Dyslipidemia Flashcards

1
Q

What are adverse effects of “statins”

A
headache
dyspepsia
myositis
elevation of hepatic transaminase levels
non serious and reversible cognitive side effects
increases in blood glucose
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2
Q

What are monitoring parameters for “statins”

A

Baseline ALT&raquo_space;> ALT as clinically indicated

Creatine kinase test as needed for myositis

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3
Q

What are adverse effects of Fibric Acids

A
Nausea
Diarrhea
Vomiting
Dyspepsia
Flatulence
Abdominal distress
Fatigue
Headache
Rash
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4
Q

What are monitoring parameters for Fibric Acids

A
  • Baseline ALT
  • alk phos. ALT
  • alk phos 6-12 wks x 2, q12mo therafter
  • fasting lipid profile 6-12 wks after dose change, q12mo thereafter
  • creatine kinase test as needed for myositis
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5
Q

What are adverse effects of Bile Acid Resins

A
Indigestion
bloating
nausea
constipation
abdominal pain
flatulence
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6
Q

What are monitoring parameters for Bile Acid Resins

A

Fasting lipid profile 6-12 wks after stable dose then q12mo thereafter

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7
Q

What are adverse effects of Nicotinic Acid (Niacin)

A
flushing
itching
tingling
headache
naseau
gas
heartburn
fatigue
rash
elevation serum glucose and uric acid
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8
Q

What are monitoring parameters for Nicotinic Acid

A
  • Baseline ALT
  • alk phos. ALT
  • alk phos 6-12 wks x 2, q12mo therafter
  • after stable dose acheived X2 month fasting lipid profile, uric acid and glucose, fasting lipid profile q12mo thereafter
  • creatine kinase test as needed for myositis
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9
Q

How do statins effect lipid levels?

A

They lower LDL synthesis and increase LDL breakdown by:

Inhibiting HMG CoA reductase, an enzyme that is important in the conversion of HMG CoA to Mevalonate, a vital step in cholesterol synthesis within the liver.

Therefore, statins help REDUCE the amount of endogenous cholesterol produced.

They also stimulate hepatic LDL receptors to enhance LDL clearance from plasma.

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10
Q

How do Bile Acid Resins effect lipid levels?

A

Increase in LDL breakdown, and a decrease in cholesterol absorption by:

Binding to bile acids within the GI tract and prevent their reabsorption, excreting the bile acids in the feces. A drop in bile acids signals the liver to generate bile acids from existing cholesterol.

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11
Q

How do Fibrates effect lipid levels?

A

Increases VLDL clearance and decreases LDL absorption by:

Activating nuclear receptors that are involved in cellular function, ultimately causing a decrease in the production of TG-rich lipoproteins VLDL and IDL and an increase in HDL.

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12
Q

How does Nicotinic Acid (Niacin) work on lipid levels?

A

Lowers VLDL and LDL synthesis and TG levels by:

Inhibits FA release from adipose tissue and inhibits FA and TG production in the liver.

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13
Q

How does Ezetimibe effect lipid levels?

A

Inhibits cholesterol absorption by:

Interacting with a transporter located in the brush boarder membrane of the enterocytes. This limits the cholesterol content within chylomicrons and thus reduces liver cholesterol stores, upregulates LDL receptors and lowers serum cholesterol levels.

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14
Q

If a patient is considered high risk by NCEP guidelines what is their LDL goal and when do you consider meds for them?

A

LDL goal = /= to 100,
if their LDL is < 100 but they have other CV risk factors (like high TG or low HDL), you can consider combining a fibrate or nicotinic acid with an LDL-lowering drug

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15
Q

What is the LDL goal of a patient with moderately high risk (greater than 2 and 10 year risk of 10-20%), and when do you consider drug therapy

A

LDL goal= 130

100-129= at baseline or with TLC, LDL lowering drug is get LDL <100 is an option

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16
Q

What is the LDL goal of a moderate risk patient? And when do you consider drug therapy?

A

LDL goal= / = to 160

17
Q

What is the LDL goal of a low risk patient and when do you consider drug therapy?

A

LDL goal: 190

160-189 drug therapy optional

18
Q

According to ACC/AHA what 4 criteria are considered when placing a patient in the Statin Benefit Group?

A
  1. Patients with clinical ASCVD
  2. Patients with LDL >/= to 190
  3. patients age 40-75 with diabetes but without ASCVD and LDL 70-189
  4. Patients without clinical ASCVD or diabetes with LDL 70-189, with an estimated 10 year risk of ASCVD >/= 7.5%
19
Q

What other factors can be considered if there is clinical suspicion that a statin would be beneficial

A
LDL >/= 160 or other evidence of hyperlipidemia
CVD in 1st degree male relative /=2
ankle-brachial index < 0.9
elevated lifetime risk of ASCVD
Coronary artery calcium score >/=300 Agatston units, or >/= 75th percentile for age, gender and ethnicity
Statin adverse effects
statin drug interactions
patient preference