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BIOCHEMISTRY > BIOCHEMISTRY- Processes Videos > Flashcards

BIOCHEMISTRY- Processes Videos Flashcards

1
Q

From where is energy extracted?

A

From food via oxidation

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2
Q

Which are the processes of energy extracted from food?

A
  1. Hydrolyzed in the GI tract to a diverse set of monomeric building blocks
  2. Building blocks are degraded to a common metabolic intermediate, acetyl CoA
  3. Citric acid cycle oxidizes acetyl CoA to CO2
  4. Extraction of energy from food is oxidative phosphorylation in which the energy of NADH and FADH2 is released via the ETC and used by an ATP synthase to produce ATP
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3
Q

Which cycle oxidizes acetyl CoA to CO2?

A

Citric acid cycle

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4
Q

What is increased every time metabolism is increased?

A

CO2

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5
Q

What is the first substrate of TCA cycle?

A

Acetyl CoA

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6
Q

Which are the products of TCA cycle?

A

2 CO2, 3 NADH and FADH2

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7
Q

What activates NADH and FADH?

A

Dehydrogenases

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8
Q

What do NADH and FADH2 produce?

A

Electrons

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9
Q

What happens to the electrons produced by NADH and FADH?

A

The electron transporter chain take them

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10
Q

Where does Electron Transporter chain work?

A

In the inner mitochondrial membrane

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11
Q

Who is the acceptor of electrons?

A

O2

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12
Q

Which is the most common cause of damage tissue?

A

Hypoxia–> Decrease the production of energy

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13
Q

Three main causes of hypoxia

A

Vessels
Heart/lung
Red blood cells

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14
Q

Which enzyme derives the energy of the electron transport chain?

A

ATP synthase

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15
Q

What is the function of ATP synthase?

A

Derives the energy of the E;ectron Transport chain to make ATP

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16
Q

Which is the process of how ATP is produced by ATP synthase?

A

By oxidative phosphorylation

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17
Q

What are the main sources of Acetyl CoA?

A

Carbohydrate → Glucose → Pyruvate
Fat → Fatty acids
Protein → Aminoacids

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18
Q

Which is the process where GLucose becomes Pyruvate?

A

Glycolysis

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19
Q

What else is produce in Glycolysis?

A

ATP (in the abscense of Oxygen)

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20
Q

From where is ATP produce in the abscense of Oxygen?

A

From anaerobic Glycolysis

Substrate Level phosphorylation

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21
Q

Which enzyme is required from pyruvate conversion to Acetyl CoA?

A

PDH

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22
Q

When do Carbohydrates produce Acetyl CoA?

A

After a meal

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23
Q

When do Fat produce Acetyl CoA?

A

Between meals

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24
Q

Process that leads from fatty acids to Acetyl CoA?

A

β oxidation

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25
Q

Which hormone is present after a meal?

A

Insulin

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26
Q

Which hormones are present between meals?

A

Glucagon, Cortisol, epinephrine

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27
Q

Who are the main source of Acetyl CoA when you are between meals?

A

Fatty acids

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28
Q

Which is the only organ that uses Fatty acids after a meal?

A

Heart

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29
Q

What is GLycogen?

A

Taking a lot of glucose and forming a large chain of glucose

Storage form of glucose

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30
Q

Which hormone forms glycogen?

A

Insulin

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31
Q

What controls the formation of glycogen?

A

Insulin

High levels of ATP from burning sugar

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32
Q

Which is the starting point of Gluconeogenesis?

A

In the liver starting from pyruvate

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33
Q

From where can we get pyruvate?

A

From aminoacids, alanine by alanine transmaminase

From lactate coming from Red blood cells by cori cycle

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34
Q

Which organ produces Ketone bodies?

A

Liver

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35
Q

Which organs use ketone bodies to make Acetyl CoA?

A

Heart, kidneys

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36
Q

Once ATP is high, what is the effect of insulin?

A

Make glycogen or make fat

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37
Q

Once ATP is high, what is the effect of Glucagon?

A

Make ketones
Make glucose thorugh gluconeogenesis
Release glucose from glycogen through gluconeogenesis

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38
Q

Which food are high carb meals?

A

Starch, sucrose, lactose

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39
Q

After digestion of starch, sucrose and lactose by amylase… What are the results?

A

Maltose, isomaltose, sucrose, lactose

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40
Q

Who breaks maltose, ismolatose, sucrose and lactose?

A

Brush border disaccharidases

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41
Q

What are the products of brush border disaccharidases?

A

Glc, Gal, Fru (Monosacharides)

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42
Q

Which forms of carbohydrates can’t be absorbed?

A

Disacharides, they have to be monosacharides

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43
Q

How are monosacharides absorbed in the intestinal lumen?

A

By active transport by Na+/ Gl symporter

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44
Q

Which are the insulin dependent tissues?

A

Liver, adipocytes anb muscle

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45
Q

Which GLUT is very associated with insulin?

A

GLUT 4

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46
Q

What is the effect of increased insulin related to GLUT 4?

A

Increases the number of plasma membrane GLUT 4 transporters

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47
Q

Where are GLUT 4 found?

A

In muscle and adipose tissue

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48
Q

What is the effect of GLUT 4?

A

Glucose removal out of Blood

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49
Q

How are GLUT 4 made?

A

Cytoplasmic vesicles with membrane bound GLUT 4 transporters

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50
Q

Which is the sign for GLUT 4?

A

Insulin effect, opening the vesicle to free GLUT 4

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51
Q

How is responsable of opening the vesicle who frees GLUT?

A

Insulin binds to the receptor → All the systems activated → PI3 kinase → Open vesicles

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52
Q

What is the effect of insulin in the adipose tissue?

A

↑ LPL (lipoproteinlipase) → break down tryglycerides and Fatty acids

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53
Q

Why do we require LPL?

A

Because Tryglycerides can’t go into the membrane; so membrane they break down to fatty acids pass thorugh the membrane and once again inside the adipocyte become tryglyceride and stored

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54
Q

Where do we find GLUT 1?

A

Most tissues (brain, red cells)

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55
Q

Where do we find GLUT-2?

A

Liver, Pancreatic β cells

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56
Q

Where do we find GLUT 3?

A

Most tissues

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57
Q

Where do we find GLUT 4?

A

Skeletal muscle

Adipose tissue

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58
Q

Which GLUT manage basal uptake of glucose?

A

GLUT-1 and GLUT-3

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59
Q

What is the function of GLUT-2?

A

Uptake and release of glucose by the liver; β cell glucose sensor

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60
Q

It’s function is insulin stimulated glucose uptake; stimualted by exercise in skeletal muslce

A

GLUT 4

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61
Q

Which are the normal glucose concentration?

A

4-6 mM (72-110 mg/ dL)

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62
Q

Which are the GLUT that transport GLucose at a constant rate regardless of blood GLucose?

A

GLUT 1 and GLUT 3 (1mM value)

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63
Q

km glucose levels of GLUT 2

A

15 mM

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64
Q

Which GLUT serves as a glucose sensor in the pancreas?

A

GLUT 2 in β pancreatic cells

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65
Q

What is the process of glucose once it gets to the pancreas?

A
  1. Enter β cell by GLUT 2
  2. GLucokinase phosphorylate GLucose
  3. Glucose phosphate enters glycolysis in Mitochondrion
  4. Oxidation is done making a lot of ATP
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66
Q

What is the effect of high ATP levels in β pancreatic cells?

A

Closes K ATP channel → Decreased membrane depolarization → Opens Ca2+ channel (calcium enters pancreatic cells) → Activates ATPases → COnversion of proinsulin to insulin → insulin is released out of the pancreas into blood stream

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67
Q

How is insulin secretion?

A

Biphasic:

  1. Preformed insulin (occurs within 10-15 minutes)
  2. Newly synthesized insulin (last up to 2 hours)
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68
Q

Which enzyme converts Glucose to Glucose 6 P?

A

Hexokinase

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69
Q

Who regulates Hexokinase?

A

The product which is Glucose 6P

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70
Q

Which enzyme is found in the liver and has the same activity as Hexokinase?

A

Glucokinase

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71
Q

What is the function of Kinase?

A

Phosphorylate the product = ATP → ADP

72
Q

Who regulates Glucokinase?

A

Insulin

73
Q

Which is one of the most important enzymes in glycolysis?

A

PFK-1 (Phosphofructokinase- 1 )

74
Q

What is the effect of PFK 1?

A

Conversion of Fructose 6P to Fructose 1,6 bis P

75
Q

What is the importance of PFK-1?

A

Is highly regulated by a lot of things but the main ones: AMP (+), ATP (-) and Citrate (remember this last one is pruduced during Kreb cycle)

76
Q

From all the processes of glycolysis, how do we get to Pyruvate?

A

From Phosphoenolpyruvate, thanks to Pyruvate kinase effect it becomes pyruvate

77
Q

Which enzyme makes Acetyl CoA from Pyruvate?

A

Pyruvate dehydrogenase

78
Q

Which are the main pathway that Acetyl CoA can cause?

A

TCA of Fatty acid synthesis

79
Q

Type of enzyme defect found with Pyruvate defect?

A

Partial defect

80
Q

Pathologies associated with Pyruvate kinase

A

Hemolytic anemia
Increased BPG
NO HEINZ BODIES

81
Q

What is the function of Pyruvate kinase?

A

It catalyzes the transfer of a phosphate group from phosphoenolpyruvate (PEP) to ADP, yielding one molecule of pyruvate and one molecule of ATP

82
Q

Second most common cause of Hemolytic anemia

A

Pyruvate kinase deficiency

83
Q

Which are the only metabolic pathway remain in Erythrocytes?

A

Glycolysis

Hexomonophosphate shunt

84
Q

Why do RBC require GLycolysis?

A

Because they require energy for the pumps of channels in the memebrane to maintain a gradient, of not the cells shape is lost which leads to hemolytic anemia

85
Q

Why do erythrocytes require NADH?

A

Antioxidant
Conversion of Methemoglobin to hemoglobin. Remember that NADH gives electrons and those electrons are required for the conversion of Fe+3 (methemoglobin) to Fe2+ (normal hemoglobin)

86
Q

What is the effect of 2,3 BPG in the RBC?

A

↓ O2 affinity for Hb

↑ O2 unloading

87
Q

What is found in erythrocytes structure in G6P deficiency?

A

Heinz bodies

88
Q

Most common cause of Hemolytic anemia

A

G6P deficiency

89
Q

What are the effects after high carb meal?

A

↑ ATP
↓ PFK-1
↓ GLycolysis

90
Q

Where is PFK-2 6-P found?

A

Liver

91
Q

What is the result of PFK-2?

A

Fructose 6P → Fructore 2,6 P

92
Q

What is the function of PFK-2?

A

Force PFK-1 to work in the liver to conclude forming fatty acids

93
Q

Who regulates positively PFK-2?

A

Insulin

94
Q

Who turns off PFK-2?

A

Glucagon

95
Q

How many ATP are generated in anaerobic glycolysis?

A

2

96
Q

Where does 2,3 BPG bind in the RBC?

A

To β subunits

97
Q

?What is the function of 2,3 BPG

A

Kick out the oxygen of the erythrocyte in order to oxygenate tissues

98
Q

Does 2,3 BPG bind to HbF?

A

NO

99
Q

What is the function of Lactase?

A

Convert Lactose to Glucose and Galactose

100
Q

Where does Galactose enters?

A

Liver and Brain

101
Q

Which enzyme catabolizes Galactose?

A

Galactose kinase and the product is Galactose 1-P in the liver and the brain

102
Q

What enzyme is required for galactose1-P to become Glucose 1-P?

A

Gal 1- P Uridyl transferase

103
Q

Which enzymes might be deficient in Galactosemia?

A

Galactokinase

Gal 1- P Uridyl transferase

104
Q

Clinical findings of Glacatokinase deficiency

A

Cataracts early in life

105
Q

Clinical findings of Gal 1- P Uridyl transferase deficiency

A 
Cataracts early in life
Vomiting, diarrhea after lactose ingestion
Letharghy
Liver damage, hyperbilirubinemia
Mental retardation
106
Q

If galactose accumulate where does it go?

A

To the lens

107
Q

Once galactose goes to the lens what happens?

A

Aldose reductase catabolizes it, becoming Galactiol (Polyol)

108
Q

What is the effect of Galactiol in the lens?

A

It gets trapped causing cataracts and swelling

109
Q

What explains cataracts in diabetics?

A

Glucose accumulate in the lens becoming sorbitol thanks to aldolase reductase

110
Q

What are the components of Sucrose?

A

Glucose+ Fructose catalized by sucrase

111
Q

Where does Fructose go?

A

Liver and kidney

112
Q

In fructose metabolism which are the main enzymes?

A

Fructokinase and aldolase B

113
Q

What does Fructokinase catalize?

A

Fructose to Fructose 1-P (phosphorylates)

114
Q

What does Aldolase B catalize?

A

Fructose 1P → Glyceraldehyde or DHAP

115
Q

Alternative name for fructokinase deficiency

A

Essential fructosuria

116
Q

Findings of Aldolase B deficiency

A 
Lethargy, vomiting
Liver damage, hyperbilirubinemia
Hypoglycemia
Hyperuricemia
Renal proximal tubule defect (Fanconi)
117
Q

Alternative name for Aldolase B deficiency

A

Hereditary Fructose Intolerance

118
Q

Which enzyme catalizes the conversion of Pyruvate to Acetyl CoA?

A

Pyruvate dehydrogenase

119
Q

Where is Pyruvate dehydrogenase located?

A

In the Mitochondria

120
Q

What does Pyruvate dehydrogenase do?

A

Two paths:
Take the electrons of Pyruvate; from NAD form NADH and generate 3 ATP and CO2
Becomes Acetyl CoA enters TCA cycle and form more ATP

121
Q

Which is the main characteristic of Pyruvate Dehydrogenase?

A

Highly regulated

122
Q

Who regulates Pyruvate dehydrogenase?

A

Acetyl CoA (the product- negatively)

123
Q

What does Pyruvate Dehydrogenase need to work?

A 
Tender Loving Care For Nancy
Thiamine pyrophosphate (TPP) form vitamin Thiamine
Lipioc acid
Coenzyme A (CoA) from panthothenic
FAD (H2) from riboflavin
NAD (H) from niacin
124
Q

Which enzymes require the mnemonic “Tender Loving Care For Nancy”?

A

Pyruvate Dehydrogenase
α ketoglutarate
Branched-chain ketoacid dehydrogenase

125
Q

Why can IV glucose solution kill alcoholic patients?

A

Because of Lactic acidosis

126
Q

Why IV solution cause lactic acidosis in alcoholic patients?

A

Thiamine deficiency → Bad function of Pyruvate dehydrogenase → Pyruvate not becoming Acetyl CoA → Pyruvate accummulate out of mitochoncria in the cytoplasm → Lactic dehydrogenase start working on accumulated Pyruvate → Lactic Acidosis → Dead

127
Q

How many ATPs are generated by Acetyl CoA in Kreb Cycle?

A

12 ATP per Acetyl CoA, but glucose generate 2 acetyl CoA so 24 ATP total

128
Q

In TCA cycle what is the function of α ketoglutarate dehydrogenase?

A

Catabolize α ketoglutarate to Succinyl CoA producing CO2 and NADPH

129
Q

What does α ketoglutarate need to work?

A 
Tender Loving Care For Nancy
Thiamine pyrophosphate (TPP) form vitamin Thiamine
Lipioc acid
Coenzyme A (CoA) from panthothenic
FAD (H2) from riboflavin
NAD (H) from niacin
130
Q

Which is the most important enzyme of Kreb cycle?

A

Isocitrate dehydrogenase

131
Q

What regulates Isocitrate dehydrogenase?

A

ATP, NADH (low ATP, NADH → ↑ Isocitrate dehydrogenase; High ATP, NADH → ↓ Isocitrate dehydrogenase)

132
Q

Once Isocitrate dehydrogenase is inhibited what is the effect?

A

Isocitrate accummulates in the mitochondria → Citrate spills out to cytoplasm → Citrate accumulation on cytoplasm → Inhibition of PFK 1 (Top regulator of glycolysis)

133
Q

Alternative names for Coenzyme Q

A

Ubiquinone
CoQ
CoQ10

134
Q

What is Coenzyme Q?

A

A lipid

135
Q

In oxidative Phosphorylation pathway in electron chain reaction which are the bypass reaction for Ubiquinone?

A

Succinate dehydrogenase FADH2 Complex II (krebs cycle)
Fatty Acyl CoA dehydrogenase FADH2 (β oxidation)
GLycerol-P shuttle FADH2 (Glycolysis)
NADH dehydrogenase Comple I

136
Q

Which enzyme does β oxidation?

A

Fatty Acyl CoA dehydrogenase FADH2

137
Q

During Oxidative phosphorylation on the mitochondria which drugs inhibit NADH dehydrogenase Complex I?

A 
Barbiturates
Rotenone (an insecticide)
138
Q

How do Barbiturates and Rotenone inhibit the production of ATP?

A

Stop electron flow from NADH dehydrogenase Complex I to Coenzyme Q (Ubiquinone)

139
Q

In oxidative Phosphorylation who affects complex IV cytochrome oxidase?

A

Cyanide

140
Q

How does cyanide kill?

A

Because it binds Fe in its Fe3+ form in Complex IV, then when electrons come down in electron transport when they get in complex IV, electrons can’t go to complex IV in the Fe3+ because there is cyanide, so electrons back up (electrons flow stop) so no ATP is made

141
Q

What are the antidotes for cyanide poisoning?

A

1) Nitrite

2) Thiosulfate

142
Q

How does Nitrite work as antidote for Cyanide poisoning?

A

1) Nitrite (oxidative agent, removes electrons) → making Methemoglobin
Hb (Fe2+) + Nitrite → Hb (Fe3+)
Once Methemoglobin is formed (thanks to nitrite), cyanide will look for Fe3+ and bind to it, instead of binding to the Fe3+ of the Complex IV

143
Q

How does Thiosulfate work as antidote for Cyanide poisoning?

A

Will convert cyanide to thiocyanate (less toxic)

144
Q

What does CO bind to?

A

To Fe2+ form

145
Q

How does CO affect Complex IV?

A

Because it binds to Fe2+ form of the complex IV, preventing the electron to bind to Fe2+, so no ATP generated

146
Q

What is the function of the F0 channel?

A

Transportation of protons to the F1 compartment in the phosphorylation of ADP to ATP

147
Q

How does Oligomycin inhibit ATP formation?

A

By inhibiting F0 channel, so no proton transportation to F1 compartment, so no ADP Phosphorylation to ATP

148
Q

Which drug inhibits F0 channel in Mitochondrioa in ATP formation?

A

Olygomycin

149
Q

Which antiporter system moves ATP out of the mitochondrioa?

A

ATP/ ADP translocase

150
Q

What is the function of ATP/ADP translocase?

A

Works as Antiporter moving ATP out of the mitochondria and introducing ADP once again into the mitochondria

151
Q

Who regulates Oxidative phosphorylation?

A

ADP (controls rate- respiratory control)

152
Q

In the oxidative phosphorylation process who works as an uncoupler?

A

2,4 DNP

153
Q

What is the effect of 2,4 DNP?

A

Weak base which allows H+ back in matrix, so no ATP production, because protons do not reach F1 compartment

154
Q

Which drugs are consider uncouplers?

A

Aspirin (High dose)

Thermogenin

155
Q

How is glycogen formed?

A

By α 1, 4 glucose attachment to another α 1,4 glucose, thanks to glycogen synthase
After 12-13 glucose residues, a branching enzyme make it α 1,6 glucose linkage

156
Q

Who positively regulates glycogen synthase? Where?

A

Insulin, in the liver and muscle

157
Q

Who turns off glycogen synthase?

A

Glucagon

158
Q

Which enzyme breaks down Glycogen in order to form Glucose 1 P?

A

Glycogen Phosphorylase

159
Q

What is the function of Glycogen Phosphorylase?

A

Adds inorganic phosphate to cleave sugar bonds converting Glycogen to Glucose 1-P

160
Q

Which are the two most important phosphorylases?

A

Glycogen phosphorylase

Purin Nucleoside Phosphorylase

161
Q

Which is the accesory enzyme that helps Glycogen Phosphorylase?

A

Debranching enzyme, which debranch the α 1,6 Glucose, depolarizing

162
Q

Who regulates Glycogen Phosphorylase?

A

Glucagon (Liver)
Epinephrine (liver, muscle)
AMP (muscle)

163
Q

Who inhibits or dephosphorylates Glycogen Phosphorylase?

A

Insulin

164
Q

Which enzyme catabolizes the conversion of Glucose 6 P to Glucose?

A

Glucose 6 Phosphatase

165
Q

Where can we find glucose 6 Phosphatase?

A

In the liver

166
Q

In the muscle what happens to GLucose 6 P?

A

Enters glycolysis, becoming pyruvate in the end generating Lactate or ATP, CO2 + H20

167
Q

Where is glycolysis made?

A

In the muscle

168
Q

What is purpose of glucose 6- Phosphatase found only in the liver?

A

Because it maintains glucose in the body

169
Q

Glycogen storage diseases

A

von Gierke
Pompe
Cori disease
Andersen disease

170
Q

Which pathology is associated to GLucose 6 phosphatase deficiency?

A

von Gierke disease (GLycogen storage disease)

171
Q

Cardinal clinical features of von Gierke disease

A

Severe hypoglycemia, lactic acidosis, hepatomegaly, hyperlipidemia, hyperuricemia, short stature, doll like facies, protruding abdomen, emanciated extremities

172
Q

How is glycogen synthesis in von Gierke disease?

A

Normal

173
Q

Deficient enzyme in Pompe disease

A

Lysosomal α 1,4 glucosidase

174
Q

Cardinal clinical features Pompe disease

A

Cardiomegaly, muscle weakness, death by 2 year

175
Q

How is glycogen synthesis in Pompe disease?

A

Glycogen like material in inclusions bodies

176
Q

Deficient enzyme in Cori disease

A

Glycogen debranching enzyme

BIOCHEMISTRY (12 decks)

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