Lecture 10 (HTN)-Exam 3

Question 1

HTN:
* MC reason for what?
* How many people have it?
* Increases significance with what?
* Roughly half of those diagnosed w/ hypertension still have what?

Answer 1

Question 2

What are the modifable RF?(6)

Answer 2

Question 3

What are the relatively fixed risk factor?

Answer 3

Question 4

Answer 4

Question 5

Measure BP:
* What does the patient have to do?
* What method should be used?
* What should be avoided for at least 30 mins?
* Use of appropriate what?

Answer 5

• Seated quietly for 5 minutes in a chair with feet on the floor and arm at heart level
• The auscultatory method should be used.
• Caffeine, exercise, and smoking should be avoided for at least 30 minutes before BP measurement.
• Use appropriate sized cuff. Cuff bladder to encircle at least 80% of the arm circumference

Question 6

BP is dx based on what?

Answer 6

Diagnosis based on the mean of 2 or more measured readings at 2 or more office visits

Question 7

Answer 7

Question 8

Answer 8

Question 9

What are out of office BP measurements used for?

Answer 9

I A recommendation: Out-of-office BP measurements are recommended to confirm the diagnosis of hypertension and for titration of BP-lowering medication, in conjunction with telehealth counseling or clinical interventions.

Bc of white coat HTN or stress at home (masked HTN)

Question 10

Answer 10

Question 11

Detection of White Coat Hypertension or Masked Hypertension in Patients Not on Drug Therapy

Answer 11

ABPM indicates ambulatory blood pressure monitoring; BP, blood pressure; and HBPM, home blood pressure monitoring

Question 12

Detection of White Coat Effect or Masked Uncontrolled Hypertension in Patients on Drug Therapy

Answer 12

Question 13

Answer 13

Question 14

Answer 14

JNC 8= HTN is over 140/90 where ACC/AHA is stage 2

Question 15

Prehypertension:
* What is the the BP?
* How do you txt them?
* 50% of them will develop with what?

Answer 15

• 120-129/ <80
• Individuals who are prehypertensive are not candidates for drug therapy but should be firmly advised to practice lifestyle modification.
• 50% of people with pre-hypertension will develop HTN in 4 years.

Question 16

Answer 16

capsured more patients: shows patients are at risk

Question 17

What is the cause of 95% of cases of HTN?

Answer 17

~95% have no identifiable cause of hypertension
* This is PRIMARY/ESSENTIAL/IDIOPATHIC hypertension

Question 18

Primary causes of HTN:
* What can be some causes?

Answer 18

• Remember some of your physiology pathways that regulate blood pressure
• Sympathetic nervous system (fight or flight)
• RAAS system
• Blood volume
• Genetics

Question 19

Primary factors contributing to high blood pressure

Answer 19

Question 20

What is the basic testing and optional testing for HTN?

Answer 20

Question 21

Types of hypertension: Primary hypertension
* How many cases?
* What are all the terms?
* What are the causes?

Answer 21

Question 22

Types of hypertension: Secondary hypertension
* Accounts for 5%
* Secondary to what?

Answer 22

• Accounts for ~5% of cases
• Secondary to potentially curable/treatable conditions (modifiable)

Question 23

What are the causes of secondary hypertension?(9)

Answer 23

• Medications
• Intrinsic renal or renovascular disease
• Sleep apnea
• Hyperaldosteronism
• Drugs, EtOH
• Pheochromocytoma
• Cushing’s
• Coarctation of aorta
• Hyper/hypothyroidism

Question 24

Fill in for Causes of Secondary Hypertension

Answer 24

Question 25

Who gets screened for secondary hypertension?

Answer 25

Question 26

TOD indicates what?

Answer 26

TOD indicates target organ damage (e.g., cerebrovascular disease, hypertensive retinopathy, left ventricular hypertrophy, left ventricular dysfunction, heart failure, coronary artery disease, chronic kidney disease, albuminuria, peripheral artery disease).

Question 27

Screening tests for secondary hypertension

Answer 27

Question 28

# Common causes of secondary hypertension(90%) Renal parenchymal disease * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 28

Question 29

# Common causes of secondary hypertension(90%) Renovascular disease: * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 29

Question 30

# Common causes of secondary HTN Primary aldosteronism: * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 30

Question 31

# Common causes of secondary HTN Obstructive Sleep Apnea: * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 31

Question 32

# Common causes of secondary hypertension Drug or alcohol induced: * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 32

Question 33

# Uncommon causes of secondary HTN Pheochromocytoma/paranglioma * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 33

Question 34

# Uncommon causes of 2 HTN Cushing's * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 34

Question 35

# Uncommon causes of 2 HTN Hypothroidism: * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 35

Question 36

# uncommon causes of 2nd HTN Hyperthyroidism: * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 36

Question 37

# Uncommon causes of 2 HTN Aortic coarctation: * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 37

Question 38

# Uncommon causes of 2 HTN Primary hyperpara-thyroidism: * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 38

Question 39

# Uncommon causes of 2nd HTN Congenital adrenal hyperplasia: * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 39

Question 40

# Uncommon causes of 2nd HTN Mineralocorticoid excess syndromes other than primary aldosteronism: * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 40

Question 41

# uncommon causes of 2nd htn Acromegaly: * What are the clinical indications? * What does the physical exam show? * What is the screen test? * What are additional/confirmatory tests?

Answer 41

Question 42

End organ damage caused by chronic hypertension * What can happen to the heart and brain?

Answer 42

Question 43

End-Organ Damage Caused by Chronic Hypertension: * What are some other issues besides heart and brain?(5)

Answer 43

* Chronic kidney disease * Peripheral arterial disease * Retinopathy, choroidopathy, optic neuropathy

Question 44

Adequate blood pressure reduces the incidence of what (3)

Answer 44

* Acute Coronary Syndromes by 20-25% * Stroke by 30-35% * Heart failure by 50%

Question 45

How does HTN have effects on the CVS? (4)

Answer 45

* Left ventricular hypertrophy, dysfunction (systolic and diastolic) and heart failure. * **Arrhythmias (atrial fibrillation)** MC * Coronary artery disease, Acute MI * Arterial aneurysm, dissection, and rupture.

Question 46

How does HTN have effects on the renal system? (2)

Answer 46

* Glomerular sclerosis leading to impaired kidney function and finally end stage kidney disease. * Ischemic kidney disease especially when renal artery stenosis is the cause of HTN (renal artery stenosis is present in 1-2 % of HTN patients- treatment of it is not straight forward)

Question 47

What are the effects of HTN on nervous system? (2)

Answer 47

* Stroke, intracerebral and subaracnoid hemorrhage. * Cerebral atrophy and dementia

Question 48

How does HTN have effects on the eyes (3)

Answer 48

* Retinopathy, retinal hemorrhages and impaired vision. * Vitreous hemorrhage, retinal detachment * Neuropathy of the nerves leading to extraoccular muscle paralysis and dysfunction

Question 49

What is this?

Answer 49

Question 50

What is this?

Answer 50

AV nicking you see in HTN patients?

Question 51

Fill in for the grades of HTN retinopathy?

Answer 51

Question 52

Goals of treatments: Fill in

Answer 52

Question 53

Txt for HTN: * What is the txt for low risk patients (ASCVD <10%)?

Answer 53

Lifestyle modifications at 130/80, start medication at 140/90 with a goal of 130/80 once on medication.

Question 54

What is the txt of High-risk patients (ASCVD risk >10%) OR CKD, DM, CVD?

Answer 54

Starting medications and lifestyle modifications at 130/80 or above

Question 55

Answer 55

Question 56

10-year risk for ASCVD is categorized as what?

Answer 56

* Low-risk (<5%) * Borderline risk (5% to 7.4%) * Intermediate risk (7.5% to 19.9%) * High risk (≥20%) -> Tech over 10 is high risk!

Question 57

What is apart of the ASCVD Risk Estimator Plus ?

Answer 57

Question 58

Best Proven Nonpharmacological Interventions for Prevention and Treatment of Hypertension i.e. lifestyle modifications

Answer 58

Question 59

Best Proven Nonpharmacological Interventions for Prevention and Treatment of Hypertension i.e. lifestyle modifications

Answer 59

Question 60

Best Proven Nonpharmacological Interventions for Prevention and Treatment of Hypertension i.e. lifestyle modifications

Answer 60

Question 61

Best Proven Nonpharmacological Interventions for Prevention and Treatment of Hypertensioni.e. lifestyle modifications

Answer 61

Question 62

Pharmacologic management * What are the first line agents for HTN?

Answer 62

For initiation of antihypertensive drug therapy, first-line agents include thiazide diuretics (hydrochlorothiazide or chlorthalidone), CCBs (DHP or Non-DHP), and ACE inhibitors or ARBs. * Class IA recommendation

Question 63

When do you Initiate antihypertensive drug therapy with 2 first-line agents of different classes?

Answer 63

Initiation of antihypertensive drug therapy with 2 first-line agents of different classes, either as separate agents or in a fixed-dose combination, is recommended in adults with stage 2 hypertension and an average BP more than 20/10 mm Hg above their BP target. * Class IC recommendation

Question 64

Adults initiating a new or adjusted drug regimen for hypertension should have what? What should that include?

Answer 64

Adults initiating a new or adjusted drug regimen for hypertension should have a follow-up evaluation of adherence and response to treatment at monthly intervals until control is achieved. Follow-up and monitoring after initiation of drug therapy for hypertension control should include systematic strategies to help improve BP, including use of HBPM, team-based care, and telehealth strategies. * Class IA recommendation

Question 65

Fill in the HNC htn guidelines

Answer 65

Question 66

Urgency versus emergency * What is the difference?

Answer 66

* Hypertensive urgency is SBP >180mmHg and/or DBP >120mmHg WITHOUT signs of end-organ damage * Hypertensive emergency is SBP >180mmHg and/or DBP >120mmHg WITH signs of end-organ damage

Question 67

Answer 67

Question 68

Hypertensive Urgency * BP? * Without what? * What are examples? * Usually due to what? * What txt is preferred?

Answer 68

* Severely elevated BP ( >180/120). * Without progressive end-organ dysfunction. * Examples: Highly elevated BP without symptoms (no headache, shortness of breath or chest pain) * Usually due to poorly-controlled HTN. * Oral medications preferred (decrease BP to stage 2 over serveral hours to day) via increase maintence medications, add new agent or treat hypertension

Question 69

Hypertensive emergency * What is the BP level? * What do they have? * What are examples? * What does it require?

Answer 69

Question 70

Hypertensive emergency Treatment * What is the process of getting the BP down? * What happens if the BP drops fast?

Answer 70

Get BP down in 1 hour * Not more than 25% within first hour * Then to 160/100 hours 2-6 * Normotension 24-48 * Exception is aortic dissection Faster reductions can have consequences * AKI, decreased coronary (MI), cerebral perfusion (stroke)

Question 71

# Dr. V sides Hypertensive emergencies exceeptions to BP lowing over 24 hours: * What do you do for acute phase of ischemic stroke? * Acute aortic dissection? * Spontaneous hemorrhagic stoke?

Answer 71

Question 72

# Dr. V slides? What are the drugs that you can give for hypertensive emergency?

Answer 72

Question 73

# Dr. V slides Hypertensive retinopathy (malignant htn) * Characterized by what? * If untreated, what can happen? * What are the first line agents?

Answer 73

Question 74

* What is hyperlipidemia? Common or not? * Alternatively, a more objective definition describes hyperlipidemia as what?

Answer 74

* Hyperlipidemia is a condition that incorporates various genetic and acquired disorders that describe elevated lipid levels within the human body. * Hyperlipidemia is extremely common, especially in the Western hemisphere, but also throughout the world. * Alternatively, a more objective definition describes hyperlipidemia as low-density lipoprotein (LDL), total cholesterol, triglyceride levels, or lipoprotein levels greater than the 90th percentile in comparison to the general population, or an HDL level less than the 10th percentile when compared to the general population.

Question 75

* Lipids include what? * Through a vast array of trials and studies, it has been consistently shown that elevated levels of LDL cholesterol increase a person's risk for the development of what? * Estimates are that over 50% of American adults have what?

Answer 75

* Lipids include cholesterol levels, lipoproteins, chylomicrons, VLDL, LDL, apolipoproteins, and HDL * Through a vast array of trials and studies, it has been consistently shown that elevated levels of LDL cholesterol increase a person's risk for the development of atherosclerotic plaques and subsequent vascular disease. * Estimates are that over 50% of American adults have elevated LDL levels, and it is speculated that under 35% of those patients adequately manage their high LDL levels, clearly depicting an undertreated disease

Question 76

What is primary lipid disorders/hyperlipidemia?

Answer 76

* Familial/hereditary * Genetically determined

Question 77

What is secondary lipid disorders/hyperlipidemia?

Answer 77

Acquired * Hypercholesterolemia: hypothyroidism, nephrotic syndromes, drugs * Hypertriglyceridiema: DM, alcohol, gout, chronic renal failure

Question 78

What are the secondary causes of dyslipidemia?

Answer 78

Question 79

fill in for the types of lipid disorders/hyperlipidemia

Answer 79

Question 80

Lipid disorders potentiate what?

Answer 80

atherosclerotic disease

Question 81

What is the pathophysio of atherosclerotic disease?

Answer 81

* Circulating monocytes are recruited to the subendothelial space. * These monocytes undergo differentiation, becoming macrophages, which are scavenger cells that recognize and accumulate oxidized LDL. * The lipid-laden macrophages then become foam cells, which cluster under the endothelial lining to form a bulge into the artery. * This bulge is called a fatty streak and is the first overt sign of atherosclerotic change.

Question 82

Why is dyslipidima bad: * When does plaque narrow the lumen? * When arterial cross-sectional area is narrowed by 40% have progressive decrease in what? * When luminal cross-sectional area is narrowed by 75% you reach what? * Thus, patients with stenoses greater than 75% can have what?

Answer 82

* Because atherosclerotic plaques first expand the blood vessel wall outward, it is not until >40% of the blood vessel area is plaque that lumen narrowing occurs. * When arterial cross-sectional area is narrowed by 40% have progressive decrease in coronary flow * When luminal cross-sectional area is narrowed by 75% you reach critical coronary stenosis which significantly limits coronary flow. * Thus, patients with stenoses greater than 75% can have reliable stable angina.

Question 83

* What is a slow process? What is a fast/sudden event? * Dyslipidemia present in over 70% of what?

Answer 83

* Atherosclerosis, with narrowing resulting in critical coronary stenosis, is a SLOW process. * Unstable atherosclerotic plaque rupture is a FAST/SUDDEN event that causes myocardial infarction. * Dyslipidemia present in over 70% of premature CAD!

Question 84

What are the tools for identifying patients at risk for ASCVD?

Answer 84

* Fasting lipid profile * Identify risk factors predisposing patients to ASCVD * ASCVD risk calculators * Using these tools to determine treatment goals

Question 85

Who are we screening for dyslipid disease?

Answer 85

* In general, adults over 20 years old, fasting lipid panel recommended * Younger if known hx of familial lipid disease

Question 86

Answer 86

Question 87

The fasting lipid profile * What does it include? * Generally fasting in preferred as what can happen?

Answer 87

Includes measurements of total cholesterol, LDL-C, HDL-C, triglycerides Generally fasting in preferred as triglycerides may be falsely elevated w/ food however this is debated * The effect is very small, and likely wouldn’t change the decision to treat except only in a small population

Question 88

What are the five major lipoproteins in blood?

Answer 88

* chylomicrons * very low density lipoprotein (VLDL) * intermediate density lipoprotein (IDL) * low density lipoprotein (LDL) * high density lipoprotein (HDL)

Question 89

Which class carries the majority of cholesterol and triglycerides?

Answer 89

Each of these classes of lipoproteins carries cholesterol and triglyceride to a varying degree, with LDL carrying the majority of cholesterol, and VLDL carrying the majority of triglyceride.

Question 90

Answer 90

Question 91

What can induce the development of atherosclerosis even in the absence of other risk factors?

Answer 91

Elevated plasma concentrations of apo B-100 containing lipoproteins (low density and very low density lipoprotein [LDL and VLDL]) can induce the development of atherosclerosis even in the absence of other risk factors. It has been proposed that the initiating event in atherogenesis is the subendothelial retention of apo B-100-containing lipoproteins. 

Question 92

HDL, in contrast to LDL and VLDL, does what?

Answer 92

HDL, in contrast to LDL and VLDL, has antiatherogenic properties that include macrophage cholesterol efflux, antioxidation, protection against thrombosis, maintenance of endothelial function, and maintenance of low blood viscosity through a permissive action on red cell deformability.

Question 93

Lp(a), the specialized form of LDL, is a risk factor for what?

Answer 93

Lp(a), the specialized form of LDL, is a risk factor for the development of atherosclerotic events and evidence strongly suggests that it is causative. This issue is discussed separately.

Question 94

What are Other ASCVD risk factors aside from ldl?

Answer 94

Question 95

10-year risk for ASCVD is categorized as what for dyslipidemia

Answer 95

* Low-risk (<5%) * Borderline risk (5% to 7.4%) * Intermediate risk (7.5% to 19.9%) * High risk (≥20%)

Question 96

What to know regarding ASCVD calculators * This calculator helps predict the 10-year risk of what? * This calculator may overestimate what? * This calculator has only been validated for what ages? * Lifetime Risk is only calculated for what patient ?

Answer 96

This calculator helps predict the 10-year risk of the following hard ASCVD events: * First occurrence of nonfatal myocardial infarction * CHD death * Fatal or nonfatal stroke This calculator may overestimate risk and a discussion with the patient needs to ensue if there are any questions. This calculator has only been validated for ages 40 to 79 years. Lifetime Risk is only calculated for patient 20 to 59 years

Question 97

* Risk estimates were developed from cohorts primarily comprising White and African-American subjects. Risk may be underestimated in what populations? Overestimated? * ASCVD Plus is updated, more sensitive calculator, what does it include?

Answer 97

* Risk estimates were developed from cohorts primarily comprising White and African-American subjects. Risk may be underestimated in Native Americans, Asian Americans of South Asian ancestry, and Puerto Ricans. Risk may be overestimated in Asian Americans of East Asian ancestry and some Mexican Americans. * ASCVD Plus is updated, more sensitive calculator: Includes LDL Cholesterol, Taking a Statin or not, and Taking an ASA or not

Question 98

What is the primary prevention of ascvd/hyperlipidemia (3)

Answer 98

* Methods to avoid occurrence of disease * Review lifestyle habits (e.g., diet, physical activity, weight or body mass index, and tobacco use). * Endorse a healthy lifestyle and provide relevant advice, materials, or referrals. (e.g., CardioSmart, AHA Life’s Simple 7, NLA Patient Tear Sheets, PCNA Clinicians’ Lifestyle Modification Toolbox, cardiac rehabilitation, dietitian, smoking cessation program).

Question 99

Answer 99

Question 100

# Primary prevention of dyslipid What are the three higher risk groups? what do you tx them with?

Answer 100

Question 101

# Primary Prevention Baseline LDL-C >190mg/dl * What is first line? * What goals do you want to hit? What can you add if you do not hit goals?

Answer 101

Question 102

# dyslipid For intermediate risk of ASCVD: What do you initate?

Answer 102

Question 103

# dyslipid Medical therapy will be determined by what?

Answer 103

Question 104

# dyslipid Secondary prevention

Answer 104

Question 105

# dyslipid For secondary prevention

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Question 106

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Question 107

Secondary prevention: Very high risk ASCVD or under 75 years without very high risk * What is first line, second on add, third add on? * What is the LDL goal?

Answer 107

Question 108

Secondary prevention: Not at very high risk ASCVD and age over 75 * What is the first line txt?

Answer 108

mod to high intensity statin

Question 109

High-Risk ASCVD Patient Treatments * Patients with cardiovascular disease (CVD), all of whom are at high risk of a CVD event, should be recommended what? * Statin refractory lipid disease should be what?

Answer 109

* Patients with cardiovascular disease (CVD), all of whom are at high risk of a CVD event, should be recommended lifestyle (modification) interventions that are associated with improved clinical outcomes as well as lifelong statin therapy. * Statin refractory lipid disease should be referred to a lipid specialist

Question 110

Where does statins work

Answer 110

Question 111

Answer 111

Question 112

Statins: * What causes the greatest change in LDL-C? Who should get this?

Answer 112

Rosuvastatin, atorvastatin, and simvastatin cause the greatest percentage change in LDL-C; they are preferred in patients who require a potent statin because of high cardiovascular risk or who require >35 percent reduction in LDL-C.

Question 113

In patients with severe renal impairment, it is suggested treatment with what to lower lipids?

Answer 113

In patients with severe renal impairment, it is suggested treatment with atorvastatin or fluvastatin. These medications do not require dose adjustment.

Question 114

In patients with chronic liver disease who require a statin because of high cardiovascular risk, it suggested to have have the patient do what?

Answer 114

In patients with chronic liver disease who require a statin because of high cardiovascular risk, it suggested to have complete abstinence from alcohol and the use of pravastatin at a low dose.

Question 115

Fewer pharmacokinetic drug interactions are likely to occur with which statins? why?

Answer 115

Fewer pharmacokinetic drug interactions are likely to occur with pravastatin, fluvastatin, rosuvastatin, and pitavastatin because they are not metabolized through the CYP3A4.

Question 116

What are the SE of statins?

Answer 116

* Myalgias (CK normal) * Myositis/myopathy (CK > ULN) with concerning symptoms or objective weakness * Rhabdomyolysis (CK >10× ULN + renal injury) * Statin-associated autoimmune myopathy (HMGCR antibodies, incomplete resolution) * New-onset diabetes mellitus * Transaminase elevation 3× ULN * Hepatic failure * Memory/cognition * Cancer

Question 117

What are the RFs of SAMS?(7)

Answer 117

Question 118

how do you manage SAMS?

Answer 118

Question 119

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Question 119

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Question 120

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Question 122

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Question 123

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Question 124

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Question 125

LDL related ASCVD risk

Answer 125

Question 126

LDL related ASCVD risk

Answer 126

Question 127

# Non-statin cholesterol lowering drugs Bile acid sequestrants * What is an example * What is the MOA? * What are the SE?

Answer 127

* e.g: Questran (cholestyramine) * Impairs reabsorption of bile acids by binding to negatively charged acids and salts which forms a insoluble complex with bile acid. This increases teh excretion of bile acids which increases demand for production. Bile acids are made of cholesterol. Liver senses the decreased cholesterol and increase Raise LDL receptor activity which brings in more LDL and decreases cholesteral levels * SE: Constipation, GI distress, Increases TG

Question 128

# Non-statin cholesterol lowering drugs Bile acid sequestrants * Effects on plasma lipids? * What happens to LDL?

Answer 128

Question 129

# Non-statin cholesterol lowering drugs Ezetimibe: * What is the MOA?

Answer 129

MOA: Impairs absorption of cholesterol via binding to NP1L1 and inactivates its ability to interact with clatrin AP2 which is needed for endocytosis. Decreases delivery of intestinal cholesterol to liver which raises LDL receptor activity

Question 130

# Non-statin cholesterol lowering drugs Ezetimibe * Effects on Plasma Lipids? * LDL-C Lowering?

Answer 130

Question 131

# Non-statin cholesterol lowering drugs Bempedoic acid * What is the MOA? * What are the SE?

Answer 131

* MOA: Inhibitor of ATP-citrate lyase leading to decreased cholesterol synthesis and an increase in LDL receptor activity * SE: Increases uric acid leading to gout and Tendon rupture has been reported

Question 132

Bempedoic acid * Effects on plasma lipids? * LDL-c lowering?

Answer 132

Question 133

# Non-statin cholesterol lowering drugs Niacin * What is the MOA? * What are the SE?(4)

Answer 133

* MOA:Reduces hepatic secretion of VLDL * SE: Flushing, rash, raise plasma glucose, hepatic dysfunction, others

Question 134

Niacin: * Effects on plasma lipids? * LDL-C lowering?

Answer 134

Question 135

# Non-statin cholesterol lowering drugs MTP inhibitors * Approved for treatment of what? * What is the MOA? * What are the SE?

Answer 135

* homozygous familial hypercholesterolemia * MOA: Reduces hepatic secretion of VLDL * SE: Fatty liver

Question 136

MTP inhibitors * Effects on plasma lipids? * LDL C lowering?

Answer 136

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Question 139

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Question 140

PCSK9 inhibitors * Alirocumab and evolocumab: used for what?

Answer 140

Alirocumab and evolocumab: 1) ↓ LDL-C in adults with primary hyperlipidemia (including HeFH) as adjunct to diet, either alone or in combination with other lipid-lowering therapies

Question 141

PCSK9 inhibitors * Alirocumab used for what?

Answer 141

Alirocumab: 1) ↓ risk of MI, stroke, and unstable angina requiring hospitalization in adults with ASCVD; 2) ↓ LDL-C in adults with HoFH as adjunct to other LDL-C–lowering therapies

Question 142

PCSK9 inhibitors * Evolocumab used for what?

Answer 142

1) ↓ risk of MI, stroke, and coronary revascularization in adults with ASCVD; 2) ↓ LDL-C in pediatric patients (aged ≥10 years) with HeFH as adjunct to diet and other LDL-C–lowering therapies; 3) ↓ LDL-C in adults and pediatric patients (aged ≥10 years) with HoFH as adjunct to diet and other LDL-C–lowering therapies

Question 143

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Question 144

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Question 145

# Top 10 take home messages In all individuals, emphasize what? Why?

Answer 145

Question 146

# Top 10 take home messages In patients with clinical ASCVD, reduce what? How?

Answer 146

Question 147

# Top 10 take home messages In very high-risk ASCVD, use a LDL-C threshold of what? What should you consider?

Answer 147

Question 148

# Top 10 take home messages In patients with severe primary hypercholesterolemia (LDL-C level ≥ 190 mg/dL[≥4.9 mmol/L]) without calculating 10-year ASCVD risk, begin what? * What do you do if levels do not decrease?

Answer 148

Question 149

* In patients 40 to 75 years of age with diabetes mellitus and LDL-C ≥70 mg/dL (≥1.8 mmol/L), start what? * In patients with diabetes mellitus at higher risk, especially those with multiple risk factors or those 50 to 75 years of age, it is reasonable to use what?

Answer 149

Question 150

# Top 10 take home messages * In adults 40 to 75 years of age evaluated for primary ASCVD prevention, have a clinician do what? * Risk discussion should include what?

Answer 150

Question 151

# Top 10 take home messages * In adults 40 to 75 years of age without diabetes mellitus and with LDL-C levels ≥70 mg/dL (≥1.8 mmol/L), at a 10-year ASCVD risk of ≥7.5%, start what? * Risk-enhancing factors favor what? * If risk status is uncertain, consider using what?

Answer 151

Question 152

# Top 10 take home messages * In adults 40 to 75 years of age without diabetes mellitus and 10-year risk of 7.5% to 19.9% (intermediate risk), what favors? * What does Risk-enhancing factors include ?

Answer 152

Question 153

# Top 10 take home messages * In adults 40 to 75 years of age without diabetes mellitus and 10-year risk of 7.5% to 19.9% (intermediate risk), What is favored? * Risk-enhancing factors include what?

Answer 153

Question 154

# Top 10 take home messages * Assess adherence and percentage response to LDL-C–lowering medications and lifestyle changes with what? * Define responses to lifestyle and statin therapy by what? * In ASCVD patients at very high-risk, triggers for adding what?

Answer 154

Question 155

What is normal, moderate, severe triglycerides?

Answer 155

* Normal: <150 mg/dL (1.7 mmol/L) * Moderate: 150 to 885 mg/dL (1.7 to 10 mmol/L) * Severe: >885 mg/dL (≥10 mmol/L)

Question 156

* Hypertriglyceridemia is common in what? * There were also racial and ethnic differences?

Answer 156

* Hypertriglyceridemia is common in clinical practice, with a prevalence of about 10 percent, depending on the population being studied. In individuals with established cardiovascular disease, the prevalence will be higher. * There were also racial and ethnic differences, with non-Hispanic African Americans having lower fasting TG levels than in non-Hispanic Caucasians and Mexican Americans.

Question 157

hypertriglyceridemia * Elevated fasting plasma TG levels are associated with what? * The risk of ASCVD events begins to rise above a TG level of what? * However, when levels of TG are adjusted for other related variables, what is the issue?

Answer 157

* Elevated fasting plasma TG levels are associated with atherosclerotic cardiovascular disease (ASCVD) burden and events such as myocardial infarction and stroke. * The risk of ASCVD events begins to rise above a TG level of 150 mg/dL (1.7 mmol/L). * However, when levels of TG are adjusted for other related variables (eg, components of the metabolic syndrome), the relationship is weakened if not absent. ## Footnote A causal relationship has not been established. Thus, levels of fasting or nonfasting TG are not included in ASCVD risk prediction models.

Question 158

What are the medications associated with hypertriglyceridemia

Answer 158

Question 159

What are some other causes of hypertriglyceridemia?

Answer 159

Question 160

Clinical Presentation of hypertriglyceridemia * Most patients with hypertriglyceridemia have what?

Answer 160

hypertriglyceridemia have no symptoms or signs associated with the biochemical abnormality.

Question 161

What are the exceptions to asymptomicatic hypertriglyceridemia patient?

Answer 161

* In patients with hereditary disorders, skin lesions such as eruptive xanthomas and xanthelasmas may be present. They also may exhibit lipemia retinalis or hepatosplenomegaly. * In patients with very high triglyceride levels (above 1000 mg/dL [11.3 mmol/L]), pancreatitis may develop. It should be kept in mind that the diagnosis of triglyceride-mediated pancreatitis cannot be made in the absence of chylomicronemia.

Question 162

What is xanthelasma? What is a xanthoma?

Answer 162

* A xanthelasma is a sharply demarcated yellowish collection of cholesterol underneath the skin, usually on or around the eyelids. * Strictly, a xanthelasma is a distinct condition, being called a xanthoma only when becoming larger and nodular, assuming tumorous proportions

Question 163

Lipemia retinalis * What is it?

Answer 163

Question 164

hypertriglyceridemia txt: * What is the txt?

Answer 164

Question 165

Answer 165

Question 166

Answer 166

Question 167

Answer 167

Question 168

Answer 168

Question 169

Answer 169