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44 Cards in this Set
- Front
- Back
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What are the dietary sources of Cholesterol?
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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. |
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What are the endogenous sources of Cholesterol?
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Liver, intestine, adrenal cortex and reproductive tissues.
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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 |
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Smith-Lemli-Opitz syndrome (SLOS) is a Autosomal recessive condition caused by deficiency of ___________
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7-dehydrocholesterol-7-reductase
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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 |
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Cholesterol synthesis is regulated by the ___________ gene and the __________ binding to the gene
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sterol regulatory element (SRE)
sterol regulatory binding protien (SRBP) |
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cholesterol-lowering drugs like statins reduce Cholesterol synthesis by acting as an anolog of _________ that can not be converted to ___________
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HMGCoA
Mevalonic Acid |
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one of the functions of Cholesterol is to make _________ which is used to make vit A, E, & K
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isopentyl pyrophosphate
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Cholesterol is also used to make vitamen __
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D
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cholesterol is also used to make ________,________, & _______
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cholesteryl esters, membranes & plasma lipoprotiens, & bile acids
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7-dehydrocholesterol is converted in the ______ by UV light into ___________
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Cholecalciferol (vit D3)
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Cholecalciferol (vit D3)is converted in the _______ by 25 hydroxylase into _________
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liver
25-hydroxycholecalciferol |
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25-hydroxycholecalciferol is converted in the _______ by 1 alpha hydroxylase into _____
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Kidney
1,25 DHCC |
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Cholesterol is modified to make two sets of bile acids with the addition of ______ & _______
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taurine & glycine
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the mnemonic "PVT TIM HALL always Argues, never Tires".
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Phenylalanine
Valine Tryptophan Threonine Isoleucine Methionine Histidine Arginine Lysine Leucine always argenine never tiresine |
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bile acids form fats by forming a ______
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mycell
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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
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Cholesterol makes up ________, & ________ carry cholesterol.
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plasma lipoproteins
plasma lipoproteins |
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Chylomicron is a type of _________
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plasma lipoproteins
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Describe the structure of cholesterol.
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Chol is 4 ringed C molecule that has C tail
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Identify the dietary and endogenous sources of cholesterol
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Dietary: Eggs, milks, meats --- endogenous: liver what tissue types?
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Identify the substrate-product-enzyme of the rate limiting step of cholesterol synthesis.
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HMG Co A (substrate) turned into Melamalonic acid ( product) by the enzyme HMG Co A reductase (RLS)
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Identify the enzyme deficiency in Smith-Lemli-Opitz syndrome.
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7 dehydro cholesterol reductase
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Describe 4 regulatory mechanisms of cholesterol synthesis.
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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 |
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Describe the structure of the cholesterol storage molecule.
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Esterify it with FA
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Recognize the mechanism of Vitamin D activation.
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Three tissue types: skin, liver, kidney ;know enzyme name for each tissue type.
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Describe the structure and function of bile acids.
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Bile acid has hydrophilic and hydrophobic side – can form a mycell to corrall hydrophobic FA in center to break them down
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Identify the mechanism of bile acid sequestrants.
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Fx: carry dietary and endogenous sources of cholesterol in bloodstream
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Describe the structure and function of lipoproteins.
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Sx:Lipoprotien is a lipid (covering & cargo) & protein (stick on outside as license plate)
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Recognize the presentation and the biochemical profile of a patient with Smith-Lemli-Opitz syndrome.
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Congenital malformations (palm of hand, etc.)
Elevations in substrate, enzyme decreased(7 dehydrocholesterol reductase) measured by enzyme activity. |
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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. |
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Describe the structure of cholesterol.
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Chol is 4 ringed C molecule that has C tail
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Describe the structure of cholesterol.
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Chol is 4 ringed C molecule that has C tail
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Describe the structure of cholesterol.
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Chol is 4 ringed C molecule that has C tail
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Identify the dietary and endogenous sources of cholesterol.
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Dietary: organ meats, the yolk of eggs
Endogenous: Liver, intestine, adrenal cortex, reproductive tissues |
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Identify the substrate-product-enzyme of the rate limiting step of cholesterol synthesis.
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HMG Co A (substrate) turned into Melamalonic acid (product) by the enzyme HMG Co A reductase (RLS)
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Identify the enzyme deficiency in Smith-Lemli-Opitz syndrome
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7 dehydrocholesterol 7 reductase (7-DHCR)
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Describe 4 regulatory mechanisms of cholesterol synthesis.
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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. |
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Describe the structure of the cholesterol storage molecule.
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For cholesterol to be a storage molecule we simply need to esterify it with a FA
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Recognize the mechanism of Vitamin D activation.
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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++ |
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Describe the structure and function of bile acids.
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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
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Identify the mechanism of bile acid sequestrants.
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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
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Describe the structure and function of lipoproteins.
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Sx: lipid covering & cargo with protein stuch on outside as license plate
Fx: carry dietary and endogenous sources of cholesterol in bloodstream |
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Recognize the presentation and the biochemical profile of a patient with Smith-Lemli-Opitz syndrome.
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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 |
