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Advanced Pharm 1 -- Exam 6 > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

What are Lipoproteins?

A

Droplets of fats surrounded by a single layer of phospholipid molecules.

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2
Q

What are phospholipids?

A

Molecules of fats what are attached to a phosphorus-containing group

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3
Q

What does Amphipathic mean?

A

Having both polar and non-polar ends.

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4
Q

Why is it important that Lipoproteins are Amphipathic?

A

-The polar ends face outwards and interact with water. The lipoprotein can be carried in the blood rather than rising to the top, like cream on milk
-Non-polar fat is balled up inside the phospholipid layer
-Allows fat to be transported through the blood to the place where it must be stored or metabolized despite being insoluble in blood

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5
Q

How are lipoproteins differentiated?

A

Differentiated based on specific proteins attached to the phospholipid outer layer.
-Apolipoprotein, Apoprotein

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6
Q

What are the two major sequelae associated with increased Lipoproteins? (Blue Box!)

A

-Acute Pancreatitis
-Atherosclerosis

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7
Q

What is the leading cause of death for both men & women in the US? (Blue box!)

A

Atherosclerosis

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8
Q

What are Chylomicrons?

A

-The largest and least dense of the lipoproteins
-Originate in the intestines in intestinal lymphatics and deliver fats and cholesterol from the intestines to the muscles, fat cells, and the liver
-Have a protein component synthesized in the liver, which wraps around diet-derived cholesterol and fats.
-Travel from the intestinal lymphatics to the large veins
-Stick to the inner surface of the tiny capillary blood vessels inside the muscles and the fat storage cells in various parts of the body
-Triglycerides are digested & the cholesterol remains
-Cholesterol remnant travels to the liver for metabolism
-Highest triglyceride content (associated with pancreatitis!!)
-The higher the triglycerides, the lower the density

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9
Q

What are VLDL Lipoproteins?

A

-Composed of protein, fats and cholesterol synthesized in the liver.
-5 different apoproteins
-Converted to IDL and LDL by removal of the apoproteins and the esterification of the cholesterol.
-2nd highest triglyceride count

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10
Q

What is esterification?

A

Converting cholesterol to cholesterol, allowing more to become packed inside (becomes more dense).

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11
Q

What are IDL lipoproteins?

A

Created by the metabolism of VLDL

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12
Q

What are LDL Lipoproteins?

A

-Created by the metabolism of VLDL
-Contains chiefly cholesterol
-Only one apoprotein (ApoB-100).
-More dense than VLDL as it goes through esterification process.
-Known for bulking up artery walls and decreasing ability to dilate. Involved with plaques in arteries.

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13
Q

What are HDL Lipoproteins?

A

-Have the highest protein:lipid ratio (densest)
-“Good Cholesterol”
-Carries cholesterol away from the tissues to the liver
-Lowering blood cholesterol levels
-⬆HDL levels are associated with ⬇ risk of cardiovascular disease

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14
Q

What are ways to increase HDL levels?

A

-Exercise
-Higher estrogen levels
-Alcohol consumption (red wine)
-Weight loss
(technically, smoking cigarettes also does but not recommended)

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15
Q

T/F: With LDLs and Triglycerides, the higher amount the better.

A

False; want these to be low and HDLs to be high.

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16
Q

What are the disorders associated with Primary Hypertriglyceridemias?

A

-Primary Chylomicronemia
-Familial Hypertriglyceridemia (Severe or Moderate)
-Familial Combined Hyperlipoproteinemia
-Familial Dysbetalipoproteinemia

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17
Q

What are the disorders associated with Primary Hypercholesterolemias?

A

-Familial Hypercholesterolemia
-Familial Ligand-Defective Apolipoprotein B-100
-Familial Combined Hyperlipoproteinemia
-Lp(a) Hyperlipoproteinemia

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18
Q

Before primary disorders can be diagnosed, ______ causes must be considered.

A

Secondary

Primary diagnosis is of exclusion - have to rule out other secondary causes.

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19
Q

With secondary causes, the lipoprotein abnormality usually ______ if the underlying disorder can be treated.

A

Resolves

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20
Q

What are the most common secondary causes of hypertriglyceridemia (Hyperlipoproteinemia)?

A

-Diabetes Mellitus
-Alcohol ingestion
-Severe nephrosis
-Estrogens
-Uremia
-Corticosteroid excess
-Myxedema
-Glycogen storage disease
-Hypopituitarism
-Acromegaly
-Immunoglobulin-lipoprotein complex disorders
-Lipodystrophy
-Protease inhibitors

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21
Q

What are the most common secondary causes of hypercholesterolemia (Hyperlipoproteinemia)?

A

-Hypothyroidism
-Early nephrosis
-Resolving Lipemia
-Immunoglobulin-lipoprotein complex disorders
-Anorexia nervosa
-Cholestasis
-Hypopituitarism
-Corticosteroid excess

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22
Q

What are the treatments for Hyperlipoprotein diseases?

A

1) Dietary measures always initiated first. But, issues with compliance.
-Unless they have CAD or PVD, then go straight to pharmacologic intervention in addition to dietary
-Familial issues ALWAYS require drug therapy as well
-Weight has to stabilize for 1 month - don’t want them to go on a crash diet and lose weight fast then gain it all back. Establish healthy eating habits.

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23
Q

What increases LDL?

A

-Cholesterol
-Saturated fats
-Trans fats

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24
Q

What increases triglycerides?

A

-Total fat
-Alcohol
-Excess calories

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25
What increases VLDL?
-Sucrose -Fructose
26
The conclusion that diet suffices for management can only be made after weight has stabilized for at least _____ month. (Blue Box!)
The conclusion that diet suffices for management can only be made after weight has stabilized for at least 1 month.
27
What populations are c/i with the use of meds for Hyperlipoproteinemia?
-C/I in pregnant and lactating women and women looking to conceive. -Has drug interactions with anticoagulants (monitor and adjust warfarin and indadione anticoagulants) -Typically not used until after the age of 16, but can be used after age 7/8 if you ensure that the neuro system has had time for complete myelination -Need robust H&P on these people
28
The ____ is central to cholesterol metabolism.
The Liver is central to cholesterol metabolism.
29
Hepatic Cholesterol can be synthesized from __________ in a multi-step enzymatic process, whose rate-limiting enzyme, _______, is inhibited by _________.
Hepatic cholesterol can be synthesized from acetyl coenzyme A (CoA) in a multi-step enzymatic process, whose rate-limiting enzyme, 3-hydroxy-3- methylglutaryl CoA reductase, is inhibited by Statins such as atorvastatin.
30
What is the rate-limiting enzyme for hepatic cholesterol?
3-hydroxy-3- methylglutaryl CoA reductase (3HMG CoA Reductase)
31
Hepatic Cholesterol is used in part to synthesize _____ that are destined, with sterols, for secretion in bile.
Hepatic cholesterol is used in part to synthesize bile acids that are destined, with sterols, for secretion in bile.
32
The luminal sterol pool in the upper portion of the small intestine comes from both ________ and ________ sterols.
The luminal sterol pool in the upper portion of the small intestine comes from both dietary and biliary sterols.
33
Intestinal luminal sterols are transported into enterocytes and repackaged into ______________ for secretion into lymph and, ultimately, ______.
Intestinal luminal sterols are transported into enterocytes and repackaged into chylomicrons for secretion into lymph and, ultimately, plasma.
34
T/F: Bile acids advance through the intestinal lumen and facilitate intestinal cholesterol absorption. Unbound bile acids are normally recycled through the terminal ileum into the enterohepatic circulation. Bile acid- binding resins, such as colestipol, prevent this recycling and force more hepatic cholesterol into bile acid synthesis.
True
35
To compensate for the depletion of hepatic cholesterol stores induced by all of these drugs, the liver increases expression of _________________________________________________ receptors to extract more cholesterol from the plasma by receptor-mediated endocytosis.
To compensate for the depletion of hepatic cholesterol stores induced by all of these drugs, the liver increases expression of cell-surface low- density lipoprotein (LDL) receptors to extract more cholesterol from the plasma by receptor-mediated endocytosis.
36
What are the HMG-CoA Reductase Inhibitors?
-The "Statins" -Structural analogs of HMG-CoA -Most effective in ⬇LDL -⬇ Oxidative stress (less imbalance of free radicals) -⬇ Vascular inflammation -⬆ Stability of atherosclerotic lesions (prevents thrombotic events)
37
When is statin therapy initiated in acute coronary syndrome? (Blue Box!!)
Statin therapy is initiated immediately after acute coronary syndromes regardless of lipid levels
38
What are the examples of the HMG-CoA Reductase Inhibitors that you need to know?
-Lovastatin (Mevacor) - parent drug -Atorvastatin (Lipitor) - most lipophilic -Simvastatin (Zocor) -Rosuvastatin (Crestor) - least lipophilic (most lipophobic)
39
Which two drugs are the Reductase Inhibitors that are inactive, lactone prodrugs and also are hydrolyzed in the GI tract?
-Lovastatin -Simvastatin
40
Which two drugs are the Reductase Inhibitors that are Fluorine containing congeners and are active as given?
-Atorvastatin -Rosuvastatin
41
Absorption of the Statins varies from ___% to ____%.
Absorption of the Statins varies from 45%-75%
42
How are all Statins metabolized/excreted?
-All are metabolized in the liver by CYP3A4 and CYP2C9 -All are excreted mostly in the bile with 5-20% in the urine
43
Which 2 Reductase Inhibitors have half-lives of 1-3 hours?
-Lovastatin -Simvastatin
44
Which Reductase Inhibitor has a half-life of 14 hours?
Atorvastatin
45
Which Reductase Inhibitor has a half-life of 19 hours?
Rosuvastatin
46
What is the therapeutic use for the Reductase Inhibitors (Statins)?
-Used in mono or combination therapy to reduce LDLs -Can be used in combo with Resins, Niacin, or Ezetimibe
47
When are Reductase Inhibitors (Statins) contraindicated?
C/I in pregnant/lactating women or women likely to become pregnant
48
What are the administration facts to know regarding Reductase Inhibitors (Statins)?
Administer at night b/c cholesterol production happens at night -Exceptions: Atorvastatin & Rosuvastatin Absorption is enhanced by food -Exception: Pravastatin
49
Why can you administer Atorvastatin and Rosuvastatin anytime?
Atorvastatin & Rosuvastatin have longer half-lives, so don't have to be administered at a certain point in time.
50
What are the toxicity S/Sx associated with the Reductase Inhibitors (Statins)?
-Elevated serum aminotransferase activity (up to 3xs normal levels) -Elevated CK -Myopathies (!), muscle pain, cramps, weakness, stiffness, spasms -Metabolized by CYP 450 (other drugs that inhibit or induce will change concentration) -D/C for serious illness, trauma, or major surgery
51
What is important to know regarding Statins and serum aminotransferase activity?
-Can cause Elevated serum aminotransferase activity (up to 3xs normal levels) -Therapy may be continued if patient asymptomatic -Malaise, Anorexia, & Precipitous decrease in LDL = D/C Immediately due to liver injury -Measure baseline➜ 1-2 months ➜ 6-12 months (if stable)
52
What is important to know regarding Statins and CK levels?
-Can cause elevated CK -Minor elevations common -Marked elevations rare ➜ may progress to myoglobinuria & renal injury, Rhabdomyolysis
53
T/F: If patient experiences myopathy, don't switch them to another Statin because they won't help.
False: Myopathy doesn’t occur in every statin. If they’re experiencing it, switch them to another Statin.
54
What are the clinical effects of Niacin (Nicotinic Acid) = Vitamin B3?
-⬇ LDL, VLDL & Lp(a) levels in most patients -⬆ HDL levels significantly -Inhibits VLDL secretion from liver to the blood, decreasing production of LDL, and increasing hepatic clearance of VLDLs, leading to decreased triglycerides. -Converted in the body to an amide builder for NAD (NAD = Niacinamide Adenine Dinucleotide) -Excreted in the urine unmodified & as several metabolites
55
What is the most effective agent for increasing HDLs, and the only agent that may reduce Lp(a)? (Blue Box!)
Niacin (Nicotinic Acid) AKA Vit B3
56
What are the therapeutic uses for Niacin (Nicotinic Acid) AKA Vit B3?
-Mono or combination therapy with Resin or Statin -Hypercholesterolemia (Heterozygous Familial Hypercholesterolemia) -Severe mixed lipemia incompletely responsive to diet -Dysbetalipoproteinemia -Hypertriglyceridemia
57
What are the toxicity symptoms associated with Niacin (Nicotinic Acid) AKA Vit B3?
-Cutaneous vasodilation (flushing) -Pruritis, rashes & dry skin -Dry mucous membranes -Acanthosis Nigricans (brown/black hyperpigmentation of the skin),C/I Niacin use 2/2 insulin resistance -May ⬆insulin resistance -Nausea & ABD pain (Alleviated with antacid therapy) -Potentiate Anti-HTN Agents -Hyperuricemia (Allopurinol PRN) -Elevated serum aminotransferase (Rarely associated with true hepatotoxicity) -Impaired carbohydrate tolerance -Red cell macrocytosis -Platelet deficiency (rare) -Atrial arrhythmias (rare)!! -Macular Edema!!
58
What is important to know regarding Niacin therapy and Acanthosis Nigricans?
-Acanthosis Nigricans: brown/black velvety hyperpigmentation of the skin. Usually in folds: armpits, neck folds -D/c therapy immediately if developed. -Prone to happen in pts with insulin resistance
59
The occurrence of which two toxicity symptoms would cause you to d/c Niacin therapy?
-Atrial Arrhythmias (rare) -Macular Edema (monitor vision)
60
What are the two example drugs of the Fibric Acid Derivatives?
-Gemfibrozil (Lopid) -Fenofibrate (Tricor) Older drugs, not used as often anymore.
61
What is Gemfibrozil (Lopid)?
-Protein bound -Absorption improved with food -Enterohepatic circulation -Crosses the placenta (C/I in pregnancy) -Half-life 1.5 hours -70% kidney elimination (Unchanged)
62
What is Fenofibrate (Tricor)?
-Isopropyl ester that is hydrolyzed in the intestine -Half-life 20 hours -60% urine excretion -25% feces excretion
63
Which of the Fibric Acid Derivatives has a longer half life?
Fenofibrate: 20 hrs Gemfibrozil: 1.5 hrs
64
What is the MOA for the Fibric Acid Derivatives?
Function primarily as ligands for the nuclear transcription receptor PPAR-α -⬆ Oxidation of fatty acids in the liver & striated muscle -⬆ Lipolysis of lipoprotein triglycerides -⬇ VLDL, modest reductions in LDL -Moderate ⬆ in HDL Tells Liver not to secrete LDLs
65
What are the uses for the Fibric Acid Derivatives?
-Hypertriglyceridemias in which VLDL predominates -Dysbetalipoproteinemia
66
What are the RARE toxicity effects associated with the Fibric Acid Derivatives?
-Rashes -GI symptoms -Myopathy -Hypokalemia -Arrhythmias -⬆ aminotransferase -⬆ alkaline phosphatase -⬇ WBC or HCT (!!!) -Rhabdomyolysis
67
What are the other toxicity effects associated with Fibric Acid Derivatives?
-Potentiate actions of Coumadin and Indanedione Anticoagulants (Adjust doses) -⬆ Myopathy risk with statins -Avoid in hepatic/renal dysfunction -⬆Risk of cholesterol gallstones: Caution in pts with obstructed biliary tract. High risk = women, obese patients and Native Americans
68
Which patients are high risk for gall stones?
Women, obese patients, Native Americans
69
What is the use for Bile-Acid Binding Resins?
-Used for isolated ⬆ in LDL only -If ⬆ Triglycerides ➜ ⬆ VLDL
70
What is the MOA of the Bile-Acid Binding Resins?
-Bile acids = metabolites of cholesterol -Bind bile acids in the intestines -Prevent reabsorption -Excretion ⬆ 10 x’s -Feedback loop tells body to break down more cholesterol into bile acids -Also stops the reuptake of bile acids from the gut to the liver -Taken BID or TID with meals -Ex: Colestipol, Cholestyramine, Colesevelam
71
What are the clinical conditions that Bile-Acid Binding Resins are utilized in?
-Primary Hypercholesterolemia -Combined Hyperlipidemia (Must add Niacin) -Can be combined with other agents to maximize effect -Helpful in relieving pruritus from cholestasis & bile salt accumulation
72
What are the toxicity S/Sx of Bile-Acid Binding Resins?
-Impairs the absorption of other drugs (Give other meds 1 hr before or 2 hrs after) -Constipation & bloating (C/I in Diverticulitis!!!!) -Malabsorption of Vit K (Monitor PT in pts taking anticoagulants like Coumadin that are Vit K dependent)
73
What is the MOA of the Inhibitor of Intestinal Sterol Absorption (Ezetimibe)?
Selective inhibitor of intestinal absorption of cholesterol and phytosterols. -Targets the transport protein NPC1L1 -Inhibits the reabsorption of cholesterol excreted in the bile -⬇LDL with minimal ⬆HDL -Half-life = 22 hours
74
What are Phytosterols?
Saturated plant steroid alcohol. Similar to cholesterol
75
What are the therapeutic uses of the Inhibitor of Intestinal Sterol Absorption (Ezetimibe)?
Primary Hypercholesterolemia & Phytosterolemia -Can be used in combo with Statins. -Synergistic with Statins
76
What is the toxicity associated with Ezetimibe?
Low incidence of reversible hepatic dysfunction. -If you stop therapy, can reverse liver dysfunction that occurred due to toxicity.

Advanced Pharm 1 -- Exam 6 (6 decks)

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