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Week 14- SHANE > Dyslipidemia TBL > Flashcards

Dyslipidemia TBL Flashcards

1
Q

Bilateral xanthelasma palpebrarum, corneal arcus, and thickened achilles tendons are clinical signs of what?

A

familial hypercholesterolemia

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2
Q

Bilateral xanthelasma palpebrarum, corneal arcus, and thickened achilles tendons are clinical signs of what?

A

familial hypercholesterolemia

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3
Q

What are xanthelasma palpebrarum?

A

deposits of cholesterol in the eye of patients with FH

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4
Q

Are thickened achilles tendons common in kids or adults with FH?

A

adults

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5
Q

Total cholesterol over what level would indicate potential FH?

A

300mg/dL

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6
Q

What is the optimal level for total cholesterol?

A
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7
Q

What is the optimal level for TAG?

A
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8
Q

What is the optimal level for HDL?

A

> 40mg/dL

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9
Q

What is the optimal level for LDL?

A
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10
Q

Most patients with FH have what defect?

A

some defect in LDL receptor, function, although defects in apoB are possible, or gain of function of PCSK9

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11
Q

What is the mode of inheritance of FH?

A

autosomal dominant

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12
Q

What is the prevelance of heterozygous FH?

A

1:500

increased risk for premature coronary disease

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13
Q

What is the prevelance of homozygous FH?

A

1:1000000

develop atherosclerosis or coronary disease in childhood

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14
Q

If you have a defect in the signal sequence of the LDL receptor, will you have defect in the function or number of receptors?

A

number; defect would inhibit the mRNA transcription of the gene of the receptor

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15
Q

What are some of the treatment approaches for patients with FH?

A

diet (Reduce total fat to

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16
Q

What are Bilateral retinitis pigmentosa (caused by vitamin E deficiency),
decreased DTR’s in upper and lower extremities, truncal ataxia, positive Romberg sign (problems with balance), Hepatomegaly, and acanthocytes, and lipids in the liver during fasting state signs of?

A

MTP protein defect- Abetalipoproteinemia

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17
Q

MTP defect causes what?

A

inability to make VLDL or chylomicrons so very low cholesterol blood levels in the liver so fat accumulates in intestinal cells and in the liver

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18
Q

As patients with Abetalioproteinemia able to process fat and cholesterol better with age?

A

yes, they can absorb enough dietary fat to live by making alternative pathways of absorbing fat/cholesterol without having to make chylomicrons

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19
Q

What are some approaches for treating Abetalipoproteinemia?

A

Early diagnosis is essential to prevent irreversible ocular and neurologic impairment

Supplementation with large doses of vitamins E, D, A and K

Supplementation with essential fatty acids (linoleic and linolenic acids)

Patients generally learn to regulate fat intake to control GI symptoms

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20
Q

What is the mode of inheritance of Abetalipoproteinemia?

A

autosomal recessive; thus, heterozygotes are normal

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21
Q

Visceral fat drains to what?

A

portal vein to the liver so fatty acids from visceral fat can cause fatty liver

22
Q

What are the guidelines for diagnosing abdominal obesity in men and women?

A

Waist size:

Women

23
Q

What is the optimal level for apoB?

A
24
Q

How does insulin resistance cause fatty liver?

A

insulin resistance causes increased fatty acid release from adipose which goes to the liver. The increase of fatty acids in the liver causes the liver to make more VLDL so TAG levels go up. When the output of VLDL from the liver is exceeded by the input from adipose, you get non-alcoholic fatty liver disease (NAFLD). When VLDL levels are high, CPST facilitate the transfer of TAG from VLDL to circulating HDL particles. These TAG-enriched HDL are then acted upon by hepatic TAG lipase (HTGL) in the liver which removes the TAG from the particle and in the process of doing that it causes APoA1 to dissociate from HDL (and it then cleared by the kidney). The result is lowered amounts of HDL in the body. Also, VLDL becomes cholesterol enriched and becomes more like an LDL that is susceptible to becoming oxidized and atherogenic

25
Q

What are xanthelasma palpebrarum?

A

deposits of cholesterol in the eye of patients with FH

26
Q

Are thickened achilles tendons common in kids or adults with FH?

A

adults

27
Q

Total cholesterol over what level would indicate potential FH?

A

300mg/dL

28
Q

What is the optimal level for total cholesterol?

A
29
Q

What is the optimal level for TAG?

A
30
Q

What is the optimal level for HDL?

A

> 40mg/dL

31
Q

What is the optimal level for LDL?

A
32
Q

Most patients with FH have what defect?

A

some defect in LDL receptor, function, although defects in apoB are possible, or gain of function of PCSK9

33
Q

What is the mode of inheritance of FH?

A

autosomal dominant

34
Q

What is the prevelance of heterozygous FH?

A

1:500

increased risk for premature coronary disease

35
Q

What is the prevelance of homozygous FH?

A

1:1000000

develop atherosclerosis or coronary disease in childhood

36
Q

If you have a defect in the signal sequence of the LDL receptor, will you have defect in the function or number of receptors?

A

number; defect would inhibit the mRNA transcription of the gene of the receptor

37
Q

What are some of the treatment approaches for patients with FH?

A

diet (Reduce total fat to

38
Q

What are Bilateral retinitis pigmentosa (caused by vitamin E deficiency),
decreased DTR’s in upper and lower extremities, truncal ataxia, positive Romberg sign (problems with balance), Hepatomegaly, and acanthocytes, and lipids in the liver during fasting state signs of?

A

MTP protein defect- Abetalipoproteinemia

39
Q

MTP defect causes what?

A

inability to make VLDL or chylomicrons so very low cholesterol blood levels in the liver so fat accumulates in intestinal cells and in the liver

40
Q

As patients with Abetalioproteinemia able to process fat and cholesterol better with age?

A

yes, they can absorb enough dietary fat to live by making alternative pathways of absorbing fat/cholesterol without having to make chylomicrons

41
Q

What are some approaches for treating Abetalipoproteinemia?

A

Early diagnosis is essential to prevent irreversible ocular and neurologic impairment

Supplementation with large doses of vitamins E, D, A and K

Supplementation with essential fatty acids (linoleic and linolenic acids)

Patients generally learn to regulate fat intake to control GI symptoms

42
Q

What is the mode of inheritance of Abetalipoproteinemia?

A

autosomal recessive; thus, heterozygotes are normal

43
Q

Visceral fat drains to what?

A

portal vein to the liver so fatty acids from visceral fat can cause fatty liver

44
Q

What are the guidelines for diagnosing abdominal obesity in men and women?

A

Waist size:

Women

45
Q

What is the optimal level for apoB?

A
46
Q

How does insulin resistance cause fatty liver?

A

insulin resistance causes increased fatty acid release from adipose which goes to the liver. The increase of fatty acids in the liver causes the liver to make more VLDL so TAG levels go up. When the output of VLDL from the liver is exceeded by the input from adipose, you get non-alcoholic fatty liver disease (NAFLD). When VLDL levels are high, CPST facilitate the transfer of TAG from VLDL to circulating HDL particles. These TAG-enriched HDL are then acted upon by hepatic TAG lipase (HTGL) in the liver which removes the TAG from the particle and in the process of doing that it causes APoA1 to dissociate from HDL (and it then cleared by the kidney). The result is lowered amounts of HDL in the body. Also, VLDL becomes cholesterol enriched and becomes more like an LDL that is susceptible to becoming oxidized and atherogenic

47
Q

What is Acanthosis nigricans?

A

thickened epidermis on the back of the neck due to insulin resistance (seen more in African americans)

48
Q

What is CRP?

A

is an acute phase reactant induced in liver by IL-1 and IL-6 and is an index of inflammation

CRP levels are as predictive as LDL levels for heart attack and stroke

Statin therapy lowers CRP levels (aka anti-inflammatory) independently of its effect on lipid levels

49
Q

How do you treat Metabolic Syndrome?

A 
Diet and Exercise
Achieve ideal body weight
Treat hypertension
Treat hyperlipidemia
Treat diabetes
Statins (w/ Niacin and fibrates)
50
Q

What is a common problem with statin drugs?

A

muscle pain (myopathy) or uncommonly muscle cells can lyse and clog the kidneys, causing renal failure

Week 14- SHANE (11 decks)

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