Physiology 1A Flashcards
homeostasis
keeping the internal environment of the body constant
dynamic equilibrium
kept within narrow limits
positive feedback
divergence from the equilibrium in an explosive or blocking way
negative feedback
maintenance of equilibrium
set point
optimal environment
components of negative feedback mechanism
controlled variable
receptors/ sensors
set point processor
effector mechanism processor
controlled variables in the body
core body temperature
blood glucose
osmolarity of blood plasma
blood oxygen levels
blood pressure
effector mechanisms in the body
heart rate
insulin levels
urine concentration
respiratory rate
illnesses caused by disturbances to homeostasis
heat stroke
diabetes
how may homeostatic disease/ illness be treated
behavioural adaptation
what % of the body is water
60%
ratio of ECF to ICF
20:40
importance of differences in ECF and ICF
electrical activity in the nervous system
muscle contraction
formation of urine in the kidney
brownian motion
random thermal motion of particles
speed of particles is inversely related to their size
molecules continuously collied and change direction
fick’s law of diffusion
J = P([X]outside - [X]inside) = net flux
P - permeability coefficient
X - difference in concentration across membrane
transport: pores
simple diffusion
always open, non-selective
transport: examples of pores
porins
perforins
transport: channels
simple diffusion
non-gated or gated
specific to ions
transport: examples of channels
Na+
K+
transport: carriers
facilitated diffusion
specific binding of solute causes change of conformation
release of solute
transport: examples of carriers
uniport
symport
antiport
transport: pumps
active transport
use energy from hydrolysis of ATP
net transport against electrochemical gradient
transport: examples of pumps
Na+/K+ ATPase
transport: secondary active transport
specific binding of 2 solutes
change of conformation
release of solute
simple diffusion on a rate-conc graoh
linear
carrier mediated diffusion on a rate-conc graph
saturation kinetics
when is equilibrium potential
electrical gradient and concentration gradient are equal for one ionm
clinical importance of electrochemical gradients of K+
hypokalaemia - muscle weakness
hyperkalaemia - cardiac arrythmia
molarity
unit of concentration
osmole
unit of quantity
number of particles rather than molecules
osmolarity
measure of activity of the solvent
number of osmoles per unit volume
what does an increase in osmolarity result in
decrease in solvent activity
calculating osmolarity
osmolarity = g * molar concentration of osmolyte particles
g = osmotic coefficient
osmosis
movement of water from an area of higher solvent activity to an area of lower solvent activity across a semipermeable membrane
lower osmolarity to a higher osmolarity
osmotic pressure
pressure required to exactly stop osmosis
activity of a solvent can be increased by applying hydrostatic pressure
reflection coefficient
sigma
sigma = 1, impermeable
sigma = 0.1, semipermeable
sigma = 0, permeable
tonicity
effect of bathing a solution on a cell membrane
volume changes based on movement of water
determined by osmolarity of solution and permeability of membrane
chromatin
DNA packaged with proteins, arranged in chromosomes
nuclear envelope
double membrane continuous with endoplasmic reticulum
nucleolus
site of RNA synthesis and ribosome assembly
SER
lipid and steroid biosynthesis
peroxisomes
contain oxidative enzymes
microfilaments
tracks for motor proteins - mysoin
cell-cell adhesion
microvilli
microtubules
tracks for motor proteins - kinesins
components of cilia and flagella
spindles
intermediate filaments
provide structural integrity and strength
cell-cell adhesion
apoptosis
programmed cell death
necrosis
killed by bacteria
polyploid
> 2 sets of chromosomes
aneuploid
atypical chromosome numbers
telomere
protects chromosomes from shortening during cell division
regulatory region
capable of modulating the expression of a gene
promotor region
upstream region that binds to RNA polymerase
properties of neurones: excitable cells
charge which changes when they are activated to generate action potentials
action potentials
very fast change in membrane potential from negative inside to positive and back again
properties of neurones: directional
information spreads along the membrane as a wave of electrical charge
properties of neurones: neurotransmitters
small quantities of specialised chemicals which allow communication between the nerve cells
properties of neurones: integration
able to integrate information from multiple sources and generate an action potential
afferent neurone
towards brain
efferent neurone
away from brain
interneurones
receive and process signals within the brain
vagus nerve corresponds to which segments of the spinal chord
cervical
thoracic
lumbar
sacral
which part of the spinal chord to efferent nerves leave
ventral roots
where are ventral roots located
ventral horns
where do afferent nerves enter
dorsal horns
why is the spinal chord shorter than the spinal column
bones grow faster than nerves
what does the lumbar level of the spinal chord consist of
mainly roots
nervous system nuclei
associations of high density clusters of neurones in the braoin
ganglia
associations of high density neurones in the periphery
how can someone with a severed spinal chord experience stimuli
very strong stimulus via central horn
Na+/K+ pump
3Na+ bind on outside
2K+ bind on inside
uses 1 ATP
resting membrane potential
K+ diffuses down conc gradient through leaky K+ channels
inside becomes more negative, electrical gradient builds up
as K+ leave they become more attracted to inside due to developing electrochemical gradient
the nernst equation
Eion = 61.5/z * log([ion out]/[ion in])
z = valence/ charge
goldman-hodgkin-katz equation
Em=61.5*log(sum of P[ions out]/sum of P[ions in])
P = relative permeability
ionic basis of action potential
Na+ for depolarisation
K+ for repolarisation
activation of Na+ channels
voltage sensor and activation mechanism detects voltage
narrow selectivity filter opens, Na+ move into cell
inactivation of Na+ channels
positive membrane potential reached
inactivation gate closes
why does repolarisation speed up
K+ conductance
K+ channels do not have inactive/ active states just open or closed
factors responsible for rapid action potential termination
inactivation of Na+ channels
delayed activation of K+ channels
VGNa+ structutre
single protein with 4 subunits
VGK+ structure
4 individual protein subunits
oligodendrocyte
provide myelin
Ca2+ dependent exocytosis
IC Ca2+ kept low
Ca2+ enters via VGCa2+
vesicles of NT move to fuse with membranes
nicotinic acetylcholine receptor
ligand gated ion channel
2ACh bind
Na+ enter K+ leave
can become desnsitised after prolonged exposure
graded endplate potentials
multiple vesicles fuse after presynaptic action potential
miniature graded endplate potentials
unitary signal
quantal transmitter release
single vesicles fuse
why is the endplate potential kept short
rapid action potential
post synaptic excitation
graded depolarisation
membrane potential kept closer to threshold for firing action potential
termination of trans synaptic signal
AChE
gap junction
connexin from cell 1 to connexon in cell 2
ion flow carries electrical charge from cell to cell
pendritic spines
increase surface area for synaptic contacts
neurotransmitters and neuromodulators: amino acids
glutamate
GABA
glycine
neurotransmitters and neuromodulators: biogenic amines
dopamine, NA, adrenaline, serotonin, histamine
neurotransmitters and neuromodulators: neuropeptides
opioids, oxytocin, angiotensin 2
neurotransmitters and neuromodulators: purines
ATP
adenosine
neurotransmitters and neuromodulators: gases
NO
dale’s principle
the nature of the chemical function is characteristic for each particular neurone
ionotropic glutamate receptor
post-synaptic excitation
2-4 glutamate bind
Na+ or Ca2+ enter, K+ leaves
graded depolarisation
GABA A receptor
synaptic inhibition
2 GABA bind to receptor
chlorides move in
graded hyperpolarisation
purpose of synaptic delay
allows for integration of incoming signals
post synaptic integration
summation to decide whether to action potential or not
spatial summation
different synaptic inputs arrive at the post synaptic neurone
temporal summation
many arriving in rapid succession
autonomic nervous system
control of the function of internal organs, biochemical composition of the body and metabolism
sympathetic nervous system: piloerection
rising hair
contraction of pilomotor muscles
sympathetic nervous system: salivation
anticipation
sympathetic nervous system: pupils dilate
see more
circular muscles relax and radial muscles contract
sympathetic nervous system: trachea and bronchi
dilate
more air flow
sympathetic nervous system: heart rate
increases
sympathetic nervous system: force of contraction
increases
sympathetic nervous system: arterioles
distribute blood to critical organs
constriction around skin
relaxation around heart
sympathetic nervous system: veins
constrict
more blood returns to heart for faster circulation
parasympathetic nervous system: pupils constrict
reduce light on retina
parasympathetic nervous system: lens rounds
near vision
parasympathetic nervous system: secretion
salivary and GI tract
parasympathetic nervous system: trachea and bronchi
constrict
parasympathetic nervous system: heart
decrease in rate and force
properties of skeletal muscle
skeleton
striated
voluntary
movement
properties of cardiac muscle
heart
striated
involuntary
pump blood
properties of smooth muscle
hollow organs
non-striated
involuntary
control organ size
calculating lever action of muscle and bones
m * (A+B) = F*A
m = mass
F = force down
A & B = lengths
Vn = x * Vm
Vn = hand velocity
Vm = muscle contraction velocity
M line
middle line
H zone
M line and mysosin
A band
M line, myosin and overlap of myosin and actin
I band
actin only
Z line
ends
structure of myosin
head - light chain region
hinge - heavy chain region
tail - heavy chains
function of myosin head
acting binding site
ATP binding site
function of myosin neck
essential and regulatory light chain
myofilament structure
actin thin filament
troponin complex > Ca2+ binding site
myosin thick filaments form helix
tropomyosin forms helix around actin
sarcomere length during contraction
shortens
actin filaments slide along between myosin filaments
sliding filament mechanism
crossbridges generate force independent of each other
total force produced by one sarcomere determined by number of crossbridges formed
total force determined by amount of overlap between myosin and actinq
cross bridge cycle
crossbridge binds to actin
cross bridge power strokes
ATP binds to myosin detaching crossbridge
hydrolysis of ATP energises crossbridge
role of ATP in muscle contraction: allosteric regulator
ATP binds to one site causing change in conformation to another site
allows myosin to detach from actin
role of ATP in muscle contraction: energy source
ATP hydrolysis provides energy for cross bridge movement
TnC
binds Ca2+
TnI
inhibits crossbridge formation
TnT
binds tropomyosin
activating muscle contraction
TnC binds Ca2+ - 4 binding sites but only 2 lower affinity site used
troponin complex changes conformation]
tropomyosin moves away from myosin binding sites
what triggers muscle contraction
action potential
function of the sarcoplasmic reticulum
store high concentrations of Ca2+ in calsequestrin
rapidly release Ca2+ into myoplasm in response to action potential
rapidly remove Ca2+ from myoplasm
function of transverse tubules
conducts action potential from sarcolemma deep into muscle fibre
conveys action potential to sarcoplasmic reticulum causing release of Ca2+
what is the voltage sensor on T tubules
dihydropyridine receptor
Ca2+ release channel on T tubules
ryanodine receptor
components in contraction against time graph order of peaks
action potential
myoplasmic Ca2+
Ca2+ troponin complex
twitch force
relationship of tension to myoplasmic Ca2+
Ca2+ always higher over time
isometric contraction
constant length regardless of tension
isotonic contraction
muscle changes length while maintaining constant tension
eccentric contraction
load exceeds muscle tension pulling muscle to longer length
accessory proteins
maintain architecture of myofibrils
accessory proteins: titin
largest protein in the body
determines optimal position of thick filament relative to thin filament
accessory proteins: nebulin
molecular ruler
bind to actin determining length of actin thin filaments
structure of heart muscle
microfibrils and intercalated
desmosomes hold cells together
gap junctions between cells
plateau for duration of twitch (no tetanus)
contractile apparatus of smooth muscle
contractile fibres contain actin and myosin
supporting fibres contain intermediate filaments
dense plasma menbrane sites
cytoplasmic dense bodies
organisation of smooth muscle: unitary
muscle fibres act together as a functional unit
gap junctions co ordinate contractions
organisation of smooth muscle: multiunit
muscle fibres act independently
electrical isolation allows finer motor control
regulation of contraction: cardiac and skeletal muscle
cytosolic ca2+ increases
ca2+binds troponin
tropomyosin moves out of blocking position
myosin cross bridges bind to actin
contraction
regulation of contraction: smooth muscle
cytosolic ca2+ increase
ca2+ binds to calmodulin
ca2+-calmodulin complex binds to MLCK
MLCK used ATP to phosphorylate myosin cross bridges
phosphorylated cross bridges bind to actin
contraction
cardiac conduction
SAN
AVN
bundle of His
right and left bundle branches
ventricular action potentials: phase 0
activation of voltage gated na+ channels
inward current moving cell towards Ena
ventricular action potentials: phase 1
early repolarisation due to inactivation of na+ channels
ventricular action potentials: phase 2
plateau phase due to inward current through Ca2+ channels
slow in/activation
ventricular action potentials: phase 3
repolarisation phase due to inactivation of ca2+ channels and increase in permeability to K+
ventricular action potentials: phase 4
resting membrane potential determined by permeability of K+
importance of plateau phases in ventricular action potentials: phase 1
ca2+ influx through VG channels
Ca2+ released from sarcoplasmic reticulum
contraction
inward current delays repolarisation maintaining plateau
importance of plateau phases in ventricular action potentials: phase 2
refractory period
cell is electrically inexcitable during depolarisation to only generate one twitch
absolute refractory period
Na+ recover from inactivation of membrane repolarises
why does the SAN show unstable resting membrane potential
slow inward movement of Ca2+ currents
sympathetic activity of pacemaker potential
accelerates heart
noradrenaline binds to beta 1 adrenoreceptors
increased slope of pacemaker potential
parasympathetic activity pacemaker potential
slows heart rate
ACh binds to muscarinic receptors
decrease in slope and slight hyperpolarisation
conduction velocity: atrial myocytes
1ms-1
conduction velocity: AVN
0.05ms-1
conduction velocity: pukinje fibre
3-5ms-1
conduction velocity: ventricular myocyte
0.5-1ms-1
electrocardiograms: P wave
atrial depolarisation
electrocardiograms: QRS complex
ventricular depolarisation
electrocardiograms: T wave
ventricular repolarisation
deflection of ECG waves: depolarisation towards electrode
+
deflection of ECG waves: repolarisation towards electrode
-
deflection of ECG waves: depolarisation away from electrode
-
deflection of ECG waves: repolarisation away from electrode
+
PR wave
atrial depolarisation
AV conduction through His
branches to purkinje
QT wave
ventricular depolarisation and repolarisation
darcy’s law
Q = deltaP/R
Q = flow
poiseuille’s law
8viscositylength/pi*radius^4
combine darcy’s and poiseuille’s law
Q = delaPpir^4/8viscositylength
vascular tone
degree of vasoconstriction/dilation of vessel
bayliss/ myogenic response
contraction of a blood vessel that occurs when intravascular pressure is elevated
compliance
degree to which a blood vessel can be stretched
deltaV/deltaP
capacitance
ability of veins to increase volume at low pressures
depends on tone of smooth muscle
controlled by sympathetic nervous system
total peripheral resistance
sum of all resistors in series
calculating MABP
MABP = DBP + PP/3
calculating cardiac output from MABP
CO = MABP/TPR
function of pulmonary circulation
perfuse alveoli for gas
intrinsic control of cardiac output
myogenic response
paracrine
physical factors
extrinsic control of cardiac output
vasodilator nerves
sympathetic vasoconstrictor nerves
endocrine factors
active/ metabolic hyperaemia
increased blood flow
release of vasodilatory metabolites affecting arterioles
hypoxia does the same
post-exercise hyperaemia
oscillation on v-t graph
contracted muscles have higher resistance to blood flow
pulmonary hypoxic vasoconstriction
hypoxia causes vasoconstriction of pulmonary blood vessels
must match alveolar perfusion to alveolar ventilation to optimise Q
sympathetic vasoconstriction
NA binds to a1 adreno
increased cytosolic ca2+
MLCK activated, contraction occurs
action potentials not necessary for electrical mechanical coupling
vascular smooth muscle does not generally produce action potentials
b adrenoreceptor mediated vasodilation
adrenaline binds to b adrenergic receptor
fall ca2+
MLCK deactivated
relaxes
baroreceptor function
sensitive to stretch
changes in pressure result in stretch/ relaxation of vessel wall
information sent to medulla oblongata via vagal anf glosso-pharyngeal nerve
baroreceptor afferent fibres
increase in pressure stretched carotid sinus wall
increase in firing of afferent fibres
reduction in pressure produces relaxation of carotid sinus wall
decrease in firing of afferent fibres
afferent fibres as a dynamic reponse
frequency of firing is highest as pressure changes
sensitivity and setting of the baroreceptor reflex
slope of relationship gives sensitivity of reflex
reflex strives to reach set point pressure
altered by interaction with CNS
veno-atrial receptors
on venous side blood pressure ,onitored by mechanoreceptors of atria and veins and pulmonary arteries
arterial chemoreceptors
carotid and aortic bodies
control breathing
respond to hypoxia and hypercapnia and acidosis
produce increase in sympathetic activity
continuous capillary
no large gaps
fenestrated capillary
fenestrations
discontinuous capillary
large gaps
metabolite and gas exchange in capillaries
occurs across capillary wall by diffusion
as blood travels down the capillary metabolite conc falls with exponential relation
starling’s principle
balance between forces causing movement of water into and out from capillary lumen
starling’s forces
forces tending to cause bulk movement of water across capillary wall
net filtration and lymphatic drainage
starling’s forces vary along length of the capillary
tend to net filtration at arteriolar end
tend to net absorption at venous end
excess fluid drainage by lymphatics
lymphoedema
surgery in groin to remove testicular cancer
severed lymphatic drainage
elephantiasis
parasitic nematode blocks lymphatic drainage
local oedema
venous/ lymphatic obstruction
inflammation
generalised oedema
heart failure
arterial-pressure time graph
sharp peak for painful stimulus and sex
general drop during sleep
orthostasis
response to change in posture
response to metabolite concentration
build up of metabolites causing vasodilation
darcy’s law applies
baroreceptor reflex in exercise
slope of relationship gives sensitivity
reflex strives to set point
set point altered by interaction of CNS during exercise
cardiovascular responses to exercise
metabolic vasodilation
coronary vasodilation
SV increase
renal vasoconstriction
skin blood flow
dynamic exercise
alternating contraction and relaxation
SBP increases, DBP decreases
vasodilation
static exercise
sustained contraction
SBP and DBP increase
compression of muscles impairs blood flow
the central command hypothesis
anticipation of excercise
cerebral cortex influences autonomic and respiratory neurones
HR increases before effort commences
acral skin and thermal regulation
fingers, toes, palms, soles
heat loss via radiation, conduction, convection and evaporation
dilation of arteriovenous anastomoses increase skin blood flow
