physiology
Created @December 6, 2022 1:01 PM
Reviewed
Homeostasis
Explain the underlying principles of physiological homeostasis, including the
importance of negative feedback
homeostasis = dynamic maintenance of physiological variable (PVs) eg.
HR within range of set point (basal, temporarily adjusted for circumstance)
PV out of range = death/illness
PVs hierarchy eg. bp increases to keep plasma osmolality stable as more
important short term
neg feed - sensors detect change to PV from set point > afferent to
integrating centre (IC) > integrating centre compares signal to set point
and elicits response > efferent to effector > response bringing back to set
point
Describe the role of the autonomic nervous system in physiological control
for temp, bp, blood gas, breathing, osmolality
neuronal ICs in midbrain/stem eg. hypothalamus, pons, medulla
autonomic SNS and PSNS are antagonistic allowing fine tuning
Describe the role of endocrine systems in physiological control
more/less hormone circulates in blood, bind to receptors on target organ =
response
hormone classes
peptides = ADH and oxytocin (posterior pit)
polypeptides = insulin (pancreas) growth hormone (anterior pit)
glycopeptides = FSH, LH, TSH (anterior pit)
physiology 1
, steroids = cholesterol (liver), testosterone (testes), estradiol (ovaries),
cortisol and aldosterone (adrenal cortex)
tyrosine derivatives = thyroxine T4 (thyroid) adrenaline (adrenal medulla)
receptors
plasma membrane - peptides, catecholamines (adrenaline), glycoproteins
= 2nd messengers change enzyme activity = rapid
intracellular - steroids, thyroids = alter gene transcription = slow
Describe the role of paracrine homeostatic signalling in physiological control
local neg feed - sensors, ICs, effectors all same tissue
substance secreted and diffuses to neighbouring cell eg.
endothelium/smooth muscle of skeletal muscle arterioles
parallel or independent to neuronal/endocrine
Describe feed-forward and positive feedback control mechanisms
feed forward = anticipation brings about response before it is detected by
neg feed eg. saliva before meal
positive feedback = change causes further change, amplification not
normalisation eg. pregnancy contractions
muscle cell
Describe the basic structure of cardiac, skeletal and smooth muscle.
skeletal = voluntary, motor unit innervation, striated, unbranched, 20-
100um diam <12cm long, multinuc
cardiac = spontaneous (conduction - no motor nerve) involuntary, striated,
branched syncytium, brick 10-20um diam 100um long, intercalated discs
smooth = involuntary, unstriated, line vessels/organs, spindle 5um diam
200um long
striated = A (thick myosin), t tubules along z
myofibril extends length of fibre (85%) surrounded by SR, sarcomere
between z, 6 a around each m, sarcolemma membrane
physiology 2
, Describe how the membrane potential changes in different muscle types and
its role in triggering contraction.
skeletal - motor neurone > NMJ = short AP 500us/refractory 2ms but
longer relative refractory = tetany/summation (more APs so more Ca)
cardiac - sinoatrial node excitation (spontaneous) triggers long
AP/refractory (200-400ms) = allow diastole, prevents tetany/vfib
smooth
eg. ileum - time dependent (v/ligand gated) channels > long AP >5s,
less neg resting potential, stronger
eg. aorta, vascular smooth- time independent (v/ligand) channels > no
AP, graded depolarisation (proportional to stimulus), constrictor
depolarises/dilator hyper
Recognise the central role of Ca in muscle contraction.
actin-myosin mechanism = Ca binds troponin c > pulls tropomyosin out of
actin groove allowing myosin with ADP and P attached to bind (cross
bridge) > head swings (power stroke) and ADP and P released > new ATP
attaches causing myosin to detach > ATP hydrolysed to ADP and P
returning mysoin to cocked position ready to rebind
changing contraction strength
size of Ca transient - more = more bridges = more tension larger
contraction
sensitivity of filament to ca - temp, pH, drugs, Pi
skeletal - motor unit all or nothing (stimulation = full fibre contraction),
more units = more tension
physiology 3
, cardiac - graded, more Ca/sensitive = more tension, ionotropes (affect
SV/contractility), chronotropes (affect HR)
Describe the process by which changes in membrane potential elevate Ca and
trigger contraction in cardiac, skeletal and smooth muscle – the process of
excitation-contraction coupling.
excitation contraction coupling = electrical excitation > calcium >
mechanical contraction
cardiac
calcium induced calcium release
contract: AP along sarcolemma and down t > v gated l type Ca channel in t
tubule opens > extracellular Ca influx = intracellular Ca inc transient > Ca
diffuses across dyadic cleft > binds to and opens RyR receptor > Ca influx
from sarcoplasmic reticulum (SR) > contraction induced
relax: SERCA and phospholipase B actively transports CA back into SR
store, Na/Ca exchanges original Ca out
skeletal
voltage induced calcium release
contract: similar to cardiac but AP triggers RyR to release Ca without initial
extracellular Ca entry (across triadic cleft)
concentric = power stroke pulls actin towards centre causing shortening,
eccentric stronger
relax: same except all Ca back to SR
smooth:
contract: v/ligand 2nd mess/stretch channels allow Ca influx from
extracellular or intracellular SR store > Ca binds calmodulin > activates
MLCK > phosphorylates myosin light chain = contraction
relax: K channel opens > hyperpolarised > ca channels inactivated
action potentials occur when membrane depolarises to threshold and v
gated channels open
physiology 4
Created @December 6, 2022 1:01 PM
Reviewed
Homeostasis
Explain the underlying principles of physiological homeostasis, including the
importance of negative feedback
homeostasis = dynamic maintenance of physiological variable (PVs) eg.
HR within range of set point (basal, temporarily adjusted for circumstance)
PV out of range = death/illness
PVs hierarchy eg. bp increases to keep plasma osmolality stable as more
important short term
neg feed - sensors detect change to PV from set point > afferent to
integrating centre (IC) > integrating centre compares signal to set point
and elicits response > efferent to effector > response bringing back to set
point
Describe the role of the autonomic nervous system in physiological control
for temp, bp, blood gas, breathing, osmolality
neuronal ICs in midbrain/stem eg. hypothalamus, pons, medulla
autonomic SNS and PSNS are antagonistic allowing fine tuning
Describe the role of endocrine systems in physiological control
more/less hormone circulates in blood, bind to receptors on target organ =
response
hormone classes
peptides = ADH and oxytocin (posterior pit)
polypeptides = insulin (pancreas) growth hormone (anterior pit)
glycopeptides = FSH, LH, TSH (anterior pit)
physiology 1
, steroids = cholesterol (liver), testosterone (testes), estradiol (ovaries),
cortisol and aldosterone (adrenal cortex)
tyrosine derivatives = thyroxine T4 (thyroid) adrenaline (adrenal medulla)
receptors
plasma membrane - peptides, catecholamines (adrenaline), glycoproteins
= 2nd messengers change enzyme activity = rapid
intracellular - steroids, thyroids = alter gene transcription = slow
Describe the role of paracrine homeostatic signalling in physiological control
local neg feed - sensors, ICs, effectors all same tissue
substance secreted and diffuses to neighbouring cell eg.
endothelium/smooth muscle of skeletal muscle arterioles
parallel or independent to neuronal/endocrine
Describe feed-forward and positive feedback control mechanisms
feed forward = anticipation brings about response before it is detected by
neg feed eg. saliva before meal
positive feedback = change causes further change, amplification not
normalisation eg. pregnancy contractions
muscle cell
Describe the basic structure of cardiac, skeletal and smooth muscle.
skeletal = voluntary, motor unit innervation, striated, unbranched, 20-
100um diam <12cm long, multinuc
cardiac = spontaneous (conduction - no motor nerve) involuntary, striated,
branched syncytium, brick 10-20um diam 100um long, intercalated discs
smooth = involuntary, unstriated, line vessels/organs, spindle 5um diam
200um long
striated = A (thick myosin), t tubules along z
myofibril extends length of fibre (85%) surrounded by SR, sarcomere
between z, 6 a around each m, sarcolemma membrane
physiology 2
, Describe how the membrane potential changes in different muscle types and
its role in triggering contraction.
skeletal - motor neurone > NMJ = short AP 500us/refractory 2ms but
longer relative refractory = tetany/summation (more APs so more Ca)
cardiac - sinoatrial node excitation (spontaneous) triggers long
AP/refractory (200-400ms) = allow diastole, prevents tetany/vfib
smooth
eg. ileum - time dependent (v/ligand gated) channels > long AP >5s,
less neg resting potential, stronger
eg. aorta, vascular smooth- time independent (v/ligand) channels > no
AP, graded depolarisation (proportional to stimulus), constrictor
depolarises/dilator hyper
Recognise the central role of Ca in muscle contraction.
actin-myosin mechanism = Ca binds troponin c > pulls tropomyosin out of
actin groove allowing myosin with ADP and P attached to bind (cross
bridge) > head swings (power stroke) and ADP and P released > new ATP
attaches causing myosin to detach > ATP hydrolysed to ADP and P
returning mysoin to cocked position ready to rebind
changing contraction strength
size of Ca transient - more = more bridges = more tension larger
contraction
sensitivity of filament to ca - temp, pH, drugs, Pi
skeletal - motor unit all or nothing (stimulation = full fibre contraction),
more units = more tension
physiology 3
, cardiac - graded, more Ca/sensitive = more tension, ionotropes (affect
SV/contractility), chronotropes (affect HR)
Describe the process by which changes in membrane potential elevate Ca and
trigger contraction in cardiac, skeletal and smooth muscle – the process of
excitation-contraction coupling.
excitation contraction coupling = electrical excitation > calcium >
mechanical contraction
cardiac
calcium induced calcium release
contract: AP along sarcolemma and down t > v gated l type Ca channel in t
tubule opens > extracellular Ca influx = intracellular Ca inc transient > Ca
diffuses across dyadic cleft > binds to and opens RyR receptor > Ca influx
from sarcoplasmic reticulum (SR) > contraction induced
relax: SERCA and phospholipase B actively transports CA back into SR
store, Na/Ca exchanges original Ca out
skeletal
voltage induced calcium release
contract: similar to cardiac but AP triggers RyR to release Ca without initial
extracellular Ca entry (across triadic cleft)
concentric = power stroke pulls actin towards centre causing shortening,
eccentric stronger
relax: same except all Ca back to SR
smooth:
contract: v/ligand 2nd mess/stretch channels allow Ca influx from
extracellular or intracellular SR store > Ca binds calmodulin > activates
MLCK > phosphorylates myosin light chain = contraction
relax: K channel opens > hyperpolarised > ca channels inactivated
action potentials occur when membrane depolarises to threshold and v
gated channels open
physiology 4
