125 Flashcards
superior
above
inferior
below
anterior or ventral
front
posterior or dorsal
back
close to (midline) anatomical term
medial
away from/next to (midline) anatomical term
lateral
sagittal
side of head (side profile
transverse
top of head
coronal
back of head
components of CNS
brain and spinal cord
components of PNS
cranial and peripheral nerves
(peripheral nervous system)
sensory function of nervous system
detect external and internal changes
integrative function of the nervous system
analyses and makes decisions based on voluntary and involuntary responses
motor functions of the nervous system
initiates motor movement and glandular secretions
cerebrum simple anatomy
largest part of the brain. It contains the cerebral cortex and subcortical regions
cerebellum
located in the posterior region of the brain, it is mainly responsible for balance and coordination
brainstem
contains the midbrain, pons and medulla oblongata. It communicates with the PNS to control involuntary processes such as breathing and heart rate.
what separates the 2 hemispheres of the cerebrum
connected by a large fibres bundle called the corpus callosum
whats the outer layer of the cerebrum composed of
cerebral cortex
4 lobes of the cerebral cortex
frontal
parietal
temporal
occipital
cortical lobes- frontal lobe
higher cognitive functions
decision making
problem-solving
some features of language and voluntary movement
parietal lobe
integrates info from visual pathways
coordinates motor movement and interpretation of sensory info
temporal lobe
interpreting speech and hearing, object recognition and emotion
occipital lobe
processing primary visual info
where are the subcortical regions located
brain regions that lie underneath the cortex
examples of subcortical structures
hypothalamus
amygdala
hippocampus
thalamus
basal ganglia
what are the subcortical regions responsible for
memory
emotions
motor movement
processing sensory info
what serves as a connection between the brainstem and subcortical regions
midbrain
what does the midbrain consist of
colliculi- eye movements towards interest objects
tegmentum-coordination of movement, alertness/sleep
cerebral peduncle- control of ocular muscles
what are the 5 main sections of the spinal cord
cervical- neck
thoracic- chest
lumbar- lower back
sacral-hip
coccygeal- tail
what does enteric system regulate
water and solutes between gut and tissue
PNS- autonomic system
what does somatic system control
voluntary
skeletal muscle
sensory info from the body and from the outside world
is it parasympathetic or sympathetic system that controls fight or flight
sympathetic- fight-flight
parasympathetic- rest-digest
what pathway carry sensory info from the periphery up to the brain
afferent pathway via ascending nerve tracts
where does brain send signals down to peripheral nerves
down efferent descending nerve tracts to control motor output
leg jerk response- reflex arc
hit- sensory afferents- dorsal column of spinal cord- interneurons in spinal cord- muscles of legs via efferents nerve that originate in ventral horn- efferent fibres communicate with muscles causing them to contract- jerk
NO INPUT FROM BRAIN
4 cells of the CNS
neuron
astrocytes
microglia
oligodendrocytes
2 main cell groups in CNS
neurons-nerve cells
glia- support cells
4 subdivisions of glial cells
microglia
astrocytes
oligodendrocytes
ependymal cells
in neurons how is input from other cells received
via finger like dendrites
relay info to the cell body
3 types of neuron
bipolar
unipolar
multipolar
bipolar neuron
1 main dendrite and axon
e.g. retina, inner ear, olfactory area of brain
unipolar neurons
1 process from the cell body, part way down the axon
alwasy sensory enurons - pain, temp, touch
multipolar neurons
many dendrites
1 axon
most neurons in CNS
microglia
immune cells that survey CNS and respond to sites of infection or damge
exist in wide range of morphologies depending on activation state
surveillant state
activated state
surveillant microglia
smaller
multiple processes
activated microglia
larger
rounded cell body
shorter processes
what shape are astrocytes
small star shaped
what do astrocytes do
provide support for the development and homeostatic maintenance of the nervous system and cerebral blood vessels
form a glial scar after sever injury
heterogeneity across different brain regions
oligodendrocytes
Schwann cells in PNS
lipid-rich sheath of myelin that wraps around neurons to increase speed of transmission
white matter
contain myelin
grey brain matter
unmyelinated cell bodies
neurovascular unit
blood vssels in brain made up of astrocytes, pericytes, smooth muscle cells, neurons
blood-brain barrier
endothelial cells form tight junction proteins
brain creates physical barrier between blood and the brain
cerebrospinal fluid (CSF)
contained within ventricles in subarachnoid spaces
provides buoyancy for brain and cushions it
produced from filtered blood by choroid plexus in ventricles
what forces move ions across membranes
chemical- conc differences
electrical- interior cell - so + cations are retained and negative ions expelled
2 broad categories of ion channels that facilitate ion movement
- gated channels and require stimulus
- channels always open and allow free movement
at resting conditions is Na+ higher inside or outside neuron
10x higher outside
but k+ is 15x higher inside neuron
potassium movement in neuron
constant k+ flow from inside to outside neuron through leaky (open) channels
how is ion gradient maintained in neuron
na+/K+ ATPase pump
moves 3 Na+ out the cell
2K+ moved into cell at same time
at rest in neuron is there more of a positive charge inside or outside of cell
outside
as a result of the Na+/K+ ATPase pump
this is known as polarisation
resting membrane potential
most neurons its -70mV
the difference in voltage across the PM when neuron at rest
electrochemical gradient of sodium
when Na+ channels open ions move into cell- chemical
electrical forces pulls ions into cell
both chemical and electrical act in same direction so Na+ moved into cell
reaching equilbirum in Na+ neuron movement
na moves into cell and the cell charge becomes more positive
so electrical and chemical gradients decrease
eventually it’ll all be in balance so no net flow through any open channel
equilibrium potential defintion
the membrane potential required to exactly counteract the chemical forces acting to move 1 particular ion across the membrane
electrochemical gradient of potassium
when k channels open the chemical gradient move ions out the cell
but electrical forces pull them into cell
2 forces acting in different direction
but chemical force> electrical so k moves out neuron
equilibrium of potassium movement of neuron
k moves out
cell becomes more negative so electrical gradient becomes stronger
until chemical forces thats moving k out= electrical trying to move it in
so no net flow
how is the equilibrium potential calcualted
Nernst equation
61/z log Co/ Ci
z= charge of ion
Co= conc of ion out cell
Ci= conc of ion in cell
If the membrane potential is depolarised beyond a certain critical level (threshold potential = -55mV) then an action potential is triggered in the neuron
t/f
true
when do voltage-gated ion channels open
when the voltage in the cell reaches a certain value
found in PM of neuron and are sensitive of the cell
Voltage-gated Na+ channels have both an activation gate and an inactivation gate. At rest, the activation gate is closed and the inactivation gate is open
t/f
true
Voltage-gated K+ channels have two activation gate, which opens to allow the flow of K+ ions through the channel and closes to stop the flow of K+ ions
t/f
only 1 activation gate
what happens when a neuron is initially stimulated
ligand-gated ion Na+ channels open
small amounts of Na+ move down conc grad into the neuron and resting potential becomes more psoitive
depolarisation step of action potential
membrane reaches critical threshold (-55mV)
voltage-gated activation gates in Na+ channel open quickly
Na+ moves into the neuron
neuron loses negative charge undergoing depolarisation
when inside of neuron becomes highly positive what happens to voltage-gated Na+ channel
it is plugged by inactivation gate and flow of Na+ into neuron is stopped
repolarisation
voltage-gated K+ channels open slowly
K+ flows down conc out of cell
causes neuron to regain negative charge
hyperpolarisation
response to reapid increase in negative charge
voltage-gated k channels close but as this is a slow process some k still moves into cell making it more negative than it needs to be
refractory period
during hyperpolarisation period
neuron cant fire another ap
Na+/K+ ATPase pump will restore hyperpolarisation state to -70mV
where are action potentials initiated
at base of neuron in the region called axon hillock
what are the small gaps in the myelin called
nodes of ranvier
and allow ion movement across axon membrane
saltatory conduction
nodes of ranveir
allow ap to jump from node to node very quickly
is information coded by the frequency of AP or the size of the potential
the frequency
the number of spikes over a given time rather than size
how do neurons communicate with one another
via synapses
electrical synapses use gap junctiosn that connect the cytoplasm between 2 cells
chemical synapses involves release of neurotransmitter
chemcial are more common
what happens when ap reaches end of neuron
influx of ca+
fusion of vesicles with pre-synaptic membrane
release neurotransmitter itno synaptic cleft
whats the amount of neurotransmitter in 1 vesivle called
quantum
what happens when neurotransmitter enters synaptic cleft
diffuse across
binds to receptors on postsynaptic neuron
for excitatory neurotransmitter causes Na+ influx
triggers ap
what are excitatory neurotransmitters
if they raise membrane potential towards the critical threshold
what are inhibitory neurotransmitters
if they lower the membrane potetnial away from the critical threshold
summation
where neuron ‘sums u[’ all the excitatory and inhibitory signals it receives over a period of time
criteria for transmitter substance
- synthesised in neuron
- present at presynaptic terminals in vesicles
- exogenous susbtance at reasonable concentration mimics exactly the action of endogenously released neurotransmitter
- mechanism for removing transmitter from celft
ionotropic receptors
transmitter binding= direct opening of ion channel
ligand-gated ion channels
always stimulatort
fast
metabotropic receptors
transmitter binding= indirect activation of G-protein
GPCR
trigger opening or closing of separate ion channel down from signalling cascade
slow effect
ionotropic receptors structure
4 or 5 subunits around central pore
receptors can be made up of different combinations of subunits increasing diversity
examples- GABAa, ACh, glycine, 5-HT3 receptors
structure of metabotropic receptors
single protein with 7 membrane-spanning regions
7 transmembrane receptors
examples- muscarinic acetylcholine, rhodopsin, all 5-HT receptors except 5-HT3
inotropic receptors how it works when binding to neurotransmitter
at rest= channel pore closed
binding of neurotransmitter causes channel to open
ions flow down conc grad
channels will be permeable to anions (na,k)or cations(cl-)
metabotropic receptors when binding to neurotransmitter
when it binds activates g-protein
g-protein acts on ion channel causing ion pore to open
g-protein activates second messenger
second messenger can bind to and open an ion channel or initiate a signalling cascade
agonists
drugs that mimic the actions of neurotransmitter
binding to receptor= activation
antagonists
a drug that block the action of neurotransmitter
binding to receptor= no activation
first neurotransmitter to be discouvered
acetylcholine
in 1912
synthesis of acetycholine
Acetyl coA + acetylcholine
synthesised by choline acetyl transferase
2 types of acetylcholine
nicotinic - neuromuscular, brain, autonomic nerves
muscarinic- smooth muscle, exocrine glands, brain
whats alzheimers
onset of dementia
problems with memory
loss of brain weight
enlargement of ventricles
numerous senile plaques and neurofibrillary tangles in the brain
cholinergic death in alzheimers disease
acetylcholine is important for memory and attention
cholinergic neurons die in early AD
what drugs are approved for treatment of AD
AChE inhibitors
- donepezil-1997
- rivastigmine- 2000
- galantamine- 2001
wahts catecholamines synthesised from
tyrosine
which is transported into brain from blood
what enzymes does catabolism of catecholamines
monoamine oxidase (MAO) and catechol 0-methyltransferase (COMT)
2 major families of dopamine receptors
D1-like= D1 and D5- coupled stimulatory g-proteins
D2-like= D2, D3, D4- coupled to inhibitory g-proteins
what do D1-like dopamine receptors stimulate
adenylate cyclase
what do D2-liek dopamine receptors inhibit
inhibit adenylate cyclase
parkinsons disease
onset age- 60+
affects 1-2% over 65
muscle stiffness
slow movements
tremor at rest
pathology of parkinsons disease
degeneration of dopaminergic neurons
in substantia nigra pars compacta
loss of dopamine in the caudate-putamen
>50% dopamine depletion
treatment of Parkinsons disease
motor symptoms- L-dopa (converts to dopamine in brain)
COMPT and MAO-B given to inhibit dopamine degradation
peripherally active Dopa decarboxylase inhibitor given to prevent premature conversion of L-dopa to dopamine
what is serotonin synthesised from
tryptophan by tryptophan hydroxylase and 5-hydroxytryptophan decarboxylase
what is serotonin broken down into
5-hydroxyindoleacetic acid by MAO and aldehyde dehydrogenase
serotonin signalling
5-HT can bind to 14 diff receptors- all are g-coupled except for 5-HT3
some excitatory and others are inhibitory
action terminated mainly by reuptake from the synapse via the 5-HT transporter on the presynaptic neuron
SSRI treatment
can treat depression, anxiety, OCD, PTSD, etc
example- citalopram(cipramil)
fluoxetine (prozac, oxactin)
amino acid transmitters
glutamate and aspartate= excitatory
glycine and GABA= inhibitory
what type of receptor is GABA A
ionotropic receptors coupled to cl-
what type of receptor is GABA B
metabotropic receptor
coupled to ca and k ions cannels via g-protein and second messenger systems
what modulatory binding sites does GABA A have
for benzodiazepines
barbiturates
neurosteroids
ethanol
3 types of glutamate receptors
NMDA
non-NMDA
mGlut
NMDA receptor
bidn glutamate , glycine, mg, zn and polyamines
form channels that are permeable to cations
non-NMDA receptors(kainate and AMPA)
interact only with glutamate and their specific agonists - Na+ and K+> Ca+
mGlut receptors
g-protein receptors that trigger a second messenger cascade
8 types
drug to treat alzheimers
memantine
it blocks mg2+ binding site on the glutamate NMDA receptors
whats the most common type of neurotransmitter in the hypothalamus
peptide neurotransmitter
peptide neurotransmitter synthesis
large precursor proteins
transported to synaptic release site- activated by proteolytic cleavage
do peptide neurotransmitters include opioids
yes
endorphins
enkephalins
dynorphins
do peptide neurotransmitters have slow or fast postsynaptic effects
slow
how long is gi tract
approx 4.5metres when living
9metres when dead
4 process (basic) of digestion system
digestion
absorption
motility
secretion
4 layers of gi tract inorder centre to outside
mucosa- epithelium
submucosa- connective tissue
muscularis-circualar and longitudinal layer
sreosa- connective tissue
nerve plexus
from centre to outside layer of gi tract
enteric nervous system
what does the mucosa consist of
-mucous membrane- epithelial cells or enterocytes include absorptive, exocrine/endocrine, goblet cells
-lamina propria
-muscularis mucosae
exocrine definition
secretion of enzymes into a duct directed at target
endocrine definition
secretion of hormones into the bloodstream
how much saliva secreted per day
0.75-1.5
what is saliva stimulated by
autonomic nervous system
what does saliva contain
a-amylase and lingual lipase
functions of saliva
lubrication
buffering noxious substances
antibiotic action
taste
cleans teeth
fluoride, calcium uptake into teeth
breaks down food
How long is oesophagus
approx 25cm
what connects pharynx to stomach
oesophagus
what type of muscle is upper 1/3 of oesophagus
skeletal muscle
what type of muscle is lower 2-3 of oesophagus
smooth muscle
how much can stomach expand
from 50ml to 1-2 litres
what do gastric glands contain
parietal cells and cheif cells
what do parietal cells secrete
HCL
what do chief cells secrete
pepsinogen
how much HCL is secreted by stomach
2 litres per day
in the stomach what is required for absorption of vitamin B12 in the ileum
intrinsic factor= glycoprotein
what does rennin coagulate
milk
what triggers the release of pepsinogen and HCl
gastrin and vagus nerve
is vagus nerve parasympathetic or sympathetic
parasympathetic
involved in rest and digest
HCL secretion mechanism in stomach
h+ made from co2 and water by carbonic anhydrase
actively transported to lumen in exchange for k+
bicarb ions exchanged for cl- which diffuse into lumen
- HCL
activation of pepsinogen in stomach
not activated till it encounters HCL
first 44 removed to make pepsin
pepsin then activate more pepsinogen
is pepsin an endopeptidase
yes it breaks internal peptide bonds of proteins to create smaller fragments
what does an exopeptidase do
remove 1 amino acid at a time from either end of a polypeptide
activation of chymotrypsinogen
chymotrypsinogen - trypsin–>
chymotrypsin –chymotrypsin–> a-chymotrypsin (3 chains linked by interchain disulphide bonds )
how long is small intestine
2.5-3 metres
parts of si
first 30cm = duodenum
then jejenum and ileum
does Duodenum receives chyme from stomach, enzymes from pancreas, and bile from liver & gallbladder
yes
what part of si is responsible for digestion
duodenum
what part of si is responsible for absorption of nutrients, water, vitamin, minerals
all parts
where are crypts of lieberkuhn foudn and waht do they secrete
found in SI
secrete bicarb rich fluid to neutralise chyme from stomach
parts of the colon
cecum
rectum
anal canal
appendix- attached to cecum
crypts of lieberkuhn but no villi
area of large intestinal mucosa of an adult in colon
2m^2
wheres the principle location of commensal microflora
colon
how is the pancreas
20cm long
100g
what are digestive enzymes made by in pancreas
acinar cells (exocrine cells)
and released into duodenum via secretory duct
what are chymotrypsin, trypsin, carboxypeptidase, elastase made as
zymogens
what do islets of langerhans make
hormones which are secreted into the blood
in pancreas
b-cells make insulin
a-cells- make glucagon
s-cells- somatostatin - regulate digestion, absorption and release of other hormones
how many amino acids are removed from proinsulin to get insulin
4
proinsulin has 86AA
type 1 diabetes
autoimmune disease
loss of insulin secretion from islets of Langerhans
treated with insulin administration
type 2 diabetes
associated with obesity, sedentary lifestyle
loss of responsiveness to insulin
reduced insulin secretion
what are long chain fatty acids and monoglycerides converted into in the si
synthesised into triglycerides
packed into chylomicrons
which enter lacteals and into the lymphatic system
how are monoglycerides and AAs absorbed
blood capillaries of villi then to liver
how are fats absorbed
emulsified into fat droplets by bile salts
then susceptible to digestion by pancreatic lipase
what does microbiota include
bacteria
archaea
protists
fungi
viruses
predominant phyla of microbiota
bacteriodetes
firmicutes
actinobacteria
proteobacteria
does diet influence presence and abundance of microbiota
yes
where does fibre predominantly digest
colon
metabolites in microbiota
vit k
butyrate
thiamine
folate
biotin
riboflavin
panthothenic acid
is fasting induced adipocyte factor activation modulated by microbiota
yes
has a role in obesity and metabolic syndrome development
where does the thoracic duct drain into
left subclavian vein
what lymphatic vessel drain from the intestine
mesenteric lymph vessels
what is transported to liver via mesenteric and hepatic portal vein
monosaccharides
AAs
electrolytes
water
are bile salts recirculated
yes
where is the heart located
in the mediastinum with the lungs
level of the 2nd rib
roughly central
base pointing towards the right and the apex towards th left
pericarditis
problems with the pericardium
impact the movement and function of the heart
3 main layers of pericardium
fibrous pericardium
serous pericardium
epicardium
why does the heart sit in a bag - pericardium
lubrication- serous
mechanical protection
protects it allow it to move smoothly
3 muscular layers of the heart wall
epicardium- outer
myocardium
endocardium
why do heart valves open and close
in response to pressure change as the heart relaxes and contracts
where does atrioventricular valves prevent backflow
prevent backflow from atria to ventricles
where do semilunar valves prevent back flow
aorta/pulmonary artery into the ventricles
tricuspid
release of contraction close valves
what stops valves acting like a swingdoor in both directions
chordae tendinae
problems with heart valves
incompetent valves- valves dont fully close so regurgitant flow
valvular stenosis- stiffened valves caused by repeated infection- congenital disease or calcium deposits- opening is narrows
3 layers of blood vessels
-tunica externa
- tunica media
- tunica intima - inner layer
tunica media
helps move blood along arteries
vasoconstriction and vasodilation
and lumen size affects blood flow and blood pressure
continuous capillaries
most common
gaps only between endothelial cells- tight junction
CNS, lungs, muscle tissue, skin
fenestrated capillaries
pore 70-100nm in the capillary wall
choroid plexus, kidneys, endocrine glands, villi, ciliary processes of the eye
sinusoid capillaries
wider gaps in the vessel walls - lets blood cells through
bone marrow, endocrine glands placenta
are veins or arteries under less pressure
veins are under less pressure
do veins or arteries have less smooth muscles
veins has less smooth muscles
are veins stretchy
yes
do large veins have valves
yes to prevent blood flowing backwards
do capillaries drain into venules
yes
do veins lose or gain bp on the way to vena cava
lose bp, almost 0 by the time it gets to the vena cava
where is the blood located when upright and supine
in supine
less blood in peripheral veins
more blood in central volume
when blood leaves heart what 3 systems is it split into
- pulmonary circulation (RHS)
- systemic circulation (LHS)
- coronary circulation (from aorta)
RHS pulmonary circulation shape and location
crescent-shaped
positioned towards back of heart
blood in through venae cavae and back out through pulmonary artery
LHS- systemic circulation
at front and apex in heart
more circular
in through pulmonary veins and out through aorta to aortic arch
how many blood groups are there
43 blood groups
4 main blood groups
A
AB
B
O
Blood plasma will have Antibodies to the surface molecules that your RBCs do not have.
t/f
true
what happens blood transfusion are done with incompatible blood
antibodies bind to the RBCs expressing different antigen
causes clumping of RBCs and antibodies
causes severe volume
universal blood group donor
type O
make antibodies A and B
cannot receive any other bloo types
universal blood group receiver
AB
do not make any A or B antibodies
wont agglutinate donor blood
their blood can only be given to AB recipients
3 blood type allesl
IA, IB, IO
mother - baby blood incompatibility
RBCs are broken down causing jaundice, anaemia and death if severe
as mothers antibodies linger after birth and destroy baby RBCs causing icnrease in bilirubin
cardiac cycle in 1 heart beat
t/f
true
systole is contraction
t/f
true
generally means ventricular contraction
diastole is relaxation
t/f
true
ventricular relaxation and filling
at a heart rate of 75bpm how long does each cardiac cycle last
0/8 seconds
diastole for 0.4 secs
atrial systole- 0.1
ventricular systole- 0.3
how many heart sounds aer there
4
but only 2 loud enough to be heard (auscultation)
the first heart sound (LUBB)
turbulence caused by closure of the AV valves (when ventricles contract)
whats the second heart sound (DUPP)
turbulence caused by semilunar valves cloing (when ventricles stop contracting
3rd and 4th heat sound
from ventricular filling and atrial systole
4th sound audible when ventricles are stiff
atrial systole
atria contract
squeeze blood into ventricles
AV valves open, pulmonic and aortic closed
slight increase in atrial pressures
isovolumetric contraction
all valves closed
beginning of systole
increase in intraventricular pressure
heart shape change but no blood ejection
pushes AV valves closed- first sound
rapid ejection step in cardiac cycle
AV valve closed other open
when intraventricular p> aortic and pulmonary p, valves open and blood ejected
atria continue to fill
no heart sound in healthy patient
reduced ejection step of cardiac cycle
aortic and pulmonary valve stay open
AV closed still
no blood movement
ventricular muscle relaxation
ventricular p decrease slightly but no blood leaves heart
atria p increasing as its filling
isometric relaxation step of heart cycle
valves close (heart sound 2)
ventricle vol remains the same as valves are closed (dicrotic wave)
atrial pressure and volume increase from venous return
end systolic ejection
volume remaining in the ventricles after ejection
rapid filling step of heart cycle
AV valves open
aortic and pulmonary valves close
ventricular filling- relaxation phase
amount of filling decrease with increasing hr
third sound
reduced filling step of heart cycle
difficult to distinguish these phases
when filling is nearly finished
ventricles at full stretch so P rises
p in large vessels drops as blood flows into circulation
7 steps of cardiac cycle
- atrial systole
- isovolumetric contraction
3.rapid ejection
4.reduced ejection - isovolumetric relaxation
6.rapid filling - reduced filling
SV equation
stroke volume = end diastolic vol (EDV) - end systolic vol (ESV)
edv= amount of blood collecting in ventricle
esv= amount remaining after contraction
how to calculate cardiac output
co= stroke volume x heart rate
/ 1000 to get in L
is cardiac output affected by the control of heart rate
yes
what regulates cardiac output
-neural control- physical or emotional stress
-ion levels
how does neural control affect cardiac output/hr
sympathetic nervous system stimulates heart rate (SA node) up to 100-200%
parasympathetic nervous system steadies HR
how do ion levels regulate cardiac output/hr
calcium- too little= too weak, too much= long contractions
potassium- involved in muscle contraction and nerve conduction
can increase CO to point
CO is not proportional to HR increase
frank starling law
bigger SV ejected if there is a larger degree of filling at the end of diastole
^ sympathetic input= ^ HR
^ parasympathetic= dec HR
preload
how stretchy is the heart at max fill
afterload
pressure against which the heart need to pump to expel blood
the higher the arterial pressure the lower the stroke volume
contractility
the ability of the muscle to produce a force
the more forcefully the muscle contract the more blood expelled
the skeletal muscle pump
lack of muscle in veins limits the force of venous return
contraction of skeletal muscle in the tissue surrounding the veins compresses them
blood pressure equation
bp= cardiac output x total peripheral resistance
peripheral resistance
the degree of friction encountered by blood
what causes friction
- constriction/narrowing
^bv
viscosity
pulse pressure equation
PP= systolic BP - diastolic BP
massively increases as arteries become less stretchym
mean arterial pressure (MAP)
more useful to work out the pressure at which blood is actually delivered to the tissues
MAP= DP + (PP/3)
where are baroreceptors found
arterial carotids and aortic arch
baroreceptors
detect pressure changes
small changes increase firing frequency
each receptor is sensitive to different pressure
control bp
where are chemoreceptors found
peripheral chemoreceptors= carotid bodies in carotid artery. none in veins
central chemoreceptors- medulla
what do chemoreceptors do
detect changes in PO2, PCO2, pH
vasoconstriction
contraction of smooth muscle in vessel walls
activation of sympathetic nervous system
narrows diameter of blood vesse;
increase blood flow resistance
increase blood pressure
vasodilation
relaxation of smooth muscle in vessel walls
widening of diameter
caused by withdrawal of sympathetic nerve activity
decreases resistance of blood vessels
decreases blood pressure
reasons to increase blood pressure
stress
exercise
orthostatic hypotension- getting up too quick
haemorrhage
how to decrease blood pressure
low salt diet
decrease stress
therapeutically with ACE inhibitors- interact with RAAS
myogenic
cells contract spontaneously
cardiac pacemakers
SAN cells slowly depolarise spontaneously (funny channels)- causes resting membrane potential to decrease - once threshold reached an AP in stimulated
AVN node spontaneously depolarize slowly but usually triggered by SAN
neural control of hr
1.sensory info from sensors is processed in medulla
2. triggers ANS response
sympathetic NS increases HR and contractability
what increase sympathetic stimulation
-muscarinic receptor antagonist
- b adrenergic receptor agonist
- circulating catecholamines
- hyperkalaemia
- hyperthermia
- hyperthyroidism
things that decrease SA node firing (increase parasympathetic stim)
-muscarinic receptor agonist
- b blocker
ischaemia/hypoxia
-hypokalaemia
- sodium and calcium channels
hypothermia
regulators of HR
hormones
age
fitness
sex
body temp
tachycardia
increased hr
stress
drugs
heart disease
if persists leads to death
bradycardia
under 60bpm
low temp
drugs
endurance training
if not athlete poor circulation
indictive of head trauma
fibrillation
rapis
regular
and unco-ordinated contraction
what does an ECG measure
an electrical trace of the action potentials in all the heart muscle fibres
what does p wave on ECG show
depolarisation of atrial muscle
what does QRS show on ECG
depolarisation of ventricular muscle
t wave show on ECG
contraction of ventricular muscle
whats the highest peak on ECG
R
whats the lowest peak on ECG
S
at rest whats the average human breaths per min
12 to 15
how many lobes are in each lung
right has 3 lobes
left lung has 2 lobes
how much area to alveoli make for gas exchange
70m2
conducting zone of respiratory system
transfer of air into lungs
nasal cavity
pharynx
layrnx
bronchi
bronchiole
terminal bronchioles
respiratory zone in respiratory system
gas exchange between blood and air
respiratory bronchioles
alveolar ducts
alveolar sacs
alveoli
atmospheric pressure
760mmHg
alveolar pressure
760mmHg
intrapleural pressure
756mmHg
always pressure is always negative
help the lungs to expand and stay inflated
inhalation steps
diaphragm contracts
external intercostal muscles contract
chest cavity and lung vol expand
alveolar pressure drops to 758mmHg
so atmospheric pressure is higher
air drawn in down con grad
exhalation steps
diaphragm and external intercostal muscles contract
lungs spring back and chest cavity contracts
contraction increases alveolar pressure to 762mmHg
air flow out lungs own conc grad
boyles law
volume of gas varies inversely with pressure
e.g. squash it and pressure increases
lung compliance
how stretchy the lungs are
surface tension in lungs
surfactant reduces surface tension
without it alveoli would collapse
airway resistance
airflow = (p alveoli - p atmosphere)/ resistance
resistance increases on exhalation as bronchioles diameter decreases
neural control of breathing
respiratory centres in medulla oblongata and midbrain control breathing
pontine respiratory group in mid brain
dorsal and ventral respiratory group in medulla
dorsal respiratory group
active phase- diaphragm and intercostal muscles contract= normal quiet inhalation
inactive phase- diaphragm and intercostal muscles relax= normal quiet ahalation
dorsal respiratory group
diaphragm contract- forceful breathing
ventral respiratory group
accessory inhalation muscles contract leading to forceful breathing
ventral respiratory grou[ accessory exhalation
internal intercostal muscles
scalene pectoralis minor
external oblique
transverse abdomis
rectus abdominis
motor cortex influence on breathing
info from motro cortex related to level of effort involved in exercise
CNS on influences of breathing control
ventilation increased or decreased for gasping sobbing etc
voluntary control of breathing
useful for communication
speaking
limited in extent
anatomical dead space in lungs
not all air reaches the alveoli but ventilates the trachea , bronchi and bronchioles filling the conducting zone
theres no perfusion of these areas so gas exchange cannot occur
tidal volume
amount taken in and exhaled on a normal breathin
inspiratory reserve volume
amoutn taken in after deap breath
expiratory reserve volume
amount exhaled in a forced exhalation
residual volume
air not exchanged but stays in lungs to keep inflated
inspiratory capacity
tidal vol+ inspiratory reserve vol
vital capacity
Inspiratory Reserve Volume+ Tidal Volume+ Expiratory Reserve Volume
total lung capacity
lung capacity + residual volume
external respiration
o2 diffuses from alveoli into pulmonary capillaries
carbon dioxide moves in the opposite direction
occurs across respiratory membrane - alveolar and blood vessel walls
internal respiration
o2 diffuses from the systemic capillaries into the tissues and co2 in the opposite direction
how long is blood in contact with the alveoli
0.75 seconds
partial pressure definition
the pressure of an individual gas
can be measured by multiplying the % of that gas by the total pressure
partial pressure of o2
o2= 760 x 21%= 159mmHg
o2 makes up 21% of atmosphere
what do alveolar contain
elastic fibres for movement and stretch
macrophages (dust cells) for filtration
alveoli are lined by type 1 and type 2 alveolar epithelial cells
t/f
true
what do type 2 alveolar epithelial cells release
lipid-rich surfactant
lowers surface tension
an increase in SA on lung inflation would ordinarily increase surface tension and cause lung collapse- surfactants prevents this
respiratory distress syndrome
surfactant produced from 26weeks . so premature babies are vulnerable to collapsed lungs
cortisol treatment from mother can help stimulate surfactant production
infants treated with o2 to resolve
respiratory membrane structure
type 1 alveolar cells
alveolar basement membrane
interstitial space- elastic fibres
capillary basement membrane
capillary endothelium
factors affecting gas exchange
surface area
diffusion distance
diffusion gradient- ficks law
diffusion distance in healthy lungs
0.4 to 2nm
can be 0.6um
If alveolar PO2 is low or the diffusion resistance is high, capillary PO2 may not reach equilibrium with alveolar PO2
t/f
true
i.e not enough difference between 2 to allow diffusion
ficks law
means that diffusion of gas is slow if the diffusion thickness increases
R= D x A x triangle p/t
r= rate of diffusion
d= diffusion constant for gas
a- surface area
p= difference in pp
t= thickness of respiratory membrane
diffusion in terms of ficks law
diffusion is proportional to sa and conc difference
its inversely proportional to diffusion distance
diffusion rate will decrease if area of diffusion decreases and/or the diffusion distance increases
ventilation definition
amount of air reaching the alveoli/min
perfusion definition
amount of blood reaching the alveoli/min
what does V/P ration determine
determines blood O2 and CO2 concentration
mismatch leads to respiratory failure
why does apex of lung have higher V/Q ratio
theres more ventialtion here
why does base of lungs have lower V/Q
gravity means more blood at base so higher perfusion
when is V/Q 0
if there is perfusion but no ventilation
average V/Q ratio for entire lung
0.8
>0/8 at apex
what is perfusion affected by
cardiac output
pulmonary vascular resistance
decreased V/Q
- decreased ventilation in lung
- no effect on blood flow
-low arterial PO2 - associated with increased PCO2
- chronic bronchitis, asthma, acute oedema
increased V/Q
- increases PO2 and dead -space in lungs (high ventilation)
-decrease in arterial o2 sat - in emphysema where lots of ventilation but small area for blood exchange
internal envirnonemnt
the environment required for life and metabolism
includes
temp
pH
gas levels
it is in the blood plasma and interstitial fluid
why does the internal environment have to be kept stable
to maintain the correct conditions for cellular functions
e.g. prevent cellular and protein damage- damage to proteins is usually irreversible effecting enzymes, cellsurface receptors and transporters resulting in cell death
different forms of haemoglobin
fetal
adult A
adult A2
do males or females have more more haemoglobin
males
linked to menstruation and iron levels
how many mls of o2 can 1g Hb carry
1.34mls o2
alveoli PO2 and affinity
104mmHg
almost 100% saturated
high affinity
in systemic veins whats teh pp and affinity
49mmHg
Hb around 77% saturated
low affinity for oxygen
when PCO2 is high what happens to Hb affinity for 02
o2 affinity falls
curve shifts right
if blood pH is low which way does curve shift
right
how is co2 carried out of blood
8% dissolved in blood
20% binds to amines in Hb to form carbaminohaemoglobin
72% (the rest) reacts with water in the cytoplasm of the RBC
how is pH of arterial blood maintained
buffers
H+ loss in urine by kidney
breathing out co2
pH of arterial blood
7.35-7.45
why does the blood have a narrow range of pH
it can change structures like DNA
damage enzymes
changes the amount of o2 carried by bllod
bicarboante buffer system defnition
reversible chemical reaction that can absorb or release hydrogen ions in response to changes in system
H + HCO3- –> H2CO3
when pH decreases it combines with bicarb to form carbonic acid to raise pH levels
Increased metabolism means less carbonic acid
t/f
false
it means more carbonic acid
More carbonic acid means more breakdown into Hydrogen and Bicarbonate (decrease in pH)
t/f
true
chemical control of breathing
increased h+, chemoreceptors
respiratory control centre (medulla)
respiratory muscles
change in frequency and depth of breathing
what stops overinflation of lungs
Hering-Bruer inflation reflex
during extreme exercise
but normal for infant breathing
hering-bruer infaltion reflex
when activted lung stretch
slow adapting stretch receptors fire
high receptors activity inhibits further inflation and expiration begins
what receptos in muscles sense movemnt
proprioceptors
where are irritant receptors located
airways and lungs
stimulate coughing and sneezing
