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Step 1 - Biochemistry > Metabolism > Flashcards

Metabolism Flashcards

1
Q

Reactions that take place in the mitochondria: 6

A
  1. Beta oxidation
  2. Actetyl-CoA production
  3. TCA cycle
  4. Oxidative phosporilation
  5. Ketogenesis
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2
Q

Reactions that take place in the cell’s cytoplasm

A
  1. Glycolisis
  2. HMP shunt: ruta pentosas
  3. Synthesis:
    - Steroids (SER)
    - Proteins (RER)
    - Fatty acids
    - Cholesterol
    - Nucleotides
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3
Q

Reactions that take place both in the mitochondria and the cytoplasm

A

HUGs take two
Heme synthesis
Urea cycle
Gluconeogenesis

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4
Q

Combines 2 molecules into 1 using an energy source

A

Synthase

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5
Q

Combines 2 molecules into 1 without using an energy source

A

Synthetase

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6
Q

Rate-determing enzyme of glycolisis

A

Phosphofructokinase-1 (PFK-1)

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7
Q

Rate-determing enzyme of gluconeogenesis

A

Fructose -1,6 - biphosphatase

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8
Q

Rate-determing enzyme of TCA cycle

A

Isocitrate dehydrogenase: It’s the citrate cycle

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9
Q

Rate-determing enzyme of glycogenesis

A

Glycogen synthase

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10
Q

Rate-determing enzyme of glycogenolysis

A

Glycogen phosphorylase

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11
Q

Rate-determing enzyme of HMP shunt

A

G6PD

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12
Q

Rate-determing enzyme of de novo pyrimidine synthesis

A

Carbamoyl phosphate synthetase II

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13
Q

Rate-determing enzyme of urea cycle

A

Carbamoyl phosphate synthetase I

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14
Q

Rate-determing enzyme of de novo purine

A

Glutamine-PRPP amidotransferase

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15
Q

Rate-determing enzyme of fatty acid synthesis

A

Acetyl-CoA carboxylase

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16
Q

Rate-determing enzyme of Ketogenesis

A

HMG-CoA synthase

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17
Q

Rate-determing enzyme of Cholesterol synthesis

A

HMG-CoaA reductase

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18
Q

Regulator of PFK-1

A

Fructose-2,6-biphosphate

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19
Q

Arobic metabolism of glucose yelds

A

32 net ATP: malate-aspartate shuttle (heart and liver)

30 net ATP: glycerol-3-phosphate shuttle (muscle)

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20
Q

Anaerobic metabolism of glucose yelds

A

2 ATP

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21
Q

Toxic that causes glycolysis to produce zero net ATP

A

Arsenic

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22
Q

TPP carries

A

Aldehydes

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23
Q

Biotin carries

A

CO2

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24
Q

Tetrahydrofolates carry

A

1-carbon units

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25
Q

S-adenosylmethionine carries

A

Ch3 groups

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26
Q

Product of the HMP shunt

A

NADPH

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27
Q

NAD is used in

A

catabolic processes

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28
Q

NADH is used in

A

Anabolic processes

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29
Q

At low glucose concentrations

A

Hexokinase sequesters glucose in the tissue

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30
Q

At high glucose concentrations

A

Excess glucose is stored in the liver

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31
Q

Location of glucokinase

A

Liver

Beta cells of pancreas

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32
Q

Location of hexokinase

A

Most tissues

Except liver and beta cells of pancreas

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33
Q

Km of hexokinase

A

Lower: higher affinity

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34
Q

Km of glucokinase

A

Higher: lower affinity

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35
Q

Vmax of hexokinase

A

Lower: lower capacity

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36
Q

Vmax of glucokinase

A

Higher: higher capacity

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37
Q

Induced by insuline: hexokinase or glucokinase?

A

Glucokinase

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38
Q

Feedback-inhibited by glucose-6-phosphate

A

Hexokinase

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39
Q

Feedback-inhibited by fructose-6-phosphate

A

Glucokinase

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40
Q

Reactions that require ATP for glycolisis

A

Glucose to glucose-6-P (hexokinase)

Fructose-6-P to fructose-1,6-BP (PFK1)

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41
Q

Glucagon enhances FBPase-2 or PFK2?

A

FBPase2

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42
Q

Insulin enhances FBPase-2 or PFK2?

A

PFK2

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43
Q

Fructose-2,6-biphosphate acts as a positive alosteric regulator for

A

PFK-1: produce more fructose-1,6,BP for glycolysis

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44
Q

Mitochondrial enzyme complex linking glycolisis and TCA cycle

A

Pyruvate dehydrogenase complex

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45
Q

Pyruvate dehydrogenase active in fasting/fed state?

A

Fed

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46
Q

Pyruvate dehydrogenase complex cofactors

A 
The Lovely Coenzimes For Nerds:
Tiamine
Lipoic acid
CoA
FAD
NAD
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47
Q

Arsenic inhibits

A

Lipoic acid (cofactor for pyruvate dehydrogenase complex)

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48
Q

Arsenic poisoning clinical findings

A
  1. Vomiting
  2. Rice-water stools
  3. Garlic breath
  4. QT prolongation
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49
Q

Pyruvate dehydrogenase complex deficiency: heredability

A

X-linked

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50
Q

Findings of a pyruvate dehidrogenase complex deficiency

A
  1. Neurologic defects
  2. Lactic acidosis
  3. High serum alanine (starting infancy)
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51
Q

Pyruvate dehydrogenase complex deficiency: consequences

A

Excess pyruvate gets shunt to lactate (LDH) and alanine (ALT)

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52
Q

Tratment of Pyruvate dehydrogenase complex deficiency:

A

Intake of ketogenic nutrients:

  • Intake of lysine and leucine
  • High fat content
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53
Q

the onLy pureLy ketogenic aminoacids

A

Lysine

Leucine

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54
Q

Lactic acid dehydrogenase is the end of anaerobic glycolisis. This is the major pathway in

A 
RBC
WBC
Kidney Medulla
Lens
Testes
Cornea
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55
Q

TCA cycle yelds per glucose

A 
6 NADH
2FADH2
4CO2
2GTP= 
20ATP
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56
Q

TCA cycle substrates

A

Citrate is Kreb’s Starting Substrate For Making Oxaloacetate:

Citrate
alpha ketoglutarate
Succinyl-CoA
Succinate
Fumarate
Malate
Oxaloacetate
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57
Q

1 NADH via ATP synthase yields

A

2.5 ATP

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58
Q

1 FADH2 via ATP synthase yields

A

1.5 ATP

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59
Q

Rotenone inhibits

A

Complex ONE inhibitor

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60
Q

Antimycin inhibits

A

Complex 3: an-3-micyn

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61
Q

Cyanide and CO inhibit

A

Complex 4: COCN: 4 letters

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62
Q

ATP synthesase complex V inhibitor

A

Oligomycin

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63
Q

Uncoupling agents of AT synthase

A

2,4 Dinitrophenol
Aspirin
Thermogenin (brown fat)

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64
Q

Gluconeogenesis irreversible enzymes

A

Pathway Produces Fresh Glucose

  1. Pyruvate carboxylase
  2. Phophoenolpyruvate carboxylkinase
  3. Fructose-1,6-biphosphatase
  4. Glucose-6-phosphatase
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65
Q

Gluconeogenesis takes place in

A

Liver mainly
Kidney
Intestinal epithelium

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66
Q

Fatty acids that can participate in the TCA cycle

A

Odd-chain fatty acids: they yeld 1 propionyl CoA

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67
Q

Process that doesn’t use or produce ATP

A

HMP shunt

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68
Q

HMP shunt yelds

A

NADPH

Ribose

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69
Q

HMP shunt takes palce in

A

Cytoplasm

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70
Q

Phases of HMP shunt

A

Oxidative: irreversible
Nonoxidative: reversible

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71
Q

Rate limiting step of HMP shunt

A

Glucose 6P dehydrogenase

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72
Q

Why is G6PD so important in RBC

A

It produces NADPH necessary to keep glutathione reduced to detoxify free radicals: its lack leads to hemolytic anemia due to poor RBC defense against oxidising agents

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73
Q

Oxidising agents important in G6PD deficiency

A

Fava beans: favismo
Sulfonamides
Primaquine
Antituberculosis drugs

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74
Q

Heredability in G6PD deficiency

A

X linked

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75
Q

G6PD deficiency is more common in

A

African Americans: it offers more resistance to malaria

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76
Q

Anatomopathological findings in G6PD deficiency

A

Bite into some Heinz ketchup

  1. Heinz bodies: denatured Hb precipitates inside cell
  2. Bite cells: splenic macrophages phagocyte Heinz bodies
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77
Q

Disorders of fructose metabolism

A
  1. Essential fructosuria

2. Fructose intolerance

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78
Q

Disorders of galactose metabolism

A
  1. Galactokinase deficiency

2. Classic galactosemia: G-uridyltransferase

79
Q

Essential fructosuria is due to a defect in…

A

Fructokinase

80
Q

Fructose intolerance is due to a defect in

A

Aldolase B

81
Q

Symptoms of fructose intolerance

A
  • Hypoglucemia: fructose 1 P accumulates causing a deficit of phosphate which results in inhibition of glycogenolysis and gluconeogenesis
  • Jaundice
  • Cirrhosis
  • Vomiting
82
Q

Treatment of fructose intolerance

A

No intake of fructose and sucrose (glucose+fructose): fruit, juice, honey

83
Q

May present as a failure to track objects or develop a social smile

A

infantile cataracts: galactokinase deficiency

84
Q

Absence of galactose-1-phosphate-uridyltransferase

A

Classic galactosemia

85
Q

Toxic substance that accumulates in galactosemia

A

Galactitol

86
Q

Symptoms of classic galactosemia

A
  1. Failure to thrive
  2. Jaundice
  3. Hepatomegaly
  4. Infantile cataracts
  5. Intellectual disability
87
Q

Urine dipstick in fructose intolerance

A

Negative: it tests for glucose only

88
Q

High blood levels of galactose result in the conversion of

A

Galacticol via aldose reductase:

Danger it is osmotically active

89
Q

Glucose transforms into Sorbitol via

A

Aldose reductase

90
Q

Sorbitol transforms into Fructose via

A

Sorbitol dehydrogenase

91
Q

Aldose reductase is present in

A 
LuRKS
Lens
Retina
Kidneys
Schwann cells
92
Q

Aldose reductase
Sorbitol dehydrogenase
Both present in

A

Liver
Ovaries
Seminal vesicles

93
Q

Primary lactase deficiency

A

Age dependent decline after childhood: asians, african and native americans

94
Q

Secondary lactase deficiency

A

Loss of brush border lactase due to GE

95
Q

Congenital lactase deficiency

A

Rare

Defective gene

96
Q

Findings in lactase deficiency study

A

Stool: low pH
Breath: high H content with lactose hydrogen breath test
Intestinal biopsy: normal mucosa if hereditary lactose intolerance

97
Q

Clinical findings in lactase deficiency

A

Bloating
Cramps
Flatulence
Osmotic diarrea

98
Q

Essential amino acids, glucogenic

A

I MET HIS VALentine, she is so SWEET
Methionine
Histidine
Valine

99
Q

Basic Aa

A

His lies are so basic:
Histidine
Lysine
Arginine

100
Q

Urea compounds

A

CO2
NH3
Aspartate

101
Q

Allosteric activator of Carbamoyl phosphate synthetase I

A

N-acetylglutamate

102
Q

Ammonia is transported by

A

Alanine in the Cahill Cycle

103
Q

Cori cycle

A

Glucose-Piruvate-Lactate from liver to muscle

104
Q

Hyperammonemia results in

A

Excess NH3 which deplets alpha-ketoglutarate, leading to inhibition of TCA cycle

105
Q

Treatment of hyperammonemia

A
  1. Limit protein in diet
  2. Lactulose to acidify the GI tract and trap NH4
  3. Rifaximine to low down colonic ammoniagenic bacteria
    Benzoate/phenylacetate/phenylbutirate: form renally excretable products
106
Q

Symptoms of hyperammonemia

A
  1. Tremor: asterixis
  2. Slurring of speech
  3. Somnolence
  4. Vomiting
  5. Cerebral edema
  6. Blurring of vision
107
Q

Most common urea cycle disorder

A

Ornithine transcarbamylase deficiency

108
Q

Ornithine transcarbamylase deficiency: heridability

A

X-linked

109
Q

Consecuence of Ornithine transcarbamylase deficiency

A
  1. Interferes with body’s ability to eliminate ammonia

2. Excess carbamoyl phophate is converted to orotic acid

110
Q

Findings of Ornithine transcarbamylase deficiency

A
  1. High orotic acid in blood and urine
  2. Low BUN
  3. Symptoms of hyperammonemia
    NO MEGALOBLASTIC ANEMIA vs Orotic aciduria!
111
Q

What aa is required for heme synthesis?

A

GLycine

112
Q

What aa is required for creatinine synthesis?

A

Arginine

113
Q

What aa is required for Melatonin synthesis?

A

Serotonin

114
Q

What aa is required for Histamine synthesis?

A

Histidine

115
Q

What aa is required for urea synthesis?

A

Arginine

116
Q

What aa is required for NO synthesis?

A

Arginine

117
Q

Phenylketonuria is due to

A

Low phenylalanine hydroxilase

118
Q

Malignant Phenylketonuria is due to

A

Low tetrahydrobiopterin BH4 cofactor

119
Q

Tyrosin Aa becomes essential

A

Phenylketonuria

120
Q

Tratment of Phenylketonuria

A

Low phenylalanine and high tyrosine in diet

Tetrahydrobiopterin supplementation

121
Q

Maternal Phenylketonuria

A 
Lack of proper dietary therapy during pregnancy:
Children with microcephaly
intellectual disability
growth retardation
congenital heart defects
122
Q

Screening for Phenylketonuria takes place

A

2-3 days after birth: normal at birth because of maternal enzyme during fetal life

123
Q

Musty body odor

A

Phenylketonuria: disorder of AROMATIC amino acid metabolism

124
Q

Artificial sweetener aspartame to be avoided in

A

Phenylketonuria, it contains phenylalanine

125
Q

Findings of Phenylketonuria

A
  1. Intellectual disability
  2. Growth retardation
  3. Seizures
  4. FAIR SKIN
  5. Eczema
  6. MUSTY BODY ODOR
126
Q

Maple syrup urine disease

A

Blocked degradation of branched amino acids: Isoleucine, Leucine, Valine: I Love Vermont maple syrup from maple trees with b1ranches
Due to low branched-chain alpha ketoacid dehydrogenase (B1)

127
Q

Maple syrup urine disease: blood analysis

A

High alpha ketoacids (s/t leucine)

128
Q

Presentation of Maple syrup urine disease

A

Vomiting
Poor feeding
Urine smells like maple syrup

129
Q

Treatment Maple syrup urine disease

A

Restriction of isoluecine, leucine and valine in diet

Thiamine supplementation

130
Q

Alkaptonuria, cause

A

Deficiency of homogentistate oxidase

131
Q

Error in the Degradative pathway of tyrosine to fumarate

A

Alkaptonuria

132
Q

Bluish-black connective tissue in alkaptonuria is due to

A

Pigment forming homogentisic acid

133
Q

Findings in alkaptonuria

A
  1. Ochronosis: Bluish-black connective tissue, ear cartilage and sclerae
  2. Urine turs black on prolonged exposure to air
  3. Debilitating arthralgias!
134
Q

Albinism is due to

A

Deficiency of tyrosinase: metabolising DOPA into melanin

135
Q

HOMOCYstinuria findigns

A
  1. Homocysteine in urine
  2. Osteoporosis
  3. Marfanoid habit
  4. Ocular changed: lens subluxation
  5. Cardiovascular effects
  6. Kyphosis
  7. Intellectual disability
136
Q

Types of homocystinuria

A
  1. Cystathione synthase deficiency
  2. Lower affinity to cysthatione synthase for B6
  3. Methionine synthase deficiency
137
Q

What form of homocystinuria requires to rise levels of methionine in diet

A

Deficiency of methionine synthase

138
Q

What form of homocystinuria requires to lower levels of methionine in diet, rise cysteine, B6 and B12?

A

Cystathione synthase deficiency

139
Q

What form of homocystinuria requires to rise levels of B6 and cysteine in diet?

A

Lack of affinity of cystation synthase for B6

140
Q

Cystinuria is due to?

A

Hereditary defect of renal PCT and intestinal Aa transporter that prevents reabsorption of Cysteine, Ornithine, Lysine and Arginine (COLA)

141
Q

Treatment of cystinuria

A

Urinary Alkalinization and chelating agents increase solubility of cysteine stones

142
Q

Diagnostic test for cystinuria

A

Urinary cyanide nitroprusside test

143
Q

Glucagon and epinephrine: regulation on glycogen

A
  1. Activate PKA
  2. Activate glycogen phosphorylase kinase
  3. Activate Glycogen phophorylase
  4. Glucogenolysis
144
Q

Insulin: regulation on glycogen

A
  1. Binds to TK receptor
  2. Activates protein phosphatase
  3. Activates glycogen synthase
  4. Glycogenesis
145
Q

Bond in glycogen branches

A

alpha 1,6

146
Q

Limit dextrin

A

One to four residues remaining on abranch after glycogen phosphorlylase has already shortened it

147
Q

Type I glycogen storage disease

A

Von Gierke

148
Q

Type II glycogen storage disease

A

Pompe disease

149
Q

Type III glycogen storage disease

A

Cori disease

150
Q

Type V glycogen storage disease

A

McArdle disease

151
Q

Deficient Skeletal muscle glycogen phosphorylase

A

Myophosphorylae= Mc Ardle disease

152
Q

Deficient Enzyme in Von Gierke disease

A

Glucose-6-phosphatase

153
Q

Deficient debranching enzyme (glucogen storage diseases)

A

Cori disease

154
Q

Findings in Von Gierke disease

A 
Severe fasting hypoglycemia
Accumulates Glycogen in liver
High blood lactate
High triglycerides
High uric acid (gout)
Hepatomegaly
155
Q

Lysosomal storage diseases

A
  1. Tay-Sachs
  2. Fabry
  3. Metachromatic leukodystrophy
  4. Krabbe
  5. Gaucher
  6. Nieman-Pick
  7. Hurler syndrome
  8. Hunter syndrome
156
Q

Cherry red spot on macula

A

Tay Sachs

Niemann-Pick

157
Q

Hepatosplenomegly in Tay Sachs

A

No

158
Q

Hepatosplenomegaly in Niemann-Pick

A

Yes

159
Q

Deficient enzyme in tay-sachs

A

Hexosaminidase A (tAy-saX)

160
Q

Angiokeratomas

A

Fabry disease

161
Q

Triad in fabric disease

A
  1. Angiokeratomas
  2. Peripheral neuropathy
  3. Hypohidrosis
162
Q

Most common lysosomal storage disease

A

Gaucher

163
Q

Lipid-laden macrophages resembling crumpled tissue paper

A

Gaucher cells

164
Q

Gaucher disease findings

A
  1. Hepatosplenomegaly
  2. Pancytopenia
  3. Osteoporosis
  4. Avascular necrosis of femur
  5. Bone cries
  6. Gaucher cells
165
Q

Nieman Pick disease finding

A

Progressive neurodegeneration: deffect in sphingomyelinase

166
Q

Hurler syndrome- is there corneal clouding?

A

Yes

167
Q

Hunter syndrome - is there corneal clouding?

A

No: hunters see clearly

168
Q

X linked lysosomal storage diseases

A

Fabry

Hunter: hunters aim for the X

169
Q

Fatty acid synthesis requires transport of citrate from mitochondria to cytosol through

A

The citrate shuttle

170
Q

Fatty acid degradation requires transport into the mitochondrial matrix through

A

Carnitine shuttle

171
Q

Ketone bodies

A

Acetone
Acetoacetate
Beta hydroxybutyrate

172
Q

Urine test for ketones detects

A

Acetoacetate

NOT beta hydroxybutirate

173
Q

Ketogenesis takes place in the _____ and uses ______ and _____ as substrates

A

Liver
Fatty acids
Amino acids

174
Q

1g carb yields

A

4 kcal

175
Q

1g alcohol yields

A

7 Kcal

176
Q

1g fatty acid yields

A

9 Kcal

177
Q

RBC use ketones

A

False, they lack mitochondria

178
Q

Function of hormone sensitive lipase

A

Degradation of TG stored in adipocytes

179
Q

Function of Lipoprotein Lipase

A

Deagradation of TG circulation in Qm and VLDL in vascular endothelial surface

180
Q

Function of pancreatic lipase

A

Degradation of dietary triglycerides in small intestine

181
Q

Apo E function

A

Mediates remnant uptake (everything except LDL)

182
Q

Apo A-1 function

A

Activates LCAT

183
Q

Apo C-2 function

A

Lipoprotein lipase cofactor that catalyzes cleavage

184
Q

Apo B-48 function

A

Mediates chylomicron secretion into lymphatics

185
Q

Apo B100 function

A

Binds to LDL receptor

186
Q

Transports cholesterol from periphery to liver

A

HDL

187
Q

Deficiency in Apo B48 and Apo B100

A

Abetalipoproteinemia

188
Q

Findings in abetalipoproteinemia

A 
Severe fat malabsorption
Steatorrhea
Failure to thrive
Retinitis pigmentosa!
Spinocerebellar degeneration: lack of vit E
Ataxia
Acanthocytosis
189
Q

Treatment of abetalipoproteinemia

A

Middle chain fatty acids

Oral vit E

190
Q

Tuboeruptive xanthomas

A

III: dysbetalipoproteinemia: defective apo E

191
Q

Hereditary hypertriglyciridemia

A

IV: hypertrygliceridemia: AD

192
Q

Absent or defective LDL receptors

A

II: FAmilial hypercholesterolemia

193
Q

Tendon achilles xanthomas

A

II: FAmilial hypercholesterolemia

194
Q

Familial dyslipidemias

A

I: Hyperchylomicronemia
II:Familial hypercholesterolemia
III: Dysbetalipoproteinemia
IV: Hypertriglyceridemia

Step 1 - Biochemistry (7 decks)

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