Gen Med: Ednocrine > Lipid pathologies > Flashcards

Lipid pathologies Flashcards

(49 cards)

Study These Flashcards
1
Q

What is the fate of lipids?

A

Fats that are either absorbed from foods or synthesized by liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where are trigs stored?

A

Triglycerides store energy in adipocytes & muscle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the role of cholesterol?

A

constituent of cell membranes, steroids, bile acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is cholesterol transported?

A

Most cholesterol is carried in LDL and HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How are most triglycerides transported?

A

transported in chylomicrons or VLDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 5 major classes of lipoproteins?

A
  1. Lipoproteins are divided into five major classes, based on density:
    A. Chylomicrons
    B. Very low-density lipoproteins (VLDL)
    C. Intermediate-density lipoproteins (IDL)
    D. Low-density lipoproteins (LDL)
    E. High-density lipoproteins (HDL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define hyperlipidemia

A

A group of disorders characterized by an excess of serum cholesterol, especially excess LDL-C &/or excess triglycerides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What causes abnormal lipoprotein metabolism? What follows?

A
  1. Defects in lipoprotein synthesis, processing & clearance
  2. Accumulation of lipids in plasma & vessel endothelium
  3. High LDL & low HDL associated with increased risk for ASHD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes primary dyslipidemia/hyperlipoprooteinemia?

A
  1. Gene mutations
  2. Familial combined hypercholesterolemia most common primary
    A. ↑ Triglycerides & cholesterol & ↓ plasma HDL-C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Are secondary or primary dyslipidemia/hyperlipoprooteinemia?

A

Secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the secondary causes of hyperlipidemia?

A
  1. DM
  2. Glycogen storage diseases
    A. Genetic or acquired enzyme defic. disorders
  3. Lipodystophies
    A. Abn. or degenerative conditions of adipose tissue
  4. Excessive steroid use
  5. ETOH
  6. OCP’s
  7. Renal Dz
  8. Hepatic dysfunction
  9. Hypothyroidism
  10. Cushing’s Syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is isolated hypercholesterolemia?

A

due mostly to high LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is mixed dyslipidemia?

A

– high total or LDL cholesterol + high triglycerides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is isolated hypertriglyceridemia?

A

inc trig

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Low HDL cholesterol?

A

alone or w/ high total cholesterol or high triglycerides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the epidemiology for lipid pathologies?

A
  1. T chol & LDL-C levels are similar in whites and blacks
  2. Trig lower & HDL-C levels higher in African-Americans
  3. Asian-Indians have the highest risk
  4. Chinese have the lowest risk
  5. Europeans have intermediate risk
  6. Differences in lipid levels can be partly explained by dietary & lifestyle differences
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the risk factors for lipid disorders?

A
  1. Habitual excessive alcohol use
  2. Obesity
  3. Lack of exercise
  4. M > W
  5. Ethnic groups adopting a ‘western’ lifestyle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the most typical sxs of lipid pathologies?

A
  1. Typically asymptomatic

A. Incidental diagnosis from routine blood work

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What sxs are indicative of lipid pathologies?

A 
1. Xanthelasmas
A. Yellow plaques on medial aspect of eyelids
2. Arcus (Senilis) Corneae
A. Onset <45 y/o
B. White/gray ring around corneal margin
3. Eruptive xanthomas
A. Subcutaneous nodules along tendons/ligaments
4. GI manifestations
A. Pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the dx studies for lipid pathologies?

Study These Flashcards
A
  1. Screening total cholesterol & HDL (+/- fasting)
21
Q

When is a fasting lipid profile performed?

Study These Flashcards
A
  1. Abnormal screening test

2. (+) CHD

22
Q

When does the US Preventive Services Task Forcerecommend screening for lipid pathologies?

Study These Flashcards
A 
1. Based on risk factors, age and sex
A. (+) Risk factors for CAD
Begin: M @ 25 yr 
               F @ 35 yr
B. (-) Risk factors for CVD 
Begin: M @ 35 yr, 
               F @ 45 yr
23
Q

What is step one in management of abnormal fasting lipid profile?

Study These Flashcards
A

Evaluate results of LDL, total & HDL cholesterol levels

24
Q

What is step two in management of abnormal fasting lipid profile?

Study These Flashcards
A
  1. Identify CHD and CHD risk equivalents
  2. Clinical CHD
  3. Symptomatic carotid artery disease (TIA/Stroke of carotid source)
  4. PAD
  5. AAA
  6. DM
25
What is step three in management of abnormal fasting lipid profile?
``` 1. Evaluate for other major risk factors (other than LDL) A. HTN B. Cigarette smoking C. FH premature CHD -M < 55 yr -F < 65 yr D. Low HDL -High HDL >60 subtract 1 risk factor E. Patient age -M ≥ 45 yr -F ≥ 55 yr ```
26
What is step four in management of abnormal fasting lipid profile?
1. If 2+ risk factors (in addition to ↑ LDL) & no CHD or CHD risk equivalents A. Assess 10yr CHD risk (Framingham tables)
27
What is step five in management of abnormal fasting lipid profile?
1. Determine risk category using ATP III to A. Establish LDL goal therapy B. Determine need for therapeutic lifestyle changes (TLC) C. Determine level for drug consideration
28
What is step six in management of abnormal fasting lipid profile?
``` 1. Initiate TLC if LDL above goal A. Diet low in saturated fats & cholesterol B. ↑ Soluble fiber C. Weight reduction D. ↑ Physical activity ```
29
What is step seven in management of abnormal fasting lipid profile?
1. Consider drug therapy | 2. See STEP V guidelines
30
What is step eight in management of abnormal fasting lipid profile?
1. Identify Metabolic Syndrome A. Abdominal obesity, ↑ triglycerides, ↓ HDL, HTN, Impaired FBS 2. Treat triglycerides/HDL if remains abnormal after 3 mo lifestyle changes 3. Treat underlying metabolic syndrome A. Weight loss, physical activity B. HTN C. ASA if CHD
31
What is step nine in management of abnormal fasting lipid profile?
Treat elevated triglycerides if present
32
What are the treatment recommendations for Individuals w/ clinical ASCVD?
receive high-intensity statin therapy (moderate-intensity for those patients >75 years)
33
What are the treatment recommendations for Individuals w/ primary elevations of LDL–C ≥190 mg/dL?
receive high-intensity statin therapy
34
What are the treatment recommendations for Individuals 40 to 75 yr w/ DM & LDL-C 70 to 189 mg/dL?
receive at least moderate-intensity statin therapy
35
What are the treatment recommendations for Individuals 40 to 75 yr w/out clinical ASCVD or DM w/ LDL-C 70 to 189 mg/dL & estimated 10-year ASCVD risk of 7.5% or higher?
receive moderate- or high-intensity statin therapy
36
What is high intensity statin therapy?
1. daily dose lowers LDL on average by approximately >50% 2. Ex. Atorvastatin (lipitor) 40-80 mg Rosuvastatin (crestor) 20-40 mg
37
What is moderate intensity statin therapy?
1. daily dose lowers LDL on average by approximately 30-50% 2. Ex. Atorvastatin (Lipitor) 10–20 mg Rosuvastatin (Crestor) 5–10 mg Simvastatin (Zocor) 20–40 mg   Pravastatin (Pravachol) 40–80 mg
38
What is low intensity statin therapy?
``` daily dose lowers LDL on average by approximately <30 2. Ex. Simvastatin 10 mg Pravastatin 10-20 Fluvastatin 20-40 ```
39
What is the moa of HMG CoA Reductase Inhibitors statins?
1. Inhibit enzyme used in cholesterol synthesis 2. Upregulate LDL receptors 3. Increase LDL clearance
40
What are the se of statins?
1. Myositis, myalgias, rhabdomyolysis (risk ↑ when used w/ niacin or fibrate) 2. Elevated LFT’s
41
What are the statins?
Lovastatin (Mevacor), Atorvastatin (Lipitor), Simvastatin (Zocor) Fluvastatin (Lescol), Pravastatin (Pravachol), rosuvastatin (Crestor)
42
What is the moa of the bile acid sequestrants?
1. Bind bile acid in intestine preventing reabsorption | 2. Lower hepatic cholesterol
43
When are bile acid sequestrants used?
Used w/ statin or nicotinic acid | Synergistic effect
44
What are the bile acid sequestrants?
Cholestyramine (Questran/Light), colestipol (Colestid), colesevelam (Welchol)
45
What is the moa of nicotinic acid (Vit. B3) What can it be used with?
1. Decreases hepatic LDL/VLDL production 2. Can be used with statins/bile acid sequestrants 3. Niacin, Niaspan
46
What is the moa and effects of fibric acid?
1. MOA unknown 2. Inhibits trig synthesis & stimulates catabolism of trig-rich lipoproteins 3. ↑ HDL 4. Gemfibrozil (Lopid), fenofibrate (Tricor), finofibric acid (Trilipix)
47
What is the moa of Ezetimibe (Zetia)?
1. Inhibits cholesterol absorption in small intestine | 2. Used alone or w/statin
48
What homeopathic remedies are available for high cholesterol?
1. Red Yeast Rice 2. Psyllium 3. Coenzyme Q-10
49
What pt education needs to take place?
1. For each 1% reduction in the level of LDL-C, there is a 1% to 1.5% reduction in the risk of major cardiovascular events 2. Lifestyle modifications A. Weight loss, exercise, & dietary changes B. Key in long-term management
Gen Med: Ednocrine
flashcards
Decks in class (8)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions