Biochemistry Lecture Davidson (Lan)

Front 1

What is bioenergetics?

Back 1

physical science dealing with energy changes

Front 2

Definition of living things:

Back 2

open systems
non equilibrium
steady state
isothermal
usually constant P

Front 3

1st law of thermo

Back 3

consevation of energy

Front 4

2nd law of thermo

Back 4

all processes goes to an increase in entropy in the universe

Front 5

What is free energy?

Back 5

can do work at constant temp and P

Front 6

What is the gibbs free energy equation?

Back 6

G = H - TS
H = enthalpy

Front 7

What is standard free energy change?

Back 7

* all rxn proceed w/ change in energy

* it is a constant - can calculate Keq under std conditions

Front 8

What constitutes standard conditions?

Back 8

T = 298 K; P = 1 atm; 1 M reactants/products

Front 9

What is the standard free energy equation?

Back 9

ΔG° = -RTlnKeq

ΔG° = G°(product) - G°(reactant)

Front 10

What does the prime ' on free energy "ΔG°" mean?

Back 10

standard free energy is working at pH 7

Front 11

What determines the direction of a reaction?

Back 11

the actual ΔG not ΔG° that determines spontaneity

Front 12

What is the difference between ΔG° and ΔG?

Back 12

ΔG is "actual" free energy change for rxn under existing cellular conditions

Front 13

What is the actual free energy change equation?

Back 13

ΔG = ΔG° + RTln (prod/rctant)

Front 14

What are some compound that has higher energy than ATP?

Back 14

Phosphoenolpyruvate (glyco)
1,3 bis P glycerate (glyco)

Front 15

Why do you have large amt release of energy when you hydrolyze ATP?

Back 15

Release energy in the unstable molecule (ATP).

Front 16

Name 2 thioesters and their use:

Back 16

Acetyl-CoA and succinyl CoA (TCA cycle)

energy is used to ATP or GTP or transfer acyl group

higher energy than ATP

Front 17

What is creatine-P used for?

Back 17

restore ATP

5x the amt than ATP in muscle

reversible rxn

Front 18

What is the importance of adenylate kinase in metabolism?

Back 18

ATP -> AMP + PPi

Front 19

What is the function of adenylate kinase?

Back 19

phosphorylate AMP to ADP
AMP + ATP = 2 ADP
reversible

Front 20

ATP -> AMP + PPi

Back 20

the PPi are rapidly hydrolyze to ensure a forward rxn.

common reaction in biochem

Front 21

What is the importance of coupling reaction?

Back 21

not all rxn are negative
sum of the ΔG for coupled rx'ns must be (-)

energy from exergonic can be used to drive another rxn

Front 22

What are roles of ATP?

Back 22

donate phosphate group to substrate

activates substrate for rxn

push biosynthetic rxn

gamma-phosphoryl group forms high energy intermediate

Front 23

How to make ATP?

Back 23

Use metabolites with higher potential energy than ATP

Front 24

substrate vs oxidative phosphorylation?

Back 24

oxidative made in electron transport chan

substrate is the transfer of P from a reactive intermediate
Ex - glycolysis or creatine kinase

Front 25

What is total body water separated into?

Back 25

Intracellular fluid (ICF) and extracellular fluid (ECF)

Front 26

What is extracellular fluid separated into?

Back 26

interstitial fluid and blood

Front 27

What ions are predominent in ECF?

Back 27

Na+, Cl- and HCO3-

Front 28

What ions are predominent in ICF?

Back 28

K+, phosphate and protein

Front 29

ICF and blood have similar electrolytes except for?

Back 29

proteins
blood has more
interstitial has none

Front 30

What can cause edema?

Back 30

high capillary P
low plasma protein
lymphatic obstruction
high cap permeability
kidney disease

Front 31

What is hypo and hypernatremia?

Back 31

low and high osmolaity in plasma

Plamsa concentration is important rather htan total body Na+

Front 32

What are some causes of hyponatremia?

Back 32

loss of Na+; low aldosterone
overhydration
renal failure - low urine volume
dietary deficiency

Front 33

What are some consequeces of hyponatremia?

Back 33

low osmolaity
swelling of cells
neuromuscular effects (weakness, convulsions/seizures, coma, and death)
pulmonary edema

Front 34

What is the main cause of hypernatremia?

Back 34

dehydration
minor: diabetes insipidus (defect ADH)

Front 35

What are some consequences of hypernatremia?

Back 35

* increase osmolality
* cell shrinkage
* neurological symptoms, convulsions, coma

Front 36

Hypovolemia vs. hypervolemia

Back 36

dehydration (low volume) vs. hypervolemia (high volume)

Front 37

List consequences of dehydration:

Back 37

low volume -> low supply of blood to tissues -> unconc -> coma -> death

symptoms: tiredness, lethargy, altered reflexes

Front 38

List consequences of overhydration:

Back 38

high volume
burden on heart, pulmonary edema

neuromuscular fxn due to low electrolye conc'n

Front 39

How do determine if an acid is strong?

Back 39

large Ka value means they fully disassociate

Front 40

What is the henderson hasselbalch equation?

Back 40

It relates the pH of a sol to hte pKa and the ratio of the conjugate base to acid

pH = pKa + log (base/acid)

Front 41

What is the basic mechanism of buffer action?

Back 41

Buffer is a sol of weak acid or weak base and its conjugate form.

Ex: OH- into buffer will form weak conjug base (H2O) so the change is not as much.

Front 42

What are 3 roles of the kidneys in regulating pH?

Back 42

1. Secretion of H+ (prox and dist)
2. conservation of filtered bicarbonate
3. regeneration of consumed bicarbonate and H+ excretion

Front 43

What are two types of H+ metabolism?

Back 43

non volatile acids and volatile acid (ex by lungs)

Front 44

What enzyme convert CO2 to carbonic acid?

Back 44

carbonic anhydrase

Front 45

Describe CO2 transport in blood:

Back 45

1. CO2 diffuse into plasma --> rbc
2. inside, H2CO3 --> H+ and HCO3-

3. HCO3- moves out in exchange for Cl-

Front 46

Describe CO2 transport for lungs:

Back 46

high pO2 means release of H+ from rbc to fuse with HCO3- to form CO2 and H2)

2. CO2 is blown off

Front 47

What are some physiological ways to regulated acid/base balance?

Back 47

1. respiratory
2. metabolic
3. mixed

Front 48

Name 4 basic acid/base disorders?

Back 48

1. respiratory acidosis (high CO2)
2. respiratory alkalosis (low CO2)
3. metabolic acidosis (low base)
4. metabolic alkalosis (high base)

Front 49

What is the compensatory reaction of a metabolic acidosis?

Back 49

hyperventilation to get rid of H+ (quick response)

Front 50

What is the compensatory rxn of a respiratory acidosis?

Back 50

increase H+ excretion and HCO3- reabsorption in kidney (slow response)

Front 51

Name some causes of metab acidosis and metab alkalosis

Back 51

acid:
1. loss of HCO3-
2. excess met acids
3. impraid H+ excretion
4. exogenous acid

alkalosis:
1. loss of H+
2. K+ deficiency (absorb more bicarbonate)
3. diuretics
4. ingestion of alkali

Front 52

What happens in hyperaldosteronism?

Back 52

increase Na+ reabsorption means more H+ excretion

Front 53

What happens in hyperkalemic patient?

Back 53

competition at distal tubule with H+ for secretion --> acidosis

K+ moves out b/c high concen and H+ moves in

Front 54

Name aliphatic R groups:

Back 54

Glycine, alanine, valine, leucine, isoleucine

Front 55

Name hydroxyl R groups:

Back 55

Serine and threonine

Front 56

Name sulfur containing R groups:

Back 56

cysteine and methionine

Front 57

Name aromatic R groups:

Back 57

pheynylalanine, tyrosine, tryptophan

Front 58

Name acidic R groups:

Back 58

aspartic acid, glutamic acid, and asparagine

Front 59

What are the functions of lutathione?

Back 59

1. conjugate and excretion of toxic xenobiotic
2. decomp H2O2
3. keep S-S in reduced form
4. transfer certain AA to kidney