Theme: dark red
Mood: bloody hell... angry
Motivated level: i'll get better marks than u bish.
Music: kissin you - miranda cosgrave
Details: angry and there is test tml, and there is exam on sat.. WTF.
Wednesday, 23 December 2009
1. blood oxigen capacity
2. content of air in atmostphere
3. purpose of ventilation
4. content of alveoli gas
5. draw oxigen-haemoglobin saturation disassociation graph
6. diff forms of transport of CO2 and O2 in blood
7. func of carbonic anhydrase
8. partial pressure of O2 in our cells
1. 10-20ml per 100ml blood
2. O2 : CO2 : N2 : H2O :: 20.87% : 0.03% : 78.6 : 0.5
3. no idea, figure out urself >,<"! just crap something lar.
4. O2 : CO2 : N2 : H2O :: 13.5% : 5.3% : 74.9% : 6.3%
5. uhm, its the bloody sigmoid thing.. saturation % vs oxigen pressure graph
curve goes left if temp down, presure down, ph up.
curve goes right if temp up, pressure up, ph down
6. transport of O2
1.5% in plasma
98.5% in hb-o2 [ in rbc]
transport of Co2
7% in plasma
23% in hb-co2 [in rbc]
70% in form of HCO3
7. function of carbonic anhydrase
IN RBC, it catalyses the binding of H2O with CO2 and forms H2CO3.
H2CO3 is then converted into HCO3.
HCO3 then goes into the venous blood.
H+ from H2CO3 goes to dispose other Hb-O2 and makes it Hb-H. The O2 goes into the tissues.
8. according to lecture it is
Po2 = 10
Pco2 = 60
according to my reference it is
Po2 = 40
Pco2 = 45
bie bie ..gluck
reference for answers are mostly lecture of last week.
Wednesday, 16 December 2009
so, until now i only managed to create this..
2. White muscles usually only perform aerobic glycolysis because postural maintainance movements hardly leads muscle to exhaustion. In addition to that, white muscles has a high fatique rate. In general, skeletal muscles are able to perform glycolysis even during anaerobic conditions. However the end product would be lactate. Why lactate? Due to the production of NADH2 during the 6th glyceraldehyde dehydrogenase reaction.Then it requires a place for NADH2 to be oxidised. In a normal senario we are able to send the NADH2 into respirative phosphorylation chain for oxidation. However, in anaerobic situation it is not possible. Thus, the lactate dehydrogenase[LDH] oxidises the NADH2 at reaction 11 of glycolysis.
inhibition of LDH would then result accumulation of NADH2. which probably will allosterically inhibit enzyme 6.
4. glycogen phosphorylase of skeletal muscles has higher Vmax due to the requirement to induce a huge amount of glucose-6-phosphate release at the spur of the moment that muscle action is needed. The glycogen phosphorylase of liver has alot of time to slowly release glucose because there is no real dire need for glucose, it is just to maintain the body's blood glucose rate.
5. not very possible due to no ATP production from those processes.
6. treat bicarbonate as the CO2 that is required for the 1st reaction of pyruvate decarboxylase.
7.From the view of glycolysis:
A rising ATP conc means that AMP is yet to be present to activate PFK I complex. However, ATP will be used by PFK 2 to catalyse fructose2,6-bisphosphate. The F2,6-bp will then allosterically activate PFK 1 and change its conformation into a conformation rather similar if the AMP activates it. Now, why do AMP is the activator of PFK 1? This is due to AMP is the signal of used ATP, which is followed by the excessive usage of ATP in muscles, which in turn signify that muscle has been put to much work. Thus, F 2,6-biphos will help the degeneration of glycogen to provide glucose.
a rising AMP conc will allosterically activate PFK 1 complex.
From the view of gluconeogenesis:
ATP increase will activate gluconeogenesis and AMP increase will activate glycolysis
10. 2 NADH2 molecules are formed. In the case of aerobic condition, NADH2 = 3 ATP. Thus 6 ATP is generated and outweights the ATP used in glucokinase and phosphofructokinase reactions. Net ATP = 4.
11. through oxidative phosphorylation pathway 3 ATP is generated of each NADH2. So 2 NADH2 will generate 6 ATP and the net ATP gain is 4 ATP.
12. Synthesis of glucose will increase due to
14. could this substance be protein kinase c???
16. This procedure saves the 1 ATP that is used by hexokinase aka glucokinase to add the phosphate back to glucose that results the formation of glucose 6- phosphate. This process is only possible due to sm glycolysis is used up at the time of release. Thus, saving the 1 single ATP does not affect the blood glucose levels unlike in liver.
17. glucose lvl blood drop , glycolysis drop, glycogen decomp drop, glycogen synthesis up.
1. Myocardium infaction = no oxygen. This results the anaerobic affinity of LDH to work [LDH4,5 which is at muscles]
2. Acute hepatitis = ???
20. glucose levels will go up due to glycolysis. Glycolysis by epineprine is possible to be activated by 2 receptors which have their own diff pathways.
1. Receptor alpha does the PIP2 CA2+ signal transduction method. [which ultilizes IP3 DAG + calcimodulin,it is an intracellular receptor pathway]
2. Receptor beta does the typical glucagon pathway. Which is cAMP signal transduction method [ intracellular, which requires adenylate cyclase]
21. insulin. For which test, maybe check ur biochem workbook.
22. its all about PFK 1. The increase in AMP due to continuous usage will result allosteric activation at PFK 1. [ATP]/[AMP] ratio will also decrease and the less ATP is a signal for PFK 2 to convert fructose 6 phosphate into fructose 2,6 phosphate that binds to the simillar purine allosteric site at PFK 1 and creates a change in conformation that resembles the allosteric activation of PFK1. In both bindings, rate of PFK 1 converting fructose 6 phosphate to glucose 2,6-phosphate with the usage of 1 ATP results in speeding up the glycolysis.
Wednesday, 25 November 2009
Regulation of physiological functions.
1. Concept about physiological functions and their regulation. Homeostasis and homeokinetics
Physiological function is the manifestation of vital activity of a living organism by means of adaptation. It is about how the organism adapts itself to its external environment, and how it adjusts its internal environment to meet its own requirements.
This involves exchange of matter and energy, complex physical and chemical changes, transformations between matter and energy. It is a continuous process that takes place constantly in every living organism.
Homeostasis and homeokinesis
a) any self-regulating process by which biological systems tend to maintain stability while adjusting conditions that are optimal for survival.
b) If homeostasis is successful, life continuous… if it isn’t, disaster or death ensues.
c) The continuous utilization and dissipation of energy create emergent phenomena and then maintain them by homeostasis.
d) Homeostasis is about maintaining a constant and stabile internal environment. Its perimeters are constant PH, pressure, and temperature. This is to maintain blood, lymph, tissue fluid and cell and enzyme activities.
3. Humoral regulation. Types of humoral regulation
It is based on action, diff biological substances[liquid,extracellular fluid, lymph and blood] The change of activity within out organism is due to metabolites[between biological substances]
There are ions CO2 , hormones etc.
Humoral mechanisms are divided into 3 types.
a) Autocrine – change in activity of cell under chemical substance released by itself. Only cells that detects this substance has change of its cell activity.
b) Paracrine – changes activity of cells in response to substances released by neighbouring cells. Exp: vasoconstrictor factor NO, prostagladins, growth factors and many other cytokine.
c) Endocrine – release of biological substance to specific cell. A release through blood. Exp: adrenaline. Released by diffused glands[APUP system]
Pecularities: slow spreading. Might be crushed by other enzymes before arriving upon location.
4. Nervous regulation. Reflex as basic mechanism of nervous regulation.
This is also known as neural mechanisms. Regulating effect formed by neural activity of nervous system. It is in general a very precise set of regulations. Characterized by:
I) Very high velocity of spreading.
II) Very high accuracy. Due to nerve fibres bring specific impulses.
III) Very high reliability
Its basic principle is reflex. Which reflex is a response reaction of an organism for the change of internal and external environment with participation of CNS. It is based on the reflex arch. *draw plz reflex arch.
6. the systemic organization of functions [IP Parlov and PK Anokhin]
Firstly definition of functional system is different organs which coorperate with each another to perform the same function although anatomical and histological structures are different.
Exp: origin of nutrient lung takes part in supplying O2. GIT absorbs nutrients from food. Liver changes the chemical composition of many substances. Musculoskeletal system help you to take food and eat.
According to Parlov, some organs function together to get +ve results only. [at that time Parlov didn’t’ know about –ve mechenisms. Anokhin however said that functional systm is a conceptual scheme of behavior where interaction of central and peripheral structures is directed in achievement of purposeful result.
Control mechanisms of functional systems of regulation are:
a) Genetic control system
b) Control systems tru out the entire organ
c) Control systems in organ that functions to control individual parts
Physiology of central nervous system
1. general structure of CNS
The CNS includes brain and the spinal cord.
2. functions of CNS
a) regulation of all organs and systems within the body and adaptation to the external environment.
b) Integration or coordination of all systems of an organism.
c) Purposeful behavior with integration of the external environment.[I think quite like voluntary]
3. reflex principle of CNS activity. The importance of R.Decart, I.M Sechenov, I.P Parlov, P.K. Anokhin works. Principles of reflex theories of Sechenov-Parlov.
a) principle of determination – any reflex act is based on the motivation.[ Purposeful behavior]There is a reason of each action
b) principle of structure – each reflex response and its reaction has specific structured and neuron network.
c) Principle analysis and synthesis – CNS analyses any information and submit all information and produces new information and stores significant info within our memory.
d) Parlov’s principle [ Anokhin principle] – there is +ve and –ve feedback.
4. Classification of reflexes.
a) according to biological importance
- nutritional , sex-orientation
b) according to location of receptors
- exteroceptive, viscera
c) parts of CNS involved
- bulbar, mesencephalic
d) according to character of response
-motor, sensory, vasomotor.
5. Neuron, its structure and functions.
Neuron is the basic conducting unit in the NS. Its main function is the production and regeneration of AP within the NS. It consists of
short variable processes
function: getting into body by means of conduction.
include all subcellular organels
function: integrity function (analyse and synthesis)
only 1 process
function: conduct impulse to other cells.
Components of neurons:
Hillock = very low membrane pressure, high excitability.
collateral branches = extra axon branches.
related cells: astrocytes, oligodendrocyte
There are 2 types of neurons:
6. brain glial cells and their functional important
Neuroglia are several cell types in N.tissue that is associated with neurons and play an auxillary role on support,metabolic, and protective functions.
its cell processes branch upon neuron surface.
function to remove waste products of metabolism, supply O2, energy substates,pathway for neuron and modulate synaptic transmission.
Form protective barrier around neurons.
Function: making myelin and unmyelin sheaths of nervous fibers.
c) Epidimal cyte
Lines central canal of spinal cord and ventricles of brain which are filed with cerebrospinal fluid.
Functions as barrier and supporting framework for Nervous tissues.
7. synapse. Its structure and functions.
Synapse has the function of conduction of impulses between 2 neurons. There are 2 types of synapse, electric synapse and chemical synapse. The chemical synapses is dominant within humans. Consists of :
I) Presynaptic membrane –vesicles, active sites
II) Synaptic cleft – 10nm in electric, 40-60nm in chemical
III) Post synaptic membrane – ionotrophic receptor aka channels, metabotrophic receptor.
Classification of synapses:
d) Neuromuscular junction
8. the mechanism of transmission of excitation in chemical and electric synapses. The mechanism of neuron excitation.
I) AP opens Ca2+ voltage dependant channels.
II) Ca2+ inflow into cell, stimulating movement of vesicles with active site near to Ca2+ channels.
III) pores and exocytosis of neuro transmitters into synaptic cleft. There is a quantum/fixed amount of neurotransmitters.
IV) neurotransmitters then binds to post-synaptic receptors.
V) the binding allows opening of ionic channels and increase in permeability of post synaptic membrane to diff ions.
VI) As a result of permeability change, potential of membrane will change too.
VII) Change in membrane potential grants 2 kinds of local respose:
a) Local depolarization – coz Na and Ca inflow
b) Local hyperpolarization
VIII) AP will arise and accumulate in hillock.
IX) Neurotransmitters are removed from synaptic cleft.
9. character of spreading of excitation in CNS [ divergence,convergence and circulation]
These are all types of neuron joins.
An impulse will spread from 1 neuron to a few neurons.
An example would be sense impulse, irradiation, and reflex arch.
Happens when many stimulus results only 1 reaction.
This sis due to many neurons combining into 1 neuron.
A known scenario is innervations.
When a chain of neuron has multiple axons that returns signals to the presynaptic neuron.
Results in a cycle of impulse.
It is how impulses spreads within networks.
An example would be short term memory that circulates within the network for about 5 minutes.
11. irradiation, facilitation and occlusion on excitation in the CNS
Is about the spreading of an impulse to the neighbouring channels. It follows the principle of divergence.
It can be inhibited by lateral inhibition.
Is the stimulation of a sub-normal excitable neuron. Such neurons are not usually activated due to its resting potential being lower or its excitation potential is far greater than common neurons. Thus, a normal strength of excitation does not activate it. However, a combination of 2 or more exicitatory neurons might generate enough EPSP that exceed its critical potential and result in AP formation.
In other words it can only be activated by convergence of 2 or more excitatory neurons.
14. inhibition in CNS. History of central inhibition discovery
Inhibition is a diminishing of activity. It is an active self dependant process that is provoked by excitation at inhibitory neuron and is reveal in the organism as a depression or diminished action by another excitation. It is a reversible process.
Its history is :
Firstly Brothers Wever discovered nerve valves and inhibition of heart activity. Sachenov is the first to discover central inhibition of CNS. However his 1st experiment was wrong. Work 27.
15. mechanisms of inhibition
2 primary inhibitions:
Firstly neurons consist of 3 types, excitatory, inhibitory, and effector neuron.
The inhibition occurs on postsynaptic membrane of specific inhibitory neuron. Glysine and GABA will be released at the pre-synaptic end aka the axon part of inhibitory neuron. This will result post synaptic effector neuron opening Cl- channels. The Cl- ions will enter the effector neuron and result in a prolonged but weak hyperpolarization through the cell membrane and as a result accumulation of IPSP within the axonal hillock. The summation of IPSP would decrease excitability and hillock is unable to generate AP even if EPSP gathers. Due to the resting membrane potential goes lower than -70mV.[check graph,lec 10]
Inhibitor neuron might have 2 axons. The axon that acts upon the effector neuron and a collateral that is directed to the excitatory neuron. In this inhibition, a long but weak impulse takes place by that collateral axon. Due to this weak impulse, subtreshold and weak depolarization occurs, and results the accumulation of EPSP at the hillock of exicitatory neuron. However EPSP is subthreshold.
Following this, a stimulus is received and AC travels along the nerve fiber and reaches the presynaptic excitatory neuron. No excitation is further transmitted due to the inability of the presynaptic membrane to further depolarize due to its inactivated ion channels across its membrane.
2 secondary inhibitions[both are postsynaptic style] :
Frequent threshold excitations on postsynaptic membrane that achieves AP generation, but results fatique and an accommodation reaction of membrane by the increase in critical potential levels. This results in a decrease in excitability.
Inhibition after excitation
Certain specific neurons have the ability to generate long , hyperpolarizing after-potential at the hillock. Prerequisites is an excitation.
16. Significance of inhibition
EXHAUSTATION NORMAL COORDINATION
i) To prevent excessive excitation and EXHAUSTATION
ii) To limit irradiation of excitation to make sure CNS has NORMAL response to stimulation
iii) To take part in COORDINATION of reflex and function (aka all physiological functions, exp : movement, respiration.
17. coordination of reflex acts. Main principles of coordination [principles of interaction of nervous centers]: reciprocal inhibition, dominant, common final pathway and feedback.
Interaction between neurons are necessary to ensure the right sequence work is done within the nerve centre. There are many principles, mainly is
a) reciprocal inhibition [postsynaptic]
the excitation of an effector neuron is the inhibition of antagonist of is the latter.
Example : flexor and extensor ; abductor and adductor
b) Dominant inhibition
Has the highest excitability and suppresses other nerve centres. It subcoordinate them to their work. Results a few nerve fibers working for 1 stimuli.
Its advantages is the
- ability of summation to increase strength of excitation
- remained stimulated longer
c) Common final pathway
It is according to convergence principle.
Different sensory neurons connect to a single nerve centre although they have diff stimuli.
18. muscle tone. The mechanism of muscle tone
Muscle tone is visible as a result of prolonged muscle contraction with very low chance to fatigue. We can say that muscle tone only occurs in tonic muscles aka red muscles with high level of mitochondria. These muscles contain 2 specialized receptors in the form of Golgi Tendon Organ [GTO] and muscle spindle. Resting muscle tone which is different from muscle tone due to alpha neurons not generating any tonic impulses. Resting muscle tone is due to thixotropy to conserve energy.
Function: to maintain decent posture of a human being.
Mechanism: when a muscle is extended or stretched, type Ia affector neurons will send impulses to the spinal cord and generate a response. This process occurs very fast due to being a monosynaptic neuron and it has the highest latency in all spinal transmitions. The response generated is contraction of the extrafusal by efferent motor neuron alpha and contraction of muscle spindle by efferent gama motor neuron. As mentioned above this happens at a reflex speed which is for maintaining original length of muscle fibers. Following that, II type afferent neurons aka secondary neurons will fire impulses directed towards higher centers of regulation. GTO is a tension receptor located in intrafusal muscles that will send impulse to 2 locations to dorsal of spinal cord that leads to CNS and inhibition collateral branch that will act on the alpha motor neuron to reduce the excessive tone of the muscle.
19. regulation of muscle tone. The role of spinal cord, the medulla oblongata, midbrain, cerebellum, basal ganglia and cerebral cortex in formation and regulation of muscle tone.
The spinal cord serves generates reflex muscle tone
The medulla oblongata can generate involuntary muscle tone.
The midbrain is the centre which is located nucleus rubra, this nucleus can inhibit the muscle tone. Without it, muscles will be in extended state.
Cerebellum participates in the reflex arch, and can control the level of muscle tone involuntarilly. Sickness at this level is dystonia, dysmetria.
Basal ganglia sickness at this level is Parkinson’s.
Cortex has formation and control over muscle tone and phasic movements. It controls tone voluntarily.
20. righting-tonic reflexes and their importance
It is also known as postural reflexes. It functions to maintain posture in change of conditions.
It is divided into static and kinetic type.
a) postural – appear when slight change in body, for example head movement.
b) Restorative tone –when change in body posture.
a) linear- up and down movement for example in a lift. This depends on the acceleration. To reduce stress on skeleton.
b) Rotational – angle acceleration. To prevent dizziness.
21. muscle disorders:
Is the situation of weakening of a muscle. It thought as an active contraction with less force and fatigues faster than of a normal muscle
The situation where muscles are activated by gama motoneurons and has higher resistance to stretch. It could be due to muscle spasm, Emre defined
muscle spasm as an “involuntary and inappropriate, reversible,
prolonged bracing of a muscle or group of muscles,
attributable to overactivity of motor units or changes
of excitability of muscle fibers”.
1 Limbic dysfunction – muscle hypertonicity due to dysfunction
of the limbic system that is usually not spontaneously
painful. Muscle tension from emotional stress
is an example.
2 Impaired function at the segmental (interneuronal) level
– characterized by an altered balance between physiologically
antagonistic muscles. Muscle tension asymmetry
in joint dysfunction would fall into this category.
3 Impaired coordination of muscle contraction – this type
leads to increased tone in part of a muscle where the rest
of the muscle remains normal. Trigger points (TrPs)
may be included in this category.
4 Response to pain irritation – a defense reaction meant to
immobilize an injured part of the body. Splinting spasm
from viscera and flexor or nociceptive reflexes are examples.
5 Overuse – muscle tightness, involved in “muscle imbalance”
syndromes. Janda believes this type of hypertonicity
is due to long-term overuse and finds the active
muscle fibers are replaced by non-contractile tissue.
Active muscle hypertonicity also includes other diagnostic/
descriptive categories, including focal dystonia,
antalgia, trigger points, cramp, spasticity and rigidity.
Focal dystonia is probably about the loss of type Ia neurons if movement and leaves only type II neurons which is responsible for length of muscle
Antalgia is the weird stretching or positioning of a muscle due to the antagonic reaction would result in pain.
Trp is about the damage of the coordination between the muscle spindle and the extrafusal. Might be due to a strong sretching force that overcomed muscle in contraction.
Cramp is a sudden painful muscle spasm