevelam, colestipol

69
Q

Only medication for lipid lowering that is safe in pregnancy

A

Bile Acid-Binding Resins
* Cholestyramine, colesevelam, colestipol

70
Q
  • 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
A

Fibric Acid Derivatives

71
Q
  • 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
A

Niacin (Nicotinic Acid)

72
Q

treatment for any patient requiring a lipid-modifying medication

A

statins

73
Q

treatment for any patient requiring a lipid-modifying medication Combination therapy indicated for

A
  • 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
Q
  • Risk for pancreatitis when serum TG >1000 mg/dL
  • Pathophysiology is not certain
  • Most clinicians treat fasting levels >500 mg/dL
A

high blood triglycerides

75
Q

Primary therapy for high blood triglycerides

A
  • 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
Q

cholesterol absorption inhibitor (ezetimibe) used for

A

LDL

77
Q

PCSK9 inhibitors used for

A

LDL

78
Q

bile acid binding resins (cholestyramine, colestipol, colesevelam) used for

A

LDL

79
Q

fibrates (gemfibrozil, fenofibrate, fenofibric acid) used for

A

TG

80
Q

omega 3 fatty acids used for

A

TG

81
Q

niacin used for

A

HDL

cardiology (6 decks)

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