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Clinical Medicine 3 > Lecture 10 (HTN)-Exam 3 > Flashcards

Lecture 10 (HTN)-Exam 3 Flashcards

1
Q

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

A
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2
Q

What are the modifable RF?(6)

A
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3
Q

What are the relatively fixed risk factor?

A
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4
Q
A
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5
Q

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?

A
  • 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
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6
Q

BP is dx based on what?

A

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

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7
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A
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8
Q
A
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9
Q

What are out of office BP measurements used for?

A

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)

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10
Q
A
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11
Q

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

A

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

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12
Q

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

A
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13
Q
A
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14
Q
A

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

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15
Q

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

A
  • 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.
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16
Q
A

capsured more patients: shows patients are at risk

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17
Q

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

A

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

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18
Q

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

A
  • Remember some of your physiology pathways that regulate blood pressure
  • Sympathetic nervous system (fight or flight)
  • RAAS system
  • Blood volume
  • Genetics
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19
Q

Primary factors contributing to high blood pressure

A
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20
Q

What is the basic testing and optional testing for HTN?

A
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21
Q

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

A
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22
Q

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

A
  • Accounts for ~5% of cases
  • Secondary to potentially curable/treatable conditions (modifiable)
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23
Q

What are the causes of secondary hypertension?(9)

A
  • Medications
  • Intrinsic renal or renovascular disease
  • Sleep apnea
  • Hyperaldosteronism
  • Drugs, EtOH
  • Pheochromocytoma
  • Cushing’s
  • Coarctation of aorta
  • Hyper/hypothyroidism
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24
Q

Fill in for Causes of Secondary Hypertension

A
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25
Q

Who gets screened for secondary hypertension?

A
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26
Q

TOD indicates what?

A

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).

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27
Q

Screening tests for secondary hypertension

A
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28
Q

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?

A
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29
Q

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?

A
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30
Q

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?

A
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31
Q

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?

A
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32
Q

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?

A
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33
Q

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?

A
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34
Q

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?

A
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35
Q

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?

A
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36
Q

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?

A
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37
Q

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?

A
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38
Q

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?

A
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39
Q

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?

A
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40
Q

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?

A
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41
Q

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?

A
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42
Q

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

A
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43
Q

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

A
  • Chronic kidney disease
  • Peripheral arterial disease
  • Retinopathy, choroidopathy, optic neuropathy
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44
Q

Adequate blood pressure reduces the incidence of what (3)

A
  • Acute Coronary Syndromes by 20-25%
  • Stroke by 30-35%
  • Heart failure by 50%
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45
Q

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

A
  • Left ventricular hypertrophy, dysfunction (systolic and diastolic) and heart failure.
  • Arrhythmias (atrial fibrillation) MC
  • Coronary artery disease, Acute MI
  • Arterial aneurysm, dissection, and rupture.
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46
Q

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

A
  • 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)
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47
Q

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

A
  • Stroke, intracerebral and subaracnoid hemorrhage.
  • Cerebral atrophy and dementia
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48
Q

How does HTN have effects on the eyes (3)

A
  • Retinopathy, retinal hemorrhages and impaired vision.
  • Vitreous hemorrhage, retinal detachment
  • Neuropathy of the nerves leading to extraoccular muscle paralysis and dysfunction
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49
Q

What is this?

A
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50
Q

What is this?

A

AV nicking you see in HTN patients?

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51
Q

Fill in for the grades of HTN retinopathy?

A
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52
Q

Goals of treatments: Fill in

A
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53
Q

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

A

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

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54
Q

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

A

Starting medications and lifestyle modifications at 130/80 or above

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55
Q
A
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56
Q

10-year risk for ASCVD is categorized as what?

A
  • 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!
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57
Q

What is apart of the ASCVD Risk Estimator Plus ?

A
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58
Q

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

A
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59
Q

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

A
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60
Q

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

A
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61
Q

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

A
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62
Q

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

A

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

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63
Q

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

A

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

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64
Q

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

A

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

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65
Q

Fill in the HNC htn guidelines

A
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66
Q

Urgency versus emergency
* What is the difference?

A
  • 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
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67
Q
A
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68
Q

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

A
  • 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
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69
Q

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

70
Q

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

A

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)

71
Q

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?

72
Q

Dr. V slides?

What are the drugs that you can give for hypertensive emergency?

73
Q

Dr. V slides

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

74
Q
  • What is hyperlipidemia? Common or not?
  • Alternatively, a more objective definition describes hyperlipidemia as what?
A
  • 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.
75
Q
  • 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?
A
  • 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
76
Q

What is primary lipid disorders/hyperlipidemia?

A
  • Familial/hereditary
  • Genetically determined
77
Q

What is secondary lipid disorders/hyperlipidemia?

A

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

78
Q

What are the secondary causes of dyslipidemia?

79
Q

fill in for the types of lipid disorders/hyperlipidemia

80
Q

Lipid disorders potentiate what?

A

atherosclerotic disease

81
Q

What is the pathophysio of atherosclerotic disease?

A
  • 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.
82
Q

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?

A
  • 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.
83
Q
  • What is a slow process? What is a fast/sudden event?
  • Dyslipidemia present in over 70% of what?
A
  • 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!
84
Q

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

A
  • Fasting lipid profile
  • Identify risk factors predisposing patients to ASCVD
  • ASCVD risk calculators
  • Using these tools to determine treatment goals
85
Q

Who are we screening for dyslipid disease?

A
  • In general, adults over 20 years old, fasting lipid panel recommended
  • Younger if known hx of familial lipid disease
87
Q

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

A

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

88
Q

What are the five major lipoproteins in blood?

A
  • chylomicrons
  • very low density lipoprotein (VLDL)
  • intermediate density lipoprotein (IDL)
  • low density lipoprotein (LDL)
  • high density lipoprotein (HDL)
89
Q

Which class carries the majority of cholesterol and triglycerides?

A

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.

91
Q

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

A

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.

92
Q

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

A

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.

93
Q

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

A

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.

94
Q

What are Other ASCVD risk factors aside from ldl?

95
Q

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

A
  • Low-risk (<5%)
  • Borderline risk (5% to 7.4%)
  • Intermediate risk (7.5% to 19.9%)
  • High risk (≥20%)
96
Q

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 ?

A

This calculator helps predict the 10-year risk of the followinghardASCVD events:
* First occurrence of nonfatal myocardial infarction
* CHD death
* Fatal or nonfatal stroke

This calculator may overestimate riskand 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

97
Q
  • 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?
A
  • 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
98
Q

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

A
  • Methods to avoid occurrence of disease
  • Review lifestyle habits (e.g., diet, physical activity, weightor 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).
100
Q

Primary prevention of dyslipid

What are the three higher risk groups? what do you tx them with?

101
Q

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?

102
Q

dyslipid

For intermediate risk of ASCVD: What do you initate?

103
Q

dyslipid

Medical therapy will be determined by what?

104
Q

dyslipid

Secondary prevention

105
Q

dyslipid

For secondary prevention

107
Q

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?

108
Q

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

A

mod to high intensity statin

109
Q

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?

A
  • 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
110
Q

Where does statins work

112
Q

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

A

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.

113
Q

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

A

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

114
Q

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

A

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.

115
Q

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

A

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

116
Q

What are the SE of statins?

A
  • 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
117
Q

What are the RFs of SAMS?(7)

118
Q

how do you manage SAMS?

125
Q

LDL related ASCVD risk

126
Q

LDL related ASCVD risk

127
Q

Non-statin cholesterol lowering drugs

Bile acid sequestrants
* What is an example
* What is the MOA?
* What are the SE?

A
  • 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
128
Q

Non-statin cholesterol lowering drugs

Bile acid sequestrants
* Effects on plasma lipids?
* What happens to LDL?

129
Q

Non-statin cholesterol lowering drugs

Ezetimibe:
* What is the MOA?

A

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

130
Q

Non-statin cholesterol lowering drugs

Ezetimibe
* Effects on Plasma Lipids?
* LDL-C Lowering?

131
Q

Non-statin cholesterol lowering drugs

Bempedoic acid
* What is the MOA?
* What are the SE?

A
  • 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
132
Q

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

133
Q

Non-statin cholesterol lowering drugs

Niacin
* What is the MOA?
* What are the SE?(4)

A
  • MOA:Reduces hepatic secretion of VLDL
  • SE: Flushing, rash, raise plasma glucose, hepatic dysfunction, others
134
Q

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

135
Q

Non-statin cholesterol lowering drugs

MTP inhibitors
* Approved for treatment of what?
* What is the MOA?
* What are the SE?

A
  • homozygous familial hypercholesterolemia
  • MOA: Reduces hepatic secretion of VLDL
  • SE: Fatty liver
136
Q

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

140
Q

PCSK9 inhibitors
* Alirocumab and evolocumab: used for what?

A

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

141
Q

PCSK9 inhibitors
* Alirocumab used for what?

A

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

142
Q

PCSK9 inhibitors
* Evolocumab used for what?

A

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

145
Q

Top 10 take home messages

In all individuals, emphasize what? Why?

146
Q

Top 10 take home messages

In patients with clinical ASCVD, reduce what? How?

147
Q

Top 10 take home messages

In very high-risk ASCVD, use a LDL-C threshold of what? What should you consider?

148
Q

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?

149
Q
  • 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?
150
Q

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?
151
Q

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?
152
Q

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 ?
A
Top 10 take home messages
153
Q

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?
154
Q

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?
155
Q

What is normal, moderate, severe triglycerides?

A
  • 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)
156
Q
  • Hypertriglyceridemia is common in what?
  • There were also racial and ethnic differences?
A
  • 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.
157
Q

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?

A
  • 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.

A causal relationship has not been established. Thus, levels of fasting or nonfasting TG are not included in ASCVD risk prediction models.

158
Q

What are the medications associated with hypertriglyceridemia

159
Q

What are some other causes of hypertriglyceridemia?

160
Q

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

A

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

161
Q

What are the exceptions to asymptomicatic hypertriglyceridemia patient?

A
  • 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.
162
Q

What is xanthelasma? What is a xanthoma?

A
  • Axanthelasmais a sharply demarcated yellowish collection of cholesterol underneath the skin, usually on or around the eyelids.
  • Strictly, axanthelasmais a distinct condition, being called axanthomaonly when becoming larger and nodular, assuming tumorous proportions
163
Q

Lipemia retinalis
* What is it?

164
Q

hypertriglyceridemia txt:
* What is the txt?

Clinical Medicine 3 (27 decks)

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