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BIOCHEMISTRY > BIOCHEMISTRY- Raymon Videos > Flashcards

BIOCHEMISTRY- Raymon Videos Flashcards

1
Q

What is the Nitrogen balance?

A

Is the normal condition in which the amount of nitrogen incorporated into the body each day exactly equals the amount excreted

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2
Q

What is associated to negative Nitrogen balance?

A 
Protein malnutrition (Kwashiorkor)
Dietary Deficiency of even one essential aminoacid
Starvation
Unconroled diabetes
Infection
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3
Q

Positive Nitrogen Balance situations

A

Growth
Pregnancy
Recovery phase of injury or surgery
Recovery from condition associated with negative nitrogen balance

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4
Q

What are the products of Glucose+ O2?

A

CO2 + H2O

With a lot of energy release production

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5
Q

Does Glucose+ O2 –> CO2 + H2O occur spontaneously?

A

Yes, it doesn’t tell how long it will take to happen

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6
Q

Does Glucose+ O2 –> CO2 + H2O occur immediatly?

A

NO

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7
Q

What determines spontaneous biochemichal reactions?

A

Energy (Δ G)

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8
Q

What determines speed of biochemichal reactions?

A

Rate (V)

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9
Q

What increases speed of biochemichal reactions?

A

By enzymes

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10
Q

What is the Δ G++ energy activation?

A

Energy that is needed to the highest level on top of reaction until it runs forward

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11
Q

What does Δ G

A

Thermodynamically spontaneous (energy released, often irreversible)

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12
Q

What does Δ G >0 mean?

A

Thermodynamically nonspontaneous (energy required)

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13
Q

What does Δ G = 0 mean?

A

Reaction at equilibrium (free reversible)

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14
Q

What does Δ G0 mean?

A

Energy involved under standarized conditions

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15
Q

What is the effect of enzymes related to Energy?

A

Decrease energy of activation, Δ G++

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16
Q

In what does Vmax depend on?

A

of enzymes (more enzymes more Vmax, less enzymes less Vmax

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17
Q

What does Michaelis-Menton plot determine?

A

Kinetics of reactions

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18
Q

Parameters on Michaelis-Menton plot

A 
Substrate concetration (what the enzyme digest)
V (speed of reaction)--> vmol/sec
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19
Q

Which is the rule of kinetic of reactions?

A

The more substrate you give the more product make, but there a limit on how much you are going to make per unit of time depending in the number of enzymes

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20
Q

What does the plateu of the curve mean in Kinetic Reactions?

A

Means saturation, the activity of the enzyme is saturated

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21
Q

What does Km in Kinetic Reactions mean?

A

Substrate Concetration

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22
Q

How is Km calculated?

A

Is 1/2 Vmax

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23
Q

What is related to Km?

A

Affinity

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24
Q

What does Km determines?

A

How well substrate and enzyme like each other, if they each other that is affinity

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25
Q

Who is irreversible proportional to affinity?

A

Km

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26
Q

So… ↑ affinity translate as…

A

↓ Km

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27
Q

And ↓ affinity means…

A

↑ Km

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28
Q

What determines the affinity of a substrate to an enzyme?

A

The shape

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29
Q

In what does km depends on?

A

Number of enzymes

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30
Q

In Michealis Menton plot what does the right shift of the curve means?

A

+ competitive inhibitor, increased (substrate, Km)

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31
Q

Which drugs shift the curve of Michealis Menton plot to the right?

A

Competitive inhibitors (Antagonist) just like ACE (-), COX (-) except Aspirin

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32
Q

Which is the only COX (-) that does not shift the curve of Michealis Menton plot curve to the right?

A

Aspirin

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33
Q

What effect do Competitive inhibitors have on kinetic reactions?

A

↑ Km, No effect on Vmax

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34
Q

What effect fo Non competitive inhibitors have in Kinetic reactions?

A

No effect on Km, and decreases Vmax

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35
Q

Characteristic of Non competitive inhibitors

A

Irreversible

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36
Q

Alternative name for Irreversible

A

Allosteric (Characteristic of non competitive inhibitors)

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37
Q

Example of non competitive irreversible drug

A

Aspirin
ACE inhibitors (organo phosphorade)
Cianide, CO

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38
Q

In which situation do we see increased of enzymes?

A

Gene induction expression–> ↑ Vmax

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39
Q

What is the result of increase of enzymes in kinetic reactions?

A

↑ Vmax

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40
Q

In kinetic reactionswhat does activation means?

A

↑ Affinity

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41
Q

What is the effect of ↑ Affinity in kinetic reactions?

A

↓ Km

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42
Q

In Michealis Menton plot… what shifts the curve to the left?

A

Activator

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43
Q

In Michealis Menton plot… what shifts the curve up?

A

Inducers

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44
Q

In Michealis Menton plot… what shifts the curve to the right?

A

Competitive inhibitors

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45
Q

In Michealis Menton plot… what shifts the curve down?

A

Non competitive inhibitors

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46
Q

In the old days how was methanol posioning treated?

A

With ethanol administration

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47
Q

What explains ethanol is used to treat methanol intoxication?

A

Both are substrates for alcohol dehydrogenase (ADH), with ethanol having a much lower km for the enzyme compare to methanol
This prevents methanol from being converted to formaldehyde, which is toxic and not metabolized further

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48
Q

Which is the selected treatment for methanol or ethylenglycol intoxication?

A

Use of Fomepizole, old management ethanol

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49
Q

Mechanism of action of Fomepizole

A

Dehydrogenase inhibitor

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50
Q

Characteristics of paracrine hormones

A

Are secreted into the interstitial space

Very short half life

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51
Q

Example of paracrine hormones

A

Prostaglandins and neurotransmitters

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52
Q

Characteristics of Water Soluble hormones

A

Can’t cross membrane of cells
Receptor in cell membrane
Second messengers often involved (Protein kinase activated)
Protein phosphorylation to modify activity of enzymes (requires minutes)

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53
Q

Characteristics of lipid Soluble hormones

A

Receptor inside cell
Hormone receptor complex binds hormone response elements (HRE of enhancer regions) in DNA
Can get into the cell

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54
Q

Which hormones are lipid soluble?

A

Steroids, Calcitriol, Thyroxines, Retinoic Acid

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55
Q

What is the effect of lipid soluble hormones?

A

Control of gene expression (requires hours)

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56
Q

How do water soluble hormones regulate gene expression?

A

Through proteins such as cAMP response element binding (CREB protein) (requires hours)

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57
Q

Example of water soluble hormones

A

Insulin, Glucagon, Catecholamines

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58
Q

Process of signal transduction by water soluble hormones

A

Receptor –> G protein –> enzyme –> Second messenger —> Protein Kinase

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59
Q

What is the purpose of protein Kinase?

A

Take a phosphorylated Protein using ATP –> ADP, then phosphorylate a protein

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60
Q

Example of dephosphorylated Proteins

A

Gene regulator proteins

Enzymes (rate limiting)

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61
Q

Which enzyme converts a phosphorylated protein to devephosphorylated?

A

Protein Phosphatase

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62
Q

What does Protein Phosphatase use?

A

H2O –> Pi

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63
Q

Which hormone turns on Protein kinase?

A

Glucagon, phosphorylates everything

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64
Q

Which hormone turns on Protein phosphatase?

A

Insulin, dephosphorylates everything

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65
Q

How are G proteins consider?

A

Trimeric proteins, conform by α β γ subunits

66
Q

Why are G proteins called that way?

A

Because they bind to GTP

67
Q

Which subunit of G protein binds to GTP and obteins energy?

A

α, converting GTP to GDP

68
Q

How is the process of Trimeric G protein cycle?

A
  1. Inactive G protein (means α subunit with GDP)
  2. Active G protein (means α subunit with GTP)
  3. Splitting of subunits α- GTP and β-γ
  4. α subunit has two types (αs- stimulates, αi- inhibits)
  5. Either way αs stimulates Adenylate cyclase or αi inhibits adenylate cyclase
  6. α subunit returns to GDP and the cycle is started again
69
Q

How many transmemebrane domains do G protein coupled receptors have?

A

7 transmembrane domains

70
Q

What is the outside cell terminus of transmembrane domain?

A

NH3 (Amino gropu)

71
Q

What is the inside cell terminus of transmembrane domain?

A

COO- (carboxyl group)

72
Q

How do we know is a G protein cell receptor?

A

By the 7 transmembrane domains

73
Q

Example of Gs receptors

A

Glucagon
Epinephrine
Vasopressin in Kidney (ADH)

74
Q

Example of Gi receptors

A

Epinephrine α2

ACh M2

75
Q

What is the result of Gs?

A

↑ cAMP (second messenger)

76
Q

In G protein stimulation which is the first messenger?

A

Hormone

77
Q

In G protein stimulation which is the second messenger?

A

cAMP

78
Q

What is the effect of Gi?

A

↓ cAMP

79
Q

Once cAMP is increased what happens?

A

+ stimulation of Protein kinase A

80
Q

Which protein kinase is stimulated with cAMP pathway?

A

Protein Kinase A

81
Q

What is the action of Protein Kinase A?

A

Phosphorylates (examples Serine and Treonin) Phosphorylates CREB

82
Q

Once CREB is stimulated, what happens next?

A

Goes to the nucleus and stimulate gene production

83
Q

Which kind of receptors does PIP2 system have?

A

G protein cell receptor

84
Q

What binds to G protein receptor in PIP2 system?

A

Vasopressin vacular
Epinephrine α1
ACh muscarinic 1 or 3

85
Q

In PIP2 system instead of Gs what is the stimulant protein?

A

Gq

86
Q

What does Gq stimulates in PIP2 system?

A

Phospholypase C

87
Q

What is the function of Phospholypase C?

A

Breaks into two second messengers PIP2 (portion of the membrane-becoming DAG) and IP3 (which goes inside the cell)

88
Q

What is the intracellular effect of IP3?

A

Goes to ER and increases Ca2+

89
Q

In PIP2 system how is protein kinase C activated?

A

By increased intracellular Ca2+ (by IP3 stimualtion) and with DAG stimulation

90
Q

Which protein Kinase is activated in PIP2 system?

A

Protein Kinase C

91
Q

What is the effect of Protein Kinase C?

A

Gene expression

Enzymes phosphorylated

92
Q

What is the final effect of energy Gq protein?

A

Increase Ca2+

93
Q

Which are the second messengers in PIP2 system?

A

DAG, IP2, Ca2+

94
Q

Which is the substrate to produce Nitric Oxide (NO)?

A

Arginine

95
Q

Enzyme that converts Arginine to Nitric Oxide?

A

Nitric Oxide Synthase

96
Q

Where is the NO synthase primarily found?

A

In endothelium

97
Q

What characteristics of NO allows it to cross membrane?

A

That is a Gas, lipid soluble

98
Q

Do NO requires receptor?

A

No, because it crosses membrane as a gas

99
Q

After crossing membrane what is the effect of Nitric Oxide?

A

Stimulates soluble Guanylate Cyclase (Heme containing group)

100
Q

What is the effect of Guanylate cyclase?

A

Converts GTP to cGMP

101
Q

What is stimualted by cGMP?

A

Protein kinase G

102
Q

In NItric Oxide pathway which is the second messenger?

A

cGMP

103
Q

What is the final effect of Protein Kinase G?

A

Relaxation of smooth muscle (vasodilation)

104
Q

Drugs that work at the nitric oxide pathway

A

Nitroprusside
Nitroglycerine
Isosorbide dinitrate
Hydralazine

105
Q

Which is the drug of choice in hypertensive emergencies?

A

Nitroprusside

106
Q

What is the secondary effect of Nitroprusside?

A

The prusside portion causes cianide toxicity

107
Q

What is recommended when administering Nitroprusside?

A

Never administering more than a day or two days

108
Q

What is the primarily effect of Nitroglycerine and Isosorbide dinitrate?

A

↓ venous pressure (venodilate) → decrease preload, oxigen demand for contraction, decrease cardiac output
Primary NO release in large veins, no effect on arteries

109
Q

When is isosobide dinitrate recommended?

A

As antianginal drug, to prevent myocardial infarction

110
Q

Mechanism of action of hydralazine?

A

Works releasing NO in arteries, antihypertensive medication pregnanacy

111
Q

Characteristics of Guanylate cyclase

A

1 transmembrane domain

112
Q

Does Receptor Guanylate cyclase have G protein?

A

No

113
Q

For what is Receptor Guanylate cyclase?

A

For atrial Natriuretic Factor (ANF)

114
Q

Which is a endogenous Diuretic?

A

Atrial Natriuretic Factor

115
Q

How does Atrial Natriuretic factor works?

A

Stimulates Receptor guanylate cyclase–> ↑cGMP –> ↑ Protein Kinase G –> Relaxation of smooth muscle (vasodilation)

116
Q

Which smooth muscle are relaxated by the effect of Atrial Natriuretic factor?

A

Afferent Arterioles of kidney

117
Q

What is the effect of Atrial Natriuretic Factor?

A

Diuretic, ↑ Diuresis of Na+

118
Q

Which drug is a recombinant form of Atrial Natriuretic Factor?

A

Nesirittide

119
Q

What kind of receptor does Insulin have?

A

Two separetly receptors that become a dimer

120
Q

What is activated once insulin is bind to the receptor?

A

Tyrosine kinase activity (Protein kinase)

121
Q

Which aminoacid is phosphorylated once insulin is bind to a receptor?

A

Tyrosine

122
Q

Where can we find Tyrosine kinase?

A

Bind to the dimeric receptor of insulin

123
Q

After Tyrosine kinase is activated in insulin receptor what happens next?

A

Autophosphorylation of receptor (which is Tyrosine Kinase itself) inside the cell

124
Q

What is the effect of Tyrosine kinase after phosphorylation?

A

Insulin receptor substrate (IRS) binds receptor and is phosphorylated on tyrosine residues

125
Q

After IRS are phsophorylated, what is the result?

A

SH2 domain proteins bind phosphotyrosine residues on IRS

126
Q

Which is the final step of Tyrosine kinase activation by binding insulin to the receptor?

A

Protein phosphatase activation which leads to enzymes dephosphorylated

127
Q

Which mechanism does insulin follow in order to produce gene expression in nucleus?

A

p21 ras G protein stimulation

PI-3 kinase (important)

128
Q

Which is the most common affected gene in cancer?

A

ras protein —> too much work, cause growth of everything including cancer

129
Q

Which enzyme is important for insulin translocation of GLUT-4 tom membrane?

A

PI-3 kinase

130
Q

In which cells membrane is GLUT-4 found?

A

Adipose and Muscle

131
Q

Example of Insulin Growth factors

A

Insulin, IGF, PDGF, EGF

132
Q

Which is the main factor related to all types of growth?

A

Tyrosine Kinase

133
Q

Which drug inhibits Tyrosine Kinase?

A

Imatinib

134
Q

Gene affected in CML

A

t (9:22)

bcr-abl

135
Q

What is bcr-abl?

A

A Tyrosine kinase

136
Q

When do we do Glycogen synthesis?

A

When glucose is high, when insulin is present (Store Glucose)

137
Q

Which is the enzyme that forms glycogen?

A

Glycogen synthase

138
Q

When is Glycogen Active?

A

When it does not have any phosphate, when insulin is around

139
Q

What is the effect of Glucagon to Glycogen synthase?

A

Phosphorylates it, making it less active

140
Q

What is the effect of Glucagon to Glycogen?

A

Glycogenolysis (release Glucose)

141
Q

When is Glycogenolysis done?

A

When Glucose is low, when glucagon is present

142
Q

Which is the enzyme activated by glucagon in order to make glycogenolysis?

A

Glycogen Phosphorylase

143
Q

Which protein mutation is related ti cancer?

A

p21 ras (ras)

144
Q

Which cancers are related to ras mutation?

A

Colon, lung, breast, bladder tumors

145
Q

Which is the numer 1 cancer killing?

A

Breast cancer

146
Q

Which is the numer 2 cancer killing?

A

Lung cacer

147
Q

Which is the numer 3 cancer killing?

A

Colon

148
Q

What predisposes to bladder cancer?

A

Smokers, aniline dyes–> ethylenalonamide, chronic inflammation due to cystosomises

149
Q

What is associated to ras protein?

A

GTP

150
Q

Which Exotin cause ADP ribosylation?

A

Cholera Toxin
E. Coli
Pertusis Toxin

151
Q

Which Toxins affect Gs α?

A

Cholera toxin

E. ColiToxin

152
Q

Which toxins affect Gi α?

A

Perutssis toxin

153
Q

Type of diarrhea caused by E. Coli

A

Watery diarrhea (Travelers diarrhea)

154
Q

Type of diarrhea caused by Cholera toxin

A

Rise water stoles

155
Q

How is the mechanism of watery diarrhea caused by E. Coli and cholera?

A
  1. Stimulation od Gs α protein with toxin (Increased cAMP)
  2. Activation of Protein Kinase A
  3. Phosphorylation of CFTR channels in epithelium cells
  4. Leads to Cl- excretion (salt) by CFTR channels to the intestinal lumen
  5. Dilution of Cl- in intestinal lumen with water causing watery diarrhea
156
Q

Type of toxins produce by Bordetella pertusis, E. Coli, Vibrio Cholera

A

Exotoxins

157
Q

Type of diarrhea caused by E. Coli and Vibrio Cholera

A

Secretory Diarrhea

158
Q

Toxins of E. Coli

A

Heat labile of LT

159
Q

What effect foes Cortisol have when binding to response elements?

A

It binds to the enhancer region of the phosphoennolpyruvate

Carboxykinase (PEPCK) gene

160
Q

How does Cortisol cause hyperglycemia?

A

By increasing the amount of PEPCK in the hepatocytes, Cortisol can increase the capacity for gluconeogenesis

BIOCHEMISTRY (12 decks)

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