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Biochem 3 Flashcards

1
Q

Kwashiorkor

A

Protein malnutrition! Skin lesions, edema, liver malfunction (fatty change due to dec. apolipoprotein synthesis). Small child with swollen belly.

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2
Q

Kwashiorkor mnemonic

A

MEAL: Malnutrition (protein), Edema, Anemia, Liver (fatty)

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3
Q

Marasmus

A

Total calorie malnutrition resulting in tissue and muscle wasting, loss of SubQ fat, and variable edema

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4
Q

How much net ATP via malate-aspartate shuttle

A
  1. because NADH is used in cytosol and matrix so you don’t lose anything.
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5
Q

Net ATP via glycerol-3-phosphate shuttle

A
  1. because you end up with reduced FADH2, so you end up losing 2 ATP per glucose (2.5(NADH)-1.5(FADH2)=1 (the loss of energy from one pyruvate formed)
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6
Q

Malate-aspartate shuttle

A

Needed because NADH can’t cross the inner mitochondrial membrane. In cytosol OAA is converted to malate and this then enters matrix to produce a new NADH in the TCA cycle. Aspartate is the way OAA can move from matrix to cytosol.

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7
Q

Glycerol-3-phosphate shuttle

A

DHAP formed in glycolysis is reduced to glycerol-3-phosphate which is then oxidized by glycerol-3-phosphate dehydrogenase which gives its electrons to FADH2, hence the loss. It also is a way of regenerating NAD+ for glycolysis.

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8
Q

Glycolysis net ATP production

A

2 net

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9
Q

Arsenic effect

A

Causes glycolysis to produce 0 net ATP

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10
Q

What does CoA and lipoamide carry

A

Acyl groups

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11
Q

What does Biotin carry

A

COOH (carboxylic acid group)

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12
Q

What does THFs carry

A

1-carbon units

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13
Q

What does SAM carry

A

Methyl (CH3) groups

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14
Q

What does TPP carry

A

Aldehydes

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15
Q

What family of molecules in NAD+ and NADP+

A

Nicotinamides from vitamin B3 (Niacin)

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16
Q

What family is FAD+

A

Flavins (Riboflavin B2)

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17
Q

NAD+ for what general reactions

A

Catabolic (for energy production)

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18
Q

NADPH+ for what general reactions

A

Anabolic processes (steroid and fatty acid synthesis), Respiratory burst,
Cytochrome P-450 system
Glutathione reductase

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19
Q

First step of glycogen synthesis in the liver?

A

Glucose to glucose-6-phosphate

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20
Q

Know all the differences between Hexokinase vs. Glucokinase…

A

Location, Km, Vmax, Induced by Insulin, Feedback-inhibited by glucose-6-P, gene mutation associated with maturity onset diabetes of the young (MODY)

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21
Q

What does it mean that hexokinase is feedback-inhibited by glucose6P

A

Excess glucose-6-P will stop hexokinase which makes sense in muscles where you only use the pathways to make energy. In liver, you’ll have excess glucose-6-P but you don’t want to slow it down so it does not feedback-inhibit.

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22
Q

What is MODY

A

Aut. dom. gene disrupting insulin production. (monogenic diabetes) Type I and Type II are multigenic

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23
Q

What does phosphofructosekinase-1 reaction do

A

Fructose-6-P to Fructose-1,6-bisphosphate

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24
Q

What reactions in glycolysis produce ATP?

A

1,3-BPG to 3-PG by phosphoglycerate kinase AND

Phosphoenolpyruvate to pyruvate by Pyruvate Kinase

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25
Q

Why does fructose-2,6-BP induce PFK-1?

A

Because when glucose is in high supply it is produced by PFK-2 and activates PFK-1

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26
Q

Why does alanine slow down pyruvate kinase?

A

alanine is made from pyruvate so if you have too much alanine, you probably have a lot of pyruvate, hence pyruvate kinase not needed.

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27
Q

Know regulation by F2,6BP

A

…..

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28
Q

Are Fructose bisphosphatase-1 and PFK-1 the same enzyme with different phosphorylations too?

A

No. They are not the same. PFK-1 reaction is unidirectional.

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29
Q

Where is pyruvate dehydrogenase complex and what does it do?

A

it is mitochondrial and links glycolysis to TCA cycle

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30
Q

When is PDH active?

A

In fed state

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31
Q

PDH has how many enzymes

A

3

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32
Q

Name the PDH cofactors

A
  1. Pyrophosphate (B1, thiamine; TPP)
  2. FAD (B2, riboflavin)
  3. NAD (B3, niacin)
  4. CoA (B5, pantothenate)
  5. Lipoic acid
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33
Q

What activates PDH

A

Exercise which also increases Ca2+, ADP, and NAD+/NADH ratio which all increase PDH

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34
Q

What is the basic reaction for PDF

A

pyruvate+NAD+ +CoA leads to acetyl-CoA+CO2+NADH

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35
Q

PDH is like what TCA cycle complex

A

alpha-ketoglutarate dehydrogenase complex (same cofactors, simlar substrate and action)

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36
Q

Arsenic does what to PDH

A

Inhibits lipoic acid

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37
Q

Arsenic presentation

A

Vomiting, rice-water stools, garlic breath

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38
Q

What happens if PDH is deficient

A

Buildup of pyruvate that shunts to form lactate (via LDH) and alanine (via ALT)

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39
Q

PDH def. findings

A

neurologic defects, lactic acidosis, increased serum alanine starting in infancy

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40
Q

PDH def. tx

A

Increased intake of ketogenic nutrients (e.g. high fat content or inc. lysine and leucine)

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41
Q

Lysine and Leucine are what…

A

The only purely ketogenic amino acids

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42
Q

Write out the pathways for pyruvate metabolism.

A

…..

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43
Q

Lactic acid dehydrogenase is used where

A

Major pathway in RBCs, leukocytes, kidney medulla, lens, testes and cornea

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44
Q

Mnemonic for TCA

A

Citrate Is Kreb’s Starting Substrate For Making Oxaloacetate

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45
Q

Write out steps for TCA

A

…..

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46
Q

Know the balanced equation for TCA cycle

A

1 Acetyl-CoA creates 3 NADH (7.5 ATP) + 1 FADH2 (1.5 ATP) + 1 GTP = 10 ATP….x2 equals 10

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47
Q

Where does FADH2 deposit it’s electrons

A

At succinate dehydrogenase which is complex II, it does not pump protons

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48
Q

What does CoQ do?

A

Shuttles electrons from Complex I and II to Complex III

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49
Q

What does cytochrome C do?

A

Shuttle electrons from complex III to IV

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50
Q

Rotenone

A

Stops Complex I

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51
Q

Antimycin A

A

Stops Complex III

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52
Q

Cyanide, CO

A

Stops Complex IV

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53
Q

Oligomycin

A

Stops Complex V

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54
Q

Final electron acceptor?

A

Complex IV: combines O2 + H2 to produce H2O with the elctrons

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55
Q

2,4-Dinitrophenol

A

Destroys proton gradient by making membrane more permeable

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56
Q

Where are the protons pumped into?

A

Into the intermembrane space of the mitochondria

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57
Q

Where does electron transport chain occur??

A

Inner mitochondrial membrane

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58
Q

What side is ATP formed on?

A

Inside the mitochondrial matrix, protons leak through ATP synthase into the matrix

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59
Q

Where does TCA cycle take place

A

In the mitochondrial matrix

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60
Q

What are examples of uncoupling agents

A

2,4-dinitrophenol (weight loss), aspirin, thermogenin in brown fat

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61
Q

What is the effect of uncoupling agents?

A

Increase O2 consumption, ATP production stops, but electron transport continues and makes heat

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62
Q

Why can’t muscle contribute to GNG?

A

No glucose-6-phosphatase

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63
Q

What are the irreversible enzymes of GNG?

A
  1. Pyruvate carboxylase (pyruvate + biotin (CO2) and ATP to produce OAA) in Mitochondria
  2. Phosphoenolpyruvate carboxykinase (OAA to phosphoenolpyruvate via GTP) in cytosol
  3. Fructose-1,6-bisphosphatase (Frcutose1,6BP to fructose6P) in cytosol
  4. Glucose6P to glucose in ER
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64
Q

Where can you find GNG enzymes?

A

Mostly liver, but also kidney, intestinal epithelium

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65
Q

How do fatty acids contribute to the metabolic pathways

A

Odd-chain fatty acids yield propionyl-CoA (3 C remnant of fatty acid) which can go into succinyl CoA and go into GNG. Even-chain fatty acids yield acetyl-CoA equivalents, cannot be used in GNG.

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66
Q

HMP stands for

A

Hexose Monophosphate, also known as the pentose phosphate pathway

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67
Q

HMP shunt contributes to

A

Glutathione reduction, ribose production, glycolytic intermediates

68
Q

HMP shunt uses how much ATP

A

No ATP is used

69
Q

Where does HMP shunt take place

A

lactating mammary glands, liver, adrenal cortex (sites of fatty acid or steroid synthesis), RBCs

70
Q

What is the oxidative step of HMP shunt?

A

Irreversible. Glucose-6-P forms Ribulose-5-P with the production of 2 NADPH and 1 CO2. This is via Glucose-6-P dehydrogenase and is the rate limiting step.

71
Q

What is the nonoxidative step of HMP shunt?

A

Ribulose-5-P forms Ribose-5-P, Glyceraldehyde3P, and fructose-6-P. It requires B1 (thiamine. The enzymes are phosphopentose isomerase, transketolases

72
Q

Explain respiratory burst…

A

NADPH is in phagolysosomes which reduce O2 to form superoxide which then can form H2O2 via superoxide dismutase. The H2O2 combines with chloride to form HOCL-, hypocholrite ion (bleach) to destroy the bacterium….

73
Q

What is myeloperoxidase

A

Blue-green heme-containing pigment that gives sputum its color

74
Q

What makes superoxide

A

NADPH oxidase

75
Q

What makes H2O2

A

Superoxide dismutase

76
Q

What makes HOCl

A

Myeloperoxidase

77
Q

Explain the glutathione cycling steps

A

Glutathione peroxidase oxidizes it to reduce the free radical, gluathione reductase with NADPH reduces it to GSH

78
Q

How is H2O2 broken down…

A

In bacteria, catalase

In humans, by glutathione peroxidase (glutathione is oxidized, reducing H2O2 to H2O)

79
Q

What is pyocyanin

A

From P. aeruginosa that generates ROS to kill competing microbes

80
Q

What is lactoferrin

A

Protein in secretory fluids and PMNs that inhibits microbial growth via iron chelation

81
Q

Chronic granulomatous disease patients are at increased infection from what

A

Catalase + species (they can’t use the bacteria’s H2O2 because the bacteria break their own down)

82
Q

is the breakdown of H2O2 oxidation or reduction?

A

H2O2 is reduced to H2O

83
Q

What are some oxidizing agents in G6PD deficiency

A

Fava beans, sulfonamides, primaquine, antituberculosis agents. INFECTION: free radicals from inflammatory response

84
Q

G6PD def. is due to what

A

Can’t produce enough NADPH

85
Q

G6PD def. genetics, ethnicity, benefits

A

X-linked recessive, most common human enzyme deficiency, more prevalent among blacks. Increased malarial ressitance.

86
Q

Pathology of G6PD def.

A

BITE into some HEINZ ketchup

87
Q

What is the end product of G6PD?

A

6-phosphogluconate

88
Q

Essential fructosuria

A

Defect in fructokinase. Benign, asymptomatic condition since fructose is not trapped in cells.

89
Q

Ess. fructosuria Genetics and presentation

A

Aut. rec.

Asymptomatic, but fructose in blood and urine

90
Q

Fructose or galactose disorders are worse?

A

Galactose disorders are worse for the analogous conditions

91
Q

Fructose intolerance genetics and path

A

Aut. rec. deficiency of Aldolase B. Fructose-1-P accumulates, sequestering pshophate, which inhibits glycogenolysis and GNG.

92
Q

Fructose intolerance presentation

A

After consuming fruit, juice, or honey. Hypoglycemia, jaundice, cirrhosis, and vomiting.

93
Q

Fructose intolerance lab work

A

Urine dip negative (glucose tested only); reducing sugar in urine positive (nonspecific)

94
Q

Fructose intolerance tx

A

Decrease fructose and sucrose intake

95
Q

how does fructose bypass PFK

A

by triose kinase which turns glyceraldehyde into glyceraldehyde-3-P which can then enter glycolysis

96
Q

Galactokinase deficiency genetics and path

A

Aut. rec. deficiency of galactokinase. Galactitol accumulates if galactose is present in diet.

97
Q

Galactokinase deficiency presentation

A

Relatively mild. Galactose in bloond and urine. Infantile cataracts. Failure to track objects or develop a social smile.

98
Q

Classic galactosemia genetics and path

A

Aut. rec. absence of galactose-1-phosphate uridyltransferase. Accumulation of toxic substances (including galactitol (accumulates in eye))

99
Q

Classic galactosemia presentation

A

failure to thrive, juandice, hepatomegaly, infantile cataracts, intellectual disability

100
Q

Classic galactosemia tx

A

exclude galactose and lactose from diet

101
Q

Mnemonic for galactose and fructose metabolism problems

A

FAB GUT

Fructose is to Aldolase B as Galactose is to Uridyl-Transferase

102
Q

Classic galactosemia and neonate condition

A

E. coli sepsis in neonates

103
Q

What causes the serious defects of fructose and galactose metabolism (general mechanism)

A

Depletion of phosphate

104
Q

sorbitol metabolism

A

it is the sugar alcohol of glucose made by Aldose reductase (uses NADPH), can be turned to Sorbitol Dehydrogenase using up a NAD+

105
Q

Too much sorbitol??

A

From chronic hyperglycemia: can cause cataracts, retinopathy, and peripheral neuropathy

106
Q

What creates sugar alcohols

A

Aldose reductase (with NADPH)

107
Q

What cells have both aldose reductase and sorbitol dehydrogenase

A

Liver, ovaries, and seminal vesicles

108
Q

What cells have only aldose reductase

A

Scwann cells, retina, and kidneys. lens has primarily aldose reductase

109
Q

Causes of lactase deficiency

A

Primary: age-dependent decline after childhood (absence of lactase-persistent allele), common in Asians, Blacks, and Native Americans.
Secondary: Loss of brush border due to gastroenteritis (e.g. rotavirus), autoimmune disease
Congenital lactase deficiency: rare

110
Q

Lactase deficiency lab tests

A

Low stool pH and positive hydrogen breath test with lactose tolerance test. Normal mucosa on biopsy with heriditary lactose intolerance.

111
Q

Lactase deficiency presentation

A

Bloating, cramps, flatulence, osmotic diarrhea

112
Q

Lactase def. tx

A

Avoid dairy products or add lactase pills to diet; lactose-free milk

113
Q

Name the essential Amino Acids

A

Methionine, valine, histidine, isoleucine, phenylalanine, threonine, tryptophan, leucine, lysine (9 total)

114
Q

What are the glucogenic amino acids

A

Methionine, valine, histidine

115
Q

What are the glucogenic/ketogenic amino acids

A

isoleucine, phenyalanine, threonine, and tryptophan

116
Q

What are the ketogenic amino acids

A

Leucine and Lysine

117
Q

What are the acidic amino acids

A

Glutamic acid and aspartic acid (neg. at body pH)

118
Q

What are the basic amino acids

A

Arginine, lysine, histidine

119
Q

What is the most basic amino acid

A

Arginine

120
Q

What basic amino acid has no charge at body pH

A

Histidine

121
Q

What basic amino acids needed during periods of growth

A

Arginine and histidine

122
Q

Know the steps of the urea cycle

A

….

123
Q

What makes up each urea molecule

A

NH3, CO2, and aspartate

124
Q

Explain how ammonia is transferred from muscle to liver

A

Amino acids give the amino group to alpha ketoglutarate forming alphaketoacids and glutamate. Glutamate gives its amino group to pyruvate to form alanine, alanine can then go to the liver, add its amino to alphaketoglutratae to form glutamate which participates in the urea cycle.

125
Q

What is the cori cycle

A

It is how lactate is recycled from the muscle to the liver. From lactate to pyruvate to glucose and then pumped back out.

126
Q

What is the path of hyperammonemia

A

Depletes alphaketoglutarate so TCA stops

127
Q

Ammonia intoxication

A

tremor (asterixis), slurring of speech, somnolence, vomiting, cerebral edema, blurring of vision.

128
Q

Treating hyperammonemia

A

Limit protein in diet. Benzoate or phenylbutyrate which bind amino acid and lead to excretion. Lactulose to acidify GI tract and trap NH4 for excretion

129
Q

What happens if you have a deficiency of N-acetylgutamate

A

You get hyperammonemia because you can’t use carbamoyl phosphate synthetase I

130
Q

N-acetylglutamate deficiency presentation

A

Presentation identical to carbamoyl phosphate synthetase I deficiency.

131
Q

N-acetylglutamate deficiency diagnosis

A

elevated ornithin with normal urea cycle enzymes suggets hereditary n-acetylglutamate deficiency

132
Q

most common urea cycle disorder

A

ornithine transcarbamylase deficiency

133
Q

OTC def. genetics and path

A

X linked rec. excess carbamoyl phospahte converted to orotic acid (part of pyrimidine synthesis pathway)

134
Q

OTC def. presentation

A

Evidence in first few days of life, but may present with late onset.

135
Q

OTC def. lab work

A

elevated orotic acid in blood and urine, low BUN, symptoms of hyperammonemia. No megaloblastic anemia (vs. orotic aciduria)

136
Q

How to make histamine

A

From histidine with B6

137
Q

How to make heme

A

From porphyrin which is made from glycine with B6

138
Q

How is GABA made

A

From glutamate with B6

139
Q

How is glutathione made

A

From Glutamate

140
Q

Where does Creatine, urea, and nitric oxide come from

A

From arginine. NO uses BH4

141
Q

Know the pathway of phenylalanine metabolism

A

………

142
Q

What does DOPA stand for

A

Dihydroxylphenylalanine

143
Q

What is responsible for causing albinism

A

Defective tyrosinase which turns DOPA into melanin

144
Q

What does carbidopa block

A

DOPA decarboxylase

145
Q

What causes alkaptonuria

A

Defective homogentisate oxidase

146
Q

Homogentisic acid comes from what

A

Tyrosine

147
Q

Alkaptonuria genetics and path

A

Aut. rec. congenital deficiency of homogentisate oxidase in the degradative pathway of tyrosine to fumarate.

148
Q

Alkaptonuria presentation

A

Benign disease. Dark connective tissue, brown pigmented sclerae, urine turns black on prolonged exposure to air. May have debilitating arthralgias. (homogentisic acid toxic to cartilage)

149
Q

what is Cahill cycle also called

A

the alanine cycle

150
Q

Why does lactic acid fermentation happen

A

To regenerate NAD+ to continue glycolysis because either 1. TCA has stopped because of anaerobic conditions or 2. Too much pyruvate for TCA or 3. Too much NADH

151
Q

Glyceraldehyde-3-phosphate in heavy alcohol consumption goes through what process

A

Because of excess NADH, it turns to glycerol-3-phosphate and combines with fatty acids to make TGs and you get hepatosteatosis

152
Q

Where does Pyruvate Dehydrogenase occur

A

Inside the mitochondrial matrix (pyruvate is actively shuttled into the matrix with a proton)

153
Q

Know the basic pathway for GNG

A

Pyruvate to OAA via pyruvate carboxylase and moving with every normal enzyme of glycolysis backwards until you reach PFK-1 stage, where instead you use fructose-1,6-bisphosphatase and then use glucose-6-Phosphatase.

154
Q

what does DHAP stand for

A

dihydroxyacetone phosphate

155
Q

How many atoms in malonyl CoA vs. Acetoacetyl CoA

A

Malonyl CoA has 3 carbons but gives 2 to FA synthesis.

AcetoacetylCoA also has 3 carbons, but lacks the carboxylic acid tail

156
Q

Describe outer mitochondrial emmbrane

A

Has porins that allow for anything smaller than 5000 daltons to move through, hence it is essentially cytosol for all these molecules.

157
Q

What is the permeability of the inner membrane

A

Freely permeable only to oxygen, carbon dioxide and water.

158
Q

Difference between OAA and aspartate

A

Aspartate has an amino group on it via aspartate aminotransferase.

159
Q

MODY presentation

A

Because it’s aut. dom. 50% of first degree relatives have it. it presents in second to fifth decade.

160
Q

What is LADA

A

latent autoimmune diabetes of adults (late Type I)

161
Q

LADA presentation

A

Non-obese Type II person is typical.

162
Q

Distinguish LADA from type II

A

Low C-peptide vs. high C-peptide. They have islet cell autoantibodies.

163
Q

What is GSH vs. GSSG

A

When glutathione is oxidized, it forms a disulfide bond (GSSG), the reduced form is a sulfhydryl (GSH)

164
Q

What is the basic explanation of GNG

A

Glycolysis has two irreversible reactions, pyruvate kinase and PFK-1, which are the only things that need a bypass in GNG. (you do this with OAA via PC and PEP carboxykinase)

165
Q

Why can’t citrate participate in GNG?

A

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