wk 8 - Lipoprotein receptors Flashcards
Friedewald equation can estimate the value of
a) Cholesterol
b) HDL
c) LDL
d) Triglycerides
c) LDL
The Friedewald formula has the following limitations EXCEPT
a) When chylomicrons are present
b) When plasma TG concentration exceeds 400 mg/dL (4.52 mmol/L)
c) In patients with type III hyperlipoproteinemia
d) When measured in fasting state
d) When measured in fasting state
Patients with Familial hypetriglyceridemia will tend to have a predominant elevated plasma _________
a) HDL
b) LDL
c) VLDL
d) LDL & VLDL
e) VLDL & Chylomicrons
Patients with Familial hypetriglyceridemia will tend to have a predominant elevated plasma VLDL
A disorder in lipoprotein metabolism is considered as a _________ cause of hyperlipidemia, whereas, diabetes is considered as a __________ cause of hyperlipidemia.
a) Primary
b) Secondary
A disorder in lipoprotein metabolism is considered as a primary cause of hyperlipidemia, whereas, diabetes is considered as a secondary cause of hyperlipidemia.
Cholesteryl ester is formed from cholesterol using ______.
Cholesteryl ester is formed from cholesterol using LCAT (Lecithin–cholesterol acyltransferase)
Diagnosis of dyslipidemia is dependent upon the measurement of the following EXCEPT:
a) Chylomicron
b) HDL
c) LDL
d) Tg
e) Total cholesterol
a) Chylomicron
According to Friedewald equation, the equation is not valid if:
a) Cholesterol > 4.5 mmol/L
b) Chylomicron > 4.5 mmol/L
c) HDL > 4.5 mmol/L
d) LDL > 4.5 mmol/L
e) Triglycerides > 4.5 mmol/L
e) Triglycerides > 4.5 mmol/L
LDL receptor recognizes VLDL, IDL and LDL through their ________
a) ABCA1
b) Apo B100
c) Apo 48
d) SRB1
b) Apo B100
A patient with high cholesterol and high LDL and normal triglycerides is more likely to have ___________ due to a genetic deficiency in ___________. Whereas, a patient with high triglycerides and normal cholesterol is more likely to have ____________ due to a deficiency in ___________.
a) Hypercholesterolemia
b) Hyperlipidemia
c) LDL receptor
d) lipoprotein lipase
A patient with high cholesterol and high LDL and normal triglycerides is more likely to have Hypercholesterolemia due to a genetic deficiency in the LDL receptors. Whereas, a patient with high triglycerides and normal cholesterol is more likely to have Hyperlipidemia due to a deficiency in Lipoprotein lipase
name the disease
Hypercholesterolemia
Given a serum HDL-C of 0.8 mmol/L, a total cholesterol of 6.0 mmol/L and a Triglyceride of 5.5 mmol/L, what is the most likely calculated LDL-C by the Friedwald formula?
a) 3.0 mmol/L
b) Not valid
c) 4.5 mmol/L
d) 5.0 mmol/L
e) 5.5 mmol/L
b) Not valid
- Tc > 4.5 mmol/L
Hyperlipidaemia is the term used due to high concentration of plasma _________.
a) Cholesterol
b) Chylomicron
c) HDL
d) LDL
e) Triglycerides
Hyperlipidaemia is the term used due to high concentration of plasma triglycerides.
The commonly measured lipids in serum are all the following EXCEPT
a) Cholesterol
b) Chylomicrons
c) HDL
d) LDL
e) Triglycerides
b) Chylomicrons
In the reverse __________ pathway for HDL to get rid of cholesterol, Cholesteryl ester transfer protein (CETP) exchanges ________ in VLDL for the _________ in HDL.
a) Cholesterol
b) Cholesteryl ester
c) Triglycerides
d) Direct
e) Indirect
In the reverse indirect pathway for HDL to get rid of cholesterol, Cholesteryl ester transfer protein (CETP) exchanges triglycerides in VLDL for the cholesteryl esters in HDL.
A patient with combined ____________ has elevated levels of serum cholesterol and triglycerides.
a) Hypercholestrolemia
b) Hyperlipoproteinemia
c) Hyperglycemia
d) Familial hypercholestrlemia
A patient with combined Hyperlipoproteinemia has elevated levels of serum cholesterol and triglycerides.
The enzyme HMG-CoA reductase plays a central role in the production of __________.
The enzyme HMG-CoA reductase plays a central role in the production of cholesterol.
Hypercholesterolemia could be regarded to any of the following EXCEPT
a) Mutation in Apo B100
b) Excess production of LDL
c) Mutation in LDL receptor
d) Increased production of HDL
d) Increased production of HDL
Patients with Familial hypetriglyceridemia will tend to have a predominant elevated plasma _________
a) HDL
b) LDL
c) VLDL
d) LDL & VLDL
e) VLDL & Chylomicrons
Patients with Familial hypetriglyceridemia will tend to have a predominant elevated plasma VLDL
________ carries ~2/3 of cholesterol in plasma.
a) HDL
b) LDL
c) IDL
d) Lipoprotein lipase
e) Lipoprotein receptors
b) LDL
In children, ________ are effective at reducing cholesterol levels in those with familial hypercholesterolemia.
In children, inulins are effective at reducing cholesterol levels in those with familial hypercholesterolemia.
How does cholesterol bind to HDL?
________ activated __________ which phosphorylates the ABC transporters. Phosphorylation induces a conformational change which permits binding of ATP and opening the channel for cholesterol to bind to __________.
a) cAMP
b) HDL
c) LDL
d) Protein kinase A
e) Insulin
How does cholesterol bind to HDL?
cAMP activated PCA (protein kinase A) which phosphorylates the ABC transporters. Phosphorylation induces a conformational change which permits binding of ATP and opening the channel for cholesterol to bind to HDL.
Hypercholesteremia means high _______
a) Chylomicron
b) HDL
c) IDL
d) LDL
e) VLDL
Hypercholesteremia means high LDL
_____________ is a protein best known for its role in the direct reverse pathway, facilitating the uptake of Cholesteryl ester-HDL in the ____________.
a) CETP
b) Extrahepatic cells
c) Liver
d) LCAT
e) Reverse Scavenger (SR-BI)
Reverse Scavenger (SR-BI) is a protein best known for its role in the direct reverse pathway, facilitating the uptake of Cholesteryl ester-HDL in the liver.
Given a serum HDL-C of 1.5 mmol/L, a total cholesterol of 6.0 mmol/L and a Trigyceride of 1.0 mmol/L, what is the most likely calculated LDL-C by the Friedewald formula?
a) 3.0 mmol/L
b) 4.0 mmol/L
c) 4.5 mmol/L
d) 5.0 mmol/L
e) 5.5 mmol/L
b) 4.0 mmol/L
LDL = Total Cholesterol – HDL – Trig/2.17 for mmol/L
A patient with familial hypercholesterolemia could be the result of a deficiency in ________. Thus the cells do not absorb _________ and it will be high in plasma.
a) LDL
b) LDL receptor
c) HDL
d) HDL receptor
A patient with familial hypercholesterolemia could be the result of a deficiency in LDL receptor Thus the cells do not absorb LDL and it will be high in plasma.
VLDL-c is estimated to be equal to ___________ in mmol/L
a) Triglyceride/2
b) Triglyceride/3
c) Triglyceride/4
d) Triglyceride/5
e) Triglyceride/6
d) Triglyceride/5
Reverse Scavenger (SR-BI)is a receptor on the liver facilitating the movement of cholesterol fromPeripheral tissuestowards theliver for excretion.
a) Reverse Scavenger (SR-BI) Cholesteryl ester
b) LCAT
c) CETP
d) Liver
e) Peripheral tissues
Reverse Scavenger (SR-BI) is a receptor on the liver facilitating the movement of cholesterol from Peripheral tissues towards the liver for excretion.
A patient with familial hypertriglyceridemia could be the result of a deficiency in _________. Thus the triglycerides won’t get hydrolysed and it will be high in plasma.
a) LDL
b) LDL receptor
c) Lipoprotein lipase
d) HDL receptor
A patient with familial hypertriglyceridemia could be the result of a deficiency in lipoprotein lipase Thus the triglycerides won’t get hydrolysed and it will be high in plasma.
In a clinical biochemistry lab, the ________ lipid profile is measured
In a clinical biochemistry lab, the fasting lipid profile is measured
A patient with Tangier disease is expected to have ___________
a) Hypercholestrolemia
b) Hypolipoproteinemia
c) Hyperglycemia
d) Familial hypercholestrlemia
A patient with Tangier disease is expected to have Hypolipoproteinemia
Excess cholesterol in the cells stimulates the liver to synthesise __________
a) HDL
b) LDL
c) IDL
d) VLDL
e) Lipoprotein lipase
a) HDL
In the reverse ______ pathway for HDL to get rid of cholesterol, LDL excreted its content of cholesterol to the ________ via interacting with its LDL receptors.
a) Kidney
b) Liver
c) Direct
d) Indirect
In the reverse indirect pathway for HDL to get rid of cholesterol, LDL excreted its content of cholesterol to the liver via interacting with its LDL receptors.
A patient with familial hypercholesterolemia could be the result of a normal synthesis of LDL, but lack of LDL ________.
A patient with familial hypercholesterolemia could be the result of a normal synthesis of LDL, but lack of LDL receptors.
________ _____ is the storage form of cholesterol in the body.
Cholesteryl ester is the storage form of cholesterol in the body.
__________ or HMG-CoA reductase inhibitors are a class of cholesterol lowering drugs that inhibit the enzyme HMG-CoA reductase which plays a central role in the production of _________ and prevent cardiovascular disease.
a) Cholesterol
b) Cholesteryl ester
c) Clathrin
d) LPL
e) Statins
Statins or HMG-CoA reductase inhibitors are a class of cholesterol lowering drugs that inhibit the enzyme HMG-CoA reductase which plays a central role in the production of cholesterol and preventing cardiovascular disease.
_______ mediates binding of LDL to the LDL-receptor.
a) ABCA1
b) Apo B100
c) Apo 48
d) SRB1
e) LCAT
b) Apo B100
Hyperlipidemia is measured in the _________ state.
a) Feeding
b) Fasting
Hyperlipidemia is measured in the fasting state.
In a ________ state, no chylomicrons are present in the blood.
a) Fasting
b) Feeding
In a fasting state, no chylomicrons are present in the blood.
After the ________ state, we expect to see high chylomicrons in the blood.
a) Fasting
b) Feeding
After the feeding state, we expect to see high chylomicrons in the blood.
Triglycerides are degraded by hepatic ________ so that, finally, small HDL particles are left, which restart the uptake of _________ from __________.
a) Cholesterol
b) Cholesteryl ester
c) Cells
d) Hydrolase
e) Lipase
Triglycerides are degraded by hepatic lipase so that, finally, small HDL particles are left, which restart the uptake of cholesterol from cells.
__________ on the cell surface binds to _________ in the blood to bring it inside the cell using __________. Both the LDL receptor and LDL could be recycled inside the cell. LDL is hydrolysed into amino acids, fatty acids and _________, which is converted to ___________ via LCAT for storage. Alternatively, _________ could go back to the cell surface. Excess LDL can inhibit the production of __________.
a) Cholesterol
b) Cholesteryl ester
c) Clathrin
d) LDL
e) LDL receptor
LDL receptor on the cell surface binds to LDL in the blood to bring it inside the cell using Clathrin. Both the LDL receptor and LDL could be recycled inside the cell. LDL is hydrolysed into amino acids, fatty acids and cholesterol which is converted to cholesteryl ester via LCAT for storage. Alternatively, LDL could go back to the cell surface. Excess LDL can inhibit the production of LDL receptors.
______________ could be regarded to mutation in
- Apo B100
- Apo A-I
- Apo A-II
- Apo C-III
- LPL
hypercholesterolemia could be regarded to mutation in
- Apo B100
- Apo A-I
- Apo A-II
- Apo C-III
- LPL
A patient with familial hypercholesterolemia could be the result of a _____ synthesis of LDL.
A patient with familial hypercholesterolemia could be the result of a high synthesis of LDL.
HDL ___________helps collecting fatty acids from the cells and convert it to HDL __________ in the _________ via enzyme lecithin-cholesterol acyltransferase (LCAT).
a) Cholesterol
b) Cholesteryl ester
c) Kidney
d) Liver
HDL cholesterol helps collecting fatty acids from the cells and convert it to HDL cholesteryl ester in the liver via enzyme lecithin-cholesterol acyltransferase (LCAT).
Hyperlipidaemias are abnormally elevated levels of any or all __________ or ___________ in the blood or both in ______________.
a) Combined hyperlipidaemia
b) Lipids
c) Lipoproteins
Hyperlipidaemias are abnormally elevated levels of any or all lipids or lipoproteins in the blood or both in combined hyperlipidemia
A patient with Tangier disease is expected to have absence of the transporter _________ thus, accumulation of cholesterol in the cell, and consequently, low cholesterol and _________ in the serum.
a) ABCA1 transporter
b) Cholesterol
c) HDL
A patient with Tangier disease is expected to have absence of the transporter ABCA1 transporter thus, accumulation of cholesterol in the cell, and consequently, low cholesterol and HDL in the serum.
_____________ is abnormally elevated levels of any or all lipids or lipoproteins in the blood.
Hyperlipidaemia is abnormally elevated levels of any or all lipids or lipoproteins in the blood.
i.e. Hyperlipoprotaeinaemia is a sub-class of hyperlipidaemia.
VLDL-c is estimated to be equal to ________ in mg/dL
a) Triglyceride/1.17
b) Triglyceride/2.17
c) Triglyceride/3.17
d) Triglyceride/5
e) Triglyceride/5.17
b) Triglyceride/2.17
HDL is synthesized by the liver and it picks ___________ in the cell by interaction with the ATP-binding cassette transporter A1 (ABCA1).
a) Cholesterol
b) Cholesteryl ester
HDL is synthesized by the liver and it picks cholesterol in the cell by interaction with the ATP-binding cassette transporter A1 (ABCA1).
