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44 Cards in this Set

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What are the dietary sources of Cholesterol?
High cholesterol: Organ meats, eggs.
Moderate cholesterol: Meats, milk
products with medium to high fat
content.
Low cholesterol: Milk products with
low fat content.
Very low cholesterol: Skim milk
products.
No cholesterol: Plant foods.
What are the endogenous sources of Cholesterol?
Liver, intestine, adrenal cortex and reproductive tissues.
What is the rate-limiting step in Cholesterol synthesis?

HMG CoA is turned into __________ by _________ whose expression is limited by cholesterol.
Mevalonic Acid
HMG CoA reductase
Smith-Lemli-Opitz syndrome (SLOS) is a Autosomal recessive condition caused by deficiency of ___________
7-dehydrocholesterol-7-reductase
Smith-Lemli-Opitz syndrome (SLOS) is characterized by the following:
Etiology discovered 1993
Congenital Malformations
Low plasma cholesterol
_______ 7 DHC (precursor)
_______ 7 DHCR (enzyme)
Increased
Decreased
Cholesterol synthesis is regulated by the ___________ gene and the __________ binding to the gene
sterol regulatory element (SRE)

sterol regulatory binding protien (SRBP)
cholesterol-lowering drugs like statins reduce Cholesterol synthesis by acting as an anolog of _________ that can not be converted to ___________
HMGCoA
Mevalonic Acid
one of the functions of Cholesterol is to make _________ which is used to make vit A, E, & K
isopentyl pyrophosphate
Cholesterol is also used to make vitamen __
D
cholesterol is also used to make ________,________, & _______
cholesteryl esters, membranes & plasma lipoprotiens, & bile acids
7-dehydrocholesterol is converted in the ______ by UV light into ___________
Cholecalciferol (vit D3)
Cholecalciferol (vit D3)is converted in the _______ by 25 hydroxylase into _________
liver
25-hydroxycholecalciferol
25-hydroxycholecalciferol is converted in the _______ by 1 alpha hydroxylase into _____
Kidney
1,25 DHCC
Cholesterol is modified to make two sets of bile acids with the addition of ______ & _______
taurine & glycine
the mnemonic "PVT TIM HALL always Argues, never Tires".
Phenylalanine
Valine
Tryptophan

Threonine
Isoleucine
Methionine

Histidine
Arginine
Lysine
Leucine

always argenine never tiresine
bile acids form fats by forming a ______
mycell
How do bile acid sequestrant drugs reduce blood Cholesterol?

Bile acids are made in liver. They are then sent to the gall bladder to store. After eating a fatty meal bile acids get sent to the intestine where they form mycells capture the fatty acids. Some FA are disposed of in the feces.

Bile acids sequestering drugs cause _______ of FA in feces.
excretion
Cholesterol makes up ________, & ________ carry cholesterol.
plasma lipoproteins
plasma lipoproteins
Chylomicron is a type of _________
plasma lipoproteins
Describe the structure of cholesterol.
Chol is 4 ringed C molecule that has C tail
Identify the dietary and endogenous sources of cholesterol
Dietary: Eggs, milks, meats --- endogenous: liver what tissue types?
Identify the substrate-product-enzyme of the rate limiting step of cholesterol synthesis.
HMG Co A (substrate) turned into Melamalonic acid ( product) by the enzyme HMG Co A reductase (RLS)
Identify the enzyme deficiency in Smith-Lemli-Opitz syndrome.
7 dehydro cholesterol reductase
Describe 4 regulatory mechanisms of cholesterol synthesis.
1.Cholesterol dependant (-) feedback on binding protein to inhibit transcription and translation
2. local control: AMP means we need energy – no cholesterol should be made
3. hormonal: insulin world (enzymes phosphorylated) want to make cholesterol, enzyme is on/glucagon world (enzymes phosphorylated) = don’t want to make cholesterol, enzyme-P is off
4. Pharmicalogic – statin drugs– competitive, reversable inhibitor on the enzyme HMG CoA-reductase
Describe the structure of the cholesterol storage molecule.
Esterify it with FA
Recognize the mechanism of Vitamin D activation.
Three tissue types: skin, liver, kidney ;know enzyme name for each tissue type.
Describe the structure and function of bile acids.
Bile acid has hydrophilic and hydrophobic side – can form a mycell to corrall hydrophobic FA in center to break them down
Identify the mechanism of bile acid sequestrants.
Fx: carry dietary and endogenous sources of cholesterol in bloodstream
Describe the structure and function of lipoproteins.
Sx:Lipoprotien is a lipid (covering & cargo) & protein (stick on outside as license plate)
Recognize the presentation and the biochemical profile of a patient with Smith-Lemli-Opitz syndrome.
Congenital malformations (palm of hand, etc.)
Elevations in substrate, enzyme decreased(7 dehydrocholesterol reductase) measured by enzyme activity.
Identify a patient with Vitamin D deficiency and evaluate a specific patient for treatment types.
3 organ problems and what type of suppliment can be given – 3 scenarios & 3 tx types.
--
Describe the structure of cholesterol.
Chol is 4 ringed C molecule that has C tail
Describe the structure of cholesterol.
Chol is 4 ringed C molecule that has C tail
Describe the structure of cholesterol.
Chol is 4 ringed C molecule that has C tail
Identify the dietary and endogenous sources of cholesterol.
Dietary: organ meats, the yolk of eggs
Endogenous: Liver, intestine, adrenal cortex, reproductive tissues
Identify the substrate-product-enzyme of the rate limiting step of cholesterol synthesis.
HMG Co A (substrate) turned into Melamalonic acid (product) by the enzyme HMG Co A reductase (RLS)
Identify the enzyme deficiency in Smith-Lemli-Opitz syndrome
7 dehydrocholesterol 7 reductase (7-DHCR)
Describe 4 regulatory mechanisms of cholesterol synthesis.
1. Excess cholesterol leads to (-) feedback via blocking to the the binding protein that stops the sterol regulatory elements from inhibiting transcription and translation
2. local control: AMP stimulates the protien kinase that phosphorylates HMG Co A reductase, rendering it inactive.
3. In glucagon world enzymes are phosphorylated rendering them inactive (See above)
4. Pharmicalogic –The statin drugs mimic HMG CoA.
Describe the structure of the cholesterol storage molecule.
For cholesterol to be a storage molecule we simply need to esterify it with a FA
Recognize the mechanism of Vitamin D activation.
7-DHC is converted by UV LIGHT in the SKIN to
VITAMEN D3 (CHOLECALCIFEROL) where it is converted by 25-HYDROXYLASE in the LIVER to become
25-HCC where it is converted by 1-ALPHA HYDROXYLASE in the KIDNEY to become
1,25 DHCC where it goes to the INTESTINES and helps to increase Ca++
Describe the structure and function of bile acids.
Bile acid has hydrophilic and hydrophobic side this enables formation of mycell which are water soluble yet can corral hydrophobic FA in center for break them down
Identify the mechanism of bile acid sequestrants.
Bile acids are made in liver & stored in gall bladder-. BA get sent to Intestine & form mycells to capture the fat acids. Some FA are exreted into the feces. Bile acid sequestering drugs aid in the excretion of bile acids into feces
Describe the structure and function of lipoproteins.
Sx: lipid covering & cargo with protein stuch on outside as license plate
Fx: carry dietary and endogenous sources of cholesterol in bloodstream
Recognize the presentation and the biochemical profile of a patient with Smith-Lemli-Opitz syndrome.
PE will show thick alveolar ridges of gums. No palate.
Simean crease on palms (lines meet)
Ambiguous genetals
4th & 3rd toe fused together
LAB TESTS:
Elevated 7DHC (substrate)
Decreased 7DHCR