cholest Flashcards

1
Q

strcuture of cholestrol

A

cyclic rings with a hydrophobic tail

The steroid ring structure is planar

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2
Q

function of cholestrol

A

is that it can increase and decrease membrane stiffness, depending on the temperature and the nature of the membrane

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3
Q

formation of c

A

liver through de novo synthesis of cholesterol from acetyl-CoA.

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4
Q

3 main steps Cholesterol Synthesis

A

1) Synthesis of isopentenyl pyrophosphate
2) Condensation of 6 moleclies of iso to form squalene
3) Cyclisation and demethylation to get cholestrol

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5
Q

how bile salts are formed

A

major breakdown products of cholesterol

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6
Q

what are the primary bile salt

A

glycocholate and also taurocholate.

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7
Q

what makes sterioids

A

…cholesterol…

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8
Q

what does chol generate using demolase

A

pregnenolone

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9
Q

what is pregnenolone

A

All five classes of steroid hormones come from pregnenolone: Progestagens, glucocorticoids, mineralocorticoids, androgens and oestrogens.

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10
Q

what is vitiman d

A

collective term for a group of steroids which are vital for the intestinal absorption of important ions needed for bone development

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11
Q

examples of vitimin d

A

calcium, phosphate and magnesium.

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12
Q

main source of vitimin d

A

our main source is from the activity of UV light upon 7-dehydrocholesterol in the epdermis of the skin.



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13
Q

what is `Calcitriol

A

most active vitamin D metabolite

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14
Q

function

A

plays a key role in calcium metabolism. It functions as a steroid hormone, binding to vitamin D response elements (VDREs) in the promoter of target genes and inducing key genes involved in bone metabolism

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15
Q

lack of calcitrol causes

A

in childhood leads to rickets

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16
Q

is Familial hypercholesterolaemia (FH) dominant

A

yes

17
Q

what happens if a person is hetrozygotes

A

have cholesterol levels approximately 2-3 times higher than in normal people and are susceptible to atherosclerosis (hardening of the arteries) in middle age

18
Q

and homozygotes

A

serum cholesterol levels are five times higher than in healthy individuals and severe atherosclerosis and coronary infarction may be observed in adolescence.

19
Q

severe fh causes

A
lacked functional LDLRs
LDL receptor (LDLR)
Mutations in several domains of the LDL receptor lead to FH
20
Q

what is hypercholesterolaemia

A

high cholesterol

21
Q

how to control hypercholesterolaemia

A

Inhibition of de novo cholesterol synthesis by the liver, or the reduction of dietary cholesterol absorption by the intestines

22
Q

resins method

A

These bind or sequester bile acid-cholesterol complexes preventing their reabsorption by the intestine

23
Q

HMG-CoA-Reductase inhibitors/

statin

A

is that of a competitive inhibitor of HMG-CoA Reductase.

24
Q

step 1

Formation of acetoactyl coA

A

2 acteyl coA to it

25
Q

step 2 to HMG coA

A

acetoacetyl coa + acetyl coa

26
Q

step 3 form melovonate

A

uses HMG coA reductase which can be controlled by negative feedback cholestrol bile salts and melavonate