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FORGOTTEN
PAPER 2
TOPIC 6
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Jasmine Singh
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Cards (23)
RECEPTORS IN THE EYE?
ROD
CELLS
120 million
per eye,
periphery
of
retina
black
and
white
images (cannot
distinguish
different
wavelengths
of light)
poor visual acuity
(
clarity
)
sensitive to
low intensity light
only
one
type (
rhodopsin
)
demonstrate
retinal
convergence
,
multiple rod cells
link to
one bipolar cell
so
more
likely to
exceed threshold
and create a
generator potential
CONE
CELLS
6 million
per eye,
fovea
colour
images (
three
types of
pigment
each receptive to different
wavelengths
of light)
good visual acuity
not sensitive to
low intensity light
(
iodopsin
)
no convergence
,
one cone cell
links to
one bipolar cell
(
separate impulses
make easier to
differentiate different wavelengths
)
so
less
likely to
exceed threshold
and create a
generator potential
so only responds to
high intensity light
STRUCTURE OF PACINIAN CORPUSCLE?
capsule
blood capillary
layers
of
connective tissue
with
viscous gel
between
neurone
ending
neurone
HEART RATE CONTROL?
Wave
of
electrical excitation spreads
out from
SAN
across
both atria
Atria contract
Atrioventricular septum
prevents
wave
crossing to
ventricles
Wave
of
excitation
enters
AVN
Short delay
AVN
conveys
wave
of
electrical excitation
between
ventricles
along
bundle
of
His
Bundle
of
His
conducts
wave
through
atrioventricular septum
to
base
of
ventricles
Bundle branches
into
smaller fibres
of
Purkyne tissue
Wave released
from
tissue
Ventricles contract quickly
at
same time
from
bottom
CHANGING HEART RATE?
detect change
send impulses
to
medulla
more impulses
to
SAN
by
sympathetic
/
parasympathetic nervous system
WHERE ARE DIFFERENT RECEPTORS FOUND?
CHEMORECEPTORS:
carotid artery walls
BARORECEPTORS:
carotid artery
/
aorta walls
OSMORECEPTORS: hypothalamus (
posterior pituitary gland
)
REFRACTORY PERIOD?
inward movement
of
Na+
prevented
as
voltage-gated Na+ channels
are
closed
action potentials
propagated
in
one direction
only
discrete impulses
limits
number
of
action potentials
(detect
stimulus strength
)
MUSCLE FIBRES?
SLOW TWITCH
contract more
slowly
less
powerful
longer
period
adapted to
endurance
and
aerobic respiration
large myoglobin store
rich supply
of
blood vessels
numerous
mitochondria
FAST TWITCH
contract more
rapidly
more
powerful
shorter
period
adapted to
intense exercise
and
anaerobic respiration
thicker
more numerous myosin filaments
high concentration
of
glycogen
high concentration
of
enzymes
required for
anaerobic respiration
store
of
phosphocreatine
NEUROMUSCULAR JUNCTION VS SYNAPSE?
NMJ
excitatory
, cholinergic excitatory or inhibitory
NMJ links neurones to
muscles
, cholinergic links neurones to
neurones
/
neurones
to
effector organs
NMJ only involves
motor neurones
, cholinergic involves
motor
/
sensory
/
relay
neurones
at NMJ
action potential ends
, at cholinergic a
new action potential
may be
produced
at NMJ acetylcholine binds to
receptors
on
sarcolemma
, at cholinergic acetylcholine binds to
receptors
on
post-synaptic membrane
EVIDENCE OF SLIDING FILAMENT MECHANISM?
changes occur to
sarcomere
:
I band
becomes
narrower
Z lines
move
closer together
(
sarcomere
shortens
)
H zone
becomes
narrower
A band
stays same width
FEEDBACK?
NEGATIVE
change produced by
control system
causing change in
stimulus detected
by
receptors
turns system off
POSITIVE
deviation
from
optimum
causing change leading to
greater deviation
from
normal
INSULIN?
Binds
to
complementary insulin receptor
Activates
tyrosine kinase
Stimulates
GLUT4
protein vesicles
to
fuse
with
cell-surface membrane
Inserted
Glucose
in
blood
enters
by
facilitated diffusion
down concentration gradient
Converted to
glycogen
via
glycogenesis
Stored
as
lipids
Used
in
increased respiration
Required
to
maintain concentration gradient
Blood glucose concentration lowers
and returns to
normal
(
negative feedback
)
GLUCAGON?
Binds
to
complementary glucagon receptor
Activates adenyl cyclase
ATP
converted to
cAMP
Stimulates phosphorylation
of
enzymes
to
activate
them, e.g.
protein kinase A
Cascade
of
enzyme reactions
Glycogen
converted to
glucose
via
glycogenolysis
Glycerol
and
AAs
converted to
glucose
via
gluconeogenesis
Glucose moves out cell
down concentration gradient
via
facilitated diffusion
Blood glucose concentration increases
and returns to
normal
(
negative
feedback
)
ADRENALINE?
Binds
to
complementary
adrenaline receptor
Activates
adenyl cyclase
ATP
converted to
cAMP
Stimulates
phosphorylation
of
enzymes
to
activate
them, e.g.
protein kinase A
Cascade
of
enzyme
reactions
Glycogen
converted to
glucose
via
glycogenolysis
Glucose
moves out cell
down concentration gradient
via
facilitated diffusion
Blood glucose concentration increases
and returns to
normal
(
negative feedback
)
REGULATING BLOOD GLUCOSE?
PANCREAS
:
Islets
of
Langerhans
(
hormone-producing cells
)
alpha
=
glucagon
beta
=
insulin
LIVER
:
hepatocytes
glycogenesis
glycogenolysis
gluconeogenesis
DIABETES?
TYPE 1
unable to
produce
insulin
immune system attacks
beta cells
insulin injections
TYPE 2
glycoprotein
receptors
on
body cells
lose responsiveness
to
insulin
or
inadequate supply
of
insulin
from
pancreas
regulating carbohydrate intake
in
diet
,
match
to
exercise
supplementary insulin injections
NEPHRON?
afferent arteriole
into
,
efferent arteriole out
(
narrower
)
cortex
:
outer
region,
convoluted tubules
and
blood vessels
(
top
)
medulla
:
inner
region,
loop
of
Henle
,
collecting ducts
,
blood vessels
(
bottom
)
ULTRAFILTRATION?
PROCESS
Blood
enters Bowman's Capsule
Build up
of
hydrostatic pressure
in
glomerulus
Water
,
mineral ions
and
glucose
squeezed out
glomerular capillary
=
glomerular filtrate
RBCs
and
large proteins
too large
to pass across into
renal capsule
RESTRICTED BY
connective tissue and endothelial cells of blood capillary
epithelial cells of
renal capsule
hydrostatic pressure
of
fluid
in
renal capsule space
low water potential
of
blood
in
glomerulus
REDUCED BY
podocytes
(
inner
layer of
renal capsule
,
highly specialised cells
with
gaps
between them)
capillary endothelium
(
gaps
)
REABSORPTION OF GLUCOSE?
Na+
actively transported
out of
epithelial cells
lining
PCT
Concentration gradient
Na+ diffuse down
concentration gradient
from
PCT lumen
into
epithelial lining cells
(
facilitated diffusion
,
co-transporter proteins
)
Co-transporters
carry
glucose
/
AAs
too into
cells
of
PCT
Diffuse
into
blood
by
facilitated diffusion
LOOP OF HENLE?
DESCENDING LIMB
thin
walls
permeable to
water
, not ions
ASCENDING LIMB
thick
walls
impermeable to
water
,
only ions
DETAILS
countercurrent multiplier
opposite directions
STAGES
Na+
and
Cl-
actively transported
out ascending limb
into
interstitial fluid
=
concentration gradient
in
medulla
Water
cannot move out of
ascending limb
(
impermeable
to water)
Water
moves out of
descending limb
via
osmosis
Filtrate concentration increases
At
base
of
loop
,
filtrate
it very
concentrated
so
Na+
diffuse out
at
ascending limb
Filtrate
at
top
of
ascending limb
is
dilute
again
Water
can be
reabsorbed
in
DCT
Filtrate drains
into
collecting duct
, which flows back through
concentrated medulla
ROLE OF LOOP OF HENLE?
create
low water potential
in
medulla
so
more water
can be
reabsorbed
from
fluid
in
collecting duct
HOW DO MUSCLES ACT?
in
antagonistic pairs
against an
incompressible
skeleton
REGIONS OF SARCOMERE?
M LINE
:
middle
Z LINES
:
end
of
actin
A BAND
: both
actin
and
myosin
H ZONE
: just
myosin
I BAND
: just
actin
HOMEOSTASIS?
involves
physiological control systems
that
maintain
the
internal environment
within
restricted limits