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NUTR 344 > Dislipidemias > Flashcards

Dislipidemias Flashcards

1
Q

What is the changes in CVD prevalence in Canada in the last decade?

A
  • 40% ↓ in mortality from CVD due to
  • Improvements in control of CVD risk factors and medical management of patients with CVD, less invasive surgeries
  • New clinical data available → may enhance prevention and management of CVD
  • Despite these improvements, CVD remains a major societal burden - still very prevalent, but the mortality has decreased
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2
Q

Role of the Cardiovascular System

A

– Regulates blood flow to tissues

  • Delivers oxygenated blood and nutrients
  • Retrieves waste products

– Thermoregulation

– Hormone transport

– Maintenance of fluid volume

– Regulation of pH

– Gas exchange

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3
Q

Major Forms of Cardiovascular Disease

A
  • Hypertension
  • Atherosclerosis
  • Coronary heart disease (CHD)- also know as cardiac disease-> affects artery of the heart
  • Peripheral vascular disease

– Cerebrovascular disease (stroke)

– Deep vein thrombosis- mainly in the lower part of the leg

• Congestive heart failure- can lead to cardiac cachexia

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4
Q

Atherosclerosis definition

What does it result it?

A

Thickening of the blood vessel walls caused by presence of atherosclerotic plaque – Results in restriction of blood flow

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5
Q

What are the conditions associated with Atherosclerosis

A
  • Myocardial infarction (MI)- clot in the artery, or just restricted artery
  • Cerebrovascular accident (CVA; stroke)
  • Peripheral vascular disease (PVD)
  • Coronary heart disease (CHD)
  • Congestive heart failure (CHF) when severe CHD or MI occurs
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6
Q

Atherosclerosis – Pathophysiology

A
  • Complex and incompletely understood process
  • Involves endothelial cells, smooth muscle cells, platelets, and leukocytes
  • Begins as a response to endothelial lining injury that results in an inflammatory process
  • Results in restriction of arterial blood flow
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7
Q

When do the symptoms of Atherosclerosis develop?

A

Asymptomatic until it progresses to ischemic heart disease

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8
Q

What are the steps of Formation of the atherosclerotic plaque

A

increase in LDL to HLD ratio-> increased risk of atherosclerosis LDL particles bind to LDL receptors in the epithelial cells

Superoxide anion will act upon trapped LDL monocytes contact with arterial wall and monocyte enters the sub-endothelial space

‘Monocytes differentiate into macrophages and take up oxidized LDL-> intracellular accumulation of cholesterol and foam cell formation

Macrophages activate T cell which produce inflammatory chemicals-> increased inflammatory responses

Cytokines are also being released-> more inflammation

Growth factors attract smooth muscle cells

Smooth muscles cells migrate to the sub-endothelial cells and differentiate

Free cholesterol is released into entima

Cytokines stimulate smooth muscle cell proliferation and collagen is made-> fibrous gap

Smooth muscle cells can accumulate lipids and can turn int smooth muscle derived foam cells -> plaque blood vessels grow into the plaque

Calcium salts are attracted to the plaque, leading to calcification and hardening of the plaque

This plaque cna then rapture and release it’s contents-> can lead to thrombosis

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9
Q

Potential primary causes of atherogenesis

A
  • High blood pressure
  • Chemicals from tobacco
  • Oxidized LDL
  • Glycated proteins-

!!chronic!! hyperglycaemia such as in Diabetes e.g. glycated Hb; these glyctaed proteins induce stress on arterial walls

  • Decreased nitric oxide (NO)- NO is produced within our cells and has vasodilation effect less No-> smaller arterial radius
  • Angiotensin II- causes vasoconstriction all these factors can lead to Damage to the endothelial wall
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10
Q

What is a biochemical biomarker of atherosclerosis? What are the levels?

A

CRP is a biomarker fo atherosclerosis; people with CVD have slightly elevated values of CRP (low grade inflammation): below 10, more than 3-> different from acute inflammation

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11
Q

Atherosclerosis – Risk Factors

A

A lot overlap with HTN •

Risk factors have an additive effect

  • Family history - Especially a first-degree relative — a parent, sibling or child — who experienced a heart attack or stroke or developed peripheral artery disease at a relatively young age
  • Age and sex – More prevalent over the age of 65 and in men - estrogen is protective against atherosclerosis - post-meonpausal women show increase in CVD occurence
  • Obesity – Positively associated with dyslipidemia, hypertension, physical inactivity, and diabetes
  • Hypertension – May initiate an atherosclerotic lesion – Can also cause plaque to rupture
  • Physical inactivity (can be reversed)
  • Diabetes mellitus
  • Impaired fasting glucose/metabolic syndrome (aka pre-diabetes)
  • Cigarette smoke
  • Obstructive sleep apnea as there’s a lack of oxygen being delivered to cells and cause endothelial damage
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12
Q

What is the age/sex demographic that experiences hihger risk of CVD?

A

More prevalent over the age of 65 and in men

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13
Q

What is obesity associated with such that there’s increased risk of atherosclerosss?

A

Positively associated with dyslipidemia, hypertension, physical inactivity, and diabetes

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14
Q

How is atheroscleorsis connected with hypertension?

A

Hypertension may initiate an atherosclerotic lesion

– Can also cause plaque to rupture

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15
Q

how is Obstructive sleep apnea connected to atherosclerosis?

A

less oxygen in developed to cells-> can result in cell damage

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16
Q

Major risk factors for atherosclerosis- organized by non-reversible/reversible characteristic

A
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17
Q

WHat are the cut-offs for low HDL-C levels?

Can they be reversed?

A

<1.0 mmol/L men

<1.3 mmol/L women

Can be reversed

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18
Q

Where can chylomcirons be formed and what do they contain?

A

Can be formed by the intestinal cells only

Carriers of ingested fat

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19
Q

What are chylomicrons made of?

A

Chylomicrons: the core is mostly TG, some CE and non-esterified cholesterol on the surface of the chylomicron

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20
Q

Surface of all lipoproteins is made of _-

A

Surface of all lipoproteins is made of phospholipids

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21
Q

Where are chylomicrons released into?

A

lymph, not blood!!

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22
Q

What is the role of LPL and where is it found?

A

on the lining of our vessels we have LPL-> will hydrolyze TG into FA and glycerol to be taken up by the cells (mainly taken up by adipose cells)
`

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23
Q

Whtat happens to the chylomicron as it circualtes around the body?

A

It’s TGs content gradually gets depleted by LPL-> > chylomicron remnant will have less TG in proportion to more of cholesterol esters

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24
Q

What is the activator LPL?

A

ApoC-II

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25
Q

What will occur to the chylomicron remnant in the end? WHat is the next step?

A

will be taken up by the liver and degraded

TGS from the diet and endogenous sources will be repackaged into VLDL

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26
Q

What are the sources of TGs in VLDL

A

both exogenous and endogenous

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27
Q

Chylomicron vs VLDL

A

Chylomicrons and VLDL particles each contain surface apolipoprotein-B (apoB). Chylomicrons are assembled primarily in the intestine and contain a smaller version, apoB-48, whereas VLDL particles contain the larger apoB-100 surface protein and are primarily assembled in the liver.

Chylomicrons only have exogneous fats; VLDL as both enogenous and exogenous

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28
Q

What happens to VLDL as it circulates

A

VLDL will circulate into tissues, will exchange with HDL (cholesterol from HDL, TGs to HDL)
LPL will be activated by ApoC-II on the VLDL-> hydrolysis of TGs occurs-> FA are taken up by tissues
VLDL remnant will be created -> less TGs, more CE (similar to chylomicrons)
VLLD receptors found in the liver and other tissues (e.g. endothelium) will recognize this VLDL remnant, and will take it up

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29
Q

What are the 2 fates of VLDL?

A
  • Most of circulating VLDL will be picked up by the receptors through the recognition of ApoE
  • The rest will be recognized by hepatic lipase found in the liver-> will continue to degrade TGs in the core of VLDL remnant-> LDL will be created (has mostly cholesterol esters, vert little TGs)
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30
Q

__ is responsible for the inverse transport of cholesterol - from tissue to liver

A

HDL is responsible for the inverse transport of cholesterol - from tissue to liver

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31
Q

maturation of HDL:

A

When they are secreted, they are secreted as nascent HLD- not a globular particle yet-> have an empty core- phospholipid layer wiith ApoA-I and ApoE attached to it
as it circulates-> will accumulate cholesterol in the core
Cholesterol will Be esterified in CE by LCAT-> will become a globular HDL2 particle

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32
Q

WHat is CETP and it’s function?

A

CETP (cholesterol ester transfer) step
Cholesterol-ester transfer protein - will transfer CE from HDL to VLDL; TGs from VLDL to HDL

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33
Q

LPL results in chylomicron remnants

A

__ results in chylomicron remnants

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34
Q

Overview of Endogenous and Exogenous Cholesterol Transport

A
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35
Q

LDL can be picked up by __

A

LDL can be picked up by both liver and extra-hepatic tissues

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36
Q

Characteristics of chylomicrons

Lipid type + apo proteins

A
  • More TG in the core,
  • B-48, E, A-I, A-IV, C-II, C-III
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37
Q

Characteristics of VLDL

Lipid type + apo proteins

A
  • B-100, E, C
  • More TG
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38
Q

Characteristics of LDL

Lipid type + apo proteins

A
  • Mostly CE
  • B-100
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39
Q

Characteristics of HDL

Lipid type + apo proteins

A
  • mostly PL, CE
  • A-I, A-II, C, E
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40
Q

Cut-offs for normal total cholesterol levels

A

< 5.2 mmol/L

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41
Q

Cut-offs for normal HDL-C levels

A

The higher the better (has protective properties)

1-1.5 mmol/l

>1.0 men

>1.3 women- women tend to have higher levels of HDL->thus higher recommendations

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42
Q

Cut-offs for normal LDL-C levels

A

<2.6 mmol/L

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43
Q

Cut-offs for normal TG levels

A

<1.7 mmol/L

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44
Q

Which components are measured in Plasma Lipoprotein levels lab tests

A

these 4 are obtained in routine measurements for lipid profiles
Total cholesterol
LDL
HDL
TG

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45
Q

Apoproteins: Functions

A

Synthesis/secretion of specific lipoproteins

Stabilize surface coat of lipoproteins

Activate enzymes (e.g. apo C-II activates LPL)

Interact with cell surface receptors (B-100 and LDL receptors)

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46
Q

What is the primary determinant of metabolci fate of lipoproteisn

A

apoproteins

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47
Q

What are the aporproteins serve as markers/diagnostics of?

A
  • Reflect changes in lipoprotein composition
  • Indicative of # of lipoproteins in plasma (concentration)
  • Apoprotein levels maybe better predictors of heart disease than lipid levels and may correlate with the severity of the disease
  • Aid in diagnostic of lipoprotein disorders and risk for developing CHD or CVD
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48
Q

which market is now being used to measure lipid profile?

A

ApoB

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49
Q

Relative frequency of genotypes of Apo-E

A

ApoE has different has 3 allleles

ApoE 2 is the least common, ApoE 3 is the most common

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50
Q

What is the influence of Apo E-2/E-2 on VLDL?

A

Apo E-2/E-2 does not bind to LDL receptorsà↑ VLDL remnants

marker of increased risk of displipidemia as ApoE-II cannot bind to LDL receptor-> VLDL that has ApoE-II will remain in the circulation-> resultign in high levels of VLDL in the circulation

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51
Q

ApoE-4 is associated with an increased risk of_

A

ApoE-4 is associated with an increased risk of Alzheimer

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52
Q

What are the 2 categories of Dyslipidemia Classification?

A

primary and secondary

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53
Q

Primary vs secondary dislipidemia causes

A

Primary: single or poly-genetic abnormalities affecting lipoprotein function resulting in hyperlipidemia or hypolipidemia

Secondary: environmental causes +/- predisposition

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54
Q

Primary vs secondary dislipidemia- which is more common?

A

secondary

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55
Q

Primary vs secondary dislipidemia- when do they occur?

A

primary -> happens early in life (due to genetic bases)
secondary -> happens later in life

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56
Q

What is diagnosis of primary dyslipidemia based on?

A

• History (age at onset, family members,…)

  • Physical signs (e.g. xanthomas- happen mostly at joints and elbows )
  • Lab analysis: lipid profile, apoproteins, LPL activity
  • Appearance of serum
  • Genetic sequencing for rare cases
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57
Q

Synonym for pirmary Dyslipidemias

A

Familial

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58
Q

Name hypolipoproteinemias

A

– Abetalipoproteinemia

– Familial hypobetalipoproteinemia

– Familial alpha-lipoprotein deficiency (Tangier disease)

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59
Q

Describe Abetalipoproteinemia

A
  • Defect in apoprotein B synthesis-> no ApoB is made
  • No chylo, VLDL, LDL formed and TGs accumulate in liver and intestine
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60
Q

Describe Familial hypobetalipoproteinemia

A

some ApoB is made, but lower than needed-> Lower LDL levels

• LDL concentration is 10-50% of normal but chylomicron formation occurs

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61
Q

Describe Familial alpha-lipoprotein deficiency (Tangier disease)

A
  • Virtual absence of HDL (Apo-AI), CE accumulate in tissues
  • Chylo, VLDL, LDL are all normal
  • Moderate hyperTG
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62
Q

Are Hyperlipoproteinemias or Hyporlipoproteinemias more common

A

Hyperlipoproteinemias

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63
Q

I-

  • Name
  • CVD risk-
  • Main lipoprotein affected
  • Serum lipids-
  • Main symptoms-
  • Specific marker-
A
  • Hyperchylomicronemia
  • CVD risk- 0
  • Main lipoprotein affected- Chylomicrons (↑ chylo fasting)
  • Serum lipids- ↑↑ TG (>11 mM vs the norm of ,1.7mmol/L), ↓HDL-C
  • Main symptoms- early, skin xanthomas, pancreatitis, lipemia retinalis, hepatosplenomegaly
  • Specific marker- absence or deficiency of LPL or apo C-II
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64
Q

IIa –name

  • CVD risk-
  • Main lipoprotein affected-
  • Serum lipids-
  • Main symptoms-
  • Specific marker-
A
  • Hypercholesterolemia
  • CVD risk- +
  • Main lipoprotein affected- ↑LDL-C TG: N or H
  • Serum lipids- high LDL
  • Main symptoms- vascular diseases xanthelasma (eye)
  • Specific marker- Mutation of LDL receptor or polygenic
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65
Q

IIb –name

  • CVD risk-
  • Main lipoprotein affected-
  • Serum lipids-
  • Main symptoms-
  • Specific marker-
A
  • Combined hyperlipoproteinemia
  • CVD risk- +++
  • Main lipoprotein affected- ↑LDL and VLDL ↑apo-B
  • Serum lipids- ↑Chol (8-15 mM) and ↑TG (2-11 mM); ↓HDL-C
  • Main symptoms- Variable, vascular diseases
  • Specific marker- Mutation of LDL receptor or apo B
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66
Q

III –name

  • CVD risk-
  • Main lipoprotein affected-
  • Serum lipids-
  • Main symptoms-
  • Specific marker-
A
  • Dysbetalipoproteinemia
  • CVD risk- +++
  • Main lipoprotein affected- ↑ b-VLDL; ↑LDL and VLDL
  • Serum lipids- ↑Chol (by a lot) and ↑TG (significant increase); ↓HDL-C
  • Main symptoms- Tuberoeruptive and palmar xanthomas
  • Specific marker- Apo E2/E2
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67
Q

IV –name

  • CVD risk-
  • Main lipoprotein affected-
  • Serum lipids-
  • Main symptoms-
  • Specific marker-
A
  • Hypertriglyceridemia
  • CVD risk- +
  • Main lipoprotein affected- High VLDL
  • Serum lipids- ↑TG (4.5-11 mM) ↓HDL-C
  • Main symptoms- Similar to I; Exacerbated by alcool and diabetes
  • Specific marker-
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68
Q

V-name

CVD risk-

Main lipoprotein affected-

Serum lipids-

Main symptoms-

Specific marker-

A
  • mixed hyperlipidemia
  • CVD risk- n/a
  • Main lipoprotein affected- high VLDL and chylomicrons
  • Serum lipids- ↑↑TG (very hihg); ↓HDL-C
  • Main symptoms- Similar to I; Exacerbated by alcool and diabetes
  • Specific marker-serum aspect: chylo band over VLDL
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69
Q

Serum patterns of hyperlipoproteinemia

A

I- Hyperchylomicronemia (lot’s of chylomicrons)-> band of TGs, milky appearance
IIA high LDL, less TGs- normal looking serum
IIB- TGs accumulation from high VLDL-> pale colour
III- Beta VLDL accumulation causes white band due to TGs; also a paler color
IV- mixed typed, high VLDL -> white
V- white-> mixture of VLDL and chylomicron

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70
Q

Secondary dyslipidemia may exacerbate __

A

• May exacerbate primary dyslipidemia

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71
Q

Effects on Tot-Chol, LDL-C, HDL-C, TG

of a diet high in CH

A

Increased Tot-Chol,

Increased LDL-C,

Same HDL-C

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72
Q

Effects on Tot-Chol, LDL-C, HDL-C, TG

of a diet high in saturated fat

A

Inceased Tot-Chol,

Icnreased LDL-C,

Increased HDL-C- that’s why saturated fats are actually not that critically bad

TG-> same

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73
Q

Effects on Tot-Chol, LDL-C, HDL-C, TG

of a diet high in trans fat

A

Increased Tot-Chol,

Increased LDL-C,

Decreased HDL-C

TG-> same

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74
Q

Effects on Tot-Chol, LDL-C, HDL-C, TG

of a diet high in sugars

A

Same total CH and LDL-C

Decreased HDL-C

Inceased TG

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75
Q

Effects of alcohol, smoking and lack of physical activity n lipid profiles

A

Alcohol increases HDL-C and TG

Smoking- increases or doesn’t affect Tot CH and LDL-C, but decreases HDL-C

Physical inactivity decreases HDL-C and increased TG

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76
Q

Effects of diabetes, hypothyrodism, renal failure, obesity, choleastasis, cirrhosis, myelomas, cushings sndrome on lipid profiles

A
  • increase total Chol is increased by diseases , but have varied effects of HLD and LDL
  • All diseases increase Total CH, but have different impacts on HDL and LDL
  • mostly increase TG
  • mostly decrease HDL
  • Cushing’s, hypothyroidism and diabetes increase LDL-C, which is the most atherogenic-> will increase the risk of CVD
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77
Q

Effects of

thiazide diuretics, beta-blockers, corticosteroids, estrogens, progesterone, benzodiazepine, retinoic acid, antiretroviral drugs on lipid profiles

A

Most of the drugs, apart form progesterone increase TG

Thiazide diuretics elevate all the markers, but maybe HDL-C ( can either elevate or leave unchanged)

Retinoic acid increase all the markers, but HDL-C (it decreases HDL-C)

Corticosteroids elevate all the markers

Estrogens increase HDL-C and TG and lower the others

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78
Q

Why is there an increased substrate flux to the liver in both postprandial and postabsortive states in obesity

A

Postprandial:

  • Due to excess calories (lipids and carbohydrates)
  • Most commonly there’s an increased substrate flux to liver observed in obese individuals as people with excess weight tend to eat more, especially CHO and fat

Postabsorptive

  • Due to high adipose tissue and hormone-sensitive lipase (HSL) activity (because of insulin resistance) resulting in increased FFA flux to liver (situation of insulin resistance is commonly seen in obesity)
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79
Q

Affect of alcohol on TG is nthe circulation

A

when ethanol is present-> excess alcohol-> blockage of oxidation of Acyl-Coa-> promotion of conversion of Acyl-CoA into TGs-> increases TGs in circulation due to alcohol presence

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80
Q

What are the 3 intake factors that need to be regualted in individuals with dislipidemia

A

diet high in sugar, fat and alcohol contributes to TGs elevation in circulation
to manage lipid levels-> manage these factors

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81
Q

What hapens when there’s excess fatty acid and CHO intake and how can it lead to Hypertriglyceridemia of Obesity

A

having excess fatty acid and CHO coming to the liver-> will lead to excess LDL production
this results in more lipolysis by LPL and uptake of TGs into tissues and their storage->
increase in fat and body weight
if increased lipolysis levels by the liver equal to increased level of fat production, LDL levels can still be normal
thus not all obese people will have elevated LDL levels (this is still however accompanied by higher fat stores)

Hypercholesterolemia of Obesity:

  1. The increase in overproduciton is higher than the chnages in lipolysis (absence of lypolitic effect)
    this can be due to e.g. problems with LPL-> no lipolytic effect on VLDL and TGs-> accumulation of LDL and TGs in the circulation
    2.
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82
Q

Hypercholesterolemia of Obesity

A

starts with excess total calories (either from fat or sugar)-> overproduction of VLDL
increase in lipolysis, creating VLDL remnant and being converted into LDL
the problem is at the uptake of LDL particles due to reduced activity of LDL receptors-> LDL accumulation
there are many reasons for them to be effected: e.g. diet high in saturated fat and CH
results in VLDL particle accumulation in the circulation -> Higher LDL-C

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83
Q

Possible mechanisms for HDL-cholesterol lowering in obesity

A

this has to do with higher production of VLDL-TG and increased transfer of CH form HDL to VLDL; and increase TG transport from VLDL to HDL
This results in a decrease in HDL-C
this will result in an increased catabolism of HDL by excess adipose tissue and increased uptake by the liver-> decreased HDL levels

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84
Q

Both the severity (high BMI) and distribution (abdominal) obesity are associated with low __

A

Both the severity (high BMI) and distribution (abdominal) obesity are associated with low HDL-C

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85
Q

The connection of BMI and HDL-C/LDL connection

A

– Inverse linear relationship between BMI and HDL

– Stronger association of BMI with HDL than LDL

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86
Q

Abdominal fat/totoal fat and HLD connection

A

– Stronger association with HDL than total body fat

– Stronger association in men and post-menopausal women: as accumulation of visceral fat is mostly seen in men and PM women

• e.g. 5 times more likely to have low HDL with high visceral fat

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87
Q

Possible mechanisms of reduced HDL-C in obesity

A

– Association with hyperTG:

More VLDL-> more transfer of CE from HDL; TG from VLDL ->

HDL will become richer in TGs than CE-> this will trigger hepatic lipase (which usually recognizes VLDL)-> will recognize TG-rich HDL and hydrolyse those TG-> this will stimulate HDL particle uptake by the liver-> decreased HDL levels

But not the only mechanism, also:

– ↑ uptake of HDL2 by adipocytes

– ↑ clearance of apolipoprotein A-1-> HDL catabolism

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88
Q

Who to screen?

A
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89
Q

What are the screeening tests used for everyone?

A
  • History and physicla exams
  • Standard lipid panel (TC, LDL-C, HDL-C, TG)
  • Non HDL-C ( non-HDL= Total CH-HDL-C (includes all lipoproteins that are not HDL)
  • Glucose- as diabetes is such an important factor for CBD, glucose levels are also measured
  • eGFR- to have and indication of renal problems, as it’s a big risk factor
    *
90
Q

How is LDL-C calculated?

A

LDL-C is calculated by difference (LDL-C= TC-HDL-C), there’s no specific measure for LDL-C

91
Q

FAsting vs non-fasting lipid measures

A

non-fastign are ok as well

92
Q

How often shoudl a cardiovascular risk assessment be completed?

What are the acceptable methods?

A
  • cardiovascular risk assessment be completed every 3 to 5 years for men and women age 40 to 75.
  • A risk assessment may also be completed whenever a patient’s expected risk status changes.
  • Options include using the 10 Year Risk (Framingham Model) or Cardiovascular Age (Cardiovascular Life Expectancy Model).
  • the results should be shared with the patient to support shared decision making and improve the likelihood that they will reach lipid targets
93
Q

What are the risk factors the FRS is based on?

A

diabetes, smoking, systolic blood pressure, total cholesterol, HDL-C, Age are the most important CVD factors-> included into the tool

94
Q

What does the 2nd step of FRS determine?

A

the 10-year CVD risk

95
Q

what is the modified Framingham Risk Score?

A

Double cardiovascular disease risk percentage for individuals between the ages of 30 and 59 without diabetes if the presence of a positive history of premature cardiovascular disease is present in a first-degree relative before 55 years of age for men and before 65 years of age for women.
This is known as the - this takes family history into account-> brings the risk into a high zone, thus family history is a very strong risk factor

96
Q

What does step 3 of FRS determine?

A

the heart age

97
Q

What are the FRS cut-offs for high, intermediate and lwo

A

High >20%

Intermediate: 10-19%

Low <10%

98
Q

WHat are Statin-indicated conditions?

A
  • Clinical atherosclerosis*
  • Abdominal aortic aneurysm
  • Diabetes mellitus Age ≥ 40 years
  • Chronic kidney disease (age ≥ 50 years) eGFR 3 mg/mmol
  • LDL-C ≥5.0 MMOL/L
99
Q

What are the pirmary target (LDL-C)

A

• ≤2 mmol/L or ≥50% decrease in LDL-C (Strong, M

100
Q

What is the Apo-B level which would signal to initiate treatment?

A

equal to or above 1.2g/L

101
Q

What are the Statin-indicated Conditions?

A
  • Clinical atherosclerosis*
  • Abdominal aortic aneurysm
  • Diabetes mellitus (age ≥40; 15 yrs duration for age ≥30 yrs (DM1); Microvascular disease)
  • Chronic kidney disease
  • LDL-C ≥5.0 MMOL/L (tipically indicates familiar hyperlipidemia as this is very high)
102
Q

What is the 1st line of treatment for hyperlipidemias?

A

statins

103
Q

Describe Primary Prevention Conditions

high risk vs intermediate risk

A

Meds can be considered to prevent the development of CVD

104
Q

WHen are meds not prescribed

A

For low risk: when FRS <10%

105
Q

What is presribed all the time for hyperlipidemia treatment, no matter what si the risk level?

A

the base of the treatment is the lifestyle change- diet and PA
add meds to it, if needed

106
Q

What are the alternative criteria of blood biomarkers to LDL-C?

A

Non-HDL-C and apo-B as alternate targets to LDL-C

107
Q

Describe Lp(a)

A

Lp(a)- small and dense, very atherogenic; not measured routinely; but are part of non-HDL-c, thus this is the benefit of measurign non-HDL-c instead of LDL-C

108
Q

How are LDL-c and ApoB measured?

A

LDL-C: Calculated from standard Lipid Profile

ApoB: Measeured separately

109
Q

Are the meds that target HDL levels?

A

no

110
Q

What is the FRS % for high risk level

When woudl we initiate therapy at this risk level?

What are the primary target?

Alternate target?

A
  • High- FRS ≥20%
  • Consider treatment in all
  • Primary traget: <2 mmol/L or >50% decrease in LDL-C
    • Consider <1.8 mmol/L if coronary disease (2016)
  • Alternate target: Apo B <0.8 g/L or
    • Non-HDL-C <2.6 mmol/L
111
Q

What is the FRS % for intemediate risk level

When woudl we initiate therapy at this risk level?

What are the primary target?

Alternate target?

A
  • Intermediate: FRS 10-19%
  • Initiate theraphy if: LDL-C ≥3.5 mmol/L
    • For LDL-C <3.5 mmol/L consider if: Apo B ≥1.2 g/L OR Non-HDL-C ≥4.3 mmol/L
  • Primary target: <2 mmol/L or >50% decrease in LDL-C
  • Alternate target: Apo B <0.8 g/L or; Non-HDL-C <2.6 mmol/L
112
Q

What is the FRS % for low risk level

When woudl we initiate therapy at this risk level?

What are the primary target?

Alternate target?

A

Low: FRS <10%

Initiate therapy if LDL-C ≥5.0 mmol/L; Familial hypercholesterolemia

Primary target: >50% decrease in LDL-C

Alternate target: N/A

113
Q

As VLDL circulates in blood, it picks up __ and additional __ donated from high-density lipoprotein (HDL)

A

As VLDL circulates in blood, it picks up apolipoprotein C-II (apoC-II) and additional apoE donated from high-density lipoprotein (HDL)

114
Q

Metabolic Fate of chylomicrons

A
115
Q

Metabolic fate of HDL

A
116
Q

What are the benefits of moderate (2-7kg) weight loss for lipid profiles?

A
  • ↓ LDL-C by 0.1 mmol/L initially, variable afterwards
  • ↓ HDL-C by 0.03 mmol/L during loss, then ↑ by 0.04 mmol/L during maintenance
  • ↓ TG by 0.07 mmol/L- bounces back after some time after the weigth loss

the higher the weight loss-> the bigger the impact

117
Q

PA effects on lipid profiles

A

Variable effects- exercise mostly affects TGs (lowers), impacts HDL a bit
no impact of exercise on LDL levels
additive effects of diet

– At exercise levels of 1200-2200 kcal/week:

  • ↓ TG by 4-37%
  • ↑ HDL-C by 2-8%
  • ↓ LDL-C by 0-7%

– Improvements accentuated with weight loss

  • it’s more the volume and time that has the benefit

– Volume/intensity of exercise has greatest benefits (kcal spent) – Resistance exercise has little effect
– Modest exercise can prevent deterioration

118
Q

Relationship between increases in cholesterol in diet and rises in serum cholesterol levels

A

Almost linear relationship between dietary CH and increase in serum CH

119
Q

What are the key ideas form predictive Equations of Effects of Diet on Serum Total Cholesterol

A

equations to predict the change in serum cholesterol based on the amount of CH in the diet and saturated and unsaturated fats

  • > amount of saturated fat in the diet minus the % of Polyunsaturated Fatty Acids + Dietary Cholesterol predicts the serum CH levels
  • *saturated fat has the highest influence, not the cholesterol**

From this equation developed concept of ideal P:S ratio >1- more poly vs saturated fat should be consumed

120
Q

Limitations of Predictive Equations

A
  • Different SFA have different effects
  • Predicts total cholesterol only – not lipid fractions which is not entirely true
  • Assumes MUFA and carbohydrates are neutral
  • Effects on total cholesterol may not be linear
121
Q

What was the fundament of mediterannean diet?

A

Create from the 7 country study- Crete is an outlier in the Mediterranean-> high serum cholesterol, but low mortality-> the origin of Mediterranean diet

122
Q

Describe lipid profile response to dietary CH

A

– Compensators (2/3) vs non- (1/3)

Compensators: high CH intake-> less is produced endogenously no regulation -> effect of dietary CH will be greater

– Effect less pronounced in humans vs. other primates

– 100 mg/d decrease in dietary cholesterol results in 0.05-0.2 mmol/L decrease in total-C not significant

Less of an effect on raising blood cholesterol than saturated fats, BUT may be significant in some individuals

123
Q

What is the main effect of Cholesterol consumption?

A

Decreased activity of LDL receptors

Also CH content of chylomicrons will increase due to increased amount of CH in the diet-> more atherogenic chylomicrons

124
Q

Dietary Cholesterolo independent mechanisms

A

– Decreased synthesis and activity of hepatic LDL receptors

– Increased cholesterol in chylo and chylo remnants-> more atherogenic and increased chol delivery to liver

– Increased cholesterol in VLDL and VLDL remnants-> more atherogenic

– Interferes with ability of HDL to clear cholesterol

125
Q

cholesterol content is __ proportional to fat content

A

cholesterol content is not directly proportional to fat content

126
Q

WHich organ has the highest conent of CH? FIsh?

A

brain

shrimp

127
Q

Recommendations for fat intake

Are we consuming the recommended amounts?

A

25-35% of calories is goal – also helps to reduce total calorie and saturated fat intakes

Current intake in North America: 34-37% of total kcal; it’s more the quality that matters, not the quantity

128
Q

What is the effect of very low-fat diet on lipid profiles?

A

• Very low-fat diet may decrease HDL-C, in addition to lowering LDL

129
Q

Mechanisms of action of diets rich in saturated FA

A

restricted synthesis and activity of LDL receptor (ApoB activated)-> decreased clearance of LDL from the diet-> increased circulatory levels

Also decreased clearance of VLDL by decreased activity of VLDL receptor (ApoE activated)

130
Q

How do saturated Fatty acids decrease the activity of LDL receptor?

A

By:

– Decreasing transcription of LDL receptor gene

– Altering PL composition of cell membranes to decrease binding -> decreased LDL clearign from concentration

more saturated fat as a part of phospholipid membrane-> more rigid membrane-> can alter LDL bindign capacity to the receptor

– Altering LDL itself and delays binding to receptors

131
Q

Goal saturated FA intake vs the actual intake

major sources?

A

Goal was less than 10% of total calories - no such recommendations in the new canadian food guide as by following the recommendations, you wil stay below the target

  • Average intake in Canada is about 10% of energy
  • Major sources (US): highly processed foods, processed meats, baked goods (cakes, cookies, donuts), pizza, cheese, ice cream.
132
Q

What are the impacts of trans fatty acid consumption?

A
  • Increase LDL-C, similar to saturated fats, but reduce LDL size (more atherogenic)
  • Reduce HDL-C
  • May ↑inflammatory markers and endothelial damage
133
Q

What are the reasons and sources of trans fats

A

Occur as a result of partial hydrogenation.

Food Sources: hard margarines, partially hydrogenated oils used in many foods, small amounts in dairy (which may not have the same effects)

134
Q

Are EPA and DHA essential?

A

EPA and DHA are not considered essential as we produce them, but at a very low reate

135
Q

Omega 3 fatty acids formulas

A

Linolenic acid- 18:3w3

Eicosapentaenoic acid(EPA)- 20:5w3

Docosahexaenoic acid (DHA)- 22:6w3

136
Q

Omega-6 PUFAs effects on lipid profiles

A
  • Passive increase in LDL and VLDL clearance by counteracting the suppressive effect on LDLR of SFA (similar to that of CHO and oleic acid)
  • Decrease in HDL

High intakes of omega-6

  • When intake is above 10% it may lead do decreased HDL-C and/or decreased ApoA-I
  • Increased risk of inflammation, oxidative damage to LDL and possibly cancer
137
Q

HDL is associated with__

A

HDL is associated with Apo-AI

138
Q

What can high PUFA intake also lead to?

A

– Inflammation (cancer risk?- not proven yet), increased oxidative damage to LDL, increased oxidative stress

  • increased oxidation and inflammation results in increased risk of atherosclerosis
139
Q

GOAL for PUFA intake? Is it achievable?

A

Goal is 5-10% of calories- achievable

140
Q

PUFA food sources?

A

corn, sunflower, safflower, soybean oils, walnuts, sunflower seeds

141
Q

Intake goal for Mono-unsaturated (MUFAs)

A

Goal is no more than 20% of total calories – assuming a lower saturated fat intake

142
Q

Effect of PUFA vs oleic acid on HDL-C

A

Compared to PUFA, oleic acid does not lower HDL-C

143
Q

SF vs oleic acid effect in LDL-C

A

Compared to saturated fats (C:12 – C:16) oleic acid lowers LDL-C

144
Q

MUFAs can lower LDL-C withoiut lowering HDL-C but what is a downside fo them?

A

MUFAs are often consumed with saturated fats

145
Q

MUFA food sources

A

Food sources: olive and canola oils, peanuts, meat and poultry

146
Q

MUFA effect on lipid profile

A
  • Compared to SFA, oleic acid lowers LDL-C; compared to PUFAs and CHOs, MUFAs do not lower HDL
  • Enhance clearance of VLDL and LDL
  • MUFAs are also less susceptible to oxidation, compared to PUFAs
147
Q

Which type of FA is typical for mediterannean diet>

A

MUFA

148
Q

WHat are the advantages of MUFA?

A

– Do not decrease HDL as does PUFA and carbohydrates, thus it’s better to replace SFA with MUFAs rather than CHOs

– Less susceptible to oxidation than PUFA
– Do not increase triglycerides as carbohydrates often do

– Do not increase cancer risk as high PUFA intakes could

149
Q

What is high oleic oil? Name examples

A

High oleic oil is any oil that is high in monounsaturated fats

  • Sunflower seed oil
  • Safflower oil
  • Soybean oil
150
Q

Dietary Sources of Linoleic Acid

A

Safflower oil

Soybean oil

Sunflower seed oil

Corn oil

151
Q

Dietary Sources of Oleic Acid

A 
Olive oil
Canola oil (rapeseed)

Peanut oil

Avocados

Nuts

152
Q

Name 3 types of Omega-3 PUFAs

A

EPA: eicosapentanoic acid (fish)
DHA: docosahexanoic acid (fish)
ALA: Alpha-linolenic acid (canola, linseed, soybean oil)

153
Q

Effects of omega-3 PUFAs on TGs

A
  • Decrease TG in hyperlipidemic and hyperTG patients
    • May reduce risk of mortality in those with CVD (but not in those people who don’t have CVD)
154
Q

Are omega-3 supplements recommended to reduce CVD events?

A

CCS recommendations do not promote use of omega-3 PUFA supplements to reduce CVD events

155
Q

Omega-3 effect on LDL and VLDL

A
  • Do not reduce the number of VLDL particles being secreted by the liver but rather decrease the TG content of these particles
  • Omega-3 PUFAs do not lower LDL-C concentrations except as their PUFA replace SFA in the diet
156
Q

beneficial effects of Omega-3 intake (non-lipid profile related)

A
  • Omega-3 PUFAs interfere with platelet aggregation and thereby prevent coronary thrombosis; delay proliferation of fibroblasts
  • Reduce plaque formation and growth as they reduce adhesion molecules
157
Q

Dietary fiber recommendations and benefits

A
  • Goal is 20-30 g/day; about 50% of which should be as soluble fiber is better at preventing CH absorption by creating a gel in the intestine
  • Soluble fibers decrease total-C and LDL-C – may be dependent on initial level of hypercholesterolemia- the higher the initial level, the higher the decrease

Higher fiber intakes usually results in lower energy and fat intakes

158
Q

CHO intake effect on lipid profile levels + disadvanatges of CHO diet

A
  • Overproduction of VLDL-TG especially if excess sucrose, fructose, or high-fructose corn syrup
  • Decrease HDL-C levels linked to the transfer of TGs from HLD and LDL

Decreased synthesis and activity of LDL receptors

Chylomicrons accumulate more cholesterol and become more atherogenic

Increased Cholesterol delivery to the liver

Increased VLDL and LDL remnants-> more atherogenic

Interferes with the ability of HDL to clear cholesterol

all of this doesn’t apply if the diet is rich in complex CHO

159
Q

Alcohol effect on lipid profiles

A
  • Elevates HDL-C
  • Red wine in particular may inhibit cell-mediated oxidation of lipoproteins – due to resveratrol (polyphenol) NOT alcohol –FRENCH PARADOX
  • Alcohol inhibits acylCoA oxidation in liver: avoid completely if hypertriglyceridemia
160
Q

Alcohol consumption recommendations

A

OK if consumed in moderation: 1-2 drinks/d

Consumption of alcohol not specifically recommended especially for those with established CHD

HyperTG and familial hyperTG alcohol should be avoided at all as it increases TGs

161
Q

Beneficial impacts of soy protein + mechanism

A

Reduces TC, LDL-C, and TG without an effect on HDL-C in patients with or without CVD

Due to isoflavones and phytoestrogens, other?

162
Q

US health claim about soy

A

25 grams of soy protein, as part of a diet low in saturated fat and cholesterol, may reduce the risk of heart disease Also in Canada since 2015.

163
Q

What are the recommednations for soy intake?

A

Optimal level not yet established

164
Q

Name antioxidants and their imapcts in relation to CHD

Is supplementation recommended?

A

Vit C, E, β-carotene

May inhibit LDL oxidation thereby decreasing atherosclerosis risk

Supplementation with these vitamins is inconclusive ->

165
Q

Vitamin E supplements and CHD risk

A

– Benefits in 3 studies
– No effect in 5 studies
– Deleterious effects in 1 study

166
Q

diet deficient in Folate and B6 is a risk factor for __, which increases the risk for __

A

diet deficient in Folate and B6 is a risk factor for Hyperhomocysteinemia, which increases the risk for CVD

167
Q

What are the normal fasting levels of monocysteine?

Which levels increase the risk of CVD?

A

Normal: 6-12 umol/L

Increased: >14 umol/L

168
Q

What is the prevalence of Hyperhomocysteinemia

A

1:70

169
Q

Is b12 deficiency related to Hyperhomocysteinemia?

A

no

170
Q

Each increase of __ of fasting concentrations increases the incidence of CVD by __ fold

Elevated homocysteine levels appear in up to __ of patients with CVD

A

Each increase of 5 umol/L of fasting concentrations increases the incidence of CVD by 1.6-1.8 fold

Elevated homocysteine levels appear in up to 40% of patients with CVD

171
Q

Low levels of _- especially are associated with high homocysteine levels

A

Low levels of folate especially are associated with high homocysteine levels

172
Q

WHat are the recommednations for folate levels? Supplements?

A

Recommendations: to increase food sources of folates

Supplement only in persons with high levels or family history of

CVD: 500 μg folate/day (once B12 deficiency is ruled out )

173
Q

Food sources of folate

A

fortified cereals, vegetables, citrus fruits/juices, legumes, organ meats

174
Q

Phytosterols

Effect on lipid profiles

Fortiifcation benefits

A
  • Equivalent to plant cholesterol
  • Compete with cholesterol absorption: increase fecal excretion
  • Diet enriched with 2-2.5 g sterols/stanols reduced LDL-C by 6- 14%
  • This amount is almost impossible to obtain from normal foods: fortified margarines are the main source
175
Q

WHat are Nuts good sources of?

A
  • Rich in mono- and polyunsaturated FA, most low in SFA
  • High in plant protein, soluble fibers, folic acid, antioxidants, arginine (NO precursor)
176
Q

recommended nut intake for CHD reduction/lipid profiles

A

High intake (30-60 g/d) reduces risk of CHD,

moderate intake reduces LDL-C and improves endothelial function

177
Q

What is Dietary approach for dyslipidemia based on?

A

Based on global cardiovascular risk (Framingham)

178
Q

What is the first target of Based on global cardiovascular risk (Framingham)?

A

LDL-C, then factors of the metabolic syndrome

179
Q

What is the TLC model for dyslipidemia

A

TLC model = therapeutic lifestyle changes

  • Decrease saturated fats and dietary cholesterol
    • Step I: <10% SFA and <300 mg cholesterol
    • Steps II and III: <7% SFA and <200 mg cholesterol
  • Increase physical activity
  • Weight managment to reduce coronary risk
180
Q

Dietary recommendations for of dyslipidemia- both NCEP III and Canadian guidelines

A
181
Q

What are the characterstics of mediterranean diet?

A

– high in oleic acid (olive oil)

– high in fruits, vegetables, legumes

– high in fish, low red meat, moderate dairy (mostly cheese and yogurt)

– regular but moderate wine consumption

182
Q

What are the results of mideterannean diet?

A

– Primary prevention:

  • PREDIMED trial: 30% ↓ in CV events, favorable lipid profile compared to low fat diet: ↓ LDL-C, apo-B and TG, ↑HDL-C
  • Other studies: additive effects to statins, ↓ inflammatory markers, favors weight loss, 25% ↓mortality (highest effect on mortality by a diet)

– Secondary prevention: Lyon Study: 70% ↓mortality post-MI (people who had a CV event-> prevention of second CV)

183
Q

What are the characteristics of portfolio diet?

A
  • low in saturated fats
  • vegetarian
  • high in phytosterols (1 g, margarine), soy protein (21 g), soluble fibers (10 g), almonds (14 g) (all/1000 kcal)
184
Q

results of portfolio diet

A

– ↓ 29% in LDL-C vs. 31% with low-fat diet +statins vs. 8% low-fat diet, ↓CRP vs. low-fat diet, under controlled conditions

– In a clinical study: ↓13% in LDL-C in portfolio intensive vs. 13% in portfolio routine vs. 3% in diet low in SFA. 11% ↓ in FRS.

– But adherence to portfolio diet is low: about 40-45%

185
Q

CCS Guidelines 2016- Dietary recommendations

A
  • advice about healthy eating and activity and adopt the Mediterranean dietary pattern to lower their CVD risk
  • omega-3 PUFA supplements should not be used to reduce CVD events
  • avoid the intake of trans fats and decrease the intake of saturated fats for CVD disease risk reduction: replace saturated fats with polyunsaturated fats emphasizing those from mixed omega-3/omega-6 PUFAs and target an intake of saturated fats of <9% of total energy. If saturated fats are replaced with MUFAs and carbohydrates, then choose plant sources of MUFAs (e.g. olive oil, canola oil, nuts, and seeds) and high-quality sources of carbohydrates (e.g. whole grains and low glycemic index carbohydrates)
  • All should be encouraged to moderate energy intake to achieve and maintain a healthy body weight and adopt a healthy dietary pattern to lower their CVD risk:
186
Q

Accordign to CCS Guidelines 2016-dietary recommendations what are healthy dietary patterns?

A

– Mediterranean dietary pattern other healthy diet patterns are OK as well

– Portfolio dietary pattern

– DASH dietary pattern fruits, veggies, fiber, enough protein

– Dietary patterns high in nuts (≥ 30 g/day)

– Dietary patterns high in legumes (≥ 4 servings/week)

– Dietary patterns high in olive oil (≥ 60mL/day)

– Dietary patterns rich in fruits and vegetables (≥ 5 servings/day)

– Dietary patterns high in total fibre (≥ 30 g/day) and whole grains (≥ 3 servings/day)

– Low-glycemic load (GL) or low-glycemic index (GI) dietary patterns

– Vegetarian dietary patterns

187
Q

Dietary goals for treatment of severe hyperlipidemia and hypertriglyceridemia- blood levels and diet therapy

A
188
Q

Factors that increase HDL-C

A
  • Saturated fats
  • Dietary cholesterol
  • Alcohol (less or euqal to 2 drinks daily)

not linked to diet:

  • Long-term aerobic exercise program
  • Estrogens
  • Female sex
189
Q

Factors that decrease HDL-C

A

Diet-related: Simple sugars/high carb diet; high intake of Polyunsaturated fat; Obesity

non Diet-related: Androgens, Male sex, Anabolic steroids, Some antihypertensive drugs, Diabetes mellitus, Cigarette smoking

190
Q

Statins

Predicted effect

Mechanism

A

Main predcited effect: decrease in LDL-C (18-55%)

Also: decrease in TG (17-30%), decrease in HDL-C (5-15%)

Mechanism: Block cholesterol synthesis; increases LDL receptor mediated removal

191
Q

Cholesterol absorption inhibitors

Drug examples

Predicted effect

Mechanism

A
192
Q

What are the main drugs used for hyperlipidemia and hypertriglyceridemia treatment; what are the other drugs

A

Main drugs for hyperlipidemia: statins, Cholesterol absorption inhibitors

Others: Bile acid sequestrants (BAS), PCSK9 inhibitors

Drugs for hypertriglyceridemia treatment: Fibrates, Nicotinic acid

193
Q

Bile acid sequestrants

Drug names

Predicted effect

Mechanism

A
194
Q

PCSK-9 inhibitors

Drug names

Predicted effect

Mechanism

A
195
Q

FIbrates

Drug names

Predicted effect

Mechanism

A

For use in highly elevated TG (familial hyperTG)

196
Q

Nicotinic acid

Drug names

Predicted effect

Mechanism

A

It hihg dose of Vit B5, higher than can be obtained from the diet

197
Q

What is the rational for use of statin for 1st line of treatment?

A

Meta-analysis of statin trials show: 1mmol/L decrease in LDL-C-> 20 to 25% rr reduction

198
Q

Are statins generally well-tolerated?

What are the side effects?

A
  • Generally well-tolerated
  • Adverse effects: myalgia (muscle pain) and myopathy, increased liver enzymes and low risk of diabetes (liver enzymes should be monitored semi-annually)

It is imporant to check for normal liver function

199
Q

Statins- food and drug interactions

A

Simvastatin: interaction with grapefruit juice

Vitamins, minerals or supplements for myalgia should not be used

200
Q

Approach to Risk Management

A
  1. Always start with lifestyle changes: smoking cessation, diet and excercise
  2. Based on the conditions, prescribe statins to achieve the target of LDL-C <2.0 mmol/L or >50% reduction
  3. Isthe target is acieved on the max tolerated dose:
    1. Yes-> monitor for 3-4 month
    2. No-> Discuss add on therapy
201
Q

What are the statin add-on therapy?

A

Primary prevention conditions: first add on is ezetimibe (most accessible and least side-effects) or BAS as an alternative

High risk of statin-indicated conditions: ezetimibe (BAS as an alternative); PCSK9 inhibitors as 2nd line

202
Q

Ezetimibe

  • Mechanism
  • When is it prescribed
  • Possible side effects and contrinidcation
A
  • Mechanism: decreases intestinal absorption of cholesterol
  • Recommended as second-line Tx in patients with clinical CVD and targets not reached by maximal statin dose
  • Possible side effects: diarrhea, rash, fatigue, muscle weakness or pain
  • Contra-indications: liver disease or failure
    • most medications are metabolized in the liver and kidneys-> has to be kept in mind if there are related conditions
203
Q

Bile Acid Sequestrants (cholestyramine)

  • Mechanism
  • effects on lipid profile
  • Side effects
  • contradicitons
A
  • Mechanism: bind bile acids in the GI tract and prevents their reabsorption
  • Combined with diet, a dose of 20-24 g/day may reduce total cholesterol by 20% and LDL cholesterol by 30%
  • May increase VLDL-C and VLDL –TG transiently (3-4 weeks)
  • May decrease absorption of fat and liposoluble vitamins, Ca, Fe, Zn, Mg (chelating agents can also increase this effect of meds)
  • Side effects: significant constipation -> pain and hemorrhoids
  • Contraindications: existing hemorrhoids, peptic ulcer, hiatus hernia, multiple drug use, extensive travel, hypertriglyceridemia
204
Q

How is PCSK9 administred?

A

injection

205
Q

When are PCSK9 inhibitors recommended?

A

Recommended for primary (familial) hypercholesterolemia with high LDL-C despite maximal statin dose

206
Q

PCSK9 inhibitors side effects

A

diarrhea, muscle or joint pain, bruising around injection site

207
Q

Triglycerides: recommendation for treatment

A
  • No specific target level for high-risk
  • Lower triglyceride levels are associated with decreased CVD
  • risk
  • Health behavior interventions are first-line (diet + PA)
  • Fibrates may prevent pancreatitis in patients with extreme hypertriglyceridemia (>10 mmol/L)
208
Q

HDL-C: recommendation for treatment

A

Low HDL-C may pose no risk, depending on genetic type

Medications may not increase HDL-C to a clinically significant extent

Health behavior interventions increase HDL-C

209
Q

When are fibrates not recommended

Side effects, contraindications

A
  • Not recommended to add to statin for CVD prevention when target has been reached
  • Side effects: GI reactions (taste changes, abdominal pain), muscle toxicity
  • Contraindications: hepatic or renal dysfunction, gallbladder disease, combination Tx with simvastatin
210
Q

Nicotinic acid

What is it used for and what is the dose

A

Used for primary hypercholesterolemia and/or hypertriglyceridemia, and hypoalphalipoproteinemia

• Dosage of 3-6 grams/day

211
Q

Can nicotinic acid be used with statins?Not recommended as add-on to statins

A

Not recommended as add-on to statins

212
Q

Nicotinic acid side effects and contrindications

A
  • Side effects: only 50-60% tolerate nicotinic acid: GI distress, skin flushing and itching, hepatotoxicity, arrhythmias
  • Contraindications: active peptic ulcer, hepatic disease, gout, hyperuricemia
213
Q

Statins- safety and monitoring

A

Well-tolerated

Most common side- effects:

  • Myopathy
  • GI distress

• Semi-annual liver enzyme

monitoring recommended

214
Q

Niacin- safety and monitoring

A
  • May elevate ALT and/or blood glucose levels
  • Extended-release niacin is better tolerated
  • ASA 325 mg 30-60 min before niacin attenuates flushing
  • Small risk of hepatotoxicity
  • Monitor uric acid levels
  • Semi-annual follow-up`recommended
215
Q

Fibrates- safety and monitoring

A
  • May cause reversible increases in plasma creatinine
  • Monitor renal function and lipid parameters → avoid in renal insufficiency or dose adjust
216
Q

What is cardiac cachexia?

A

Cardiac cachexia is a condition that can happen to people who have heart failure. It means you lose a serious amount of body fat, muscle, and bone.

217
Q

LCAT found on __ converts HDL into __

A

LCAT found on the surface of endothelium converts HDL into IDL

218
Q

Which SFA increase LDL-C?

A

– Lauric: may increase HDL-C more, thus ↓LDL/HDL ratio

– Myristic

– Palmitic: may ↑LDL-C only in presence of high dietary cholesterol

219
Q

Benefits of replacing SFA with CHO for CVD

A

no benefit on CVD risk

220
Q

What shoudl SFAs be substitued with? Why?

A

When 5% of energy from SFAs is substituted by PUFAs-> 10% reduction in CVD risk (but no effect on mortality risk)

Replacing SFA with carbohydrates-> no benefit on CVD risk

Replacing SFA with MUFAs and PUFAs -> improved lipid profile and reduced CVD risk

221
Q
A
222
Q

NCEP III vs Canadian guidelines for treatmetn of dyslipidemia

A

NUTR 344 (22 decks)

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