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Cardio > Lipoprotein and Lipid disorders for M2 discovery curriculum > Flashcards

Lipoprotein and Lipid disorders for M2 discovery curriculum Flashcards

1
Q

ASCVD

what does it stand for and what does it include

A

atherosclerotic cardiovascular disease

MI+Stroke+peripheral arterial disease

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2
Q

What is the key determinant of CVD?
What else matters?
What are some factors for increased CVD?

A

LDL:HDL ratio; lifestyle is also important

DM, Smoking, HTN, obd obesity

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3
Q

What are three things that can guard against CVD?

A

exercise, eating fruits and veggies, and some alcohols

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4
Q

6 lifestyle related factors contributing the ASCVD and what values are disease inducing?

A 
BMI >35
BP >135/85
FBS >100 AKA Dm
Tobacco any/second hand
Exercise less than 30 minutes/day
Alcohol none or excess
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5
Q

lifestyle ways to increase LDL and Trigs

A

LDL: eat high fat, high cholesterol diets (thereby increasing chylomicrons)
Trigs/cause insullin resistance: eat SAD, drink sodas, sedentary lifestyle, and smoke

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6
Q

What’s included in the classic lipid profile? (5)

What are 2 other factors you can measure?

A 
Total cholesterol
triglycerides
HDL
LDL
non HDL

ApoB, and LDL-Particle

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7
Q

Which lipoprotein amounts are calculated?

How are they calculated?

A

LDL and non-HDL
TC-(HDL+VLDL-C)=LDL
TC-HDL=nonHDL

called Friedewald equation

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8
Q

CVD pathologic limits of the following:

LDL-C
HDL
Trigs

A

LDL-C >100

HDL 1000 is risk for pancreatitis

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9
Q

What are optimal values for

TC, TG, HDL, LDL, nonHDL?

A

40M >50F, «100

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10
Q

What are normal values for TC, TG, HDL, LDL, nonHDL

A

40M/ >50F, <160

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11
Q

Two pillar determinants of lipid disorders.

What is the more realistic picture?

A

Genetics (recess or dom)
environment (diet, exercise, and drugs)

Genetics unmasked by lifestyle

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12
Q

Which subtypes of lipid disorder are mainly genetic and involves very little lifestyle changes? (2)

A

I and IIA

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13
Q

Which lipid disorder subtypes are heavily influenced by lifestyle? (4)

A

IIB, III, IV, V

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14
Q 
Type I Hyperlipidemia
Common Name
Clinical Presentation
what's in excess?
What's defective?
common or rare?
abnormal lab value
A 
severe Hypertriglyceridemia or Hyperchylomicronemia
baby with >2,000 TG
Chylomicrons are in excess
defective LPL, apoC2, or apoC3
very rare
TG is >2,000
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15
Q 
IIa
Common name 
clinical presentation
what's in excess?
What's defective?
common or rare?
abnormal lab value
A

Familial Hypercholesterolemia

CAD 275, LDL-C >190

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16
Q 
IIb
common name
clinical presentation
what's in excess?
What's defective?
common or rare?
abnormal lab value
A

familial combined hyperlipidemia with metabolic syndrome
CAD risk 2x normal despite borderline nl lipid numbers
LDL and VLDL are in excess
due to ApoB100 over production
common
LDL 100, trigs 200-500, HDL <40

17
Q 
III
common name
clinical presentation
what's in excess?
What's defective?
common or rare?
abnormal lab value
A 
dysbetalipoproteinemia
premature CAD
VLDL, IDL in excess
due to ApoE2 over production 
rare
TC and trig both are 200-500
18
Q 
IV
Common Name
presentation
what's in excess?
What's defective?
common or rare?
abnormal lab value
A 
Hypertriglyceridemia
pancreatitis
VLDL in excess
due to LPL or apoC3 defect
common
Trigs are 500-1000
19
Q 
V 
common name
presentation
what's in excess?
What's defective?
common or rare?
abnormal lab value
A 
Hypertrigliceridemia
pancreatitis, usually with DM
VLDL and chylomicrons in excess due to LPL or apoC3 defect
uncommon 
trigs >1000
20
Q

Type IIb-dyslipidemia

-major factors

A

western diet
metabolic syndrome/DM
diabesity

21
Q

metabolic syndrome –>2x risk for CAD despite not having DM.

What lipoproteins are prominent?

A

VLDL remnants
LDL

These are atherogenic

22
Q

MEtabolic syndrome (3/5)

A
  1. Waist >40 men, >35 women
  2. BP >135/85
  3. Glucose >100
  4. Trigs >150
  5. HDL men <50
23
Q

Type IIB pathogenesis

A

increase in glucose–>storage in liver –>VLDL biosynthesis upreg–>CETP conversion between HDL, VLDL, and LDL. Increase in LDL content in general, and HL converts some LDL to small LDL which have even worse affinity for LDLR…
THEREFORE increased LDL–>atherosclerosis

HDL gets smaller due to CETP–>apoA1 and AII fall off and renal excretion…
THEREFORE less HDL

24
Q

atherogenic dyslipidemia
caued by what?
what are the lipoprotein characteristics

A 
caused by metabolic syndrome. 
characteristics:
high TRIGS
low HDL
LDL-particles are wayyyyyyyy more than LDL-cholesterol

Cardio (6 decks)

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