Lipid metabolism disorders / Questions and case reports

Questions

 * 1) Which of the following statements about LDL is true?
 * 2) * A – is involved in the supply of triacylglycerols to peripheral tissues
 * 3) * B – the main component of the surface part are cholesterol esters
 * 4) * C – apolipoprotein C is needed for its function
 * 5) * D – this particle is removed from the circulation by receptor-mediated endocytosis
 * 6) Which of the following does not participate in esterification in the centripetal transport of cholesterol?
 * 7) * A – lecithin-cholesterol acyltransferase (LCAT)
 * 8) * B – phosphatidylcholine
 * 9) * C – apolipoprotein A
 * 10) * D – apolipoprotein B
 * 11) Squalene is an intermediate metabolite in biosynthesis:
 * 12) * A – cholesterol
 * 13) * B – β-hydroxybutyrate
 * 14) * C – unsaturated fatty acid
 * 15) * D – sphingomyelin
 * 16) * E – acylcarnitine
 * 17) The following does not apply to triacylglycerol hormone-sensitive lipases:
 * 18) * A – catalyzes the degradation of triacylglycerols, which are transported in the nucleus of VLDL particles
 * 19) * B – is induced by insulin
 * 20) * C – is regulated by phosphorylation and dephosphorylation
 * 21) * D – is an integral part of HDL
 * 22) What results in the complete absence of apolipoprotein B-48??
 * 23) * A – VLDL cannot be formed
 * 24) * B – chylomicrons cannot be formed
 * 25) * C – LDL particles cannot be formed
 * 26) * D – cholesterol synthesis in the liver is impaired
 * 27) Fatty acids released from adipose tissue are transported by circulation::
 * 28) * A – in relation to albumin
 * 29) * B – as chylomicron-transferred triacylglycerols
 * 30) * C – as lecithin on the surface of HDL particles
 * 31) * D – none of the above mechanisms
 * 32) Fatty acid catabolism stimulates gluconeogenesis in all of the following ways except:
 * 33) * A – by contributing to the production of NADH
 * 34) * B – by providing carbons for the glucose skeleton
 * 35) * C – by activating pyruvate carboxylase
 * 36) * D –by contributing to the production of ATP
 * 37) Fatty acid serves as a source of energy for (list all):
 * 38) * A – liver
 * 39) * B – brain
 * 40) * C – muscles
 * 41) * D – red blood cells
 * 42) Which statement about HDL is correct?
 * 43) * A – has an antiatherogenic effect
 * 44) * B – arise in adipose tissue
 * 45) * C –transfer triacylglycerols in their nucleus
 * 46) * D – enable centripetal transport of cholesterol
 * 47) * E – in the circulation, they transmit apolipoprotein E and C to chylomicrons
 * 48) Multiplication of LDL particles is more dangerous in terms of atherogenicity than a multiplication of chylomicrons or VLDL because:
 * 49) * A – LDL particles are smaller than VLDL or chylomicron, so they penetrate the pores of the blood capillary wall and reach the target cells to which they supply cholesterol.
 * 50) * B – contain lecithin-cholesterol acyltransferase, which esterifies cholesterol to non-polar cholesteryl esters.
 * 51) * C – are taken up by target cells by endocytosis driven by specific receptors
 * 52) * D – their increased amount in the circulation stimulates endogenous cholesterol production in the endothelium of vascular capillaries
 * 53) Why are VLDL particles increased in alcoholics?
 * 54) Which lipoprotein particles are elevated in the absence of lipoprotein lipase?

Patient with hypertension and ischemic heart disease
A 52-year-old woman with hypertension (drug-controlled), coronary heart disease was examined for a lipid profile. The finding showed an increase in LDL-cholesterol (4.62 mmol / l), a decrease in HDL-cholesterol (0.90 mmol / l) and an increase in triacylglycerols (2.85 mmol / l). Her brother had mild hypercholesterolemia but a significant reduction in HDL cholesterol and normotriacylglycelemia, and her sister had severe triacylglycerolemia.

Questions:
 * 1) What are the main risk factors for coronary heart disease?
 * 2) What adverse effects can poorly treated diabetes have on lipoprotein metabolism?
 * 3) What induces oxidized LDL particles?

Patient after acute IM
A 53-year-old man who had an acute myocardial infarction was monitored by a attending physician. Triacylglycerol level: 1.6 mmol / l, HDL-cholesterol: 0.89 mmol / l, cholesterol: 9.5 mmol / l, calculated LDL-cholesterol also significantly increased. A "high cholesterol" has been reported in his younger brother's family history.

Questions:
 * 1) What is the most likely form of hyperlipoproteinemia in this patient?
 * 2) What is the mechanism of action of cholestyramine (bile acid sequestrant) and statins

Patient with hyperlipidemia
In a 65-year-old man, hyperlipidemia was detected at the routine examination: cholesterol: 8.8 mmol / l, triacylglycerols: 2.4 mmol / l. The patient had periorbital edema, dry skin and hair, had no family history of cardiovascular disease.

Questions: Note: thyroid disorder should be treated primarily, hyperlipoproteinemia usually resolves.
 * 1) What can be the causes of combined hyperlipoproteinemia?
 * 2) What other tests do you recommend for differential diagnosis?

Patient with xanthomas and hypercholesterolemia
A 55-year-old obese woman came to the GP with nodules about 2 cm in diameter on her forearms. She had yellowish streaks (palmar striae) on her palms.

Laboratory examination:
 * cholesterol: 11,9 mmol/l
 * triacylglycerides: 8,7 mmol/l
 * Lipoprotein ELFO: broad β fraction

Questions:
 * 1) What type of hyperlipoproteinemia is it?

46-year-old manager on a preventive check-up
He had a father's history of acute myocardial infarction at the age of 57 but lived to the age of 79. The patient is obese (104 kg, 175 cm), blood pressure 170/100 mmHg.

Laboratory examination: Question:
 * cholesterol: 6,5 mmol/l
 * triacylglycerols: 2,9 mmol/l
 * HDL cholesterol: 0,84 mmol/l
 * 1) What are the health risks of this patient?

Related articles

 * Cholesterol
 * Other chapters from the book MASOPUST, J., PRŮŠA, R .: Pathobiochemistry of metabolic pathways

Source

 * MASOPUST, Jaroslav and Richard PRŮŠA. Pathobiochemistry of metabolic pathways. 1st edition. Prague: Charles University, 1999. 182 pp. 80-85.  ISBN 80-238-4589-6.


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