BIOCHEMISTRY- Raymon Videos Flashcards
(160 cards)
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
2
Q
What is associated to negative Nitrogen balance?
A
Protein malnutrition (Kwashiorkor) Dietary Deficiency of even one essential aminoacid Starvation Unconroled diabetes Infection
3
Q
Positive Nitrogen Balance situations
A
Growth
Pregnancy
Recovery phase of injury or surgery
Recovery from condition associated with negative nitrogen balance
4
Q
What are the products of Glucose+ O2?
A
CO2 + H2O
With a lot of energy release production
5
Q
Does Glucose+ O2 –> CO2 + H2O occur spontaneously?
A
Yes, it doesn’t tell how long it will take to happen
6
Q
Does Glucose+ O2 –> CO2 + H2O occur immediatly?
A
NO
7
Q
What determines spontaneous biochemichal reactions?
A
Energy (Δ G)
8
Q
What determines speed of biochemichal reactions?
A
Rate (V)
9
Q
What increases speed of biochemichal reactions?
A
By enzymes
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
11
Q
What does Δ G
A
Thermodynamically spontaneous (energy released, often irreversible)
12
Q
What does Δ G >0 mean?
A
Thermodynamically nonspontaneous (energy required)
13
Q
What does Δ G = 0 mean?
A
Reaction at equilibrium (free reversible)
14
Q
What does Δ G0 mean?
A
Energy involved under standarized conditions
15
Q
What is the effect of enzymes related to Energy?
A
Decrease energy of activation, Δ G++
16
Q
In what does Vmax depend on?
A
of enzymes (more enzymes more Vmax, less enzymes less Vmax
17
Q
What does Michaelis-Menton plot determine?
A
Kinetics of reactions
18
Q
Parameters on Michaelis-Menton plot
A
Substrate concetration (what the enzyme digest) V (speed of reaction)--> vmol/sec
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
20
Q
What does the plateu of the curve mean in Kinetic Reactions?
A
Means saturation, the activity of the enzyme is saturated
21
Q
What does Km in Kinetic Reactions mean?
A
Substrate Concetration
22
Q
How is Km calculated?
A
Is 1/2 Vmax
23
Q
What is related to Km?
A
Affinity
24
Q
What does Km determines?
A
How well substrate and enzyme like each other, if they each other that is affinity
25
Who is irreversible proportional to affinity?
Km
26
So... ↑ affinity translate as...
↓ Km
27
And ↓ affinity means...
↑ Km
28
What determines the affinity of a substrate to an enzyme?
The shape
29
In what does km depends on?
Number of enzymes
30
In Michealis Menton plot what does the right shift of the curve means?
+ competitive inhibitor, increased (substrate, Km)
31
Which drugs shift the curve of Michealis Menton plot to the right?
Competitive inhibitors (Antagonist) just like ACE (-), COX (-) except Aspirin
32
Which is the only COX (-) that does not shift the curve of Michealis Menton plot curve to the right?
Aspirin
33
What effect do Competitive inhibitors have on kinetic reactions?
↑ Km, No effect on Vmax
34
What effect fo Non competitive inhibitors have in Kinetic reactions?
No effect on Km, and decreases Vmax
35
Characteristic of Non competitive inhibitors
Irreversible
36
Alternative name for Irreversible
Allosteric (Characteristic of non competitive inhibitors)
37
Example of non competitive irreversible drug
Aspirin
ACE inhibitors (organo phosphorade)
Cianide, CO
38
In which situation do we see increased of enzymes?
Gene induction expression--> ↑ Vmax
39
What is the result of increase of enzymes in kinetic reactions?
↑ Vmax
40
In kinetic reactionswhat does activation means?
↑ Affinity
41
What is the effect of ↑ Affinity in kinetic reactions?
↓ Km
42
In Michealis Menton plot... what shifts the curve to the left?
Activator
43
In Michealis Menton plot... what shifts the curve up?
Inducers
44
In Michealis Menton plot... what shifts the curve to the right?
Competitive inhibitors
45
In Michealis Menton plot... what shifts the curve down?
Non competitive inhibitors
46
In the old days how was methanol posioning treated?
With ethanol administration
47
What explains ethanol is used to treat methanol intoxication?
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
48
Which is the selected treatment for methanol or ethylenglycol intoxication?
Use of Fomepizole, old management ethanol
49
Mechanism of action of Fomepizole
Dehydrogenase inhibitor
50
Characteristics of paracrine hormones
Are secreted into the interstitial space
| Very short half life
51
Example of paracrine hormones
Prostaglandins and neurotransmitters
52
Characteristics of Water Soluble hormones
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)
53
Characteristics of lipid Soluble hormones
Receptor inside cell
Hormone receptor complex binds hormone response elements (HRE of enhancer regions) in DNA
Can get into the cell
54
Which hormones are lipid soluble?
Steroids, Calcitriol, Thyroxines, Retinoic Acid
55
What is the effect of lipid soluble hormones?
Control of gene expression (requires hours)
56
How do water soluble hormones regulate gene expression?
Through proteins such as cAMP response element binding (CREB protein) (requires hours)
57
Example of water soluble hormones
Insulin, Glucagon, Catecholamines
58
Process of signal transduction by water soluble hormones
Receptor --> G protein --> enzyme --> Second messenger ---> Protein Kinase
59
What is the purpose of protein Kinase?
Take a phosphorylated Protein using ATP --> ADP, then phosphorylate a protein
60
Example of dephosphorylated Proteins
Gene regulator proteins
| Enzymes (rate limiting)
61
Which enzyme converts a phosphorylated protein to devephosphorylated?
Protein Phosphatase
62
What does Protein Phosphatase use?
H2O --> Pi
63
Which hormone turns on Protein kinase?
Glucagon, phosphorylates everything
64
Which hormone turns on Protein phosphatase?
Insulin, dephosphorylates everything
65
How are G proteins consider?
Trimeric proteins, conform by α β γ subunits
66
Why are G proteins called that way?
Because they bind to GTP
67
Which subunit of G protein binds to GTP and obteins energy?
α, converting GTP to GDP
68
How is the process of Trimeric G protein cycle?
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
How many transmemebrane domains do G protein coupled receptors have?
7 transmembrane domains
70
What is the outside cell terminus of transmembrane domain?
NH3 (Amino gropu)
71
What is the inside cell terminus of transmembrane domain?
COO- (carboxyl group)
72
How do we know is a G protein cell receptor?
By the 7 transmembrane domains
73
Example of Gs receptors
Glucagon
Epinephrine
Vasopressin in Kidney (ADH)
74
Example of Gi receptors
Epinephrine α2
| ACh M2
75
What is the result of Gs?
↑ cAMP (second messenger)
76
In G protein stimulation which is the first messenger?
Hormone
77
In G protein stimulation which is the second messenger?
cAMP
78
What is the effect of Gi?
↓ cAMP
79
Once cAMP is increased what happens?
+ stimulation of Protein kinase A
80
Which protein kinase is stimulated with cAMP pathway?
Protein Kinase A
81
What is the action of Protein Kinase A?
Phosphorylates (examples Serine and Treonin) Phosphorylates CREB
82
Once CREB is stimulated, what happens next?
Goes to the nucleus and stimulate gene production
83
Which kind of receptors does PIP2 system have?
G protein cell receptor
84
What binds to G protein receptor in PIP2 system?
Vasopressin vacular
Epinephrine α1
ACh muscarinic 1 or 3
85
In PIP2 system instead of Gs what is the stimulant protein?
Gq
86
What does Gq stimulates in PIP2 system?
Phospholypase C
87
What is the function of Phospholypase C?
Breaks into two second messengers PIP2 (portion of the membrane-becoming DAG) and IP3 (which goes inside the cell)
88
What is the intracellular effect of IP3?
Goes to ER and increases Ca2+
89
In PIP2 system how is protein kinase C activated?
By increased intracellular Ca2+ (by IP3 stimualtion) and with DAG stimulation
90
Which protein Kinase is activated in PIP2 system?
Protein Kinase C
91
What is the effect of Protein Kinase C?
Gene expression
| Enzymes phosphorylated
92
What is the final effect of energy Gq protein?
Increase Ca2+
93
Which are the second messengers in PIP2 system?
DAG, IP2, Ca2+
94
Which is the substrate to produce Nitric Oxide (NO)?
Arginine
95
Enzyme that converts Arginine to Nitric Oxide?
Nitric Oxide Synthase
96
Where is the NO synthase primarily found?
In endothelium
97
What characteristics of NO allows it to cross membrane?
That is a Gas, lipid soluble
98
Do NO requires receptor?
No, because it crosses membrane as a gas
99
After crossing membrane what is the effect of Nitric Oxide?
Stimulates soluble Guanylate Cyclase (Heme containing group)
100
What is the effect of Guanylate cyclase?
Converts GTP to cGMP
101
What is stimualted by cGMP?
Protein kinase G
102
In NItric Oxide pathway which is the second messenger?
cGMP
103
What is the final effect of Protein Kinase G?
Relaxation of smooth muscle (vasodilation)
104
Drugs that work at the nitric oxide pathway
Nitroprusside
Nitroglycerine
Isosorbide dinitrate
Hydralazine
105
Which is the drug of choice in hypertensive emergencies?
Nitroprusside
106
What is the secondary effect of Nitroprusside?
The prusside portion causes cianide toxicity
107
What is recommended when administering Nitroprusside?
Never administering more than a day or two days
108
What is the primarily effect of Nitroglycerine and Isosorbide dinitrate?
↓ venous pressure (venodilate) → decrease preload, oxigen demand for contraction, decrease cardiac output
Primary NO release in large veins, no effect on arteries
109
When is isosobide dinitrate recommended?
As antianginal drug, to prevent myocardial infarction
110
Mechanism of action of hydralazine?
Works releasing NO in arteries, antihypertensive medication pregnanacy
111
Characteristics of Guanylate cyclase
1 transmembrane domain
112
Does Receptor Guanylate cyclase have G protein?
No
113
For what is Receptor Guanylate cyclase?
For atrial Natriuretic Factor (ANF)
114
Which is a endogenous Diuretic?
Atrial Natriuretic Factor
115
How does Atrial Natriuretic factor works?
Stimulates Receptor guanylate cyclase--> ↑cGMP --> ↑ Protein Kinase G --> Relaxation of smooth muscle (vasodilation)
116
Which smooth muscle are relaxated by the effect of Atrial Natriuretic factor?
Afferent Arterioles of kidney
117
What is the effect of Atrial Natriuretic Factor?
Diuretic, ↑ Diuresis of Na+
118
Which drug is a recombinant form of Atrial Natriuretic Factor?
Nesirittide
119
What kind of receptor does Insulin have?
Two separetly receptors that become a dimer
120
What is activated once insulin is bind to the receptor?
Tyrosine kinase activity (Protein kinase)
121
Which aminoacid is phosphorylated once insulin is bind to a receptor?
Tyrosine
122
Where can we find Tyrosine kinase?
Bind to the dimeric receptor of insulin
123
After Tyrosine kinase is activated in insulin receptor what happens next?
Autophosphorylation of receptor (which is Tyrosine Kinase itself) inside the cell
124
What is the effect of Tyrosine kinase after phosphorylation?
Insulin receptor substrate (IRS) binds receptor and is phosphorylated on tyrosine residues
125
After IRS are phsophorylated, what is the result?
SH2 domain proteins bind phosphotyrosine residues on IRS
126
Which is the final step of Tyrosine kinase activation by binding insulin to the receptor?
Protein phosphatase activation which leads to enzymes dephosphorylated
127
Which mechanism does insulin follow in order to produce gene expression in nucleus?
p21 ras G protein stimulation
| PI-3 kinase (important)
128
Which is the most common affected gene in cancer?
ras protein ---> too much work, cause growth of everything including cancer
129
Which enzyme is important for insulin translocation of GLUT-4 tom membrane?
PI-3 kinase
130
In which cells membrane is GLUT-4 found?
Adipose and Muscle
131
Example of Insulin Growth factors
Insulin, IGF, PDGF, EGF
132
Which is the main factor related to all types of growth?
Tyrosine Kinase
133
Which drug inhibits Tyrosine Kinase?
Imatinib
134
Gene affected in CML
t (9:22)
| bcr-abl
135
What is bcr-abl?
A Tyrosine kinase
136
When do we do Glycogen synthesis?
When glucose is high, when insulin is present (Store Glucose)
137
Which is the enzyme that forms glycogen?
Glycogen synthase
138
When is Glycogen Active?
When it does not have any phosphate, when insulin is around
139
What is the effect of Glucagon to Glycogen synthase?
Phosphorylates it, making it less active
140
What is the effect of Glucagon to Glycogen?
Glycogenolysis (release Glucose)
141
When is Glycogenolysis done?
When Glucose is low, when glucagon is present
142
Which is the enzyme activated by glucagon in order to make glycogenolysis?
Glycogen Phosphorylase
143
Which protein mutation is related ti cancer?
p21 ras (ras)
144
Which cancers are related to ras mutation?
Colon, lung, breast, bladder tumors
145
Which is the numer 1 cancer killing?
Breast cancer
146
Which is the numer 2 cancer killing?
Lung cacer
147
Which is the numer 3 cancer killing?
Colon
148
What predisposes to bladder cancer?
Smokers, aniline dyes--> ethylenalonamide, chronic inflammation due to cystosomises
149
What is associated to ras protein?
GTP
150
Which Exotin cause ADP ribosylation?
Cholera Toxin
E. Coli
Pertusis Toxin
151
Which Toxins affect Gs α?
Cholera toxin
| E. ColiToxin
152
Which toxins affect Gi α?
Perutssis toxin
153
Type of diarrhea caused by E. Coli
Watery diarrhea (Travelers diarrhea)
154
Type of diarrhea caused by Cholera toxin
Rise water stoles
155
How is the mechanism of watery diarrhea caused by E. Coli and cholera?
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
Type of toxins produce by Bordetella pertusis, E. Coli, Vibrio Cholera
Exotoxins
157
Type of diarrhea caused by E. Coli and Vibrio Cholera
Secretory Diarrhea
158
Toxins of E. Coli
Heat labile of LT
159
What effect foes Cortisol have when binding to response elements?
It binds to the enhancer region of the phosphoennolpyruvate
| Carboxykinase (PEPCK) gene
160
How does Cortisol cause hyperglycemia?
By increasing the amount of PEPCK in the hepatocytes, Cortisol can increase the capacity for gluconeogenesis
