L12: pH measurement®ulation

pH:influences most enzymes within body

physiological pH=7.4= -log[H+]=0.00004mEq/L or 40nEq/L : varry:10-160

pH regulation: 3 mechanisms:

1(seconds) Chemical ACID-BASE BUFFER system of body fluids

buffer+H+ ↔HBuffer

• Bicaronate buffer system

CO2+H2O↔↓H2CO3↔↑H+ +↑CO3-

Ionizes almost completely Na+

↑Acidosis: If Add acid: CO2 stimulates respiration removes it from system
↑Alkalosis: If Str.Base: ↓respiration to reserve CO2, ↑renal excretion: HCO3

H-H Eqn: pH=^.1+log HCO3-/(0.03*PCO2)

METABOLIC A-B DISORDERS:

M. Acidosis: ↓HCO3

M. Alkalosis: ↑HCO3

RESPIRATORY A-C DISORDERS:

R.Acidosis: ↑PCO2

R.Alkalosis: ↓PCO2

• Phosphate buffer system: important in TUBULAR system of kidneys

A: HCl + Na2HPO4 ↔ NaH2PO4 + NaCl

B: NaOH+ NaH2PO4 ↔ Na2HPO4 +H2O

• MAINLY: Cellular Protein buffer system

slow reaction, take several hrs to buffer changes in extracellular fluid due to slow movement of bicarbnate+ protons across plasma membr. (with exception of RBCs)

2 (minutes): Respiratory centre-regulation of pH

control of extracellular fluid: PO2

↑ [H+]->↑ alveolar ventilation-> ↓ PO2 (-feedback to [H+]) ↓ ventilation->↑ PO2

Abnormalities in respiration-> change in A-B balance&alter extracellular pH

e.g. emphysema: ↓ ability eliminate CO2-> build CO2->extracellular pH becomes acidic-> R.ACIDOSIS

3 (hrs-days) Kidneys-Renal Control ->pH regulation: regulation of extracellular fluid: [H]: 3 ways:

• Reabsorption of 85% HCO3 -->>contributes to:
• Generation of new HCO3 inside tubule cells
• Secretion of H+

if person suffering ACIDOSIS additional buffering can be gained with new bicarb. ions synthesized in the tubule cells, as long as a sink for H+ (HPO4-2) is available.

2nd way: from catalysis of a.a. glutamine

ACIDOSIS/ALKALOSIS:

better look handwritten notes

L11: Blood

Functions of bl:

1. Transport: O2+Hb(RBCs) v.little in plasma, CO2-> RBCs+plasma, nutrient: glu&lipids, -waste products (urea&bilirubin)
2. Regulation: HORMONES (site prod->target tissue), T regulatio-DIVERSION: bl. deeper-superficial vessels
3. Protection: Role of LEUKOCYTES-> INFECTION, CLOTTING

Components of Bl.:

Plasma: H2O, ions, proteins, nutr., horm. wastes

7%pl.w: PROTEINS:

albumins (liver synthesis), globulins (buffers, transport lipids, hormones, vit. metals, clotting enzymes, antibodies), fibrinogens (clot formation, forms bridges between activated pl.)

ELECTROLYTES (Na, K, Ca, Mg,Cl, HCO3, HPO4, SO4):

keep H2O extracellular comp., buffers, bl.clotting role, membrane Xcitability

Leukocytes:WBCs+A/B dye (Leishmans satin): 4000-11000/mm3

Leukopenia >4000/mm3, Leukocytosis<20000/mm3

according to granules:

• GRANULOCYTES (70%): granular : dye blue

neutrophils/polymorphocytes: ↑count->INFECTION, 2-5lobes, IF <3%:>

contain enzymes->breakdown egulfed bac.-> cytoplasm, amaeboid movement, phagocytosis, inflammatory mediators

eosinophils:2lobes, (3lobed), spherical granules, larger than neutro, phagocytic action, Inflammation-ASTHMA

Basophils: granules: HIS, HEPARIN, degranulation: ALLERGIC REACTIONS (skin rash, anaphylactic shock, urticara)

• AGRANULOCYTES: monocytes (2-8%), lymphocytes:large/small (20-40%)

Lymphocytes: Large nucleus, small #granules, lysosomal enzymes

• B-cells: antibody production
• T-cells: Regulation of antibody production
• NK (natural killer) cells: immune responce: lyse target cells

Monocytes: LARGEST OF Bl. cells, irregular, often lobed nucleus, phagocytic-SICKLE CELL ANEAMIA, egulf bac+MALARIA parasites, migrate tissues->differentiate->macrophages

Hematocrit: %RBCs/Bl.V pH: 7.35-7.45, 280-295mOSM

Erythrocytes 120 days life span: Erythropoiesis: regulated (hormone): Eryhtropoietin, O2 delivery-> kidneys, ↓O2-> EPO production-> altitude, lung disease, insuffisient heart pumping, anemia

transport of gases: O2-Hb, CO2

ANEMIA: ↓ ability of O2 transport-> ↓RBCs, ↓[Hg]/RBC

dietary iron deficiency, bone marrow failure: cancer/toxicity, poor EPO production from kidneys, ↑destruction RBCs, SICKLE CELL ANEMIA (Genetic mutation-HbS instead of HbA, Heterocyte≠Malaria, Abnormal Hb forms fibres @ ↓O2, RBS shapes distorted, Capillaries blockage, pain, ↓RBCs lifespan)

Platelets/Thrombocytes: no nucleus, discoid

from Megakaryocytes(multinucleus-> bone marrow)

When ↓pl. # ->↑TPO-> release Thrombopoietin (hormone) from Liver -->> pl. production

ROLE IN DISEASE:

↓pl.count (thrombocytopenia), pl.adhesion/aggregation (Scotts),pl.metabolism

Bl.clotting:

Hematoma: acumulatn of bl. in tissues

Hemostasis: prevent bl.loss in ↓P/small vessels, difficult staunch bl.loss from arteries

THESE CAUSE:

1)PLATELET AGGREGATION (Adherence of platelets to each other)

• Adhension to surface: vessel injury->conformationally changed collagen+
• Pl., Pl.activation: adenosine&serotonin (e-dense granules), adhesive proteins (a-granules): (+) feedback more pl.

(ACTIVATION from collagen (subendothelium), mol. (serotonin) made by themselves)

on activtn: pl. active sites exposed: fibrigonen can bind

• Pl.aggregation
• PLATELET PLUG

2)BL.COAGULATION=CLOTTING/Thrombus around plPLUG: Transformation of bl->solid gel

2Clotting Pathways:

Intrinsic:Begins in bl when exposed to collagen (from traumat. vessels)

Extrinsic: Trauma->vascular membr.: phospholipids+lipoprotein comples

Both lead to formation of :

F13 (XIII)

Prothrombin-> thrombin-> XIIIa

Fibrinogen ->Fibrin monomers -> Stabilised Fibrin

In an UNINJURED vessel: thrombin bound to thrombomodulin activates PROTEIN C: blocks clotting response

Limiting CLOT FORMATION: Plasminogen activators

Plasminogen------Fibrin------->> plasmin

Soluble Fibrin Fragments formed

Liver: critical role: producing&modifying bl.borne proteins (clotting pathways)

bile salts from liver facilitate absorption lipids: diets, VIT.K REQUIRED fro PROTHrombin Synthesis

BLEEDING DISORDERS: CL.factors: liver, Deppresion of Cl.system, NO VIT.K, HEMOPHILIA (male)- abnormality in XIII

HAEMOPOIESIS:bl. cells not replicate, constnt formation: stem cells->foetal liver->bone marrow

Leukopoiesis: (only LYMPHOCYTES): lympoid tissue: lymph, nodes,spleen e.tc.

Erythropoiesis: (+other bl.cells): myeloid tissue: red bone marrow, bones, ribs e.t.c.

PRODUCTION OF BLOOD CELLS: bone marrow (w~liver)- >thrombopoietin, erythropoietin

pluripotent stem cells-> precursors of any bl.cells: 1st differentiation: Lympoid + Myeloi stem cells

HAEMOPOIETIC GROWTH FACTORS: CYTOKINES: regulate production of bl.c. from st.cells, also Thrombopoietin (pl.prod.) from megakaryocytes, reagulate proliferation&differentiation, prevent normal programmed cell death (apoptosis)

Lec 7: Autonomic nervous system

Visceral motor: no conscious control
(Smooth muscle, rather than skeletal)

• Sympathetic: fight/flight: ↑heart rate
• Parasympathetic:Rest&Digest: relaxed

preganglionic cell bodies in thoracic lumbar region of spinal cord send projections to puravertebral SNS chain
postaganglionic cell bodies in SNS chain send long axonal projections that synapse on taget organ
output from sp.cord: collection to ganglion close to sp.cord

pregangionic cell bodies in cranial&sacral regions spinal cord send long axonal projections to PNS ganglia
postganglionic cell bodies send short axonal projections which synapse on target organs
ganglion close to effector

HYPOTHALAMUS decide whether
SNS
controlled brainstem emotions
dilation of pupil=>better vision=>greater field of view=>wasted E=> if neede for sth else
more bl. circulation
store (liver) glu.
inhibit insulin
gland releases hormonal response relax bladder

PNS
Design to relax
salive->food digestion
major output of neuron from cranial
stimulate insulin: abs. glu.

Neurotransmitters (chemical) &receptors (chemical)->ANS

Somatic efferent inovate skeletal muscles

CNS----------------------------<>ACh NIC Sk.muscle

Sympathetic

----------<>ACh NIC----------<>NA Adr heart, bl.vessels e.t.c.

---------------------<>ACh NIC-----<> ACh Musc heart, smooth, glands

1)Nicotinic ACh receptos, glutamate, GABA: ligand gated ion channels

2)Adrenoreceptors&muscarinic receptors: G-protein-coupled receptors

• Adrenoreceptors subtypes (SNS): α, β

α1: constriction bl.vessels

α2: inhibit NE release

β1:↑heart rate

β2: opening bl.vessels

β3:break down lipids if E needed

• Muscarinic (PNS)

M1:neural, CNS

M2: cardia, heart

M3:grandular, smooth muscle

Physiological effects of ANS

Efficacy of heart-> quick pumping of heart

S:↑heart rate, P:↓ heart rate

Bl.vessels

controlled most by S (α1 constriction less bl.supply, β2 dilation)

lungs: S: relaxation, P: constriction

GI tract: S:↓motility,secretion,contriction, ability to digest food, P: ↑ ability digestion

sex organs: S: ejaculation, P: erection

bladder: S: constriction, motility, P: Dilation, ↑motility

skin: S: secretion, constriction

eye: S: dilation, better peripheral vision, P: relaxation

liver, fat cells, adrena medulla: S mostly

pancreas: S: inhibited, P: stimulated

Lec 6: Overview of Human Brain

• Brain->
• Cerebral cortex*: mood&concept memory
• Diacephalon: involved-> emotions, coordinating complicated, more sophisticated movements
• Midbrain
• Pons: brain stem
• Medulla
• Cerebellum

*occipital lobe, parietal lobe, central sulcus, frontal lobe, tempral lobe
gap run through brain
motor, somatic sensory, visual, put electrodes figure out what happens to brain (used:stroke victims), what part of brain destroyed



Input to SOMATOSENSORY cortex--> into brain axons
from muscle reach sp.cord->medulla-thalamus(diacephalon)->reach somatonsensory cortex

Humunculus: toc which part of it receives info from what body part
Mainly FACE!-> more brain imput->more sophisticated movement (HANDS)=>sense

MOTOR cortex- Humunculus: huge amt of brain->HANDS sophisticated movement&FACE

Output from motor cortex: Desceding pathway: coordinated movement rather than reflex
from brain m.c.AP generated travels down axon -->medulla->spinal cord->periphery

Control of voluntary movement
motor/somatic sensory
Brodmanns area:
coordination of movements/ processing visual info: visual cortex: signal from eye in response to eye/motivation, emotion, movement, make decisions/talk speech, make sound/Werniches area: language center: processing of sound decoding, understanding language

Importance of midbrain: linked to control movement
Thalamus, caudate nucleus, putamen, globus pallidus, subthalamic nucleus, substantia nigra

Cerebellum (millions neurons, billions synapses) &synaptic integration (summation: each synapse causes AP to control v.complex processes)

Neurotransmitters in brain:
FAST: ligand-gated
Glutamate->excitatory opens ligand-gated Na+ channel local depolarising potential
GABA ->inhibitory opens ligand-gated Cl- channel local hyperpolarizing potential

SLOW: activate G-protein coupled receptors

• 5HT (serotonin):turkey, ecstasy, sleep, beer, alcohol, Prozac nerve terminal inhibitor of reuptake
• ACh : memory (?)/ ANS
• Dopamine : If destroyed 90% symptoms PARKINSONS: stratum activated by natural: eating, exercise, sex
• Noradrenaline/Norepinephrine

Lec 5: The nervous system: structure and function

Afferent (input) Sensory

Efferent (outpout) Somatic (consious movement:s.motor neuron: skeletal muscle)/

Autonomic (no control: visceral motor neiron: cardiac muscle)

to spinal cord (some directly to brain-12nerves)

spinal nerves-nerve enter gaps: cervical, thoracic, lumbar, sacral

cranial nerves: olfactory, optic, oculomotor (eyes), trochlear, trigeminal (face sesnsory), abducens, facial, auditory vestibular, glossopharyngeal, vagus (πνευμονογαστρικο), spinal, accessory, hypoglossal

INPUT:

• touch&visceral -->> mechanoreceptors (movement), proprioreceptors (posture&balance), nocireceptors (noxus stimulus/pain receptors), chemoreceptors ( ↑A/B)
• sight, sound, smell, taste

unipolar: spinal cord, multipolar: every neuron in brain

Reflex: sth happens u don't have any control of!
Reflex Arc:
Receptor>------Afferent fibre---- Spinal cord----Efferent fibre---->Receptor responses


Dorsal back, ventral front
Dorsal root ganglion=> Αβ axon: AP comes in through dorsal root: mechanoreceptor/msg go str8 to brain


muscle stretch: tendon quadriceps (front): pulls on muscle, muscle spindle: sense muscle all of sudden been stretched, activation of muscle from motor neurone (α) causes contraction.

sensory neurones:
Aα, Αβ, Αδ, C
I, II, III, IV
←-------------
increasing diameter/speed
proprioreceptors(posture-balance) of skeletal muscles, skin mechanoreceptors, pain/T, pain/T/itch

Ascending vs Desceding pathways (e.g. control of pain)
1 up spinal cord->2 into brain medulla-> 3 thalamus-> 4 somatosensory cortex

dorsal column-medial (lemnisal pathway) spinothalamic pathway

evetyrhing right side of body sensed by left side of brain+ vice versa

visual neuroanatomy left->right

≠ brain through spinal cord to peripheral
PAG->midbrain-> Raphe nuclei (medulla)-> Dorsal horn (spinal horn)

Nervous system full of other cells-> Glial cells:

• provide myelin in brain cells, astrocytes*
• support, insulation buffering, guide developing neurones, scavenging (αφαιρω καταλοιπα), immune response, brain barrier

CereboSpinal Fluid (CSF):

• aqueous NaCl+glucose--> fuel/E
• surrounds cell neurones&brain+gives them food
• produced by choroid plexus, ~120ml, clear colourless solutn
• buoyancy&cushioning/compensation of changes in brain V/ diagnosis: lumbar puncture (needle test take fluid from sp.cord), drug delivery (inject pain relief--> delivery), hydrocephalus

Bl. supply to CNS&Bl. Brain Barrier:

separates bl. from CNS

stoping viruses&bac enter brain

also drugs getting in

antianxiety have pass bl.-brain Barrier

microglia act as white bl.cells

L4: Synapses&neurotransmitters

Types of neurones: motor neurones, pyramidal neurone (hippocampus), purkinje neurone (cerebellum)

Synaptic Trasmission (chemical): e.g. neuromuscular junction (synapse between motor neurones&skeletal muscle)

neurotrasmitters are released resting neuromuscular junction
voltage gated Ca++ channel: open in response to changes in membr. depolarisation

ACheR=> ligand gated ion channels, non-specific cation channels

vesicles containing neurotransmitter (ACh)

activated neuromuscular junction:

1) AP generated <>

2) depolarisation

3) open Ca++ cause: Ca++ entry to presynaptic

4) cause ACh vesicles fuse with membr. to release ACh in synapse

5) let Na+ ion generates local potential /AP

6) when open -->> muscle-->>contraction

7)in skeletal muscle Ca++ release=>contraction

Neurotransmitters:

a.a.=>γ-aminobutyric acid (GABA), Glutamate, Glycine

amines=>ACh, Dopamine, Histidine, Noradrenaline, 5-HT (Hydroxytryptamine)

peptides=> Cholecystokinin, Dynorphin, Enkephalins, Neuropeptide Y, Somatostatic

gases=> NO, (CO)

Criteria for Identifying neurotransmitter:

1) Localisation

2) Synthetic/catabolic mechanisms: occurs in dif.ways

• Neurotr. synthesis:e.g. peptide neuron/DNA protein (all body), RER, Golgi apparatus, vesicle, transported in axon terminal, synaptic vesicles nerve terminal



• synthesis&degradation of ACh: catalyses synthesis ACh transporter=>

ChAT(cholic acetyl transferase)--> formation of Ach<Ch+Ac.CoA

AChE (acetyl choline esterase) breakdown ACh-->> acetic acid+choline (recycled for synthesis of ACh)

Ach=> package up inside vesicle to be trnsferred release<>

3)Release from terminal

release of neurotransmitter (e.g. ACh)by exocytosis: synaptic vesicle: protein-protein interactions binding to membr., once membrane depolarised, entry Ca++ allows vesicles to release content, neurotrasmitter molecules molecules : vesicle pinches back to presynaptic.

neurotransmitter receptors:

• ACh: ligand-gated ion channel=> ionotropic receptors: allow movements of ions: 1) signal proteins open, 2)allow ions in, 3) causes hyperpolarisation/depolarisation


• G-protein-coupled receptors => metabotropic: reflecting much slower on cellular metabolism, more time consuming process

Active G: activate ions->change in excitability-> cellular effects

Active G: activate E-> cause 2nd msg->Ca++ release/protein phosphorylation

4) Synaptic mimicry->stimulate nerve

5) Pharmacological identity of action: block effect of suspected neurotr. in the same way of directly stimulating nerves

Synapses in the CNS:

1) Variety-Types of synapses in the CNS:

2)Size &Shape of CNS synapses:

• presynaptic terminals contain vesicles arranged @ active zones => RELEASE
• postsynaptic membr.=> specialized&contains clusters of neurotransmitters receptor&signalling molecules

3) Excitatory/inhibitory synapses:

e.g. glutamate generates excitatory post synaptic potential (EPSP) Na+ entry causes local/ small depolarisation

/ e.g. γ-aminobutyric acid generates inbitory post synapric potential (IPSP) entry to cell more (-) inside cell, hypepolarisation

4)Synaptic integration:

temporal summation: adding 2gether local potentials that occur @ same synapse, but dif. times

spatial summation: adding 2gether local potentials that occur @ dif. sites on neurone=> more often cuase loc. potentials dont travel v. far

5)Electrical synapses: --> gap junctions: brain&heart

apart<>

formed<>

elec. synapses affect integration: generate elec. pot. although no enzyme released: If record Vm of cell 1 and cell 2 elect. PSP

lower curve than AP @ same time

6) network of neurones: convergence/ divergence

L3: Action Potential and conduction

Structure of ion channels:

• K channels: 4 subunits (transmembrane domain) proteins arranged in a barrel to form a pore htat spans the membr, are selective for K+ cuase of polypeptide sequence lines the pores of the ion

• Sodium Channels: single (only 1) subunit made up of 4 times repeating 6transmembr. segments, have pore-lining region-->> determines selectivity, lets Na+ pass through, contain voltage sensing domain rotate&moves up causing pore to open by conformational change!
  
  

Activation State of ion Channels
3 states of conformational change:

• resting state: closed- no ion flow
• activated state: open-ion flow (Na+ influx)
• inactivated state: closed-no ion flow :

*Refractory period: Na+channels become inactivated as the membr. depolarizes and cannot be activated again until the membr. is repolarized.

membr. hyperpolarized until K+ channels close, so more current required to depolarize membr. potential to more positive

• absolute refractory period: when during AP a 2nd stimulus no matter how strong will not produce a 2nd AP, inactivated closed channels
• relative refractory perod: can last 1-15ms, coincides with after hyperpolarisation, interval during which 2nd AP can be produced ONLY if stimulus strength = greater than treshold.

Action Potential/ Spike/Nerve impulse discharge:

rapid large alterations in membr. potential up to 100mV from -70 to +30mV, inside cell becomes more (+)!
Only EXCITABLE (nerve, muscle, endocrine, immune, reproductive) CELLS produce AP

≠ ALL CELLS can produce local potentials

Threshold: point where all Na+ channels open
Overshoot: always go above OmV~ENa+
All or nothing event: once pass threshold always generate this size of potentia, Always get same height, amplitude in graph every cell same Na channels=>same size eq.,
Refractory period:*
Propagate: act of ion potential
No decrement
undershoot: ~EKa+

Conduction velocity: propagation/A.P. conduction, A.P. travels down axon, no backwards cause absolute refractory period inactivated closed channels, SIGNAL<>> MUSCLES

Myelin: ↑diameter of axon, ↑myelin (stimulating substance, round axon, insulation to speed up flow of AP membr.)=> better, faster AP

Nodes of Ranvier (Saltatory=jumping conduction:

node/gaps in myelin, clusters of Na+ channels

Local Potentials: confined to a small region of cell membr., small response,

size: vary,

dicited. stimuli

dif.names depending on location/function

depolarization/hyperpolarization

graded-size/duration

decay rapidly,

travel small distances

show summation

e.g. endplate, synapric, pacemaker, receptor potential

polarized: outside/inside cell=> dif. net charge

depolarized: potential ↓ (-) than resting potential level (Na+ influx)

overshoot: reversal of membrane potential polarity, inside of cell becomes (+) relative to outside

repolarizing: when a membr. potential that has been depolarized returns toward the resting value (K+ Efflux)

hyperpolarized: when potential is more (-) than restin lvl

undershoot: E~K+ r.m.p.

Graded potentials (cause magnitude of potential change can vary): changes in membrane potential that are confined to a relatively small region of the plasma membr. produced < some specific change in cells environment acting on a specialized region of membr. they are given various names related to location of potential/function perform.

L2: MEMBRANE POTENTIAL

Equilibrium potential
Nerst eqn: E=60logCo/Ci (mV)
Eq.pot. for a particular ion, [ion] out/in, 60: constant taking into account: R, T, valance of ion, Faraday elec. constant
If [ ] changes =>E changes
E for K+ ~-80mV, Na+ ~ +60mV

Ion movements once s.s. has been achieved:although few open Na+, Na+ larger e-chemical force acting upon it, that is, it is far <>> ↑ membr. permeability -->> ion species-->> ↑ contribution of ion species to membr. potential

Resting membrane potential =-70mV*
Goldman eqn: Vm=60log (PK[K]o+PNa[Na]o+PCl[Cl]i)/PK[K]i+PNa[Na]i+PCl[Cl]o)2.303RT/F=60Pion-->> relative permeability of ion
K+=1, Na+=0.035, Cl-=0.001 (more permeable to K+ because for K + channels found on those membranes <>
*neither Na+, nor K+=> Epotential, but r.m.p. is closer to K+ Epotential, because membr. more permeable to K+
K+ moves out through open leak K+ channels
inside cells becomes (-)K+flux has more import on r.m.p. than Na+ flux,
but Na+ (small no) channels also open in resting state
Na+move in cell, cancelling effect on equivalent no of K+ions simultaneously moving out.
there is a NET movement <>
Over time, [ ] of intracellular Na+, K+ ions does not change because Na+K+ATPase pump maintains&helps to establish [Na+, K+] gradients @ stable lvls, as they move 3Na+ out & 2K+ in.
This unequal transfer contributes directly to membr. potential.

Note: In a resting cell, the no of ions that move in the opposite direction through membr. channels down their [ ] and/or elec. gradients. As long as the [ ] gradients remain stable and ion permeabilities of the plasma membr. do not change, elec. potential across the resting membr. will also remain constant.

Excitable cell
Neurones, muscle cells, grandular tissue, fertilised eggs, plant cells-->>RMP
Express correct ion channels: VOLTAGE GATED ION CHANNELS

Different types of ion channels (sensory system: mechanosensitive ion channes, phosphorylation sensitive ion channels, poring for H2O channels. 2 of the most characteristics:)

• Ligand-gated ion channels: (e.g. ACh Receptor) change from close to open, protein shape change to open
• Voltage-gated ion channels: passive down elec.gradient, rapid, important for signalling in nervous system, cation channels, relatively selective for: K+, Na+, Ca++(40/40-12/12dif.channels)/ anion channels: realtively selective for Cl-

proteins exist in open, inactivated, closed states depending on membrane depolarization.

change in charge induces change!

L1: CELL MEMBRANE&SOLUTE MOVEMENT

Body Fluid Compartments:
70kg person (x 60% or 2/3 body weight H2O) 42L H2O:

• 2/3 inside cells
• 1/3 outside cells : 20% plasma, 80%between cells

Stable composition: functional consequnces of the [ ] gradients on nerve cells:

• IN: HIGH: K+, LOW: Na+, Cl-, Ca++ (really low)
• OUT: LOW: K+, HIGH: Na+, Cl-, Ca++ (acts as a signalling molecule-->>important how muscles contract: CARDIAC)

Cell membrane function:

boundaries cellular components within cell, cells&environment, specialised for functions they perform, selective permeability

larger/charged molecules,need proteins--small/uncharged/polar molecules,no proteins, pass easily

Na+, K+, Cl-, glu/tryptophan, urea, glycerol, H2O/alcohols

LOW permeability HIGH permeability

Passive Transport

Diffusion: flow of particles (O2, CO2) <>> areas of ↓ [ ]

dependent on 1) [ ]gradients (may require E to establish them)

2) passive process/membrane impermeable to glu: proteins r required

Simple Diffusion: membrane, Osmosis (↑ H2O/ ↓osmolatiry-->> ↑osmolairty ↓H2O): porins,

Facilitated diffusion: transporters: carriers=integral membr. proteins where solutes bind changing shape protein&solute released on the other side of membrane down gradient

diffusion rate determined<>> ethanol ↑ permeability

NET FLUX

Active transport pumps (carriers) against gradient, requires ATP

direct use (HYDROLYSIS) of ATP-->>ADP+Pi: Primary active transport: from α subunit of Na+K+ATPase 3Na+ out, 2K+ in

Secondary active transport: nutrient absorption in gut oupled to Na+ transport

Physiology

This is just a blog to summarize my physio notes for exam in an interesting which I lately really enjoy! And just to start Physio is all about maintaining homeostasis in the body and more specifically:

• bl.P.
• body T.
• heart rate
• ph
• nutrients (glu)
• H2O
• Na+
• Ca++
• O2
• osmolarity
• hormones

are some of the external&internal factors-->>loss of homeostasis-->> compensatory mechanisms (+/- feedback)--->> RESTORE homeostaris / DISEASE!

e.g. ↑ heart rate -->> loss homeostasis-->> stop running

fright-->>↑heart rate-->>↑adrenalin-->> loss hoemostasis-->> stop fright-->> back to normal

except if disease: ↑bl.P.