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CV > 7 and 10 Lipid Disorders and Case review > Flashcards

7 and 10 Lipid Disorders and Case review Flashcards

1
Q

2 yo with severe abdominal pain and rash, draw blood and and overnight in fridge seperates out to blood and fat. Why

A

Hyperchylomicronemia

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2
Q

Rare disease of childhood or seen in Type V adults

Genetically absent or redueced LPL or apoC2 or apoC3

A

Hyperchylomicronemia

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3
Q

What do we expect to see for TG in hyperchylomicronemia

A

TG from 2000 to 25000

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4
Q

Function of chylomicrons

A

carry mostly TG from gut to liver

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5
Q

Long term tx for hyperchylomicronemia

A

near total fat restriction and use of medium chain fatty acids to bypass more common long chain FAs

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6
Q

What happens microscopically during atherosclerosis

A

LDL crosses into endothelium into the intima
Monocytes phagocytize cholesterol
Cholesterol gets oxidixed
Vascular adhesion and metalloporoteinases activated to remodel the artrial wall
SMS migraiton
foam cell formation

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7
Q 
Pt history:
nonsmoking, asymptomatc female athlete, had high cholesterol since college, father had heart stents placed in mid 50s but didn't have a heart attack
BP: 118/72 and BMI of 23
TC; 305    TG:55    HDL:85     LDL:209
Whats her risk for ASCVD?
A

Increased and we need to start tx today

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8
Q 
Pt history:
nonsmoking, asymptomatc female athlete, had high cholesterol since college, father had heart stents placed in mid 50s but didn't have a heart attack
BP: 118/72 and BMI of 23
TC; 305    TG:55    HDL:85     LDL:209
DX?
A

Type IIA Familial Hypercholesterimia

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9
Q

Whats the metabolic issue with Type IIA Familial HYpercholesterimia?

A

LDL-R is defective, won’t remove cholesterol form circulation
–mutation in LDL-R, ApoB or PSCK9 GOF mutation

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10
Q

Tx recommendation for Type IIA Hypercholesterimia

A

High dose high intensity statins to decrease intracellular cholesterol, activate nuclear receptors and upregulate production of LDL-R

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11
Q

Pt goes undiagnosed with Type IIA Familial Hypercholesterimia until age 42. Comes in with chest pain, dyspnea on exertion: Dx?

A 
Myocardial infarction (heart issues)
see on EKG and enZ that pt had an infarct...recommend emergency angiogram and place stents
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12
Q

What tx do you recommend to a pt that has children and is diagnosed with Type IIA familial hypercholesterimia

A

Have kids on heart healthy diet and exercise as well as have lipids checked and tx if elevated (if over 12 years)

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13
Q

Pt Hx
45yo male smokes 1ppd
BP: 135/85 BMI:32 Waist:39 FBS:94
Exercise; none and has 2-4 beers a day
TC is 210 TG:165 HDL:40 LDL:137 nonHDL:170
What is he most at risk for?

A

Atherosclerotic heart disease

smoking causes more heart disease then cancer

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14
Q

What is the leading cause of disease and death

A

ASCVD

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15
Q

ASCVD stands for what diseases?

A

Aterosclerotic CV Disease

Heart attacks + STrokes + Peripheral Arthery Disease

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16
Q

CAD stands for

A

Coronary Atheroscloerotic Disease

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17
Q

Whats the biggest RISK of MI

A

LDL:HLD (then diabetes, smoking, HTN..)

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18
Q

Lifestyle can make a ____ differenct from lowest to highestl quintile in lifetime ASCD risk

A

10 fold

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19
Q

What are Heart healthful meausures for
BMI
BP
FBS

A

BMI <100

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20
Q

LDL-C >100

HDL <40

A

risk for ASCVD

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21
Q

TRIG 200-499 risk for

>1000 at risk for

A

CAD

risk for pancreatitis

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22
Q 
Normal vs Optimal for:
HDL
LDL
TC
TG
A

Normal HDL: M>40 and F>50~ same for optimal

Normal LDL: <75

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23
Q

Which types of lipid disorders are predominantely genetic with minimal lifestyle influence?

A

Type I and IIA

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24
Q

Which lipid disorders are dormand until lifestyle (diabesity) or other disease (diabetes) unmask them

A

Type IIB, III, IV, and V

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25
Q

What lipoprotein is in excess in Type I severe hypertriglylceridemia?

A

Excess chylomicron bc we can’t off load TG they pick up in enterocyte d/t LPL or apoC2/C3 defect

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26
Q

What defect do we see in Type I hyperTG?

A

LPL or apoC2/C3

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27
Q

In a lipid panel, you see TG in chilld >2000, what do you suspect?

A

Type I hyperTG d/t LPL or apoC2/3 defect

28
Q

Common presentation of IIa Familial Hypercholesterimia

A

see CAD < age of 60

29
Q

In IIa familial hypercholesterolemia, what is the primary defect… what does this result in?

A

Defect of LDL-R–> end up with excess LDL

30
Q

What lipid panel would we see in someone with IIa?

A

TC>275 and LDL-C >190 d/t LDL-R defect

31
Q

Do we see TG abnormalities in IIa?

A

NOPE. just elevated LDL and TC

32
Q

What risk are you at with CAD if you have IIb familial combined hyperlipidemia or with Metabolic syndrome?

A

CAD is 2x normal risk despite borderline lipid numbers

33
Q

What lipoproteins are in excess in IIb familial combined hyperlipidemia or with metabolic syndrome

A

Excess LDL and VLDL

also more LDL-P

34
Q 
lipid panel:
LDL 100
TG: 200-500
HDL <40
pt at 2x risk for CAD
A

This is IIb familial combined hyperlipidemia or with metabolic syndrome

35
Q

What is the primary defect in IIb?

A

overproduciton of apoB100

36
Q

What is the role of Hepatic lipase in IIb familial combined?

A

Pt has High TGS that drive CETP
CETP moves TG to LDL and HDL
When you have LDL with lots of TG, Hepatic lipase is all like, wow, too much and then makes sdHDL and sdLDL

37
Q

What is the funciton of CETP?

A

Takes VLDL to HDL or LDL

see increased VLDL in high central adiposity or insulin resistance

38
Q

Type III Dysbetalipoproteinemia causes premature CAD and is d/t :

A

overproduction of ApoE2/E2 + envirornment

39
Q

What is the role of ApoE2 in Type III Dybetalipoproteinimeia?

A

ApoE2/E2 is poorly recognized on IDL by the LDL-R so doesn’t get taken up

40
Q

What abnormal lipids do we expect to see in Type III Dybetalipoproteiniemia

A

TC and TG bonth 200 to 500

41
Q

pts comes in with TC andn TG both 200 to 500 and excess VLDL and IDL with nodules on knees and orange creases on hands. Dx

A

Type III

42
Q

What lipoproteins are in excess in pt with type III dybetaliporoteinmia

A

excess VLDL and IDL

43
Q

Type IV hypertriglyceridemia can lead to

A

pancreatitis (not diabetic releated)

44
Q

What lipoprotein is in excess in pt with Type IV hyperTG?

A

excess VLDL

45
Q

What is our primray defect in type IV hyperTG?

A

defect of LPL or ApoC3 (means VLDL will accumulate)

46
Q

What lpids are abnormal in pt with type IV hyperTG

A

TGS between 500-1000

47
Q

Pt comes in with TG between 500-1000 and and exces VLDL, what is the primary defect

A

Type IV hyperTG:

defect is ApoC2 or LPL thus can’t break down VLDL

48
Q

Pt comes to clinic with TC>275 and LDL-C >190 with an excess LDL level. What is the primary defect

A

LDL-R; patient has IIa familial hypercholesterolemia

49
Q

YOung pt comes in with TG over 2000, what lipoprotein would you expect to be in excess?

A

has Type I severe hypterTG

mutation in LPL or apoC2/C3 thus very high chylomicrons bc they can’t offload

50
Q

Pt comes in with excess LDL and VLDL.

His LDL is around 100 but had TG 200-500 with low HDL, what is the defect

A

Overproduction of apoB100:

Type IIB famililal hyperlipidemia or with metabolic syndrome

51
Q

Pt comes in with elevated TC and TG both between 200-500. Here VLDL and IDL are elevated. DX?

A

Type III Dysbetalipoproteinemia,

Dt ApoE2 overproduction

52
Q

Type V Familial hyperTG is dt defect where?

A

On the ApoC2 or C3 on BOTH VLDL and chylomicron

53
Q

What Lipoproteins are elevated in Type V familial hyperTG?

A

VLDL and chylomicron

54
Q

What does a lipid panel for pts with Type V familial hyperTG look like

A

TGs >1000

also have elevated chyomicrons and VLDL

55
Q

Pt comes in with TG>1000 and elevated chylomicrons and VLDL, what do you expect primary defect is?

A

ApoC2 or C3 on both chylomicron and VLDL isn’t fnx properly

56
Q

VLDL, chylomicrons and IDL are primary filled with:

A

TGs

57
Q

elevated LDL, smoking, high BP and Family Hx all CV risk factors that cause:

A

LDL infiltrate into intima

58
Q

90% of circulating cholesterol is

A

LDL

59
Q

What lipoproteins are risk factors for atherosclerosis

A

IDL (VLDL remnants) and LDL

IDL and VLDL remntants as well

60
Q

pt had apoA1 mutation means they cannot make

A

HDL = increased risk for disease

61
Q

most potentially lethal inherited disease in world; see heterozygotes 1/500 and is autosomal dominant most often

A

famililal hypercholesterolemia
–> 50% males have MI or die from MI by 55, females by 65
LDL is 2X to 5X normal since birth
tx with statins to lower LDL by 12 yo to decrease risk

62
Q

What catabolized LDL-R

A

PCSK9

63
Q

Metabolic syndrome_____ risk of CAD even in absence of diabetes

A

doubles risk
increases LDL-P
increases VLDL remnants
can cause atherogenic dyslidemia

64
Q 
AHA criteria for Metabolic syndrome
waist for men and women
TG for men and women
HDL for men and women
BP
FBG
A

waist men: >40 in and women >35
TBS for both >150
HDL for men 135/85 and women 135/85
FBG for both >100

65
Q

Visceral adiposity and insulin resistance drive FFA to liver where TG-rich_____ are pushed into circulation

A

VLDL

66
Q

What enZ acts on VLDL to make HDL and LDL

A

CETP

67
Q

what enZ acts on LDL and HDL to make them sdHDL and sdLDL?

A

hepatic lipase

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