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Biochem Flashcards

1
Q

Signal transduction of alpha1 receptors

A

IP3 –> Ca2

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2
Q

Signal transduction of Beta receptors

A

cAMP –> Protein kinase A

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3
Q

Signal transduction of M1 and M3 recptors

A

IP3 –> Ca2 + protein kinase C

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4
Q

Signal transduction of M2 receptors

A

cAMP

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5
Q

Signal transduction of nicotinic receptors

A

Voltage gated Na Ca and K channel

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6
Q

Cytokines that induce systemic inflammatory response

A

IL 1, IL 6, and TNFa

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7
Q

DNA Pol I

A

Works on the lagging strand, synthesizes 5’ to 3’ and is an exonuclease at 5’ to 3’
Degrades RNA primers

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8
Q

DNA Pol III

A

Works on both lagging and leading strand. Synthesizes 5’ to 3’ but is an exonuclease at 3’ to 5’

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9
Q

Xeroderma pigmentosum

A

deficient endonuclease for thiamine dimer repair due to UV radiation

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10
Q

Base excision repair process

A

Alteration to a single nucleotide usually by carcinogen

Glycolsylase removes altered base
Lyase and endonuclease repair 3’ and 5’ ends
DNA pol adds in new base
Ligase completes the chain

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11
Q

Mismatch repair

A

MutS and MutL recruit Endonuclease to the mismatch which removes the surrounding DNA
DNA pol replaces the sugars and ligase completes the process

Defective in lynch syndrome

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12
Q

Homologous end joining

A

Sister chromosome used as template

Associated with Fanconi anemia and gynecological malignancy

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13
Q

Nonhomologous end joining

A

Many proteins required, no sister chromosome template
increased risk of errors
associated with ataxia telangiectasia

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14
Q

Amatoxins inhibit

A

RNA pol II

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15
Q

Amino acids bind this portion of tRNA

A

3’ acceptor stem sequence CCA

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16
Q

D arm of tRNA

A

binds aminoacyl tRNA synthetase which adds amino acids to tRNA

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17
Q

T arm of tRNA

A

binds the ribosome

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18
Q

Mutations in introns are commonly associated with

A

B thal

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19
Q

E2F

A

Promotes G1 to S phase transition

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20
Q

Rb protein

A

Binds E2F and prevents transition to S phase. When phosphorylated by Cyclin-CDK complex it will release E2F. Mutation can result in retinoblastoma or osteosarcoma.

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21
Q

Cyclin-CDK complex

A

Phosphorylates Rb, releasing E2F and allowing progression to S phase. This action is blocked by p21.
Mutations in Cyclin D1 result in Mantle Cell Lymphoma

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22
Q

p21

A

Prevents Cyclin-CDK from phosphorylating Rb. This action is promoted by p53.

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23
Q

p53

A

Further activates p21’s inhibition of Cyclin-CDK

mutations in p53 are associated with Li-Fraumeni syndrome. DNA damage UP REGULATES p53 to prevent cancer.

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24
Q

I cell disease

A

Defect in N-acetylglucoasminyl-1-phosphotranferase
Proteins become secreted instead of transported to lysosomes

Presentation:
Failure to thrive
Coarse facial features
Cognitive impairment
Corneal clouding
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25
Q

Clathrin

A

associated with transport between the cell membrane and golgi

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26
Q

COP1

A

transport from golgi to RER

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27
Q

COP2

A

transport from RER to golgi

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28
Q

Zellweger syndrome

A

Dysfunction in peroxisome activity, increased very long chain fatty acids

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29
Q

X-linked adrenoleukodystrophy

A

Impaired transport of very long chain fatty acids to peroxisome
Accumulation in brain (cognitive impairment) and adrenal glands (adrenal insufficiency)

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30
Q

Desmin

A

Intermediate filament associated with rhabdomyosarcoma

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31
Q

Vimentin

A

intermediate filament associated with sarcomas

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32
Q

GFAP

A

intermediate filament associated with astrocytomas

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33
Q

Neurofilaments

A

intermediate filaments associated with neuroblastomas.

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34
Q

Scurvy mechanism

A

VitC is required for the hydroxylation of pro alpha chains of collagen

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35
Q

Osteogenesis imperfecta mechanism

A

Faulty assembly of 3 collagen pro alpha chains into procollagen

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36
Q

Osteogenesis imperfecta

A

Autosomal Dominant
COL1A1/COL1A2 gene mutations
Multiple fx, blue sclera, hearing loss, abnormal teeth

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37
Q

Ehlers-Danlos mechanism

A

Deficiency of procollagen peptidase or lysyl oxidase

Decreased cross linking of collagen

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38
Q

Menkes Dz

A

Decreased Cu absorption which is a cofactor of lysyl oxidase resulting in decreased cross linked collagen

  • Brittle hair
  • Hypotonia
  • Growth Restriction
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39
Q

Marfan mechanism

A

Fibrillin 1 is a scaffold protein for elastin

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40
Q

Hexokinase

A

Converts glucose to G6P
Present in most tissue, not Beta cells or liver
Not induced by insulin
Low Km, Low Vmax

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41
Q

Glucokinase

A 
Converts glucose to G6P
Found in B cells and liver
Induced by insulin
High Vmax
High Km
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42
Q

Phosphofructokinase-2

A

Converts F6P to F2,6BP

Upregulated by insulin

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43
Q

Phosphofuctokinase-1

A

Converts F6P to F1,6BP
Upregulated by F26BP
Downregulated by Citrate and ATP

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44
Q

Fructose 2,6 Bisphosphatase

A

Converts F26BP to F6P

Upregulated by Glucagon

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45
Q

Fructose 1,6 Bisphosphatase

A

Converts F16BP to F6P

Inhibited by F26BP

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46
Q

BPG mutase

A

converts 13BPG to 23BPG
takes place in RBCs when O2 levels are low
23BPG decreases Hb affinity for oxygen

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47
Q

2,3 BPG phosphatase

A

Converts 23BPG to 3 phosphoglycerate

After recovery from low oxygen state, returns 23BPG to glycolysis

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48
Q

Pyruvate Kinase

A

Converts phosphoenolpyruvate to pyruvate
Produces ATP
Deficiency results in hemolysis

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49
Q

4 Molecules pyruvate can be converted into

A

Alanine
Oxaloacetate
Acetyl-CoA
Lactate

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50
Q

Lactate dehydrogenase

A

Converts pyruvate into Lactate

Requires NADH, Niacin

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51
Q

Pyruvate Dehydrogenase

A

Converts Pyruvate to Acetyl Coa
Inhibited by NADH and AcetylCoa
Requires NAD, Thiamine (B1), Riboflavin (b2), Niacin(B3), and Pantothenic acid (B5)

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52
Q

Pyruvate carboxylase

A

converts pyruvate to oxaloacetate
Requires Biotin
promoted by AcetylCoA

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53
Q

Citrate synthase

A

converts Acetyl CoA and Oxaloacetate to Citrate

Inhibited by ATP

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54
Q

Isocitrate dehydrogenase

A 
Converts Isocitrate and NAD to a-Ketogluterate, NADH, and CO2.
Requires Niacin (B3)
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55
Q

a-Ketoglutarate dehydrogenase

A

Converts a-ketoglutarate and NAD to Sucinyl-CoA, NADH, and CO2
Activated by Ca2+ in skeletal muscle
Requires B1, B2, B3, and B5

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56
Q

Cytochrome C oxidase

A

Complex 4 of the ETC

Fe goes between 2+ and 3+ states making it a target for CN- (3+) and CO (2+) poisoning.

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57
Q

PEPCK

A

Converts oxaloacetate to Phosphoenolpyruvate
requires GTP
used in Gluconeogenesis

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58
Q

Von Gierke disease

A

Deficiency of Glucose 6 phosphatase
Hypoglycemia and hepatomegaly and lactic acidosis
Gierke breaks Gluconeogenesis

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59
Q

a-1,4 glucosidase

A

Converts glycogen into glucose within lysosmes

Deficient in Pompei Dz

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60
Q

Pompe Disease

A 
Deficient a-1,4 glucosidase
Build up of glycogen within lysosomes
Cardiomegaly, hepatomegaly, and hypotonia
Normal blood sugars
"PomPe breaks the PumP" 4 Ps = 1.4
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61
Q

Glycogen Phosphorylase

A

Cleaves alpha-1,4 links in glycogen
Deficient in McArdles Dz
Activated by Ca2+, AMP, and cAMP

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62
Q

McArdle Disease

A

Deficient glycogen phosphorylase in skeletal muscle
Muscle cramps, weakness, rhabdomyoslysis
Liver unaffected
“McArdle breaks the Muscle”

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63
Q

a-1,6-glucosidase

A

Breaks the branches of glycogen

deficiency causes Cori Dz

64
Q

Cori Disease

A

Deficient a-1,6-glucosidase
Accumulation of glycogen causes hepatomegaly, hypotonia, and hypoglycemia.
Compensation by fat metabolism causes ketoacidosis

Cori breaks the Corner

65
Q

Fructokinase

A

Converts fructose to F1P

Deficient in Essential fructosuria

66
Q

Essential Fructosuria

A

Deficiency of fructokinase
relatively benign as Fructose can be converted to F6P by hexokinase
Detected by copper reduction test

67
Q

Aldolase B

A

Converts F1P to dihydroxyacetone phosphate and glyceraldehyde
Deficient in Fructose intolerance

68
Q

Fructose intolerance

A

Deficient Aldolase B
Accumulation of F1P within cells
Hypoglycemia, hepatomegaly, and liver failure
detected with copper reduction test

69
Q

Polyol Pathway

A

Conversion of glucose into sorbitol into fructose
Increase in hyperglycemia
soribitol can be damaging to the eyes causing cataracts.

70
Q

Lactase

A

Converts lactose to glucose and galactose

deficient in lactose intolerance

71
Q

Galactokinase

A

Converts galactose to G1P

Deficiency causes accumulation of galactitol which can cause infantile cataracts

72
Q

Galactose-1-phosphate uridyltransferase

A

Convers Galac-1-P to Glucose 1 P

Deficiency causes classic galactosemia.

73
Q

classic galactosemia

A

Deficient Gal1P uridyltransferase
Accumulation of Galac1P causes liver damage, cataracts, and hypoglycemia.
These patients are also at an increased risk of e coli sepsis due to preference of galactose

74
Q

G6P dehydrogenase

A

Converts G6P to 6 phosphogluconate
Part of the PPP
Creates NADPH
Deficiency causes hemolysis

75
Q

NADPH

A

Created in PPP
Used in FA, steroid, and cholesterol synthesis
Used in production in glutathione for oxidative damage reduction
Used in oxidative burst

76
Q

Transketolase

A

PPP
Converts Fructose 6 phosphate to ribose 5 phosphate
Preserves PPP in those with G6PD deficiency

77
Q

Carnitine shuttle

A

Combination of Carnitine and Acyl CoA during fatty acid metabolism allows the Acyl CoA to enter the mitochondria

78
Q

Acyl-CoA Dehydrogenase

A

Converts Acyl CoA eventually into Acetyl-CoA
Creats FADH2 and NADH
Deficient in Medium chanin acyl-CoA dehydrogenase deficiency (MCAD)

79
Q

Systemic primary carnitine deficiency

A

Low carnitine, impairing carnitine shuttle
Hypoglycemia (Acetyl CoA not made, cannot promote gluconeogenesis)
Hypokentonia due to lack of B oxidation
Accumulation of long chain fatty acids in liver and brain

80
Q

Medium chain acyl CoA dehydrogenase Deficiency

A

Impaired beta oxidation
Hypoketotic, hypoglycemia
Liver damage, encephalopathy
Carnitine levels are normal.

81
Q

Ethanol metabolism (NADH) effects

A

Metabolism of etoh causes an accumulation of NADH
This causes an inhibition of the TCA cycle
AcetylCoA from EtOh is shunted to ketone bodies
High NADH also promotes pyruvates conversion to lactate
High NADH also inhibits the breakdown of fatty acids, causing fatty liver.

82
Q

Vitamin D metabolism step 1

A

7 dehydrocholesterol is converted to Vitamin D3 (Cholecalciferol) by UV light

83
Q

Vitamin D metabolism step 2

A

Cholecalciferol (Light or diet) is converted to 25 Hydroxvyvitamind D by 25 hydroxylase in the liver

84
Q

VitD metabolism step 3

A

25 hydroxyvitamind D is converted to 1,25 dihydroxyvitamin D by 1 alpha hydroxylase in the kidney
This process is regulated by PTH

85
Q

Effects of 1,25 dihydroxyvitamin D

A

Increases bone mineralization, increases calcium absorption in SI, increases calcium and phosphate reabsorption in kidneys, decreases PTH secretion

86
Q

ApoB48

A

Only found on chylomicrons, allows entering of enterocytes

87
Q

ApoC-II

A

Transfered to chylomicron by HDL

Cofactor for LPL

88
Q

ApoE

A

Transfered to chylomicron by HDL
Facilitates binding to the hepatic remnant receptors
Found on HDL, chylomicros, HDL, VLDL, IDL

89
Q

Lipoprotein lipase

A

Frees fatty acids from Chylomicros and VLDL converting them into Chylomicron remnants and IDLs

90
Q

ApoB100

A

Allows VLDL to exit the liver and LDL to re enter the liver

91
Q

Fibrates, Niacin, Fish oil

A

all block excretion of VLDL by the liver

92
Q

Hepatic lipase

A

Converts IDL to LDL, freeing fatty acids and removing ApoE

93
Q

Abetalipoproteinemia

A

Lack of ApoB100 and ApoB48
Inability to secrete VLDL and chylomicrons
Steatorrhea, fat soluble vitamin deficiency, acanthocytosis

94
Q

Acanthocytosis

A

lack of lipids in RBC membrane, making them appear spiny

95
Q

Famililial hyperchylomicronemia (type I)

A

Deficiency ApoC-II
Increased Chylomicrons and VLDL
Labs: TGs

96
Q

PCSK9 inhibitors

A

Decrease LDL receptor degradation on the liver, allowing for increased LDL reabsorption
evolocumab

97
Q

Lecithin choldesterol acyl transferase

A

Allows HDL to absorb cholesterol

98
Q

Cholesterol ester transfer protein

A

Allows transfer of cholesterol from HDL to VLDL and LDL

99
Q

Familial hypercholesterolemia (Type II)

A

ApoB 100 Defect or LDL receptor defect
LDL cannot re enter the liver
Labs: LDL

100
Q

Familial dysbetalipoproteinemia (Type III)

A

Defect in ApoE3 and ApoE4
Chylomicrons, VLDL, IDL cannot enter the liver
Labs: Tgs, VLDL, IDL

101
Q

Familial hypertriglyceridemia (Type IV)

A

Overproduction of VLDL

Labs: TG

102
Q

Cystathionine synthase

A

Converts homocysteine to cystathionine
reqiuires B6
Deficient in homocysteinuria

103
Q

Homocysinuria

A

Usually due to a deficiency in cystathionine synthase
elevated homocysteine in the urine
Cysteine becomes an essential AA
ID, hypercoag, ectopia lentis, and marfanoid habitus
B6 can improve symptoms

104
Q

Methionine synthase

A

Converts homocysteine to methionine.
Requires 5-methyl THF
Requires B12
Indirectly requires folate for turnover of THF
Deficiency can be an alternative cause of homocystinuria

105
Q

Uses of Methionine

A

Can be made into SAM for methylation reactions

Can be converted to propionyl Coa –> MMA –> Succinyl CoA (requires folate)

106
Q

PRPP amidotransferase

A

Used in purine synthesis to create IMP which can become AMP or GMP

107
Q

UMP Synthase

A

Converts PRPP and orotic acid to UMP for pyrimadine synthesis
Deficient in Orotic aciduria

108
Q

Orotic Aciduria

A

Deficient UMP synthase
Megaloblastic anemia
No hyperammonemia
Tx: Uridine

109
Q

Thymidylate Synthase

A

Converts dUMP to dTMP
Requires 5,10-methylene THF
Indirectly requires folate
Inhibited by 5FU

110
Q

Dihydrofolate Reductase

A

Converts DHF to THF
requires folate
Inhibited by methotrexate, Primethamine, and TMP

111
Q

HGPRT

A

Converts Hypoxanthine/Guanine and PRPP to IMP or GMP

Deficiency causes lesch-nyhan syndrome

112
Q

Adenosine daminase

A

Converts adenosine to Inosine

Deficiency causes SCID (adenosine metabolites are toxic to T cells)

113
Q

Lesch-Nyhan Syndrome

A

Deficient HGPRT

Gout, Self mutilation, and ID

114
Q

Carbamoyl phosphate synthase I

A

Combines NH3 CO2 and ATP to form Carbamoyl Phosphate

115
Q

Orinithine transcarbamylase

A

Converts carbamoyl phosphate and ornithine to citrulline

116
Q

Ornithine transcarbamylase deficiency

A

Decreased urea cycle activity
Hyperammonemia
Increased Orotic acid

117
Q

NH3 effects on the nervous system

A

Glutamine is converted to glutamate in presynaptic neurons.
Glutamate is used as an excitatory neurotransmitter
Once released, glutamate is eventually reabsorbed by a nearby astrocyte and combined with NH3 from the bllod to be converted back to Glutamine. This is then returned to the presynpatic neuron.

In situations with increased NH3 in the blood, increased amounts of glutamine are created in astrocytes. This acts as an osmotic agent, drawing water into the astrocyte. When the astrocyte is swollen it is no longer able to transfer its glutamine to the presynaptic neuron.

118
Q

Connexins

A

Gap junctions

119
Q

Claudins, occludin

A

Tight junction

120
Q

Cadherins

A

Adherens junction

121
Q

desmogleins, desmoplakins

A

Desmosomes

122
Q

Integrins

A

Hemidesmosomes

123
Q

Maple syrup urine disease

A

Deficiency in branched chain a ketocaid dehydrogenase complex
Defective metabolism of isoleucine leucine and valine
Cannot produce proprionyl CoA
B1 B2 B3 B5
accumulation of alpha keto acids
ID, seizures, irritability
Thiamine can improve symptoms

124
Q

Phenylalanine hydroxylase

A

COnverts phenylalanine to tyrosine
Requires BH4
Deficiency of this is one cause of PKU

125
Q

Dihyrobiopterin reductase

A

Converts BH2 to BH4

Deficiency of this is one cause of PKU

126
Q

PKU

A

Defiency of Phenylalanine hydroxylase or Dihydrobiopterin reductase
Results in deficiency of neurotransmitters (dopamine, epi, NE)
Tyrosine becomes essential

127
Q

Tyrosinase

A

Converts DOPA to melanin

Deficiency causes albinism

128
Q

Homogentisic acid dioxygenase

A

Converts homogentisate to maleylacetoacetate

Deficient in Alkaptonuria

129
Q

Alkaptonuria

A

Homogentisic acid dioxygenase deficiency
Homogentisic acid accumulates in the connective tissue (ears and sclera, joint pain) and in the urine. When urine is exposed to air it will turn black.

130
Q

Fabry Dz

A

lack of a-galactosidase A
accumulation of Ceramide Trixhexoside
Palm and sole neuropathy, anhydrosis, renal and CV failure in adulthood, angiokeratomas
X linked recessive

Fa br A

131
Q

Niemann Pick Dz

A

Deficient sphingomyelinase
accumulation of sphingomyelin
Weakness, Chery red spot, HSM, foam cells
Autosomal recessive

132
Q

Tay Sachs Disease

A 
Deficient Hexoasaminidase A
Accumulation of GM2 Ganglioside
Weakness cherry red spot lysosomes with onion skin
autosomal recessive
A GANG of six jews
133
Q

Gaucher Disease

A 
Glucocerebrosidase deficiency
Accumulation of glucocerebroside
Bone dz, lipid laden macrophages, pancytopenia
Autosomal recessive
gaUcher
134
Q

Arginase Deficiency

A

Normally converts Arginine to ornithine and urea.

Causes spastic diplegia, abnormal movements, and growth delay. No/mild hyperammonemia.

135
Q

Huntingtin protein

A

In Huntington dz there is a gain of function which causes increased histone deacetylation, which silences genes necessary for neuron survival

136
Q

AAT

A

AAT is the primary inhibitor of neutrophil and macrophage elastin degradation protein

Results in panacinar empysema
Accelerated by smoking and 2nd hand smoke

137
Q

Gq G protein

A

IP3 and DAG –> PKC

Used by H1, a1, va,M1, and M3 (HAV 1 M&M)

138
Q

Gi G protein

A

Decreases cAMP

Used by M2, a2, D2 (MAD 2)

139
Q

Gs G protein

A

Increases cAMP –>PKA

used by everything besides HAV1 M&M and MAD 2

140
Q

cGMP

A

ANP BNP NO and EDRF activate guanylate cyclase creating cGMP
cGMP increased Protein Kinase G
Protein Kinase G causes vasodilation

141
Q

Receptor Tyrosine Kinases

A

Insulin, IGF-1, EGF, PDGF, FGF

Act on RAS/MAP kinase pathway

142
Q

Nonreceptor tyrosine kinases

A

IL-2, IL-6, prolactin, thrombopoietin, erythropoeitin, GH, GCSF
Acts on the JAK/STAT Pathway

143
Q

alpha 1

A

Mydriasis, vasocontriction

144
Q

alpha 2

A

Decrease NE release, decrease aqueous humor production

145
Q

Beta 1

A

Increase heart rate, increase contractility, increase Renin

146
Q

Beta 2

A

Vasodilation in Skeletal muscles, bronchodilation, increased aqueous humor production

147
Q

M3 sympathetic

A

Sweating, only sympathetic M receptor

148
Q

M3 parasympathetic

A

Miosis, lens accomodation, bronchoconstriction, increased gastric acid, increased salivation, increased parastalsis, bladder contraction

149
Q

M2

A

Decreased HR, decreased contractility

150
Q

H1

A

Increased mucous production, bronchoconstriction, and vasodilation

151
Q

H2

A

Increased HCl secretion

152
Q

V1

A

Vasoconstriction

153
Q

V2

A

Increased aquaporins in collecting tubule –> increased H20 reabsorption

154
Q

GLUT4

A

Transporter found in myocytes and adipose tissue

Responsive to insulin

155
Q

Ornithine shuttle

A

Transport of proteins into mitochondria for urea cycle

Step 1 (23 decks)

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