Biochem Post-midterm Packet 1

1. 1Metabolism of a Beta-hydroxybutyrate leads to the production of how many ATP?

   1. A24
   2. B21
   3. C27
   4. D12
   5. E15
2. 2A deficiency in which of the following will result in failure of Beta-oxidation activation?

   1. AThiolase
   2. BThiophorase
   3. CAcyl CoA dehydrogenase
   4. DThiokinase
   5. EHMG CoA lyase
3. 3A biotin deficiency would most likely affect which of the following?

   1. ACPT-1 activity
   2. BCPT-2 activity
   3. CCarnitine/acylcarnitine translocase activity
   4. DOmega-oxidation
   5. EOxidation of odd chain fatty acids
4. 4Dr. House is volunteering his time at a clinic in West Africa. One afternoon, a man frantically carries his unresponsive child into the clinic. After inspecting the child, Dr. House immediately administers glucose intravenously. With careful monitoring, the child makes a full recovery. What is the most likely cause of the child's symptoms?

   1. AFailure of beta-oxidation of short chain fatty acids.
   2. BZellweger syndrome
   3. CFailure of beta-oxidation of medium chain fatty acids.
   4. DIngestion of the ripe Ackee fruit, leading to hypoglycin A toxification.
   5. EFailure of beta-oxidation of long chain fatty acids.
5. 5Choose the incorrect statement.

   1. AWe need linoleic acid for the production of arachidonic acid, for the production of eicosanoids, which include prostaglandins, thromboxanes and leukotrienes.
   2. BATP citrate lyase is required for the indirect transport of acetyl CoA from the mitochondrial matrix into the cytosol.
   3. CThe conversion of malate into pyruvate by malic enzyme results in the oxidation of 1 NADPH.
   4. DAcetyl CoA carboxylase (ACC), is a biotin requiring, rate-limiting enzyme of the first step of fatty acid synthesis, which requires 1 ATP/malonyl CoA formed.
   5. ECitrate allosterically activates ACC by promoting the polymer formation, while palmitoyl CoA allosterically inhibits ACC by promoting the dimer formation.
6. 6Choose the correct statement.

   1. AShort term hormonal regulation of ACC includes its activation by phosphorylation.
   2. BHigh fat diets can lead to increased synthesis of ACC.
   3. CThe fatty acid synthase (FAS) enzyme is most active in its dimeric form.
   4. DEach addition of two carbons from malonyl CoA to the growing fatty acid by FAS requires 1 ATP and 1 NADPH.
   5. EIn the fifth reaction of fatty acid synthesis, the growing chain is dehydrated to form a cis-monounsaturated fatty acyl group.
7. 7Palmitate elongation and desaturation primarily take place:

   1. Ain the cytosol and ER, respectively.
   2. Bin the cytosol.
   3. Cin the ER membrane.
   4. Din the ER and mitochondrial matrix, respectively.
   5. Ein the ER and cytosol, respectively.
8. 8Choose the correct statement.

   1. AErythrocytes synthesize eicosanoids.
   2. BAll eiocosanoids function locally via G-protein receptors, leading to either increased cAMP or increased intracellular calcium.
   3. CTypically, arachidonic acid resides at the C-2 position of membrane phospholipids and is released by phospholipase A2.
   4. DOther phospholipids, including A, C and D are frequently found in humans.
   5. EBoth 'b' and 'c' are correct.
9. 9Lipoxygenase:

   1. Ais inhibited by glucocorticoids.
   2. Bplays a role in converting PGH2 into leukotrienes.
   3. Cplays a role in converting PGH2 into PGE2.
   4. Dplays a role in converting arachidonic acid into leukotrienes.
   5. Eplays a role in converting arachidonic acid into PGE2.
10. 10Choose the incorrect statement.

    1. ACyclooxygenase plays a role in converting arachidonic acid into PGH2.
    2. BCyclooxygenase plays a role in converting arachidonic acid into PGI2 (prostacyclin).
    3. CCelebrex is a selective inhibitor of the nonconstitutive COX.
    4. DCortisol directly inhibits both COX-1 and COX-2.
    5. ECorticosteroids inhibit phospholipase A2.

11. 11Aspirin can promote vascular health in some individuals by:

    1. Aincreasing the ratio of TXA2/PGI2.
    2. BIncreasing both TXA2 and PGI2 production significantly.
    3. CDecreasing both TXA2 and PGI2 production significantly.
    4. DDecreasing the ratio of TXA2/PGI2.
    5. EBy inhibiting lipooxygenase.
12. 12Choose the incorrect statement.

    1. ATXA3 (from EPA) is less potent than TXA2 in platelet aggregation.
    2. BPGI3 (from EPA) has about the same potency as PGI2.
    3. C5-Hyroperoxyeicosatetraeinoic acid (HPETE) is created from arachidonic acid by 5-lipoxygenase (LOX) in leukotriene synthesis.
    4. DConcerning leukotriene synthesis, LTC4 has glutamate removed to produce LTE4, and subsequently, glycine removed to produce LTD4.
    5. ELTA4 is used in mast cells and eiosinophils to form LTC4 by addition of the tripeptide GSH (glutathione).
13. 13Choose the incorrect statement concerning cholesterol synthesis.

    1. AActivation, and subsequent decarboxylation of mevalonate (6-C) into isopentyl pyrophosphate (IPP 5-C) requires 3 high energy bonds.
    2. BThe condensation of IPP + DPP -------> geranyl pyrophosphate (GPP 10-C).
    3. CThe condensation of GPP + DPP -------> farnesyl pyrophosphate (FPP 15-C)
    4. DFPP + FPP -------> squalene (noncyclic) with the oxidation of NADPH.
    5. EFPP is also important in the production of ubiquinones and dolichol pyrophosphate.
14. 14Choose the incorrect statement.

    1. A The correct sequence of cholesterol synthesis is as follows: 2 acetyl CoA -------> acetoacetyl CoA -------> HMG CoA -------> mevalonate -------> 5-pyrophosphomevalonate -------> IPP -------> DPP -------> GPP -------> FPP -------> squalene -------> ianosterol -------> cholesterol.
    2. BThe total metabolic cost of producing 1 mole of cholesterol from acetyl CoA is 3 mole ATP and 4 mole NADPH.
    3. CPyrophosphate is required to keep the pathway intermediates of cholesterol synthesis soluble.
    4. DIanosterol is converted to cholesterol by a series of reactions in the cytosol by many enzymes, the details of which haven't been worked out as of yet.
    5. EThe most regulated enzyme in cholesterol synthesis is located in the ER membrane.
15. 15Choose the correct statement.

    1. AThe use of statins in competitively inhibiting HMG CoA reductase is only effective for short term treatment, as it leads to increased production of new HMG CoA reductase enzyme.
    2. BGlucagon leads to AMP kinase phosphorylation inhibition of HMG CoA reductase.
    3. CHigh intracellular concentrations of AMP stimulate AMP kinase which phosphorylates HMG CoA reductase thereby inactivating it.
    4. DHigh cholesterol stimulates the release of SREBP from the ER.
    5. EOnly high levels of cholesterol can lead to rapid degradation of HMG CoA reductase by the ubiquitin system in proteosomes.
16. 16Choose the incorrect statement.

    1. A Intestinal bacteria can convert primary bile salts into secondary bile salts, lithocholic and deoxycholic from cholic and chenodeoxycholic, respectively.
    2. BSLOS, an autosomal recessive disorder, is caused by a partial deficiency in 7-dehydrocholesterol reductase, which results in microencephaly and profound mental disabilities of the affected individual.
    3. CCholestanol and coprostanol are formed from free cholesterol by bacteria in the intestines.
    4. DACAT converts cholesterol to cholesteryl esters.
    5. EThe rate-limiting enzyme of bile synthesis is 7-alpha-hydroxylase, which is inhibited by one of its products, cholic acid.
17. 17Choose the correct statement.

    1. AThe synthesis of steroid hormones is affected by fed vs. unfed state.
    2. BAldosterone is unique among the steroid hormones in that it contains a phenol ring.
    3. CWhen ACTH binds its G-protein coupled receptor, it leads to production of cAMP which activates PKA which activates cholesterol esterase.
    4. DStAR facilitates the transport of cholesterol into the ER.
    5. EThe conversion of progesterone to cortisol takes place in the cytosol.
18. 18Choose the incorrect statement.

    1. AThe "multi-named" rate limiting enzyme of steroid synthesis, desmolase, requires 2 NADPH per pregnenolone produced from dihydroxycholesterol.
    2. BCortisol inhibits phospholipase A2.
    3. COnly unbound cortisol is physiologically active and can enter cells.
    4. DLH receptors in leydig cells lead to testosterone synthesis, while sertoli cells produce DHT, which is more potent than testosterone.
    5. EThe mixed function oxidase is cytochrome P450 dependent, and requires 2 NADPH to convert Cholesterol into dihydroxycholesterol.
19. 19Concerning congenital adrenal hyperplasias (CAH):

    1. A3-Beta-hydroxy steroid dehydrogenase deficiency leads to a massive production of progesterone.
    2. B17-Alpha-hydroxylase deficiency results in increased glucocorticoid production.
    3. C21-Alpha-hydroxylase deficiency is the most common CAH and it leads to overproduction of androgens as the glucocorticoid and mineralocorticoid intermediates are shunted towards androgen production.
    4. D11-Beta-hydroxylase deficiency leads to exorbitant renin levels.
    5. ETestosterone is produced in the zona fasciculata.
20. 20Choose the incorrect statement.

    1. ACushing's syndrome is usually caused by an adrenocortical tumor, resulting in hyperfunction of the adrenal cortex.
    2. BCushing's syndrome leads to increased cortisol and decreased ACTH concentration in plasma.
    3. CCushing's syndrome leads to glucocorticoid excess which leads to protein gain and characteristic fat distribution.
    4. DAddison's disease is usually caused by autoimmune destruction of the adrenal cortex.
    5. EIn addison's disease, patient's present with low aldosterone and cortisol levels, but high ACTH.
21. 21Glycosaminoglycans are homopolysaccharides made up of repeating disaccharide units.

    1. ATrue
    2. BFalse
22. 22GAGs account for the resilience of synovial fluid and aqueous humor of eye.

    1. ATrue
    2. BFalse
23. 23GAGS are made up of the following repeating disaccharide unit: [acidic sugar –amino sugar]n where the amino sugar is either D-glucosamine or D-galactosamine and the acidic sugar is either D-glucuronic acid or its C-5 epimer: L- iduronic acid. The exception to this is keratan sulfate where galactose is present instead of an acid sugar.

    1. ATrue
    2. BFalse
24. 24What is the only GAG not found covalently attached to proteins in proteoglycans?

    1. AHyaluron
    2. BChondroitin sulfate
    3. CKeratan sulfate
    4. DDermatan sulfate
    5. EHeparin
    6. FHeparan sulfate
25. 25What is the most abundant GAG (found in cartilage, bone and heart valves)?

    1. AHyaluron
    2. BChondroitin sulfate
    3. CKeratan sulfate
    4. DDermatan sulfate
    5. EHeparin
    6. FHeparan sulfate
26. 26Keratan sulfate is typically found aggregated with which type of GAGs?

    1. AHyaluron
    2. BChondroitin sulfate
    3. CDermatan sulfate
    4. DHeparin
    5. EHeparan sulfate
27. 27In addition to being similar in structure to heparin, heparan sulfate also contains more sulfate groups.

    1. ATrue
    2. BFalse
28. 28Unlike the other five types of GAGs, heparin is found intracellularly.

    1. ATrue
    2. BFalse
29. 29GAGs are linked to a protein core through a trihexoside and a Serine residue (X-Y-Z-Ser). What is the composition of X-Y-Z?

    1. AGalactose-galactose-xylose
    2. BXylose-galactose-galactose
    3. CGlucose-glucose-xylose
    4. DXylose-glucose-glucose
    5. EGalactose-glucose-xylose
30. 30Mucins are large glycoproteins with negatively charged sialic acid and N-acetyl neuraminicacid (NANA). They occupy a large space, trap water and serve as protective barriers which can trap pathogens.

    1. ATrue
    2. BFalse
31. 31The oligosaccharide part of glycoproteins is a mixture of:

    1. AD-hexoses
    2. BNANA
    3. CL-fucose
    4. DL-hexoses
    5. ED-fucose
    6. FGABA
32. 32The oligosaccharide part of a glycoprotein is attached to a protein through either an N-glycosidic link, which is the ____________ group of ____________, or an O-glycosidic link, which is the ____________ group of ____________.

    1. AAmide; asparagine; hydroxyl; serine or threonine
    2. BAmine; glutamine; carbonyl; serine or tyrosine
    3. CAmide; glutamine; carboxyl; threonine or tyrosine
    4. DAmine; asparagine; hydroxyl; serine or tyrosine
    5. EAmide; asparagine; hydroxyl; serine or tyrosine
33. 33O-linked and N-linked glycoside synthesis both take place in the ER and golgi. In contrast to O-linked glycosides, N-linked glycoside biosynthesis involves the use of both dolichol (lipid) and dolichol phosphate (phosphorylated lipid), both of which are derived from FPP (farnesyl pyrophosphate).

    1. ATrue
    2. BFalse
34. 34Choose the incorrect answer.

    1. AChylomicrons have the highest percentage of TAGs in lipoproteins while VLDLs have the second highest.
    2. BHDLs have the lowest percentage of cholesterol in lipoproteins.
    3. CLipoprotein lipase is an extracellular enzyme anchored by heparan sulfates mainly to the capillary walls of heart , skeletal muscle and adipose tissue.
       
    4. DLipoprotein lipase cleaves TAGs in chylomicrons and VLDLs and needs apo C-II for activation.
    5. ELipoprotein lipase is active as a dimer.
35. 35Choose the incorrect answer.

    1. AThe cardiac isozyme of lipoprotein lipase has a smaller Km for TAGs than adipose lipoprotein lipase.
    2. BThe release of chylomicrons from the intestinal mucosal cells into the lymph needs apo B-48
       
    3. C Chylomicrons obtain apo C-II and apo E in blood from HDL, which are required for activation of lipoprotein lipase (LPL) and entry into liver (as chylomicron remnants), respectively.
    4. DIn intestinal mucosal cells, mRNA editing of the apo B-100 transcript by cytidine deaminase results in the structure of apo B-48 which is the C-terminal 48% of apo B-100.
    5. EThe microsomal triglyceride transfer protein MTP is needed to assemble TAG-rich apo B containing lipoproteins.
36. 36Choose the incorrect answer.

    1. A VLDLs obtain apo C-II and apo E from HDLs in blood (as did CMs). LPL cleaves TAGs in VLDLs containing apo C-II. IDLs, the remnants of VLDLs, are formed and apo C-II is given back to HDLs.
       
    2. B Apo E of IDLs is given back to HDLs and the formed LDLs have only the large apo B-100. About 70% of these LDLs are taken up into the liver via the LDL-receptors which recognize apo B-100.
    3. COne of the principal functions of hepatic lipase is to convert intermediate-density lipoprotein (IDL) to low-density lipoprotein (LDL).
    4. DAt high free cytosolic cholesterol levels, the SCAP-SREBP complex is released in the ER membrane and SREBP can enter the nucleus.
    5. EAt high free cholesterol levels, the cytosolic enzyme (fatty) acyl CoA cholesterol acyl transferase (ACAT) is activated and a reservoir of cholesteryl esters is formed.
37. 37Choose the incorrect answer.

    1. ACETP is the cholesteryl ester transfer protein and allows the transfer of TAGs from VLDL into HDL in exchange for cholesteryl esters.
    2. BLCAT uses the fatty acid in position-2 of lecithin of the HDL monolayer.
    3. CHereditary CETP deficiency or inhibition by medical drugs, leads to higher LDL cholesterol and lower HDL cholesterol
    4. DHepatic lipase is a very unusual enzyme as it contains both lipase activity acting on TAGs in IDLs (HTGL) and it has also phospholipase activity.
    5. ETangier disease is related to a defective cholesterol ABC transporter in the plasma membrane which leads to very low serum HDL and coronary heart disease in childhood.
38. 38Choose the incorrect answer.

    1. AAbetalipoproteinemia is due to a defect in the microsomal TAG transfer protein (MTP) which normally interacts with apo B and is needed for the formation of VLDL or CM.
    2. BMTP (or MTTP) is essential for the assembly of chylomicrons and VLDL.
       
    3. CAbetalipoproteinemia is characterized by very low amounts of serum VLDL, LDL and chylomicrons. The name refers to LDL that are nearly absent in blood.
    4. DFeatures of abetalipoproteinemia include fat malabsorption and TAG accumulation in liver and intestine, retinitis pigmentosa and peripheral neuropathy.
    5. EAbetalipoproteinemia effects apo E containing lipoproteins.
39. 39Choose the incorrect answer.

    1. AHypercholesterolemia is often related to defective LDL-receptors or apo E deficiency.
    2. BThe Friedewald equation is especially useful in calculating the VLDL-C of obese patients.
    3. CType I hyperlipidemia: Hyperchylomicronemia, is often caused by a genetic deficiency of LPL (Type Ia) or of apo C-II (Type Ib) or presence of a LPL inhibitor protein (Type Ic).
    4. DFamilial Hypercholesterolemia (type IIa hyperlipidemia) is an autosomal dominant disorder which results in a defective LDL-receptor.
    5. EDysbetalipoproteinemia (type III hyperlipidemia) is a rare disease characterized by palmar xanthomas and tubereruptive xanthomas over the elbows and knees.
40. 40Choose the correct association(s) concerning hyperlipidemias.

    1. AType I results in increased chylomicron levels.
    2. BType IIa results in increased LDL.
    3. CType IIb results in increased VLDL and LDL.
    4. DType III results in increased IDL remnants as well as increased chylomicron remnants.
    5. EType IV results in increased VLDL.
    6. FType V results in increased VLDL and chylomicrons.
41. 41Choose the incorrect answer.

    1. AStatins are used to treat hyperlipidemias by inhibiting HMG CoA reductase.
    2. BCholestyramine is use to treat hyperlipidemias by binding bile acids and leading to their excretion.
    3. CNiacin reduces LDL-cholesterol and TAGs, but has the unintended consequence of lowering HDL.
    4. DFibrates lower VLDL concentration in blood via decreased VLDL synthesis and increased LPL activity.
    5. ELp(a) is very similar to LDL, but it has an additional apo(a) which shows the unusual structure of “kringles."

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Quiz on Biochem Post-midterm Packet 1, created by mbkatz21 on 24/03/2014.

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