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Endocrine > Lipid Disorders - Exam 4 > Flashcards

Lipid Disorders - Exam 4 Flashcards

1
Q

What are lipids composed of? What are the two main lipids?

A

glycerol and fatty acids

main lipids: cholesterol and triglycerides

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2
Q

What is the role of cholesterol? Triglycerides?

A

essential element of all animal cell membranes and forms the backbone of steroid hormones and bile acids synthesis

assist in the transfer of energy into cells

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3
Q

What is the function of apolipoproteins? Where are they found? Where are they synthesized?

A

activate enzymes for lipoprotein metabolism and act as ligands for cell surface receptors

proteins found on the surface of lipids that

synthesized: liver and small intestine

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4
Q

Where is the primary source, lipoprotein association and function of the following: ApoB-48, ApoB-100, ApoC-I, ApoC-II, ApoC-III, ApoE

A
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5
Q

What are lipoproteins composed of? What is their role?

A

are complex molecules made up of lipids and apolipoproteins.

transporting cholesterol, triglycerides and fat-soluble vitamins to and from tissues

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6
Q

What is the core of a lipoprotein made out of?
What is the shell composed of?

A

core: hydrophobic liquid
triglyceride (aka triglycerols)
Free cholesterol
cholesterol esters (bound to free fatty acids)

shell: hydrophilic lipids
phospholipids
apolipoproteins (apo)

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7
Q

How are lipoproteins classified? How is that determined?

A

based on density

Density is determined by the presence of triglycerides and apolipoproteins

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8
Q

Which is more dense, triglycerides or apolipoproteins? What are the 5 types?

A

triglycerides are less dense; apolipoproteins are more dense

chylomicrons
VLDL - Very-low-density
IDL - Intermediate-density
LDL - Low-density
HDL - High-density

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9
Q

What are the 2 lipoprotein metabolic pathways? Give a short summary of each

A

Exogenous lipid pathway: absorption of dietary lipids and formation of chylomicrons

Endogenous lipid pathway: secretion of VLDL by the liver, transition to IDL and LDL

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10
Q

Exogenous pathways Step 1:

Dietary TG’s, cholesterol, fatty acids and retinol (vit. A) are absorbed in small intestine combined with _____ to form _____. They then pick up ____ and ____ from HDL and travel to the capillaries.

A

apolipoprotein (apoB-48)

chylomicrons

apoC

apoE

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11
Q

Exogenous pathways Step 2: These _____ are absorbed into capillaries where they are utilized in the _____ via ____. TG’s are broken down by ______ into FFA which can be converted to energy for use/storage in muscle and adipose tissue

A

chylomicrons

peripheral tissue

apoC

lipoprotein lipase (LPL)

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12
Q

Exogenous pathways Step 3: The ____ remnant then travels to the ____ where it is taken up via _____ with the help of ____. _____ is also lost in this process to another receptor

A

chylomicron

liver

LDL receptors (LDLR)

apoE

ApoB48

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13
Q

Endogenous Pathway Step 1: ____ and _____ are combined in the liver along with ____ to create VLDL

Step 2: ____ acquires apoE and ____ via transfer from ____molecules when leaving the ___

A

Cholesterol

triglycerides

apoB-100

VLDL

apoC

HDL

liver

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14
Q

Endogenous pathway Step 3: VLDL is utilized in the _____ as TG’s are broken down by ____ for energy (lipolysis) and now are referred to as _____

Step 4: 40-60% of ___ is taken up by the liver (via _____, the remaining IDL is further broken down by ____ during systemic circulation to form ____

A

peripheral tissues (apoC)

LPL

IDL

IDL

apoE and the LDLR

hepatic lipase (HL)

LDL

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15
Q

Endogenous pathway Step 5: 70% of the ____is removed from circulation by the liver _____ , the remaining 30% is used up by the ______.

Step 6: ____ removed from circulation by the ____ is broken down and the _____ is excreted in the bile

A

LDL

(via apoB & LDLR)

peripheral tissues (lipolysis)

LDL

liver

cholesterol

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16
Q

HDL: Immature HDL with ____ sees the macrophages full of ____ and “sweeps” up the ____ → HDL matures

A

ApoA1

LDL

excess LDL

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17
Q

Mature ____ can drop off ____ into peripheral tissues to create more ____ as well as take ____ from lower density lipoproteins

A

HDL

cholesterol

hormones

triglycerides

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18
Q

Finally, HDL can deposit _____ cholesterol in the ____ for breakdown/excretion and process starts over. What is an additional function of HDL?

A

“sweeped up”

liver

other functions of HDL include “donating”
apoproteins for lipid metabolism

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19
Q

What are some key differences between LDL and HDL?

A

LDL: bad
-deposits cholesterol in the blood vessel wall which build up can impede blood flow
-High level of cholesterol esters

HDl: good
-can “sweep” cholesterol out of the blood vessel keeping them clear of build-up
-Picks up cholesterol from peripheries to deposit into the liver
-High protein levels

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20
Q

Watch ninja nerd video included in the lecture about lipoprotein metabolism

A

DO IT!!

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21
Q

What are 4 pathways that lead to dyslipidemia

A
  1. Excessive hepatic secretion of VLDL
  2. Impaired lipolysis of triglyceride-rich lipoproteins
    chylomicrons and VLDL
  3. Impaired hepatic uptake of ApoB containing lipoproteins
    all lipoproteins except HDL
  4. Inherited low levels of HDL-C
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22
Q

**______ is one of the MC cause for dyslipidemia. Will fasting TG and HDL be high or low? What are some factors that increase VLDL secretion? **What is the major one?

A

Excessive Hepatic Secretion of VLDL

elevated fasting TGs
low HDL-C levels

factors:
Obesity
Insulin resistance
High-carb diet
**Nephrotic syndrome
ETOH use
Cushing’s Syndrome

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23
Q

_____ results from a dysfunction in lipoprotein lipase (LPL). What does TGs and HDL look like? What are 2 causes?

A

Impaired Lipolysis of Triglyceride Rich Lipoproteins aka impaired breakdown

elevated TGs
low HDL-C

**genetic disorder
insulin resistance

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24
Q

______ a down regulation of the LDL receptor (LDLR) in the liver leads to elevated serum LDL-C. What are some common causes?

A

Impaired Hepatic Uptake of ApoB Containing Lipoproteins

saturated fat intake reduces LDL activity
hypothyroidism
estrogen deficiency
chronic kidney and liver disease
**multiple drugs
thiazides, cyclosporin, carbamazepine
genetic disorders

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25
Q

_____ accelerated catabolism of HDL and its apoA. What are 3 causes?

A

Disorders of low HDL cholesterol

causes:
obesity
insulin resistance
genetic disorders

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26
Q

**How is dsylipidemia defined? What are 2 contributing factors? Increases risk for ______.

A

as elevated levels of LDL-C and triglycerides as well as low HDL aka due to increased LDL, more foam cells = increased risk of heart attack

genetics and environmental factors

increases risk for atherosclrotic cardiovascular disease (ASCVD)

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27
Q

patches on skin (MC -buttock) due to lipid deposition
yellow, pink, brown, or skin-colored
can be pruritic or painful

What am I?
What values are normally high?

A

Eruptive Xanthomas

extremely high chylomicrons (TG’s) or VLDL

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28
Q

_____ are lipid deposit nodules in the tendons of the hands, feet, and heel. What value is high?

A

tendinous xanthomas

seen with high LDL

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29
Q

_____ milky appearance of the veins and arteries of the retina. What value is high?

A

lipemia retinalis

extremely high triglycerides

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30
Q

Serum changes in the blood after it is drawn are due to high _____. Describe it

A

triglycerides

often look opalescent or milky serum

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31
Q

When do you start screening for ASCVD? What test do you order?

A

adults starting at age 20

or kids beginning at age 2 if family hx of early CVD or significant primary hypercholesterolemia

textbook answer: Total cholesterol (TC) and HDL (fasting sample is preferred but non-fasting is acceptable)

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32
Q

What are the indications if a full lipid panel should be ordered?

A

Total Cholesterol > 250
HDL-C is < 40
non-fasting may result in higher TG’s leading falsely elevated results

33
Q

**What are the normal ranges for : TC, LDL, HDL, TG. How long do they need to fast?

A

TC < 200 mg/dL
LDL < 100 mg/dL - UNLESS THEY HAVE EXISTING ASCVD!
HDL 40-59 mg/dL (> 60 mg/dL is cardioprotective)
TG’s < 150 mg/dL

9-12 hours prior to collection

34
Q

How often should you screen for hyperlipidemia?

A

~5 years for the average adult
3 years for lipid levels close to those warranting therapy - if they’re borderline
Annually for those on treatment

not a definitive answer! guideline only

35
Q

What are some secondary causes of hyperlipidemia?

A

hyperglycemia
nephrotic syndrome/chronic renal insufficiency
hepatitis/cholestasis
hypothyroidism

36
Q

What effect does oral contraceptives have on lipids? alcohol use?

A

increase triglycerides and total cholesterol

increased triglycerides and HDL due to carbs and sugar, liver dysfunction

37
Q

What are the 4 guidelines we need to consider about statin therapy?

A

clinical ASCVD
DM
LDL > or equal to 190mg
primary prevention with ASCVD risk of over 7.5%

38
Q

** What are the 6 risk factors for ASCVD?

A
  1. Tobacco use
  2. DM
  3. HTN
  4. Obesity (BMI ≥ 30)
  5. Family hx of premature heart disease
    55 y/o in males
    65 y/o in females
  6. Personal hx of CAD or non-coronary atherosclerosis: abdominal aortic aneurysm, peripheral artery disease, carotid artery stenosis
39
Q

**What are the 4 major ASCVD events that put you in the VERY high risk category? How many of the MAJOR event do you need to be considered VERY high risk?

A

ACS within past 12 months
History of MI (other than ACS above)
History of ischemic stroke
Symptomatic PAD

2+

40
Q

**What are the high risk conditions? What is the second way to be considered VERY high risk?

A

Age ≥ 65 years
CKD (GFR 15-59 mL/min)
Coronary bypass or percutaneous intervention
Current smoker
Diabetes
Hereditary Familial Hyperlipidemia
History of heart failure
Hypertension
LDL-C ≥ 100 mg/dL despite max tolerated statin + ezetimibe

1 of the major and 2+ of the high risk conditions to be very high risk

41
Q

When should you start high intensity versus moderate intensity statin therapy?

A

High intensity statin - Very high risk ASCVD or ≤ 75 years of age

Moderate intensity statin - Not “Very High Risk” and older than 75

42
Q

**What drugs (with dosages) are considered high-intensity statins? What percent do they lowered LDL? Which one has mild evidence to decrease existing plaque?

A

Rosuvastatin 20mg 40mg
Atorvastatin 40mg 80mg

greater than 50%

Rosuvastatin

43
Q

How much does moderate statin therapy decrease LDL? Low intensity? What are the low intensity statins with dosages?

A

Moderate: 30-49%

Low: 30%
Simvastatin 10mg
Pravastatin 10mg 20mg
Lovastatin 20mg
Fluvastatin 20-40mg

44
Q

What are the 2 goals of lipid management? How often should you monitor?

A

Reassess lipid panel after 4-12 weeks then every 3-12 months

45
Q

For a person WITHOUT ASCVD and LDL at or above 190? What is the tx? monitoring? goals?

A

tx: high intensity statin
Rosuvastatin 20mg 40mg
Atorvastatin 40mg 80mg

monitor: Reassess lipid panel after 4-12 weeks then every 3-12 months

goals:
Goal #1 - 50% reduction in LDL-C
Goal #2 - LDL-C of <100 mg/dL

46
Q

For a pt age 40-75 with DM and LDL 70-190, what is the protocol?

A

Step 1: Calculate an estimated 10-year ASCVD risk
Step 2: Review diabetes-specific high-risk features

47
Q

What is the ASCVD risk estimator calculator tool? What are the criteria?

A

Predicts 10-year risk for first ASCVD event among patients who are between 20 and 79 years of age

Sex, Age, Race
TC/HDL
SBP
Tx for HTN/DM
Smoking status

48
Q

Picking statin therapy for pts 40-75 with DM and LDL between 70-190 depends on what two factors? Do they have to have both or one?

A

ONE FACTOR

**10 year risk ≥ 7.5% or (+) Diabetes specific risk enhancers

know greater than or equal to 7.5% risk

49
Q

**Picking statin therapy for pts 40-75 with DM and LDL between 70-190 and the answer is YES! What is the tx? What are the 2 goals?

A
50
Q

**Picking statin therapy for pts 40-75 with DM and LDL between 70-190 and the answer is no. What is the tx? What are the 2 goals?

A
51
Q

For borderline pts between 40-75 without ASCVD or DM and LDL is between 70-189. What are the next steps?

A
  1. calculate ASCVD risk

tx depends on risk %

52
Q

**Aged 40–75 without clinical ASCVD or DM and whose LDL-C is between 70–189 mg/dL and ASCVD risk is between 7.5 and 19.9 need to consider _____. What is it? What do the results indicate?

A

measuring coronary artery calcium (CAC)

CAC - utilizes a low dose CT scan of the heart, assessing the amount of calcium plaque build up on the vascular walls. Score ranges from 0-400.

CAC ≥100 - consider adding statin
CAC 1-99 - consider adding statin if age ≥ 55 years
CAC score of zero - focus on lifestyle modifications
reassess in 5-10 years, indicates low 10-15 year risk

53
Q

What are the 3 lifestyle modifications? How long does it take to see an effect?

A

aerobic exercise

weight loss

diet changes

3-6 months

54
Q

**______ inhibit HMG-CoA, a key enzyme in cholesterol synthesis in the liver
increases the number of LDL receptors on the hepatocyte cell membrane. Where are they metabolized? What do you need to order before starting?

A

statins

in the liver

need to order baseline LFTs, 2-3 months after starting/changing dose and annually

55
Q

What is the MC SE of statins? What drugs have LESS likelyhood of SE?

A

Myalgias- normal CK
Myopathy/Rhabdomyolysis- with elevated CK

pravastatin and fluvastatin

56
Q

_____ occurs in those predisposed to DM and use of high intensity statin

A

hyperglycemia

57
Q

What are the CI to statin therapy?

A

active liver dz

preg and nursing mothers

58
Q

What is the effect of taking statin and CYP450 meds together?

A

worsening the SE of statins

59
Q

What if a pt cannot tolerate a statin or its not doing its job, then what?

A

try a different statin, fluvastatin, pravastatin - most likely to be tolerated but not as effective

2nd line: ezetimibe, PCSK9 inhibitors, bempedoic acid, inclisiran
3rd: -bile acid sequestrants, fenofibrate, niacin (kinda)

60
Q

______ : blocks appx 60% of dietary cholesterol absorption. Works best when ?? What does it NOT have an effect on?

A

Ezetimibe (Zetia)

works best in combo with statin

no effect on HDL or TG but statins do

61
Q

_____ monoclonal antibodies inhibit PCSK9 from binding to LDL receptors decreasing LDL receptor degradation and increasing LDL clearance. What is the route? Any CI?

A

PCSK9 Inhibitors
alirocumab (Praluent), evolocumab (Repatha)

injection q 2 weeks

no limitation in renal or liver impairment

62
Q

______ inhibits adenosine triphosphate-citrate lyase (ACL) inhibiting cholesterol synthesis in the liver.
increases the number of LDL receptors on the hepatocyte cell membrane
stimulates LDL catabolism. When it is commonly used?

A

Bempoic Acid (Nexletol)

Used as adjunct therapy when we need additional LDL reduction after maximally tolerated statin therapy

63
Q

bempoic acid/ezetimibe = ____. What is the effect? What are the SE? (includes just normal bempoic acid)

A

Nexlizet

synergistic effect with statins

gout/hyperuricemia, cold/flu s/s, tendon rupture, muscle spasms, abdominal pain

64
Q

_____ Blocks the production of mRNA needed for PCSK9 production resulting in less LDL. What is the route?

A

Inclisiran (Leqvio)

Injection day 1, then at 3 months, then q6m thereafter (must be in a clinical setting)

65
Q

_____ Binds bile acids in the intestines requiring the liver to excrete more bile. The liver uses hepatic cholesterol to make bile which results in the liver taking up more LDL-C from the systemic circulation. What % reduction in LDL? What is the pt education?

A

Bile Acid Sequestrants
cholestyramine, colestipol and colesevelam (Welchol)

10-24%

take it by itself NOT with other drug. take other drugs 1 hour before or 4 hours after bile acid sequestrants

66
Q

What is the preferred lowing lipid med for preg pts?

A

Bile Acid Sequestrants:
cholestyramine, colestipol and colesevelam (Welchol)

67
Q

**How do you define hypertriglyceridemia? **What is a complication?

A

Defined by a plasma/serum level >150 mg/dL

pancreatitits: triglycerides over 400

68
Q

what is the tx for pts older than 20 with triglycerides between 175-499?

A

treat underlying conditions
Avoid medications that worsen lipid levels
**Avoid refined carbohydrates, saturated and trans fatty acids
**Watch your “white” foods!
Avoid alcohol

69
Q

**When is statin therapy indicated for hypertriglycerdimia?

A

40-75 y/o with severe hypertriglyceridemia ≥ 500 mg/dL with an ASCVD risk of ≥ 7.5%

Severe hypertriglyceridemia >1000 mg/dL alone

70
Q

_____ stimulate LPL activity (enhances TG clearance from blood)
reduce apoC-III synthesis (enhances lipoprotein remnant clearance)
promote breakdown of fatty acids
may reduce VLDL-TG production
How much do they reduce TGs?

A

Fibrates: gemfibrozil (Lopid), fenofibrate (Trilipix, Tricor)

by 50% or more

71
Q

dyspepsia, increase risk of gallstones, myopathy, hepatotoxicity are all SE of _____

A

fibrates: gemfibrozil (Lopid), fenofibrate (Trilipix, Tricor)

72
Q

**What is a drug interaction of gemfibrozil (Lopid), fenofibrate (Trilipix, Tricor)? When do you need to be cautious?

A

Drug interaction: increases warfarin

caution in CKD pts: excreted by the kidneys - dose reduction required

73
Q

______ inhibit the release of TG’s from the liver (reducing VLDL). Stimulates LPL (increases clearance of TG’s from the plasma).

A

Omega 3 Fatty Acids

74
Q

Where are Omega 3 Fatty Acids naturally found? What dose is beneficial?

A

Naturally found in fish and flaxseed, OTC supplement

can reduce TG’s by 50% or more - requires up to 4 grams a day to be beneficial

75
Q

_____ stronger version of omega 3 fatty acid - contains >95% omega 3 fatty acids in comparison to 30-50% in OTC combinations

A

Vascepa (Icosapent ethyl)

expensive

76
Q

What is considered severe for a fasting triglyceride level?

A

TG greater than or equal to 500

elevated VLDL and chylomicrons

77
Q

______ inhibits breakdown of TG in adipose tissue. Increases LPL activity (increases clearance of TG’s). Inhibits synthesis of TG in liver (reduces VLDL secretion and subsequently LDL levels). Reduces clearance of apoA-I. What are the SE? What is a way to combat it?

A

Niacin

SE: niacin flush-> give ASA 81mg 30min prior to reduce flush
also raises uric acid levels- avoid with hx of gout

78
Q

_____ is approved for use in Europe for patients with genetically confirmed monogenic chylomicronemia but is not approved for clinical use in the United States.

A

APO C3 Inhibitor

79
Q
A

Endocrine (14 decks)

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