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Biochemisty Flashcards

1
Q

What is the HH equation?

A

pH = pKa + log (base/acid)

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2
Q

What is the equation that relates pCO2 to H2CO3?

A

0.03*pCO2 = H2CO3

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3
Q

What is the modified HH equation for blood pH?

A

pH = [HCO3] / (0.03* pCO2)

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4
Q

What is the normal pH range of blood?

A

7.35-7.45

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5
Q

What is the equation for anion gap?

A

Na - (HCO3 + Cl)

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6
Q

What is the normal range of the anion gap?

A

12 +/- 4

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7
Q

What is the mnemonic for anion gap acidosis?

A 
Methanol
Uremia
DKA
Phenyl alcohol
Isoniazid / Iron
Lactic acid
Ethanol
Rhabdo
Salicylates
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8
Q

What is the mnemonic for non-anion gap acidosis?

A 
H = hyperalimentation (e.g., starting TPN).
A = acetazolamide use.
R = renal tubular acidosis (Type I = distal; Type II = proximal; Type IV = hyporeninemic hypoaldosteronism.
D = diarrhea
U = uretosigmoid fistula (because the colon will waste bicarbonate).
P = pancreatic fistula (because of alkali loss--the pancreas secretes a bicarbonate-rich fluid).
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9
Q

What is represented by the anion gap?

A

Unmeasured anions

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10
Q

What is the difference between a fixed and a volatile acid?

A

Fixed = cannot be blown off through the lungs

Volatile = can be

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11
Q

What happens to the following with emphysema:

  • pCO2
  • HCO3
  • pH
A
  • Increased pCO2 (can’t blow off)
  • Increased HCO3 (kidney compensation)
  • Normal pH (maintained by the ratio)
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12
Q

All polymerases add nucleotides from the 3’ or 5’ end? How do they progress along the strand (3’ to 5’ or vice versa)?

A
  • 3’ end

- Move from 3’ to 5’

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13
Q

What replaces the T in RNA?

A

Uracil

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14
Q

What is the major start codon?

A

AUG (school starts in AUGust)

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15
Q

What are the three major stop codons?

A

UGA (you go away)
UAA (you are away)
UAG (you are gone)

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16
Q

the 5’ end of the DNA pairs with which side of the RNA?

A

3’

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17
Q

The mRNA is almost identical to what DNA strand: sense or antisense strand?

A

Sense strand

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18
Q

What, generally, are thalassemias?

A

Structural variants of Hb, that produce unstable Hb molecules

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19
Q

What are the three major abnormal structural variants of Hb? What gene do they all impact?

A
  • Hb S (sickle cell)
  • Hb C (Hb C disease)
  • Hb E (Hb E disease)

All impact the beta globin gene

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20
Q

What chromosome is the beta globin gene found on?

A

11

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21
Q

What is meant by the term Hb S (or Hb C, E, etc) trait?

A

One mutant allele of beta globin gene and one wild -type allele

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22
Q

What is the amino acid change in sickle cell disease?

A

Glutamate at position 6 is exchanged for a valine (charge to uncharged amino acid)

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23
Q

When does sickle cell Hb precipitate into solution?

A

When deoxygenated

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24
Q

What is a sickle cell crises?

A

Severe bone pain precipitated by dehydration or infx

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25
Q

What is the medication that can be used to treat sickle cell anemia? How does it work?

A
  • Hydroxyurea

- Boosts Hb F (alpha2, gamma2)

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26
Q

What is Hb C disease? What ethnicity is this more common in ?

A
  • Glutamate changes to lysine at position 6, causing form crystals (as opposed to polymerizing like with sickle cell dz)
  • West african origin
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27
Q

Why don’t patients with Hb C disease have episodic crises? What s/sx do they have?

A

Hb C does not polymerize– form crystals that can cause splenomegaly or cholelithiais

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28
Q

How can you distinguish between Hb S and Hb C?

A

Electrophoresis

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29
Q

True or false: Hb C/s compound disease is relatively common

A

True

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30
Q

What is Hb E disease? What ethnicity is it found in?

A
  • E to K at position position 26, causing not enough beta globin chain synthesis
  • Southeast asia
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31
Q

What type of anemia does patients with Hb E disease? Mild or severe?

A

Mild microcytic anemia

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32
Q

What is the treatment for Hb E disease?

A

None needed–mild disease

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33
Q

What are the three major prion diseases?

A
  • CJD
  • vCJD
  • Kuru
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34
Q

What are prions?

A

Proteinaceous infectious particle

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35
Q

What is the pathophysiology of prion disease?

A

Seeding and propagation of abnormal proteins

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36
Q

What is the protein change that occurs with prion diseases?

A

PrP^C changes to PrP^Sc

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37
Q

What is the inheritance pattern of CF?

A

AR

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38
Q

What is the defect in CF?

A

Defect In CFTR gene encoding a chloride channel

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39
Q

What is the diagnostic test for CF?

A

Increased NaCl in sweat

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40
Q

What is the most common mutation for CF? What does this cause?

A
  • Deletion of a single phenylalanine residue at position 508
  • Interferes with protein folding and glycosylation
  • Mutant protein fails to route to the cell membrane
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41
Q

What is the inheritance pattern of HD?

A

AD

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42
Q

What is the trinucleotide repeat with HD? What protein is added to the gene?

A
  • CAG

- Adds glutamine residues and thus misfolded aggregates

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43
Q

What part of the brain is damaged with HD?

A

Caudate nucleus

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44
Q

What is the gene that is affected with HD?

A

Huntingtin (HTT disease)

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45
Q

What is the MM equation?

A

V = Vmax[S] / (Km = [S])

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46
Q

What does the Km value represent in the MM equation?

A

Represents the substrate concentration where v Vmax / 2

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47
Q

What are the neurotransmitters that are lost with HD?

A

Loss of ACh and GABA

“Caudate loses ACh and GABA (CAG)”

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48
Q

Which is dependent on substrate concentration: Vmax or Km?

A

Vmax (Km is independent)

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49
Q

Does a large or a small Km indicate a high affinity for a substrate?

A

Small = higher affinity

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50
Q

What happens to Vmax and Km with competitive inhibitors?

A

Vmax is normal

Km is shifted

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51
Q

What happens to Vmax and Km with non-competitive inhibitors?

A

Vmax is lower

Km is unchanged

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52
Q

What is the modification that is made with non-competitive inhibitors of an enzyme?

A

Forms covalent bond that cannot be washed away

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53
Q

What is the difference in MOA of ASA vs IBU?

A
  • ASA = irreversible COX inhibitor

- IBU = reversible COX inhibitor

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54
Q

What are allosteric enzymes inhibitors? Do they follow MM kinetics?

A
  • Enzymes with multiple subunits that exhibit positive / negative cooperativity (e.g. Hb tetramer)
  • No
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55
Q

What is the MOA of diphtheria toxin?

A

ADP ribosylation of EF-2

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56
Q

How is the ribosomal subunit deactivated?

A

Phosphorylation of eIF2a

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57
Q

What is the MOA of pseudomonas?

A

ADP ribosylation of EF-2

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58
Q

What is the MOA of ricin?

A

Remove adenine bases from 28s rRNA

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59
Q

What is the MOA of shiga toxin?

A

Remove adenine bases from 28s rRNA

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60
Q

What is the abx that causes gray baby syndrome? How?

A

Chloramphenicol

Cannot UDP

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61
Q

Where does N and O linked glycosylation occur?

A 
N = ER
O = Golgi
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62
Q

Where in the cell does trimming of N/O glycosylation occur?

A

Golgi

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63
Q

What is the pathophysiology of scurvy? Where in the cell does this occur?

A

Inability to hydroxylation of proline in the rER

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64
Q

What are the amino acids that are O linked glycosylated?

A

Y and S

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65
Q

What is Menke’s disease?

A
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66
Q

What are congenital disorders of glycosylation?

A

Rare, protein losing enteropathy

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67
Q

What is prenylation? What proteins need this to become activated?

A

G-Ras proteins

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68
Q

What drugs inhibit isoprenoid synthesis?

A

Statins d/t loss of cholesterol

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69
Q

What is the signal on proteins that move proteins from the ER to the golgi?

A

Phosphorylation of Mannose

70
Q

What is I cell disease?

A

Deficiency of Phosphorylation of mannose on glycoproteins leads to accumulation of undegraded molecules in the lysosomes

71
Q

What is the difference between euchromatin and heterochromatin?

A
  • Euchromatin = open to transcription

- Heterochromatin = not open to transcription

72
Q

Histone acetylation leads to what effect on transcription?

A

Facilitates transcription

73
Q

DNA methylation leads to what effect on transcription?

A

Inhibits transcription

74
Q

Where are enhancer / suppressor regions found in DNA?

A

Anywhere

75
Q

Where are promoter elements found on DNA?

A

Near to, and just prior to the DNA region being transcribed

76
Q

What are the different types of transcription factors?

A
  • Steroid
  • CREB
  • PPAR
  • NFkappaB
  • Homeodomain proteins
77
Q

What are CREB proteins/?

A
78
Q

What are PPARs?

A

Peroxisome proliferator activated receptors that regulate lipid metabolism (activated by fibrates)

79
Q

What are the HOX genes for?

A

Regulate development

80
Q

What is the general role of NF-kappa-B?

A

Regulates gene expression in the immune system

81
Q

What is the key regulatory step of gluconeogenesis? What stimulates it? (2)

A
  • PEP carboxykinase
  • Cortisol stimulates via cortisol receptor and
  • Glucagon stimulates expression via cAMP / CREB
82
Q

What are the steps involved with Gs? What is activated with the glucagon pathway?

A

Stimulates cAMP, and protein kinase A

CREB is activated

83
Q

Which are short and which are long lived: water soluble vs lipophilic

A 
Water = short lived
Lipid = long lived
84
Q

Where is the receptor for water soluble hormones? Lipid hormones?

A

Water soluble = plasma membrane

Lipid = in the cytoplasm or nucleus

85
Q

Which typically acts through a second messenger, or has enzymatic activity: water or lipid soluble

A

Water soluble for both

86
Q

Which modulate the activity of enzymes, vs modulates the transcription of enzymes: water vs lipid soluble hormones

A

modulate the activity of enzymes = water soluble

modulates the transcription of enzymes = lipid soluble

87
Q

What is the MOA of G proteins?

A

GDP bound alpha subunit of the G protein changes to GTP, and activates adenylate cyclase

88
Q

What is the MOA of adenylate cyclase?

A

ATP to cAMP

89
Q

What is the protein that is the target of Gs pathway?

A

Turns on PKA, which can phosphorylate phosphorylase kinase, which phosphorylates other stuff

90
Q

What is the major advantage of Gs protein, as opposed to having a signal molecule directly activate PKA?

A

Signal amplification

91
Q

What are the two second messengers of Gq pathway? What does each do?

A
  • IP3 and DAG

- DAG remains in plasma membrane, IP3 goes releases Ca from the sER

92
Q

What is the MOA of PKC? How is it activated?

A

Ca released from the sER from IP3 leads to activation

93
Q

What is the role of calmodulin?

A

Binds Ca and modulates Ca control

94
Q

What is type of receptor is the insulin receptor? MOA?

A
  • Protein tyrosine kinase

- phosphorylates IRS1, which serves as a binding site for other molecules

95
Q

What does CREB bind to?

A

CRE element on DNA

96
Q

What is the function of B1 (thiamine)

A
  • Decarboxylation of alpha-ketoacids
  • Transketolase rxn

(alpha-KG dehydro, Transketolase, Pyruvate dehydrogenase)

97
Q

What are the diseases that result from B1 deficiency?

A
  • BeriBeri

- Wernicke-Korsakoff syndrome

98
Q

What are the physiological effects of Vit B1 deficiency?

A

Impaired glucose production

99
Q

What are the s/sx of Beriberi?

A
  • Pain and paresthesias
  • Impaired cardiac energy metabolism
  • Peripheral neuritis
100
Q

What is the triad classic for Wernicke encephalopathy?

A
  • Horizontal nystagmus
  • Encephalopathy
  • ataxia
  • ophthalmoplegia
101
Q

What is the classic triad for NPH?

A

wacky, wobbly and wet

102
Q

What is B2 (riboflavin) needed for?

A

Component of FAD and FMN

103
Q

What are the s/sx of riboflavin deficiency?

A
  • Cheilosis
  • Corneal vascularization

-Two C’s of B2

104
Q

What is Niacin (b3) used for?

A

Dehydrogenase reactions

-NAD (B3 = 3 ATP)

105
Q

What is the disease caused by niacin deficiency? S/sx?

A

Pellagra

  • Dermatitis
  • Dementia
  • Diarrhea
  • Death
106
Q

Niacin can be synthesized from what amino acid? What does this synthesis require?

A

Tryptophan, which requires B6

107
Q

What are the s/sx of excess niacin?

A

Facial flushing

108
Q

What is the function of B5?

A

Required for amino acid metabolism and heme synthesis

109
Q

What are the s/sx of B5 deficiency? (4)

A
  • Dermatitis
  • Enteritis
  • alopecia
  • Adrenal insufficiency
110
Q

What are the hematological abnormalities that can be had with B5 deficiency?

A

Sideroblastic anemia

111
Q

What is the function of B9 (folate)? (2)

A
  • THF generation

- Thymidylate synthase

112
Q

Where is folate from?

A

Foliage

113
Q

What are the s/sx of folate deficiency? Why?

A
  • Macrocytic, megaloblastic anemia

- Thymidylate synthase inhibition leads to inability to synthesize DNA

114
Q

What are the only 2 reactions that B12 is needed for?

A
  • Methionine synthase

- Methylmalonyl-CoA mutase

115
Q

What is the only source of B12?

A

Bacteria

116
Q

What is the parasite that causes B12 deficiency?

A

Diphyllobothrium latum

117
Q

What are the s/sx of B12 deficiency? (3)

A
  • Demyelination of the dorsal columns
  • Methylmalonic aciduria
  • Megaloblastic anemia
118
Q

How does B12 cause megaloblastic anemia?

A

Lack of B12 blocks methionine synthase rxn takes away the only reaction to convert N5-methylTHF to more oxidized forms

119
Q
A
120
Q

What is the most common cause of cobalamin deficiency?

A

Pernicious anemia, which causes a severe intrinsic factor deficiency

121
Q

Where is B12 + IF absorbed in the intestines?

A

Ileum

122
Q

What, besides the synthesis of collagen, is Vit C needed for?

A

Dopamine-beta-hydroxylase (converts Dopamine to NE)

123
Q

What are the s/sx of excess vitamin C?

A
  • n/v
  • diarrhea
  • fatigue
124
Q

What is B7 (biotin) needed for?

A

Cofactor for the carboxylation

125
Q

What is the protein in eggs that prevent biotin (B7) uptake?

A

Avidin

126
Q

What is the disease that can result in biotin deficiency?

A

biotinidase deficiency

127
Q

What are the s/sx of biotin deficiency?

A
  • facial rash
  • Alopecia
  • Keto-lactic acidosis
  • hypotonia
128
Q

What can be detected in the urine with biotin deficiency?

A

3-hydroxyisovaleric acid

129
Q

What is B5 needed for?

A

fat synthesis

CoA synthesis

130
Q

What are the s/sx of B5?

A
  • Dermatitis
  • enteritis
  • alopecia
  • Adrenal insufficiency
131
Q

What is vitamin A required for?

A
  • Retinaldehyde in vision

- Retinoic acid as a hormone

132
Q

What is the major source of vitamin A?

A

Beta-carotene in vegetables

133
Q

What are the s/sx of vitamin A deficiency?

A
  • Night blindness
  • Xerophthalmia (keratinization of the cornea)
  • Infections
134
Q

What are the s/sx of acute vitamin A excess? (3)

A
  • Increased ICP
  • Szs
  • Exfoliative dermatitis
135
Q

What are the s/sx of chronic vitamin A excess? (4)

A
  • Dryness of skin
  • Alopecia
  • Glossitis
  • Cheilosis
136
Q

What is the effect of excess vitamin A in pregnancy?

A

Birth defects and abortions

137
Q

What is D2 and D3 respectively?

A 
D2 = ergocalciferol
D3 = Cholecalciferol
138
Q

What is the storage and active form of Vit D?

A 
25-D = storage
1,25 = active
139
Q

What are the s/sx of vitamin D excess?

A

Hypercalcemia

Stones

140
Q

Why is there excess Ca with sarcoidosis?

A

increased activation of macrophages

141
Q

What is the name of vitamin E?

A

alpha tocopherol

142
Q

What is the function of vitamin E?

A

antioxidant

143
Q

What is the effect of vitamin E on WArfarin?

A

Increases effects

144
Q

What are the s/sx of vitamin E deficiency?

A

Hemolytic anemia

acantholysis

145
Q

What is the function of vitamin K?

A

Synthesis of various clotting factors (carboxylation of glutamate residues in various proteins)

146
Q

What is the primary source of vitamin K?

A

Green leafy vegetables

147
Q

What are the s/sx of vitamin K deficiency?

A

neonatal hemorrhage with increased PT and PTT

-Bleeding, bruising, hemorrhage

148
Q

Why are neonates given vitamin K injections at birth?

A

They don’t have intestinal flora that produces it yet

149
Q

What causes warfarin necrosis?

A

Protein C and S are depleted fasters, causing a hypercoagulable state, and resulting necrosis

150
Q

What is the MOA of warfarin?

A

Inhibits Vitamin K epoxidase

151
Q

True or false: you cannot convert acetyl-Coa into glucose

A

True

152
Q

What is the overall purpose of the CAC?

A

take acetyl-coa to NADH, FADH and GTP

153
Q

What are the three major control points of the CAC?

A
  • Citrate synthase
  • Isocitrate dehydrogenase
  • alpha-KG
154
Q

What is citrate synthase controlled by?

A

availability of OXA

155
Q

What is isocitrate dehydrogenase controlled by?

A

Activated by ADP and inhibited by NADH

156
Q

What is alpha-KG dehydrogenase controlled by?

A

Inhibited by NADH and succinyl-CoA

157
Q

What is the function of citrate?

A

-Exported to cytoplasm, and cleaved by citrate lyase to release acetyl-CoA for fat synthesis

158
Q

What is the function of malate?

A

Exported to cytoplasm to serve as a substrate for gluconeogenesis

159
Q

What is the function of succinyl-CoA?

A

Substrate for Heme synthesis

160
Q

What is the drug that inhibits complex I of the ETC?

A

Rotenone (barbiturates)

161
Q

What is the drug that inhibits complex III of the ETC?

A

Amtimycin

162
Q

What is the drug that inhibits complex IV of the ETC?

A

Cyanide

163
Q

What is the drug that inhibits ATP synthase of the ETC?

A

Oligomycin

164
Q

What is the sequence of complexes in the ETC? (5)

A 
I
CoQ
III
Complex C
IV
165
Q

Where is NADH oxidized in the ETC?

A

Complex I

166
Q

Where is FADH2 oxidized in the ETC?

A

Complex II

167
Q

How many ATP are generated from NADH and FADH2 respectively?

A
  1. 5 for NADH

1. 5 for FADH2

168
Q

What is the treatment for CN toxicity? MOA?

A

Amyl Nitrate + sodium nitrite

-Nitrate oxidizes some of the Fe from ferrous to ferric state, to cause CN to release CN from Cytochrome oxidase

169
Q

What is the MOA of dinitrophenol?

A

Uncoupler of ETC

170
Q

What is the protein in brown fat the uncouples ETC?

A

Thermogenin

171
Q

What is the major source of ROS in the ETC?

A

Ubiquinone

172
Q

What is ischemia reperfusion injury?

A

Low ATP and high NADH after transient ischemia

All the Small Things (29 decks)

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