1
Q
Cell theory
A
- animals and plant made of eukaryotic
- cells can change into other cells later on
- cell represents the smallest unit which performs physiological processes
- every cell has its own homeostasis
2
Q
how is physiological processes performed and homeostasis maintained
A
- body uses biomolecules such as proteins, lipids and sugars to produce energy to perform..
3
Q
cell metabolism
A
- chemical process converts carbs, fats, proteins into energy for cellular functions.
4
Q
what is energy needed for from cell metabolism
A
- muscle contraction
- membrane transport
- synthesis of enzymes, hormomes.
5
Q
ATP
A
- unit of currency transfers enegry in living cells.
- ATP hydrolysed to form ADP
6
Q
plasma membrane -physical barrier outside n inside of cell
A
- barrier prevents general ingress, preserves cells status
- controls movement of desirable material into a cell
- excretes waste material out of the cell
- communicates with whats outside of the cell, has various receptors that bind with sepcific chemical messengers changing activity of cell
- makes physical connections
7
Q
Transporters
A
- carrier proteins specialized membrane - soanning proteins that assist in movement of ions, peptides, small molcules, lipids and macromolecul;es acrosss biological membrane.
- passive transport, no energy as transprort follows concentration gradient.
8
Q
diffusion
A
random movement of membrane permeable substance across membrane down the conc gradient from an area of high concentration to an area of low concentration.
9
Q
facilliated transport
A
the movement of a membrane impermeable substance across the membrane via transporters down the concentration gradient
10
Q
Active transport
A
requires ATP to transport substaces into a cell
11
Q
primary active transport
A
- transport protein containd an ATPase which hydrolyses ATP to generate energy for transport. e.g ion pump
12
Q
Secondary active transport
A
no direct coupling of ATP with transporter, useses electrochemical potential between cell and fluid. pups ions out of the cell by primary active transport
- creates electro chemical potential and ATP is still consumed by mode of transport
13
Q
Concentration gradient affects diffusion across a membrane
A
if molecule can pass through a membrane there is a natural flow from areas of high con to an area of low conc
14
Q
surface area
A
SA of membrane increases the rate of diffusion increases, more space for molecules to diffuse across the membrane.
15
Q
molecular size
A
smaller the molecule the easier it can move through a membrane by passive diffusion
16
Q
state of ionisation
A
most drugs are weak acid bases which exist in ionised and unioinised form depending on the pH
- it is the lipid - soluble, non - ioinised from of the drug that readily diffuses across the membrane.
17
Q
cytoskeleton
A
- cells structural suppourt
- influences shape, strength and flexibility of the cell and movement of the cell
- made up of proteins such as actin and tubulin
- cells such as flagella and cilia have extracellular structures built around core of cytoskeletal proteins
18
Q
ribosomes
A
- 25nm
- small and large ribosomal sub - unit which comes together for protein synthesis where mRNA is translated to protein.
- manufacturers proteins destined for the cytosol.
19
Q
endoplasmic reticulum
A
- network of membranes with responsibilities for the synthesis and storage of proteins, carbohydrate and lipids,
- transportation of molecules within its enclosure and the detoxification of dangerous materia.
20
Q
rough endoplasmic reticulum
A
- Receives newly manufactured protein chains from ribosomes, and secondary / tertiary structures are achieved
- Modification of proteins into glycoproteins
-Packaging of proteins / glycoproteins into transport vesicles, to be sent to Golgi apparatus
21
Q
Smooth endoplasmic reticulum
A
-Synthesis of phospholipids and cholesterol for endoplasmic reticulum, nuclear membrane, Golgi apparatus
-Synthesis of steroid hormones,
- Synthesis & storage of (tri)glycerides and glycogen
- Detoxification of drugs and alcohol
22
Q
lysomes
A
- roving vesicles that engulf and digest their targets, acting as the “stomach” of the cell.
- clear damaged organelles, invading bacteria / viruses or other organic waste
23
Q
peroximes
A
- group of digestive vesicles. - responsible for the digestion of large fatty acids and are the site of β-oxidation: larger numbers of peroxisomes are present in cells involved in lipid metabolism (e.g. liver cells). The reactive oxygen species hydrogen peroxide is generated during fatty acid breakdown.
- damaging material is kept safe inside the peroxisome and further degraded to water and oxygen before release.
24
Q
Mitochondria
A
- organelles responsible for energy generation, and as such their numbers are higher in cells with a large energy requirement.
25
nucleus
- vast majority of a cells DNA
-nucleus is surrounded by a double membrane called the nuclear envelope,
-dotted with pores that allow ions and small molecules (such as RNA) to pass, but keeps larger molecules outside and the DNA inside. - -Almost all cells have a nucleus, but one notable exception is red bloods cells, which do not have a nucleus
26
prokaryotic cells
-differ from eukaryotes as they have no membrane bound organelles.
- all DNA, proteins, nutrients, ions and non-membrane bound organelles are held within a single cytoplasm inside the prokaryotic cell membrane
27
mitosis
- produces identical duaghter cells
28
process
interphase
prophase
metaphase
anaphase
telophase
cytokinesis
29
Sickle cell anaemia
- affects 1 in 2000 live births in the UK.
- a genetic disorder which causes red blood cells to be more rigid and mis-shaped.
- makes it harder for them to move through smaller blood vessels. This causes painful ischemia (restricted blood flow) and can also result in organ damage. Sickle cell anaemia is caused by a single substitution mutation in the HBB haemoglobin gene
30
meiosis
daughter cells are not identical
diploid --> haploid to form gametes which contain half the DNA of the parent cells and then in sexual reproduction a sperm and an ovum combine to form a new diploid cell, which grows to become a new organism.
31
recessive inherited disorder
- disorder is recessive, means that a healthy version of the gene will make up for the faulty copy
- if you have one good and one faulty copy of the gene you will be a carrier of the faulty gene but you won’t have the disorder yourself.
32
endocrine factors
Released from cells and enter circulation to “act at a distance” e.g. Hormones, cytokines
33
Paracrine factors
Released from cells and have local (nearby) site of action e.g. Neurotransmitters,
34
Autocrine factors:
Released from cells and act on the same cells e.g. hormones
35
membrane potential
A potential difference exists across the cell membrane because ions are distributed unevenly outside and inside cells.
-a high concentration of sodium (Na+) and chloride (Cl-) ions outside the cell (extracellular),
- and a high concentration of potassium (K+) and various anions inside the cell (intracellular), creating an electrochemical gradient across the cellular plasma membrane.
- the membrane acts as a barrier as the ions want to be equally spread across both sides
36
resting membrane potential
Cells vary in their resting membrane potential.
around -70mV.
37
change
- change in membrane potential happens because the cell becomes more permeable to particular ions, and so those ions are able to move across the membrane.
38
Equilibrium potential
-potassium (EK) is approximately80mV, -equilibrium potential for sodium (ENa) is approximately +60mV. Remember the resting membrane potential of a neuron is -70mV, which is quite close to the equilibrium potential of potassium. This is because the membrane is more “leaky” to potassium than it is for sodium, and so the resting membrane potential is quite close to EK. If the membrane suddenly became more permeable to sodium, the membrane potential would rise closer to ENa.
39
facilitated diffusion.
ion channel opens, it allows ions to flow down their concentration gradient. e.g with sodium ion concentrations being high outside the cell, these ions want to move into the cell, but they can’t as they aren’t able to freely pass through the membrane. If a sodium ion channel opens, this provides a path for the sodium ions to cross the membrane.
40
Ligand-gated ion channels
binding site on them where particular specific substances (ligands) can attach to the ion channel and cause it to open. These could be endogenous ligands, such as neurotransmitters, or they could be drugs.
41
Voltage-gated ion channels
sensitive to the membrane potential of the cell. VG sodium channels will be closed at the resting membrane potential, but if the membrane potential rises this will cause the protein which make up the channel to shift, opening the channel.
42
neurons
are critical to your thoughts, feelings, sensations, and movement.
43
Dendrites:
receive input from other neurons
44
Cell body:
nucleus endoplasmic reticulum and mitochondria as well as all the organelles found in cells
45
Axon
carries information in the form of electrical signal known as the action potential. The axon meets the cell body at the axon hillock. Axons can be myelinated or unmyelinated. Myelinated axons have a faster conduction speed.
46
Axon Terminals
output region, release of neurotransmitter
47
action potential
triggered by a rise in membrane potential.
48
overview of action potential
- Cell starts at a resting state (resting membrane potential, RMP). A stimulus large enough to reach the threshold membrane potential (typically -55mV) will initiate an action potential.
- This is because sufficient voltage-gated Na+ channels open to cause a large depolarisation.
- During the rising phase and overshoot, there is depolarisation to a peak of ~ +30mV known as the equilibrium / reversal potential for Na+.
- a repolarisation to~ -90mV: the overshoot at the end of the repolarisation phase is known as hyperpolarisation.
- RMP is restored by sodium-potassium ATPase which pumps 3 Na+ ions out of the cell for every 2K+ ions back across the plasma membrane to restore the cell’s resting membrane potential.
49
conduction of action potenial
- alteration in membrane potential spreads along the membrane to open other sodium channels, propagating a wave of depolarisation along the membrane.
- fast process
- action potential will move in a single direction along the membrane; this is because the refractory period of the membrane prevents the action potential turning back in the direction it has already travelled
- AP will travel from the cell body, along the axon, and down to the axon terminals.
50
AP
Local potential
Threshold state Depolarisation phase (rising phase)
Peak
Repolarisation phase (falling phase)
Hyperpolarisation phase (undershoot)
Resting state.
51
initiating
- If lots of these ligand-gated ion channels are activated together, then the local potential will rise more due to the increased amount of sodium ions entering the cell. If this local potential is strong enough, it will reach the threshold for generating an action potential.
- VGSC open when the membrane reaches -55mV. if the local potential reaches -55mV (threshold), then the voltage-gated channels open and cause further depolarisation of the membrane and initiating an action potential.
52
Depolarisation
Na+ flows into the cell down its chemical gradient and its electrical gradient until it reaches its reversal potential (at +30 mV) when the Na+ channels close
53
repolarisation
Voltage-gated K+ channels open, allowing K+ to flow out of the cell down its chemical gradient and its electrical gradient. This repolarises the membrane, bringing the membrane potential back towards the equilibrium potential Ek (approximately -80mV).
54
hyperpolarisation
end of AP the membrane potential lowers than usual resting phase as some K= ions remian open so ions can pass through the membrane.
- refactory period occurs during this when when the neuron typically cannot fire another action potential, even if it is stimulated.
55
absolute refractory period
immediately after the action potential. In this phase the voltage-gated sodium channels are still deactivated, so even if there is a local potential depolarising the membrane, the voltage-gated sodium channels are not ready to initiate another action potential.
56
relative refractory period;
the voltage-gated sodium channels ready to generate another action potential, but the membrane is still hyperpolarised.
the membrane potential is still lower than the normal resting membrane potential, a bigger stimulus is required to reach the threshold of -55mV.
57
salatory conduction
- neurons have a myelin sheath
- myelin sheath acts as an insulator to prevent the change in membrane potential diminishing along the axon, and it allows the signal to travel faster.
58
nodes of ranvier
VGSC at NOR where no myelin
AP generated at Node thus the impulse “skips” the length of the axon rather than depolarising the entire membrane surface.
59
drugs affect synaptic transmission
-Stop the chemical reactions that create neurotransmitters, inhibit enzymes.
Increase / decrease availability of precursor.
Storage (stored in synaptic vesicles in the axon terminal)
* Block neurotransmitters from entering or leaving vesicles.
* Empty neurotransmitters from the vesicles where they're normally stored and protected from breakdown by enzymes.
Release (released in response to the arrival of an action potential and the influx of Ca2+ into the presynaptic terminal).
* Blockade of Ca2+ channels on the presynaptic terminals.
Activation of receptors (activate autoreceptors on the presynaptic terminal and/or diffuse across the synapse to activate postsynaptic receptors).
* Bind to receptors in place of neurotransmitters, e.g. agonists / antagonists.
* Interaction with presynaptic receptors that control neurotransmitter release
Inactivation/Reuptake (neurotransmitters are broken down enzymes and/or taken back up into the presynaptic terminal by specific transporters).
* Inhibit enzymes that breakdown neurotransmitters.
* Prevent neurotransmitters from returning to the presynaptic neuron (i.e. block the reuptake system).
60
- An action potential reaches the presynaptic terminal, opening voltage-gated calcium channels and allowing calcium ions (Ca2+) to enter the cell.
2) NM in the presynaptic terminal are stored in vesicles; these are like bubbles of phospholipid bilayer within the cell. The increase in Ca2+ inside the cell cause the vesicles to merge with the presynaptic membrane, releasing the neurotransmitter into the synaptic cleft.
3) NM crosses the synaptic cleft to bind with receptors on the postsynaptic membrane.
4) The receptors initiate a response in the postsynaptic cell. The response will depend on the type of receptor present; in the example shown here the receptor is a ligand-gated ion channel
61
ionotrophic receptors
very rapid responses
msecs> secs
used in NTransmission processes
agonist efficacy relates to mean channel open time
62
metaphobric receptors
slower responses
secs>MINS>hrs
used in slower NTransmission processes
agnoist efficaicy relates to ability to activate g protein
63
kinase - linked receptors
slower responses
mins > hours
Endogenous agonists include hormones and growth factors
involved in regualtion pf growth, differentiation and response to metabolic signals
64
intracellular receptors
very slow responses
hours > days
response long lasting and remain long lasting after agonist binding
65
Increases the synthesis of a neurotransmitter?
RAPS
flashcards
Decks in class (8)
# Cards
