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Clinical Exercise Prescription > Dislipedeamia > Flashcards

Dislipedeamia Flashcards

1
Q

what is a lipid

A

organic molecule, poorly souble in water
carbon containing, few oxygen molecules
hygrophilic head, hydrophobic tail

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2
Q

what is a TAG

A

3 FA attached to a glycerol
less O2
more hydrophobic

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3
Q

what is cholestrol ester (CE)

A

cholestrol and FA

no oxygen

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4
Q

why do we need fat

A 
energy 
cell membrane 
protection of organs 
thermal insulation 
neural insulation
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5
Q

why do we need cholestrol

A 
acts as a membrane stiffner 
present between TAG tails 
uses in 
- steriods 
- vit D 
- bile acid
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6
Q

what is the role of lipoproteins

A

make cholestrol and TAG souble
has a hydrophobic core made up of TAG and cholestrol
hydrophilic outside

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7
Q

what is the only way the body can get rid of cholestrol

A

through excretion

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8
Q

name the 4 lipoproteins

A

chylomicrons
VLDL
LDL
HDL

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9
Q

describe chylomicrons in terms of lipid, protein and density

A

high lipid
low protein
low density

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10
Q

describe VLDL in terms of lipid, protein and density

A

high ish density
lowish protein
low ish lipid

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11
Q

describe LDL in terms of lipid, protein and density

A

low ish lipid
highish protein
highish density

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12
Q

describe HDL in terms of lipid, protein and density

A

high protein
low lipid
high density

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13
Q

how do short and medium chain Fats enter the blood

A

TAG and CE broken down in FA and glycerol in the intestinal lumen
enter portal vien

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14
Q

Postprandial

what does HDL donate to Chylomicron

A

Apo protein C2 and Apo E

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15
Q

Postprandial

how does the chylomicron bind to the tissue

A

via Apo C2 and lipoprotein lipase

TAG absorbed

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16
Q

Postprandial

what is produced after chylomicron binds

A

a chylomicron remant

more cholestrol dense, less TAG

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17
Q

Postprandial

what happens to the chylomicron remant

A

ApoC2 goes back to HDL
ApoE binds to receptor on liver
chlyomicron remnant stored in liver

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18
Q

Fasted

how much of the VLDL remant bind to the liver

A

50%

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19
Q

Fasted

what happens to VLDL

A

leaves the liver
recieves ApoC2 and ApoE
binds to tissue via ApoC2 and lipoprotein lipase

20
Q

what is produced after VLDL binds to tissue

A

VLDL remant

21
Q

what happens to other 50% of VLDL

A

LDL synethsis
docks to hepatic lipase - removes any TAG left
new LDL
LDL taken up by cell

22
Q

what is the problem of LDL

A

half life of a couple of days so spends longer in the blood exposing it to free radicals and toxins
gets unfavourably modified

23
Q

what happens to unfavourably modifide LDL

A

macrophages do not recognize it

  • express SR-a Receptor
  • takes up LDL
  • macrophage has no internal feedback, so has a build up of C
  • becomes a foam cell
  • atherosclerosis
24
Q

phamaological treatments for cholestrol

A

treat underlying disease if appropriate (diabetes)
lifestyle modifications - diet, smoking, exercise
Drugs
- statins
- resins
- exetimibe

25
Q

how do statins work

A

statins stop cell producing its own C

upregulates expression of LDL receptors

26
Q

how do resins work

A

prevents recycling of bile acids
so you lose more C
express more receptors

27
Q

how do exetimbe work

A

knocks out C transporter in SI

prevents C getting into the system

28
Q

effect of high fat diet on chylomicrons

high fat diet

A

high fat = more chylomicrons

29
Q

describe the interaction between chylomicrons and LDL

high fat diet

A

chylomicron exchanges some C for fat from LDL via CET
produces chylomicorn with more cholestrol in it
LDL with small amount of fat in it

30
Q

what is the effect of TAG rich chylomicrons from high fat diet
(high fat diet)

A

leads to oxidative stress
causes endothelial to stop working
LDL can get through endothelial wall and settle in wall

31
Q

what happens to the small LDL after interacting with Chylomicron
(high fat diet)

A

binds to hepatic liapse, pass on small amount of TAG to become a smaller LDL remant

32
Q

what is the effect of small LDL remant

high fat diet

A

easier for it to be damaged
macrophages collect
endothelial wall damaged so macrophage can pass through

33
Q

what happens to HDL following high fat diet

high fat diet

A

same thing as LDL
takes some TAG from VLDL
binds to liver and delivers TAG
becomes a smaller HDL remant

34
Q

what happens to smaller HDL remant

high fat diet

A

more rapidly removed from the blood
less HDL to give ApoC2 and ApoE to chylomicron
leads to impaired clearence of TAG
oxidative stress happening at the same time

35
Q

what is the relationship between HDL and chlyomicrons

A

inversely proportinate

36
Q

possible dietary inverventions

A 
reducing dietary C 
reduce fat intake 
reduce salt fat 
increase fibre intake
limit sugar consumption 
limit alcohol
37
Q

effect of increasing fibre

A

increases C loss through gut

38
Q

effect of limiting alcohol

A

decreased VLDL
80% of alcohol metabolised by the liver
up to 31% of an alcohol bolus ends up as VLDL
leads to fatty liver

39
Q

effects during exercise

A

increase delivery and use of TAG

- reduce TAG blood pool

40
Q

effects post exercise

A 
increase HDL production 
increase lPLase expression and activity 
increase hepatic fatty acid oxidation 
increase size of VLDL 
improves endothelial function 
improves redox state
41
Q

effect of increase HDL production

A

increase ApoC2 and ApoE availibilty

42
Q

effect of increase lPLase expression and activity

A

enchances TAG clearence

43
Q

effect of increase hepatic fatty acid oxidation

A

decrease hepatic TAG output

44
Q

effect of increase size of VLDL

A

VLDL TAG hydrolysed more quickly

45
Q

effect of improved endothelial function

A

preventing infiltraion of lipoprotein/macrophages into the sub endothelial space

46
Q

ACSM guidelines for improving blood lipid profile

A

start 3 days a week, increase to 5-7
40-80% age predicited HRmax
11-24 RPE
150-300 mins a week

Clinical Exercise Prescription (12 decks)

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