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BPM II-DM > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

L1.1 Outline the classifications of monosaccharides based on number of carbons atoms and functional group

A

By number of carbons:

triose, tetrose, pentose, hexose, heptose

By functional group:

  1. Aldose (C=O at C1): faster reducing power
  2. Ketose (ke “twose”; C=O at C2); slower reducing power
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2
Q

L1.2 Differentiate between: Pyranoses & furanoses; reducing and non-reducing sugars

A

pyranose: 6 membered saccharide ring containing 5 carbon molecules and 1 oxygen

furanose: 5 membered saccahride ring containing 4 carbon molecules and 1 oxygen

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3
Q

L1.3 Differentiate between L- and D-, alpha and beta anomers of glucose

A

L- &; D- glucose are enatiomers (mirror images). Indicates left and right position of OH in chain

Alpha and beta glucose anomers indicate downward position or upward position of -OH on ring, respectively. Forms are a result of cyclization and are interconvertible (mutarotate)

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4
Q

L1.4 Define the terms enantiomer and epimer with examples of each

A

enatiomer: mirror image; “reflection”

epimer: carbohydrate isomers that varying around one carbon only. i.e. glucose and galactose or glucose and mannose

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5
Q

L1.5 Differentiate between and indicate the bonds present in each of the examples listed: Monosaccahrides (glucose, galactose, fructose, ribose, deoxyridbose) Disaccharides (maltose, sucrose, and lactose) Oligosaccharides Polysaccharides (glucosamine and galatosamine)

A

Monosaccharides:

  1. Glucose: aldose
  2. Fructose: ketokexose
  3. Galactose: aldose
  4. Ribose & Deoxyribose: furan; components of nucleic acids; B-N-glycosidic linkage

Disaccharides:

  1. Sucrose: glucose + fructose - non reducing sugar - a-1,2 glycosidic bond
  2. Maltose: glucose + glucose - reducing sugar - a-1,2 glycosidic linkage
  3. Lactose: galactose + glucose - reducing sugar - B-1, 4 glycosidic linkage

Polysaccharides:

  1. glucosamine & glycosaminoglycans: sugar acid + amino sugar
  2. galatosamine: amino sugar
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6
Q

L1.6 Compare sucrose with HFCS regarding composition and monosaccharides

A

HFCS55: 55% fructose and 42% glucose (sucrose substitute) - can be digested as fructose and glucose

Sucrose can only be digested by sucrase

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7
Q

L1.7 Identify the linkage present in nucleosides

A

B-N-glycosidic linkage

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8
Q

L1.8 Identify the linkages in glycoproteins: O-linked glycosylation and N-linked glycosylation

A

O-linked: glycosylation of Ser/Thr

N-linked: glycosylation of Asn residue

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9
Q

L1.9 Review the glycolipids (or shingolipids or glucosphingolipids) Cerebrosides Sulfatides Globosides Gangliosides

A
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10
Q

L1.10 Identify the various carbohydrates present in urine in diabetes mellitus and in the inherited disorders of fructose and galactose metabolism

A

Diabetes Mellitus: glucose & sorbitol (prolonged elevation of glucose)

Fructosuria/hereditary fructose intolerance: fructose

Galactosemia: galactose

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11
Q

L2.1 Pentose Phosphate Pathway

A

purpose: produce NADPH & ribose phosphate for purine/pyrimidine synthesis

location: cytosol

key enzyme: glucose 6 phosphate DH

co-factor: TPP

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12
Q

L2.2 Define glycolysis and explain its role in generation of metabolic energy

A

breakdown of glucose to for pyruvate under aerobic or anaerobic conditions.

Generates net 2 ATP, 2 Pyruvate, 2 NADH per glucose (aerobic)

Generates 2 ATP & 2 Pyruvate per glucose (anaerobic)

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13
Q

L2.3 Compare and contrast the action of glucokinase and hexokinase. Use graph.

A

glucokinase: high Vmax; high Km (low affinity) found in liver and beta-cells of pancreas

hexokinase: low Vmax, low Km (high affinity) found in most other tissues. Add picture

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14
Q

L2.4 List the reactions and enzymes that convert the glucose into pyruvate. Key enzymes & irreversible enzymes.

A
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15
Q

L2.5 Define substrate level phosphorylation and identify the glycolytic reactions

A

substrate level phosphorylation:

  • formation of ATP without the use of the mitochondria
  • direct transfer of phosphate from high energy molecule to ADP to form ATP.

Reactions:

  1. phosphoglycerate kinase: 1,3BPG –> 3 PG
  2. pyruvate kinase: PEP –> pyruvate
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16
Q

L2.6 Explain significance of lactate production in anaerobic glycolysis. Indicate the further fate of lactate formed in muscle (Cori cycle)

A

Lactate production allows for pyruvate to be converted back into glucose in the liver, since there is no O2 for use of TCA in anearobic conditions

Cori Cycle: glucose –> pyruvate –> lactate via LDH in muscle/tissues lactate –>pyruvate –> glucose via LDH-5 in liver glucose then released back into blood stream for use by tissues

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17
Q

L2.7 Describe the regulation of glycolysis indicating the regulatory enzymes

A

3 regulatory enzymes: all irreversible reactions

  1. Gluco/Hexokinase
  2. PFK-1: committed step
  3. Pyruvate kinase
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18
Q

L2.8 Appraise the role of AMP, ATP, and fructose 2,6 bisphosphate on glycolysis

A

AMP: favors glycolysis

ATP: favors gluconeogenesis

F-2,6BP: favors glycolysis (PFK-2); activates PFK-1 slide

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19
Q

L2.9 Highlight regulation of pyruvate kinase

A

fructose 1,6 BP feeds forward to pyruvate kinase upregulating activity phosphorylation of PK decreases activity

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20
Q

L2.10 Outline the function of glycolysis in specific tissues (liver, brain, muscle, eye, tumor cells)

A

brain & skeletal: glucose –> pyruvate –> acetyl CoA –> TCA –> complete oxidation

liver: only active when the blood glucose is high and less active when low

adipose: formation of DHAP used for TAG formation

retina, lens, & RBCs: no mitochondria; use of anerobic glycolysis

tumor cells: main source of energy from glycolysis; prefer FDG glucose analog

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21
Q

L2.11 Analyze the effect of pentavalent arsenate on glycolytic enzymes

A

inhibits glyceraldehyde 3-phosphate DH, PDH complex, and alpha-ketoglutarate DH complex

22
Q

L2.12 Identify the biochemical mechanisms involved in the occurrence of lactic acidosis in states of poor tissue perfusion/oxygenation and metabolic states where aerobic metabolism is hindered

A

lactic acidosis is a metabolic acidosis:

  • low pH due to decresaed HCO3-
  • compensation via hyperventilation to decrease PCO2

Due to an increased conversion of pyruvate to lactate increasing the NADH/NAD+ ratio;

important for driving glycolysis forward to maitain energy demands

23
Q

L2.13 Explain the role of NADPH generated by pentose phosphate pathway in metabolism.

A

NADPH required for FA synthesis, cholesterol synthesis, steroid hormone synthesis in liver, adipocytes, and endocrine synthesizing hormones.

***Also formed by malic enzyme

24
Q

L11.1 Indicate how pyruvate is transported from the cytosol into the mitchondrial matrix

A

Pyruvate is converted to Acetyl-CoA via PDH, which then enters the TCA cycle to produce 3 NADH, 1 FADH2, and 1 GTP

25
Q

L11.2 summarize the overall reaction catalyzed by the PDH complex

A

oxidative decarboxylation reaction:

Net equation:

Pyruvate + NAD+ + CoASH –> Acetyl CoA + NADH + CO2

  1. Pyruvate is Decarboxylated and is bound to thiamine pyrophosphate(TPP)
  2. TPP is oxidized by transfer to Disulfide form of Lipoic acid bound to Dihydrolipoyl transacetlyase.
  3. Acetyl group of lipoic acid is transferred to CoA
  4. Sulfhydrl form of lipoic acid is oxidized by dihydrolipoyl dehydrogenase-> Lipoic acid is reformed
  5. Reduced FADH by dihydrolipoyl dehydrogenase
26
Q

L11.3 Outline the multi-enzyme nature of PDH complex and the cofactors that it requires

A

3 catalytic domains:

  1. Pyruvate decarboxylase - E1
  2. Dihydrolipoyl transacetylase - E2
  3. Dihydrolipoyl dehydrogenase - E3

Cofactors:

prosthetic groups:

  • Thiamine pyrophosphate (TPP) - from B1
  • Lipoic acid - from octanoic acid
  • FAD - from B2

cofactors:

  • NAD+ - from B3
  • CoA - from B5
27
Q

L11.4 Outline the regulation of PDH complex:

  • role of NADH
  • role of Acetyl CoA
  • role of phosphorylation of PDH complex
  • regulation of phosphorylation
A
  • NADH & Acetyl CoA inhibit the activation of PDH
  • ATP, Acetyl CoA, and NADH activate PDH kinase, which phosphorylates PDH, inactivating PDH
  • Pyruvate inhibits PDH kinase, allowing PDH to be active
  • Ca2+ activates PDH phosphatase, allowing phosphatase to de-phosphorylate PDH, enabling its active form
  • *Activation:**
    1. Dephosphorylation
    2. Insulin in adipocytes and liver
    3. Catecholamines in Cardiac muscle
    4. Ca+2 in skeletal muscle
  • *Inhibition:**
    1. Phosphorylatin
    2. Acetly CoA, ATP, NADH
28
Q

L11.5 Indicate the inhibitory effects of trivalent arsenic compounds on PDH

A
  • Arsenic binds to lipoic acid, inhibiting interaction with dihydrolipoyl transacetylase
  • Results in Lactic acidosis, neurological defect, and death.
29
Q

L11.6 Discuss the consequences of thiamine deficiency:

  • Wernicke-Korsakoff syndrome
  • Beri-Beri
  • PDH and alpha-KG
A

PDH/a-ketogluterate DH/Branched chain a-ketoacid DH ALL require thiamine.

Deficiency of thiamine: (low PDH activity)
- Werneke-Korsakoff: Ataxia, Ophthalmolplagia, Memory loss, cerebral hemorrhage.

*alcoholics and malnourished individuals at risk
- Wet beri-beri: Heart failure, Decrease ATP, Increased cardiac output

  • PDH deficiency: increased pyruvate and lactic acid and alanine (transamination); decreased production og acetyl CoA; severe decrease in ATP production
30
Q

L11.7 Summarize the congenital abnormalities affecting the action of PDH complex and their clinical consequences.

A
  • increased pyruvate, lactic acid, and alanine
  • decreased Acetyl CoA production
  • severe decreased in ATP production

Presentations:

  • frontal prominence
  • wide nasal bridge
  • flares nares
  • long philtrum
  • Brain malformation: corpus callosum agenesis and cerebral adn basal ganglia cysts
31
Q

L11.8 Explain the central role of the TCA cycle in metabolism, including both its catabolic and anabolic functions (amphibolic role)

A
  • amphibolic (catabolic & anabolic): provides precursors for biosynthetic pathways and replaces used biosynthesis molecules
  • Catabolism: Energy producing/Oxidative phosphorylation
  • Anabolic: Pyruvate, a-Ketogluterate, oxaloacetate can be used for the synthesis of amino acids (alanine, aspartate, glutamine)
32
Q

L11.9 Outline the intermediates and the enzymes of the TCA cycle

L11.10 Explain the energetics of the cyle, including reactions where reducing equivalents (NADH and FADH2) are produced and the production of GTP by substrate level phsophorylation

A

NADH producing reactions:

  • Isocitrate dehydrogenase
  • alpha-ketoglutarate dehydrogenase complex
  • malate dehydrogenase

FADH2 producing reaction:

  • succinate dehydrogenase

GTP producing reaction:

  • succinate thiokinase
33
Q

L11.11 Explain why aerobic metabolism of glucose using the TCA cycle is much more efficient than anaerobic glycolysis

A

Aerobic metabolism of glucose using TCA give a total ATP production of 38 ATP (24 from TCA; 6 from PDH; 6 from Glycolysis)

Anaerobic glycolysis will only yield 2 ATP & 2 Pyruvate, but the pyruvate would not be able to be used in oxidative phosphorylation.

34
Q

L11.12 Explain the regulatory mechanism for the TCA cycle. Indicate the effect of NADH, ATP, succinyl CoA, Ca2+, and OAA

A

Regulation of TCA

Citrate Synthase:

  • irreversible reaction
  • product inhibition (citrate); activation by substrate (Acetyl CoA & OAA)

Isocitrate Dehydrogenase:

  • irrevesible reaction
  • allosteric activation by ADP & Ca2+
  • inhibition by ATP and NADH

Alpha-ketoglutarate Dehydrogenase:

  • requires 5 coenzymes (TPP, Lipoic Acid, FAD, NAD+, CoA)
  • activation by Ca2+
  • inhibition by NADH and succinyl CoA
35
Q

L11.13 Indicate the effect of fluorocitrate and malonate on TCA cycle

A

Fluorocitrate:

  • inhibits aconitase

Malonate:

  • competitive inhibitor of succinate dehydrogenase
36
Q

L12.1 Outline the aspartate-malate and glycerophosphate shuttles and their significance in regenerating cytoplasmic NAD+

A
  • Inner mitochondrial membrane is impermeable
  • Shuttle needed to deliver electrons from NADH from glycolysis to inner mitochondrial membrane.
  • *2 Shuttles:**
  • *1. Glycerol phosphate shuttle: (2 ATP synthesized)**
  • DHAP is reduced by Cystolic glycerol phosphate dehydrognase with 2e- from NADH+H to form Glycerol 3 phosphate
  • Glycerol 3-phosphate enters the inner mitochondrial membrane and is oxidized by Mitochondrial Glycerol Phosphate dehydrogenase to form DHAP and FADH2 which is used with CoQ
  • *2. Malate asparate shuttle: (3 ATP synthesized)**
  • Malate can enter the inner mitochondrial membrane and be oxidized with Mitochondrial malate dehydrogenase to form Oxaloacetate and NADH+H which interacts with Complex I of ETC
  • Oxaloacetate with glutamate and amino transferase forms aspartate and a-ketoglutarate and leave the mitochondria.
  • In the cytosol Aspartate and a-ketoglutarate converterd to OAA and glutamate by amino transferase, respectively. Glutamate is recycled back into mitochondria. OAA is converted to malate by cytosolic malate DH with the use of NADH.
37
Q

L12.2 Describe the role of the inner mitochondrial membrane in electron transport and oxidative phosphorylation

A
  • ETC results when NADH and FADH2 donate e- to complexes in the inner mitochondrial membrane. Eventually donated to oxygen forming water.
  • Impermeability allows the formation of the H+ gradient for ATP synthase.
  • ATP synthase causes H+ to flow from intermembrane space and into the matrix forming ATP by phosphorylation of ADP
38
Q

L12.3 Outline the different types of electron carriers found in the ETC complexes and follow the path of electrons from NADH and FADH2 to O2

A

Complex I (NADH DH):

  • prosthetic group: FMN (riboflavin deriv.)

Complex II (succinate DH):

  • prosthetic group: FAD (riboflavin deriv.)

CoQ: lipid mobile electron carrier

Complex III (cytochrome reductase):

  • prosthetic group: heme groups (Fe3+)

Cyt C: mobile protein

Complex IV (cytochrome oxidase):

  • prosthetic group: Cu2+ and hemer groups

Flow of electrons:

  1. NADH oxidized by CoQ at complex I; FADH2 oxidized by CoQ at complex II
  2. CoQH2 oxidized by cyt c at complex III
  3. cyt c oxidized by O2 at complex IV
  4. O2 is final electron acceptor at complex IV

Sources of NADH:

  • malate DH, a-ketoglutarate DH, isocitrate DH, PDH, b-oxidation and glycolysis

Source of FADH2:

-succinate DH

**CoQ can also accept electrons from glycerophosphate DH adn acy CoA DH

39
Q

L12.4 Discuss the mode of action/effect of specific inhibitors of the ETC:

  • antimycin A
  • azide
  • hydrogen sulphide
  • cyanide
  • rotenone
  • piercidin A
  • carbon monoxide
A

Antimycin A: inhibts cytochrome b of complex III (cytochrome reductase)

Azide, CO, H2S, and CN-: inhibit complex IV (cytochrome oxidase)

Oligomycin: inhibits ATP synthase; decreases ETC and oxygen consumption

Rotenone, piericidin A, and barbituate amytal: inhibit NADH dehydrogenase in complex I

40
Q

L12.5 Differentiate between direct inhibitors of ETC, uncouplers of oxidation phosphorylation, ATP synthase inhibitors (oligomycin), and inhibitors of the ATP/ADP translocase

A

Inhibition of ADP/ATP transport:

  • Atractyloside: toxic glycoside; binds the outward facing portion of the adenine nucleotide transporter
  • Bongkrekic acid: respiratory toxin binds inward facing portion of adenine nucleotide transporter

Uncouplers of oxidative phosphorylation:

  • DNP, ASA(aspirin), thermogenin, ionophore act by destroying the proton gradient
  • decrease ATP synthesis, increase ETC and oxygen consumption
  • uncoupling proteins create a “proton leak” allowing protons to re-enter the mitochondrial matrix without capturing any energy as ATP

ATP Synthase inhibitors:

  • Oligomycin blocks oxidative phosphorylation and the electron transport chain by inhibiting membrane bound mitochondrial ATP synthase (ATPase) and proton channel (pump, FO subunit) blocker

Thermogenin (uncoupling protein): brown adipose

  • H+ gradient generated from electron transport is uncoupled from ATP synthesis, generates heat
  • heat generation due to regulated uncoupling action of thermogenin

Ionophores:

  • makes inner membrane permeable to compounds that cannot usually cross; increas proton permeability
  • *Inhibitors of ETC can involve:**
  • Complexes of ETC (direct)
  • Decrease ATP synthesis, ETC, O2 consumption
  • Uncouplers(Creates leaks in the inner membrane->Disrupts H+gradient)
  • Decrease ATP, Increase ETC and O2 consumption
  • ATP synthase activity may be disrupted(respiratory control)
41
Q

L12.6 Explain how the electrochemical gradient is generated during electron transport to drive ATP synthesis and consider Mitchell’s Chemiosmotic theory

A
  • Electrons flowing through the ETC complexes 1,3,4 cause protons to be pumped into the intermembrane space -> pH gradient -> Complex 5 (ATP synthase pumps protons back into the mitochondrial matrix while generating ATP)
42
Q

L12.7 Describe the mode of action of the mitochondrial ATP synthase and its inhibiton by oligomycin

A
  • H+ are pumped into the matrix via ATP synthase and ADP is being phosphorylated to ATP.
  • Oligomycin binds to the inner membrane portion and blocks entry of H+ -> Stops ETC due to high gradient -> Respiratory control: Cytosol dependent ADP phosphorylation.
43
Q

L12.8 Define uncoupling of oxidative phosphorylation, uncoupling in brown adipose tissue vs other types of uncouplers (2,4 DNP, valinomycin, gramicidin A)

A
  • *Uncouplers of Oxidation phosphorylation**
  • *2 types (Both destroy H+ gradient)**
    1. Uncouplers: Specifically increase H+ permeability
  • Thermogenin/UCP: Present in Brown Fat and provides Heat
    2. Ionophores: Compounds which make inner membrane permeable to ions that cannot usually cross
  • Makes channels/pores/mobile carriers that can allow ions to cross membrane
  • Indirectly disrupts the H+ gradient
  • Gramicidin: Channel forming
  • Valinomycin: Mobile carrier(associated with K+ rich bilayers)
44
Q

L12.9 Discuss the transport of ADP into and ATP out of mitochondrion and inhibitors of this process (atractyloside adn bonbkrekic acid)

A

Adenine nucleotide translocase:

  • Antiporter exchange of ATP(out) and ADP(In)
  • *Inhibitors ADP/ATP transport:**
  • Atractyloside: Binds to outward facing(intermembrane space) portion of translocase
  • Bongkrekic acid: Binds the inward facing(matrix) portion of translocase
45
Q

L13.1 Discuss repsiratory control of ETC and the P/O ratio

A

P/O ratio= ATP formed per O2 atom reduced.

  • NADH=3ATP(Malate-asparate shuttle)
  • FADH2=2ATP(Glycerol phosphate shuttle)
46
Q

L13.2 Identify the role of oxidative phosphorylation at conditions of low oxygen

A

activity decreased, decreasing ATP synthesis and increasing lactic acid

47
Q

L13.3 Understand the inheritance pattern of mitochondrial diseases

A

Mother gives all children the disease. Only female children will give to all their children.

48
Q

L13.4 Identify common symptoms of mitochondrial diseases

A

Nervous system: seizures, movement disorders, developmental delays, deafness, dementia, stoke, visual defects, poor balance/coordination, peripheral nerve issues, migraines/headaches.

Skeletal Muscle: muscle weakness, exercise intoleracnce, pain, faitgue, carmps, low muscle tone

Liver: unexplained liver failuer

Kidneys: unexplained renal failure, nephrotic syndrome

Endocrine: diabetes, hyperthyroidism, and excess body hair

GI: difficulty swallowing, reflux, vomiting, feeling full, chronic constipation, intestinal disruption

Heart: cardiomyopathy and conduction abnormalities

Eyes: drooping, inability to move eyes, blindness

Ears: sensorineural deafness

49
Q

L13.5 List diseases involving mutations in mitochondrial DN, key symptoms, and common mutations for each.

A

Leber Hereditary Optic Neuropathy: (mitochondrial genome)

  • defective NADH DH
  • degeneration of retinal ganglion cells

Kearns Sayer: (mito deletion)

  • deletion within mitochondria (4997 bp)
  • affects systems with high energy requirements

MERRF: (tRNA mutation)

  • begin age 6-16yrs
  • myoclonus, seizures, ataxia, muscle weakness, worsening eye sight and hearin loss

MELAS: (OxPhos defect, mutation of mito tRNA)

  • stokes, myopathy, muscle twitching, dementia, and deafness
  • excess pyruvate reduces to lactic acid

Amingoglycoside Induced Deafness: (mutation of rRNA)

  • non syndromic hearing loss
  • bilateral to severe sensorineural hearing loss within a few days to weeks after admin of aminoglycoside antibiotic
50
Q

L13.6 identify the treatment options for patients with mitochondrial diseases

A
  • Physical therapy, speech therapy, and respiratory therapy, exercise
  • small frequent meals, midnight snack, and feeding at night
  • CoQ10, Vit C, high fat diet (medium chaing TGs), carnitine
  • avoid stress, alcohol, and cigarettes
  • artificial reproductive technology: taking healthy nucleus from mom’s egg and put into donor egg with healthy mitochondria, then fertilize.

BPM II-DM (5 decks)

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