ppy2

oxygen

oxygen

electron transport chain final electron acceptor

oxygen needed

to run the Krebs cycle

glycogesis

addition of a glucose to glycogen (making more glycogen)

glycogenolysis

breakdown of glycogen

beta oxidation

fatty acid/2 #-1 (14atp) 1 (10atp) add them and subtract one always an odd number

107

given 16 carbon fatty acids how many how many ATPs can be obtained (beta oxidation)

cytosol

anaerobic metabolism takes place in the

NAD - NADH

reduction reaction (endogenic)

NADH - NAD

oxidation reaction (exogenic)

FAD - FADH2

reduction reaction (endogenic)

less to more

reduction (endogenic)

more to less

oxidation (exogenic)

NADH

produces 2.5 ATP

NO

can NADH enter the mitochondria

yes

can FADH2 enter the mitochondria

FADH2

produces 1.5 ATP

transmission

conversion of one amino acid into another aa1 into aa2 using keto acids or pryvic acids

oxidative deamination

conversion of aa into a keto acid or pyretic acid - so loss of NH3 which then is converted into urea and then most is excepted as urea.

Gluconeogenesis

making glucose from an amino acid (making glucose from lactic acid)

need all 3 for Gluconeogenesis

transmission, oxidative deamination, making urea

10

how many ATPs from Krebs cycle

10atp

3NADH + 1FADH2 + 1ATP =

acetyl COA can make

proteins, fat, glycogen

polar hormones

stored in vesicles, binds to plasma membrane, small peptides (TRH, TSH, insulin, CRH, ATCH), proteins

non polar hormones

not stored in vesicles, binds to nuclear receptors, cortisol, PGG2

t3 & t4

not polar or non polar, mixture

aspirin

blocks production of PGG2 (blocks cyclooxyrgenase, make arachidonic acid but not PGG2)

arachidonic acid/PGG2 cycle

phosopholipid - arachidonic acid - cyclooxyrgenase - PGG2

calcitonin responds to

high blood Ca2+ (calcium)

calcitonin

regulate blood calcium

regulate blood calcium levels

bone, kidney (urine), gut (food/absorption)

T3/T4

synthesized from tyrosine, binds to nuclear receptors

T3

more active than T4

the 3 and 4 stand for

number of iodine molecules

T3 and 4 purpose

increased protein synthesis if mitochondria and Na/K, increase basal metabolism, increased O2 use, increased ATP formation, generation of heat (increased cold for generation of heat for cold adaptation)

high blood glucose

beta cells secrete insulin and there is a decrease of glucagon from alpha cells

low blood glucose

alpha cells release glucagon and beta cells decrease insulin secretion

glucose/insulin release

high blood glucose enters pancreatic beta cells increasing levels of ATP

glucose process

glucose comes in - increase ATP levels - ATP binds to potassium channel and blocks it - depolarizes cell, opens calcium channel (results in increase of blood glucose)

effect of glucagon on glycogen

increase in blood glucose

glucocorticoids

nonpolar, binds to nuclear receptors, not stored in vessicles

cortisol

stimulated by circadian rhythm and stress, counteracts insulin contributing to hyperglycemia, stimulates glucogenogenesis, inhabitation utilization of the glucose by decreasing the transport of glucose into cells

growth hormone

increase blood glucose

growth hormone components

liver, adipose tissue (fats), most tissue (decreased glucose uilitazation)

indirectly through liver

cartilage and bone growth, muscle, and other organs, protein synthesis growth

ADH

responds to increase in osmolarity, increase water uptake

sensory neurons

peripheral to central nervous system

pseudounipolar

organs, skin, fingers, toes

bipolar

special organs EYES

multipolar

interneurons, motor neurons

myelination

gives fast transmission down the axon (fast neurotransmission), insulates the axon (oligodendrocytes CNS, Schwann PNS)

calcium high

outside the cell

chloride high

outside the cell

sodium high

outside the cell

potassium high

inside the cell

sodium leaking out

more negative

any negative or minus

more potassium

resting membrane potential (-50)

1. sodium/potassium pump

2. net neg. charge in cell due to protein

3. potassium leak + sodium leak channels with more potassium than sodium

signals in and out of neuron

1. signals from other neurons start @ dendrites

2. summed @ hillock

3. if large enough starts an action potential

4. AP travels down axon

5. release a neurotransmitter, neurohormone @ the terminal (presynaptic terminal)

depolarization

occurs when MP becomes more positive

hyper polarization

MP becomes more negative than RMP

repolarization

MP returns to RMP

open sodium channel

depolarization

open chloride channel

hyper polarization

action potential

1. fast sodium channel opens

2. cell depolarizes

3. sodium channel opens

4. cell repolarizes

5. potassium slowly closes, RPM restored

myelinated axons

1. fast transmission

2. sodium channels clustered at nodes

3. AP only at nodes

4. AP for all axons proceed down the axon in only one direction

absolute refractory

cannot get an action potential during this period because sodium channel is inactivated (depolarization)

relative refectory

gate closes, only potassium channels, can get an action potential

IPSP

thrives in negative membrane, potassium or chloride channel opening, decrease inhibitory

EPSP

thrives in positive membrane, sodium channel opening, increase sodium

channels

faster then GPCR

channels also called

ionotropic, nicotinic

GPCR also called

metabotropic, muscarinic, adrenergic (epiprine and norepinephrine)

adrenergic

epinephrine and norepinephrine (GPCR only)

ach (cholunergic)

can be ionotropic/nicotinic, or metaboltropic/muscarinic

release of neurotransmitter or hormone from presynaptic membrane

AP depolarizes the membrane and opens a gated calcium channel, intracellular calcium stimulates vesicle fusion and release

ach finds to nicotinic receptors and opens Na channel

generates EPSP or they bind to muscarnic receptors GPCR

Cl opens

hyperpolarization

Na closes

hyper polarization

K closed

depolarization (EPSP depolarizes membrane and open calcium channel)

GABA

decrease calcium uptake which decreases neurotransmitters release which decreases postsynaptic response

GABA bind

can bind to multiple channels and block calciums stimulated vessicle fusion

post synaptic response

ach binds to nicotinic receptors and opens sodium channel, generates ESP or they bind to muscarinic receptors GPCR

norepinephrine and arc removed from cleft by

reuptake through transporters decrease the number of neurotransmitters

spacial summation

EPSP and IPSP on post synaptic membrane from several neurons that occur nearly simutaneously

temoral summation

repeated stimulation of an action potential of a single neuron can result in 2 signals (IPSP ro EPSP) arriving at the post synaptic membrane that can be summated

summation

at the hillock

PKA causes t3 and t4 to

on thyroglobulin to enter the cell (endocytosis), fuses with lysosomes which releases t3 and t4 (transporters speed up)

where is t3 and t4 stored

thyroglobulin on the colloid

K equilibrium potential

-90

Na equilibrium potential

+66

positive leak out

negative

postitive leak in

positive