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STEP 1 Review > Metabolism Review > Flashcards

Metabolism Review Flashcards

1
Q

What cellular processes happen in both mitochondria and cytoplasm

A

Urea cycle, heme synthesis, gluconeogenesis

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2
Q

What processes happen in only mitochondria

A

Beta oxidation of fatty acids, acetyl coa production, krebs cycle, oxidative phosphorylation.

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3
Q

Carboxylase enzyme cofactor

A

Add CO2 to things – require biotin

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4
Q

Rate determining enzyme of glycolysis

A

PFK-1, activated by F26bp, amp, inhibited by atp, citrate

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5
Q

Rate determining enzyme of gluconeogenesis

A

F16bisphosphatase, activated by ATP and acetyl coa. Inhibited by AMP and fructose 2,6 bisphosphate

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6
Q

Rate determining enzyme of TCA

A

Isocitrate dehydrogenase, activated by ADP

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7
Q

Rate determining enzyme of glycogenesis

A

Glycogen synthase

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8
Q

Rate determining enzyme of glycogenolysis

A

Glyogen phosphorylase

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9
Q

Rate determining enzyme of HMP shunt

A

Glucose 6 phosphate dehydrogenase

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10
Q

Rate determinign enzyme of de novo purine synthesis

A

PRPP amidotransferase

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11
Q

Urea cycle rate limiting enzyme

A

Carbamoyl phosphate synthetase

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12
Q

Fatty acid synthesis rate determining enzyme

A

Acetyl coa carbodylase

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13
Q

Fatty acid oxidation rate determining enzyme

A

Carnitine acyltranferase

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14
Q

Fatty acid oxidation rate determining enzyme

A

Carnitine acyltranferase

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15
Q

How much atp does aerobic metabolism of glucose produce?

A

32 via malate-aspartate shuttle (heart and liver), 30 via G3P shuttle (muscle

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16
Q

How much atp does anaerobic glycolysis produce

A

Costs 2, makes 4, net 2.

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17
Q

How does arsenic affect metabolism

A

Arsenic causes glycolysis to net zero ATP and also inhibits lipoic acid

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18
Q 
What do each of these active carriers produce?
ATP
NADH
CoA, lipoamide
Biotin
THF
SAM
TPP
A 
Phosphate
electrons
acyl group
(b7) CO2
1 carbon units
CH3 groups
Aldehydes (b1)
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19
Q

NAD vs NADPH

A

NAD (from b3) ususally used in catabolic processes to carry away electrons as NADH

NADPH is usually used in anabolic processes (steroid and fatty acid synthesis), the respiratory burst, cyp450, and glutathione reductase

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20
Q

Hexokinase vs glucokinase

A

Hexokinase has low Km (high affinity) and low total velocity. In muscle so it can use glucose as it exists in the body. Not induced by insulin, inhibited by G6P.

Glucokinase has high Km (low affinity) and high velocity. Only in liver. Induced by insulin after a meal to store glucose in cells for use as glycogen. Not inhibited by g6P.

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21
Q

MODY

A

Maturity onset diabetes of the young – defect in glucokinase so not enough glucose taken into liver. Hyperglycemia.

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22
Q

MODY

A

Maturity onset diabetes of the young – defect in glucokinase so not enough glucose taken into liver. Hyperglycemia.

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23
Q

Draw glycolysis out

A

Pay special attention to the steps that require ATP (G, G3P; F6P, F16BP)
and make atp (13BPG, 3PG; PEP,pyr)

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24
Q

Cofactors required in pyruvate dehydrogenase complex

A 
TPP (B1)
FAD (B2)
NAD (B3)
CoA (B5)
Lipoic Acid (inhibted by arsenic, causes vomiting, rice water stools, garlic breath).
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25
Q

Where is pyruvate dehydrogenase located?

How is pyruvate dehydrogenase activated? What is the product made?

A

Located in the mitochondrial membrane
By a exercise which causes high NAD/NADH ratio, increased ADP, increased Ca.
Acetyl CoA.

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26
Q

Pyruvate dehydrogenase deficiency findings and treatment

A

Causes lactic acidosis (via LDH) and build up of alanine (via ALT).
Neurologic symptoms too.

Treat by supplementing ketogenic amino acids (lysine and leucine) or ketogenic foods (high fat)

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27
Q

Pyruvate dehydrogenase deficiency findings and treatment

A

Causes lactic acidosis (via LDH) and build up of alanine (via ALT).
Neurologic symptoms too.

Treat by supplementing ketogenic amino acids (lysine and leucine) or ketogenic foods (high fat), which bypass PDH complex and go directly into TCA

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28
Q

Products of pyruvate metabolism

A

Lactate via LDH (anaerobic metabolism in retina, lens, RBC, renal medulla)–requires B3

Alanine via ALT (used to take amino groups from muscle to liver)– requires B6

OAA via Pyruvate carboxylase (to be used in gluconeogenesis) – requires biotin

Acetyl-CoA via Pyruvate dehydrogenase

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29
Q

TCA Products

A

3 NADH, 1 FADH2, 2 CO2, 1GTP per acetyl coa, 2x for 1 glucose.

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30
Q

Electron transport chain.

A

Electrons enter intermembrane space through complexes 1-4 from the inner mitochondrial membrane. Complex 1 is where NADH goes, complex 2 (succinate dehydrogenase) is where FADH goes. Complex 4 passes electrons to O2 to make H2O. Generates H gradient in intermembrane space which pass through ATP synthase and make ATP.

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31
Q

Electron transport chain.

A

Electrons enter intermembrane space through complexes 1-4 from the inner mitochondrial membrane. Complex 1 is where NADH goes, complex 2 (succinate dehydrogenase) is where FADH goes. Complex 4 passes electrons to O2 to make H2O. Generates H gradient in intermembrane space which pass through ATP synthase and make ATP.

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32
Q

ETC complex inhibitors

A

Rotenone inhibits complex 1
Antimycin inhibits complex 3
Cyanide/CO inhibit complex 4
Oligomycin inhibits ATPsynthase

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33
Q

Uncoupling agents

A

Aspirin overdose
Thermogenin
2,4 Dinitrophenol

increase O2 consumption because they decrease proton gradient, but No ATP generated. Energy dissipated as heat

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34
Q

Gluconeogenesis key enzymes

A

Pyruvate carboxylase (in mitochondria), requires biotin

PEPcarboxykinase in cytosol (requires GTP)

Fructose 1,6 BPase

Glucose 6 Phosphatase (not found in muscle)

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35
Q

Why can’t gluconeogenesis happen in muscle?

A

Muscle lacks glucose 6 phosphatase.

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36
Q

How do even chain fatty acids contribute to gluconeogenesis

A

They don’t. They can only yield acetyl coa equivalents.

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37
Q

How do odd chain fatty acids contribute to gluconeogenesis

A

When broken down, yield proprionyl coa, which can enter TCA as succinyl CoA, regenerate OAA.

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38
Q

How much ATP does 1 NADH produce?

FADH?

A
  1. 5

1. 5

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39
Q

HMP Shunt

A

Provides a source of NADPH when glucose is abundant to serve in fatty acid and steroid synthesis, glutathione reduction in RBC. Also used to generate ribose for nucleotide synthesis.

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40
Q

HMP Shunt

A

Provides a source of NADPH when glucose is abundant to serve in fatty acid and steroid synthesis, glutathione reduction in RBC. Also used to generate ribose for nucleotide synthesis.

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41
Q

Oxidative phase of HMP shunt

A

Irreversible phase, G6P turned into Ribulose 5 P, generating 2 NADPH, via Glucose 6 Phosphate Dehydrogenase.

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42
Q

Nonoxidative phase of HMP shunt

A

Revesible phase, ribulose 5 phosphate turned into ribose 5 phosphate by phosphopentose isomerase. G3P and F6P generated for glycolysis by transketolases.

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43
Q

Nonoxidative phase of HMP shunt

A

Revesible phase, ribulose 5 phosphate turned into ribose 5 phosphate by phosphopentose isomerase. G3P and F6P generated for glycolysis by transketolases.

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44
Q

Components of respiratory burst

A

O2 turned into O2- by NADPH oxidase, O2-turned into H2O2 by SOD, H2O2 turned into HOCl by MPO.

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45
Q

How is H2O2 neutralized?

A

By Glutathione peroxidase.

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46
Q

G6PD deficiency

A

The most common enzyme deficiency. X-linked recessive disorder. Causes Hb to be oxidized and build up in cells as heinz bodies. Bite cells from spleen especially after sulfa drugs, malaria drugs, fava beans. Hemolytic anemia.

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47
Q

Fructokinase deficiency

A

Causes fructose to build up in blood and urine (can’t be P’d to F1P and stay in cells). Totally benign.

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48
Q

Aldolase B deficiency

A

More serious (though less serious than galactose metabolism problems). F1P accumulates in cells, decrease in available phosphate, which blocks glycogenolysis and gluconeogenesis.

Hypoglycemia, jaundice, cirrhosis, vomiting, especially after fruit juices and honey.

URINE DIPSTICK NEGATIVE (only tests for glucose).

Treat by decreasing fructose and sucrose.

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49
Q

Essential Fructosuria

A

Fructokinase deficiency Causes fructose to build up in blood and urine (can’t be P’d to F1P and stay in cells). Totally benign.

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50
Q

Fructose intolerance

A

Aldolase B deficiency. More serious (though less serious than galactose metabolism problems). F1P accumulates in cells, decrease in available phosphate, which blocks glycogenolysis and gluconeogenesis.

Hypoglycemia, jaundice, cirrhosis, vomiting, especially after fruit juices and honey.

URINE DIPSTICK NEGATIVE (only tests for glucose).

Treat by decreasing fructose and sucrose.

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51
Q

Galactokinase deficiency

A

Galactose cant be turned into Galactose 1 P, so galACTitol builds up. Relatively mild.

Symptoms are: lack of a social smile, galactose in blood/urine, infantile catarACTs.

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52
Q

Classic galactosemia

A

Absence of galactose 1 phosphate uridyltransferase. Damage is caused by accumulation of galactitol.

Causes failure to thrive, jaundice, hepatomegaly, infantile catarACTs.

Treat by exclusing galactose and lactose from diet.

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53
Q

Classic galactosemia

A

Absence of galactose 1 phosphate uridyltransferase. Damage is caused by accumulation of galactitol.

Causes failure to thrive, jaundice, hepatomegaly, infantile catarACTs.

Treat by exclusing galactose and lactose from diet.

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54
Q

How to create sorbitol?
What is it used for?
Any problems with sorbitol

A

From glucose using aldose reductase. Its an alternative method of trapping glucose in cells if it is high. Many tissues have sorbitol dehydrogenase to convert it to fructose, however, schwann cells, lens, and retina don’t have it. Causes osmotic damage. This is what happens in diabetes.

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55
Q

How to create sorbitol?
What is it used for?
Any problems with sorbitol

A

From glucose using aldose reductase. Its an alternative method of trapping glucose in cells if it is high. Many tissues have sorbitol dehydrogenase to convert it to fructose, however, schwann cells, lens, and retina don’t have it. Causes osmotic damage. This is what happens in diabetes.

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56
Q

Glucogenic Essential Amino Acids

A

Valine, Histidine, Methionine

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57
Q

Glucogenic/Ketogenic Essential Amino Acids

A

Isoleucine, tryptophan, threonine, phenylalanine.

58
Q

Ketogenic Essential Amino Acids

A

Lysine/leucine

59
Q

Acidic Amino Acids

A

Glutamate, Aspartate

Negatively charged at physiologic pH

60
Q

Basic Amino Acids

A

Histidine ** , lysine, arginine.

Arginine and lysine are in histones because they bind negatively charged DNA.

Postively charged at physiologic pH

61
Q

Urea cycle purpose

A

to turn amino groups into urea for excretion. Takes place in liver, both in mitochondria and cytoplasm.

62
Q

Urea cycle purpose

A

to turn amino groups into urea for excretion. Takes place in liver, both in mitochondria and cytoplasm.

63
Q

Draw the urea cycle

A

Ordinarily, careless (created by NH3 and CO2) crappers (are) also (frivolous) about (urination)

64
Q

Draw the urea cycle

A

REQUIRES N-Acetyl glutamate to turn NH3 into carbamoyl phosphate!!!!!!!! Ordinarily, careless (created by NH3 and CO2) crappers (are) also (frivolous) about (urination)

65
Q

Transport by ammonia by alanine and glutamate.

A

Draw it.

66
Q

Hyperammonemia- cause/sxs/ treatment

A

Can be acquired (liver disease) or genetic (enzyme deficiency). Results in excess NH4 which depletes alpha ketoglutarate and inhibits TCA cycle.

Causes tremor, slurring of speech, somnolence, vomiting, cerebral edema.

Treat by limiting protein in diet, or by lactulose to acidify GI tract and trap NH4 for excretion.

Also treat with benzoate or phenyl butyrate (bind AA for excretion).

67
Q

N-Acetylglutamate deficiency

A

Required cofactor for carbamoyl phosphate synthetase I. Deficiency leads to hyperammonemia. Presentation is identical to CPS I deficiency but this has increased ornithine with normal urea cycle enzymes.

68
Q

Ornithine transcarbamylase deficiency

A

Most common urea cycle disorder. X linked recessive. Interferes with body’s ability to excrete ammonia. Often evident in first few days of life. Excess carbamoyl phosphate is converted to orotic acid which causes increased orotic acid in blood and urine, decreased BUN, symptoms of hyperammonemia. NO MEGALOBLASTIC ANEMIA (seen in orotic aciduria).

69
Q

Ornithine transcarbamylase deficiency

A

Most common urea cycle disorder. X linked recessive. Interferes with body’s ability to excrete ammonia. Often evident in first few days of life. Excess carbamoyl phosphate is converted to orotic acid which causes increased orotic acid in blood and urine, decreased BUN, symptoms of hyperammonemia. NO MEGALOBLASTIC ANEMIA (seen in orotic aciduria).

70
Q

Ornithine transcarbamylase deficiency

A

Most common urea cycle disorder. X linked recessive. Interferes with body’s ability to excrete ammonia. Often evident in first few days of life. Excess carbamoyl phosphate is converted to orotic acid which causes increased orotic acid in blood and urine, decreased BUN, symptoms of hyperammonemia. NO MEGALOBLASTIC ANEMIA (seen in orotic aciduria).

71
Q

Phenylalanine metabolism

A

Becomes tyrosine, DOPA, Dopamine, Norepinephrine, epinephrine.

72
Q

Tryptophan becomes

A

Niacin (B6 cofactor)

Serotonin (BH4, B6 cofactors)

73
Q

Histidine becomes

A

Histamine (with B6 cofactor)

74
Q

Glycine becomes

A

Porphyrin (with B6), then heme

75
Q

Glutamate becomes

A

GABA (with b6)

Glutathione

76
Q

Arginine becomes

A

urea, creatinine, nitric oxide (with BH4)

77
Q

Vitamin B6 deficiency causes

A

Sideroblastic anemia, needed for ALAS function to create ALA from succinyl CoA.

78
Q

Catecholamine synthesis

A

Draw it.

79
Q

Phenylketonuria

A

Deficiency in phenylalanine hydroxylase or a decrease in BH4 cofactor (malignant PKU), build up of phenylalanine leads to increased synthesis of phenylketones. Tyrosine becomes an essential amino acid.

Findings: intellectual disability, musty body odor, seizures, fair skin, eczema.

Treat by decreasing phe, increasing tyr in diet.

80
Q

Maternal PKU

A

Lack of proper dietary therapy during pregnancy. Causes microcephaly, intellectual disability, growth retardation

81
Q

Alkaptonuria (ochonosis)

A

Deficiency of homogentisate oxidase in the tyrosine degradation pathway. Build up of homogentisic acid

82
Q

Alkaptonuria (ochonosis)

A

benign Deficiency of homogentisate oxidase in the tyrosine degradation pathway. Build up of homogentisic acid. Causes dark connective tissue, brown sclerae, urine turns black.

May have debilitating arthralgias (homogentisic acid is tocix to cartilage).

83
Q

Homocystinuria

A

Caused by multiple things:

1) Cystathionine synthase deficiency (treat with decreasing methionine, increasing cysteine, increasing b12/folate.
2) mutation in cystathionine synthase which reduces affinity for pyridoxal phosphate (increase B6 and cysteine)
3) Homocysteine methyltransferase deficiency (treatment, increase methionine)

Causes intellectual disability, osteoporosis, tall stature, kyphosis, lens subluxation, MI

84
Q

Cystinuria

A

Defect of renal PCT and intestinal aa transporter for COLA (cysteine, ornithine, lysine, arginine).

Excess cystine in urine can cause hexagonal cystine stones.

Urinary cyanide-nitroprusside test is diagnostic. Treat with urinary alkalinization.

85
Q

Maple Syrup Urine Disease

A

Blocked degradation of branched amino acid (isoleucine, leucine, valine) due to alphaketoacid dehydrogenase. Severe CNS deficits, lethargy, seizures.

86
Q

Maple Syrup Urine Disease

A

Blocked degradation of branched amino acid (isoleucine, leucine, valine) due to alphaketoacid dehydrogenase needs B1. Severe CNS deficits, lethargy, seizures.

Treat by supplementing B1 and avoiding BCAAs.

87
Q

Phenylketonuria

A

Deficiency in phenylalanine hydroxylase or a decrease in BH4 cofactor (malignant PKU), build up of phenylalanine leads to increased synthesis of phenylketones. Tyrosine becomes an essential amino acid.

Findings: intellectual disability, musty body odor, seizures, fair skin, eczema
Also have growth retardation due to low thyroxine!

Treat by decreasing phe, increasing tyr in diet.

88
Q

Maple Syrup Urine Disease

A

Blocked degradation of branched amino acid (isoleucine, leucine, valine) due to alphaketoacid dehydrogenase needs B1. Severe CNS deficits, lethargy, seizures.

Treat by supplementing B1 and avoiding BCAAs.

89
Q

Do fat-soluble vitamins have higher or lower toxicity than water soluble vitamins?

A

Higher toxicity.

Mineral oil intake can cause fat soluble vitamin deficiencies

90
Q

What do B complex vitamin deficiencies usually cause?

A

Glossitis, dermatitis, diarrhea

91
Q

Vitamin A function

A

Retinol. Constituent of visual pigments and essential for normal differentiation of epithelial cells.

92
Q

Vitamin A deficiency

A

Night blindness, xerosis cutis, corneal degeneration (keratomalacia), immune suppression

93
Q

Vitamin A excess

A

Teratogenic (cleft palate, hox gene interference). Scaly skin, osteoporosis, PSEUDOTUMOR CEREBRI

94
Q

Vitamin B1

A

Thiamine. Used in TPP, a cofactor for severe dehydrogenase enzymes (pyruvate dyhydrogenase) AKG dehydrogenase, Transketolase (HMP shunt), and branched chain ketoacid dehydrogenase.

95
Q

Vitamin B1 deficiency

A

Can happen in alcoholics and malnutrition. Causes impaired glucose breakdown (so give B1 to alcoholics before glucose). Highly aerobic tissues like brain and heart affected first. Causes beriberi and wenicke-korsakoff syndrome. Diagnosed with increased RBC transketolase activity after B1 administration.

96
Q

Wernicke-Korsakoff Syndrome

A

B1 deficiency causes ataxia, opthamoplegia, confusion. Add confabulation and dementia/amnesia. Degeneration of mammillary bodies.

97
Q

Wernicke-Korsakoff Syndrome

A

B1 deficiency causes ataxia, opthamoplegia, confusion. Add confabulation and dementia/amnesia. Degeneration of mammillary bodies.

98
Q

Dry beriberi

A

Polyneuritis, symmetric muscle wasting

99
Q

Wet beriberi

A

High output cardiac failure (dilated cardiomyopathy) and edema.

100
Q

Wet beriberi

A

High output cardiac failure (dilated cardiomyopathy) and edema.

101
Q

Vitamin B2

A

Riboflavin. Used in FAD and FMN in redox reactions (succinate dehydrogenase).

102
Q

Vitamin B2 deficiency

A

Chielosis (inflammation of the lips and fissures at the corners), corneal vascularization.

103
Q

Vitamin B2 deficiency

A

Cheilosis (inflammation of the lips and fissures at the corners), corneal vascularization.

104
Q

Vitamin B2 deficiency

A

Cheilosis (inflammation of the lips and fissures at the corners), corneal vascularization.

105
Q

Vitamin B3

A

Niacin. Constituent of NAD/NADP used in redox reactions. Derived from Tryptophan and synthesis requires B2 and B6. Lowers levels of VLDL and increases HDL

106
Q

B3 Deficiency

A

Glossitis. Severe deficiency can be caused by Hartnup disease (decreased abs of tryptophan), carcinoid syndrome (tryptophan metabolism increased), and isoniazid (decreases B6).

Causes symptoms of pellagra: Diarrhea, dermatitis, and dementia.

107
Q

B3 Excess

A

Facial flushing (induced by prostaglandin), hyperglycemia, hyperuricemia

108
Q

Vitamin B5

A

Pantothenate. Essential component of CoA (for acyl tranfers), and fatty acid synthase.

109
Q

Vitamin B5 deficiency

A

Dermatitis, enteritis, alopecia, adrenal insufficiency

110
Q

Vitamin B6

A

Pyridoxine, converted to pyridoxal phosphate, a cofactor used in transamination (AST/ALT), decarboylation, glycogen phosphorylase. Used in the synthesis of cystathionine, heme, niacin, histamine, neurotransmitters.

111
Q

Vitamin B6 deficiency

A

Convulsions, hyperirritability, peripheral neuropathy (especially with isoniazid), SIDEROBLASTIC ANEMIA DUE TO IMPAIRED HB SYNTHESIS.

112
Q

Vitamin B6 deficiency

A

Convulsions, hyperirritability, peripheral neuropathy (especially with isoniazid), SIDEROBLASTIC ANEMIA DUE TO IMPAIRED HB SYNTHESIS.

113
Q

Vitamin B7

A

Biotin. Cofactor for carboxylation which add one carbon.

114
Q

Vitamin B7 Deficiency

A

Relatively rate, causes dermatitis, alopecia, enteritis. Caused by antibiotic use or excessive ingestion of egg whites.

115
Q

Vitamin B9

A

Folic acid, converted to THF, a coenzyme for 1 carbon transfer/methylation reactions. Needed for synthesis of bases in DNA/RNA. Found in green leafy vegetables.

116
Q

Vitamin B9 deficiency

A

Megaloblastic anemia, hypersegmented neutrophils, glossitis, no neurologic symtpoms. Increased homocysteine. Most common vitamin deficiency in the US.

Can be caused by several drugs (phenytoin, sulfonamides, methotrexate).

117
Q

Vitamin B12

A

Cobalamin. Cofactor for homocysteine methyltransferase and methylmalonyl CoA mutase.

Found in animal products. Intrinsic factor for absorption in terminal ileum

118
Q

Vitamin B12 deficiency

A

Megaloblastic anemia, hypersegmented neutrophils, paresthesias and subacute combined degenration (degeneration of dorsal columns, LCSTs, due to abnormal myelin). Increases homocysteine and methylmalonic acid.

Pernicious anemia, diphyllobothrium latum.

119
Q

Vitamin C

A

Antioxidant, facilitates iron absorption (reduces it to Fe2+). Necessary for -OH of lysine and proline in collagen synthesis. Necessary for dopamine beta hydroxylase which converts dopamine to NE.

Can treat methemoglobinemia by reducing Fe3+ to Fe2+

120
Q

Vitamin C deficiency

A

Scurvy. Swollen gums, bruising, hemarthroses, anemia, poor wound healing.

121
Q

Vitamin C excess

A

Nausea, vomiting, diarrhea, calcium oxalate nephrolithiasis.

122
Q

Vitamin D

A

D2 from plants
D3 from milk and skin (stratum basale)

Increases intestinal absorption of calcium and phosphate.

123
Q

Vitamin D deficiency

A

Rickets/osteomalatia. Hypocalcemic tetany. Breastfed infants must receive vitamin D!

124
Q

vitamin D excess

A

Hypercalcemia, loss of appetite. Seen in sarcoidosis because epitheloid histiocytes activate vitamin d.

125
Q

vitamin D excess

A

Hypercalcemia, loss of appetite. Seen in sarcoidosis because epitheloid histiocytes activate vitamin d.

126
Q

Vitamin E

A

Tocopherol. Antioxidant that protects erythrocytes and membranes from free radical damage. Can enhance effects of warfarin

127
Q

Vitamin E deficiency

A

Hemolytic anemia, acanthosis, can cause neurologic symptoms like B12 but without the megaloblastic anemia or increase in methylmalonate.

128
Q

Vitamin K

A

Cofactor for the gamma carboxylation of glutamate on coagfactors. Created by intestinal flora.

129
Q

Vitamin K deficiency

A

Neonatal hemorrhage with increased PT and PTT but normal bleeding time. Not in breast milk.

130
Q

Zinc

A

Essential cofactor. Deficiency has delayed wound healing, hypogonadism, decrease in hair.

131
Q

Zinc

A

Essential cofactor. Deficiency has delayed wound healing, hypogonadism, decrease in hair.

132
Q

Ethanol metabolism

A

EtOH turned into acetaldehyde by alcohol dehydrogenase (with NAD), in cyto. In mito, acetaldehyde turned into acetate by acetaldehyde dehydrogenase.

NAD is limiting reagent. Zero order kinetics.

Increases NADH to NAD ratio, causing pyruvate to lactate (lactic acidosis), oxaloacetate to malate (decreases gluconeogenesis – hypoglycemia), g3p makes triglycerides.

Causes ketoacidosis and lipogenesis.

133
Q

Fomepizole

A

blocks alcohol dehydrogenase. Antidote for methanol/ethylene glycol poisoning.

134
Q

Disulfiram

A

Blocks acetaldehyde dehydrogenase, leads to hangover symptoms

135
Q

Kwashiorkor

A

Protein malnutrition leads to edema, fatty change of liver. Anemia

136
Q

Marasmus

A

Total calorie malnutrition. Muscle wasting loss of fat.

137
Q

Marasmus

A

Total calorie malnutrition. Muscle wasting– loss of fat.

138
Q

Vitamin B12 deficiency

A

Megaloblastic anemia, hypersegmented neutrophils, paresthesias and subacute combined degeneration (degeneration of dorsal columns, LCSTs, due to abnormal myelin). Increases homocysteine and methylmalonic acid.

Pernicious anemia, diphyllobothrium latum.

139
Q

Vitamin K

A

Cofactor for the gamma carboxylation of glutamate on coag factors. Created by intestinal flora.

140
Q

Disulfiram

A

Blocks acetaldehyde dehydrogenase in mitochondria, leads to hangover symptoms

141
Q

Alkaptonuria (ochonosis)

A

benign Deficiency of homogentisate oxidase in the tyrosine degradation pathway. Build up of homogentisic acid. Causes dark connective tissue, brown sclerae, urine turns black.

May have debilitating arthralgias (homogentisic acid is toxic to cartilage).

STEP 1 Review (21 decks)

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