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Pharmacology > Management of Hyperlipidemia > Flashcards

Management of Hyperlipidemia Flashcards

1
Q

What are the 3 types of lipids?

A

(1) Cholesterol
(2) Triglycerides
(3) Phospholipids

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2
Q

Cholesterol

  • A ________, primary component of cell _______
  • Precursor for _____ acids which are required for _____ absorption
  • Precursor for ______ steroids (aldosterone, others)
  • Precursor of _____ hormones (estrogens, androgens)
  • 40 - 60% of cholesterol is _________, the rest comes from diet
A
  • A STEROID, primary component of cell MEMBRANES
  • Precursor for BILE acids which are required for FAT absorption
  • Precursor for ADRENAL steroids (aldosterone, others)
  • Precursor of SEX hormones (estrogens, androgens)
  • 40 - 60% of cholesterol is ENDOGENOUS, the rest comes from diet
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3
Q

Triglycerides

  • Composed of 3 _________ esterified to a single molecule
  • Free fatty acids are used as ______ sources
  • Triglycerides in the body are provided by ______ fats and _______ conversion of carbohydrates
A
  • Composed of 3 FATTY ACIDS esterified to a single molecule
  • Free fatty acids are used as ENERGY sources
  • Triglycerides in the body are provided by DIETARY fats and HEPATIC conversion of carbohydrates
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4
Q

Phospholipids

  • Lipid containing __________ acid residues in addition to fatty acids and ______
  • Major component of cell ________
  • Play a role in single __________ in nerve tissue
A
  • Lipid containing PHOSPHORIC acid residues in addition to fatty acids and ALCOHOL
  • Major component of cell MEMBRANES
  • Play a role in single TRANSDUCTION in nerve tissue
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5
Q

Lipoproteins

  • Cholesterol and triglycerides are _____phobic — cannot be transported through polar substance (i.e. ________) alone
  • Lipoproteins are globular particles of high molecular weight that are…
    - used to transport ______ lipids t/o the body
    - Composed of a _______ lipid core consisting of triglycerides and cholesterol esters surrounding by a _______ surface of phospholipids, free cholesterol and apoproteins
A
  • Cholesterol and triglycerides are HYDROPHOBIC — cannot be transported through polar substance (i.e. BLOOD) alone
  • Lipoproteins are globular particles of high molecular weight that are…
    - used to transport NON-POLAR lipids t/o the body
    - Composed of a NON-POLAR lipid core consisting of triglycerides and cholesterol esters surrounding by a POLAR surface of phospholipids, free cholesterol and apoproteins
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6
Q

What are the 6 types of lipoproteins?

A

(1) Chylomicrons
(2) Very low density lipoproteins (VLDL)
(3) Intermediate Density Lipoproteins (IDL)
(4) Low Density Lipoproteins (LDL)
(5) High Density Lipoproteins (HDL)
(6) Apolipoproteins

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7
Q

Chylomicrons

  • Formed in ________, transport dietary fat to ________ cells and ________
  • Composition = > 90% _________, 2% ___________
  • Role in disease: taken up by cells of the _______ wall, utilizing macrophages /c the end result of generation of ______ cells
A
  • Formed in INTESTINE, transport dietary fat to PERIPHERAL cells and LIVER
  • Composition = > 90% TRIGLYCERIDES, 2% CHOLESTEROL
  • Role in disease: taken up by cells of the VESSEL wall, utilizing macrophages /c the end result of generation of FOAM cells
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8
Q

Very Low Density Lipoproteins (VLDL)

  • Transport endogenous cholesterol from _______ to _______
  • Composition: 60 - 70% ________; 12% __________
  • Role in disease: Uncertain. There is an ________ relationship btw TG rich lipoprotein concentrations (VLDL and IDL) and HDL
    - it is thought that atherogenicity is more a function of low ______ as opposed to high _______
A
  • Transport endogenous cholesterol from LIVER to PERIPHERY
  • Composition: 60 - 70% TRIGLYCERIDES; 12% CHOLESTEROL
  • Role in disease: Uncertain. There is an INVERSE relationship btw TG rich lipoprotein concentrations (VLDL and IDL) and HDL
    - it is thought that atherogenicity is more a function of low HDL as opposed to high VLDL
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9
Q

Intermediate Density Lipoproteins (IDL)

  • Intermediate product of hydrolysis of ______ by lipases
  • Composition: Cholesterol esters and __________
  • Not though tot be contributory to _________
A
  • Intermediate product of hydrolysis of VLDL by lipases
  • Composition: Cholesterol esters and TRIGLYCERIDES
  • Not though tot be contributory to DISEASE
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10
Q

Low Density Lipoproteins (LDL)

  • Generated from further “_________” of IDL
  • Composition: _____ cholesterol content, ______ triglycerides (accounts for _____% of cholesterol in blood)
  • Role in Disease: major class of lipoproteins attributable to _________ disease
A
  • Generated from further “DELIPIDIZATION” of IDL
  • Composition: HIGH cholesterol content, LOW triglycerides (accounts for 60 - 70% of cholesterol in blood)
  • Role in Disease: major class of lipoproteins attributable to ATHEROSCLEROTIC disease
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11
Q

High Density Lipoproteins (HDL)
- ________ cholesterol form the peripheral tissue for transport back to the liver for conversion into ______
- Composition: 45% _________, 25% ____________, 25% ____________
Role in disease: _____________ (removes ________ from foam cells in atherosclerotic lesions)
- Often referred to as “______ cholesterol” –> the ________ the better

A
  • REMOVES cholesterol form the peripheral tissue for transport back to the liver for conversion into BILE
  • Composition: 45% PROTEIN, 25% PHOSPHOLIPIDS, 25% CHOLESTEROL
    Role in disease: PROTECTIVE (removes CHOLESTEROL from foam cells in atherosclerotic lesions)
  • Often referred to as “GOOD cholesterol” –> the HIGHER the better
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12
Q

Apolipoproteins

  • Provide __________ stability to lipoproteins and serve as ________ for enzymes
  • Role in Disease: apolipoprotein is a ________ like protein that is thought to increase risk of __________ heart disease
A
  • Provide STRUCTURAL stability to lipoproteins and serve as CO-FACTORS for enzymes
  • Role in Disease: apolipoprotein is a PLASMINOGEN like protein that is thought to increase risk of CORONARY heart disease
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13
Q
  • High level of oxidized LDL cholesterol –> _______ formation in the walls of arteries –> atherosclerosis
  • HDL cholesterol is able to _________ cholesterol from the atheroma
  • Atherogenic cholesterol —> _______, _______, ______
A
  • High level of oxidized LDL cholesterol –> ATHEROMA formation in the walls of arteries –> atherosclerosis
  • HDL cholesterol is able to REMOVE cholesterol from the atheroma
  • Atherogenic cholesterol —> LDL, VLDL, IDL
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14
Q

Causes of Hyperlipidemia

  • Diet
  • Hereditary
  • Hypothyrodism
  • Anorexia
  • Obesity
  • Diabetes _________
  • Pregnancy
  • ____________ liver disease
  • Acute ________
  • _________ syndrome
  • Systemic lupus ____________
  • __________ inhibitors
  • Atypical _________
A
  • Diet
  • Hereditary
  • Hypothyrodism
  • Anorexia
  • Obesity
  • Diabetes MELLITUS
  • Pregnancy
  • OBSTRUCTUIVE liver disease
  • Acute HEPATITIS
  • NEPHROTIC syndrome
  • Systemic lupus ERYTHEMATOUSUS
  • PROTEASE inhibitors
  • Atypical ANTIPSYCHOTICS
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15
Q

2014 NLA Guideline Summary

  • Places patients into risk categories based upon various factors such as: ASCVD, ASCVD risk factors, Diabetes, Baseline LDL-C
  • Provides target lipoprotein goals based upon risk categories
    - Low/mod/high:
A
  • Places patients into risk categories based upon various factors such as: ASCVD, ASCVD risk factors, Diabetes, Baseline LDL-C
  • Provides target lipoprotein goals based upon risk categories
    - Low/mod/high: <130 non-HDL-C; < 100 LDL-C; < 90 Apo B
    - Very high: <100 non-HDL-C; < 70 LDL-C; < 80 Apo B
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16
Q

Lifestyle Modifications

  • Heart healthy _______
  • Regular ________
  • ________ cessation
  • Maintenance of a healthy __________
A
  • Heart healthy DIET
  • Regular EXERCISE
  • SMOKING cessation
  • Maintenance of a healthy WEIGHT
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17
Q

What are the 4 Dietary Sources of Cholesterol?

A

(1) Monounsaturated
(2) Polyunsaturated
(3) Saturated
(4) Trans

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18
Q

What source of cholesterol comes from…

- Olives, olive oil, canola oil, peanut oil, cashews, almonds, peanuts and most other nuts; avocados

A

Monounsaturated

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19
Q

What source of cholesterol comes from…

- corn, soybean, safflower and cottonseed oil; fish

A

Polyunsaturated

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20
Q

What source of cholesterol comes from…
- Whole milk, butter, cheese, and ice cream; red meat; chocolate; coconuts, coconut milk, coconut oil, egg yolks, chicken skin

A

Saturated

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21
Q

What source of cholesterol comes from…
- most margarines; vegetable shortening; partially hydrogenated vegetable oil; deep-fried chips; many fast foods; most commercial baked goods

A

Trans

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22
Q

Effects of Monounsaturated Cholesterol

  • Lowers ______
  • Raises _______
A
  • Lowers LDL

- Raises HDL

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23
Q

Effects of Polyunsaturated Cholesterol

  • Lowers ______
  • Raises ______
A
  • Lowers LDL

- Raises HDL

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24
Q

Effects of Saturated Cholesterol

- Raises both _____ and ______

A
  • Raises both LDL and HDL
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25
Q

Effects of Trans Cholesterol

- Raises ______

A
  • Raises LDL
26
Q

Clinical ASCVD Statin Benefit Group

  • High-intensity statin if age less than or equal to _____ y.o.
  • Moderate-intensity statin if age greater than or equal to _____ y.o. or not candidate for high-intensity
A
  • High-intensity statin if age less than or equal to 75 y.o.
  • Moderate-intensity statin if age greater than or equal to 75 y.o. or not candidate for high-intensity
27
Q

LDL-C (greater than or equal to 190 mg/dL) Statin Benefit Group
- ______ intensity statin

A
  • HIGH intensity statin
28
Q

Diabetes (type 1 or 2, age 40 - 75 y.o.)

  • _______ intensity statin
  • High intensity statin if 10 year ASCVD risk greater than or equal to _____%
A
  • MODERATE intensity statin

- High intensity statin if 10 year ASCVD risk greater than or equal to 7.5%

29
Q

Greater than of equal to 7.5% estimated 10 year ASCVD risk and age 40 - 75 year
- ________ to _______ intensity statin

A
  • MODERATE to HIGH intensity statin
30
Q

Statin — MOA

  • inhibit enzyme responsible for converting HMG-CoA to ___________
  • __________ step in the production of cholesterol
A
  • inhibit enzyme responsible for converting HMG-CoA to MEVALONATE
  • RATE-LIMITING step in the production of cholesterol
31
Q

Statin — most common side effects

  • m_________
  • Elevated ________ enzymes
  • Monitoring: Check ___________ and __________ at baseline and then only if clinically indicated
A
  • MYOPATHY
  • Elevated LIVER enzymes
  • Monitoring: Check CREATINE KINASE and LIVER FUNCTION TESTS at baseline and then only if clinically indicated
32
Q

Statin — rare side effects

  • new onset of __________
  • ___________ stroke
A
  • new onset of DIABETES

- HEMORRHAGIC stroke

33
Q

Statin — Contraindications

  • Active _______ disease, unexplained persistent elevations in _______
  • ___________ / lactation
  • Selection medications: more common /c ________/___________
A
  • Active LIVER disease, unexplained persistent elevations in LFT’s
  • PREGNANCY / lactation
  • Selection medications: more common /c LOVASTATIN/SIMVASTATIN
34
Q

Statin — Drug Interaction

  • Fibrates = increased risk of _________ and rhabdomyolysis
  • Niacin = do not exceed dose of 1g/day d/t increased risk of _______ and rhabdomyolysis
A
  • Fibrates = increased risk of MYOPATHY and rhabdomyolysis

- Niacin = do not exceed dose of 1g/day d/t increased risk of MYOPATHY and rhabdomyolysis

35
Q

Statin

  • avoid unnecessary __________ of statins
  • obtain h/o prior or current _______ symptoms to establish baseline before initiating statin therapy
A
  • avoid unnecessary DISCONTINUATION of statins

- obtain h/o prior or current MUSCLE symptoms to establish baseline before initiating statin therapy

36
Q

Statin

  • Unexplained severe _____ symptoms or _______
  • promptly _________ statin and address possibility of ___________
  • Urinalysis, ________ levels, and _________ levels
A
  • Unexplained severe MUSCLE symptoms or FATIGUE
  • promptly DISCONTINUE statin and address possibility of RHABDOMYOLYSIS
  • Urinalysis, CK levels, and SERUM CREATININE levels
37
Q

Statin — Mild to moderate symptoms

  • Evaluate for other conditions that may increase risk of _______ symptoms
  • Establish causal relationship between ______ symptoms and _____ therapy

If causal relationship…

  • _________ original statin
  • Resume _____ dose alternative statin
  • Increase to maximum ________ dose
A
  • Evaluate for other conditions that may increase risk of MUSCLE symptoms
  • Establish causal relationship between MUSCLE symptoms and STATIN therapy

If causal relationship…

  • DISCONTINUE original statin
  • Resume LOW dose alternative statin
  • Increase to maximum TOLERATED dose
38
Q

Non-Statin Therapies

  • Niacin
  • Bile acid sequestrates (BAS)
  • Ezetimibe
  • PCSK9 inhibitors
  • Fibric acids
  • Omega 3 Fatty acids
A

Primarily for triglyceride management

  • Fibric acids
  • Omega 3 Fatty acids
39
Q

Niacin
- ________ acid, vitamin ____

MOA:

  • inhibits ____ synthesis and hepatic secretion
  • inhibits release of ________ acids from adipose tissue
A
  • NICOTINIC acid, vitamin B

MOA:

  • inhibits VLDL synthesis and hepatic secretion
  • inhibits release of FREE FATTY acids from adipose tissue
40
Q

Niacin — Clinical Uses

  • adjunctive therapy for lowering ______, can lower _________
  • most effective agent at increasing _____
A
  • adjunctive therapy for lowering LDL, can lower TRIGLYCERIDES
  • most effective agent at increasing HDL
41
Q

Niacin should NOT be used if

  • Hepatic transaminase > _______ times ULN
  • Severe _______ symptoms, persistent _________, acute ______, or unexplained _______ pain
A
  • Hepatic transaminase > 2 - 3 times ULN

- Severe CUTANEOUS symptoms, persistent HYPERGLYCEMIA, acute GOUT, or unexplained ABDOMINAL pain

42
Q

Niacin

  • may cause significant __________
    - can premeditate /c ________, take at bedtime /c food, avoid _____ beverages, _____ foods, or _____ showers around administration time
A
  • may cause significant FLUSHING
    - can premeditate /c ASPIRIN, take at bedtime /c food, avoid HOT beverages, SPICY foods, or HOT showers around administration time
43
Q

What are these products?

  • Cholestyramine
  • Colestipol
  • Colesevelam
A

Bile Acid Sequestrants

44
Q

Bile Acid Sequestrants — MOA

- binds bile in GI tract for fecal ______ to stop _________ cycling

A
  • binds bile in GI tract for fecal EXCRETION to stop ENTEROHEPATIC cycling
45
Q

Bile Acid Sequestrants

- __________ adverse effects may be limiting factor

A
  • GASTROINTESTINAL adverse effects may be limiting factor
46
Q

Bile Acid Sequestrants

  • Avoid if baseline fasting triglycerides exceed ____ mg/dL
  • Discontinue if triglycerides exceed ______ mg/dL on therapy
A
  • Avoid if baseline fasting triglycerides exceed 300 mg/dL

- Discontinue if triglycerides exceed 400 mg/dL on therapy

47
Q

Bile Acid Sequestrants

- cholestyramine / colestipol separate all drugs by __ hour before or __ hours after

A
  • cholestyramine / colestipol separate all drugs by 1 hour before or 4 hours after
48
Q

Ezetimibe (Zetia) — MOA

- inhibits the absorption of intestinal _________

A
  • inhibits the absorption of intestinal CHOLESTEROL
49
Q

Ezetimibe (Zetia) — Efficacy

  • ____ reduction of 18%
  • reduced primary composite endpoint of _____________ death, non-fatal ______, UA /c hospitalization, coronary ________, and non-fatal stroke
A
  • LDL reduction of 18%
  • reduced primary composite endpoint of CARDIOVASCULAR death, non-fatal MYOCARDIAL INFARCTION, UA /c hospitalization, coronary REVASCULARIZATION, and non-fatal stroke
50
Q

Ezetimibe (Zetia)

- monitor _______ transaminases when clinically indicated. Discontinue if persistent levels > ____ times ULN

A
  • monitor HEPATIC transaminases when clinically indicated. Discontinue if persistent levels > 3 times ULN
51
Q

What are 3 adverse effects of Ezetimibe (Zetia)?

A

(1) Overall well tolerated
(2) Abdominal pain
(3) Diarrhea

52
Q

PCSK9 Inhibitors

(1) Praluent (alirocumab) = subcutaneous injection every _____ weeks
(2) Repatha (evolucumab) = subcutaneous injection every ______ weeks

A

(1) Praluent (alirocumab) = subcutaneous injection every 2 weeks
(2) Repatha (evolucumab) = subcutaneous injection every 2-4 weeks

53
Q

PCSK9 Inhibitors — MOA
- monoclonal antibody that inhibits a protein called PCSK9 –> increased expression of ______ receptors on hepatocyte surfaces –> increased _______ clearance from the liver

A
  • monoclonal antibody that inhibits a protein called PCSK9 –> increased expression of LDL receptors on hepatocyte surfaces –> increased CHOLESTEROL clearance from the liver
54
Q

PCSK9 Inhibitors — Efficacy

  • Have been shown to lower ________ levels by 40 - 72%
  • Outcome studies have shown reduced rates of ____________ and ______ death
A
  • Have been shown to lower LDL-C levels by 40 - 72%

- Outcome studies have shown reduced rates of MYOCARDIAL INFARCTION and CARDIOVASCULAR death

55
Q

PCSK9 Inhibitors — Adverse Effect

  • _______ site reactions
  • _________ infections
A
  • INJECTION site reactions

- RESPIRATORY infections

56
Q

Fibric Acids — MOA
- Inhibits ________ of VLDL and increases _________ of VLDL, fatty acid _____, and _________ of triglyceride-rich particles

A
  • Inhibits SYNTHESIS of VLDL and increases CATABOLISM of VLDL, fatty acid OXIDATION, and ELIMINATION of triglyceride-rich particles
57
Q

What type of drugs are these…

  • Fenofibrate (Tricor, Triglie, Trillpix, Antara)
  • Gemfibrozil (Lopid)
A

Fibric Acids

58
Q

What are 4 contraindications to Fibric Acids?

A

(1) Pregnancy
(2) Severe hepatic disease
(3) Severe renal disease
(4) Gall bladder disease

59
Q

What are 2 adverse drug reactions of Fibric Acids?

A

(1) gastrointestinal

(2) myopathies /c gemfibrozil

60
Q

Triglyceride Management

  • Primary goal = prevent _________
  • non-pharmacological therapy = weight _______, e_______, avoid large amounts of ________
  • Primary treated /c _________ or _________ fatty acids
A
  • Primary goal = prevent PANCREATITIS
  • non-pharmacological therapy = weight LOSS, EXERCISE, avoid large amounts of ALCOHOL
  • Primary treated /c FIBRATES or OMEGA-3 fatty acids

Pharmacology (10 decks)

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